Diabetes is increasing in younger population, finds study: Doctors share early signs that might help in early medical intervention  Times of India

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Diabetes is increasing in younger population, finds study: Doctors share early signs that might help in early medical intervention - Times of India

Recommendation and review posted by Bethany Smith

What are vitamins?

Vitamins are essential nutrients our bodies need for a wide array of health functions. If you eat plenty of fruits and vegetables, youre on the right path to getting the vitamins you need for optimal healththats because plant-based foods tend to be great natural sources of vitamins. For example, spinach is a great way to get in vitamin A, and many whole grains are good sources of B vitamins such as folate. And lets not forget oranges and other citrus fruits, which are a rich in vitamin C. Food isnt the only way to get vitamins, however; most famously, vitamin D is nicknamed the sunshine vitamin because you get it from sun exposure.

But even if you spend a lot of time outdoors and follow the most health-conscious of diets, you likely will need to take vitamins as supplements to achieve optimum wellness. Vitamin brands offer these nutrients as capsules, tablets, fat-soluble softgels, powders, and gummies.

People often mistakenly call minerals vitamins, because both are essential to our health. Popular minerals to take in supplement form include bone strength must-have calcium, as well as iron, zinc, magnesium and selenium. Foods are a good natural source of these minerals, but just as its difficult to get enough vitamins from our diet. We also often need to take a dietary supplement to get adequate levels of minerals.

The term supplements refers to vitamins and mineral supplements, as well as amino acids such as L-carnitine, antioxidants such as coenzyme CoQ10, and also herbals like echinacea. You may also find supplement formulas called multivitamins which contain both vitamins and other nutrients necessary for wellness.

Taking vitamins and supplements is a good insurance policy to fill in any dietary gaps. Even if your diet chock full of superfoods that are brimming with nutrition, its likely that youre missing out on some important nutrients. For example, unless you eat fatty fish regularly, you will need to supplement with omega-3 to get the heart and brain health benefits of fish oil. Beyond that, you can also supplement as part of your pursuit of a specific health goalwhether its vitamin C for immune support, collagen for healthy skin and joints, lutein and astaxanthin for eye health, sports supplements, or a specific health formula to support your healthy weight journey.

To avoid a deficiency, you should take a high-quality multivitamin that includes at a minimum vitamin B-complex (consisting of vitamin B12, folic acid, biotin and other B vitamins), vitamin C, vitamin D3, and vitamin E, as well as calcium, magnesium, and other minerals. Curcumin is a great option for heart health, brain function, comfortable joints and more; prebiotics and probiotics support optimal digestive health (and who doesnt want that?). If you follow a plant-based diet, you can obtain most of these vitamins and supplements from vegetarian capsules, including vegan vitamin D3.

Be a picky consumer when shopping for vitamins online! While youll find many natural food stores and online vitamin stores that offer a dizzying array of health products, ensure youre choosing a brand that takes a science-based approach to the formulation of vitamins and supplements. Only order health products that have been tested for efficacy and can provide a Certificate of Analysis verifying quality and safety. Ensure the supplements are being shipped from a climate-controlled facility as well, since spoiling can happen in extreme heat. A final word to the wise: always check the expiration date on your supplements before consuming!

Established in 1980, Life Extension is one of the longest-standing vitamin brands and formulates every product based on scientific research, using the dosages from clinical studies. Choose from an extensive assortment of non-GMO and gluten-free vitamins and supplements, offered at affordable prices. Plus, our Premier Rewards program gives you the chance to earn rewards on every purchase. Theres no risk to order; Life Extension offers a complete one-year satisfaction guarantee return policy. Order today!

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Recommendation and review posted by Bethany Smith

This article is for my (J.P.s) sister.

Shes always been the one in my family most vocal about her concerns with the pros and cons of immortality.

Particularly the cons.

And I think the potential problems of increased life expectancy that she identifies are concerns a lot of people share.

Because once you get past the question of if radical human life extension is even possible, the inevitable next question is, Should we do it?

In fact, there are a lot of ethical arguments against life extension (as my sister is wont to remind me).

Im sure youve heard, or even thought of, many of them yourself.

What if only the rich can afford it?

What about overpopulation and the environment?

Wont you just get bored?

Who would want to live to 150 if youre just old and decrepit and in a nursing home all that time?

In this post, were going to try and address all these longevity objections, and more (Immortal dictators! Religious concerns! Social Security!), but first we should talk about that last question (being old and decrepit for decades) briefly.

Many people, when they think about life extension, assume the process will simply extend the tail-end of our lives, adding more years on to that period when we are beset with frailty and age-related mental and physical decline.

Stuck in a wheelchair, youll have to play bingo for an extra fifty years while youre forced to stay alive through uncomfortable tubes up your nose or something.

And believe me, no one, myself included, wants that.

But what spanners and other people interested in human longevity want is not just extended lifespans, but extended healthspans.

As we said in our very first article on human life extension here:

Human life extension addresses both chronological and biological aging; it asks not just how can we live longer, but how long can we live well. Healthspan, or the years of our lives when were unencumbered by disease or disability, addresses just that. What if you could have the body you had at 25 well into your 80s or 100s or 120s? What more could you do with those extra rich years of life? Who could you become?

The technical term for this is compressing morbidity: shortening the decrepit, morbid years and extending the healthy ones. And, as we also discussed in our first article, theres plenty of scientific evidence to suggest that anti-aging interventions can do just this in both animals and in humans.

So what well be talking about throughout the rest of this article on the ethics of life extension is not extending the unhealthy years of our lives, but extending our healthy, active, vibrant years and why (quite a few, actually) people think that could still be a bad thing.

Because this is a (really) long post, feel free to jump to the section youre most interested in, rather than read through everything.

Does death make life meaningless?

Tolstoy and Nietzsche would argue that thats absolutely the caseand theyve gotten plenty of attention for it, especially in Western culture, because it runs contrary to an unspoken assumption that death itself is what gives life meaning. Christians look forward to heaven. Jews see death as a terrible but necessary part of Gods plan. Buddhists believe death leads only to rebirth. In so many philosophical traditions, death is essential for life itself to have meaning.

Some even go as far to claim that death is required for life to have meaning. Theythe likes of the late Holocaust survivor Viktor Frankl and philosopher Sir Bernard Williamspresent three major arguments against life extension:

Lets break them all down.

Religious fatalism is the belief that an individuals health is predetermined by a higher power; the individual can not and should not intervene. Religious fatalism isnt something relegated only to cults or extremists. Its significantly correlated with race, people with lower incomes, and people with lower levels of education. Religious fatalism is distinct from fatalism, in that it refers specifically to healthcare decisions. Many who believe in destiny or fate will also argue that they are predetermined to suffer from an illness or disease, and recovery will not hinge on medical interventionits up to the universe.

And, if fate does have a role in medical outcomes, intervening would be foolish. Why waste the money and resources on doing so if youre just going to die anyway? Using this logic, aging should be embraced as a natural part of life.

Following that line of thinking, the medical field should cease to exist. Forget cancer researchclose the childrens hospitals and ER rooms and eliminate the FDA. Life-sustaining drugs like insulin, Albuterol, and Levothyroxine should be banned along with seatbelts and helmets.

Of course, many who believe in religious fatalism dont necessarily want to be so prescriptive to the rest of society. They might see it as an important personal choice, but not something to put on others. Orand I find this common among my circlesits the elimination of age-related death altogether thats off-putting. Theyre completely comfortable with, say, finding a cure for Alzheimers, cancer, and diabetes, but when age itself is indicated as a major precursor to all these diseases, they shrug it off. Ageing is an essential part of life. Its not to be tampered with.

Part of the reason is because being old without being healthy is horrific. Think wheelchairs, struggling to open Jell-O cups, and slowly losing your senseseach one a tragic loss for a 15-year-old but an inevitability for someone over 90. But this goes to show that we just dont consider the elderly as human as those younger than them. Frailty is a tragedy for anyone, not just for those deemed young enough for it to be uncommon.

Thus, the indefinite extension of healthspan, or the years of our lives when were unencumbered by disease or disability, is really the ultimate goal of life extension. And many find that option far more palatable; if one practices yoga or avoids processed carbohydrates in an effort for a longer healthspan, the prospect of a lengthened lifespan becomes far more palatable.

And in the end, the ethics of life extension require that no one is forcing anyone else to live longer than they would like. Just like anyone can deny medical interventions, so too can they choose not to live longer than they believe they were destined to. That is, in my view, nothing but a personal choice.

If we were immortal, we could legitimately postpone every action forever. [] But in the face of death as absolute finis to our future and boundary to our possibilities, we are under the imperative of utilizing our lifetimes to the utmost, not letting the singular opportunities whose finite sum constitutes the whole of life pass by unused.

Frankl, in the quote above, argues that with all the time of eternity, nothing could get done. One could, theoretically, indefinitely put off confessing a love, writing a novel, or starting a company. Of course, discomfort should also be a part of the conversion; while one could choose to never eat because the process takes action, hunger is a tremendous motivator, even if one is nowhere near close to dying from starvation.

Some contemporary psychological studies support Frankl. For example, a 2007 article published in Personality and Social Psychology Bulletin found that those who encounter death over a long period are more likely to be intrinsically motivated (and actually write that novel theyve always wanted to). That said, the threat of death isnt necessarily a requirement for intrinsic motivation in general. Realistically, there is a range of reasons why people do thingsfor praise, for accomplishment, or to just do it,and very few of them have to do with the inevitability of death.

In fact, philosophers like Heidegger have argued that most people live their lives in denial of their death. One study on mortality salience (awareness of ones own death) found that research participants actively tried not to engage with their own mortalitya reaction that may be a biological response. It would be tough to argue death is the sole reason for any significant actions people take throughout their lives if theyre actively avoiding considering it.

Lets say that immortality has no effect on your motivationin fact, you have the curiosity of a 25-year-old and the body to match. Youve ticked off your bucket list. You live where you want, work where you want (if you want), and you do what you want. Life is splendid. And boring.

Desperately boring.

This could be one of the major cons of immortality, but Brooke Alan Trisel points out that not all of life is meaningful. He writes, most of our lives are neither meaningless nor meaningful, but lie somewhere between these two extremes.

I would amend his argument further to say that most moments of our individual lives are neither meaningless or meaningful, but lie somewhere in between. For example, celebrating your wedding day might be tremendously meaningful, but the hours spent visiting florists might not be.

Its true that old people experience boredom, and that that boredom can be detrimental to their health. The boredom that they experience, however, often has to do with perils of aging: loneliness, immobility, and declining faculties.

I doubt anyone would advocate that we euthanize everyone over 80 because they might suffer from boredom. Finding interest in new activities, engaging with curiosity, and experiencing excitement, joy, and contentment are all pillars of mental health. Boredom, itself, is a health issue, and not necessarily a reason to prevent life extension.

Weve all seen those dystopian sci-fi stories.

While the rich lead lives of unimaginable luxury in their space stations, enjoying near-immortality and all the sexbots they can afford, the poor toil in the spice mines below, dying early from Spice Lung or malfunctioning cheap cybernetic implants.

No one wants to live in that worldand not just because it would entail having to endure more of Matt Damons terrible acting.

And with rising concerns about wealth inequality, its entirely understandable that many people ask the question:

What if only the rich can afford life-extension treatments?

Because while global wealth inequality has actually been declining for the first time in two centuriesdue largely to the rapid economic growth afforded by technological innovation and the opening of markets, particularly in Asiasome measures of wealth inequality within countries have shown worrying rises.

So is it ethical to pursue life extension if its not accessible to everyone?

A 2016 study found that, The gap in life expectancy between the richest 1% and poorest 1% of individuals was 14.6 years for men and 10.1 years for women.

However, it may not be as bad as it seems.

A more recent study that took into account income mobility (instead of assuming people kept the same income their entire lives) found a gap of only 2.4 years for men with different income levels, and just 2.2 years for women.

They did also caution that though the gap is not as large as originally thought, it has been widening slightly over the last 30 years, possibly due to differences in education levels.

In short: yes, there is already a (small) gap in the longevity of the rich versus the poor.

Will expensive life-extension treatments widen that gap so much that the poor will be doomed to die early?

The answer to that question has several components:

To answer that first component we can look at some real-world examples, both of existing anti-aging treatments already on the market, and of past medical innovations.

For instance, the diabetes drug metformin is a classic candidate for a possible anti-aging pill. According to a recent metformin meta-analysis, Diabetics taking metformin had significantly lower all-cause mortality than non-diabetics, and a host of other studies have shown other beneficial effects of the drug, like cancer protection and slower brain aging.

And the cost of this possible wonder drug?

According to GoodRx, retail costs for 60 tablets of 500mg of metformin (a 1-2 month supply) range from $9 to $16, even without insurance.

Thats about 15-25 cents a pill.

Other potential life-extension molecules are similarly cheap.

Resveratrol, another possible longevity compound, can be bought on Amazon for $16.99-$27.99 for a 30-90 supply .

Glucosamine costs as little as ten cents a pill, has been the subject of several recent studies showing it decreases all-cause mortality by as much as 39%, and may be as effective for longevity as exercise.

Aspirin (shown to extend life in male mice) costs $1 for 100 pills at my local Rite Aid.

And the list goes on.

All the ones listed above have been known about and studied for decadesin some cases over a centuryis there evidence that newly discovered and developed drugs would be similarly inexpensive?

Its likely. Take vaccines.

Vaccines are a good parallel to anti-aging medicines because they are developed to treat a deadly, widespread disease that impacts large swaths of the human population and they thus have a huge demand and a requirement to distribute to the most people possible. Both also represent huge net benefits to society compared to the costs of not treating the diseases they target (some research indicates slowing aging could save the U.S. $7.1 trillion over 50 years).

Developing a vaccine can cost as much as $2.8-$3.7 billion and yet many vaccines, including those for the most widespread diseases, are offered free-of-cost or at very low prices. For example, the flu vaccine is often free and almost always fully-covered by insurance.

Other vaccines can be had, even without insurance, for as low as $6.

Most of these vaccines have been developed only in the last few decades, and yet their cost is low enough that almost everyone can afford them. The combination of widespread demand and subsidies means that usually the obstacle to getting a vaccine is a lack of education or of desire, not of financial means.

And theres good reason to think new anti-aging treatments may be treated like vaccines. If the FDA labels aging a treatable disease (which may well happen), and since fully 100% of the population is afflicted by this disease, demand for effective longevity treatments will be so high that medical and pharmaceutical companies can afford to set prices low, since they will be selling their products to so many people.

But of course, there may be many different types of therapies and interventions that are developed to reverse and slow aging, and not all of them will be as simple or cheap as a pill or a shot.

What if more complex interventions are needed to reverse aging?

Things like gene therapy can cost millions of dollars. In fact, theres already an (unproven) gene therapy for aging on the market, similar to the procedure longevity influencer Liz Parrish of Bioviva performed on herself in 2015, and its price tag is $1 million.

Not exactly pocket change.

So lets look at how likely expensive longevity treatments are to stay expensive, such that only the wealthy can afford them.

In the last 17 years, the cost to have your whole genome sequenced has gone from roughly $1 billion in 2003, to as low as $299 today.

And most technological innovation follows this same pattern.

First an experimental, expensive innovation is developed. Wealthy early-adopters buy it (think investment bankers and car phones back in the 80s), and their purchases fund the research and development needed to improve the innovation, better distribute it, and make it less expensive. Soon, every person who wants one can afford it, and at a much higher level of quality than the original that was available only to the rich.

High initial prices of a new product are thus almost an extended form of R&D funding (and clinical testing with data provided by early adopters). The rich are essentially paying the money necessary to further develop the product and get it to the masses. What the rich pay for with money, the poor pay for with time.

Its the reason the smartphone in your pocket only costs a couple hundred dollars, and you dont need to lug a car around to use it.

Its also the reason your Apple Watch isnt the size of a room, and yet can do way more health monitoring than the early electrocardiogram machines could (and at a significantly lower price).

In fact, Elon Musks business model for Tesla was explicitly written around this principle. He designed and built an impractical, expensive electric sports car (the Roadster) and sold it at exorbitant prices to the rich, in order to fund the research and development of his more affordable mass market car, the Model 3.

And the medical market is little different from the car market (or other technology markets) in this respect. Despite lots of hand-wringing about rising medical costs, especially in the United States, most of the increase in cost is due to increased consumption, not an increase in the cost of individual medical procedures, devices, or medicines themselves (obviously there are exceptions that get lots of media coverage, but in general this is the case). As we get wealthier, it turns out, we want to buy more medical care.

Intuitively, anti-aging medicine should even help lower the total cost of medical care for people, as individuals will have to spend less on treating the very expensive chronic diseases of old-age like Alzheimers or cancer. These health-cost savings from longevity medicine are often referred to as the Longevity Dividend.

Contrary to popular belief, the real money in almost any market is not in selling boutique treatments to a few billionaires, but selling commercialized interventions to the millions (and, globally, billions) in the middle and lower classes.

Globally, the middle class accounted for $35 trillion in consumer spending, and the lower class another $8 trillion, for a combined spending power of $43 trillion. The rich (those spending over $110 a day) accounted for only $11 trillion in total consumer spending.

Globally, the middle class accounted for $35 trillion in consumer spending, and the lower class another $8 trillion, for a combined spending power of $43 trillion. The rich (those spending over $110 a day) accounted for only $11 trillion in total consumer spending.

All else equal, which market would you rather develop an anti-aging product for?

But of course, despite all this there is still a slim chance that life-extension therapies could buck every historical, technological, and market trend ever observed and somehow remain insanely expensive forever.

So if anti-aging medicines and treatments turn out to be one of those rare types of goods that will only ever be available to the super wealthy, is it moral to ban them or prevent their development?

This philosophical question can be addressed from any number of different frameworks. Its an age-old ethical question: should some people (like the rich) be afforded more opportunities than others (like the poor)?

Bioethicist John Harris offers a utilitarian perspective: If immortality or increased life expectancy is a good, it is doubtful ethics to deny palpable goods to some people because we cannot provide them for all.

Harris further analogizes, We cannot and should not seek to prevent the development of [longevity treatments], any more than we should deny kidney transplants because there are not enough kidneys to go aroundin other words, we should develop life-extension even if we cannot provide it to everyone.

Philosophy professor John Davis, in The American Journal of Bioethics, argues that,

We accept the general principle that taking from the Haves is justified only if doing so makes the Have-nots more than marginally better off. If life-extension is possible, then one must weigh the life-years at stake for those who receive the treatment against whatever burdens making such treatments available might impose on the Have-nots, who cannot afford the treatment.

The greatest burdenis that ones death is worse the earlier one dies relative to how long it is possible to live. For example, a death at 17 is much worse than a death at 97. Because life extension changes how long it is possible to live, life-extension will make death at 97 tragic in a way it has never been beforeHoweverwhen this burden is compared to the number of additional life-years the Haves will lose if life-extension is prevented from becoming available, the burden to the Have-nots is marginal compared to what is at stake for the Haves. Therefore, Inhibiting the development of life-extension is unjustified, even though it will probably not be available to everyone for a long time.

In other words, if life-extension research alleviates aggregate suffering even a little, even if only for the wealthy, anti-aging treatments are a moral good.

The rest is here:
6 Pros and Cons of Immortality: The Ethics of Life Extension

Recommendation and review posted by Bethany Smith

Condition where males and females exhibit different characteristics

Sexual dimorphism is the condition where the sexes of the same animal and/or plant species exhibit different morphological characteristics, particularly characteristics not directly involved in reproduction.[1] The condition occurs in most animals and some plants. Differences may include secondary sex characteristics, size, weight, colour, markings, or behavioural or cognitive traits. These differences may be subtle or exaggerated and may be subjected to sexual selection and natural selection. The opposite of dimorphism is monomorphism, which is when both biological sexes are phenotypically indistinguishable from each other.[2]

Common and easily identified types of dimorphism consist of ornamentation and coloration, though not always apparent. A difference in coloration of sexes within a given species is called sexual dichromatism, which is commonly seen in many species of birds and reptiles.[3] Sexual selection leads to the exaggerated dimorphic traits that are used predominantly in competition over mates. The increased fitness resulting from ornamentation offsets its cost to produce or maintain suggesting complex evolutionary implications, but the costs and evolutionary implications vary from species to species.[4][5][pageneeded] The costs and implications differ depending on the nature of the ornamentation (such as the colour mechanism involved).[citation needed]

The peafowl constitute conspicuous illustrations of the principle. The ornate plumage of peacocks, as used in the courting display, attracts peahens. At first sight one might mistake peacocks and peahens for completely different species because of the vibrant colours and the sheer size of the male's plumage; the peahen being of a subdued brown coloration.[6] The plumage of the peacock increases its vulnerability to predators because it is a hindrance in flight, and it renders the bird conspicuous in general.[6] Similar examples are manifold, such as in birds of paradise and argus pheasants.[citation needed]

Another example of sexual dichromatism is that of the nestling blue tits. Males are chromatically more yellow than females. It is believed that this is obtained by the ingestion of green Lepidopteran larvae, which contain large amounts of the carotenoids lutein and zeaxanthin.[7] This diet also affects the sexually dimorphic colours in the human-invisible ultraviolet spectrum.[8][9] Hence, the male birds, although appearing yellow to humans actually have a violet-tinted plumage that is seen by females. This plumage is thought to be an indicator of male parental abilities.[10] Perhaps this is a good indicator for females because it shows that they are good at obtaining a food supply from which the carotenoid is obtained. There is a positive correlation between the chromas of the tail and breast feathers and body condition.[11] Carotenoids play an important role in immune function for many animals, so carotenoid dependent signals might indicate health.[12]

Frogs constitute another conspicuous illustration of the principle. There are two types of dichromatism for frog species: ontogenetic and dynamic. Ontogenetic frogs are more common and have permanent color changes in males or females. Ranoidea lesueuri is an example of a dynamic frog that has temporary color changes in males during breeding season.[13] Hyperolius ocellatus is an ontogenetic frog with dramatic differences in both color and pattern between the sexes. At sexual maturity, the males display a bright green with white dorsolateral lines.[14] In contrast, the females are rusty red to silver with small spots. The bright coloration in the male population serves to attract females and as an aposematic sign to potential predators.

Females often show a preference for exaggerated male secondary sexual characteristics in mate selection.[15] The sexy son hypothesis explains that females prefer more elaborate males and select against males that are dull in color, independent of the species' vision.[16]

Similar sexual dimorphism and mating choice are also observed in many fish species. For example, male guppies have colorful spots and ornamentations while females are generally grey in color. Female guppies prefer brightly colored males to duller males.[17][pageneeded]

In redlip blennies, only the male fish develops an organ at the anal-urogenital region that produces antimicrobial substances. During parental care, males rub their anal-urogenital regions over their nests' internal surfaces, thereby protecting their eggs from microbial infections, one of the most common causes for mortality in young fish.[18]

Most flowering plants are hermaphroditic but approximately 6% of species have separate males and females (dioecy).[19] Sexual dimorphism is common in dioecious plants[20]:403 and dioicous species.[21]:71

Males and females in insect-pollinated species generally look similar to one another because plants provide rewards (e.g. nectar) that encourage pollinators to visit another similar flower, completing pollination. Catasetum orchids are one interesting exception to this rule. Male Catasetum orchids violently attach pollinia to euglossine bee pollinators. The bees will then avoid other male flowers but may visit the female, which look different from the males.[22]

Various other dioecious exceptions, such as Loxostylis alata have visibly different sexes, with the effect of eliciting the most efficient behaviour from pollinators, who then use the most efficient strategy in visiting each gender of flower instead of searching say, for pollen in a nectar-bearing female flower.[citation needed]

Some plants, such as some species of Geranium have what amounts to serial sexual dimorphism. The flowers of such species might for example present their anthers on opening, then shed the exhausted anthers after a day or two and perhaps change their colours as well while the pistil matures; specialist pollinators are very much inclined to concentrate on the exact appearance of the flowers they serve, which saves their time and effort and serves the interests of the plant accordingly. Some such plants go even further and change their appearance again once they have been fertilised, thereby discouraging further visits from pollinators. This is advantageous to both parties because it avoids damage to the developing fruit and avoids wasting the pollinator's effort on unrewarding visits. In effect the strategy ensures that the pollinators can expect a reward every time they visit an appropriately advertising flower.[citation needed]

Females of the aquatic plant Vallisneria americana have floating flowers attached by a long flower stalk that are fertilized if they contact one of the thousands of free floating flowers released by a male.[23][bettersourceneeded] Sexual dimorphism is most often associated with wind-pollination in plants due to selection for efficient pollen dispersal in males vs pollen capture in females, e.g. Leucadendron rubrum.[24]

Sexual dimorphism in plants can also be dependent on reproductive development. This can be seen in Cannabis sativa, a type of hemp, which have higher photosynthesis rates in males while growing but higher rates in females once the plants become sexually mature.[25]

Every sexually reproducing extant species of vascular plant actually has an alternation of generations; the plants we see about us generally are diploid sporophytes, but their offspring really are not the seeds that people commonly recognise as the new generation. The seed actually is the offspring of the haploid generation of microgametophytes (pollen) and megagametophytes (the embryo sacs in the ovules). Each pollen grain accordingly may be seen as a male plant in its own right; it produces a sperm cell and is dramatically different from the female plant, the megagametophyte that produces the female gamete.[citation needed]

Insects display a wide variety of sexual dimorphism between taxa including size, ornamentation and coloration.[26] The female-biased sexual size dimorphism observed in many taxa evolved despite intense malemale competition for mates.[27] In Osmia rufa, for example, the female is larger/broader than males, with males being 810mm in size and females being 1012mm in size.[28] In the hackberry emperor females are similarly larger than males.[29] The reason for the sexual dimorphism is due to provision size mass, in which females consume more pollen than males.[30]

In some species, there is evidence of male dimorphism, but it appears to be for the purpose of distinctions of roles. This is seen in the bee species Macrotera portalis in which there is a small-headed morph, capable of flight, and large-headed morph, incapable of flight, for males.[31] Anthidium manicatum also displays male-biased sexual dimorphism. The selection for larger size in males rather than females in this species may have resulted due to their aggressive territorial behavior and subsequent differential mating success.[32] Another example is Lasioglossum hemichalceum, which is a species of sweat bee that shows drastic physical dimorphisms between male offspring.[33] Not all dimorphism has to have a drastic difference between the sexes. Andrena agilissima is a mining bee where the females only have a slightly larger head than the males.[34]

Weaponry leads to increased fitness by increasing success in malemale competition in many insect species.[35] The beetle horns in Onthophagus taurus are enlarged growths of the head or thorax expressed only in the males. Copris ochus also has distinct sexual and male dimorphism in head horns.[36] These structures are impressive because of the exaggerated sizes.[37] There is a direct correlation between male horn lengths and body size and higher access to mates and fitness.[37] In other beetle species, both males and females may have ornamentation such as horns.[36]Generally, insect sexual size dimorphism (SSD) within species increases with body size.[38]

Sexual dimorphism within insects is also displayed by dichromatism. In butterfly genera Bicyclus and Junonia, dimorphic wing patterns evolved due to sex-limited expression, which mediates the intralocus sexual conflict and leads to increased fitness in males.[39] The sexual dichromatic nature of Bicyclus anynana is reflected by female selection on the basis of dorsal UV-reflective eyespot pupils.[40] The common brimstone also displays sexual dichromatism; males have yellow and iridescent wings, while female wings are white and non-iridescent.[41] Naturally selected deviation in protective female coloration is displayed in mimetic butterflies.[42]

Many arachnid groups exhibit sexual dimorphism,[43] but it is most widely studied in the spiders. In the orb-weaving spider Zygiella x-notata, for example, adult females have a larger body size than adult males.[44] Size dimorphism shows a correlation with sexual cannibalism,[45] which is prominent in spiders (it is also found in insects such as praying mantises). In the size dimorphic wolf spider Tigrosa helluo, food-limited females cannibalize more frequently.[46] Therefore, there is a high risk of low fitness for males due to pre-copulatory cannibalism, which led to male selection of larger females for two reasons: higher fecundity and lower rates of cannibalism.[46] In addition, female fecundity is positively correlated with female body size and large female body size is selected for, which is seen in the family Araneidae. All Argiope species, including Argiope bruennichi, use this method. Some males evolved ornamentation[vague] including binding the female with silk, having proportionally longer legs, modifying the female's web, mating while the female is feeding, or providing a nuptial gift in response to sexual cannibalism.[46] Male body size is not under selection due to cannibalism in all spider species such as Nephila pilipes, but is more prominently selected for in less dimorphic species of spiders, which often selects for larger male size.[47] In the species Maratus volans, the males are known for their characteristic colorful fan which attracts the females during mating.[48]

Ray finned fish are an ancient and diverse class, with the widest degree of sexual dimorphism of any animal class. Fairbairn notes that "females are generally larger than males but males are often larger in species with malemale combat or male paternal care ... [sizes range] from dwarf males to males more than 12 times heavier than females."[49][pageneeded]

There are cases where males are substantially larger than females. An example is Lamprologus callipterus, a type of cichlid fish. In this fish, the males are characterized as being up to 60 times larger than the females. The male's increased size is believed to be advantageous because males collect and defend empty snail shells in each of which a female breeds.[50] Males must be larger and more powerful in order to collect the largest shells. The female's body size must remain small because in order for her to breed, she must lay her eggs inside the empty shells. If she grows too large, she will not fit in the shells and will be unable to breed. The female's small body size is also likely beneficial to her chances of finding an unoccupied shell. Larger shells, although preferred by females, are often limited in availability.[51] Hence, the female is limited to the growth of the size of the shell and may actually change her growth rate according to shell size availability.[52] In other words, the male's ability to collect large shells depends on his size. The larger the male, the larger the shells he is able to collect. This then allows for females to be larger in his brooding nest which makes the difference between the sizes of the sexes less substantial. Malemale competition in this fish species also selects for large size in males. There is aggressive competition by males over territory and access to larger shells. Large males win fights and steal shells from competitors. Another example is the dragonet, in which males are considerably larger than females and possess longer fins.

Sexual dimorphism also occurs in hermaphroditic fish. These species are known as sequential hermaphrodites. In fish, reproductive histories often include the sex-change from female to male where there is a strong connection between growth, the sex of an individual, and the mating system it operates within.[53] In protogynous mating systems where males dominate mating with many females, size plays a significant role in male reproductive success.[54] Males have a propensity to be larger than females of a comparable age but it is unclear whether the size increase is due to a growth spurt at the time of the sexual transition or due to the history of faster growth in sex changing individuals.[55] Larger males are able to stifle the growth of females and control environmental resources.[citation needed]

Social organization plays a large role in the changing of sex by the fish. It is often seen that a fish will change its sex when there is a lack of dominant male within the social hierarchy. The females that change sex are often those who attain and preserve an initial size advantage early in life. In either case, females which change sex to males are larger and often prove to be a good example of dimorphism.

In other cases with fish, males will go through noticeable changes in body size, and females will go through morphological changes that can only be seen inside of the body. For example, in sockeye salmon, males develop larger body size at maturity, including an increase in body depth, hump height, and snout length. Females experience minor changes in snout length, but the most noticeable difference is the huge increase in gonad size, which accounts for about 25% of body mass.[56]

Sexual selection was observed for female ornamentation in Gobiusculus flavescens, known as two-spotted gobies.[57] Traditional hypotheses suggest that malemale competition drives selection. However, selection for ornamentation within this species suggests that showy female traits can be selected through either femalefemale competition or male mate choice.[57] Since carotenoid-based ornamentation suggests mate quality, female two-spotted guppies that develop colorful orange bellies during the breeding season are considered favorable to males.[58] The males invest heavily in offspring during the incubation, which leads to the sexual preference in colorful females due to higher egg quality.[58]

In amphibians and reptiles, the degree of sexual dimorphism varies widely among taxonomic groups. The sexual dimorphism in amphibians and reptiles may be reflected in any of the following: anatomy; relative length of tail; relative size of head; overall size as in many species of vipers and lizards; coloration as in many amphibians, snakes, and lizards, as well as in some turtles; an ornament as in many newts and lizards; the presence of specific sex-related behaviour is common to many lizards; and vocal qualities which are frequently observed in frogs.[citation needed]

Anole lizards show prominent size dimorphism with males typically being significantly larger than females. For instance, the average male Anolis sagrei was 53.4mm vs. 40mm in females.[59] Different sizes of the heads in anoles have been explained by differences in the estrogen pathway.[60] The sexual dimorphism in lizards is generally attributed to the effects of sexual selection, but other mechanisms including ecological divergence and fecundity selection provide alternative explanations.[61] The development of color dimorphism in lizards is induced by hormonal changes at the onset of sexual maturity, as seen in Psamodromus algirus, Sceloporus gadoviae, and S. undulates erythrocheilus.[61] Sexual dimorphism in size is also seen in frog species like P. bibronii.

Male painted dragon lizards, Ctenophorus pictus. are brightly conspicuous in their breeding coloration, but male colour declines with aging. Male coloration appears to reflect innate anti-oxidation capacity that protects against oxidative DNA damage.[62] Male breeding coloration is likely an indicator to females of the underlying level of oxidative DNA damage (a significant component of aging) in potential mates.[62]

Sexual dimorphism in birds can be manifested in size or plumage differences between the sexes. Sexual size dimorphism varies among taxa with males typically being larger, though this is not always the case, e.g. birds of prey, hummingbirds, and some species of flightless birds.[63][64] Plumage dimorphism, in the form of ornamentation or coloration, also varies, though males are typically the more ornamented or brightly colored sex.[65] Such differences have been attributed to the unequal reproductive contributions of the sexes.[66] This difference produces a stronger female choice since they have more risk in producing offspring. In some species, the male's contribution to reproduction ends at copulation, while in other species the male becomes the main caregiver. Plumage polymorphisms have evolved to reflect these differences and other measures of reproductive fitness, such as body condition[67] or survival.[68] The male phenotype sends signals to females who then choose the 'fittest' available male.

Sexual dimorphism is a product of both genetics and environmental factors. An example of sexual polymorphism determined by environmental conditions exists in the red-backed fairywren. Red-backed fairywren males can be classified into three categories during breeding season: black breeders, brown breeders, and brown auxiliaries.[67] These differences arise in response to the bird's body condition: if they are healthy they will produce more androgens thus becoming black breeders, while less healthy birds produce less androgens and become brown auxiliaries.[67] The reproductive success of the male is thus determined by his success during each year's non-breeding season, causing reproductive success to vary with each year's environmental conditions.

Migratory patterns and behaviors also influence sexual dimorphisms. This aspect also stems back to the size dimorphism in species. It has been shown that the larger males are better at coping with the difficulties of migration and thus are more successful in reproducing when reaching the breeding destination.[69] When viewing this in an evolutionary standpoint many theories and explanations come to consideration. If these are the result for every migration and breeding season the expected results should be a shift towards a larger male population through sexual selection. Sexual selection is strong when the factor of environmental selection is also introduced. The environmental selection may support a smaller chick size if those chicks were born in an area that allowed them to grow to a larger size, even though under normal conditions they would not be able to reach this optimal size for migration. When the environment gives advantages and disadvantages of this sort, the strength of selection is weakened and the environmental forces are given greater morphological weight. The sexual dimorphism could also produce a change in timing of migration leading to differences in mating success within the bird population.[70] When the dimorphism produces that large of a variation between the sexes and between the members of the sexes multiple evolutionary effects can take place. This timing could even lead to a speciation phenomenon if the variation becomes strongly drastic and favorable towards two different outcomes. Sexual dimorphism is maintained by the counteracting pressures of natural selection and sexual selection. For example, sexual dimorphism in coloration increases the vulnerability of bird species to predation by European sparrowhawks in Denmark.[71] Presumably, increased sexual dimorphism means males are brighter and more conspicuous, leading to increased predation.[71] Moreover, the production of more exaggerated ornaments in males may come at the cost of suppressed immune function.[67] So long as the reproductive benefits of the trait due to sexual selection are greater than the costs imposed by natural selection, then the trait will propagate throughout the population. Reproductive benefits arise in the form of a larger number of offspring, while natural selection imposes costs in the form of reduced survival. This means that even if the trait causes males to die earlier, the trait is still beneficial so long as males with the trait produce more offspring than males lacking the trait. This balance keeps the dimorphism alive in these species and ensures that the next generation of successful males will also display these traits that are attractive to the females.

Such differences in form and reproductive roles often cause differences in behavior. As previously stated, males and females often have different roles in reproduction. The courtship and mating behavior of males and females are regulated largely by hormones throughout a bird's lifetime.[72] Activational hormones occur during puberty and adulthood and serve to 'activate' certain behaviors when appropriate, such as territoriality during breeding season.[72] Organizational hormones occur only during a critical period early in development, either just before or just after hatching in most birds, and determine patterns of behavior for the rest of the bird's life.[72] Such behavioral differences can cause disproportionate sensitivities to anthropogenic pressures.[73] Females of the whinchat in Switzerland breed in intensely managed grasslands.[73] Earlier harvesting of the grasses during the breeding season lead to more female deaths.[73] Populations of many birds are often male-skewed and when sexual differences in behavior increase this ratio, populations decline at a more rapid rate.[73] Also not all male dimorphic traits are due to hormones like testosterone, instead they are a naturally occurring part of development, for example plumage.[74] In addition, the strong hormonal influence on phenotypic differences suggest that the genetic mechanism and genetic basis of these sexually dimorphic traits may involve transcription factors or cofactors rather than regulatory sequences.[75]

Sexual dimorphism may also influence differences in parental investment during times of food scarcity. For example, in the blue-footed booby, the female chicks grow faster than the males, resulting in booby parents producing the smaller sex, the males, during times of food shortage. This then results in the maximization of parental lifetime reproductive success.[76] In Black-tailed Godwits Limosa limosa limosa females are also the larger sex, and the growth rates of female chicks are more susceptible to limited environmental conditions.[77]

Sexual dimorphism may also only appear during mating season, some species of birds only show dimorphic traits in seasonal variation. The males of these species will molt into a less bright or less exaggerated color during the off breeding season.[75] This occurs because the species is more focused on survival than reproduction, causing a shift into a less ornate state.[dubious discuss]

Consequently, sexual dimorphism has important ramifications for conservation. However, sexual dimorphism is not only found in birds and is thus important to the conservation of many animals. Such differences in form and behavior can lead to sexual segregation, defined as sex differences in space and resource use.[78] Most sexual segregation research has been done on ungulates,[78] but such research extends to bats,[79] kangaroos,[80] and birds.[81] Sex-specific conservation plans have even been suggested for species with pronounced sexual segregation.[79]

The term sesquimorphism (the Latin numeral prefix sesqui- means one-and-one-half, so halfway between mono- (one) and di- (two)) has been proposed for bird species in which "both sexes have basically the same plumage pattern, though the female is clearly distinguishable by reason of her paler or washed-out colour".[82]:14 Examples include Cape sparrow (Passer melanurus),[82]:67 rufous sparrow (subspecies P.motinensis motinensis),[82]:80 and saxaul sparrow (P.ammodendri).[82]:245

In a large proportion of mammal species, males are larger than females. Both genes and hormones affect the formation of many animal brains before "birth" (or hatching), and also behaviour of adult individuals. Hormones significantly affect human brain formation, and also brain development at puberty. A 2004 review in Nature Reviews Neuroscience observed that "because it is easier to manipulate hormone levels than the expression of sex chromosome genes, the effects of hormones have been studied much more extensively, and are much better understood, than the direct actions in the brain of sex chromosome genes." It concluded that while "the differentiating effects of gonadal secretions seem to be dominant," the existing body of research "support the idea that sex differences in neural expression of X and Y genes significantly contribute to sex differences in brain functions and disease."[83]

Marine mammals show some of the greatest sexual size differences of mammals, because of sexual selection and environmental factors like breeding location.[84] The mating system of pinnipeds varies from polygamy to serial monogamy. Pinnipeds are known for early differential growth and maternal investment since the only nutrients for newborn pups is the milk provided by the mother.[85] For example, the males are significantly larger (about 10% heavier and 2% longer) than the females at birth in sea lion pups.[86] The pattern of differential investment can be varied principally prenatally and post-natally.[87] Mirounga leonina, the southern elephant seal, is one of the most dimorphic mammals.[88]

According to Clark Spencer Larsen, modern day Homo sapiens show a range of sexual dimorphism, with average body mass between the sexes differing by roughly 15%.[89] Considerable discussion in academic literature concerns potential evolutionary advantages associated with sexual competition (both intrasexual and intersexual) and short- and long-term sexual strategies.[90] According to Daly and Wilson, "The sexes differ more in human beings than in monogamous mammals, but much less than in extremely polygamous mammals."[91]

The average basal metabolic rate is about 6 percent higher in adolescent males than females and increases to about 10 percent higher after puberty. Females tend to convert more food into fat, while males convert more into muscle and expendable circulating energy reserves. Aggregated data of absolute strength indicates that females have, on average, 4060% the upper body strength of males, and 7075% the lower body strength.[92] The difference in strength relative to body mass is less pronounced in trained individuals. In Olympic weightlifting, male records vary from 5.5 body mass in the lowest weight category to 4.2 in the highest weight category, while female records vary from 4.4 to 3.8, a weight adjusted difference of only 1020%, and an absolute difference of about 40% (i.e. 472kg vs 333kg for unlimited weight classes; see Olympic weightlifting records). A study, carried about by analyzing annual world rankings from 1980 to 1996, found that males' running times were, on average, 11% faster than females'.[93]

In early adolescence, females are on average taller than males (as females tend to go through puberty earlier), but males, on average, surpass them in height in later adolescence and adulthood. In the United States, adult males are on average 9% taller[94] and 16.5% heavier[95] than adult females.

Males typically have larger tracheae and branching bronchi, with about 30 percent greater lung volume per body mass. On average, males have larger hearts, 10 percent higher red blood cell count, higher hemoglobin, hence greater oxygen-carrying capacity. They also have higher circulating clotting factors (vitamin K, prothrombin and platelets). These differences lead to faster healing of wounds and lower sensitivity to nerve pain after injury.[96] In males, pain-causing injury to the peripheral nerve occurs through the microglia, while in females it occurs through the T cells (except in pregnant women, who follow a male pattern).[97]

Females typically have more white blood cells (stored and circulating), as well as more granulocytes and B and T lymphocytes. Additionally, they produce more antibodies at a faster rate than males, hence they develop fewer infectious diseases and succumb for shorter periods.[96] Ethologists argue that females, interacting with other females and multiple offspring in social groups, have experienced such traits as a selective advantage.[98][99][100][101][102][excessive citations] Females have a higher sensitivity to pain due to aforementioned nerve differences that increase the sensation, and females thus require higher levels of pain medication after injury.[97] Hormonal changes in females affect pain sensitivity, and pregnant women have the same sensitivity as males. Acute pain tolerance is also more consistent over a lifetime in females than males, despite these hormonal changes.[103] Despite differences in the physical feeling, both sexes have similar psychological tolerance to (or ability to cope with and ignore) pain.[104]

In the human brain, a difference between sexes was observed in the transcription of the PCDH11X/Y gene pair unique to Homo sapiens.[105] Sexual differentiation in the human brain from the undifferentiated state is triggered by testosterone from the fetal testis. Testosterone is converted to estrogen in the brain through the action of the enzyme aromatase. Testosterone acts on many brain areas, including the SDN-POA, to create the masculinized brain pattern.[106] Brains of pregnant females carrying male fetuses may be shielded from the masculinizing effects of androgen through the action of sex hormone-binding globulin.[107]

The relationship between sex differences in the brain and human behavior is a subject of controversy in psychology and society at large.[108][109] Many females tend to have a higher ratio of gray matter in the left hemisphere of the brain in comparison to males.[110][111] Males on average have larger brains than females; however, when adjusted for total brain volume the gray matter differences between sexes is almost nonexistent. Thus, the percentage of gray matter appears to be more related to brain size than it is to sex.[112][113] Differences in brain physiology between sexes do not necessarily relate to differences in intellect. Haier et al. found in a 2004 study that "men and women apparently achieve similar IQ results with different brain regions, suggesting that there is no singular underlying neuroanatomical structure to general intelligence and that different types of brain designs may manifest equivalent intellectual performance".[114] (See the sex and intelligence article for more on this subject.) Strict graph-theoretical analysis of the human brain connections revealed[115] that in numerous graph-theoretical parameters (e.g., minimum bipartition width, edge number, the expander graph property, minimum vertex cover), the structural connectome of women are significantly "better" connected than the connectome of men. It was shown[116] that the graph-theoretical differences are due to the sex and not to the differences in the cerebral volume, by analyzing the data of 36 females and 36 males, where the brain volume of each man in the group was smaller than the brain volume of each woman in the group.

Sexual dimorphism was also described in the gene level and shown to extend from the sex chromosomes. Overall, about 6500 genes have been found to have sex-differential expression in at least one tissue. Many of these genes are not directly associated with reproduction, but rather linked to more general biological features. In addition, it has been shown that genes with sex-specific expression undergo reduced selection efficiency, which lead to higher population frequencies of deleterious mutations and contributing to the prevalence of several human diseases.[117][118]

Sexual dimorphism in immune function is a common pattern in vertebrates and also in a number of invertebrates. Most often, females are more 'immunocompetent' than males. This trait is not consistent among all animals, but differs depending on taxonomy, with the most female-biased immune systems being found in insects.[119] In mammals this results in more frequent and severe infections in males and higher rates of autoimmune disorders in females. One potential cause may be differences in gene expression of immune cells between the sexes.[120] Another explanation is that endocrinological differences between the sexes impact the immune system for example, testosterone acts as an immunosuppressive agent.[121]

Phenotypic differences between sexes are evident even in cultured cells from tissues.[122] For example, female muscle-derived stem cells have a better muscle regeneration efficiency than male ones.[123] There are reports of several metabolic differences between male and female cells[124] and they also respond to stress differently.[125]

In theory, larger females are favored by competition for mates, especially in polygamous species. Larger females offer an advantage in fertility, since the physiological demands of reproduction are limiting in females. Hence there is a theoretical expectation that females tend to be larger in species that are monogamous.Females are larger in many species of insects, many spiders, many fish, many reptiles, owls, birds of prey and certain mammals such as the spotted hyena, and baleen whales such as blue whale. As an example, in some species, females are sedentary, and so males must search for them. Fritz Vollrath and Geoff Parker argue that this difference in behaviour leads to radically different selection pressures on the two sexes, evidently favouring smaller males.[126] Cases where the male is larger than the female have been studied as well,[126] and require alternative explanations.

One example of this type of sexual size dimorphism is the bat Myotis nigricans, (black myotis bat) where females are substantially larger than males in terms of body weight, skull measurement, and forearm length.[127] The interaction between the sexes and the energy needed to produce viable offspring make it favorable for females to be larger in this species. Females bear the energetic cost of producing eggs, which is much greater than the cost of making sperm by the males. The fecundity advantage hypothesis states that a larger female is able to produce more offspring and give them more favorable conditions to ensure their survival; this is true for most ectotherms. A larger female can provide parental care for a longer time while the offspring matures. The gestation and lactation periods are fairly long in M. nigricans, the females suckling their offspring until they reach nearly adult size.[128] They would not be able to fly and catch prey if they did not compensate for the additional mass of the offspring during this time. Smaller male size may be an adaptation to increase maneuverability and agility, allowing males to compete better with females for food and other resources.

Some species of anglerfish also display extreme sexual dimorphism. Females are more typical in appearance to other fish, whereas the males are tiny rudimentary creatures with stunted digestive systems. A male must find a female and fuse with her: he then lives parasitically, becoming little more than a sperm-producing body in what amounts to an effectively hermaphrodite composite organism. A similar situation is found in the Zeus water bug Phoreticovelia disparata where the female has a glandular area on her back that can serve to feed a male, which clings to her (note that although males can survive away from females, they generally are not free-living).[129] This is taken to the logical extreme in the Rhizocephala crustaceans, like the Sacculina, where the male injects itself into the female's body and becomes nothing more than sperm producing cells, to the point that the superorder used to be mistaken for hermaphroditic.[130]

Some plant species also exhibit dimorphism in which the females are significantly larger than the males, such as in the moss Dicranum[131] and the liverwort Sphaerocarpos.[132] There is some evidence that, in these genera, the dimorphism may be tied to a sex chromosome,[132][133] or to chemical signalling from females.[134]

Another complicated example of sexual dimorphism is in Vespula squamosa, the southern yellowjacket. In this wasp species, the female workers are the smallest, the male workers are slightly larger, and the female queens are significantly larger than her female worker and male counterparts.[citation needed]

In 1871, Charles Darwin advanced the theory of sexual selection, which related sexual dimorphism with sexual selection.[136]

The first step towards sexual dimorphism is the size differentiation of sperm and eggs (anisogamy).[137] Anisogamy and the usually large number of small male gametes relative to the larger female gametes usually lies in the development of strong sperm competition,[138][139] because small sperm enable organisms to produce a large number of sperm, and make males (or male function of hermaphrodites[140]) more redundant.

This intensifies male competition for mates and promotes the evolution of other sexual dimorphism in many species, especially in vertebrates including mammals. However, in some species females compete for mates in ways more usually associated with males (usually species in which males invest a lot in rearing offspring and thus are no longer considered as so redundant).[citation needed]

Sexual dimorphism by size is evident in some extinct species such as the velociraptor. In the case of velociraptors the sexual size dimorphism may have been caused by two factors: male competition for hunting ground to attract mates, and/or female competition for nesting locations and mates, males being a scarce breeding resource.[141]

Volvocine algae have been useful in understanding the evolution of sexual dimorphism [142] and species like the beetle C. maculatus, where the females are larger than the males, are used to study its underlying genetic mechanisms. [143]

In many non-monogamous species, the benefit to a male's reproductive fitness of mating with multiple females is large, whereas the benefit to a female's reproductive fitness of mating with multiple males is small or nonexistent.[144] In these species, there is a selection pressure for whatever traits enable a male to have more matings. The male may therefore come to have different traits from the female.

These traits could be ones that allow him to fight off other males for control of territory or a harem, such as large size or weapons;[145] or they could be traits that females, for whatever reason, prefer in mates.[146] Malemale competition poses no deep theoretical questions[147] but mate choice does.

Females may choose males that appear strong and healthy, thus likely to possess "good alleles" and give rise to healthy offspring.[148] In some species, however, females seem to choose males with traits that do not improve offspring survival rates, and even traits that reduce it (potentially leading to traits like the peacock's tail).[147] Two hypotheses for explaining this fact are the sexy son hypothesis and the handicap principle.

The sexy son hypothesis states that females may initially choose a trait because it improves the survival of their young, but once this preference has become widespread, females must continue to choose the trait, even if it becomes harmful. Those that do not will have sons that are unattractive to most females (since the preference is widespread) and so receive few matings.[149]

The handicap principle states that a male who survives despite possessing some sort of handicap thus proves that the rest of his genes are "good alleles". If males with "bad alleles" could not survive the handicap, females may evolve to choose males with this sort of handicap; the trait is acting as a hard-to-fake signal of fitness.[150]

Originally posted here:
Sexual dimorphism - Wikipedia

Recommendation and review posted by Bethany Smith

If your hairline is receding or your crown is thinning, you may wonder why this is happening and what exactly is causing your thinning hair. You may also be wondering what, if anything, you can do to reverse this trend.

Read on to learn more about the reasons why men lose their hair and the treatments that may help slow down the balding process.

The vast majority of men who go bald do so because of a hereditary condition known as androgenetic alopecia, more commonly known as male pattern baldness.

According to the American Hair Loss Association, 95 percent of hair loss in men is caused by androgenetic alopecia.

This inherited trait that tends to give guys a receding hairline and a thinning crown is caused by genetic sensitivity to a byproduct of testosterone called dihydrotestosterone (DHT).

So, how exactly does this hormonal byproduct cause hair loss?

Well, hair follicles that are sensitive to DHT have a tendency to shrink over time. As the affected hair follicles get smaller, the life span of each hair becomes shorter. Eventually, the affected follicles stop producing hair, or at least the type of hair youre used to.

With male pattern baldness, hair loss typically follows a predictable pattern. The two most common patterns of hair loss include the following:

The degree and progression of balding in men is assessed by the Norwood classification system. It has seven stages that measure the severity and pattern of hair loss and balding.

If you find that your hair is thinner than it used to be, you can draw some comfort from the fact that youre not alone. Male pattern baldness affects the majority of men at some stage in their lives.

According to the American Hair Loss Association:

Although male pattern baldness is the leading cause of balding, it isnt the only condition that can trigger hair loss.

With male pattern baldness, you typically dont have other symptoms aside from thinning hair. But with other hair loss causes, you may notice you have other symptoms, too.

Also, with most other causes, there isnt always a predictable hair loss pattern like there is with male pattern baldness. Instead, hair loss is more likely to happen all over, or in a few spots.

The following conditions can cause varying degrees of hair loss. Some types of hair loss may be permanent, while others may be reversible:

Hair loss from certain medications is usually temporary and once you stop taking the medication, hair growth will likely resume. Some of the known drugs associated with hair loss include:

Hair loss treatments, for male pattern baldness in particular, range from products you rub into your scalp to more invasive treatments aimed at restoring hair growth or replacing lost hair.

Here are some of the more popular and effective treatment options for balding.

There are both prescription and over-the-counter drugs approved for the treatment of male pattern baldness.

The two medications proven to treat or stave off further male pattern hair loss are finasteride (Propecia, Proscar) and minoxidil (Rogaine, Ioniten). Finasteride comes in a pill form and is only available by prescription. Minoxidil is a topical treatment thats available over the counter.

It can take at least 6 months for either treatment to start showing results.

Low-level laser therapy can be used to help invigorate circulation in the scalp and to stimulate hair follicles. Although this is a fairly new treatment option, it has been deemed safe and tolerable. It is also a less invasive option compared to hair transplant surgery.

Although research is limited for laser therapy and hair growth, some studies have shown encouraging results.

For instance, a 2013 study that included 41 men between the ages of 18 and 48 found a 39 percent increase in hair growth for participants who had laser hair surgery.

The two most common hair transplant procedures are follicular unit transplantation (FUT) and follicular unit extraction (FUE).

FUT involves the removal of a section of skin from the back of the scalp where hair is still growing. This section of skin is then divided into hundreds of tiny pieces called grafts. These grafts are then inserted into parts of the scalp where hair currently isnt growing.

With FUE, the surgeon takes individual healthy hair follicles out of the scalp and then makes small holes, where hair isnt growing, and puts the healthy follicles into these holes.

Male pattern baldness is commonly an inherited condition. Its very difficult to nonsurgically reverse any of the hair loss thats seen with this condition.

However, preventing further hair loss at the first sign of thinning is possible. Finasteride and Rogaine are two known treatments that might prevent further hair loss seen with androgenetic alopecia.

Once you discontinue use of these medications, the hair loss may resume. Talk to your doctor about if these medications may be right for you.

To keep your hair healthy and to prevent hair loss from other causes, try the following:

If you have a bald spot or a receding hairline, its likely due to your genes.

In 95 percent of cases, balding is due to androgenetic alopecia, more commonly known as male pattern baldness, which is a hereditary condition. It can affect men of all ages, and may even start before the age of 21.

Although you cant prevent male pattern baldness, there are ways to slow down hair loss. Some options include medications such as Finasteride (Propecia, Proscar) and minoxidil (Rogaine, Ioniten), laser therapy, and hair transplant surgery.

If youre concerned about going bald, be sure to speak to your doctor or dermatologist. They can work with you to figure out the treatment options that are right for you.

Read more from the original source:
Why Do Men Go Bald: Male Baldness Causes, Treatment, Prevention

Recommendation and review posted by Bethany Smith

Ethnic group in the United States

African Americans (also referred to as Black Americans and Afro-Americans) are an ethnic group consisting of Americans with partial or total ancestry from sub-Saharan Africa.[3][4] The term "African American" generally denotes descendants of enslaved Africans who are from the United States.[5][6][7] While some Black immigrants or their children may also come to identify as African-American, the majority of first generation immigrants do not, preferring to identify with their nation of origin.[8][9]

African Americans constitute the second largest racial group in the U.S. after White Americans, as well as the third largest ethnic group after Hispanic and Latino Americans.[10] Most African Americans are descendants of enslaved people within the boundaries of the present United States.[11][12] On average, African Americans are of West/Central African with some European descent; some also have Native American and other ancestry.[13]

According to U.S. Census Bureau data, African immigrants generally do not self-identify as African American. The overwhelming majority of African immigrants identify instead with their own respective ethnicities (~95%).[9] Immigrants from some Caribbean and Latin American nations and their descendants may or may not also self-identify with the term.[7]

African-American history began in the 16th century, with Africans from West Africa being sold to European slave traders and transported across the Atlantic to the Thirteen Colonies. After arriving in the Americas, they were sold as slaves to European colonists and put to work on plantations, particularly in the southern colonies. A few were able to achieve freedom through manumission or escape and founded independent communities before and during the American Revolution. After the United States was founded in 1783, most Black people continued to be enslaved, being most concentrated in the American South, with four million enslaved only liberated during and at the end of the Civil War in 1865.[14] During Reconstruction, they gained citizenship and the right to vote; due to the widespread policy and ideology of White supremacy, they were largely treated as second-class citizens and found themselves soon disenfranchised in the South. These circumstances changed due to participation in the military conflicts of the United States, substantial migration out of the South, the elimination of legal racial segregation, and the civil rights movement which sought political and social freedom. In 2008, Barack Obama became the first African American to be elected President of the United States.[15]

African-American culture has a significant influence on worldwide culture, making numerous contributions to visual arts, literature, the English language, philosophy, politics, cuisine, sports and music. The African American contribution to popular music is so profound that virtually all American music, such as jazz, gospel, blues, disco, hip hop, R&B, soul and rock all have their origins at least partially or entirely among African Americans.[16][17]

The vast majority of those who were enslaved and transported in the transatlantic slave trade were people from Central and West Africa, who had been captured directly by the slave traders in coastal raids,[18] or sold by other West Africans, or by half-European "merchant princes"[19] to European slave traders, who brought them to the Americas.[20]

The first African slaves arrived via Santo Domingo to the San Miguel de Gualdape colony (most likely located in the Winyah Bay area of present-day South Carolina), founded by Spanish explorer Lucas Vzquez de Aylln in 1526.[21] The ill-fated colony was almost immediately disrupted by a fight over leadership, during which the slaves revolted and fled the colony to seek refuge among local Native Americans. De Aylln and many of the colonists died shortly afterward of an epidemic and the colony was abandoned. The settlers and the slaves who had not escaped returned to Haiti, whence they had come.[21]

The marriage between Luisa de Abrego, a free Black domestic servant from Seville, and Miguel Rodrguez, a White Segovian conquistador in 1565 in St. Augustine (Spanish Florida), is the first known and recorded Christian marriage anywhere in what is now the continental United States.[22]

The first recorded Africans in English America (including most of the future United States) were "20 and odd negroes" who came to Jamestown, Virginia via Cape Comfort in August 1619 as indentured servants.[23] As many Virginian settlers began to die from harsh conditions, more and more Africans were brought to work as laborers.[24]

An indentured servant (who could be White or Black) would work for several years (usually four to seven) without wages. The status of indentured servants in early Virginia and Maryland was similar to slavery. Servants could be bought, sold, or leased and they could be physically beaten for disobedience or running away. Unlike slaves, they were freed after their term of service expired or was bought out, their children did not inherit their status, and on their release from contract they received "a year's provision of corn, double apparel, tools necessary", and a small cash payment called "freedom dues".[26] Africans could legally raise crops and cattle to purchase their freedom.[27] They raised families, married other Africans and sometimes intermarried with Native Americans or European settlers.[28]

By the 1640s and 1650s, several African families owned farms around Jamestown and some became wealthy by colonial standards and purchased indentured servants of their own. In 1640, the Virginia General Court recorded the earliest documentation of lifetime slavery when they sentenced John Punch, a Negro, to lifetime servitude under his master Hugh Gwyn for running away.[29][30]

In the Spanish Florida some Spanish married or had unions with Pensacola, Creek or African women, both slave and free, and their descendants created a mixed-race population of mestizos and mulattos. The Spanish encouraged slaves from the colony of Georgia to come to Florida as a refuge, promising freedom in exchange for conversion to Catholicism. King Charles II issued a royal proclamation freeing all slaves who fled to Spanish Florida and accepted conversion and baptism. Most went to the area around St. Augustine, but escaped slaves also reached Pensacola. St. Augustine had mustered an all-Black militia unit defending Spanish Florida as early as 1683.[31]

One of the Dutch African arrivals, Anthony Johnson, would later own one of the first Black "slaves", John Casor, resulting from the court ruling of a civil case.[32][33]

The popular conception of a race-based slave system did not fully develop until the 18th century. The Dutch West India Company introduced slavery in 1625 with the importation of eleven Black slaves into New Amsterdam (present-day New York City). All the colony's slaves, however, were freed upon its surrender to the English.[34]

Massachusetts was the first English colony to legally recognize slavery in 1641. In 1662, Virginia passed a law that children of enslaved women took the status of the mother, rather than that of the father, as under common law. This legal principle was called partus sequitur ventrum.[35][36]

By an act of 1699, the colony ordered all free Blacks deported, virtually defining as slaves all people of African descent who remained in the colony.[37] In 1670, the colonial assembly passed a law prohibiting free and baptized Blacks (and Indians) from purchasing Christians (in this act meaning White Europeans) but allowing them to buy people "of their owne nation".[38]

In the Spanish Louisiana although there was no movement toward abolition of the African slave trade, Spanish rule introduced a new law called coartacin, which allowed slaves to buy their freedom, and that of others.[41] Although some did not have the money to buy their freedom, government measures on slavery allowed many free Blacks. That brought problems to the Spaniards with the French Creoles who also populated Spanish Louisiana, French creoles cited that measure as one of the system's worst elements.[42]

First established in South Carolina in 1704, groups of armed White menslave patrolswere formed to monitor enslaved Black people.[43] Their function was to police slaves, especially fugitives. Slave owners feared that slaves might organize revolts or slave rebellions, so state militias were formed in order to provide a military command structure and discipline within the slave patrols so they could be used to detect, encounter, and crush any organized slave meetings which might lead to revolts or rebellions.[43]

The earliest African-American congregations and churches were organized before 1800 in both northern and southern cities following the Great Awakening. By 1775, Africans made up 20% of the population in the American colonies, which made them the second largest ethnic group after English Americans.[44]

During the 1770s, Africans, both enslaved and free, helped rebellious American colonists secure their independence by defeating the British in the American Revolutionary War.[45] Blacks played a role in both sides in the American Revolution. Activists in the Patriot cause included James Armistead, Prince Whipple, and Oliver Cromwell.[46][47] Around 15,000 Black Loyalists left with the British after the war, most of them ending up as free Black people in England[48] or its colonies, such as the Black Nova Scotians and the Sierra Leone Creole people.[49][50]

In the Spanish Louisiana, Governor Bernardo de Glvez organized Spanish free Black men into two militia companies to defend New Orleans during the American Revolution. They fought in the 1779 battle in which Spain captured Baton Rouge from the British. Glvez also commanded them in campaigns against the British outposts in Mobile, Alabama, and Pensacola, Florida. He recruited slaves for the militia by pledging to free anyone who was seriously wounded and promised to secure a low price for coartacin (buy their freedom and that of others) for those who received lesser wounds. During the 1790s, Governor Francisco Luis Hctor, baron of Carondelet reinforced local fortifications and recruit even more free Black men for the militia. Carondelet doubled the number of free Black men who served, creating two more militia companiesone made up of Black members and the other of pardo (mixed race). Serving in the militia brought free Black men one step closer to equality with Whites, allowing them, for example, the right to carry arms and boosting their earning power. However, actually these privileges distanced free Black men from enslaved Blacks and encouraged them to identify with Whites.[42]

Slavery had been tacitly enshrined in the U.S. Constitution through provisions such as Article I, Section 2, Clause 3, commonly known as the 3/5 compromise. Because of Section 9, Clause 1, Congress was unable to pass an Act Prohibiting Importation of Slaves until 1807.[51] Fugitive slave laws (derived from the Fugitive Slave Clause of the ConstitutionArticle IV, Section 2, Clause 3) were passed by Congress in 1793 and 1850, guaranteeing the right for a slaveholder to recover an escaped slave within the U.S.[40] Slave owners, who viewed slaves as property, made it a federal crime to assist those who had escaped slavery or to interfere with their capture.[39] Slavery, which by then meant almost exclusively Black people, was the most important political issue in the Antebellum United States, leading to one crisis after another. Among these were the Missouri Compromise, the Compromise of 1850, the Dred Scott decision, and John Brown's raid on Harpers Ferry.

Prior to the Civil War, eight serving presidents owned slaves, a practice protected by the U.S. Constitution.[52] By 1860, there were 3.5 to 4.4million enslaved Black people in the U.S. due to the Atlantic slave trade, and another 488,000500,000 Blacks lived free (with legislated limits)[53] across the country.[54] With legislated limits imposed upon them in addition to "unconquerable prejudice" from Whites according to Henry Clay,[55] some Black people who were not enslaved left the U.S. for Liberia in West Africa.[53] Liberia began as a settlement of the American Colonization Society (ACS) in 1821, with the abolitionist members of the ACS believing Blacks would face better chances for freedom and equality in Africa.[53]

The slaves not only constituted a large investment, they produced America's most valuable product and export: cotton. They not only helped build the U.S. Capitol, they built the White House and other District of Columbia buildings. (See Slavery in the District of Columbia.[56]) Similar building projects existed in the slave states.

By 1815, the domestic slave trade had become a major economic activity in the United States; it lasted until the 1860s.[57] Historians estimate nearly one million in total took part in the forced migration of this new "Middle Passage." The historian Ira Berlin called this forced migration of slaves the "central event" in the life of a slave between the American Revolution and the Civil War, writing that whether slaves were directly uprooted or lived in fear that they or their families would be involuntarily moved, "the massive deportation traumatized black people."[58] Individuals lost their connection to families and clans, and many ethnic Africans lost their knowledge of varying tribal origins in Africa.[57]

The 1863 photograph of Wilson Chinn, a branded slave from Louisiana, like the one of Gordon and his scarred back, served as two early examples of how the newborn medium of photography could encapsulate the cruelty of slavery.[59]

Emigration of free Blacks to their continent of origin had been proposed since the Revolutionary war. After Haiti became independent, it tried to recruit African Americans to migrate there after it re-established trade relations with the United States. The Haitian Union was a group formed to promote relations between the countries.[60] After riots against Blacks in Cincinnati, its Black community sponsored founding of the Wilberforce Colony, an initially successful settlement of African-American immigrants to Canada. The colony was one of the first such independent political entities. It lasted for a number of decades and provided a destination for about 200 Black families emigrating from a number of locations in the United States.[60]

In 1863, during the American Civil War, President Abraham Lincoln signed the Emancipation Proclamation. The proclamation declared that all slaves in Confederate-held territory were free.[61] Advancing Union troops enforced the proclamation, with Texas being the last state to be emancipated, in 1865.[62]

Slavery in Union-held Confederate territory continued, at least on paper, until the passage of the Thirteenth Amendment in 1865.[63] While the Naturalization Act of 1790 limited U.S. citizenship to Whites only,[64][65] the 14th Amendment (1868) gave Black people citizenship, and the 15th Amendment (1870) gave Black males the right to vote (which would still be denied to all women until 1920).[66]

African Americans quickly set up congregations for themselves, as well as schools and community/civic associations, to have space away from White control or oversight. While the post-war Reconstruction era was initially a time of progress for African Americans, that period ended in 1876. By the late 1890s, Southern states enacted Jim Crow laws to enforce racial segregation and disenfranchisement.[67] Segregation, which began with slavery, continued with Jim Crow laws, with signs used to show Blacks where they could legally walk, talk, drink, rest, or eat.[68] For those places that were racially mixed, non-Whites had to wait until all White customers were dealt with.[68] Most African Americans obeyed the Jim Crow laws, to avoid racially motivated violence. To maintain self-esteem and dignity, African Americans such as Anthony Overton and Mary McLeod Bethune continued to build their own schools, churches, banks, social clubs, and other businesses.[69]

In the last decade of the 19th century, racially discriminatory laws and racial violence aimed at African Americans began to mushroom in the United States, a period often referred to as the "nadir of American race relations". These discriminatory acts included racial segregationupheld by the United States Supreme Court decision in Plessy v. Ferguson in 1896which was legally mandated by southern states and nationwide at the local level of government, voter suppression or disenfranchisement in the southern states, denial of economic opportunity or resources nationwide, and private acts of violence and mass racial violence aimed at African Americans unhindered or encouraged by government authorities.[70]

The desperate conditions of African Americans in the South sparked the Great Migration during the first half of the 20th century which led to a growing African-American community in Northern and Western United States.[72] The rapid influx of Blacks disturbed the racial balance within Northern and Western cities, exacerbating hostility between both Blacks and Whites in the two regions.[73] The Red Summer of 1919 was marked by hundreds of deaths and higher casualties across the U.S. as a result of race riots that occurred in more than three dozen cities, such as the Chicago race riot of 1919 and the Omaha race riot of 1919. Overall, Blacks in Northern and Western cities experienced systemic discrimination in a plethora of aspects of life. Within employment, economic opportunities for Blacks were routed to the lowest-status and restrictive in potential mobility. At the 1900 Hampton Negro Conference, Reverend Matthew Anderson said: "...the lines along most of the avenues of wage earning are more rigidly drawn in the North than in the South."[74] Within the housing market, stronger discriminatory measures were used in correlation to the influx, resulting in a mix of "targeted violence, restrictive covenants, redlining and racial steering".[75] While many Whites defended their space with violence, intimidation, or legal tactics toward African Americans, many other Whites migrated to more racially homogeneous suburban or exurban regions, a process known as White flight.[76]

Despite discrimination, drawing cards for leaving the hopelessness in the South were the growth of African-American institutions and communities in Northern cities. Institutions included Black oriented organizations (e.g., Urban League, NAACP), churches, businesses, and newspapers, as well as successes in the development in African-American intellectual culture, music, and popular culture (e.g., Harlem Renaissance, Chicago Black Renaissance). The Cotton Club in Harlem was a Whites-only establishment, with Blacks (such as Duke Ellington) allowed to perform, but to a White audience.[77] Black Americans also found a new ground for political power in Northern cities, without the enforced disabilities of Jim Crow.[78][79]

By the 1950s, the civil rights movement was gaining momentum. A 1955 lynching that sparked public outrage about injustice was that of Emmett Till, a 14-year-old boy from Chicago. Spending the summer with relatives in Money, Mississippi, Till was killed for allegedly having wolf-whistled at a White woman. Till had been badly beaten, one of his eyes was gouged out, and he was shot in the head. The visceral response to his mother's decision to have an open-casket funeral mobilized the Black community throughout the U.S.[80] Vann R. Newkirk| wrote "the trial of his killers became a pageant illuminating the tyranny of White supremacy".[80] The state of Mississippi tried two defendants, but they were speedily acquitted by an all-White jury.[81] One hundred days after Emmett Till's murder, Rosa Parks refused to give up her seat on the bus in Alabamaindeed, Parks told Emmett's mother Mamie Till that "the photograph of Emmett's disfigured face in the casket was set in her mind when she refused to give up her seat on the Montgomery bus."[82]

The March on Washington for Jobs and Freedom and the conditions which brought it into being are credited with putting pressure on presidents John F. Kennedy and Lyndon B. Johnson. Johnson put his support behind passage of the Civil Rights Act of 1964 that banned discrimination in public accommodations, employment, and labor unions, and the Voting Rights Act of 1965, which expanded federal authority over states to ensure Black political participation through protection of voter registration and elections.[83] By 1966, the emergence of the Black Power movement, which lasted from 1966 to 1975, expanded upon the aims of the civil rights movement to include economic and political self-sufficiency, and freedom from White authority.[84]

During the post-war period, many African Americans continued to be economically disadvantaged relative to other Americans. Average Black income stood at 54 percent of that of White workers in 1947, and 55 percent in 1962. In 1959, median family income for Whites was $5,600, compared with $2,900 for non-White families. In 1965, 43 percent of all Black families fell into the poverty bracket, earning under $3,000 a year. The Sixties saw improvements in the social and economic conditions of many Black Americans.[85]

From 1965 to 1969, Black family income rose from 54 to 60 percent of White family income. In 1968, 23 percent of Black families earned under $3,000 a year, compared with 41 percent in 1960. In 1965, 19 percent of Black Americans had incomes equal to the national median, a proportion that rose to 27 percent by 1967. In 1960, the median level of education for Blacks had been 10.8 years, and by the late Sixties the figure rose to 12.2 years, half a year behind the median for Whites.[85]

Politically and economically, African Americans have made substantial strides during the postcivil rights era. In 1967, Thurgood Marshall became the first African-American Supreme Court Justice. In 1968, Shirley Chisholm became the first Black woman elected to the U.S. Congress. In 1989, Douglas Wilder became the first African American elected governor in U.S. history. Clarence Thomas succeeded Marshall to become the second African-American Supreme Court Justice in 1991. In 1992, Carol Moseley-Braun of Illinois became the first African-American woman elected to the U.S. Senate. There were 8,936 Black officeholders in the United States in 2000, showing a net increase of 7,467 since 1970. In 2001, there were 484 Black mayors.[86]

In 2005, the number of Africans immigrating to the United States, in a single year, surpassed the peak number who were involuntarily brought to the United States during the Atlantic Slave Trade.[87] On November 4, 2008, Democratic Senator Barack Obama defeated Republican Senator John McCain to become the first African American to be elected president. At least 95 percent of African-American voters voted for Obama.[88][89] He also received overwhelming support from young and educated Whites, a majority of Asians,[90] and Hispanics,[90] picking up a number of new states in the Democratic electoral column.[88][89] Obama lost the overall White vote, although he won a larger proportion of White votes than any previous nonincumbent Democratic presidential candidate since Jimmy Carter.[91] Obama was reelected for a second and final term, by a similar margin on November 6, 2012.[92] In 2021, Kamala Harris became the first woman, the first African American, and the first Asian American to serve as Vice President of the United States.[93]

Proportion of African Americans in each U.S. state, the District of Columbia, and Puerto Rico as of the 2020 United States Census

In 1790, when the first U.S. Census was taken, Africans (including slaves and free people) numbered about 760,000about 19.3% of the population. In 1860, at the start of the Civil War, the African-American population had increased to 4.4million, but the percentage rate dropped to 14% of the overall population of the country. The vast majority were slaves, with only 488,000 counted as "freemen". By 1900, the Black population had doubled and reached 8.8million.[94]

In 1910, about 90% of African Americans lived in the South. Large numbers began migrating north looking for better job opportunities and living conditions, and to escape Jim Crow laws and racial violence. The Great Migration, as it was called, spanned the 1890s to the 1970s. From 1916 through the 1960s, more than 6million Black people moved north. But in the 1970s and 1980s, that trend reversed, with more African Americans moving south to the Sun Belt than leaving it.[95]

The following table of the African-American population in the United States over time shows that the African-American population, as a percentage of the total population, declined until 1930 and has been rising since then.

By 1990, the African-American population reached about 30million and represented 12% of the U.S. population, roughly the same proportion as in 1900.[97]

At the time of the 2000 Census, 54.8% of African Americans lived in the South. In that year, 17.6% of African Americans lived in the Northeast and 18.7% in the Midwest, while only 8.9% lived in the western states. The west does have a sizable Black population in certain areas, however. California, the nation's most populous state, has the fifth largest African-American population, only behind New York, Texas, Georgia, and Florida. According to the 2000 Census, approximately 2.05% of African Americans identified as Hispanic or Latino in origin,[10] many of whom may be of Brazilian, Puerto Rican, Dominican, Cuban, Haitian, or other Latin American descent. The only self-reported ancestral groups larger than African Americans are the Irish and Germans.[98]

According to the 2010 U.S. Census, nearly 3% of people who self-identified as Black had recent ancestors who immigrated from another country. Self-reported non-Hispanic Black immigrants from the Caribbean, mostly from Jamaica and Haiti, represented 0.9% of the U.S. population, at 2.6million.[99] Self-reported Black immigrants from Sub-Saharan Africa also represented 0.9%, at about 2.8million.[99] Additionally, self-identified Black Hispanics represented 0.4% of the United States population, at about 1.2million people, largely found within the Puerto Rican and Dominican communities.[100] Self-reported Black immigrants hailing from other countries in the Americas, such as Brazil and Canada, as well as several European countries, represented less than 0.1% of the population. Mixed-Race Hispanic and non-Hispanic Americans who identified as being part Black, represented 0.9% of the population. Of the 12.6% of United States residents who identified as Black, around 10.3% were "native Black American" or ethnic African Americans, who are direct descendants of West/Central Africans brought to the U.S. as slaves. These individuals make up well over 80% of all Blacks in the country. When including people of mixed-race origin, about 13.5% of the U.S. population self-identified as Black or "mixed with Black".[101] However, according to the U.S. census bureau, evidence from the 2000 Census indicates that many African and Caribbean immigrant ethnic groups do not identify as "Black, African Am., or Negro". Instead, they wrote in their own respective ethnic groups in the "Some Other Race" write-in entry. As a result, the census bureau devised a new, separate "African American" ethnic group category in 2010 for ethnic African Americans.[102]

Historically, African-Americans have been undercounted in the U.S. Census due to a number of factors and biases.[103][104] In the 2020 census, the African American population was undercounted at an estimated rate of 3.3%, up from 2.1% in 2010.[105]

After 100 years of African Americans leaving the south in large numbers seeking better opportunities and treatment in the west and north, a movement known as the Great Migration, there is now a reverse trend, called the New Great Migration. As with the earlier Great Migration, the New Great Migration is primarily directed toward cities and large urban areas, such as Atlanta, Charlotte, Houston, Dallas, Raleigh, Tampa, San Antonio, Memphis, Nashville, Jacksonville, and so forth.[106] A growing percentage of African-Americans from the west and north are migrating to the southern region of the U.S. for economic and cultural reasons. New York City, Chicago, and Los Angeles have the highest decline in African Americans, while Atlanta, Dallas, and Houston have the highest increase respectively.[106]

Among cities of 100,000 or more, Detroit, Michigan had the highest percentage of Black residents of any U.S. city in 2010, with 82%. Other large cities with African-American majorities include Jackson, Mississippi (79.4%), Miami Gardens, Florida (76.3%), Baltimore, Maryland (63%), Birmingham, Alabama (62.5%), Memphis, Tennessee (61%), New Orleans, Louisiana (60%), Montgomery, Alabama (56.6%), Flint, Michigan (56.6%), Savannah, Georgia (55.0%), Augusta, Georgia (54.7%), Atlanta, Georgia (54%, see African Americans in Atlanta), Cleveland, Ohio (53.3%), Newark, New Jersey (52.35%), Washington, D.C. (50.7%), Richmond, Virginia (50.6%), Mobile, Alabama (50.6%), Baton Rouge, Louisiana (50.4%), and Shreveport, Louisiana (50.4%).

The nation's most affluent community with an African-American majority resides in View ParkWindsor Hills, California with an annual median household income of $159,618.[107] Other largely affluent and African-American communities include Prince George's County in Maryland (namely Mitchellville, Woodmore, and Upper Marlboro), Dekalb County and South Fulton in Georgia, Charles City County in Virginia, Baldwin Hills in California, Hillcrest and Uniondale in New York, and Cedar Hill, DeSoto, and Missouri City in Texas. Queens County, New York is the only county with a population of 65,000 or more where African Americans have a higher median household income than White Americans.[108]

Seatack, Virginia is currently the oldest African-American community in the United States.[109] It survives today with a vibrant and active civic community.[110]

During slavery, anti-literacy laws were enacted in the U.S. that prohibited education for Black people. Slave owners saw literacy as a threat to the institution of slavery. As a North Carolina statute stated, "Teaching slaves to read and write, tends to excite dissatisfaction in their minds, and to produce insurrection and rebellion."[111]

In 1863, enslaved Americans became free citizens during a time when public educational systems were expanding across the country. By 1870, around seventy-four institutions in the south provided a form of advanced education for African American students, and by 1900, over a hundred programs at these schools provided training for Black professionals, including teachers. Many of the students at Fisk University, including W. E. B. Du Bois when he was a student there, taught school during the summers to support their studies.[112]

African Americans were very concerned to provide quality education for their children, but White supremacy limited their ability to participate in educational policymaking on the political level. State governments soon moved to undermine their citizenship by restricting their right to vote. By the late 1870s, Blacks were disenfranchised and segregated across the American South.[113] White politicians in Mississippi and other states withheld financial resources and supplies from Black schools. Nevertheless, the presence of Black teachers, and their engagement with their communities both inside and outside the classroom, ensured that Black students had access to education despite these external constraints.[114][115]

During World War II, demands for unity and racial tolerance on the home front provided an opening for the first Black history curriculum in the country.[116] For example, during the early 1940s, Madeline Morgan, a Black teacher in the Chicago public schools, created a curriculum for students in grades one through eight highlighting the contributions of Black people to the history of the United States. At the close of the war, Chicago's Board of Education downgraded the curriculum's status from mandatory to optional.[117]

Predominantly Black schools for kindergarten through twelfth grade students were common throughout the U.S. before the 1970s. By 1972, however, desegregation efforts meant that only 25% of Black students were in schools with more than 90% non-White students. However, since then, a trend towards re-segregation affected communities across the country: by 2011, 2.9million African-American students were in such overwhelmingly minority schools, including 53% of Black students in school districts that were formerly under desegregation orders.[118][119]

As late as 1947, about one third of African Americans over 65 were considered to lack the literacy to read and write their own names. By 1969, illiteracy as it had been traditionally defined, had been largely eradicated among younger African Americans.[120]

U.S. Census surveys showed that by 1998, 89 percent of African Americans aged 25 to 29 had completed a high-school education, less than Whites or Asians, but more than Hispanics. On many college entrance, standardized tests and grades, African Americans have historically lagged behind Whites, but some studies suggest that the achievement gap has been closing. Many policy makers have proposed that this gap can and will be eliminated through policies such as affirmative action, desegregation, and multiculturalism.[121]

Between 1995 and 2009, freshmen college enrollment for African Americans increased by 73 percent and only 15 percent for Whites.[122] Black women are enrolled in college more than any other race and gender group, leading all with 9.7% enrolled according to the 2011 U.S. Census Bureau.[123][124] The average high school graduation rate of Blacks in the United States has steadily increased to 71% in 2013.[125] Separating this statistic into component parts shows it varies greatly depending upon the state and the school district examined. 38% of Black males graduated in the state of New York but in Maine 97% graduated and exceeded the White male graduation rate by 11 percentage points.[126] In much of the southeastern United States and some parts of the southwestern United States the graduation rate of White males was in fact below 70% such as in Florida where 62% of White males graduated from high school. Examining specific school districts paints an even more complex picture. In the Detroit school district the graduation rate of Black males was 20% but 7% for White males. In the New York City school district 28% of Black males graduate from high school compared to 57% of White males. In Newark County[where?] 76% of Black males graduated compared to 67% for White males. Further academic improvement has occurred in 2015. Roughly 23% of all Blacks have bachelor's degrees. In 1988, 21% of Whites had obtained a bachelor's degree versus 11% of Blacks. In 2015, 23% of Blacks had obtained a bachelor's degree versus 36% of Whites.[127] Foreign born Blacks, 9% of the Black population, made even greater strides. They exceed native born Blacks by 10 percentage points.[127]

College Board, which runs the official college-level advanced placement (AP) programs in American high schools, have has received criticism in recent years that its curricula have focused too much on Euro-centric history.[128] In 2020, College Board reshaped some curricula among history-based courses to further reflect the African diaspora.[129] In 2021, College Board announced it would be piloting an AP African American Studies course between 2022 and 2024. The course is expected to launch in 2024.[130]

Historically Black colleges and universities (HBCUs), which were founded when segregated institutions of higher learning did not admit African Americans, continue to thrive and educate students of all races today. There are 101 HBCUs representing three percent of the nation's colleges and universities with the majority established in the Southeast.[131][132] HBCUs have been largely responsible for establishing and expanding the African-American middle-class by providing opportunities not usually given to African Americans.[133][134]

African Americans have benefited from the advances made during the civil rights era. The racial disparity in poverty rates has narrowed. In the first quarter of 2021, 45.1% of African Americans owned their homes, compared to 65.3% of all Americans.[136] The poverty rate among African Americans has decreased from 24.7% in 2004 to 18.8% in 2020, compared to 10.5% for all Americans.[137][138]

African Americans have a combined buying power of over $892billion currently and likely over $1.1trillion by 2012.[140][141] In 2002, African American-owned businesses accounted for 1.2million of the US's 23million businesses.[142] As of 2011[update] African American-owned businesses account for approximately 2million US businesses.[143] Black-owned businesses experienced the largest growth in number of businesses among minorities from 2002 to 2011.[143]

Twenty-five percent of Blacks had white-collar occupations (management, professional, and related fields) in 2000, compared with 33.6% of Americans overall.[144][145] In 2001, over half of African-American households of married couples earned $50,000 or more.[145] Although in the same year African Americans were over-represented among the nation's poor, this was directly related to the disproportionate percentage of African-American families headed by single women; such families are collectively poorer, regardless of ethnicity.[145]

In 2006, the median earnings of African-American men was more than Black and non-Black American women overall, and in all educational levels.[146][147][148][149][150] At the same time, among American men, income disparities were significant; the median income of African-American men was approximately 76 cents for every dollar of their European American counterparts, although the gap narrowed somewhat with a rise in educational level.[146][151]

Overall, the median earnings of African-American men were 72 cents for every dollar earned of their Asian American counterparts, and $1.17 for every dollar earned by Hispanic men.[146][149][152] On the other hand, by 2006, among American women with post-secondary education, African-American women have made significant advances; the median income of African-American women was more than those of their Asian-, European- and Hispanic American counterparts with at least some college education.[147][148][153]

The U.S. public sector is the single most important source of employment for African Americans.[154] During 20082010, 21.2% of all Black workers were public employees, compared with 16.3% of non-Black workers.[154] Both before and after the onset of the Great Recession, African Americans were 30% more likely than other workers to be employed in the public sector.[154] The public sector is also a critical source of decent-paying jobs for Black Americans. For both men and women, the median wage earned by Black employees is significantly higher in the public sector than in other industries.[154]

In 1999, the median income of African-American families was $33,255 compared to $53,356 of European Americans. In times of economic hardship for the nation, African Americans suffer disproportionately from job loss and underemployment, with the Black underclass being hardest hit. The phrase "last hired and first fired" is reflected in the Bureau of Labor Statistics unemployment figures. Nationwide, the October 2008 unemployment rate for African Americans was 11.1%,[155] while the nationwide rate was 6.5%.[156]

The income gap between Black and White families is also significant. In 2005, employed Blacks earned 65% of the wages of Whites, down from 82% in 1975.[137] The New York Times reported in 2006 that in Queens, New York, the median income among African-American families exceeded that of White families, which the newspaper attributed to the growth in the number of two-parent Black families. It noted that Queens was the only county with more than 65,000 residents where that was true.[108] In 2011, it was reported that 72% of Black babies were born to unwed mothers.[157] The poverty rate among single-parent Black families was 39.5% in 2005, according to Walter E. Williams, while it was 9.9% among married-couple Black families. Among White families, the respective rates were 26.4% and 6% in poverty.[158]

Collectively, African Americans are more involved in the American political process than other minority groups in the United States, indicated by the highest level of voter registration and participation in elections among these groups in 2004.[159] African Americans also have the highest level of Congressional representation of any minority group in the U.S.[160]

Since the mid 20th century, a large majority of African Americans support the Democratic Party. In the 2020 Presidential election, 91% of African-American voters supported Democrat Joe Biden, while 8% supported Republican Donald Trump.[161] Although there is an African-American lobby in foreign policy, it has not had the impact that African-American organizations have had in domestic policy.[162]

Many African Americans were excluded from electoral politics in the decades following the end of Reconstruction. For those that could participate, until the New Deal, African Americans were supporters of the Republican Party because it was Republican President Abraham Lincoln who helped in granting freedom to American slaves; at the time, the Republicans and Democrats represented the sectional interests of the North and South, respectively, rather than any specific ideology, and both conservative and liberal were represented equally in both parties.

The African-American trend of voting for Democrats can be traced back to the 1930s during the Great Depression, when Franklin D. Roosevelt's New Deal program provided economic relief to African Americans. Roosevelt's New Deal coalition turned the Democratic Party into an organization of the working class and their liberal allies, regardless of region. The African-American vote became even more solidly Democratic when Democratic presidents John F. Kennedy and Lyndon B. Johnson pushed for civil rights legislation during the 1960s. In 1960, nearly a third of African Americans voted for Republican Richard Nixon.[163]

"Lift Every Voice and Sing" is often referred to as the Black national anthem in the United States.[164] In 1919, the National Association for the Advancement of Colored People (NAACP) had dubbed it the "Negro national anthem" for its power in voicing a cry for liberation and affirmation for African American people.[165]

According to a Gallup survey, 4.6% of Black or African-Americans self-identified as LGBT in 2016,[166] while the total portion of American adults in all ethnic groups identifying as LGBT was 4.1% in 2016.[166]

The life expectancy for Black men in 2008 was 70.8 years.[167] Life expectancy for Black women was 77.5 years in 2008.[167] In 1900, when information on Black life expectancy started being collated, a Black man could expect to live to 32.5 years and a Black woman 33.5 years.[167] In 1900, White men lived an average of 46.3 years and White women lived an average of 48.3 years.[167] African-American life expectancy at birth is persistently five to seven years lower than European Americans.[168] Black men have shorter lifespans than any other group in the US besides Native American men.[169]

Black people have higher rates of obesity, diabetes, and hypertension than the U.S. average.[167] For adult Black men, the rate of obesity was 31.6% in 2010.[170] For adult Black women, the rate of obesity was 41.2% in 2010.[170] African Americans have higher rates of mortality than any other racial or ethnic group for 8 of the top 10 causes of death.[171] In 2013, among men, Black men had the highest rate of getting cancer, followed by White, Hispanic, Asian/Pacific Islander (A/PI), and American Indian/Alaska Native (AI/AN) men. Among women, White women had the highest rate of getting cancer, followed by Black, Hispanic, Asian/Pacific Islander, and American Indian/Alaska Native women.[172] African Americans also have higher prevalence and incidence of Alzheimer's disease compared to the overall average.[173][174]

Violence has an impact upon African-American life expectancy. A report from the U.S. Department of Justice states "In 2005, homicide victimization rates for blacks were 6 times higher than the rates for whites".[175] The report also found that "94% of black victims were killed by blacks."[175] Black boys and men age 1544 are the only race/sex category for which homicide is a top-five cause of death.[169]

In December 2020, African Americans were less likely to be vaccinated against COVID-19 due to mistrust in the U.S. medical system related to decades of abuses and anti-black treatment. From 2021 to 2022, there was an increase in African Americans who became vaccinated.[176][177][178] Still, in 2022, COVID-19 complications became the third leading cause of death for African Americans.[179]

According to the Centers for Disease Control and Prevention, African Americans have higher rates of sexually transmitted infections (STIs) compared to Whites, with 5 times the rates of syphilis and chlamydia, and 7.5 times the rate of gonorrhea.[180]

The disproportionately high incidence of HIV/AIDS among African-Americans has been attributed to homophobic influences and lack of access to proper healthcare.[181] The prevalence of HIV/AIDS among Black men is seven times higher than the prevalence for White men, and Black men are more than nine times as likely to die from HIV/AIDS-related illness than White men.[169]

African Americans have several barriers for accessing mental health services. Counseling has been frowned upon and distant in utility and proximity to many people in the African American community. In 2004, a qualitative research study explored the disconnect with African Americans and mental health. The study was conducted as a semi-structured discussion which allowed the focus group to express their opinions and life experiences. The results revealed a couple key variables that create barriers for many African American communities to seek mental health services such as the stigma, lack of four important necessities; trust, affordability, cultural understanding and impersonal services.[182]

Historically, many African American communities did not seek counseling because religion was a part of the family values.[183] African American who have a faith background are more likely to seek prayer as a coping mechanism for mental issues rather than seeking professional mental health services.[182] In 2015 a study concluded, African Americans with high value in religion are less likely to utilize mental health services compared to those who have low value in religion.[184]

Most counseling approaches are westernized and do not fit within the African American culture. African American families tend to resolve concerns within the family, and it is viewed by the family as a strength. On the other hand, when African Americans seek counseling, they face a social backlash and are criticized. They may be labeled "crazy", viewed as weak, and their pride is diminished.[182] Because of this, many African Americans instead seek mentorship within communities they trust.

Terminology is another barrier in relation to African Americans and mental health. There is more stigma on the term psychotherapy versus counseling. In one study, psychotherapy is associated with mental illness whereas counseling approaches problem-solving, guidance and help.[182] More African Americans seek assistance when it is called counseling and not psychotherapy because it is more welcoming within the cultural and community.[185] Counselors are encouraged to be aware of such barriers for the well-being of African American clients. Without cultural competency training in health care, many African Americans go unheard and misunderstood.[182]

Although suicide is a top-10 cause of death for men overall in the US, it is not a top-10 cause of death for Black men.[169]

Recent surveys of African Americans using a genetic testing service have found varied ancestries which show different tendencies by region and sex of ancestors. These studies found that on average, African Americans have 73.282.1% West African, 16.7%24% European, and 0.81.2% Native American genetic ancestry, with large variation between individuals.[187][188][189] Genetics websites themselves have reported similar ranges, with some finding 1 or 2 percent Native American ancestry and Ancestry.com reporting an outlying percentage of European ancestry among African Americans, 29%.[190]

According to a genome-wide study by Bryc et al. (2009), the mixed ancestry of African Americans in varying ratios came about as the result of sexual contact between West/Central Africans (more frequently females) and Europeans (more frequently males). Consequently, the 365 African Americans in their sample have a genome-wide average of 78.1% West African ancestry and 18.5% European ancestry, with large variation among individuals (ranging from 99% to 1% West African ancestry). The West African ancestral component in African Americans is most similar to that in present-day speakers from the non-Bantu branches of the Niger-Congo (Niger-Kordofanian) family.[187][note 2]

Correspondingly, Montinaro et al. (2014) observed that around 50% of the overall ancestry of African Americans traces back to the Niger-Congo-speaking Yoruba of southwestern Nigeria and southern Benin, reflecting the centrality of this West African region in the Atlantic Slave Trade. The next most frequent ancestral component found among African Americans was derived from Great Britain, in keeping with historical records. It constitutes a little over 10% of their overall ancestry, and is most similar to the Northwest European ancestral component also carried by Barbadians.[192] Zakharaia et al. (2009) found a similar proportion of Yoruba associated ancestry in their African-American samples, with a minority also drawn from Mandenka and Bantu populations. Additionally, the researchers observed an average European ancestry of 21.9%, again with significant variation between individuals.[186] Bryc et al. (2009) note that populations from other parts of the continent may also constitute adequate proxies for the ancestors of some African-American individuals; namely, ancestral populations from Guinea Bissau, Senegal and Sierra Leone in West Africa and Angola in Southern Africa.[187]

Altogether, genetic studies suggest that African Americans are a genetically diverse people. According to DNA analysis led in 2006 by Penn State geneticist Mark D. Shriver, around 58 percent of African Americans have at least 12.5% European ancestry (equivalent to one European great-grandparent and his/her forebears), 19.6 percent of African Americans have at least 25% European ancestry (equivalent to one European grandparent and his/her forebears), and 1 percent of African Americans have at least 50% European ancestry (equivalent to one European parent and his/her forebears).[13][193] According to Shriver, around 5 percent of African Americans also have at least 12.5% Native American ancestry (equivalent to one Native American great-grandparent and his/her forebears).[194][195] Research suggests that Native American ancestry among people who identify as African American is a result of relationships that occurred soon after slave ships arrived in the American colonies, and European ancestry is of more recent origin, often from the decades before the Civil War.[196]

Africans bearing the E-V38 (E1b1a) likely traversed across the Sahara, from east to west, approximately 19,000 years ago.[197] E-M2 (E1b1a1) likely originated in West Africa or Central Africa.[198] According to a Y-DNA study by Sims et al. (2007), the majority (60%) of African Americans belong to various subclades of the E-M2 (E1b1a1, formerly E3a) paternal haplogroup. This is the most common genetic paternal lineage found today among West/Central African males, and is also a signature of the historical Bantu migrations. The next most frequent Y-DNA haplogroup observed among African Americans is the R1b clade, which around 15% of African Americans carry. This lineage is most common today among Northwestern European males. The remaining African Americans mainly belong to the paternal haplogroup I (7%), which is also frequent in Northwestern Europe.[199]

According to an mtDNA study by Salas et al. (2005), the maternal lineages of African Americans are most similar to haplogroups that are today especially common in West Africa (>55%), followed closely by West-Central Africa and Southwestern Africa (<41%). The characteristic West African haplogroups L1b, L2b,c,d, and L3b,d and West-Central African haplogroups L1c and L3e in particular occur at high frequencies among African Americans. As with the paternal DNA of African Americans, contributions from other parts of the continent to their maternal gene pool are insignificant.[200]

Formal political, economic and social discrimination against minorities has been present throughout American history. Leland T. Saito, Associate Professor of Sociology and American Studies & Ethnicity at the University of Southern California, writes, "Political rights have been circumscribed by race, class and gender since the founding of the United States, when the right to vote was restricted to White men of property. Throughout the history of the United States race has been used by Whites for legitimizing and creating difference and social, economic and political exclusion."[65]

Although they have gained a greater degree of social equality since the civil rights movement, African Americans have remained stagnant economically, which has hindered their ability to break into the middle class and beyond. As of 2020, the racial wealth gap between Whites and Blacks remains as large as it was in 1968, with the typical net worth of a White household equivalent to that of 11.5 black households.[201] Despite this, African Americans have increased employment rates and gained representation in the highest levels of American government in the postcivil rights era.[202] However, widespread racism remains an issue that continues to undermine the development of social status.[202][203]

One of the most serious and long-standing issues within African-American communities is poverty. Poverty is associated with higher rates of marital stress and dissolution, physical and mental health problems, disability, cognitive deficits, low educational attainment, and crime.[204] In 2004, almost 25% of African-American families lived below the poverty level.[137] In 2007, the average income for African Americans was approximately $34,000, compared to $55,000 for Whites.[205] African Americans experience a higher rate of unemployment than the general population.[206]

African Americans have a long and diverse history of business ownership. Although the first African-American business is unknown, slaves captured from West Africa are believed to have established commercial enterprises as peddlers and skilled craftspeople as far back as the 17th century. Around 1900, Booker T. Washington became the most famous proponent of African-American businesses. His critic and rival W. E. B. DuBois also commended business as a vehicle for African-American advancement.[207]

Forty percent of prison inmates are African American.[208] African American males are more likely to be killed by police when compared to other races.[209] This is one of the factors that led to the creation of the Black Lives Matter movement in 2013.[210] A historical issue in the U.S. where women have weaponized their White privilege in the country by reporting on Black people, often instigating racial violence,[211][212] White women calling the police on Black people became widely publicized in 2020.[213][214] In African-American culture there is a long history of calling a meddlesome White woman by a certain name, while The Guardian called 2020 "the year of Karen".[215]

Although in the last decade Black youth have had lower rates of cannabis (marijuana) consumption than Whites of the same age, they have disproportionately higher arrest rates than Whites: in 2010, for example, Blacks were 3.73 times as likely to get arrested for using cannabis than Whites, despite not significantly more frequently being users.[216][217]

After over 50 years, marriage rates for all Americans began to decline while divorce rates and out-of-wedlock births have climbed.[218] These changes have been greatest among African Americans. After more than 70 years of racial parity Black marriage rates began to fall behind Whites.[218] Single-parent households have become common, and according to U.S. census figures released in January 2010, only 38 percent of Black children live with both their parents.[219]

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Recommendation and review posted by Bethany Smith

For Immediate Release: December 16, 2022

Espaol

Today, the U.S. Food and Drug Administration approved Adstiladrin (nadofaragene firadenovec-vncg), a non-replicating (cannot multiply in human cells) adenoviral vector based gene therapy indicated for the treatment of adult patients with high-risk Bacillus Calmette-Gurin (BCG)-unresponsive non-muscle-invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors.

This approval provides healthcare professionals with an innovative treatment option for patients with high-risk non-muscle invasive bladder cancer that is unresponsive to BCG therapy, said Peter Marks, M.D., Ph.D., director of the FDAs Center for Biologics Evaluation and Research. Todays action addresses an area of critical need. The FDA remains committed to facilitating the development and approval of safe and effective cancer treatments.

Bladder cancer, one of the more common forms of cancer, is a disease in which malignant (cancer) cells form a tumor in the tissues of the bladder. These abnormal cells can invade and destroy normal body tissue. Over time, the abnormal cells can also metastasize (spread) through the body. Most newly diagnosed bladder cancers (75% to 80%) are classified as NMIBC a type of cancer that has grown through the lining of the bladder but hasnt yet invaded the muscle layer. This type of cancer is associated with high rates of recurrence (between 30 to 80%) and the risk of progression to invasive and metastatic cancer.

Treatment and care of patients with high-risk NMIBC, including those with carcinoma in situ, or CIS (abnormal cancer cells found in the place where they first formed and that have not spread to nearby tissue), often involves removing the tumor and the use of BCG to reduce the risk that the cancer will recur. Few effective treatment options exist for patients who develop BCG-unresponsive disease. The failure to achieve a complete response, or the disappearance of all signs of cancer as seen on cystoscopy, biopsied tissue, and urine, is associated with an increased risk of death or a disease-worsening event. Without treatment, the cancer can invade, damage tissues and organs, and spread through the body. According to the Centers for Disease Control and Prevention, about 57,000 men and 18,000 women are diagnosed with bladder cancer annually, and roughly 12,000 men and 4,700 women die from the disease each year in the United States.

The safety and effectiveness of Adstiladrin was evaluated in a multicenter clinical study that included 157 patients with high-risk BCG-unresponsive NMIBC, 98 of whom had BCG-unresponsive CIS with or without papillary tumors and could be evaluated for response. Patients received Adstiladrin once every three months for up to 12 months, or until unacceptable toxicity to therapy or recurrent high-grade NMIBC. Overall, 51% of enrolled patients using Adstiladrin therapy achieved a complete response (the disappearance of all signs of cancer as seen on cystoscopy, biopsied tissue, and urine). The median duration of response was 9.7 months. Forty-six percent of responding patients remained in complete response for at least one year.

Adstiladrin is administered once every three months into the bladder via a urinary catheter. The most common adverse reactions associated with Adstiladrin included bladder discharge, fatigue, bladder spasm, urinary urgency, hematuria (presence of blood in urine), chills, fever, and painful urination. Individuals who are immunosuppressed, or immune-deficient should not come into contact with Adstiladrin.

This application was granted Priority Review, Breakthrough Therapy, and Fast Track designations.

The FDA granted approval of Adstiladrin to Ferring Pharmaceuticals A/S.

###

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The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nations food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

12/16/2022

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FDA Approves First Gene Therapy for the Treatment of High-Risk, Non ...

Recommendation and review posted by Bethany Smith

Rewind 2022: Innovative research, slew of crucial FDA approvals and new strides in genetic therapies became pivotal moments  The Financial Express

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Rewind 2022: Innovative research, slew of crucial FDA approvals and new strides in genetic therapies became pivotal moments - The Financial Express

Recommendation and review posted by Bethany Smith

Multipotent stem cell in the adult body

Adult stem cells are undifferentiated cells, found throughout the body after development, that multiply by cell division to replenish dying cells and regenerate damaged tissues. Also known as somatic stem cells (from Greek , meaning of the body), they can be found in juvenile, adult animals, and humans, unlike embryonic stem cells.

Scientific interest in adult stem cells is centered around two main characteristics. The first of which, being their ability to divide or self-renew indefinitely, and secondly, their ability to generate all the cell types of the organ from which they originate, potentially regenerating the entire organ from a few cells.[1] Unlike embryonic stem cells, the use of human adult stem cells in research and therapy is not considered to be controversial, as they are derived from adult tissue samples rather than human embryos designated for scientific research. The main functions of adult stem cells are to replace cells that are at risk of possibly dying as a result of disease or injury and to maintain a state of homeostasis within the cell.[2] There are three main methods to determine if the adult stem cell is capable of becoming a specialized cell.[2] The adult stem cell can be labeled in vivo and tracked, it can be isolated and then transplanted back into the organism, and it can be isolated in vivo and manipulated with growth hormones.[2] They have mainly been studied in humans and model organisms such as mice and rats.

A stem cell possesses two properties:

To ensure self-renewal, stem cells undergo two types of cell division (see Stem cell division and differentiation diagram). Symmetric division gives rise to two identical daughter stem cells, whereas asymmetric division produces one stem cell and one progenitor cell with limited self-renewal potential. Progenitors can go through several rounds of cell division before finally differentiating into a mature cell. It is believed that the molecular distinction between symmetric and asymmetric divisions lies in differential segregation of cell membrane proteins (such as receptors) and their associated proteins between the daughter cells.[5]

Under normal conditions, tissue stem cells divide slowly and infrequently. They exhibit signs of quiescence, or reversible growth arrest.[6] The niche the stem cell is found in plays a large role in maintaining quiescence.[6] Perturbed niches cause the stem cell to begin actively dividing again to replace lost or damaged cells until the niche is restored. In hematopoietic stem cells, the MAPK/ERK pathway and PI3K/AKT/mTOR pathway regulate this transition.[7] The ability to regulate the cell cycle in response to external cues helps prevent stem cell exhaustion, or the gradual loss of stem cells following an altered balance between dormant and active states. Infrequent cell divisions also help reduce the risk of acquiring DNA mutations that would be passed on to daughter cells.

Discoveries in recent years have suggested that adult stem cells might have the ability to differentiate into cell types from different germ layers. For instance, neural stem cells from the brain, which are derived from ectoderm, can differentiate into ectoderm, mesoderm, and endoderm.[8] Stem cells from the bone marrow, which is derived from mesoderm, can differentiate into liver, lung, GI tract and skin, which are derived from endoderm and mesoderm.[9] This phenomenon is referred to as stem cell transdifferentiation or plasticity. It can be induced by modifying the growth medium when stem cells are cultured in vitro or transplanting them to an organ of the body different from the one they were originally isolated from. There is yet no consensus among biologists on the prevalence and physiological and therapeutic relevance of stem cell plasticity. More recent findings suggest that pluripotent stem cells may reside in blood and adult tissues in a dormant state.[10] These cells are referred to as "Blastomere Like Stem Cells" (BLSCs)[11] and "very small embryonic like" (VSEL) stem cells, and display pluripotency in vitro.[10] As BLSCs and VSEL cells are present in virtually all adult tissues, including lung, brain, kidneys, muscles, and pancreas,[12] co-purification of BLSCs and VSEL cells with other populations of adult stem cells may explain the apparent pluripotency of adult stem cell populations. However, recent studies have shown that both human and murine VSEL cells lack stem cell characteristics and are not pluripotent.[13][14][15][16]

Stem cell function becomes impaired with age, and this contributes to progressive deterioration of tissue maintenance and repair.[17] A likely important cause of increasing stem cell dysfunction is age-dependent accumulation of DNA damage in both stem cells and the cells that comprise the stem cell environment.[17] (See also DNA damage theory of aging.)

Adult stem cells can, however, be artificially reverted to a state where they behave like embryonic stem cells (including the associated DNA repair mechanisms). This was done with mice as early as 2006[citation needed] with future prospects to slow down human aging substantially. Such cells are one of the various classes of induced stem cells.

Adult stem cell research has been focused on uncovering the general molecular mechanisms that control their self-renewal and differentiation.

Hematopoietic stem cells (HSCs) are stem cells that can differentiate into all blood cells.[21] This process is called haematopoiesis.[22] Hematopoietic stem cells are found in the bone marrow and umbilical cord blood.[23] The HSC are generally dormant when found in adults due to their nature.[24]

Mammary stem cells provide the source of cells for growth of the mammary gland during puberty and gestation and play an important role in carcinogenesis of the breast.[25] Mammary stem cells have been isolated from human and mouse tissue as well as from cell lines derived from the mammary gland. Single such cells can give rise to both the luminal and myoepithelial cell types of the gland and have been shown to have the ability to regenerate the entire organ in mice.[25]

Intestinal stem cells divide continuously throughout life and use a complex genetic program to produce the cells lining the surface of the small and large intestines.[26] Intestinal stem cells reside near the base of the stem cell niche, called the crypts of Lieberkuhn. Intestinal stem cells are probably the source of most cancers of the small intestine and colon.[27]

Mesenchymal stem cells (MSCs) are of stromal origin and may differentiate into a variety of tissues. MSCs have been isolated from placenta, adipose tissue, lung, bone marrow and blood, Wharton's jelly from the umbilical cord,[28] and teeth (perivascular niche of dental pulp and periodontal ligament).[29] MSCs are attractive for clinical therapy due to their ability to differentiate, provide trophic support, and modulate innate immune response.[28] These cells have the ability to differentiate into various cell types such as osteoblasts, chondroblasts, adipocytes, neuroectodermal cells, and hepatocytes.[30] Bioactive mediators that favor local cell growth are also secreted by MSCs. Anti-inflammatory effects on the local microenvironment, which promote tissue healing, are also observed. The inflammatory response can be modulated by adipose-derived regenerative cells (ADRC) including mesenchymal stem cells and regulatory T-lymphocytes. The mesenchymal stem cells thus alter the outcome of the immune response by changing the cytokine secretion of dendritic and T-cell subsets. This results in a shift from a pro-inflammatory environment to an anti-inflammatory or tolerant cell environment.[31][32]

Endothelial stem cells are one of the three types of multipotent stem cells found in the bone marrow. They are a rare and controversial group with the ability to differentiate into endothelial cells, the cells that line blood vessels as well as lymphatic vessels. Endothelial stem cells are an important aspect in the vascular network, even influencing the motion relating to white blood cells.

The existence of stem cells in the adult brain has been postulated following the discovery that the process of neurogenesis, the birth of new neurons, continues into adulthood in rats.[33] The presence of stem cells in the mature primate brain was first reported in 1967.[34] It has since been shown that new neurons are generated in adult mice, songbirds and primates, including humans. Normally, adult neurogenesis is restricted to two areas of the brain the subventricular zone, which lines the lateral ventricles, and the dentate gyrus of the hippocampal formation.[35] Although the generation of new neurons in the hippocampus is well established, the presence of true self-renewing stem cells there has been debated.[36] Under certain circumstances, such as following tissue damage in ischemia, neurogenesis can be induced in other brain regions, including the neocortex.

Neural stem cells are commonly cultured in vitro as so called neurospheres floating heterogeneous aggregates of cells, containing a large proportion of stem cells.[37] They can be propagated for extended periods of time and differentiated into both neuronal and glia cells, and therefore behave as stem cells. However, some recent studies suggest that this behaviour is induced by the culture conditions in progenitor cells, the progeny of stem cell division that normally undergo a strictly limited number of replication cycles in vivo.[38] Furthermore, neurosphere-derived cells do not behave as stem cells when transplanted back into the brain.[39]

Neural stem cells share many properties with haematopoietic stem cells (HSCs). Remarkably, when injected into the blood, neurosphere-derived cells differentiate into various cell types of the immune system.[40]

Olfactory adult stem cells have been successfully harvested from the human olfactory mucosa cells, which are found in the lining of the nose and are involved in the sense of smell.[41] If they are given the right chemical environment, these cells have the same ability as embryonic stem cells to develop into many different cell types. Olfactory stem cells hold the potential for therapeutic applications and, in contrast to neural stem cells, can be harvested with ease without harm to the patient. This means they can be easily obtained from all individuals, including older patients who might be most in need of stem cell therapies.

Hair follicles contain two types of stem cells, one of which appears to represent a remnant of the stem cells of the embryonic neural crest. Similar cells have been found in the gastrointestinal tract, sciatic nerve, cardiac outflow tract and spinal and sympathetic ganglia. These cells can generate neurons, Schwann cells, myofibroblast, chondrocytes and melanocytes.[42][43]

Multipotent stem cells with a claimed equivalency to embryonic stem cells have been derived from spermatogonial progenitor cells found in the testicles of laboratory mice by scientists in Germany[44][45][46] and the United States,[47][48][49][50] and, a year later, researchers from Germany and the United Kingdom confirmed the same capability using cells from the testicles of humans.[51] The extracted stem cells are known as human adult germline stem cells (GSCs)[52]

Multipotent stem cells have also been derived from germ cells found in human testicles.[53]

Adult stem cell treatments have been used for many years to successfully treat leukemia and related bone/blood cancers utilizing bone marrow transplants.[54] The use of adult stem cells in research and therapy is not considered as controversial as the use of embryonic stem cells, because the production of adult stem cells does not require the destruction of an embryo.

Early regenerative applications of adult stem cells has focused on intravenous delivery of blood progenitors known as Hematopetic Stem Cells (HSC's). CD34+ hematopoietic Stem Cells have been clinically applied to treat various diseases including spinal cord injury,[55] liver cirrhosis[56] and Peripheral Vascular disease.[57] Research has shown that CD34+ hematopoietic Stem Cells are relatively more numerous in men than in women of reproductive age group among spinal cord Injury victims.[58] Other early commercial applications have focused on Mesenchymal Stem Cells (MSCs). For both cell lines, direct injection or placement of cells into a site in need of repair may be the preferred method of treatment, as vascular delivery suffers from a "pulmonary first pass effect" where intravenous injected cells are sequestered in the lungs.[59] Clinical case reports in orthopedic applications have been published. Wakitani has published a small case series of nine defects in five knees involving surgical transplantation of mesenchymal stem cells with coverage of the treated chondral defects.[60] Centeno et al. have reported high field MRI evidence of increased cartilage and meniscus volume in individual human clinical subjects as well as a large n=227 safety study.[61][62][63] Many other stem cell based treatments are operating outside the US, with much controversy being reported regarding these treatments as some feel more regulation is needed as clinics tend to exaggerate claims of success and minimize or omit risks.[64]

The therapeutic potential of adult stem cells is the focus of much scientific research, due to their ability to be harvested from the parent body that is females during the delivery.[65][66][67] In common with embryonic stem cells, adult stem cells have the ability to differentiate into more than one cell type, but unlike the former they are often restricted to certain types or "lineages". The ability of a differentiated stem cell of one lineage to produce cells of a different lineage is called transdifferentiation. Some types of adult stem cells are more capable of transdifferentiation than others, but for many there is no evidence that such a transformation is possible. Consequently, adult stem therapies require a stem cell source of the specific lineage needed, and harvesting and/or culturing them up to the numbers required is a challenge.[68][69] Additionally, cues from the immediate environment (including how stiff or porous the surrounding structure/extracellular matrix is) can alter or enhance the fate and differentiation of the stem cells.[70]

Pluripotent stem cells, i.e. cells that can give rise to any fetal or adult cell type, can be found in a number of tissues, including umbilical cord blood.[71] Using genetic reprogramming, pluripotent stem cells equivalent to embryonic stem cells have been derived from human adult skin tissue.[72][73][74][75] Other adult stem cells are multipotent, meaning there are several limited types of cell they can become, and are generally referred to by their tissue origin (such as mesenchymal stem cell, adipose-derived stem cell, endothelial stem cell, etc.).[76][77] A great deal of adult stem cell research has focused on investigating their capacity to divide or self-renew indefinitely, and their potential for differentiation.[78] In mice, pluripotent stem cells can be directly generated from adult fibroblast cultures.[79]

In recent years, acceptance of the concept of adult stem cells has increased. There is now a hypothesis that stem cells reside in many adult tissues and that these unique reservoirs of cells not only are responsible for the normal reparative and regenerative processes but are also considered to be a prime target for genetic and epigenetic changes, culminating in many abnormal conditions including cancer.[80][81] (See cancer stem cell for more details.)

Adult stem cells express transporters of the ATP-binding cassette family that actively pump a diversity of organic molecules out of the cell.[82] Many pharmaceuticals are exported by these transporters conferring multidrug resistance onto the cell. This complicates the design of drugs, for instance neural stem cell targeted therapies for the treatment of clinical depression.

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Adult stem cell - Wikipedia

Recommendation and review posted by Bethany Smith

Stem cells have been the object of much excitement and controversy amongst both scientists and the general population. Surprisingly, though, not everybody understands the basic properties of stem cells, let alone the fact that there is more than one type of cell that falls within the stem cell category. Here, Ill lay out the basic concepts of stem cell biology as a background for understanding the stem cell research field, where it is headed, and the enormous promise it offers for regenerative medicine.

Fertilization of an egg cell by a sperm cell results in the generation of a zygote, the single cell that, upon a myriad of divisions, gives rise to our whole body. Because of this amazing developmental potential, the zygote is said to be totipotent. Along the way, the zygote develops into the blastocyst, which implants into the mothers uterus. The blastocyst is a structure comprising about 300 cells that contains two main regions: the inner cell mass (ICM) and the trophoblast. The ICM is made of embryonic stem cells (ES cells), which are referred to as pluripotent. They are able to give rise to all the cells in an embryo proper, but not to extra-embryonic tissues, such as the placenta. The latter originate from the trophoblast [].

Even though it is hard to pinpoint exactly when or by whom what we now call stem cells were first discovered, the consensus is that the first scientists to rigorously define the key properties of a stem cell were Ernest McCulloch and James Till. In their pioneering work in mice in the 1960s, they discovered the blood-forming stem cell, the hematopoietic stem cell (HSC) [2, 3]. By definition, a stem cell must be capable of both self-renewal (undergoing cell division to make more stem cells) and differentiation into mature cell types. HSCs are said to be multipotent, as they can still give rise to multiple cell types, but only to other types of blood cells (see Figure 1, left column). They are one of many examples of adult stem cells, which are tissue-specific stem cells that are essential for organ maintenance and repair in the adult body. Muscle, for instance, also possesses a population of adult stem cells. Called satellite cells, these muscle cells are unipotent, as they can give rise to just one cell type, muscle cells.

Therefore, the foundations of stem cell research lie not with the famous (or infamous) human embryonic stem cells, but with HSCs, which have been used in human therapy (such as bone marrow transplants) for decades. Still, what ultimately fueled the enormous impact that the stem cell research field has today is undoubtedly the isolation and generation of pluripotent stem cells, which will be the main focus of the remainder of the text.

Figure 1: Varying degrees of stem cell potency. Left: The fertilized egg (totipotent) develops into a 300-cell structure, the blastocyst, which contains embryonic stem cells (ES cells) at the inner cell mass (ICM). ES cells are pluripotent and can thus give rise to all cell types in our body, including adult stem cells, which range from multipotent to unipotent. Right: An alternative route to obtain pluripotent stem cells is the generation of induced pluripotent stem cells (iPS cells) from patients. Cell types obtained by differentiation of either ES cell (Left) or iPS cells (Right) can then be studied in the dish or used for transplantation into patients. Figure drawn by Hannah Somhegyi.

Martin Evans (Nobel Prize, 2007) and Matt Kauffman were the first to identify, isolate and successfully culture ES cells using mouse blastocysts in 1981 []. This discovery opened the doors to the creation of murine genetic models, which are mice that have had one or several of their genes deleted or otherwise modified to study their function in disease []. This is possible because scientists can modify the genome of a mouse in its ES cells and then inject those modified cells into mouse blastocysts. This means that when the blastocyst develops into an adult mouse, every cell its body will have the modification of interest.

The desire to use stem cells unique properties in medicine was greatly intensified when James Thomson and collaborators first isolated ES cells from human blastocysts []. For the first time, scientists could, in theory, generate all the building blocks of our body in unlimited amounts. It was possible to have cell types for testing new therapeutics and perhaps even new transplantation methods that were previously not possible. Yet, destroying human embryos to isolate cells presented ethical and technical hurdles. How could one circumvent that procedure? Sir John Gurdon showed in the early 1960s that, contrary to the prevalent belief back then, cells are not locked in their differentiation state and can be reverted to a more primitive state with a higher developmental potential. He demonstrated this principle by injecting the nucleus of a differentiated frog cell into an egg cell from which the nucleus had been removed. (This is commonly known as reproductive cloning, which was used to generate Dolly the Sheep.) When allowed to develop, this egg gave rise to a fertile adult frog, proving that differentiated cells retain the information required to give rise to all cell types in the body. More than forty years later, Shinya Yamanaka and colleagues shocked the world when they were able to convert skin cells called fibroblasts into pluripotent stem cells by altering the expression of just four genes []. This represented the birth of induced pluripotent stem cells, or iPS cells (see Figure 1, right column). The enormous importance of these findings is hard to overstate, and is perhaps best illustrated by the fact that, merely six years later, Gurdon and Yamanaka shared the Nobel Prize in Physiology or Medicine 2012 [].

Since the generation of iPS cells was first reported, the stem cell eld has expanded at an unparalleled pace. Today, these cells are the hope of personalized medicine, as they allow one to capture the unique genome of each individual in a cell type that can be used to generate, in principle, all cell types in our body, as illustrated on the right panel of Figure 1. The replacement of diseased tissues or organs without facing the barrier of immune rejection due to donor incompatibility thus becomes approachable in this era of iPS cells and is the object of intense research [].

The first proof-of-principle study showing that iPS cells can potentially be used to correct genetic diseases was carried out in the laboratory of Rudolf Jaenisch. In brief, tail tip cells from mice with a mutation causing sickle cell anemia were harvested and reprogrammed into iPS cells. The mutation was then corrected in these iPS cells, which were then differentiated into blood progenitor cells and transplanted back into the original mice, curing them []. Even though iPS cells have been found not to completely match ES cells in some instances, detailed studies have failed to find consistent differences between iPS and ES cells []. This similarity, together with the constant improvements in the efficiency and robustness of generating iPS cells, provides bright prospects for the future of stem cell research and stem cell-based treatments for degenerative diseases unapproachable with more conventional methods.

Leonardo M. R. Ferreira is a graduate student in Harvard Universitys Department of Molecular and Cellular Biology

[] Stem Cell Basics: http://stemcells.nih.gov/info/basics/Pages/Default.aspx

[] Becker, A. J., McCulloch, E.A., Till, J.E. Cytological demonstration of the clonal nature of spleen colonies derived from transplanted mouse marrow cells. Nature 1963. 197: 452-4

[] Siminovitch, L., McCulloch, E.A., Till, J.E. The distribution of colony-forming cells among spleen colonies. J Cell Comp Physiol 1963, 62(3): 327-336

[] Evans, M. J. and Kaufman, M. Establishment in culture of pluripotential stem cells from mouse embryos. Nature 1981, 292: 151156

[] Simmons, D. The Use of Animal Models in Studying Genetic Disease: Transgenesis and Induced Mutation. Nature Education 2008,1(1):70

[] Thomson, J. A. et al. Embryonic stem cell lines derived from human blastocysts. Science 1998, 282(5391): 1145-1147

[] Takahashi, K. and Yamanaka S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell 2006. 126(4): 663-76

[] The Nobel Prize in Physiology or Medicine 2012:

[] Ferreira, L.M.R. and Mostajo-Radji, M.A. How induced pluripotent stem cells are redefining personalized medicine. Gene 2013. 520(1): 1-6 [] Hanna J. et al. Treatment of sickle cell anemia mouse model with iPS cells generated from autologous skin. Science 2007. 318: 1920-1923

[] Yee,J.Turning Somatic Cells into Pluripotent Stem Cells.Nature Education 2010.3(9):25

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Stem cells: a brief history and outlook - Science in the News

Recommendation and review posted by Bethany Smith

Sometimes patients or my students ask me, What are the best stem cells? what information are they looking for?

I think they often are looking for the most powerful stem cells so perhaps they should be asking, What are totipotent stem cells?

Other times it seems what patients specifically want to know is what might be the best stem cells for their particular condition. The answer to that is, of course, going to depend on many factors. Im a long-time stem cell biologist so I can give them that perspective, but this should be something they discuss primarily with their physician

Todays post focuses on the question of what totipotent cells are all about and addresses more specific questions about them, including why so far there seem to be fewer clinical applications for them as compared to most other stem cell types.

Every year I give a lecture here at UC Davis School of Medicine for my medical students about stem cells. Some students seem especially fascinated by totipotent stem cells. Their interest probably is piqued because these are the most powerful cells. For example, recently a student asked me, Professor Knoepfler, are there any types of cells that totipotent stem cells cannot make?

As their name implies, totipotent stem cells are entirely potent or all-powerful from a cellular perspective. What that means is that these cells can make any other cells in the developing body in utero as well as the special cells and tissues needed during development. Those latter structures include placenta and umbilical cord.

For example, the classic kind of totipotent cell is the fertilized egg, also called a zygote. In the animal world, a newly pregnant bear has a zygote that will develop in its uterus that is totipotent. That bears zygote can make the actual new eventual baby bear including all of the several hundred kinds of bear cells and also the placenta and umbilical cord that the fetal bear will need in utero. The same goes for a totipotent human zygote. Also the zygote of a dog, cat, and so on.

You can see examples of real human totipotent stem cells in the image above of early human embryos at the 2- and 4-cell stages at the top of the figure. This material is excerpted from my book on stem cells, Stem Cells: An Insiders Guide.

Interestingly, as normal early embryo development proceeds and the fertilized egg/zygote goes from just being that one cell to divide to make 2 cells and 4 cells and then 8 cells, it is thought that all of the cells are still totipotent. What this means is that if, for example, an 8-cell human embryo for whatever reason breaks into 2 pieces of 3 and 5 cells or 1 and 7 cells, in many cases those separate totipotent cells will go on to make 2 separate embryos and ultimately babies. Congrats, you have twins. Each twin in that case can also develop their own umbilical cord and placenta too, although they sometimes share. This is all possible because these very early embryonic cells are totipotent.

After the 8-cell stage or so, the embryonic cells start to lose their totipotency and become either multipotent (can make only a few types of cells) or pluripotent stem cells. The latter are the second most powerful stem cells so lets briefly talk about them next.

Pluripotent stem cells are almost as flexible as those with totipotency, but not quite. See video above. The pluripotent cells inside a developing early embryo of a specific species can make all the cells that will become the actual body of a person, a bear, or many other animals, again depending on which animal is involved. These pluripotent cells cannot, however, make the placenta or umbilical cord. This one thing that they cannot do is what makes them different than totipotent cells.

Pluripotent stem cells include some of the most well known kinds of stem cells out there including embryonic stem cells (ES cells) and induced pluripotent stem cells, also known as IPS cells.

Pluripotent stem cells are often grown in labs and differentiated into a wide variety of other types of more specialized cells such as neurons, muscle cells including beating heart muscle (see video below), lung cells and more. Some have claimed that certain IPS cells can be totipotent but that is still being debated.

Both ES cells and IPS cells can also be made into what are called organoids, which are miniature versions of normal organs. For instance, my lab makes brain organoids regularly from IPS cells. Organoids are a very powerful technology in many ways so as being a way to find new drugs for specific diseases.

I have not heard yet of specific clinical applications for these most powerful stem cells. On the global clinical trial database Clinicaltrials.gov I found just a single trial that mentions the word totipotent and it isnt related to using such cells as a treatment.

Most of the clinical potential seems to be focused on adult stem cells as well as IPS cells and ES cells. One could imagine that totipotent stem cells will be useful for research on human development and potentially infertility.

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What are totipotent stem cells & what can they do? - The Niche

Recommendation and review posted by Bethany Smith

William W. Li MD writes in his book Eat to Beat Disease, Your immune cells are regenerated every seven days, so if your stem cells disappeared, youd likely die of an infection soon after. However, you can increase your stem cells by taking in the right foods.

We develop from stem cells. When the fathers sperm meets the mothers egg, a fertilized egg is formed. It continues to divide and by day three to five develops into an embryoconsisting of about 150 stem cells in the mothers uterus. Later, these stem cells in the embryo continue to split and form various tissues and organs in the human body. There are more than two hundred different kinds of cells in the human body, all of which grow from stem cells.

Stem cells are not only present at the embryonic development stage. When babies are born, they carry a large number of stem cells within their bodies. The average person has about 37.2 trillion cells, including about 750 million stem cells, which account for 0.002 percent of the total cells (Page 27, Eat to Beat Disease).These stem cells are stored in various parts of the body, ready to regenerate or repair body tissues and organs.

Dr. William Li, the author of Eat to Beat Disease, president of the Angiogenesis Foundation and a Harvard-trained medical doctor, elaborated on the role of stem cells in an interview with The Epoch Times. Li said stem cells are mainly stored in the bone marrow, though also found in the bodys fat, skin, hair follicles, and even in the heart. He made an analogy: The human body retains and dispatches stem cells just like we keep unused paint in the garage during renovation, which is ready for use if necessary, say, for wall repair someday.

As all human tissues and organs get renewed constantly, stem cells play a key role in this process. Specifically, we need them to produce new skin to replace damaged skin cells; and to replace damaged cells on the surface of the intestine. Besides, hematopoietic stem cells divide and replace those blood cells that are damaged while operating in the circulatory system. They, too, evolve into types of white and red blood cells, and more.

Interestingly, our small intestine is renewed every two to four days; our lungs and stomach every eight days; our skin every two weeks; our red blood cells every four months; our fat cells every eight years; and our skeleton every ten years. Dr. Li cited an example: The bodys immune cells regenerate every seven days. Therefore, if a persons relevant stem cells disappear, he or she could die soon from an infection (Page 26, Eat to Beat Disease).

In addition, he quoted a Japanese story of nuclear radiation to highlight the critical life-supporting role of stem cells in his book. During the Second World War, the atomic bombardments in the cities of Hiroshima and Nagasaki caused about 200,000 deaths. Afterward, a second wave of deaths hit certain survivors because the ability of their bone marrow to make stem cells had been destroyed due to exposure to radiation. Further, in cancer treatment, chemotherapy and radiotherapy affect the survival of stem cells while destroying cancer cells, putting patients in tremendous pain and challenges (page 26, Eat to Beat Disease).

The human body is born with mechanisms that collaborate seamlessly and automatically to keep life going.

Stem cells come into play when we need to repair cells that are damaged due to various diseases and injuries or replace dysfunctional cells. Figuratively, stem cells are sentinels in the body that are always watching out for health needs and will at times appear at designated locations in preparation for rescue operations.

Dr. Li added that a damaged organ or site in need of repair releases a certain protein that acts as a messenger, calling on stem cells stored in the bone marrow. Then, the cells will respond to the call by leaving the bone marrow and entering the bloodstream. This scenario is almost like a group of bees swarming out of their hive. Together with the blood, stem cells flow to the injured tissue and land at their precise destination. Upon arriving, they begin to divide or transform themselves to regenerate organ or tissue cells.

As is well known, the liver is regenerative. It is the repair and regeneration function of stem cells that explains exactly why the liver can grow back into its original status, even if up to 75 percent of it is removed during surgery.

Likewise, our heart depends on stem cells to keep regenerating constantly, though the rebirth rate is affected by age. A 20-year-old gets about one percent of his or her heart cells renewed every year. However, this rate slows down as he or she gets older. At 75, that person gets only 0.3 percent of the heart cells renewed each year.

Reading that, you may wonder: Will stem cells eventually be depleted as they keep flowing out of the bone marrow? Dr. Lis answer is, Stem cells are capable of regenerating themselves and replenishing their stores in the bone marrow.

Although stem cells in healthy people are equipped with self-replication and replenishment mechanisms, Dr. Li emphasized that there are three scenarios that impair their regenerative and repairing capacity, directly affecting the quality of a persons life.

When smokers inhale cigarette smoke, that leads to a lack of oxygen in the body, which will recruit stem cells into the bloodstream. Habitual smoking keeps consuming the stem cells stored in the bone marrow. A study has shown that the remaining stem cells in smokers bodies have a 75 percent drop in their self-reproduction ability and a 38 percent reduction in their involvement in regeneration. Besides active smoking, Dr. Li added, passive inhalation of secondhand smoke and exposure to heavily polluted air can be equally harmful to stem cells.

Addiction to alcohol kills stem cells. Like smoking, drinking alcohol causes stem cells to be constantly pulled out of the bone marrow into the circulatory system. Meanwhile, stem cells become damaged, negatively affecting their regeneration abilities, according to Dr, Li. Furthermore, drinking alcohol impairs the activity of stem cells in the brain, which in turn affects the hippocampusresponsible for short- and long-term memory.

Both hyperlipidemia and hyperglycemia impair stem cells. Dr. Li says in his bookthat bad cholesterol in the blood, known as low-density lipoprotein (LDL), damages liver cells while good cholesterol, known as high-density lipoprotein (HDL), delays the death of endothelial progenitor cellsa type of stem cell in the blood that maintains the health of blood vessels and repairs their inner layers.

Additionally, diabetes is a stem cell killer. Diabetics are likely to have 47 percent fewer stem cells than normal, with the remaining part of stem cells unable to function properly. This is because hyperglycemia affects stem cell replication and migration, as well as the secretion of survival factors.

Dr. Li also mentioned that high levels of stress and high salt levels in the blood also harm stem cells.

Dr. Li gives advice on how to protect the activity of stem cells in the body and actively mobilize them to repair the body from a dietary perspective. Human experiments have confirmed the following foods, which can increase the number of stem cells.

Dark chocolate contains flavanols that have biological properties. Researchers at the University of California recruited patients with coronary artery disease in a 30-day controlled trial. One group drank hot chocolate low in flavanols (only nine mg per serving) twice a day, and the other group drank hot chocolate high in flavanols (containing 375 mg per serving) twice a day. The results were surprising: the group with high-level flavanol had twice as many stem cells in their blood as that with low-level flavanol, and the formers blood flow improved twice as much as the latter.

A team of Italian researchers divided patients who had mild to moderate hypertension but did not receive medication into two groups. Group A drank plain black tea without sugar and milk twice a day while group B drank other beverages twice a day. One week later, blood tests showed the number of endothelial progenitor cells in the blood in the black-tea group rose by 56 percent, with an improved ability of blood vessel widening.

A Mediterranean diet rich in virgin olive oil is effective in boosting stem cells. A 4-week control study published in The American Journal of Clinical Nutrition showed that compared to those on a diet high in saturated fat or a diet low in fat but high in carbohydrates, those on a Mediterranean diet rich in virgin olive oil showed a significant doubling in their endothelial progenitor cell count in the blood.

Flora Zhao is a health reporter for The Epoch Times. Have a tip? Email her at: flora.zhao@epochtimes.nyc

Health 1+1 is the most authoritative Chinese medical and health information platform overseas. Every Tuesday to Saturday from 9:00 a.m. to 10:00 a.m. EST on TV and online, the program covers the latest on the coronavirus, prevention, treatment, scientific research and policy, as well as cancer, chronic illness, emotional and spiritual health, immunity, health insurance, and other aspects to provide people with reliable and considerate care and help. Online: EpochTimes.com/HealthTV: NTDTV.com/live

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Certain Foods Discovered to Increase Stem Cells, Cell Regeneration

Recommendation and review posted by Bethany Smith

Skin cells are the basic building blocks of the skin; a large, complex organ forms a protective barrier between our insides and the external environment. The most common type of skin cell is the keratinocyte, whose primary function is to form a tough, waterproof layer against UV radiation, harmful chemicals, and infectious agents.

However, the skin also contains highly specialized cells with important immunological, photoprotective, and sensory functions. The term skin cell, therefore, may refer to any of the four major types of cells found in the epidermis (or outer layer) of the skin.

The skin is the largest organ of the human body and has a range of vital functions in supporting survival. The primary function of the skin is to form a physical barrier between the internal environment of an organism and the outside world. This protects internal organs and structures from injury and infection.

The skin also helps to maintain homeostasis by preventing water loss and regulating body temperature. It protects organisms from the damaging effects of UV light and helps to produce vitamin D when exposed to the sun. Finally, the skin functions as a sensory organ, allowing us to perceive touch, temperature changes, and pain.

The skin can perform all of these functions thanks to the highly specialized cells that make up the epidermis (the outermost layer of the skin).

The skin consists of three major layers; the epidermis, the dermis, and the hypodermis (AKA the subcutaneous layer).

The epidermis is the outermost layer of the skin. This waterproof barrier protects the underlying skin layers and other internal structures from injury, UV damage, harmful chemicals, and infections by pathogens such as bacteria, viruses, and fungi. The thickness of the epidermis varies between different parts of the body. In the thin, delicate skin of the eyelids, the epidermis is only around 0.5 mm thick, whereas the more resilient skin of the palms and feet is about 1.5 mm thick.

The dermis is found directly beneath the epidermis and is the thickest of the three skin layers. This layer contains a complex network of specialized structures, including blood vessels, lymph vessels, sweat glands, hair follicles, sebaceous glands, and nerve endings. It also contains collagen and elastin, which are structural proteins that make skin strong and flexible. The main functions of the dermis are to deliver oxygen and nutrients to the epidermis and to help regulate body temperature.

The hypodermis (or subcutaneous layer) is the fatty, innermost layer of the skin. It consists mainly of fat cells and functions as an insulating layer that helps to regulate internal body temperature. The hypodermis also acts as a shock absorber that protects the internal organs from injury.

The term skin cell may refer to any of the four main types of cells found in the epidermis. These are keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Each type of skin cell has a unique role that contributes to the overall structure and function of the skin.

Keratinocytes are the most abundant type of skin cell found in the epidermis and account for around 90-95% of the epidermal cells.

They produce and store a protein called keratin, a structural protein that makes skin, hair, and nails tough and waterproof. The main function of the keratinocytes is to form a strong barrier against pathogens, UV radiation, and harmful chemicals, while also minimizing the loss of water and heat from the body.

Keratinocytes originate from stem cells in the deepest layer of the epidermis (the basal layer) and are pushed up through the layers of the epidermis as new cells are produced. As they migrate upwards, keratinocytes differentiate and undergo structural and functional changes.

The stratum basal (or basal layer) is where keratinocytes are produced by mitosis. Cells in this layer of the epidermis may also be referred to as basal cells. As new cells are continually produced, older cells are pushed up into the next layer of the epidermis; the stratum spinosum.

In the stratum spinosum (or squamous cell layer), keratinocytes take on a spiky appearance and are known as spinous cells or prickle cells. The main function of this epidermal layer is to maintain the strength and flexibility of the skin.

Next, the keratinocytes migrate to the stratum granulosum. Cells in this layer are highly keratinized and have a granular appearance. As they move closer to the surface of the skin, keratinocytes begin to flatten and dry out.

By the time keratinocytes enter the stratum lucidum (AKA the clear layer), they have flattened and died, thanks to their increasing distance from the nutrient-rich blood supply of the stratum basal. The stratum corneum (the outermost layer of the epidermis) is composed of 10 30 layers of dead keratinocytes that are constantly shed from the skin. Keratinocytes of the stratum corneum may also be referred to as corneocytes.

Melanocytes are another major type of skin cell and comprise 5-10% of skin cells in the basal layer of the epidermis.

The main function of melanocytes is to produce melanin, which is the pigment that gives skin and hair its color. Melanin protects skin cells against harmful UV radiation and is produced as a response to sun exposure. In cases of continuous sun exposure, melanin will accumulate in the skin and cause it to become darker i.e., a suntan develops.

Langerhans cells are immune cells of the epidermis and play an essential role in protecting the skin against pathogens. They are found throughout the epidermis but are most concentrated in the stratum spinosum.

Langerhans cells are antigen-presenting cells and, upon encountering a foreign pathogen, will engulf and digest it into protein fragments. Some of these fragments are displayed on the surface of the Langerhans cell as part of its MHCI complex and are presented to nave T cells in the lymph nodes. The T cells are activated to launch an adaptive immune response, and effector T cells are deployed to find and destroy the invading pathogen.

Merkel cells are found in the basal layer of the epidermis and are especially concentrated in the palms, finger pads, feet, and undersides of the toes. They are positioned very close to sensory nerve endings and are thought to function as touch-sensitive cells. Merkel cells allow us to perceive sensory information (such as touch, pressure, and texture) from our external environment.

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Skin Cell - The Definitive Guide | Biology Dictionary

Recommendation and review posted by Bethany Smith

Cryonics is the practice of freezing the body at subzero temperatures, with the hope that future technology will be able to bring it back to life. Many companies have begun offering this service, but there is little to no evidence that cryo-preserved bodies can be revived.

Who doesnt want to live as long as they can? If given the chance, some people would want to live forever!

Humans put a lot of effort into extending our individual stays on this planet. Eating greens, running, intermittent fasting, juice cleansing, turning into a teetotaler the list goes on and on. Unless you live in one of the five blue zones on Earth, where people tend to live the longest, hitting the century mark in life seems to be one hell of a challenging task. No matter how careful you are, disease will eventually come knocking at the door.

However, what if theres a way to cheat nature? What is there was a path to immortality?

For those terrified of aging and death, cryonics might be the answer. Cryonics claims to be the key to immortality. It can help you resume your life after rising from the dead, but not in the way vampires do.

So what is the science behind cryonics? Is it a sham or a scientific breakthrough?

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Imagine that youre dying due to a disease with no cure. Doctors are working to find a cure, but you just dont have enough time before it ends your life. What if you could pause the process of dying until medical research caught up with your disease and a cure became available?

This is where cryonics appears as a ray of hope for your dying body. Cryonics is the practice of freezing the body at subzero temperatures, in the hopes that future technology can bring it back to life. It sounds like a good concept for a sci-fi movie, doesnt it? Thats because movies like Passenger and Vanilla Sky have played with this very appealing idea.

Given its experimental nature and the advanced equipment required for the process, it probably wont come as a surprise that cryopreservation can cost a fortune. Then again, whats the use of all that money if it cant buy you a life?

Assuming that you have the millions of dollars required to extend your life after death, how exactly will your body be frozen?

Once youve been declared legally dead, cryopreservation can begin.

To keep the brain tissues protected, blood circulation and breathing are temporarily restored by CPR and an oxygen mask until the specialized medications can be injected into the system. A medical team then cools the body by placing it in an ice water bath, and injecting anticoagulants to prevent the blood from clotting. Within 24 hours of death, the body is taken to the cryopreservation center where the body is safely preserved.

When you fill the ice tray with water and keep it in the freezer, you have probably observed that water expands upon freezing. This is because the water molecules form a hexagonal crystalline structure when frozen, which takes up more space than liquid water.

The average human body is made of 60% water. If not frozen correctly, the water present in our cells would turn into ice. Ice expands in volume and forms crystal lattices, putting pressure on cell walls and blood vessels, which can cause the cells and tissues to crack open. If the ultimate goal of cryonics is to restore your body to a healthy living condition at some time in the future, a body full of ruptured cells wont be very helpful. This is where a process known as Vitrification comes to the rescue. Vitrification allows the body to be frozen in time.

Vitrification is the process of turning a substance into glass, a non-crystalline amorphous solid. The process is done by introducing anti-freeze chemicals known as cryoprotectants into the bloodstream. Glycerol and dimethyl sulfoxide (DMSO) are common cryoprotectants that are used before starting the freezing process.

Cryoprotectants prevent the formation of ice crystals by increasing intracellular solute concentration. This allows the water molecules to be locked in place without turning into ice crystals, even after being frozen below -100 C. No ice formation means no structural damage to the bodys cells. However, with the increase in the concentration of cryoprotectants in the body, the chances of toxicity also increase.

Once your body has been safely vitrified, it will be lowered into a cryopreservation tank, i.e., your new icy home. For the foreseeable future, your body will be kept at a toasty -196C with the help of liquid nitrogen. This will protect the body from any deterioration for potentially thousands of years so to speak.

And then?

Wait and hope that science finds a way to bring you back.

The legitimacy of cryonics is one of the main ethical concerns for practitioners, opponents, and potential people popsicles. There is no proof or guarantee that the body can bounce back to health after being frozen for years. Whos to say that resurrection after being cryogenically frozen is nothing less than a false hope? Freezing your body in the hopes of scientific advancement that will help resume life sounds a lot like science fiction.

Some argue that cryonics may also promote a trend of euthanasia, as people might prefer cryopreservation while their body remains untouched by disease and old age.

Lets consider a scenario where we find a way to bring a person back to a healthy living condition. Will the cryopreserved person retain their original personality and identity? Theres no guarantee that cryopreservation wont permanently alter brain function. Additionally, after waking up after thousands of years, people would find themselves alone, without any family or friends. The prospect of being alone can be frightening for some. Another main concern would be that such resurrected beings would further add to the population on Earth.

A century ago, a trip to outer space was an unimaginable idea. Now, astronauts frequently fly to the International Space Station, so clearly, no one can truly know what the future holds. There is a possibility that coming back to life after being cryogenically frozen for years is the real deal. Or maybe cryonics is nothing but a fantastic notion.

However, there are a few possibilities that would make cryonically freezing someone a failure. If the body is damaged before or after cryopreservation, it will be impossible to revive the brain function of that person. The most disheartening possibility, of course, is that even in the future, science may never be able to fully revive a cryopreserved body.

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Is It Possible To Freeze People And Bring Them Back To Life?

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On December 15, 1966, animation legend Walt Disney died from complications of lung cancer, for which he had undergone surgery just over a month earlier. A private funeral was held the next day, and on December 17, his body was cremated and interred at Forest Lawn Memorial Park in Glendale, California. But while Disney undoubtedly lives on through the legacy of the beloved feature films and theme parks that comprise much of his lifes work, shortly after his death, a rumor began to circulate that he might be living on in a more literal sense as well with his body suspended in a frozen state and buried deep beneath the Pirates of the Caribbean ride at Disneyland in Anaheim, California, awaiting the day when medical technology would be advanced enough to reanimate the animator.

Over the years, proponents of this seemingly absurd rumor have cited the secrecy surrounding Disneys death and burial as evidence of its veracity. They claim that news of his passing was intentionally delayed in order to give his handlers time to place his body in cryonic suspension and that both his funeral and the actual location of his burial plot have been kept secret as a means of further concealing the truth of his interment.

Disneys lifelong interest in the future, projects such as his EPCOT Center (Experimental Prototype Community of Tomorrow) and the technical innovations for which he was known throughout his career would no doubt have lent the rumor a certain air of truth, while a Time magazine article about the cryonic freezing of a 73-year-old psychology professor also lent its weight.

The assertions of two separate biographies of DisneyLeonard Moselys Disneys World (1986)and Marc Eliots Walt Disney: Hollywoods Dark Prince(1993)which claimed that an obsession with death led Disney to an interest in cryonics, surely did their part to perpetuate it through the years as well.

In a 1972 biography about her father, Disney's daughter Diane wrote that she doubted he had even heard of cryonics.

Photo: United Artists/Photofest

The exact origins of the rumor are uncertain, but it first appeared in print in a 1969 Ici Paris article in which a Disney executive attributed it to a group of disgruntled animators seeking to have a laugh at their late taskmaster employers expense.

Disneys daughter, Diane, wrote in a 1972 biography about her famous father that she doubted her father had even heard of cryonics. It has been further discredited by those pointing to the existence of signed legal documents that indicate Disney was in fact cremated and that his remains are interred in a marked plot (for which his estate paid $40,000) at Forest Lawn, the exact location of which is a matter of public record.

Further, by all accounts, Disney was known to be a very private man in life, making the quiet circumstances of his cremation and burial far from suspect, and the assertions in Moselys and Eliots biographies have been widely rejected as unfounded.

Yet despite the apparent lack of any credible evidence supporting a connection between it and Disney, the existence of cryonics is very much a reality. Since 1964, when Robert Ettinger published a work discussing the plausibility of freezing human beings for the purpose of bringing them back to life, a significant cryonics industry has developed in the United States.

Today,companies such as Suspended Animation Inc.,Cryonics Institute and Alcor Life Extension Foundation offer their clients the opportunity to have their bodies placed in a large metal tank in a state of deep freeze known as cryostasis, for the purpose of being restored to life and complete physical and mental health at a theoretical point in the future when medical science is advanced enough to do so.

According to reports, there are hundreds of people being kept in cryostasis at facilities around the country and thousands more that have already made arrangements for their own preservation. Following his death in 2004, baseball legend Ted Williams became the highest-profile person to date to be placed in cryostasis.

Cryonics is not without its detractors, however. Its science has been largely dismissed as fantastical. Still, its the futuristic stuff of science fiction that maybe even Disney himself would have appreciated.

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Is Walt Disney's Body Frozen? - Biography

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What is genetic testing?

Genetic testing is the use of medical tests to look for certain mutations (changes) in a persons genes. Many types of genetic tests are used today, and more are being developed.

Genetic testing can be used in many ways, but here well focus on how it is used to look for gene changes that are linked to cancer. (To learn about the role of genes and how mutations can lead to cancer, seeGenes and Cancer.)

Predictive genetic testing is a type of testing used to look for inherited gene mutations that might put a person at higher risk of getting certain kinds of cancer. This type of testing might be suggested for:

Most people (even people with cancer) do not need this type of genetic testing. Its usually done when family history suggests that a cancer may be inherited (see below) or if cancer is diagnosed at an uncommonly young age.

Genetic counseling and testing may be recommended for people who have hadcertain cancers or certain patterns of cancer in their family. If you have any of the following, you might consider talking to a genetic counselor about genetic testing:

If you are concerned about a pattern of cancer in your family, cancer youve had in the past, or other cancer risk factors, you may want to talk to a health care provider about whether genetic counseling and testing might be a good option for you.

You need to know your family history and what kinds of tests are available. For some types of cancer, no known mutations have been linked to an increased risk.

For more information on the types of cancer that may be linked to inherited genes,see Family Cancer Syndromes.

Genetic counseling gives you information that you and your family can use to make decisions about whether to get genetic testing (see below).

Genetic counselors have special training in the field of genetic counseling. Most are board-certified, and some might have a license depending on the rules in their state. Some doctors, advanced practice oncology nurses, social workers, and other health professionals may also provide genetic counseling, although they might have different levels of training in this field. If you are offered genetic counseling, its fair to ask about their training in this area.

Before and after genetic testing, genetic counseling can help you understand what your test results might mean, your risk of developing cancer, and what you can do about this risk. It is your decision to have testing and what steps you take after.

Its important to find out how useful genetic testing might be for you before you do it. Talk to your health care provider and plan on getting genetic counseling before the actual test. This will help you know what to expect. Yourcounselor can also tell you about the risks and benefits of the test, what the results might mean, and what your options are.

Your health care provider can refer you to a genetic counselor in your area, or you can find a list of certified genetic counselors on the website of the National Society of Genetic Counselors.

To learn more, see What Should I Know Before Getting Genetic Testing?

Sometimes after a person has been diagnosed with cancer, the doctor will order tests on a sample of cancer cells to look for certain gene or protein changes. These tests can sometimes give information on a persons outlook (prognosis), and they might also help tell if certain types of treatment may be useful.

These types of tests look for acquired gene changesonlyin the cancer cells. These tests are not the same as the tests used to find out about inherited cancer risk.

For more about this kind of testing and its use in cancer treatment, see Biomarker Tests and Cancer Treatment.

Some tests that look for gene changes can be bought without needing a doctors order. For this type of testing, you purchase a test kit and send a sample of your DNA (often from saliva) to a lab for testing.

If you are considering using a home-based genetic test (also known as a direct-to-consumer genetic test), you need to know what its testing for, what it can (and cant) tell you, and how reliable the test is.

Home-based tests do not provide information on a persons overall risk of developing any type of cancer. Sometimes these tests can sound much more helpful and certain than they have been proven to be. It may sound like the test will provide an answer to your specific health concern, such as your risk of hereditary cancer, but the test may not be able to answer that question completely. For example, a test may look for mutations in a certain gene, but it might not test for all of the possible mutations. So a negative test result, even if accurate, may miss the bigger picture regarding your cancer risk and what you can do to manage it. And you might not be provided with the important context about the test results that a genetic counselor could provide.

Home-based genetic tests should not be used instead ofcancer screeningorgenetic counselingthat may be recommended by a medical professional based on your individual risk for cancer.Always consult with your doctor if you are considering or have questions aboutgenetic testing. Trained genetic counselors can help you know whatto expect from your test results.

Link:
Understanding Genetic Testing for Cancer Risk

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Amniocentesis: A procedure in which amniotic fluid and cells are taken from the uterus for testing. The procedure uses a needle to withdraw fluid and cells from the sac that holds the fetus.

Amniotic Fluid: Fluid in the sac that holds the fetus.

Aneuploidy: Having an abnormal number of chromosomes.

Cells: The smallest units of a structure in the body. Cells are the building blocks for all parts of the body.

Chorionic Villus Sampling (CVS): A procedure in which a small sample of cells is taken from the placenta and tested.

Chromosomes: Structures that are located inside each cell in the body. They contain the genes that determine a person's physical makeup.

Cystic Fibrosis: An inherited disorder that causes problems with breathing and digestion.

Diagnostic Tests: Tests that look for a disease or cause of a disease.

DNA: The genetic material that is passed down from parent to child. DNA is packaged in structures called chromosomes.

Embryo: The stage of development that starts at fertilization (joining of an egg and sperm) and lasts up to 8 weeks.

Fetus: The stage of human development beyond 8 completed weeks after fertilization.

Fluorescence In Situ Hybridization (FISH): A screening test for common chromosome problems. The test is done using a tissue sample from an amniocentesis or chorionic villus test.

Genes: Segments of DNA that contain instructions for the development of a person's physical traits and control of the processes in the body. The gene is the basic unit of heredity and can be passed from parent to child.

Genetic Counselor: A health care professional with special training in genetics who can provide expert advice about genetic disorders and prenatal testing.

Genetic Disorders: Disorders caused by a change in genes or chromosomes.

Hospice Care: Care that focuses on comfort for people who have an illness that will lead to death.

In Vitro Fertilization (IVF): A procedure in which an egg is removed from a woman's ovary, fertilized in a laboratory with the man's sperm, and then transferred to the woman's uterus to achieve a pregnancy.

Karyotype: An image of a person's chromosomes, arranged in order of size.

Microarray: A technology that examines all of a person's genes to look for certain genetic disorders or abnormalities. Microarray technology can find very small genetic changes that can be missed by the routine genetic tests.

Monosomy: A condition in which there is a missing chromosome.

Mutations: Changes in a gene that can be passed on from parent to child.

ObstetricianGynecologist (Ob-Gyn): A doctor with special training and education in women's health.

Placenta: An organ that provides nutrients to and takes waste away from the fetus.

Preimplantation Genetic Diagnosis: A type of genetic testing that can be done during in vitro fertilization. Tests are done on the fertilized egg before it is transferred to the uterus.

Screening Tests: Tests that look for possible signs of disease in people who do not have signs or symptoms.

Sickle Cell Disease: An inherited disorder in which red blood cells have a crescent shape, which causes chronic anemia and episodes of pain.

TaySachs Disease: An inherited disorder that causes intellectual disability, blindness, seizures, and death, usually by age 5.

Trisomy: A condition in which there is an extra chromosome.

Ultrasound Exam: A test in which sound waves are used to examine inner parts of the body. During pregnancy, ultrasound can be used to check the fetus.

Uterus: A muscular organ in the female pelvis. During pregnancy, this organ holds and nourishes the fetus. Also called the womb.

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Prenatal Genetic Diagnostic Tests | ACOG

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Continuing Education Activity

DiGeorge syndrome (DGS) is a congenital disorder with a broad phenotypic presentation, which results predominantly from the microdeletion of chromosome 22 at a location known as 22q11.2. This mutation results in the failure of appropriate development of the pharyngeal pouches, which are responsible for the embryologic development of the middle and external ear, maxilla, mandible, palatine tonsils, thyroid, parathyroids, thymus, aortic arch, and cardiac outflow tract. Features of DGS include cardiac anomalies, recurrent infections, abnormal facies, thymic hypoplasia or aplasia, cleft palate, developmental delay, and hypocalcemia. This activity outlines the diagnosis, evaluation, treatment, and management of patients with DGS, and highlights the role of the interprofessional team in managing patients with this condition.

Objectives:

Summarize the etiology of DiGeorge syndrome and its broad phenotypic presentation.

Review the evaluation of patients with DiGeorge syndrome.

Explain the treatment and management options available for DiGeorge syndrome.

Outline interprofessional team strategies for improving care coordination and communication to advance the care of patients with DiGeorge syndrome and improve outcomes.

DiGeorge Syndrome (DGS) is a combination of signs and symptoms caused bydefects in the development of structures derived from the pharyngeal archesduring embryogenesis. Features of DGSwere first described in 1828 but properly reported by Dr. Angelo DiGeorge in 1965, as a clinical trialthat included immunodeficiency, hypoparathyroidism, and congenital heart disease.[1]

DGS is one of several syndromes that has historically grouped under a bigger umbrella called 22q11 deletion syndromes, which include Shprintzen-Goldberg syndrome, velocardiofacial syndrome, Cayler cardiofacial syndrome, Sedlackova syndrome, conotruncal anomaly face syndrome, and DGS.Although the genetic etiology of these syndromes may be the same, varying phenotypeshas supported the use of different nomenclature in the past, which has led to confusion in diagnosing patients with DGS, which causes potentially catastrophic delays in diagnosis.[2] Current literature supports the use of the names of these syndromes interchangeably.

Features ofDGSincludean absent or hypoplastic thymus, cardiac abnormalities, hypocalcemia, and parathyroid hypoplasia (See "History and Physical" below). Perhaps, the most concerning characteristic of DGS is the lack of thymic tissue, becausethisis the organ responsible for T lymphocyte development.A complete absence of the thymus, though very rare and affecting less than 1% of patients with DGS, is associated with a form of severe combined immunodeficiency (SCID).T-cells are a differentiated type of white blood cellspecializingin certain immune functions: destroying cells that are infected or malignant,existing as an integralpart of the innate immune system by killing viruses (e.g., Killer T-cells), helping B-cells matureto produce immunoglobulins for strongeradaptive immunity (e.g. helper T-cells), etc. The degree of immunodeficiency of patients with DGS can present differently depending onthe extent of thymic hypoplasia.

Somepatients may have a mild to moderate immune deficiency, and the majority of patients have cardiac anomalies.Other features include palatal, renal, ocular, and gastrointestinal anomalies. Skeletal defects, psychiatric disease, and developmental delay are also of concern. There are different opinions about syndrome-related alterations in cognitive development, and a cognitive decline rather than an early onset intellectual disability is observable.[3] The particularities of the clinical presentation requires observation on an individual basis, with careful evaluation and interprofessional treatment throughout the patient's life.

About 90% of DGS cases are a result of a deletion in chromosome 22, more specifically on the long arm (q) at the 11.2 locus (22q11.2). Most of these mutations arise de novo with no genetic abnormalities noted in the genome of the parents of children with DGS.[1] Researchers have identified over 90 different genes at this locus, some of which they have studied in mouse models.The most studied of these genes isT-box transcription factor 1 (TBX1), which correlates with severe defects in the development of the heart, thymus, and parathyroid glands of mouse models. TBX1 also correlates with neuromicrovascular anomalies, which may be responsible for the behavioral and developmental abnormalities seen in DGS.[4][5]

Microdeletion of 22q11.2 is the most common microdeletion syndrome, affecting approximately 0.1% of fetuses.[6]The rate of 22q11.2 microdeletion in live births occurs at an estimated rate of 1 in 4000 to 6000.[1][7] There are several explanations for the variance in fetal versus live birth prevalence. Firstly, current evidence may not comprise a large enough population. Secondly, 22q11.2 microdeletions may produceembryonically lethal phenotypes, which was observable in animal studies.

The prevalence of 22q11.2 microdeletion may be more common than supported in literature due to several factors. Firstly, not every patient with this microdeletion presents with several craniofacial abnormalities and hence does notundergo genetic testing. African-American children, for example, may not have the craniofacial abnormalities characteristic of DGS in other races. Secondly, access to healthcare, specifically genetic testing, is not available to every individual that might have the microdeletion, regardless of the severity of craniofacial dysmorphism. Further population studies are therefore needed to fully understand the extent and spectrum of 22q11.2 microdeletions in different populations.[8]

DGS results from microdeletion of 22q11.2, which encodes over 90 genes. Patients with DGS display a broad array of phenotypes, and the most common findings include cardiac anomalies, hypocalcemia, and hypoplastic thymus.

On a genetic basis, TBX1 has correlations with the most prominent phenotypes characteristic of DGS. Failure in embryologic developmentof the pharyngeal pouches, which is driven by TBX1, leads to absence or hypoplasia of the thymus and parathyroid glands.Mouse and zebrafishTBX1 knockout models have been studied to understand the embryologic basis of this disease. In mice, for instance, the absence of TBX1 causes severe pharyngeal, cardiac, thymic, and parathyroid defects as well as a behavioral disturbance.[9]Moreover, zebrafish knockouts have demonstrated defects in the thymus and pharyngeal arches as well as malformation of the ears and thymus.[10]

A 22q11.2 knockout mouse model has also been studied, with findings pertinent for molecular and behavioral changes seen in Parkinson's disease, autism spectrum disorder, attention deficit hyperactivity disorder, and schizophrenia.[11][12]These findings, as well as the neuromicrovascular pathology found in TBX1 knockout mice, suggest a molecular basis for the psychiatric pathologies associated with DGS.[4][5]Of note, individuals affected bythissyndrome have a 30-fold increased risk of developing schizophrenia.

A detailed history and physical is vital in the diagnosis and assessment of DiGeorge syndrome. A broad spectrum of disease severity exists, and suspicion of DGS from history and physical can prompt further evaluation. Although most cases get diagnosed in theprenatal and pediatric periods, diagnosis can also occur in adulthood.Delay in motor development is a common presenting feature first recognized by parentswho notice delays in rolling over, sitting up, or other infant milestones.[13]These findings can be associated with delayed speech developmentand learning disabilities. Later in life, abnormal behavior in the setting of poor developmental history may be thechief presenting symptom of DGS.[1]

A detailed history mayrevealthefollowing:

Family history of diagnosed or suspected DGS

Abnormalgenetic testing results of family members

Delays in the achievement of developmental milestones

Behavioral disturbance

Cyanosis, exercise intolerance, or symptoms

Recurrent infections secondary to T-cell deficiency

Speech difficulty

Difficulty feeding and/or failure to thrive

Muscle spasms, twitching, tetany, seizure

An examination can reveal findings consistent with severalfeatures of DGS:

A complete cardiopulmonary evaluation can reveal murmurs, cyanosis, clubbing, or edema consistent withaortic arch anomalies, conotruncal defects (e.g., tetralogy of Fallot, truncus arteriosus, pulmonary atresia with ventricular septal defect, transposition of the great vessels, interrupted aortic arch), or tricuspid atresia.

A craniofacial examination may demonstrate abnormalities such as cleft palate, hypertelorism, ear anomalies, short down slanting palpebral fissures, short philtrum, and hypoplasia of the maxilla or mandible.

Recurrent sinopulmonary infections due to T cell deficiency as a result of thymic hypoplasia

Signs of hypocalcemia, including twitching and muscle spasm, may be evident as a result of parathyroid hypoplasia. Chvostek's and Trousseau's signs may be positive.

Delayed development, unusual behavior, or signs of psychiatric disorders may be observable.

A clinician makes a definitive diagnosis of DGS in individuals with amicrodeletion of chromosome 22 at the 22q11.2 locus. Classic evaluations of genetic abnormalities, such as trisomies, including the Giemsa banding technique, are incapable of revealing microdeletions. Microdeletions responsible for DGS are therefore detected by fluorescence in situ hybridization (FISH), multiplex ligation-dependent probe amplification (MLPA),single nucleotide polymorphism (SNP) array, comparative genomic hybridization (CGH) microarray, or quantitative polymerase chain reaction (qPCR). The availability and cost of these techniques can delay diagnosis, particularly in resource-poor settings.

Patients diagnosed with or suspected of having DGS should undergo extensive evaluation, particularly if life-threatening cardiac or immunologic deficits are present. The following testsshould merit consideration:

Echocardiogram to evaluateconotruncal abnormalities

Complete blood count with differential

T and B Lymphocyte subset panels

Flow cytometry to assess T cell repertoire

Immunoglobulin levels

Vaccine titers for evaluation of response to vaccines

Serum ionized calcium and phosphorus levels

Parathyroid hormone level

Chest x-ray for thymic shadow evaluation

Renal ultrasound for possible renal and genitourinary defects

Serum creatinine

TSH

Testing for growth hormone deficiency

It is important to note that the broad spectrum of disease severity makesthe evaluationofDGS particularlychallenging. Cases involving significant cardiac, thymic, and craniofacial deficits are more easily recognizable than those lacking severe features. Implementation of advancing genomic studies and facial recognition technology in modern medicinemay assist in more effective diagnosis and evaluation of DGS patients.[14]

Treatment and management of DGS require intensive interprofessional care:

Fortunately, many patients with DGS have minor immunodeficiency, with preservation of T cell function despite decreased T cell production. Frequent follow-up with an immunologist experienced in treating primary immunodeficiencies is advisable. Immunodeficiency in neonates with complete DGS (cDGS) requires management with isolation, intravenous IgG,antibioticprophylaxis, and either thymic or hematopoietic cell transplant (HSCT).

Cardiac anomalies, if not diagnosed during the fetal ultrasound, may present shortly after birth as life-threatening cyanotic heart disease. Pediatric cardiothoracic surgery evaluation may be urgently required. Blood products, if necessary, should be irradiated, CMV negative, and leukocyte reduced to prevent transfusion-associated graft-versus-host disease. These measures also aim to reduce lung injury, particularly in surgical cases requiring cardiopulmonary bypass.

Cleft palate cases require evaluation by an otolaryngologist, plastic surgeon, or oral & maxillofacial surgeon with experience in surgical correction of palatal defects. Repair ofa cleft palate can improve feeding ability, speech, and reduce the incidence of sinopulmonary infections.

Hypocalcemia is manageable with calcium and vitamin D supplementation. Recombinant human PTH is an option in DGS patients refractory to standard therapy.

Autoimmune diseases are common in DGS patients, includingimmune thrombocytopenia(ITP), rheumatoid arthritis, autoimmune hemolytic anemia, Graves disease, and Hashimoto thyroiditis. DGS patientsshould be evaluated carefully for autoimmune symptoms regularly.

Audiologic evaluationis necessary for DGS patients experiencing difficulty with hearing. Children too young to express difficulty with hearing need assessment, particularly with a delay in cognitive and behavioral development.

Early intervention services arebeneficial for children with impaired cognitive and behavioral development.

Speech therapy isnecessary for difficulty with language secondary to craniofacial anomalies and/or cognitive impairment.

Genetic counseling is a reasonable consideration for parents of a child with DGS who desire more children, as well as for patients with DGS who may want to become parents. If a parent has the same mutation as an affected child, there is a 50% chance a new baby will also have DGS.

Advanced approaches for the management of children withcomplete DiGeorge anomaly

In the cDGS featuring no thymus function andbone marrow stem cells can not develop into T cells, childrenusually die by age 2 years due to severe infections. In this setting, the proposal is to T cellreplete HSCT. Nevertheless, because of the absence of thymus, thisstrategy can only obtain engraftment of post thymic T cells.[17]A multicenter survey on the outcome of HSCT showed a survival rate of 33% after matched unrelated donors and 60% in the case of matched sibling transplantations.[18] Recently, the FDA approved the thymus transplantation as standard care. This approach focuses on producingnaive T cellswith a broad T-cell receptor set. The procedure takes place using general anesthesia, and thymus tissue usually gets transplanted into the recipient subject's quadriceps. Studies indicateup to 75% of long-term survival but have described frequent autoimmune sequelae (e.g., autoimmune hemolysis, thyroiditis, thrombocytopenia, enteropathy, and neutropenia) in survivors.[19]

All patient findings that are part ofDiGeorge syndrome can also be present as isolatedanomalies in an otherwise normal individual.

The following conditions present with overlapping features:

Smith-Lemli-Opitz syndrome - (polydactyly and cleft palate are common findings).

Oculo-auriculo vertebral (Goldenhar) syndrome (OAVS) - (ear anomalies, heart disease, vertebral defects,and renalanomalies are present). OAVS often demonstrates a sporadic presentation.

Alagille syndrome - (butterfly vertebrae,congenital heart disease, and posterior embryotoxon arecommon to both conditions).

VATER association (heart disease, vertebral, renal, and limb anomalies present in both conditions). VATER association is a diagnosis of exclusion for which an established etiology to date remains unknown.

CHARGE syndrome - (any combination ofcongenital heart disease, palatal differences, atresia choanae, coloboma, renal, growth deficiency, ear anomalies/hearing loss, facial palsy, developmental differences,genitourinary anomalies, and immunodeficiency are present in both syndromes).

Genetic consult is essential along with the complete clinical picture to make an accurate diagnosis of DiGeorge syndrome.

Less than 1% of patients with 22q11.2 microdeletion have complete DGS, the most severe subtype of DGS with a very poor prognosis. Without thymic or hematopoietic cell transplantation, these patients die by 12 months of age. Even with a transplant, however, prognosis remains poor. In a study of 50 infants who received a thymic transplant for complete DGS, only 36 survived to two years.[20]

Patients with partial DGS do not have a defined prognosis, as this depends on the severity of the pathologies associated with the disease. While some do not survive infancy due to severe cardiac anomalies, many survive into adulthood. DGS may be vastly underdiagnosed, and many undiagnosed adults with DGS thrive in the community with undetectable congenital anomalies and minor intellectual and/or social impairment. Improvements in genetic diagnostics will hopefully improve understanding of DGS in the future.

Cardiac and craniofacial anomalies associated with DGS may require surgical repair. As with any surgical procedure, the possibility of complications, including bleeding, infection, and prolonged hospitalization, exists. These risks are particularly dangerous for DGS patients with significant immunocompromise.

Consistent follow-up of patients with DGS is necessary to evaluate for possiblecomplications: severe recurrent infections, autoimmune diseases, and hematologic malignancies.

Parents of children with DGS should receive patient education as it pertains to the severity of their child's condition. Discussion topics may include the following:

Early signs and symptoms of infection

Signs of hypocalcemia

Safe use of medications

Surgical intervention options

Immune therapy options

Genetic counseling

Speech therapy for feeding or language difficulty

Developmental milestones and warning signs of developmental delay

Benefits of early intervention programs

Signs and symptoms of psychiatric disorders

DiGeorge syndrome is easy to remember using the "CATCH-22" mnemonic:

Conotruncal cardiac anomalies

Abnormal facies

Thymic hypoplasia

Cleft palate

Hypocalcemia

22q11.2 microdeletion

Management of DGS requires an interprofessional approach by a team of healthcare professionals. Obstetricians and genetic counselors can assist in diagnosis and management prenatally. Neonatologists, primary care pediatricians, family medicine physicians, immunologists, cardiothoracic surgeons, pediatricians, craniofacial surgeons, and othermedical specialties may be involved in the care of patients with DGS. Collaboration with nurses, pharmacists, psychologists, speech therapists, and other healthcare professionals is paramount. Pharmacists can verify agent selection and dosing with medications to address the endocrine aspects of the disease. Nursing can counsel parents and monitor treatment progress. Psychological professionals can assist with developmental difficulties, as well as work with family members. Patients with DGS require lifelong, consistent follow-up. Because numerous organs are involved, close follow up with each specialist is necessary. Open communication and collaboration between all members of the interprofessional healthcare team are vital to ensure good outcomes. [Level 5]

Diagnosis and management can be challenging, and the interprofessional team can provide a collaborative effort to reduce morbidity and mortality associated with DGS. Current evidence regarding the management of DGS reflects level 5 evidence, and treatment options require a tailored approach around the individual patient's disease manifestations.

DiGeorge syndrome. Contributed by Professor Victor Grech (CC By=S.A. 3.0 https://creativecommons.org/licenses/by-sa/3.0/) Image courtesy: https://en.wikipedia.org/wiki/DiGeorge_syndrome#/media/File:DiGeorge_syndrome1.jpg

DiGeorge syndrome karyotype. Image courtesy O Chaigasame

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DiGeorge Syndrome - StatPearls - NCBI Bookshelf

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13.2.1 Induced pluripotent stem cells

Induced pluripotent stem cells are differentiated cells that have been reprogrammed into an embryonic stem cell like state by the ectopic overexpression of four stem cell specific transcription factors, Oct3/4, Klf4, Sox2, and c-Myc, collectively referred to as OKSM. Induced pluripotent stem cells were first derived in a groundbreaking experiment by Yamanaka and Takashi in 2006 [77]. The team assessed the ability of 24 pluripotency associated candidate genes to covert primarily differentiated mouse tail tip fibroblasts into an embryonic stem cell state. Candidate genes were packaged into individual retroviruses and transduced into Fbx15geo/geo cells, which were grown in G418 containing media, an aminoglycoside antibiotic with conferred resistance to the neomycin gene. If the cells converted to an ESC like fate the embryonic stem cell specific locus Fbx15 containing a -galactosidase and neomycin fused reporter cassette would become activated, thereby inoculating the cells against neomycin. Transduction with all 24 factors proved to be successful in converting the fibroblasts into ESCs. Through the process of elimination, the team narrowed the list of factors down to just four factors needed to reprogram fibroblast cells to an ESC state [77]. Yamanaka and Takashi expanded their groundbreaking discovery to human cells a year later [78].

The discovery of induced pluripotent stem cells ignited the field with possibility. It was a new research tool that could be used to analyze development and cell specialization. Additionally, the possibility of deriving pluripotent stem cells was also a new therapeutic research tool that if harnessed and understood could be used for personalized cell therapy and disease modeling. Researchers quickly began differentiating iPSCs into different cell lineages.

Induced pluripotent stem cell derived-cardiomyocytes (iPSC-CMs) were generated similarly to established methods for differentiating embryonic stem cells into cardiomyocytes [7981] (Fig.13.1C). The cells were first differentiated into embryoid bodies and then exposed to serum-containing medium, which fostered a propensity to differentiate into cardiomyocytes. After 50 or more days in culture, cells derived under these conditions stained positive for sarcomeric myosin light and heavy chains, cardiac troponin T, and alpha-actinin. Additionally, the embryoid bodies demonstrated action potentials akin to atrial, ventricular, and nodal cells, and underwent rapid adaptive response to electrical stimulation and were cable of visible contractions. Despite well-established protocols the purity of cardiomyocytes derived using this technique are often times lower than 1% [8284]. However, the efficiency and purity of cardiomyocytes generated from embryoid body differentiation could be enhanced by following a step wise induction process similar to the naturally occurring cardiac differentiation process in the developing embryo [85].

To increase purity, and the usability for downstream applications monolayer culture methods were developed to facilitate a more controllable and reproducible environment to generate iPSC-CMs [86]. Monoculture conditions consist of growth on Matrigel-coated plates with mouse embryonic fibroblast conditioned media and gradual supplementation with activin A and BMP-4 growth factors. The combination of these conditions have been shown to yield greater than 50% beating iPSC-CMs [87,88]. A variation of this method, called the matrix sandwich method exists and boasts yields of up to 98% beating iPSC-CMs [89]. However, it should be noted that this method only works for some cell lines and requires growth factor batch optimizations to maintain high yields [90]. Alternatively, modifying Wnt/-catenin signaling using shRNA and small molecules has also been shown to increase iPSC-CM yield to approximately 85% [91,92].

The need for complex culture conditions to yield high iPSC-CM outputs makes identifying the biological underpinnings of iPSC-CM differentiation difficult to elucidate. One study claims to have reduced the complexity of iPSC-CM derivation to just three components, referred to as CDM3 [93]. When used in combination with lactate selection the study authors claim to achieve a yield of 80%90% troponin T positive iPSC-CMs [94]. The simplicity of the culture conditions used in this study allowed for the first time the identification of key signaling pathways implicated in iPSC-CM carcinogenesis.

The first and only case thus far of an autologous iPSC derived cell treatment making it to the clinic was reported in 2014. In a trial lead by Takahashi and colleagues, human iPSC derived retinal pigment epithelium cell sheets were transplanted into a human patient to resolve age related macular regeneration [95]. There have been no clinical trials testing iPSC-CM safety or efficacy in repairing the injured heart. However, iPSC-CMs derived using the previously mentioned matrix sandwich technique were transplanted in a non-human primate model, where they were shown to improve cardiac function after induced myocardial infraction. However, the transplanted iPSC-CMs also induced high rates of ventricular arrhythmia [96].

Despite the great hope for patient specific treatments, it is uncertain if autologous iPSC-CM treatments for myocardial infractions will make it to the clinic within the next few years. The production of patient-specific stem cells is expensive and variable. Specifically, iPSC-CM derivation efficiency still remains low and variable without the use of complex culture systems. Streamlining human iPSC cardiomyocyte differentiation to an effective simple differentiation process is key. Large numbers of iPSC-CM cells would be needed for human clinical trials, which would be impractical to accomplish using current culture systems and methods. Currently macaque trials require about 108109 reprogrammed iPSC-CM cells. The number of cells required for a human trial is projected to be a least a magnitude higher [5,97]. Additionally, like all iPSC derived cell therapies, and even embryonic stem cell therapies there is the concern that the transplanted stem cells could develop into tumor and/or cancer cells because of the possible carryover of few highly multi- or pluripotent cells in the transplanted pool [98]. Safety assessment is key before any iPSC-CM trial can make it to the clinical setting.

However, iPSC-CMs do have the potential to be somewhat useful for in vitro screening assays and drug development. iPSC-CMs have been used to improve the identification of false positive and negative data in electrophysiological assays [99]. They have also been shown to be responsive for research purposes to several cardiac and non-cardiac drugs, a prospect that might be of interest for drug screening purposes [100103]. Furthermore, disease-specific iPSC-CMs derived from people with pre-existing heart conditions have been shown to be more responsive to cardiotoxic drugs as measured by action potential duration and drug-induced arrhythmia, consistent with what would be expected naturally in the patient [104].

While iPSC-CMs might have some usefulness for drug screening, the results should be considered in light of the fact that iPSC-CMs are not equivalent to true CMs found in the adult heart. iPSC-CMs have lower conduction velocities and shorter action potential duration. They are altogether functionally immature, disorganized, fetal-like, and are not molecularly equivalent to true cardiomyocytes found in the adult heart [90,105107]. There is a need to understand cardiomyocyte maturation to facilitate regeneration and differentiation into cardiomyocytes capable of maintaining the functions of an adult heart.

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Induced Pluripotent Stem Cell - an overview - ScienceDirect

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Stem Cells Definition

Stem cells are unique cells present in the body that have the potential to differentiate into various cell types or divide indefinitely to produce other stem cells.

Figure: Stem Cell Renewal and Differentiation. Image Source: Maharaj Institute of Immune Regenerative Medicine.

All the stem cells found throughout all living systems have three important properties. These properties can be visualized in vitro by a process called clonogenic assays, where a single cell is assessed for its ability to differentiate.

The following are some properties of stem cells:

Figure: Techniques for generating embryonic stem cell cultures. Image Source: John Wiley & Sons, Inc. (Nico Heins et al.)

Depending on the source of the stem cells or where they are present, stem cells are divided into various types;

Figure: Human Embryonic Stem Cells Differentiation. Image created with biorender.com

Figure: Preliminary Evidence of Plasticity Among Nonhuman Adult Stem Cells. Image Source: NIH Stem Cell Information.

Figure: Progress in therapies based on iPSCs. Image Source: Nature Reviews Genetics (R. Grant Rowe & George Q. Daley).

Figure: Mesenchymal stem cells (MSCs). Image Source: PromoCell GmbH.

Some of the common and well-known examples of stem cell research are:

Stem cell research has been used in various areas because of their properties. Some of the common applications of stem cells research include;

Because of different ethical and other issues related to stem cell research, there are some limitations or challenges of stem cell research. Some of these are:

Read Also:

Read more here:
Stem Cells- Definition, Properties, Types, Uses, Challenges - Microbe Notes

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Your body controls your thyroid hormone (T3 and T4) levels through a complex feedback loop. Your hypothalamus releases thyrotropin-releasing hormone (TRH), which triggers your pituitary gland to release thyroid-stimulating hormone (TSH), which stimulates your thyroid to release T3 and T4.What is thyroid hormone?

Thyroid hormone is the hormone thats mainly responsible for controlling the speed of your bodys metabolism. In infants, thyroid hormone is critical for brain development. Your thyroid, a small, butterfly-shaped gland located at the front of your neck under your skin, makes and releases thyroid hormone. Its a part of your endocrine system.

Hormones are chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, muscles and other tissues. These signals tell your body what to do and when to do it.

Metabolism is the complex process of how your body transforms the food you consume into energy. All of the cells in your body need energy to function.

Thyroid hormone actually represents the combination of the two main hormones that your thyroid gland releases: thyroxine (T4) and triiodothyronine (T3). Theyre often collectively referred to as thyroid hormone because T4 is largely inactive, meaning it doesnt impact your cells, whereas T3 is active. Once your thyroid releases T4, certain organs in your body transform it into T3 so that it can impact your cells and your metabolism.

Your thyroid also releases a hormone called calcitonin to help regulate calcium levels in your blood by decreasing it. Calcitonin isnt grouped into the thyroid hormone name, and it doesnt impact your bodys metabolism like T3 and T4 do.

The production and release of thyroid hormone thyroxine (t4) and triiodothyronine (T3) is controlled by a feedback loop system that involves the following:

Your hypothalamus is the part of your brain that controls functions like blood pressure, heart rate, body temperature and digestion.

Your pituitary gland is a small, pea-sized gland located at the base of your brain below your hypothalamus. It makes and releases eight hormones.

Your pituitary gland is connected to your hypothalamus through a stalk of blood vessels and nerves. This is called the pituitary stalk. Through the stalk, your hypothalamus communicates with your pituitary gland and tells it to release certain hormones.

To start the feedback loop, your hypothalamus releases thyroid-releasing hormone (TRH) which, in turn, stimulates your pituitary gland to produce and release thyroid-stimulating hormone (TSH). TSH then triggers your thyroid to produce T4 and T3. Of the total amount of hormones that TSH triggers your thyroid to release, about 80% is T4 and 20% is T3. Your thyroid also needs adequate amounts of iodine, a substance you get from the food you eat, to create T4 and T3.

This hormone chain reaction is regulated by a feedback loop so that when the levels of T3 and T4 increase, they prevent the release of TRH (and thus TSH). When T3 and T4 levels drop, the feedback loop starts again. This system allows your body to maintain a constant level of thyroid hormones in your body.

If there are any issues with your hypothalamus, pituitary gland or thyroid, it can result in an imbalance in the hormones involved in this system, including T3 and T4.

Once your thyroid releases thyroxine (T4) into your bloodstream, certain cells in your body transform it into triiodothyronine (T3) through a process called de-iodination. This is because cells that have receptors that receive the effect of thyroid hormone are better able to use T3 than T4. Therefore, T4 is generally considered to be the inactive form of thyroid hormone, and T3 is considered the active form of it.

Cells in the following tissues, glands, organs and body systems can convert T4 to T3:

Thyroid hormone (T3 and T4) affects every cell and all the organs in your body by:

Several blood tests can measure your thyroid levels and assess how well your thyroid is working. These tests are often called thyroid function tests and include:

Your provider may order additional tests to assess your thyroid function, including:

Several conditions can result from or cause abnormal thyroid hormone levels. Thyroid disease is very common, with an estimated 20 million people in the United States having some type of thyroid condition. A person assigned female at birth is about five to eight times more likely to have a thyroid condition than a person assigned male at birth.

Thyroid conditions include:

Issues with your pituitary gland or hypothalamus can also cause abnormal thyroid hormone levels since they help control thyroid hormone levels.

Abnormal thyroid hormone levels usually cause noticeable symptoms. Since thyroid hormone is responsible for controlling the speed of your metabolism, too much thyroid hormone can make it faster than normal and too little thyroid hormone can slow it down. These imbalances cause certain symptoms, including:

If you experience these symptoms, contact your healthcare provider. They can run some simple blood tests to see if your thyroid hormone levels are irregular.

A note from Cleveland Clinic

Thyroid hormone is an essential hormone that affects many aspects of your body. Sometimes, you can have too little or too much thyroid hormone. The good news is that thyroid conditions are highly treatable. If youre experiencing any thyroid hormone-related symptoms or want to know if you have any risk factors for developing thyroid disease, dont be afraid to talk to your healthcare provider. Theyre there to help you.

See more here:
Thyroid Hormone: What It Is & Function - Cleveland Clinic

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What is human chorionic gonadotrophin?

Human chorionic gonadotrophin (hCG) is a hormone produced by the placenta during pregnancy. Its sometimes called the pregnancy hormone because of its unique role in supporting a pregnancy. HCG is found in your urine or blood around 10 to 11 days after conception (when a sperm fertilizes an egg). Your hCG levels are the highest towards the end of the first trimester (10 weeks of pregnancy), then decline for the rest of your pregnancy. Healthcare providers measure hCG to confirm a pregnancy and provide details on how the pregnancy is progressing.

After conception occurs, a fertilized egg travels through your fallopian tubes to your uterus. The fertilized egg (called an embryo) implants (attaches) into the wall of your uterus. This triggers the placenta to form. Your placenta begins producing and releasing hCG into your blood and urine. HCG can be found in a persons blood around 11 days after conception. It takes slightly longer for hCG to register on urine tests.

HCG increases quickly (almost doubling every three days) for the first eight to 10 weeks of pregnancy. Healthcare providers look at how quickly a persons hCG levels rise in early pregnancy to determine how the pregnancy and fetus are developing.

Once your placenta begins making hCG, it triggers your body to create more estrogen and progesterone. Together with hCG, these hormones help thicken your uterine lining and tell your body to stop menstruating (or releasing eggs). The correct balance of these three hormones sustains and supports the pregnancy.

This chart shows how your hCG levels rise quickly and steadily in the first trimester before declining:

These numbers should be used as a guide only. Your levels may rise differently. Its not the number that matters as much as how the number changes. Your healthcare provider will let you know if your hCG levels need to be checked and what your test results mean for your pregnancy. Remember that healthy pregnancies may have lower than average hCG levels.

HCG can be detected in either blood or urine. However, a blood test is more accurate because it can detect smaller amounts of hCG.

There are two different types of blood tests to detect hCG:

An at-home pregnancy test will be positive if hCG is detected in your urine. A urine hCG test is performed by either peeing on a chemical strip or placing a drop of urine on a chemical strip. At-home urine tests typically require higher hCG levels to return a positive.

Keep in mind a low hCG level doesnt diagnose anything. Its a tool to detect potential issues. If your healthcare provider is concerned about your hCG level, they will test your levels again in two or three days. Then, they will compare the results to get a better picture of whats going on with your pregnancy.

HCG levels are typically not checked more than once or twice during pregnancy. Healthcare providers check hCG levels in the first trimester but usually dont need to check again. If initial hCG levels are lower than average, your provider will test hCG levels again in a few days. Assessing hCG levels is done sequentially, testing several days apart and comparing levels. Some prenatal genetic tests use hCG levels to check for the possibility of a fetus having a congenital disorder.

All people have small amounts of hCG in their bodies (almost undetectable levels). Your hCG levels rise fast and peak around 10 weeks of pregnancy. After that, they fall gradually until childbirth. In rare cases, germ cell tumors or other cancers may cause your body to produce hCG.

A low or declining hCG level may mean several things:

If your hCG level is low for the gestational age of the pregnancy, your healthcare provider will recheck your hCG levels in two or three days or perform an ultrasound to get a better look at your uterus.

High levels of hCG could indicate:

HCG injections can increase your chances of becoming pregnant when used with IVF (in-vitro fertilization) or IUI (intrauterine insemination). It works by inducing ovulation (when ovaries release an egg).

If you have a history of infertility, monitoring hCG levels early in pregnancy can help healthcare providers determine if a successful pregnancy has occurred.

HCG helps with the production of testosterone and sperm in people assigned male at birth (AMAB). Its also been used to treat undescended testicles in male infants.

Most of the time, youre unaware of your hCG levels other than when you take an at-home pregnancy test. Your healthcare provider may tell you your hCG levels are low based on the gestational age of the pregnancy. Obstetricians typically check hCG early on in pregnancy but dont continue to check it unless there are signs of problems. If your healthcare provider is concerned about how your pregnancy is progressing, they will recheck hCG levels and perform other diagnostic tests like ultrasound.

A note from Cleveland Clinic

Human chorionic gonadotropin (hCG) is known as the pregnancy hormone. Its claim to fame is that its the hormone at-home pregnancy tests check for. Your body produces a lot of hCG during the first trimester to support your growing baby. Your hCG levels provide valuable insight into your pregnancy and may alert your obstetrician to potential issues. However, if your pregnancy is going well, chances are you wont ever know what your hCG levels are. Contact your healthcare provider if you have questions about your hCG levels or what they mean.

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Human Chorionic Gonadotropin: Hormone, Purpose & Levels - Cleveland Clinic

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Overview

Menopause is the time that marks the end of your menstrual cycles. It's diagnosed after you've gone 12 months without a menstrual period. Menopause can happen in your 40s or 50s, but the average age is 51 in the United States.

Menopause is a natural biological process. But the physical symptoms, such as hot flashes, and emotional symptoms of menopause may disrupt your sleep, lower your energy or affect emotional health. There are many effective treatments available, from lifestyle adjustments to hormone therapy.

In the months or years leading up to menopause (perimenopause), you might experience these signs and symptoms:

Signs and symptoms, including changes in menstruation can vary among women. Most likely, you'll experience some irregularity in your periods before they end.

Skipping periods during perimenopause is common and expected. Often, menstrual periods will skip a month and return, or skip several months and then start monthly cycles again for a few months. Periods also tend to happen on shorter cycles, so they are closer together. Despite irregular periods, pregnancy is possible. If you've skipped a period but aren't sure you've started the menopausal transition, consider a pregnancy test.

Keep up with regular visits with your doctor for preventive health care and any medical concerns. Continue getting these appointments during and after menopause.

Preventive health care as you age may include recommended health screening tests, such as colonoscopy, mammography and triglyceride screening. Your doctor might recommend other tests and exams, too, including thyroid testing if suggested by your history, and breast and pelvic exams.

Always seek medical advice if you have bleeding from your vagina after menopause.

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Menopause can result from:

Naturally declining reproductive hormones. As you approach your late 30s, your ovaries start making less estrogen and progesterone the hormones that regulate menstruation and your fertility declines.

In your 40s, your menstrual periods may become longer or shorter, heavier or lighter, and more or less frequent, until eventually on average, by age 51 your ovaries stop releasing eggs, and you have no more periods.

Surgery that removes the ovaries (oophorectomy). Your ovaries produce hormones, including estrogen and progesterone, that regulate the menstrual cycle. Surgery to remove your ovaries causes immediate menopause. Your periods stop, and you're likely to have hot flashes and experience other menopausal signs and symptoms. Signs and symptoms can be severe, as hormonal changes occur abruptly rather than gradually over several years.

Surgery that removes your uterus but not your ovaries (hysterectomy) usually doesn't cause immediate menopause. Although you no longer have periods, your ovaries still release eggs and produce estrogen and progesterone.

After menopause, your risk of certain medical conditions increases. Examples include:

Urinary incontinence. As the tissues of your vagina and urethra lose elasticity, you may experience frequent, sudden, strong urges to urinate, followed by an involuntary loss of urine (urge incontinence), or the loss of urine with coughing, laughing or lifting (stress incontinence). You may have urinary tract infections more often.

Strengthening pelvic floor muscles with Kegel exercises and using a topical vaginal estrogen may help relieve symptoms of incontinence. Hormone therapy may also be an effective treatment option for menopausal urinary tract and vaginal changes that can result in urinary incontinence.

Sexual function. Vaginal dryness from decreased moisture production and loss of elasticity can cause discomfort and slight bleeding during sexual intercourse. Also, decreased sensation may reduce your desire for sexual activity (libido).

Water-based vaginal moisturizers and lubricants may help. If a vaginal lubricant isn't enough, many women benefit from the use of local vaginal estrogen treatment, available as a vaginal cream, tablet or ring.

Dec. 17, 2022

See more here:
Menopause - Symptoms and causes - Mayo Clinic

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Overview Polycystic ovary syndrome Open pop-up dialog box

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Polycystic ovary syndrome is a condition where you have few, unusual or very long periods. It often results in having too much of a male hormone called androgen. Many small sacs of fluid develop on the ovaries. They may fail to regularly release eggs.

Polycystic ovary syndrome (PCOS) is a problem with hormones that happens during the reproductive years. If you have PCOS, you may not have periods very often. Or you may have periods that last many days. You may also have too much of a hormone called androgen in your body.

With PCOS, many small sacs of fluid develop along the outer edge of the ovary. These are called cysts. The small fluid-filled cysts contain immature eggs. These are called follicles. The follicles fail to regularly release eggs.

The exact cause of PCOS is unknown. Early diagnosis and treatment along with weight loss may lower the risk of long-term complications such as type 2 diabetes and heart disease.

Symptoms of PCOS often start around the time of the first menstrual period. Sometimes symptoms develop later after you have had periods for a while.

The symptoms of PCOS vary. A diagnosis of PCOS is made when you have at least two of these:

PCOS signs and symptoms are typically more severe in people with obesity.

See your health care provider if you're worried about your periods, if you're having trouble getting pregnant, or if you have signs of excess androgen. These might include new hair growth on your face and body, acne and male-pattern baldness.

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The exact cause of PCOS isn't known. Factors that might play a role include:

Insulin resistance. Insulin is a hormone that the pancreas makes. It allows cells to use sugar, your body's primary energy supply. If cells become resistant to the action of insulin, then blood sugar levels can go up. This can cause your body to make more insulin to try to bring down the blood sugar level.

Too much insulin might cause your body to make too much of the male hormone androgen. You could have trouble with ovulation, the process where eggs are released from the ovary.

One sign of insulin resistance is dark, velvety patches of skin on the lower part of the neck, armpits, groin or under the breasts. A bigger appetite and weight gain may be other signs.

Complications of PCOS can include:

Obesity commonly occurs with PCOS and can worsen complications of the disorder.

Polycystic ovary syndrome (PCOS) care at Mayo Clinic

Sept. 08, 2022

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Polycystic ovary syndrome (PCOS) - Symptoms and causes - Mayo Clinic

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OverviewWhat is hypothyroidism?

Hypothyroidism is a condition where there isnt enough thyroid hormone in your bloodstream and your metabolism slows down.

Hypothyroidism happens when your thyroid doesnt create and release enough thyroid hormone into your body. This makes your metabolism slow down, affecting you entire body. Also known as underactive thyroid disease, hypothyroidism is fairly common.

When your thyroid levels are extremely low, this is called myxedema. A very serious condition, myxedema can cause serious symptoms, including:

This severe type of hypothyroidism is life-threatening.

In general, hypothyroidism is a very treatable condition. It can be managed with regular medications and follow-up appointments with your healthcare provider.

The thyroid gland is a small, butterfly-shaped organ located in the front of your neck just under the voice box (larynx). Picture the middle of the butterflys body centered on your neck, with the wings hugging around your windpipe (trachea). The main job of the thyroid is to control your metabolism. Metabolism is the process that your body uses to transform food to energy your body uses to function. The thyroid creates the hormones T4 and T3 to control your metabolism. These hormones work throughout the body to tell the bodys cells how much energy to use. They control your body temperature and heart rate.

When your thyroid works correctly, its constantly making hormones, releasing them and then making new hormones to replace whats been used. This keeps your metabolism functioning and all of your bodys systems in check. The amount of thyroid hormones in the bloodstream is controlled by the pituitary gland, which is located in the center of the skull below the brain. When the pituitary gland senses either a lack of thyroid hormone or too much, it adjusts its own hormone (thyroid stimulating hormone, or TSH) and sends it to the thyroid to balance out the amounts.

If the amount of thyroid hormones is too high (hyperthyroidism) or too low (hypothyroidism), the entire body is impacted.

Hypothyroidism can affect people of all ages, genders and ethnicities. Its a common condition, particularly among women over age 60. Women are generally more likely to develop hypothyroidism after menopause than earlier in life.

In hypothyroidism, the thyroid doesnt make enough thyroid hormone.

The difference between hypothyroidism and hyperthyroidism is quantity. In hypothyroidism, the thyroid makes very little thyroid hormone. On the flip side, someone with hyperthyroidism has a thyroid that makes too much thyroid hormone. Hyperthyroidism involves higher levels of thyroid hormones, which makes your metabolism speed up. If you have hypothyroidism, your metabolism slows down.

Many things are the opposite between these two conditions. If you have hypothyroidism, you may have a difficult time dealing with the cold. If you have hyperthyroidism, you may not handle the heat. They are opposite extremes of thyroid function. Ideally, you should be in the middle. Treatments for both of these conditions work to get your thyroid function as close to that middle ground as possible.

Hypothyroidism can have a primary cause or a secondary cause. A primary cause is a condition that directly impacts the thyroid and causes it to create low levels of thyroid hormones. A secondary cause is something that causes the pituitary gland to fail, which means it cant send thyroid stimulating hormone (TSH) to the thyroid to balance out the thyroid hormones.

Primary causes of hypothyroidism are much more common. The most common of these primary causes is an autoimmune condition called Hashimotos disease. Also called Hashimotos thyroiditis or chronic lymphocytic thyroiditis, this condition is hereditary (passed down through a family). In Hashimotos disease, the bodys immune system attacks and damages the thyroid. This prevents the thyroid from making and releasing enough thyroid hormone.

The other primary causes of hypothyroidism can include:

In some cases, thyroiditis can happen after a pregnancy (postpartum thyroiditis) or a viral illness.

In most cases, women with hypothyroidism during pregnancy have Hashimotos disease. This autoimmune disease causes the bodys immune system to attack and damage the thyroid. When that happens, the thyroid cant produce and release high enough levels of thyroid hormones, impacting the entire body. Pregnant people with hypothyroidism may feel very tired, have a hard time dealing with cold temperatures and experience muscles cramps.

Thyroid hormones are important to fetal development. These hormones help develop the brain and nervous system. If you have hypothyroidism, its important to manage your thyroid levels during pregnancy. If the fetus doesnt get enough thyroid hormone during development, the brain may not develop correctly and there could be issues later. Untreated or insufficiently treated hypothyroidism during pregnancy may lead to complications like miscarriage or preterm labor.

When youre on birth control pills, the estrogen and progesterone inside of the pills can affect your thyroid-binding proteins. This increases your levels. If you have hypothyroidism, the dose of your medications will need to be increased while youre using birth control pills. Once you stop using birth control pills, the dosage will need to be lowered.

In some cases, there can be a connection between untreated hypothyroidism and erectile dysfunction. When your hypothyroidism is caused by an issue with the pituitary gland, you can also have low testosterone levels. Treating hypothyroidism can often help with erectile dysfunction if it was directly caused by the hormone imbalance.

The symptoms of hypothyroidism usually develop slowly over time sometimes years. They can include:

If your hypothyroidism is not treated, you could gain weight. Once you are treating the condition, the weight should start to lower. However, you will still need to watch your calories and exercise to lose weight. Talk to your healthcare provider about weight loss and ways to develop a diet that works for you.

It can actually be difficult to diagnose hypothyroidism because the symptoms can be easily confused with other conditions. If you have any of the symptoms of hypothyroidism, talk to your healthcare provider. The main way to diagnose hypothyroidism is a blood test called the thyroid stimulating hormone (TSH) test. Your healthcare provider may also order blood tests for conditions like Hashimotos disease. If the thyroid is enlarged, your provider may be able to feel it during a physical exam during an appointment.

In most cases, hypothyroidism is treated by replacing the amount of hormone that your thyroid is no longer making. This is typically done with a medication. One medication that is commonly used is called levothyroxine. Taken orally, this medication increases the amount of thyroid hormone your body produces, evening out your levels.

Hypothyroidism is a manageable disease. However, you will need to continuously take medication to normalize the amount of hormones in your body for the rest of your life. With careful management, and follow-up appointments with your healthcare provider to make sure your treatment is working properly, you can lead a normal and healthy life.

Hypothyroidism can become a serious and life-threatening medical condition if you do not get treatment from a healthcare provider. If you are not treated, your symptoms can become more severe and can include:

You can also develop a serious medical condition called myxedema coma. This can happen when hypothyroidism isnt treated.

The dose of your medication can actually change over time. At different points in your life, you may need to have the amounts of medication changed so that it manages your symptoms. This could happen because of things like weight gain or weight loss. Your levels will need to be monitored throughout your life to make sure your medication is working correctly.

Hypothyroidism cannot be prevented. The best way to prevent developing a serious form of the condition or having the symptoms impact your life in a serious way is to watch for signs of hypothyroidism. If you experience any of the symptoms of hypothyroidism, the best thing to do is talk to your healthcare provider. Hypothyroidism is very manageable if you catch it early and begin treatment.

Most foods in western diets contain iodine, so you do not have to worry about your diet. Iodine is a mineral that helps your thyroid produce hormones. One idea is that if you have low levels of thyroid hormone, eating foods rich in iodine could help increase your hormone levels. The most reliable way to increase your hormone levels is with a prescription medication from your healthcare provider. Do not try any new diets without talking to your provider first. Its important to always have a conversation before starting a new diet, especially if you have a medical condition like hypothyroidism.

Foods that are high in iodine include:

Work with your healthcare provider or a nutritionist (a healthcare provider who specializes in food) to craft a meal plan. Your food is your fuel. Making sure you are eating foods that will help your body, along with taking your medications as instructed by your healthcare provider, can keep you healthy over time. People with thyroid condition should not consume large amounts of iodine because the effect may be paradoxical (self-contradictory).

In some mild cases, you may not have symptoms of hypothyroidism or the symptoms may fade over time. In other cases, the symptoms of hypothyroidism will go away shortly after you start treatment. For those with particularly low levels of thyroid hormones, hypothyroidism is a life-long condition that will need to be managed with medication on a regular schedule.

Read this article:
Hypothyroidism: Symptoms, Causes, Treatment & Medication - Cleveland Clinic

Recommendation and review posted by Bethany Smith