Archive for the ‘Male Genetics’ Category

This spring, the biotechnology company Oxitec plans to release genetically modified (GM) mosquitoes in the Florida Keys. Oxitec says its technology will combat dengue fever, a potentially life-threatening disease, and other mosquito-borne viruses such as Zika mainly transmitted by the Aedes aegypti mosquito.

While there have been more than 7,300 dengue cases reported in the United States between 2010 and 2020, a majority are contracted in Asia and the Caribbean, according to the US Centres for Disease Control and Prevention. In Florida, however, there were 41 travel-related cases in 2020, compared with 71 cases that were transmitted locally.

Native mosquitoes in Florida are increasingly resistant to the most common form of control insecticide and scientists say they need new and better techniques to control the insects and the diseases they carry. There arent any other tools that we have. Mosquito nets dont work. Vaccines are under development but need to be fully efficacious, says Michael Bonsall, a mathematical biologist at the University of Oxford, who is not affiliated with Oxitec but has collaborated with the company in the past, and who worked with the WHO to produce a GM mosquito-testing framework.

Bonsall and other scientists think a combination of approaches is essential to reducing the burden of diseases and that, maybe, newer ideas like GM mosquitoes should be added to the mix. Oxitecs mosquitoes, for instance, are genetically altered to pass what the company calls self-limiting genes to their offspring; when released GM males breed with wild female mosquitoes, the resulting generation does not survive into adulthood, reducing the overall population.

But Oxitec has been proposing to experimentally release GM mosquitos in the Keys since 2011, and the plan has long been met with suspicion among locals and debate among scientists. Some locals say they fear being guinea pigs. Critics say they are concerned about the possible effects GM mosquitoes could have on human health and the environment. In 2012, the Key West City Commissionobjected to Oxitecs plan; in a non-binding referendum four years later, residents of Key Haven where the mosquitoes would have been released rejected it, while residents in the surrounding county voted in support of the release. With the decision left up to the Florida Keys Mosquito Control District, officials approved the trial to be conducted elsewhere in the Keys.

According to Oxitec, the release was delayed due to a transfer of jurisdiction over the project from the U.S. Food and Drug Administration to the Environmental Protection Agency.

The company reapplied for approval to release a new version of the mosquitoes, called OX5034, in the Keys. In May, the EPA granted a two-year experimental use permit, which the agency can cancel at any time. State and local sign-off soon followed finally giving the project the greenlight.

Oxitecs OX5034 mosquitoes are the first GM mosquitoes approved for release in the US. The company has already conducted a trial with the OX5034 mosquitoes in Brazil and released more than a billion of a previous version, called OX513A, there and in other locations over the years including the Cayman Islands. The company says it is confident in the effectiveness and safety of the technology.

But some scientists want to hit pause on Oxitecs Florida trial, to find what they say is a fairer process in deciding to release the mosquitoes. Others want to see clearer proof that this technology is even necessary, claiming that the company has only released its most positive data with the public and has kept other key data, including whether the mosquitoes curb disease transmission, private. And if the release actually launches as planned, some Keys residents say they aim to interfere.

Critics also say that Oxitec failed to engage with local communities in Florida and get their consent to release the mosquitoes. Whats the most upsetting is that the very people that are going to be most impacted, both by the benefits or the risks of such a decision, have like the smallest voice in how these choices are made. I think thats a really big issue, says Natalie Kofler, a molecular biologist and bioethicist who founded Editing Nature, a platform that advocates for inclusive decision-making processes to steer the use of genetic technology. If Oxitec doesnt do this right, she adds, we could have a huge impact on delaying the use of other beneficial technologies like that in the future.

Oxitecs OX5034 mosquitoes are programmed to combat the transmission of mosquito-borne illnesses by suppressing local Aedes aegypti populations. Oxitec which is US-owned and based in the United Kingdom describes their mosquitoes as friendly because they will only release males, which, unlike females, do not bite humans or transmit disease.

Also read: Clever Approach: Scientists Create GM-Free Organisms Using Genetic Engineering

At Oxitecs laboratory in the UK, the company genetically engineers the mosquitoes, giving the insects the self-limiting gene that makes the females dependent on the antibiotic tetracycline. Without the drug, they will die. Eggs from these genetically-altered mosquitoes which will hatch both male and female insects will be shipped to the Keys. Mosquitoes require water to mature from an egg to an adult; when Oxitecs team adds water to the boxes the mosquitoes will be deployed in, both GM males and GM females will hatch. With no tetracycline present in the box, the GM females are expected to die in early larval stages.

The male mosquitoes will survive and carry the gene. When they leave the boxes, the insects will, hypothetically, fly away to mate with wild females to pass the gene to the next wild generation, according to Nathan Rose, head of regulatory affairs at Oxitec. Kevin Gorman, the companys chief development officer, says the local female mosquito population will be increasingly reduced which will also reduce the number of wild male mosquitoes in the treatment areas.

Gorman emphasised to Undark that the EPA and other regulators found no risk in using tetracycline in breeding their genetically-altered mosquitoes. But some scientists think the presence of this antibiotic in the environment does pose a risk. According to Jennifer Kuzma, co-founder and co-director of the Genetic Engineering and Society Centre at North Carolina State University, tetracyline is commonly used in Florida to prevent bacterial diseases in agriculture particularly in citrus groves and to treat bacteria in sewage plants.

The use of the antibiotic for these purposes may mean that it will remain in the environment, especially in water where the mosquitoes breed, which could allow Oxitecs female mosquitoes to survive. While the company does not plan to release the mosquitos near areas where the antibiotic is used, Kuzma says the EPAs risk assessment did not include testing of any standing water for tetracycline something, she adds, would have been easy enough to do for good due diligence.

Skeptics of Oxitecs GM mosquitoes include local residents, physicians, scientists and environmental activists. Many of these opponents say they arent anti-GMO, but disagree with how the approval process has been handled. One group has even kept a running list of what it sees as Oxitecs wrongdoings since it first began experimental releases. The list includes Oxitecs lack of disease monitoring in the countries where it has released mosquitoes; the unknown price of its technology; and complaints that the company has overstated the success of some of it its trials.

I cannot trust this company. I cannot trust this technology, says Mara Daly, a resident of Key Largo who says shes been following Oxitecs plans for nine years.

This is not a traditional pesticide, she adds. This is not a chemical that you can trace. This is something completely different, new emerging technology, and we need better regulation.

Phil Goodman, chairman of the Florida Keys Mosquito Control District (FKMCD), an independently-elected commission carrying out mosquito control within Monroe County, says that many of those who discredit Oxitecs evidence do not understand the technology. Theyre fear-mongering, he says.

They have very little credibility here in the Florida Keys as far as Im concerned, he adds.

But people like Daly and Barry Wray, executive director of the Florida Keys Environmental Coalition, disagree. We want to know its safe, says Wray, who notes that his group more generally supports GM technology. We dont have another Florida Keys ecosystem. We dont have another Florida Keys community. We have this one.

Daly, Wray, and others point to what they perceive as the FKMCDs disrespect for public opinion. They argue that the community wasnt given a chance to consent before the EPA approval. There was a 30-day public forum in September 2019 about Oxitecs technology application, with 31,174 comments opposing release and 56 in support. A statement emailed to Undark by Melissa Sullivan, an EPA spokesperson, noted that the agency considered these comments during the review, but critics think it happened too quickly to be of real use.

In June, Kofler and Kuzma wrote an opinion piece in The Boston Globe about the EPA approval, critiquing the agencys regulatory system and calling for a better process for evaluating new biotechnologies. The researchers expressed concern that the EPA did not convene an independent, external scientific advisory panel to review Oxitecs claims about its mosquito strategy and that the agency only publicly released its risk assessment after approving the technology. The American public, Kofler and Kuzma wrote, needs to be assured that these decisions are made free of conflicts of interest. The statement from the EPAs Sullivan noted that the agency conducted anextensive risk assessment based on the best available science.

Some critics also wanted there to be more public engagement. Kofler and Kuzma say they offered to provide their expertise, along with other outside experts, to the mosquito control district to allow more discussion about the GM mosquitoes with the Keys community. But Kofler says the district wasnt responsive. Oxitec itself launched webinars about their new product, but not until after the EPA approval. Here we are, like in the final hour, having these conversations that needed to be happening a year ago, says Kofler.

Without public trust and enthusiasm, it doesnt matter whether Oxitecs mosquito technique works, says Guy Reeves, a genetic researcher at the Max Planck Institute for Evolutionary Biology in Germany, who stresses that he doesnt think the companys approach is unsafe. If the population in Florida Keys becomes so sensitised to this issue that they can no longer cooperate with each other thats good for the mosquitoes, not good for the people, he adds.

Based on their first generation mosquito OX513A, Oxitec says it has shown that the approach reduces a targeted mosquito population in trials in both Brazil and the Cayman Islands. But theres no evidence that this new OX5034 mosquito release will actually be worth it for mosquito suppression, says Reeves. Oxitec also hasnt explained how their new mosquito will directly curb human diseases, such as dengue. Reducing disease transmission and burden should be measures of efficacy for this technology, says Kofler.

According to Gorman, independent disease suppression data has only been collected by municipalities in Brazil because thats where most of the companys trials have been released in larger scales. These municipalities have shown that Oxitec mosquitoes have reduced dengue cases in areas of release, Gorman says. In order for Oxitec to collect additional data, he adds, the company needs to release and test large areas over sustained periods of time. Gorman maintains that the company is not required to report formal health impact studies.

Reeves adds that Oxitec also hasnt explained what resources are needed to sustain this product, how long it could take to be effective, or the cost. When asked about the cost of the Florida Keys project, Oxitec responded to Undark by email: Oxitec is a pre-commercial, pre-profit company. We will not profit from this pilot project in Florida. We are paying for it ourselves.

Oxitec has released more than a billion of their OX513A mosquitoes over the past 10 years. According to independent scientists, some of those experiments did not go well.

For example, researchers at Yale University and collaborators from Brazil analysed Oxitecs 2015 release of OX513A in Brazil. The scientists confirmed that some offspring of the genetically modified mosquitoes which were supposed to die and not pass new genes to the wild population survived to adulthood and mated with their native counterparts. Between 10 and 60 percent of the native mosquitoes contained genes from Oxitec, according to the Yale study, which published in Nature in 2019. The papers authors concluded they do not know what impacts these mixed mosquitoes have on disease control or transmission, but added that their findings underscore the importance of monitoring the genetics of the insects.

Oxitec disagreed with the findings and responded on the journals website. Oxitec told Gizmodo that Yales study includes numerous false, speculative, and unsubstantiated claims and statements about Oxitecs mosquito technology. And when Kofler and three other scientists wrote about Oxitecs Brazil trial in The Conversation, Oxitec pushed to have the article retracted, says Kofler.

For this coming release, some Key Largo locals are willing to act on their anger. Daly, for instance, says that if the mosquitoes are deployed in her neighbourhood, shell try to put insecticide in any box she finds or send it to an expert to test even if it means getting in trouble with the federal authorities. I already have my arresting officer and she said shes gonna clean her handcuffs for me, she says. I dont care.

Ideally, Daly says, it wont have to come to that. She and other locals hope to stop Oxitec before the latest mosquitos are delivered. Daly says she has been busy organising protests like one that happened recently in Key Largo and giving out yard signs to residents who dont want their property used in the trial. Locals are pissed off. So I have been busy getting the press to cover the local opposition, Daly wrote in an email to Undark.

The first flying insect or animal that can actually use our human blood for a friggin trial for a product to come to market without my consent, Daly says.

Thats my blood, she adds. Thats my sons blood. Thats my dogs blood.

Taylor White is a freelance journalist based in Cape Cod, MA and a graduate of the Science, Health & Environmental Reporting Program at the NYU school of journalism. Her work has appeared in NOVA GBH, Dana-Farber Cancer Institute, the American Association for the Advancement of Science, GenomeWeb, Spectrum and Science Vs.

This article was originally published on Undark. Read the original article.

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In the US, Imminent Release of Genetically Modified Mosquitoes To Fight Dengue - The Wire Science

All young children display impulsive or defiant behavior occasionally. Sometimes, this is part of a normal emotional reaction. But if these behaviors are extreme or outside the norm for their level of development, it could be a sign of a behavioral disorder.

The most common behavioral disorders in children are:

In this article, we discuss some of the most prevalent behavioral disorders in children, their symptoms, causes, diagnosis, and management.

Sex and gender exist on spectrums. This article will use the terms male, female, or both to refer to sex assigned at birth. Click here to learn more.

The U.S. Department of Health and Human Services describes behavioral disorders as involving a pattern of disruptive behaviors in children that last for at least 6 months and cause problems in school, at home, and in social situations.

This is different from the challenging behaviors children sometimes display. Almost all children will have tantrums, or act in aggressive, angry, or defiant ways at some point.

While challenging, these behaviors are a normal part of childhood development. Often, they are the result of strong emotions that the child is expressing in the only way they know how.

As a result, healthcare professionals only diagnose a behavioral disorder when the disruptive behaviors are severe, persistent, and outside the norm for the childs developmental stage.

Behavioral disorders are also different from autism spectrum disorder (ASD), which is an umbrella term for neurodevelopmental conditions that affect how some children communicate, socialize, and process sensory stimuli.

ASD may cause behaviors in children that caregivers find unusual or challenging, but these are the result of how they experience the world.

The following sections look at some specific behavioral disorders and their symptoms.

ADHD is a disorder that causes difficulty focusing attention. It can also cause hyperactivity and impulsivity.

There are three ADHD subtypes, with the diagnosis depending on the symptoms the child displays most often. The subtypes are:

A child with inattentive type ADHD may:

A child with hyperactive-impulsive type ADHD may:

A child with combined ADHD will exhibit a mixture of the above behaviors.

Doctors often diagnose ADHD after the age of 6. This is because the symptoms can be more apparent when a child starts school, and struggles to adjust to more quiet, sedentary activities.

Learn more about how ADHD can manifest differently in girls.

Those with CD tend to violate basic social rules and the rights of others. This can have a significant impact on someones academic, social, and home life. It can develop both in childhood or in adolescence.

The symptoms of CD include:

Many young people with CD have difficulty interpreting the behavior of others. For example, they may believe a person is behaving in a hostile way toward them when they are not. This causes them to escalate toward aggressive or violent behavior.

People with CD may also have difficulty feeling empathy, or have another condition, such as anxiety or post-traumatic stress disorder that affects their thoughts and behavior.

According to Mental Health America, CD may affect 616% of boys in the general population, and 29% of girls. If CD first manifests before age 11, it is more likely to persist into early adult life.

Children and adolescents with ODD display an ongoing pattern of hostile behavior toward authority figures, such as parents, caregivers, or teachers. Unlike conduct disorder, children with ODD tend to violate minor rules, rather than major rules and social norms.

The potential signs of ODD include:

It is worth noting that some clinicians have criticized the concept of ODD, arguing that it medicalizes normal child behavior. It is common for children to behave angrily or defiantly when they are unhappy, so it can be difficult to distinguish between ODD and behavior that is related to stress.

Doctors can only diagnose ODD if the behavior has been persistent for 6 months, causes constant disruption at home or school, and is not the result of another mental health condition.

There is no single cause for behavioral disorders. It is likely that a mixture of physiological and environmental factors play a role.

But it is important to note that a child of any background, sex, or gender can have a behavioral disorder.

The following factors may influence their development:

Evidence suggests that changes in brain structure, development, and neurotransmitter levels may influence behavioral disorders. For example, areas of the brain that control attention are less active in children with ADHD.

Low serotonin and high sensitivity to cortisol, a stress hormone, may also play a role in aggression.

Additionally, conditions that affect learning ability may have an impact, as children with intellectual disabilities are twice as likely to have a behavioral disorder.

Behavioral disorders appear to be more common in children with a low birth weight, or who were born prematurely.

ODD may also be more common in children exposed to toxins in the womb, such as tobacco smoke, or in children whose parents or caregivers have substance abuse disorders.

Behavioral disorders can run in families. This could indicate a genetic predisposition for some people to develop them.

But in the case of ODD, scientists have not identified a specific gene that could explain this. Older studies have shown that people with ADHD, ODD, and CD share similar genetic traits, but none were unique to these disorders.

Male children are more likely to have behavioral disorders than female children. It is unclear if this is due to biological differences, or whether differences in gender norms and expectations influence how male children behave or develop.

For example, girls with ODD may be more likely to express aggression through words, rather than actions. This may mean the behavior is less obvious, and so less likely to receive a diagnosis.

Psychological trauma is a complex emotional and physical response to severe or chronic stress. Early exposure to trauma can impact child development.

Any experience that causes significant distress can be traumatic, but common examples that may affect children include:

Behavioral disorders are more common in people from low-income backgrounds, which may be due to increased levels of stress.

It is also possible to confuse child traumatic stress with a behavioral disorder, as they have overlapping symptoms.

It is important to consult a mental health professional if a child may have a behavioral disorder. A specialist can diagnose the disorder through an assessment process. This may include:

It is not possible for parents or caregivers to diagnose behavioral disorders themselves. An early diagnosis can significantly improve the effectiveness of treatments.

But many child psychologists will not diagnose a behavioral disorder in very young children, particularly those of preschool age or younger. This is because it can be challenging to distinguish between normal and abnormal behavior in this age group.

Over 80% of preschoolers have mild tantrums occasionally. Because young children experience huge developmental changes in a short period of time, they may outgrow short-term behavioral difficulties.

The management of behavioral disorders can vary depending on the childs needs, their familys needs, and the type and severity of their disorder. Approaches that may help include:

Patience, empathy, and encouragement are important for helping to boost self-esteem. An authoritative parenting style, which involves listening to children whilst also setting reasonable rules and boundaries, is also helpful.

It is important to note that bootcamp-style programs and tough love are not effective for behavioral disorders. In fact, they can be very damaging.

Caregivers should speak with a pediatrician if they think their child may be showing signs of a behavioral or developmental disorder. The doctor may refer the child to a specialist, such as a:

It is also important for caregivers to seek support for their own well-being. They may wish to make use of respite care, if available, or to speak with a therapist. There are also support groups where caregivers can connect with others raising children with behavioral disorders.

Most children have temper tantrums or display impulsive or defiant behavior at some point. These are usually a normal part of child development.

But in cases where the behavior is persistent and constant, or outside the norm for the childs age and level of development, it may be a sign of a behavioral disorder.

With early and appropriate treatment, families can learn to manage the behaviors. In many cases, careful treatment improves behavior over time.

Read the rest here:
Behavioral disorders in children, their symptoms, and treatment - Medical News Today

The relationship between psychosocial stress and CHD seems to be stronger in women than in men. It may also vary depending on the type of stress or stressor.

However, it is unclear how different types of psychosocial stress impact womens risk of developing CHD.

For this reason, a research team from Drexel University Dornsife School of Public Health in Philadelphia, PA, decided to investigate the association of psychosocial stressors including job strain, stressful life events, and social strain with the incidence of CHD in women.

They combed through the data collected as part of the Womens Health Initiative Observational Study (WHIOS), to assess the independent and combined impact of stressful life events, social relationships, and paid work.

Their findings, which appear in the Journal of the American Heart Association, indicate that work and social strain seem to pack a double punch, increasing womens risk of developing CHD by 21%.

Stressful life events and social strain, that is, the negative aspects of social interactions or relationships, also increased womens risk of developing CHD by 12% and 9%, respectively.

Our findings are a critical reminder to women, and those who care about them, that the threat of stress to human health should not go ignored, says Dr. Conglong Wang, the studys lead author. This is particularly pertinent during the stressors caused by a pandemic.

If true, these findings could shift the focus of preventing CHD in women from managing current stress to finding ways to prevent stress at the source.

It would also serve as a serious reminder that stress is a major threat to human beings, women in particular, and that this threat must be addressed promptly and properly.

Over the past few years, several major studies have established that psychosocial stress from different aspects of life may impact the risk of developing CHD.

This is likely because psychosocial stress can disrupt homeostasis the optimal internal functioning of organs and their systems which can lead to an illness.

As a result, stress can intensify cardiovascular inflammation and reactivity, resulting in metabolic changes that increase the risk of developing CHD.

Psychosocial stress is also linked with behavioral patterns such as alcohol consumption, smoking, or being physically inactive. Certain medical conditions, including diabetes and hypertension, affect the risk of CHD as well.

Stress may impact men and women differently. The findings from a few studies indicate that the link between psychosocial stress and CHD may be stronger in women than in men.

In one study, women were more likely than men to document high average stress levels and associated emotional and physical symptoms, including exhaustion and depression.

Another study found that women may be exposed to psychological stressors that men experience less commonly.

However, scientists still do not know how different stressors influence womens risk of having CHD. It is therefore unclear which stressors affect the risk of developing this condition the most.

This makes it difficult for healthcare professionals to advise women on the best ways to reduce their likelihood of developing CHD. It also means women cannot be sure which stressors are most important to address to keep CHD at bay.

In the new study, the research team analyzed data collected as part of the WHIOS, an initiative aimed at finding better ways to prevent heart disease, cancer, and osteoporosis in women.

The scientists analyzed data from 80,825 women living in a diverse array of states across the United States that had experienced menopause.

Participants were aged 5079 when the WHIOS started tracking them, and the average time women were tracked was 14 years and 7 months. Women assessed stressors in the WHIOS using self-reporting questionnaires.

After adjusting for variables such as job tenure, socioeconomic factors, age, and additional stressors, the researchers found a high stressful life events score increased the risk of developing CHD by 12%, and high social strain by 9%.

The team also noted that the impact of work and social strain seem to work synergistically, increasing womens CHD risk by 21%. Job strain alone was not linked with a higher CHD risk.

These findings could have important implications for how healthcare professionals and women themselves decide to best tackle stress to reduce their CHD risk.

It is of note that a disproportionately large number of participants in the study were white and held more than a high school diploma. The teams findings may also be impacted by the healthy worker bias, according to which people who are less healthy are more likely to be unemployed.

Moreover, the team did not take into account other important compounding factors, such as working hours and social support systems, which are associated with CHD.

Also, the scientists only focused on the impact of stress related to a persons most recent or current job, ignoring the change of jobs throughout life.

The researchers write that more studies are necessary to determine the impact of job demands as they align with sex.

A persons sex and socioeconomic status may also affect their ability to manage stress. That is why future studies will also have to identify subgroups of people that are more likely to benefit from preventative stress interventions than others.

However, these new findings help fuel the need for more advanced, diverse research exploring the link between stress, heart disease, and sex or gender.

They may also encourage healthcare professionals and women alike to reconsider their best options for reducing their CHD risk and improving overall health.

The COVID-19 pandemic has highlighted ongoing stresses for women in balancing paid work and social stressors. We know from other studies that work strain may play a role in developing CHD, but now, we can better pinpoint the combined impact of stress at work and at home on these poor health outcomes.

Dr. Yvonne Michael, senior author and associate professor in the Dornsife School of Public Health

My hope is that these findings are a call for better methods of monitoring stress in the workplace and remind us of the dual burden working women face as a result of their unpaid work as caregivers at home.

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How stress impacts women's heart health - Medical News Today

Leafly honors the 50th anniversary of 4:20 (aka 420 or 4/20) this April with a celebration of legendary strain families. Weve already covered famous Hazes, Tangies, Purples, and OG Kushes. Now for the headliner: Cookies and Cakes!

Why do people wait two hours in line to spend $70 on an eighth-ounce of weedin the middle of a pandemic?

Easy: the Cookies strain of cannabis transcends mere geneticsits a lifestyle.

On November 4, cannabis brand Cookies new Apples and Bananas release drew several hundred young, heavy-THC smokers to Berners on Haight in San Francisco. In less than 90 minutes, guys in crisp, white sneakers and basketball shorts bought up all the pricey, designer weed.

They Instagrammed the chic bags of chunky, fragrant, mega-potent bud, flexing on their friends. One group couldnt wait to get home. They ripped bongloads out the side seats of a dusty, parked Hyundai with no hubcaps.

Cookies and Cakes strains of cannabisincluding Sunset Sherbert, Gelato, Runtz, Wedding Cake, and GMO Cookiescomprise modern pots center of gravity. Thin Mint Cookies, Animal Cookies, Platinum Cookies, and on and onthey are the top-selling cultivars in legal stores today, and their genes appear in the lions share of hyped new weed varieties.

From 2007 to the presentand emanating out of the San Francisco Bay AreaCookies hard-hitting, hybrid indica power, and its complex, sweet- scrumptious aroma has made fans of elite pot snobs, medical marijuana patients with PTSD, all-star rappers, and now almost everyone who partakes.

Cookies got this way because breeders like Jai Jigga Chang and Mario Mr. Sherbinski Guzman hybridized the best of the early 2000s OG Kushes to some truly exotic sativas. They carved up a wave of medical marijuana and adult-use legalization with rapper/business mogul Berner and wrote the playbook for viral weed marketing.

The Cookies story spans the recent histories of cannabis, weed law reform, San Francisco, and hip-hop. Its a story of plant worship and profit-chasing, of the serendipity of city life, and the power of sharing gifts instead of hoarding them.

Grower Ghost at ABF Genetics, short for Always Be Flowering, and spreader of Forum Cut Cookies, said growing Cookies is something that changed my life.

It became that thing, he said. I challenge people to say what since Cookiesor that was not derived through that whole gene poolhas really changed cannabis.

Haters gonna hate, but the future still happens first in San Francisco.

So it went with weed strain Girl Scout Cookies, which San Francisco breeder Jigga developed for the exploding medical marijuana market in the late 2000s.

In SF, peak prohibition met surging demand for cannabis and prices bloomed. Californias police arrested smokers by the tens of thousands per year. Growers used pseudonyms only, and feared being followed home from a party and beaten and robbed, or followed home from the hydroponics store and raided by police.

Californians legalized medical marijuana in 1996, and personal defenses against cannabis prosecution had become collective defensesgreen-lighting the first dispensaries and more grows.

There was this feeling of energy in the Bay Area that there was something going on that was truly special.

The profits outweighed the risk. The Bay Areas medical and recreational consumers, including its rappers, adored weed. In that climate, wholesale pounds of OG Kush, the then-reigning champion strain, might go for $3,500-$4,000.

There was this feeling of energy in the Bay Area that there was something going on that was truly special, said Mr. Sherbinski. An industry was being born.

Just like so many other thingsmusic, or technologycannabis also had its first place there, he said.

Today most states have medical laws, and 18 have adult-use legalization, now including New York, Virginia, and New Mexico. The legal industry generates $18.3 billion and employs 321,000.

Mr. Sherbinski relates how San Francisco breeder Jigga took his favorite OG Kush, called a Flo Rida OG (pronounced Flow Rider), and crossed it to his mix of a rocket-like strain he named F1 and another strain called Durb.

Mr. Sherbinski told Leafly Durb was not Durban Poison.

Ive had the F1. And Ive had the Durb. And Ive had the Flo Rida OG, said Sherbisnki.

(In 2014, Jigga told High Times that Durb was in fact Durban Poison. Bottom line: Jigga crossed three strains, F1 Durb to Flo Rida OG, to make Cookies.)

Jigga stayed busy, too. He also crossed the F1 Durb to another leader of the day, Granddaddy Purple, thus creating Cherry Pie.

Other, more apocryphal origin stories exist, but what happens is theres little pieces of info that get out and people build on that, said Sherbinski. The above facts are what I was told by Jigga.

Jigga didnt call us back, but either way, Cookies became a sleeper hit.

And I remember grinding it up and smoking it and thinking, Wow, its a super-unique, tasty flower. And I said, Yeah, I gotta track down the cut.

Ghost at ABF Genetics said he got introduced to the strain through a friend from Jigga and Sherbinskis Sunset District clique. (Many of these guys grew up together, going to the same high schools, playing pick-up basketball, smoking weed, listening to rap.)

The veteran grower from back East had collected many, many leading strains. But he still remembered the day his buddy from the Cookies circle brought over a nug of GSC, in about 2008.

It was like curled up in a Ziploc baggy, this little, abused piece of flower, Ghost recalled. And I remember grinding it up and smoking it and thinking, Wow, its a super unique, tasty flower. And I said, Yeah, I gotta track down the cut.

Your reporter has been sampling Cookies since that time period as well.

Cookies nugs present as dense, multicolored, and resinous. It first smells flat and musty, but complex. Break it up and grind it and the smell decoheres into a rowdy mix of sweet, berry, incense, and the savory, burnt part of a sugar cookie. The exhaled smoke hit might contain a note of grape and fuel or gas from the OG.

You get real high with a heavy effect that doesnt make you fall asleep per seyoure just super-lit.

Ghost couldnt get a cut of Cookies that easily. Back then, growers kept new strains to themselves or in a tight circle.

Initial supplies of Cookies remained low, limited to small indoor grows sometimes shielded from police by a medical marijuana defense.

San Francisco rapper and entrepreneur Gilbert Berner Milam Jr. gets credit for truly marketing Cookies, first through hip-hop and rap, and later through social media. Today, Cookies Enterprises commands a global lifestyle brand with licensed stores, unique strains, and partner farms in several legal states.

Cookies benefited from the advent of social media and was the first cannabis strain mentioned relentlessly in hip-hop, said Keith Stephenson, the Oakland, CA owner of Purple Heart Patient Center, reportedly the nations oldest black-owned dispensary.

If you wanted Cookies back then, you had to schlep out to the Hemp Center on Geary Ave. in the Sunsetthis grungy lounge with a Mos Eisley cantina vibe where Berner sometimes budtended. Your fearless reporter distinctly remembers that one and only visit: Junk piled up in the lobby. The weed equivalent of old barflies stared at you from the corner. I bought a gram of GSC there back around 2013(?), and that nug was fire.

Ghost got his hands on one Cookies plant in 2008, when two buddies paid $3,500 for a cut from a relative of a grower in the original circle. He grew out the GSC cutting and verified the result. Ghosts friend who first brought him the flower said, Thats it.

Cookies got loose into the wild when Ghost shared cuttings of his plant with four close friends. Rare strains become a type of currency among high-end connoisseurs that have everything else. Ghosts cut would become known as the Forum Cut, in reference to the internet forums where they debated it.

And the next thing I know, one of them is selling cuts to people; one of them is giving them away; one of them is doing giveaways behind, like, dumpsters. And then the rest of them just kind of spread through the network, he explained. One cutting, or clone, made it to the UK.

Ghosts wholesale pounds of indoor Cookies fetched $4,000, he said, at places like the Green Door.

At this point, a weed grower might assume fame and riches lie in making something special and being the only person with it. Actually, its the opposite.

Supplies stimulate demand, which induces growers, thus increasing supplies, and supporting more demand.

If we hadnt got that cut out as much as it did, it wouldnt have become known as what Cookies is, said Ghost. If its not available, people cant see it. If they cant try it, it doesnt really exist for them. Itll just fade and die off.

If you were a dispensary back then that didnt have Cookies, you werent a dispensary, Mr. Sherbinski said.

The perpetual motion machine of growing, marketing, selling, buying, smoking, and enjoying Cookies added more and more people each harvest.

It was a huge seller for some retailers, said Stephenson at Purple Heart in Oakland, CA. He started carrying Cookies strains in 2012. It definitely deserves to be celebrated.

The core Cookies team released Animal Cookies. There was Thin Mint Cookies. Green Door had Platinum Cookies.

A strain truly arrives when counterfeiting and the name game commences, said Mr. Sherbinski. Everyone slapped a name on a cookies cultivar.

We make the strains and they change the names, he said.

At that point, it became a clusterfuck, added Ghost.

Nowadays, Cookies offspring Gelato and its descendants run the world. But we wouldnt be here without the happy accident of Sunset Sherbert.

By 2012, the original Cookies craze was well underway, and San Francisco grower Mario Guzman, now known as Mr. Sherbinsnki, stood ready to partake in it.

Out in the residential Sunset District of San Francisco, he had crossed a dark, dark, dark purple, stringy sativa Burmese to the best OG Kush around the Bay Area, where pounds sold for $4,200 and $4,300.

Mr. Sherbinksis Burmese crossed with Larry OG became his Pink Panties, due to its pink hairs, or pistils, on the buds. With Pink Panties seeds in hand, he started a crop of seedlings. For research, he stuck one six-inch baby plant into his special, flowering room at his grandmas house.

Flowering room lights are timed to make the plant bloom instead of grow. But instead of blooming a female bud that he could study, the Pink Panties matured into a male. Before Guzman noticed, the male Pink Panties pollinated the entire room of Girl Scout Cookies females in the flowering room.

I didnt realize it would pollinate in a matter of weeks, but it did. It just took off.

All of a sudden, that commercial crop of Cookies bud became a research crop of new seeds. And inside one of them? What we call Sunset Sherbert.

Mr. Sherbinski said the name came to him when he first smoked the strain, and it reminded him of Thrifty ice cream rainbow sherbet, an iconic California childhood flavor for decades. He remembered his mom buying him a scoop for about 10 cents as a kid when they did laundry.

It was a really popping strain in the Bay Area. We were promoting it. Rappers were rapping about it.

When I first smoked Sunset Sherbert I tasted berry, citrus, the lemon, the orange, a little lime, all these different flavors, and I was like, Man, this tastes like Sherbert, he recalled.

He then added the district it came from and boom, Sunset Sherbert. The strain hits smooth, sweet, but still enough power in it to hit your lungs, he said. Everyone likes it, he added, including atypical consumers like women and older smokers, and especially veterans with PTSD.

Related

Pleased as Purple Punch: A Purps family genealogy

The Cookies team applied their marketing formula to Sunset Sherbert and repeated the success of Cookies, Guzman said.

It was a really popping strain in the Bay Area. We were promoting it. Rappers were rapping about it.

Mr. Sherbinski spread small-batch, indoor harvests of sherbert around to influential stores across the statestores like Harborside Health Center in Oakland and the Vapor Room on Haight St.

Part of what created the hype, for me, was it was created with love. There was not a lot of it; I made sure to spread it around to the dispensaries and friends doing a good job of getting it out to the public, he said.

The Cookie and Sunset Sherbert formula may have reached its most evolved form with Gelato, a cross of Sunset Sherbert and Girl Scout Cookies.

For this one, Jigga and Mr. Sherbinski used a substance called colloidal silver to make a female Sunset Sherbet flower produce pollen, then pollinated a GSC.

The resulting seeds are all female, and the team grew them all out, hunting for the best-looking and smelling offspringcalled a phenotype. This pheno-hunt concluded with a private, invite-only tasting by industry heads on June 16, 2014, at a Cuban food restaurant, said Guzman.

The nights picks are so famous, the numbers on the side of the flower pots became famous and emerged as the keepers:

Again, high-quality indoor production, plus on-point influencer marketing, equaled huge demand for the elite plant. And again, rather than hoarding the strain close, Mr. Sherbinski distributed cuts of Gelato 33, sparking a national bumper crop of the stuff.

Ghost uses the word, saturation.

Its one of those things where it just spun and spun and spun, he said.

Today, theres a reason why everything contains Gelato 33 genes: because Gelato grows, looks, smells, and feels amazing. Its architects stimulated the demand and provided the supply. They didnt hoard their fire in a closet. They brought it to others, Prometheus-style, and unlocked weed god mode.

Nowadays, Cookies genes appear in everything. Quality can vary, but it often bests its rivals.

The strains are over-produced now in California. However, its something that people expect to find as a standard variety, said Stephenson.

Even the cheapest of knockoffs attest to the allure of the real thing. If imitation means flattery, the weed world bows to the Cookies strain family. Look at all the headlines:

There are just so many dimensions to Cookies, a seemingly infinite array of facets, all reflecting off this heavy remix of global genetics. Lemon Tree strains and Zkittlez certainly command attention, but theyre still fads, compared to Cookies, said Mr. Sherbinski.

I think what makes a truly good strain is when people come back to it. Its such a good strain that even if people get away from it for a while when they come back to it, shes going to be there with open arms.

David Downs

David Downs directs news and lifestyle coverage as the California Bureau Chief for Leafly.com. He's written for WIRED, Rolling Stone and Billboard, and is the former cannabis editor of the San Francisco Chronicle, as well as the author of several cannabis books including 'Marijuana Harvest' by Ed Rosenthal and David Downs. He co-hosts The Hash podcast. TW: @davidrdowns | IG @daviddowns

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Just desserts: The Cookies and Cakes family genealogy - Leafly

Timothy the hippo, otherwise known as Fiona's biggest admirer, has been known to give Fiona lavish gifts for her birthday and Valentine's Day. But on Timothy's sixth birthday Wednesday, Fiona gave Timothy quite a special gift.Timothy, who's known to write Fiona love letters on Facebook on Thursdays with the help of his friends at the San Antonio Zoo, wrote Fiona this week to thank her for giving him what he called a "kiss painting." The painting showed Fiona's mouth on a canvas in rainbow paint."Ive been practicing my kisses you know....blush! Thank you so much and remember I always think you are the most beautiful hippo Ive ever seen!" the Facebook post said.Timothy lives more than 1,100 miles away at the San Antonio Zoo, but he's been madly in love with Fiona for years now.For her birthday last year, Timothy gifted Fiona an Edible Arrangement, and clearly, by looking at the joy in her face in the image below, you can tell how happy she was.This year for Valentine's Day, Timothy stepped up his game and went the extra mile or 3,000 extra miles to be more exact to give an extra special gift to his longtime crush.Timothy purchased a small property of Scottish land in Fionas name, giving her the name Lady Fiona.The Cincinnati Caledonian Pipes and Drums Band helped in the celebration with song and dance.Fiona needs to be at least 5 years old before she starts thinking about boys, according to Wendy Rice, the head keeper at Cincinnati Zoo's Africa Department. Fiona turned 4 years old this year."The genetics are basically what's going to matter most," Rice said. "If and when Fiona were to get a breeding recommendation some day, it would be based entirely on who was genetically the best match for her -- that may or may not be Timothy."Fiona's genes are valuable in the world of Nile hippopotamuses. And eventually, Rice said, the goal is to have Fiona breed if she can. But we're talking way down the road, Rice said, when Fiona is at least 5 years old.What happens then?"We obviously don't want her going anywhere," Rice said. "We love her. She's our baby and this hometown loves her. We're fairly certain people would riot if we said Fiona was leaving. We're hopeful that if she gets a breeding recommendation, that a male would be brought here for her so she wouldn't have to leave Cincinnati."

Timothy the hippo, otherwise known as Fiona's biggest admirer, has been known to give Fiona lavish gifts for her birthday and Valentine's Day. But on Timothy's sixth birthday Wednesday, Fiona gave Timothy quite a special gift.

Timothy, who's known to write Fiona love letters on Facebook on Thursdays with the help of his friends at the San Antonio Zoo, wrote Fiona this week to thank her for giving him what he called a "kiss painting." The painting showed Fiona's mouth on a canvas in rainbow paint.

"Ive been practicing my kisses you know....blush! Thank you so much and remember I always think you are the most beautiful hippo Ive ever seen!" the Facebook post said.

Timothy lives more than 1,100 miles away at the San Antonio Zoo, but he's been madly in love with Fiona for years now.

For her birthday last year, Timothy gifted Fiona an Edible Arrangement, and clearly, by looking at the joy in her face in the image below, you can tell how happy she was.

This year for Valentine's Day, Timothy stepped up his game and went the extra mile or 3,000 extra miles to be more exact to give an extra special gift to his longtime crush.

Timothy purchased a small property of Scottish land in Fionas name, giving her the name Lady Fiona.

The Cincinnati Caledonian Pipes and Drums Band helped in the celebration with song and dance.

Fiona needs to be at least 5 years old before she starts thinking about boys, according to Wendy Rice, the head keeper at Cincinnati Zoo's Africa Department. Fiona turned 4 years old this year.

"The genetics are basically what's going to matter most," Rice said. "If and when Fiona were to get a breeding recommendation some day, it would be based entirely on who was genetically the best match for her -- that may or may not be Timothy."

Fiona's genes are valuable in the world of Nile hippopotamuses. And eventually, Rice said, the goal is to have Fiona breed if she can. But we're talking way down the road, Rice said, when Fiona is at least 5 years old.

What happens then?

"We obviously don't want her going anywhere," Rice said. "We love her. She's our baby and this hometown loves her. We're fairly certain people would riot if we said Fiona was leaving. We're hopeful that if she gets a breeding recommendation, that a male would be brought here for her so she wouldn't have to leave Cincinnati."

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Fiona gives her biggest admirer, Timothy the hippo, 'kiss painting' for his 6th birthday - WLWT Cincinnati

At any given time on The New York Times website, a quick search for gender will yield an array of articles on the ins and outs of sex personified and the endless ways biology teams up with political adversaries to oppress queer people.

One recent so-called gender headline offered A Guide To Neopronouns, those nonsensical sounds like ze and zir that break from the sex binary and thus from reality. Are you a person, place or thing? the article posed, going on to imply that identity is nothing more than an aesthetic.

How Do I Define My Gender if No One Is Watching Me? probed another title, with all the flavor of If a tree falls in a forest and no one is around to hear it, does it make a sound? without the philosophy. Instead, this article refocused on what happens to so-called gender expression when its relegated to the stay-at-home privacy of pandemic lockdown. How does gender is a social construct work when theres no social? the author probed, unintentionally revealing the utter emptiness of gender identity when one tries to separate it from biological sex.

The articles are somehow baffling yet mind-numbing. Pieces like these, which seem to be ubiquitous now, are meaningless screeds of semantic acrobatics to convey the experiences of a group of Americans so out of touch with science that they would suppress the wonders of their sex and subscribe to a new doctrine that cannot even share a common language with reality. It is sad and foreign and exhausting, but the New York Times caters to it, creating room in its scarce pages for stories about folks whose prefixes include Mx. where Mr. or Ms. should be.

The brain boggles considering how such science-devoid content can square with another recent Times article. Its a collection of frequently asked COVID-19 vaccine questions. Is the Second Dose Bad? If I Feel OK, Is It Working? Can I Take Tylenol? asked last weeks headline as more and more Americans get vaccinated.

One particular subheading stands out: Is it true that women are more likely to get worse side effects from the vaccine than men?

The answer is full of science-y explanations. Apparently, females can produce double the antibodies of men after getting flu shots or vaccines for hepatitis A or B or for measles, mumps, and rubella.

It also turns out that in aggregate, women have had worse bodily responses to the vaccine than men do, with more women than men experiencing side effects and nearly all the life-threatening anaphylactic reactions, although rare, occurring in women. The Times cites a study revealing that over nearly 30 years, women have made up 80 percent of all anaphylactic vaccine reactions among adults.

[T]he higher rate of side effects in women also has a biological explanation, the article says. While testosterone can weaken a bodys immune response, estrogen can galvanize it. Additionally, many immune-related genes are on the X chromosome, of which women have two copies and men have only one, the Times declares. These differences may help explain why far more women than men are afflicted with autoimmune disease, which occurs when a robust immune response attacks the bodys healthy tissue.

Here, the Times isnt shy about making sex distinctions. Its right there in the science: Men and women are obviously different in myriad ways, with immune and vaccine reactions just being the latest in the spotlight. If its so easy to articulate the innate differences between the sexes, why does the New York Times entertain such gender gibberish as ze/zir and moon/moonself?

For years, the left has shouted that gender has nothing to do with sex. To insist that sex is genetic and results in only men and women is to evoke the LGBT clap-backs that gender is a social construct and chromosomes dont determine your gender.

A paragraph from one of the Times gender articles, however, reveals the deep and depressing hole in that worldview. The self-termed transgender-nonbinary author writes of the pandemic experience:

I was surprised by how much my gender instead seemed to almost evaporate. No longer on the alert for how to signal a restaurants waitstaff that neither he nor she applied to me, or for whether colleagues and neighbors would use the right language devoid of anyone to signal my gender to I felt, suddenly, amorphous and undefined. It was as though when I had swapped my Oxford shoes and neckties for fuzzy slippers and soft sweatpants, I, too, had lost my sharply tailored definition. Where did my own gender reside, then, if not in sending signals of difference?

These reflections are heartbreaking. Not only do they signal the amount of energy that some queer people derive from policing the perceptions of others and the apparent pleasure this may afford them, but it exposes the emptiness of finding ones identity in finding ones identity.

Thats all this futile pursuit truly boils down to. In rejecting the scientific sex binary in favor of amorphous and transient gender theory, a trans persons identity doesnt just become the opposite sex or an association with its pronouns. Rather, his or her identity becomes the lifelong task of asserting that their identity is not what you think.

Thats because the answer to the question, Where did my own gender reside, then, if not in sending signals of difference? is in ones sex. Thats where gender resides. Thats where it has always resided.

When the performative displays inherent in normal everyday life are stolen by pandemic lockdowns, and science and truth are all that remain, were forced to look in the mirror and confront reality: Human beings are genetically male and female, and since language is made to correspond with reality, we refer to those people as either he/him or she/her, consistent with their sex. Although we differ, our identities and thus the language we use to describe them are forever linked to our immutable genetics.

Any deviation from or internal confusion about these realities warrants compassion and assistance, but as weve known since time immemorial and as has been made yet more apparent through pandemic science, social experiments, and personal anecdotes, men and women are real and immutable categories, and they are different.

For a political stripe that prides itself on faithfulness to science, the lefts media and adherents dispense with it wholesale and then cant understand the emptiness that remains. The same science that explains why men and women respond differently to COVID vaccines also explains why eschewing sex in pursuit of gender fluidity is an exercise in futility.

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The New York Times Can Tell The Difference Between Men And Women With Vaccines But Not Pronouns - The Federalist

A 23andMe study from 2015 revealed that close to 4 percent of the companys customers who identified as white Americans had at least 1 percent African ancestry, consistent with an African ancestor within the last 11 generations or so. About 12 percent of whites from Southern states like South Carolina and Louisiana had 1 percent or more of African ancestry.

The Harvard scholar Henry Louis Gates Jr. has calculated that there are millions of contemporary whites who, according to the old, notorious one- drop rule of the Jim Crow era, would have been considered legally black proof not only of the absurdity of that definition of difference, he writes, but of the power of modern science to blow up false narratives about race and about American history. If modern DNA tests had existed during the heyday of mainstream eugenics in the early 20th century, Dr. Gates and others have suggested, they might have served as direct repudiation of that pseudoscience.

So, what happens when Americans learn about the diversity within themselves? The jury is still out on whether direct-to-consumer genetic testing reinforces our sense of immutable racial categories or breaks them down.

Research by Wendy Roth, a sociologist at the University of Pennsylvania, has found that customers basic knowledge of genetics going into testing may play a role in whether tests accentuate or reduce their racial essentialism. Besides, we are not our ethnicity estimates: For a variety of reasons, including the ways in which were shaped by community, family and personal experience, DNA and identity are not the same.

But whats clear from research and from my conversations with hundreds of consumers is that genetic revelations can inspire journeys of self-discovery, helping people rewrite their understandings not only of their families but of their orientations as Americans.

Some people I spoke with recounted how theyre thinking long and hard, for the first time, about what boxes to check on medical forms asking for race. Some have legally changed their names to reflect their forebears. Others are using research to illuminate the lives of ancestors in Africa before the trans-Atlantic slave trade.

One man I interviewed discovered through DNA and genealogy that his grandfather was Black, and that his mother claimed fictional Sicilian heritage to protect her family from the discrimination shed experienced growing up. He has spent the years since researching the Vermont community where his mom grew up, meeting his Black relatives, and rethinking his place in America. The truth about the past is so important, he told me without it, We cant evolve.

Continued here:
Opinion | DNA and Race: What Ancestry and 23andMe Reveal - The New York Times

TEL AVIV While the SARS-CoV-2 coronavirus grabbed center stage over this past year, biotech startup eggXYt turned its attention to avian influenza the deadly bird flu thats led to the slaughter of millions of infected poultry and also threatens human health.

A new licensing agreement will enable eggXYt to develop genetic resistance in chickens against avian influenza virus using a technology known as gene editing induced gene silencing from U.K.-based Tropic Biosciences.

This is the latest innovation from eggXYt, which has previously been recognized for its idea to determine the sex of chicks before incubation.

Every year, the egg industry destroys some 4 billion male chicks because they can lay eggs and arent the right breed for meat. Using eggXYts automated system would spare these chicks, make 4 billion more eggs available to consumers, and save labor and money for the industry.

Our primary goal is to improve animal welfare and efficiency within the poultry industry, says Yehuda Elram, CEO and co-founder of eggXYt, which is opening a state-of-the-art R&D facility in Jerusalem and raising a Series A round of funding.

Through the gene-silencing technology, eggXYt will expand its poultry portfolio into the field of health.

Following the Covid-19 outbreak, we are all very mindful of the threat of zoonotic diseases to human health and so we are especially motivated to embark on a project that may help to prevent further pandemics, Elram said.

Lifetime resistance

Elram and neuroscientist Daniel Offen (also founder of Brainstorm Cell Therapeutics) established eggXYt in 2016. Their strategy was to build a platform, talent pool and know-how to create a variety of genetics-based solutions for the poultry and livestock industry.

Avian flu was chosen as our next target because it is the number one pain point for the industry from a health point of view, says Elram.

The current main approach is an avian influenza vaccination. However, these expensive vaccines must be individually administered and do not cover all flu strains. They can only reduce, not eradicate, outbreaks.

Our new approach will produce chickens that have intrinsic, wide-range, genetic resistance throughout their whole lifetime and on to their offspring, Elram says.

Tropics bioinformatics platform for gene silencing originally developed to protect banana plants from a fungal disease uses a gene-editing technique that doesnt require adding or deleting genes. This minimal intervention is widely considered non-GMO and safe.

Elram says other genome-editing technologies to develop influenza-resistant chickens aim to change the sequence of genes that code for proteins, and may present greater risks of harmful effects.

The GEiGS platform harnesses naturally occurring defense mechanisms to directly attack disease agents, solving the heavy burden of target gene discovery for gene-editing applications, said Eyal Maori, chief science officer and CEO of Tropic Biosciences.

This is driving extensive interest in the technology from outside parties and we are delighted to partner with eggXYt and other innovative companies from the broader agricultural and life-sciences industries.

MIT Solverecently chose eggXYt as a Solver team for its Sustainable Food Systems Challenge from a pool of 2,600 applicants from 135 countries. The year-long program provides funding and access to VCs and MIT experts.

This could speed eggXYts path to commercialization for all its products. Elram believes eggXYts product will be the first to market and may provide resistance to other pathogens as well.

We estimate it will take 40 months or so to create gene-edited, stable founder flocks of chickens, he says.

Counting chickens before they hatch

At the same time, eggXYt is advancing toward commercializing its flagship product aimed to end the culling of male chicks, usually done by grinding them alive.Consumers care more and more about how food gets onto their plate and what happens between farm and fork, says Elram. This trend is only growing.

He says the buzz started in 2014 when animal welfare activists pushed Unilever producer of Hellmanns mayonnaise, one of the largest egg consumers worldwide to issue a statement that chick culling must end.

Ever since, governments have been enacting legislation to ban chick culling, each country with a different timeline, says Elram, the grandson of Israeli egg farmers.

We are taking the best approach, as we see it. Some of the competition is working on solutions that have to start the incubation process and stop it at some point.

In contrast, eggXYts technology detects the gender of newly laid eggs by picking up a signal from a biomarker right through the shell made possible by a gene-editing technique called CRISPR that recently won a Nobel Prize in Chemistry for its developers, Jennifer Doudna and Emmanuelle Charpentier.

To complete the process of designing the device that will detect the signal from each egg of the gene-edited chickens, eggXYt has partnered with strategic investor TBG, whose operating companies make egg-grading and hatchery equipment.

We believe the world is becoming more receptive to the use of high-end technology to solve the worlds most pressing problems, says Elram. That is part of what we are doing with MITbringing together different pieces of the puzzle in the innovation ecosystem to solve big problems.

Biotech startup could end avian flu and male chick killing appeared first on ISRAEL21c.

(Edited by Matthew B. Hall and David Martosko)

Link:
Adieu, Bird Flu: Biotech Startup Could End That Virus And Male Chick Kills Free Press of Jacksonville - Jacksonville Free Press

Matthew Nussbaum| Wayne County Extension

Breed differentiation within a species is quite common. A German Shephard is certainly not equivalent to a Miniature Schnauzer in terms of purpose. There are likewise many differences between our modern beef and dairy breeds.

Yes, some dual-purpose breeds are still preferred on small farms or homesteads, but overall, maximum efficiency is reached with dairy cows that convert feed into milk and beef cattle that convert feed into muscle (meat).

So, why are we discussing the idea of merging beef and dairy genetics? It comes down to market demand and profitability. All dairy cattle will one day become beef cattle. For dairy steers that day comes sooner than for milking cows that are culled after several years of producing milk, but beef is the final destination.

With our bulk meat processing plants and standardized market, consistency is key for smooth operations. Therefore, the beef industry wants livestock that meet a set of standards tht include age, weight, marbling, ribeye shape and size,and dressing percentages at time of harvest.

Those standards are all based on our modern beef cattle profile. Thus, dairy farmers typically experience discounted payments when they sell livestock into the beef market for failure to meet one or several of those standards. Most farmers will still want their entire milking herd to be strictly dairy, as that is often more efficient.

To accomplish this, farmers would select their top milking cows and breed them exclusively with dairy sexed semen. Cows with poor genetics and at the bottom of the production lineup could all be bred to beef sires.

Additionally, all or most of the replacement heifers could be bred to beef as there is some evidence beef breeds have better calving ease than many of our dairy cattle and those replacement heifers are not yet proven producers.

The result is the farms top cows produce nearly all heifer calves for replacements, which increases the farms overall production and genetic improvement, while the bottom cows produce a crossbreed offspring that may be either a heifer or a bull calf.

Unfortunately, beef sexed semen for male dominant offspring is not readily available. While the ideal plan would also include all of our bottom cows producing male crossbreeds that could be raised for beef, selling crossbreeds of either gender is usually more profitable than selling their dairy counterparts for a non-dairy purpose.

This is especially true for dairy steers as they have little purpose outside of the beef market but do not fit the industrys mold for the ideal beef animal.

Note, some aspects of dairy genetics are favorable in the beef market. Dairy breeds naturally have better marbling scores than many of the beef breeds and also have a smaller percentage of trim fat. But the road splits from here when thinking about Holstein versus Jersey dairy cows.

Holstein frames usually are bigger than what the beef market wants. So, selecting a proven sire with a smaller frame size is ideal, and will likely yield easier calving, too.

Jersey cattle have the opposite problem. Look for beef genetics with smaller birth weights, but an increased frame size. Both breeds have great needs for genetics that promote better feed conversion to pounds of gain as we no longer need an animal that is efficient at converting feed into milk production.

Is any beef breed or beef semen good enough to get the job done? That depends on what you are trying to accomplish. If the goal is to be highly profitable by introducing beef genetics, I would answer, no.

Consider paying a little extra for the beef genetics that will best compliment your dairy herd. Essentially, the goal of crossbreeding in this scenario is to make a dairy-beef cross that looks and performs like a beef animal. While it may seem silly, the beef market prefers solid-colored animals.

Breeding Holsteins to Angus or other solid black beef is preferred and similarly, breeding Jerseys to Limousin or Charolais often produces solid cream or fawn-colored cattle. In the end, these cattle should be round and smooth, not angular, about 1200 pounds, and ideally sold before 30 months old if not 2 yrs.

One final thought: if you are trying to produce a marketable beef animal, you must feed it like a beef animal. They are not dairy heifer replacements or dry cows and will perform best on a ration designed for their purpose. This often includes a higher ration of grain with need for a separate pen/facility.

Matthew Nussbaum is an OSU Extension Agriculture and Natural Resources Program Assistant and may be reached at 330-264-8722.

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Adding value to the herd with beef and dairy crossbreeding - Wooster Daily Record

According to Dr Ritu S Santwani, Director at Pune Test Tube Baby Centre & Shyam Well Women Clinic, in several cases, enlargement of veins within the scrotum leading to sperm count deterioration is often found to be the cause. Another very important reason is stress.

Hormonal disbalance is also one of the causes of infertility, says Dr Santwani.

She says stress and pandemic have further contributed to increasing cases on male infertility.

"Many people are going to the sauna bath in the gym these days, in which the testicles are exposed to a higher temperature for a longer time. Studies have found that higher temperature also leads to a reduction in the sperm count, she adds.

According to Dr Sowjanya Aggarwal, Principal Consultant, Infertility & IVF, Obstetrics And Gynaecology, Max Hospital, Vaishali, It could be physical causes, infections, hormones-related problems. There are no common causes as such. Basically, what we can say is that there are 3 main causes genetics, prior surgery because of cancer or any other major surgery, and medication that can affect semen analysis. Alcohol, drugs, and smoking can also affect this but whether there is a particular limit for that cannot be said. Stress and being overweight can also be the be a cause.

Male infertility can be caused by excess heat, drug use, excessive alcohol consumption, exposure to toxins, stress, obesity, dietary deficiencies, prostatitis infection, varicocele, and diseases/surgery of the male genital tract, says Dr Rajinder Yadav, Director and HOD, Urology, Fortis Hospital, Shalimar Bagh

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Everything About Male Infertility: Causes, Treatment & Diagnosis - The Quint

Patrick and Diamond Platnumz [Photo: Courtesy]

Just how can people who dont share any biological lineage, ethnicity or nationality look-alike?Could be because the bible tells us on good authority that we all came from Adam and Eve and even your wife could thus be your sibling? But does everyone have a doppelganger? Theres a fairly decent chance of it, actually, thanks to the limited number of genes that influence facial features.

Michael Sheehan, an assistant professor of neurobiology and behaviour at Cornell University, USA, told the journal Nature that there is only so much genetic diversity to go around, said the scholar who studies appearance variations and genetics in species such as paper wasps and house mice. If you shuffle that deck of cards so many times, at some point, you get the same hand dealt with you twice.

Family members might look alike on average than non-related individuals due to inheritable traits but what explains the resemblance between strangers?

Dr Arthur Beaudet, a professor of molecular and human genetics at Baylor College of Medicine in Houston, also told Nature that theres a huge number of genes that contribute to things like facial structure and, of course, hair, eye and skin colour, which are all highly variable and that more genes are known to be linked to looks than to other areas of human anatomy. Human faces are more variable than we would expect them to be based on how variable other body parts are, Sheehan said.

Here are look-alikes who have recently shocked us.

I wish I could meet John Magufuli- Frank Otieno

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Frank Otieno, a former secondary teacher is an editor at KTN. He resemblances to Tanzanian President John Pombe Magufuli. The no-nonsense president came to power in 2015. Just like Magufuli Frank also wears glasses, is of dark complexion but the most notable feature which makes the two gentlemen look alike are the nose and lips.

Read Also: How entertainers gifted Magufuli with a new term

Otieno posted a photo online saying he was going to Tanzania for a pep talk with Magufuli as he was tired of the endless questions that were lingering in his mind. The post excited Kenyans on social media and they urged him take the matter seriously.President Magufuli and Frank Otieno [Photo: Courtesy]

Frank told The Nairobian when I started my TV show Dau ya Elimu my followers started saying I look like John Pombe Magufuli. My wife also had similar sentiments. There was a time I was waiting for our crew to come and pick me at Kitengela for a shoot clad in a suit. A man approached and asked me if I had any relationship with Magufuli. I was astonished. For a long time I thought people were looking me in the streets because they see me on TV but I came to learn that it was because I bear a resemblance to Magufuli.

Otieno hails from Siaya County but once worked in Tanzania as a teacher from 1999 to 2001. I remember one of by biology students called Stella Matiko telling me that I looked like Magufuli but I think its just nature and Im excited because my lookalike is a president and a man of the people but Im certain that we have no blood relationship. I wish I could meet him.

I am a carbon copy of First Lady Margaret Kenyatta- Grace Mkabili

Kenyas first lady, Margaret Kenyatta, has an immediately recognizable look. Her short hair alone makes her stand out as well as her glasses and rangi ya pesa complexion. These features have become so synonymous with her that one woman found herself courting fame for sharing the First Ladys look.

Like Margaret Kenyatta, Grace Elizabeth Mkabili is short and light-skinned, and keeps her hair short. The social activist from Voi also wears glasses. Her resemblance to the Margaret Kenyatta is so striking that she has earned the nickname First Lady herself, and is often asked whether theyre blood relations.First Lady Margaret Kenyatta and Grace Mkabili [Photo: Courtesy]

Most people are not convinced when I tell them I am not First Ladys sister, said the married mother of three. After I decided to shave my hair and dye it, everyone said I was a carbon copy of the First Lady. The saloonist handed me the mirror and I was shocked to see that I resembled the First Lady.While she met the First Lady once on a Beyond Zero campaign function in Mombasa, Elizabeth maintains she would love to take a photo with Margaret Kenyatta.

Migori preacher is approached for Presidential advise

Pastor Daudi Ojuango, who is interestingly also called Mwai, is a preacher from Migori. From his height and complexion to the shiny bald head, he bears a striking resemblance to former President Mwai Kibaki, as Migori residents were quick to point out. The two look so alike his congregation often confuse him for the President, even approaching him for advice. It has happened so much that the man of God is now used to it.

Read Also: Why Mwai Kibaki prefers living in Muthaiga to Sh400 million Nyeri home

Another man who shares the features of the former president is 63-year-old Ronald Edward Frederick Kimera Muwenda Mutebi II, the reigning Kabaka of the Kingdom of Buganda, a constitutional kingdom in modern-day Uganda. He shot into the public consciousness after photos of him surfaced online, and eagle-eyed Kenyans were quick to comment that it was like President Kibaki had stepped back in time. Seeing as both men rose to positions of power, there is clearly something special about those particular genes.

Kalonzo Musyoka wanted to meet his mirror image

When you think of former Vice President and Wiper leader Kalonzo Musyoka, the thing that immediately springs to mind is a full head of hair and a 90s era moustache.Back in 2017, Jesse Kinyanjui found himself in the public eye after photos emerged of him, sporting the same head of hair and moustache that made Kalonzo so recognizable.The young resident of Ruiru in Kiambu County, was soon trending, as Kenyans on Twitter created the hashtag #Kalonzobro and got creative with the jokes.Kalonzo and Jesse [Photo: Courtesy]

Jesse revealed he had been grooming the moustache since his high school days, and that the resemblance had not gone unnoticed by his schoolmates and neighbours. But the media attention was too much for him to handle, and he was soon craving his old life of anonymity. Kalonzo later commented on the resemblance, saying it showed Kenyans are one, and that he would like to meet Kinyanjui.

Women throw themselves Governor Hassan Joho wa Meru

Few male politicians have been able to capture womens attention as wildly as Mombasa Governor Hassan Joho. His Instagram is a shrine to his unique personal style, and he routinely leaves women drooling with his photos and expensive outfits. As the saying goes, women want to be with him and men want to be him. Well, for Lynn Ngugi, a local businessman in Meru, he got the next best thing.

Read Also: We did not have money so I dropped out of school, Governor JohoNgugi and Joho [Photo: Courtesy]

Ngugi looks so much like Joho he gets a fraction of the female attention the Governor does. He has the signature beard and the smooth-shaven head. He tries to dress like Joho too, though of course, he doesnt have the Governors flamboyance. But it is enough. According to Ngugi, women throw themselves at him because of the resemblance, and he is very proud of the association.

Diamond Platinumz vs the Bodaboda rider

Our brother-in-law Diamond has established himself as the biggest star in East Africa. He created a unique style of music that has propelled him to the top of the making him a household name with a recognizable face and chiselled physique.In 2018, we were treated to the case of a young boda boda rider from Mombasa who looks a lot like the Kanyaga hitmaker. The man, identified online only as Patrick, posted photos of himself on his bike, and Kenyans were quick to note the resemblance, down to his toned biceps.Patrick and Diamond Platnumz [Photo: Courtesy]

Grandmother met Obama from Indonesia and fainted

Ilham Anas, an Indonesian man, shook the world with his resemblance to former US president Barrack Obama. He is often mistaken for the real Obama which has seen him travel around the world. If I am wearing a suit, many people mistake me for the real Obama, he told wowzeto.com. When I was in America, a grandmother got in the elevator with me and was so shocked to see Barrack Obama. She fainted.While Obama visited Indonesia, the father of two who works as a photographer for a teen magazine was in Los Angeles pretending to be Obama.

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Mirror on the wall? Celebrity look-alikes - The Standard

The newresearchusesdatafroma 2018study,whichis stillthe largestanalysisof ancient DNAfrom Britain ever conducted,thatidentifieda >90% replacement of the genetic ancestry of people living in Britain between 2500-2100 BC. Thiscoincidedwith the introduction of Beakermaterial culture and burialpractices,andwas interpreted to indicatethat there were substantial movements of people into Britain from continental Europe during this period.

At the time it was published,popular coverage of the original studyspeculatedthat this wasa rapidevent, potentially involving invasionby male warriors, butthe new study has foundfromdetailed analysis that it was more likely a long-term process, taking place over maybe 10-16 generations,withboth men and women moving for a variety of reasons thatmight haveincluded exchange, pilgrimage, and the pasturing of animals.Incoming populationsand their descendants tended to bury their dead, but local groups probably continued to cremate their dead, which destroys the DNA, or treatthemin ways which leavenorecord.Thearchaeologically invisiblelocalpopulationare only seenwhen they have children with groups who buried their dead. Thismay be partly responsible for why this change in ancestryappearedso rapidat first.

Dr Tom Booth, archaeologist at The Francis Crick Institute has said: Initially it looks like groups of locals and incomers and their descendants lived in parallel with one anotherto some extent occupying the same landscapes, slowly integrating and only having children with each other infrequently.After around 300 yearsthey start having children together more liberally itsat this point, the older population then have a much lower genetic legacyoverall.Why they have such a small overall genetic legacy is still a mystery. It could be thattherejust werent so many people living in Britain at the time these Beaker groups move in from continental Europe.

ProfIanBarnes, Researcher and Division Lead at the Natural History Museum has said:Anissue we face is that wealsodont know how many people there were from either group,althoughpopulation size may be declining inthe localpopulation of Britain at the end of Neolithic. It may be that the reason whywe seem to pick up so many genetic relatives in the Bronze Ageis becauseonly small groups of people were moving into Britain.

The new study also highlights how genetic ties were referenced variably in death among burials in the Stonehenge landscape.A man and his juvenile son were buried next to one another in a cemetery on Amesbury Down.By contrast, aman, hisnephewand his nephews daughter were buried across three different cemeteries separated by severalkilometres.A young man was buried on Boscombe Down with the skull of his paternal cousin or half-brother at his feet.

Prof. JoannaBrck, archaeologist at University College Dublin, said: Existing interpretations of the genetic evidence paint a picture of a patriarchal society, in which male immigrants married localwomen. Our research shows that although links with paternal relatives were important, kinship organization was variable, and other relationships, including with maternal kin, were also significant.Sometimes, people who were not genetically related to each other could also be viewed as kin.

The study found that it is likely there was cultural exchange between existing local groups and incomers.Dr Booth continues Even though they have no ancestry from the older population, they incorporatetheir monuments into their belief systems very quickly. They are burying people in these areas to reference these monuments as prestigious areas to bury their dead even though itwasnttheir genetic ancestors who built them.Stonehengeand its surrounding landscapeareemblematic to a certain extent because its important toallgroups in this period and when theyintegrate,it maintains its importance.

The paper was published inCambridge Archaeological Journal on 11 February 2021.

Notes foreditors

Media contact: Tel: +44 (0)779 969 0151 Email:press@nhm.ac.uk

About the Natural History Museum:

The Natural History Museum is both a world-leading science researchcentreand the most-visited natural history museum in Europe. With a vision of a future in which both people and the planet thrive, it is uniquely positioned to be a powerful champion for balancing humanitys needs with those of the natural world.

It is custodian of one of the worlds most important scientific collections comprising over 80 million specimens. The scale of this collection enables researchers from all over the world to document how species have and continue to respond to environmental changes - which is vital in helping predict what might happen in the future and informing future policies and plans to help the planet.

The Museums 300 scientists continue to represent one of the largest groups in the world studying and enabling research into every aspect of the natural world. Their science is contributing critical data to help the global fight to save the future of the planet from the major threats of climate change and biodiversity loss through to finding solutions such as the sustainable extraction of natural resources.

The Museum uses its enormous global reach and influence to meet its mission to create advocates for the planet - to inform, inspire and empower everyone to make a difference for nature. We welcome over five million visitors each year; our digital output reaches hundreds of thousands of people in over 200 countries each month and our touring exhibitions have been seen by around 30 million people in the last 10 years.

The Francis Crick Instituteis a biomedical discovery institute dedicated to understanding the fundamental biology underlying health and disease. Its work is helping to understand why disease develops and to translate discoveries into new ways to prevent, diagnose and treat illnesses such as cancer, heart disease, stroke, infections, and neurodegenerative diseases.

An independentorganisation, its founding partners are the Medical Research Council (MRC), Cancer Research UK,Wellcome, UCL (University College London), Imperial College London and Kings College London.

The Crick was formed in 2015, and in 2016 it moved into a brand new state-of-the-art building in central London which brings together 1500 scientists and support staff working collaboratively across disciplines, making it the biggest biomedical research facility under a single roof in Europe.http://crick.ac.uk/

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Experts discover new information on cultural exchange between different genetic groups and burials of close genetic relatives in the Stonehenge...

Sperm are simple cells with a straightforward job: swim until they reach an egg, then fertilize it. But in mice, some sperm resort to divisive tactics in order to gain the advantage.

A study published on February 4 in the journal PLOS Genetics shows that a genetic variation in mouse sperm, called the t-type, can give a swimmer the upper hand. These t-type sperm are able to spread a protein called RAC1 that essentially poisons other sperm. T-type sperm plant the seeds of destruction early in their development, then fortify themselves against RAC-1, Brandon Specktor reports for Live Science. When it comes time to race for the egg, the t-type sperm can swim in a straight line while poisoned sperm swim in hapless circles until they die.

We found out that the level of this protein can be more or less active, depending on whether the sperm have the gene to make it, and whether that gene is flipped on like a light switch, says biologist Alexandra Amaral of the Max Planck Institute for Molecular Genetics to Kassidy Vavra at Inverse. The level of protein that is on has to be quite well regulated. If it is too much, sperm don't move well. And if its too low, it also doesnt move well theyre kind of in circles.

T-type sperm produce the RAC1 protein at full throttle.

If all of the sperm in a group are t-type, and theyre all making RAC1, they will all struggle because there is so much of the poisonous protein going around, Sara Rigby reports for Science Focus magazine. On the other hand, if there are no t-type sperm present, then all the other sperm remain relatively healthy and swim well because theres no overabundance of RAC1. However, if a cohort has a mix of t-type and normal sperm, then t-type will have the advantage.

"The trick is that the t-haplotype 'poisons' all sperm, but at the same time produces an antidote, which acts only in t-sperm and protects them," says Bernhard Herrmann, director of the Max Planck Institute for Molecular Genetics, in a statement. "Imagine a marathon, in which all participants get poisoned drinking water, but some runners also take an antidote."

The t-type sperm do the equivalent of poisoning the drinking water early in sperm development, affecting both themselves and their non-variant peers. All of the sperm inherit genes that make it difficult to interpret the chemical signals around them. But in the final cell division of sperm development, when half of a cells genes go to one sperm and the other half to another, only the sperm that inherit the t-type variation have an extra set of genes that reverses the poisons effect, per Live Science.

The poisoned sperm end up swimming in circles, unable to advance in their quest. But the impervious t-type sperm swim ahead. In this case, theres a 99 percent chance that the sperm that fertilizes the egg first will have the t-type variation. The research shows the importance of small genetic variations in sperms success, Amaral tells Inverse.

The study was conducted in about 100 mouse sperm cells, but not all species sperm behave the same way, University of California, Berkeley, cell biologist Polina Lishko tells Inverse. The study is preliminary, but future research could illuminate the specific molecular mechanism behind RAC1 that makes it damaging to sperm at high levels.

An earlier study showed a similar effect of RAC1 on bull sperm, which is more similar to human sperm than a mouses is. Amaral says that the team plans to conduct future research with human sperm, to see if RAC1 might be involved with some cases of male infertility.

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Mice Sperm Sabotage Other Swimmers With Poison | Smart News - Smithsonian Magazine

It is not just a mother's love that endures.

A woman's influence on her children's health persists well into late middle age, according to a study published in the November issue of the European Journal of Preventive Cardiology.

The study, which enrolled almost 2,000 men and followed their families over 46 years - from 1971 to 2017 - found that the sons of women with heart-healthy lifestyles live nearly a decade longer without developing cardiovascular disease than those whose mothers have unhealthy lifestyles.

The study looked at the influence of both parents on offspring but found that men had little influence on their children's heart health in later life apart from the genes they passed on to them.

According to Dr Rohit Khurana, senior consultant cardiologist with The Harley Street Heart and Vascular Centre at Mount Elizabeth Medical Centre, told The New Paper: "While a pregnant woman's cardiovascular health (CVH) and lifestyle choices during pregnancy can affect her offspring's CVH, long-term CVH is also affected through parental behaviours and environmental influences.

"Children observe and acquire health behaviours within the family environment, with role modelling by primary caregivers being a significant contributor to children's long-term lifestyle choices.

"If primary caregivers, usually mothers, practise and instil a healthy lifestyle of balanced diets, regular exercise and minimal to zero alcohol and tobacco intake... their children are likely to continue those behaviours in adulthood.

"Those children will then pass good habits down to their children, thereby decreasing the risk of CVD (cardiovascular disease) within families for generations."

He added: "The research shows that parents, particularly mothers, are the gatekeepers of their children's CVH during formative years, which influences adult life. Numerous studies have proved that good lifestyle choices are a greater determining factor compared with genetics when it comes to optimal CVH."

According to the study, CVD incidence rates were higher among sons than daughters, (with one reason being that) women are less likely to indulge in risky behaviours.

For example, according to the World Health Organisation, about 40 per cent of the world's male population smokes, compared with only 9 per cent of women, and men are almost twice as likely to binge drink as women.

Studies also show that women generally eat more healthily and consume more fruit and vegetables than men.

Finally, women develop CVD later in life, after menopause and typically in their 60s or older; so fewer of the female participants in the study had reached the age when we would expect to see signs of CVD.

Mothers are still the primary caretakers of young ones, with more direct daily influence on diet and behaviour than fathers. They are still more likely to be disciplining, providing emotional support and generally monitoring the daily activities of their children.

Taking good care of your CVH during pregnancy is important because the heart works harder by increasing the body's blood volume to support a growing baby.

If you are a diabetic, a smoker or have high blood pressure during pregnancy, each of these things makes it harder for your heart to pump extra blood throughout your circulatory system, increasing the likelihood of maternal and neonatal mortality and morbidity.

This does not mean women with CVD risk factors should not get pregnant - it just means they should practise good preconception heart care including smoking cessation, cutting back on alcohol and weight management through regular exercise and a healthy diet rich in fruit, vegetables and fibre.

After women give birth, they should continue practising healthy behaviours at home as good examples to help children make positive choices, which become lifelong habits.

Telling children what to do will not always work as they need to see parents walk the talk.

Read more:
Sons of heart-healthy mums more likely to live 10 years longer: Study - The New Paper

Some sperm cells are ruthless manipulators that will literally poison their competition in the race to fertilize an egg, new research shows.

In a study published Feb. 4 in the journal PLOS Genetics, researchers from the Max Planck Institute for Molecular Genetics (MPIMG) in Berlin studied mouse sperm cells under the microscope to better understand the effects of a particular DNA sequence known as the t-haplotype. The team knew from previous research that sperm cells carrying this sequence tend to swim straighter (rather than in circles of death) and faster on average than competing sperm without it.

Now, they've found that those highly-effective sperms' tactics are a little less than sportsmanly.

Related: The 7 biggest mysteries of the human body

"Sperm with the t-haplotype manage to disable sperm without it," study co-author Bernhard Herrmann, director at the MPIMG, said in a statement. "The trick is that the thaplotype 'poisons' all sperm, but at the same time produces an antidote, which acts only in t-sperm [those with the t-haplotype] and protects them."

The result, Herrmann said, is sort of like a marathon "in which all the participants get poisoned drinking water," but only some of the runners have access to the antidote.

The t-haplotype is a series of linked genes occupying chromosome 17 in house mice all over the world. (Unlike humans, who have 23 pairs of chromosomes, mice have only 20). Herrmann and other researchers have called it a "selfish" gene genetic material with a single mission: to make copies of itself. Because of the t-haplotype's ruthless effectiveness at passing from one generation to the next, according to the researchers, male mice carrying one copy of the t-haplotype will transmit it to up to 99% of their offspring.

After studying more than 100 mouse sperm cells, Herrmann and his colleagues learned more about the selfish haplotype's devious tactics. They found that the t-haplotype "poisons" all sperm cells during the early phases of sperm production, injecting every cell with certain genes that inhibit their ability to regulate movement.

It's not until a later phase, when each cell divides in half, that the "antidote" comes into play. After dividing, half of the sperm cells inherit the t-haplotype genes on chromosome 17. For those lucky sperm, the t-haplotype provides new genetic variants that reverse the inhibiting effects of the "poison" that every cell consumed during the previous phase of development.

For the other half of sperm cells, which don't carry the t-haplotype or its genetic "antidote," life becomes a lot harder. These poisoned cells have a lot more trouble moving in a straight line (an important skill for a cell whose only job is to race full-speed-ahead to an unfertilized egg). In their study, the researchers saw that many sperm without the antidote literally swam in circles until they died, while their t-haplotype competitors charged straight ahead.

"Our data highlight the fact that sperm cells are ruthless competitors," Herrmann said. "Genetic differences can give individual sperm an advantage in the race for life, thus promoting the transmission of particular gene variants to the next generation."

Originally published on Live Science.

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Devious sperm 'poison' their rivals, forcing them to swim in circles until they die - Livescience.com

I once spoke to a human geneticist who declared that the notion of intelligence was quite meaningless, so I tried calling him unintelligent. He was annoyed

Nobel Prize laureate, Peter Medawar

Of all the endless nature vs nurture arguments, the debate over intelligence and race is the most toxic. It also seeps over into wider unease with human genetic research; the fear, for example, that recent advances in ancient human DNA analysis can be used by those with nefarious intentions to resurrect problematic race folk theories.

Given this seeming potential for reviving damaging beliefs, some scholars question whether we would be better off to give up on particular lines of research in the human sciences, including the quest to trace patterns of human migration. Others, meanwhile, argue for tighter restrictions on research into cognitive differences between different human populations. That said, the impetus to explore our ancestral evolution and its impacts remains an essential scientific pursuit, as it is at the backbone of research exploring how human differences impact disease and potential targeted cures.

Such arguments about race, intelligence and possible censorship were of particular concern to US-born and educated New Zealand scientist and intelligence researcher James Flynn, who died in December 2020, aged 86. Flynn was the IQ debates great scholarly champion of environment over genes, known for his respectful rebuke of scholars who took a more deterministic view of the complex relationship of intelligence, genes, and the environment.

This century-long debate flared in 1969 following the publication of an article in the Harvard Educational Review, in which psychologist Arthur Jensen claimed that observed IQ differences between Blacks and Whites was due mainly to genetics. Jensen further argued for a reset on the poverty reforms that were then rolling out under the Johnson Administration, arguing that compensatory education programs that assumed racial groups were blank slates with environment alone the only detriment to equality of performanceHead Start, for examplewere destined to fail.

The article caused an uproar that still rages. Jensen, who died in 2012, was widely denounced as a racist, particularly in the popular press and by social scientists. Instead, Jensens critics maintained that environmental factors rather than genes passed along in ancestral cohorts almost entirely explained racial disparities in test scores, a radical environmentalist position that few hard scientists hold today.

This was also when the movement to end the use of IQ tests first emerged. Today, persistent differences in SAT or ACT results among races have been cited as a reason to stop using the exam in college admissions. Last May, many University of California colleges announced they was scrapping its SAT or ACT requirement, as have many other American universities.

Having migrated to New Zealand in 1963 to escape the political repression of the McCarthy era, Flynn, now based at the University of Otago in Dunedin, responded skeptically to Jensens claims. And understandably so. For instance, how could Jensen explain away Flynns voluminous documentation that IQ scores among racial and ethnic groups world-wide have risen considerably from one generation to the next? In the 20th century, Flynn discovered, the scores of entire countries rose by more than the Black-White disparity in the entire US. How could that be if IQ was genetically fixed? He summarized much of this research in a ground-breaking response to Jensen published in 1980.

In 1987,in an article in American Psychologist, Jensen praised Flynns criticism of his own work:

I am asked by colleagues, students, and journalists: who, in my opinion, are the most respectable critics of my position on the race-IQ issue? The name James R. Flynn is by far the first that comes to mind. His book,Race, IQ and Jensen(1980), is a distinguished contribution to the literature on this topic, and, among the critiques I have seen of my position, is virtually in a class by itself for objectivity, thoroughness, and scholarly integrity.

In a study released in 2006, Flynn and a co-author, William Dickens, concluded that Black Americans had gained as many as seven IQ points on Whites since the early 1970s and into the 1990s, a finding that is hard to explain if intelligence is genetically fixed. The theory that Flynn developed was dubbed The Flynn Effect by scholars Richard Hernnstein and Charles Murray, co-authors of The Bell Curve: Intelligence and class structure in American life, the 1994 tome that faced similar harsh criticism as Jensens earlier expressed views.

In the decades since, numerous explanations of the Flynn effect have been proposed, as well as some skepticism about what has driven it and its implications. For example, there is intense debate about whether the rise in IQ scores corresponds to a rise in general intelligence or only a rise in special skills related to taking IQ tests, as schools have been turned into test-taking hot houses, in part because teacher salaries and administrative jobs are often tied to raising test scores.

Others argue that the Flynn Effects observed gains in IQ over time are unrelated tog (also known as general intelligence) that many psychometricians believe is a fairly unchangeable mental capacity. (g-scores are used in many professions to predict performance; e.g., the US military and even the National Football League, with its Wonderlic test, utilize g-weighted tests in their evaluations).

In parallel with the measured gains in IQ scores, long-term declines have been found for mental speed, digit span backwards, the use of difficult words, and color acuity, all of which are related to intelligence. More recently, the Flynn effect appears to be fading, as the IQ measure distance between some populations and others has grown. Research suggests that there is now a decline in IQ scores, in Norway, Denmark, Australia, Britain, the Netherlands, Sweden, Finland, France and German-speaking countries, a development which appears to have started in the 1990s. The Flynn effect appeared to have most influenced people born during the mid-1970s (co-incidentally a period of dramatic social transformation on racial issues), and has significantly declined ever since.

Flynn himself relished the debates that his research had stimulated. A life-long social democrat, he was outspoken in defence of free speech, including the right indeed, the desirability of open and honest debate on possible group differences in intelligence.

And this willingness to engage with those holding different opinions readily explains the reaction to news of Flynns death by his peers. Cognitive psychologist Steven Pinker, a sharp critic of blank slate post-modernist critical theory, immediately expressed sadness at the passing of a defender of Enlightenment ideals. Of particular note was the response of The Bell Curve co-author and conservative political scientist Charles Murray:

By Americas current standards of academic discourse, Jim Flynn and I should have been at each others throats, Murray said. We did in fact have different perspectives, though more nuanced than most people thought.

But those differences hadnt the slightest effect on Jims collegiality toward me or any of the people with whom he disagreed. How else are you going to learn, Jim thought, except by engaging with people who see things differently? Jim represented what a scholar is supposed to beopen, curious, passionate about his beliefs but without either self-righteousness or rancor, determined above all else to get it right.

Unfortunately, while scholars are supposed to be open and curious, much of the passion and argument over race and IQ has been self-righteous and rancorous. As Flynn himself readily acknowledged, those least open to discussion and most ready to censor opposing opinions, frequently came from his own leftist end of the political spectrum.

These were the ones, he argued, who boycott debate and put their money on indoctrination and intimidation, thereby forfeit[ing] a chance to persuade. (Here, Flynns position reflects characterizations of critical theory proponents that conservatives see as promoters of cancel culture.)

In his recent bestselling book, How to Argue With a Racist, geneticist Adam Rutherford emphasises the need to equip [people] with the scientific tools necessary to tackle questions on race, genes and ancestry and to provide a foundation to contest racism that appears to be grounded in science.

Jim Flynn, too, had long pointed to this danger that without an understanding of the scientific arguments, humane-egalitarian idealists would flounder against informed and articulate racists.

Censoring debate about the subject would then be doubly counter-productive, further removing the knowledge needed to challenge genuinely racist arguments or, more importantly, the political conclusions that arise from racist misinterpretations of human biological research.Thats the thrust of the argument made in GLP founders Jon Entine controversial but critically-praised book, 2000 Taboo: Why Black Athletes Dominate Sports and Why We are Afraid to Talk About Them, in which he wrote:

Although discussing racial differences is likely to provoke strong reactions, on balance and in proper context strong emotions are healthy.

The why of human differencesblack/white, male/female, Italian/Irish, between Slavic ethnic groups or one African tribe and anotheris likely to remain only crudely measurable. Racemarked by skin color, ethnicity, and geographyis a fuzzy concept. The challenge is in whether we can conduct the debate so that human diversity might be cause for celebration of our individuality rather than fanning distrust.

In one of his last essays on this topic, Flynn re-emphasised what Those who want to forbid discussion and scientific investigation ignore, for instance, the ability to defend your position with facts rather than just right opinion and the opportunity to hone your argument by having its weaknesses revealed. [T]ruth gains vitality from being challenged rather than being an unquestioned inheritance, he argued.

To kill an idea is to forfeit all rewards that may flow from reaction to that idea. If I had not read about [research into group differences], with its emphasis on IQ and the general intelligence factor, I would never have documented massive IQ gain over time, or urged a revolution in the theory of intelligence, or connected cognitive gains and moral gains

In contrast to Flynn, those who argue against open discussion of contentious science fear it will breathe new life into socially harmful ideas, akin to publicising the details of how to build massively destructive bombs or to create deadly viruses. And on their side of the argument is the undeniable fact that past beliefs about racial superiority/inferiority caused incalculable harm.

Nevertheless, the analogy with socially destructive bombs and viruses implies that everyone, regardless of existing political beliefs or values, would suffer through public debate of sensitive issues. Yet is this really the case? If, for example, evidence of genetic differences between racial populations was more widely discussed, would this inevitably lead more people to become racists? We believe not; the egalitarian moral belief that people should be treated equally is not dependent on people actually being equal in all respects.

Of course, given the odious history of twisted interpretations of Darwinian theories of race, some form of use or abuse analysis of proposed research is warranted. As part of this, though, the detrimental consequences of creating taboos on discussion must also be taken into account (for instance, conceding the argument to racist ideologues who may present themselves as simply telling the unpalatable truth that others are too scared to discuss).

In the absence of a scientifically accurate account of racial diversity, we cannot adequately challenge pseudo-scientific racist arguments. In addition, avoiding discussion of human biological diversity may limit our understanding of the genetic basis of disease and hamper medical research that could improve peoples lives.

The problem here is egalitarians tying their political values to actual facts about human biology; the mistaken belief that moral equality is dependent on all people being biologically or psychologically the same. Yet as Pinker argued in The Blank Slate: The modern denial of human nature, when scientific evidence appears to conflict with political values, people are tempted to suppress the facts and to clamp down on debate leav[ing] us unequipped to deal with just those problems for which new facts and analyses are most needed.

Geneticist David Reich has made much the same point about those who decry genetic research into human diversity as inherently racist. The well-meaning people who deny likely genetic differences between different human populations, Reich suggested, are digging themselves into an indefensible position, one that will not survive the onslaught of science.

And Flynn too emphasises where attempts at censorship miss their mark: Suppressing free inquiry is by its nature an expressive of contempt for truth by power. The truth can never be racist.

With regard to intelligence research, far from being massively destructive, such studies could, in future, prove hugely beneficial, especially in education. Without a clear understanding of human cognitive development, and how it is determined by both genes and environment, we are hamstrung in our attempts to improve an existing education system that persistently frustrates so many. Indeed, by ignoring the biological side of the interplay between genes and environment, we may be simply setting up many young people to fail, generation after generation. Those promoting practical uses of personal genomics, for instance, see the potential for tailoring education to reflect the needs and the abilities of individual learners, rather than forcing all learners into a one-size-fits-all system.

As for Flynn, he admitted to having no illusions that the debate over race and IQ will end.

And I do not deny that it could have social and political consequences. Perhaps someday we will conclude that a portion of the present gap will prove to be genetic in origin. I do not want to sugar the pill but will only say I am not too alarmed.

Yet even if the worst case scenario of ineluctable differences in cognitive ability proved to be the case (which is far from certain), this does not destroy the humane-egalitarian desire to create a better future society. After all, if everyone had a decent standard of living, much of the heat linking biology with racial inequality would fade a point Flynn illustrated with joking reference to his own Irish ancestry:

Assume that the lower job profile of Irish Americans compared to Chinese Americans is due in part to genes: I do not know one Irishman who cares (the English would be a different matter).

For the first time in history science, promises a glimpse of how the worlds different populations popularly and simplistically called races have evolved. Going forward, the tsunami of information genetic research is now unlocking will revolutionize medicine, as we develop targeted, personalized response to diseases based on individual and group inheritance. Research on the brain is just part of that mostly-promising and optimistic enterprise.

In his reflections on Human Diversity, a book that came out shortly before Flynns death, Charles Murray pointedly suggested that many of those most opposed to research on the brain and IQ mistakenly equate human intelligence with human worth. Thats understandable. With these caveats in mind, it is perhaps fitting here to leave the last word to Murray, Flynns supposed great adversary: in losing Jim Flynn, he says, We have lost an exemplar.

Disclosure: James Flynn was the external examiner of Patrick Whittles PhD thesis, looking at the implications of human evolutionary theory for egalitarian political ideas.

Patrick Whittle has a PhD in philosophy and is a New Zealand-based freelance writer with an interest in the social and political implications of biological science. Follow him on his website patrickmichaelwhittle.com or on Twitter @WhittlePM

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Can we have an open debate about IQ, genes, and group differences? Reassessing the legacy of James Flynn - Genetic Literacy Project

Introduction

Obesity is a common metabolic disorder and its prevalence is increasing worldwide.1 In Korea, the prevalence of obesity is rapidly increasing because of westernized diet and sedentary lifestyle; consequently, it has become a serious socioeconomic problem.2 According to an obesity fact sheet of Korea, the occurrence of obesity in adults increased from 29.7% in 2009 to 35.7% in 2018.3 Further, obesity is closely associated with increased risks of various chronic metabolic disorders, including diabetes mellitus (DM), hypertension, dyslipidemia, and cardiovascular diseases.1 According to the diabetes fact sheet in Korea, half of the patients with DM suffer from obesity.4 Therefore, the assessment and management of obesity is important to reduce obesity-related complications in a population.

Obesity results from the interactions between environmental and genetic factors. A previous study reported that genetic factors are responsible for approximately 4070% of the etiology of obesity.5 Moreover, advanced technologies such as genome-wide association studies have led to the identification of some candidate obesity-related genes.6

The vitamin D endocrine system plays a central role in bone and calcium homeostasis. Apart from its classical involvement, vitamin D also plays an important role in other metabolic pathways in immune system, cancers, and other endocrine systems.7 Although vitamin D deficiency has been associated with obesity,8,9 the exact underlying mechanisms leading to obesity have not been fully determined yet; regardless, some possible explanations, such as insulin resistance and lipolysis have been suggested.10

Vitamin D receptor (VDR; a member of the steroid/thyroid hormone receptor superfamily)11 in complex with vitamin D serves as a transcription activator and regulates gene transcription by binding to vitamin D responsive elements, which are located in the promoter region of the target genes. Therefore, genetic alterations of VDR gene can alter gene activation, and lead to various diseases.7 Furthermore, VDR gene is also expressed in adipocytes and pancreatic beta cells linked to insulin resistance and therefore it might be associated with body composition as well.12,13 More than 470 VDR polymorphisms have been identified in the VDR gene.14 Among them, the well-established VDR polymorphisms are as follows: FokI (rs2228570 C > T), BsmI (rs1544410 A > G), ApaI (rs7975232 C > T), TaqI (rs731236 T > C), and Cdx2 (rs11568820 A > G).15 A previous study has demonstrated that TaqI and BsmI polymorphisms are associated with obesity in French patients with type 2 diabetes mellitus (T2DM).16 In another study performed in the Thai population, the Cdx2 polymorphism was associated with a higher waist circumference; however, the four common polymorphisms (FokI, BsmI, ApaI, and TaqI) of the VDR gene did not show any association with BMI.17 In contrast, the VDR BsmI polymorphism has shown a significant association with vitamin D deficiency but not with the obesity phenotype in adolescents residing in Malaysia.8

So far, the previous studies have shown inconsistent results pertaining to the associations between VDR polymorphisms and obesity. Furthermore, there is a lack of data regarding the same in the Korean population, especially the data of patients with T2DM who have a higher risk of obesity. Therefore, in this study, we evaluated the association between BsmI and ApaI polymorphisms of the VDR gene and obesity in Korean patients with T2DM.

This was a single-center, casecontrol study. Patients who were diagnosed with T2DM and treated at the Chungbuk National University Hospital, Korea, were included in the study. The diagnosis of T2DM was performed by the World Health Organization criteria. Patients with type 1 DM and other types of DM were excluded from this study. The demographic data including age, sex, height, weight, BMI, duration of DM, and family history of DM were collected through reviewing of medical records. Further, the laboratory data, such as fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), C-peptide, insulin, and liver function, kidney function, and lipid metabolism parameters, were also investigated for each patient.

BMI was used to evaluate obesity. The BMI (kg/m2) was calculated as baseline body weight (kg) divided by the square of the height (m2). Obesity was defined as a cutoff value of 25 kg/m2 BMI, according to Asian-Pacific guidelines.18

The two polymorphisms of VDR, BsmI and ApaI, were analyzed in this study. Peripheral leukocytes were isolated from ethylenediaminetetraacetic acid-treated whole blood obtained from each patient. Then, the genomic DNA was extracted for subsequent polymerase chain reactions (PCR). All the included T2DM patients were genotyped using PCR-restriction fragment length polymorphism method, for two restriction sites in the VDR gene, BsmI and ApaI using specific primer sequences. The following BsmI and ApaI primers were used for amplification: (BsmI) forward 5-CAA CCA AGA CTA CAA GTA CCG CGT CAG TGA-3 and reverse 5-AAC CAG CGG AAG AGG TCA AGG G-3. (ApaI) forward 5- GGG ACG CTG AGG GAT GGC AGA GC-3 and reverse 5-GGA AAGGGGTTAGGTTGGACAGGA-3. The primers of the VDR gene were designed based on previous literature.19 The PCR condition used for Bsm I as followed: an initial denaturation of 3 min at 94 C, followed by denaturation of 30 s at 94 C, annealing of 30 s at 62 C, and extension of 1 min at 72 C for 30 cycles, and a final extension of 5 min at 72 C. The PCR condition used for amplification of Apa1 as follows; 94 C for 10 min, and 30 cycles using the following temperature profile: 94 C for 1 min, 62 C for 1 min, 72 C for 1 min, and final elongation for 5 min. The PCR products were digested overnight at 37 C by Fermentas restriction enzymes, and then resolved in 1.5% agarose gel electrophoresis for the genotype analysis. We analyzed three genotypes for each polymorphism: BB, Bb, and bb for BsmI and AA, Aa, and aa for ApaI.

The probability of HardyWeinberg equilibrium was tested using the chi-squared test. The data were expressed as the mean standard deviation or as percentages for the categorical variables. The baseline characteristics were compared using Students t-test for the continuous variables and chi-squared test for categorical parameters. Multiple logistic regression analyses were performed to evaluate the relationship between obesity and the following variables: genotype, sex, age, duration of DM, hypertension, dyslipidemia, and HbA1c. All statistical analyses were performed using SPSS for Windows software 22.0 (IBM Corp., Armonk, NY, USA). The significance was set at P < 0.05.

The study was approved by the International Review Board of Chungbuk National University Hospital (IRB No. 201803-034-001) and conducted in accordance with the Declaration of Helsinki. All procedures were carried out with adequate understanding, and all patients gave their informed consent prior to being included in the study.

A total of 506 patients (266 males and 240 females) were included in this study. The demographic and biochemical characteristics of the patients are shown in Table 1. The mean age and BMI of the patients were 62.6 10.6 years and 25.1 3.5 kg/m2, respectively. The mean duration of DM was 14.7 7.5 years and approximately 51% of the patients had a family history of DM. The mean HbA1c and FPG values were 7.6 1.4% and 145.1 55.4 mg/dL, respectively. The patients were categorized into obesity group and normal weight group depending upon their BMI values. The mean BMI was 27.9 2.9 kg/m2 in the obesity group and 22.7 1.7 kg/m2 in the normal weight group (P <0.001). The proportion of females and prevalence of hypertension and dyslipidemia were higher in the obesity group than in the normal weight group. The duration of DM was shorter in the obesity group than in the normal weight group; however, family history of DM and serum HbA1c levels did not show significant differences between the two groups. The serum triglyceride levels were 172.6 120.3 mg/dL in the obesity group and 146.0 78.0 mg/dL in the normal weight group (P = 0.004). Finally, the liver enzymes, including aspartate aminotransferase (AST) and aspartate aminotransferase (ALT), were significantly higher in the obesity group than in the normal weight group.

Table 1 Baseline Characteristics of the Patients

Table 2 presents various parameters according to BsmI genotypes. Patients with the bb genotype (bb group) showed significantly higher BMI (25.2 3.5 kg/m2) than patients with BB or Bb genotypes (BB + Bb group; 24.1 3.1 kg/m2; P = 0.034). However, no significant differences were observed between the glucose metabolism, lipid metabolism, and liver enzyme parameters of the two groups.

Table 2 Various Parameters According to BsmI Genotypes

The clinical parameters according to ApaI genotypes are shown in Table 3. The mean BMI was 25.1 3.5 kg/m2 in patients with the Aa or aa genotypes (Aa + aa group) and 24.1 2.4 kg/m2 in patients with AA genotype (AA group); however, the difference was not significant (P = 0.180). Other laboratory findings were not significantly different between these two groups.

Table 3 Various Parameters According to ApaI Genotypes

The frequencies of BsmI genotypes in the patients were as follows: BB, 2.0% (n = 10); Bb, 10.3% (n = 52); and bb, 87.7% (n = 444). The frequencies of the ApaI genotypes in the patients were as follows: AA, 4.5% (n = 23); Aa, 46.8% (n = 237); and aa, 48.6% (n = 246; Supplementary Table 1). The bb group was significantly associated with a higher prevalence of obesity compared with the BB + Bb group (48.4% vs 33.9%; P = 0.031; Table 4). Moreover, the Aa + aa group showed a higher prevalence of obesity than the AA group (47.6% vs 26.1%; P = 0.043; Table 4). Furthermore, we performed a logistic regression analysis of the risk factors associated with obesity, and the related data are shown in Table 5. The non-B allele of BsmI was significantly associated with obesity, and the odds ratio (OR) was 2.132 (P = 0.014). The a-allele of ApaI also showed a significantly high risk of obesity (OR was 2.711, P = 0.048). Among other parameters, female sex, hypertension, and dyslipidemia were identified as the risk factors for obesity.

Table 4 Association Between Genotypes of VDR Polymorphisms and Obesity

Table 5 Logistic Analysis of Risk Factors to Determine Their Association with Obesity According to VDR Polymorphisms

In this study, we investigated the association between BsmI and ApaI polymorphisms in VDR gene and obesity in Korean patients with T2DM. We found that patients with T2DM carrying the bb genotype of VDR BsmI polymorphism were associated with higher BMI and increased risk of obesity than the BB or Bb genotypes. Although patients with the Aa or aa genotypes did not show significant differences in BMI (compared with the patients with AA genotype), the a-allele showed a significant correlation with obesity in the study population.

Recently, non-classical roles of vitamin D such as regulation of hormone secretion, immune function, cellular proliferation, and differentiation have emerged.20 Interestingly, previous studies have associated the effects of vitamin D with obesity. For instance, in a study of mixed-ethnicity participants, the individuals with obesity and those who were overweight showed a significant inverse correlation of serum 25-hydroxyvitamin D (25(OH)D) level with body weight, BMI, and waist circumference.21 Another study demonstrated that vitamin D affects energy expenditure through the upregulation of leptin gene expression.22 Further, the previous meta-analysis has reported that vitamin D deficiency is associated with obesity.23 Moreover, vitamin D improves insulin sensitivity; therefore, vitamin D deficiency may lead to the development of T2DM.24,25 Thus, these studies imply that vitamin D may play a possible role in obesity and obesity-related metabolic disorders.

Vitamin D binds to VDR to induce transcription pathways and gene expression. Therefore, genetic alterations of the VDR gene may hinder the gene activation and functions.7 As VDR expression has been found in adipose tissues, the association between obesity and VDR polymorphisms has also been investigated.8,9,16 In a study performed in French subjects with T2DM, BsmI and TaqI polymorphisms were associated with obesity; whereas ApaI did not show any significant correlation.16 This is in accordance with the results of our study. Another study showed that BsmI polymorphism was significantly associated with a higher BMI.26 Interestingly, conflicting results have been observed with respect to the association of obesity and ApaI polymorphisms. In a Chinese population, positive associations were observed between ApaI polymorphism and obesity (assessed by body fat percentage and skinfold thickness).27 In contrast, these associations were not observed in another study, which involved a study group of young Chinese males.28 In adolescents and young adults from Spain and Malaysia, no significant associations were observed between the VDR gene polymorphisms and obesity-related phenotypes.8,9 In recently published data, ApaI polymorphism appears to be correlated with overweightness and obesity in Chinese children.29 There are many ongoing studies and new SNP in VDR gene (rs3847987) have been shown an association with obesity phenotypes.30 Thus, to date, inconsistent results have been observed with respect to VDR polymorphisms and obesity. We believe that these differences may be attributed to different parameters such as sex, age, ethnicity, and behavioral characteristics. Further studies are needed and obesity is closely related to the development of T2DM and has been attributed to the progression of diabetic complications via various mechanisms.31,32 Therefore, it is possible that VDR polymorphisms, which are related to obesity, may be responsible for these complications in patients with T2DM. Previous studies have reported an association between VDR polymorphisms and diabetic complications.33,34 Results from the logistic regression analysis showed that BsmI and ApaI polymorphisms were strong risk factors for obesity. Thus, our data imply a possible effect of VDR polymorphisms on obesity in patients with T2DM, which is in accordance with the results of previous studies.16,26

To our knowledge, this is the first study to assess the association between the VDR polymorphisms and obesity in Korean patients with T2DM. The present study was performed in relatively homogenous subjects with similar ethnicities and disease statuses. However, there are several limitations of our study. First, we did not evaluate the serum 25(OH)D level, therefore, we could not determine whether the patients had vitamin D deficiency. Second, the clinical characteristics related to obesity such as physical activity and diet were not evaluated. Moreover, other parameters assessing obesity including waist circumference and body composition could not obtain due to the retrospective study design. Third, there was no control group of individuals without T2DM. Finally, not all VDR polymorphisms were investigated. Thus, we cannot rule out that other VDR polymorphisms may also be associated with obesity in the studied population.

In conclusion, the present study demonstrated that BsmI and ApaI polymorphisms of the VDR gene were associated with obesity in Korean patients with T2DM. However, further studies with larger multiethnic cohorts and experimental models are required to validate our results.

Parts of this study were presented at the International Congress on Obesity and Metabolic Syndrome, Seoul, Korea, 69 September 2018.

All retrospective data involving human participants were in accordance with the ethical standards and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Ethical approval was obtained by the Local Ethics Committee.

All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work. Everyone participated in the final approval of the manuscript.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

The authors received no funding and report no conflicts of interest for this work.

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14. Uitterlinden AG, Fang Y, Van Meurs JB, Pols HA, Van Leeuwen JP. Genetics and biology of vitamin D receptor polymorphisms. Gene. 2004;338(2):143156. doi:10.1016/j.gene.2004.05.014

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19. Eltahir Khalid K. Vitamin D receptor gene polymorphisms in Sudanese children with type 1 diabetes. AIMS Genetics. 2016;3(3):167176. doi:10.3934/genet.2016.3.167

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23. Manousopoulou A, Al-Daghri NM, Garbis SD, Chrousos GP. Vitamin D and cardiovascular risk among adults with obesity: a systematic review and meta-analysis. Eur J Clin Invest. 2015;45(10):11131126. doi:10.1111/eci.12510

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26. Hasan HA, AbuOdeh RO, Muda W, Mohamed H, Samsudin AR. Association of vitamin D receptor gene polymorphisms with metabolic syndrome and its components among adult Arabs from the United Arab Emirates. Diabetes Metab Syndr. 2017;11(Suppl 2):S531S537. doi:10.1016/j.dsx.2017.03.047

27. Shen F, Wang Y, Sun H, et al. Vitamin D receptor gene polymorphisms are associated with triceps skin fold thickness and body fat percentage but not with body mass index or waist circumference in Han Chinese. Lipids Health Dis. 2019;18(1):97. doi:10.1186/s12944-019-1027-2

28. Gu JM, Xiao WJ, He JW, et al. Association between VDR and ESR1 gene polymorphisms with bone and obesity phenotypes in Chinese male nuclear families. Acta Pharmacol Sin. 2009;30(12):16341642. doi:10.1038/aps.2009.169

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30. Yu S, Li X, Yu F, et al. New evidence for associations between vitamin D receptor polymorphism and obesity: case-control and family-based studies. J Hum Genet. 2020;65(3):281285. doi:10.1038/s10038-019-0702-5

31. King GL. The role of inflammatory cytokines in diabetes and its complications. J Periodontol. 2008;79(8 Suppl):15271534. doi:10.1902/jop.2008.080246

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34. Hong YJ, Kang ES, Ji MJ, et al. Association between Bsm1 polymorphism in vitamin D receptor gene and diabetic retinopathy of type 2 diabetes in Korean population. Endocrinol Metab. 2015;30(4):469474. doi:10.3803/EnM.2015.30.4.469

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[Full text] The Associations Between Vitamin D Receptor BsmI and ApaI Polymorphism | DMSO - Dove Medical Press

By Karina Shah

Science History Images/Alamy

Sperm have one goal to reach the egg and fertilise it and it seems that some mouse sperm cells carrying a certain genetic mutation may boost their chances of doing so by sabotaging their rivals.

Bernhard Herrmann at the Max Planck Institute for Molecular Genetics in Berlin, Germany, and his colleagues analysed sperm samples from mice. They found that sperm from some mice, carrying a genetic variant called the t haplotype, move faster and swim in straight lines. Other sperm without this variant from the same mice swim less productively, often moving slower and in circles.

Previous research has shown that mice with two copies the t haplotype genetic variant are more likely to be infertile, but this new study suggests that males with one copy of the genetic variant produce these t haplotype sperm cells that are more motile than those without.

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This t haplotype genetic variant is a selfish genetic element, because it can increase its likelihood of being passed on to offspring to higher than the usual odds of 50 per cent, and now Hermann and his team have figured out how these sperm gain their advantage.

The sperm cells carrying one t haplotype variant produce certain molecules that are able to disturb other sperm cells. The gene variants make it difficult for the rival sperm cells to interact with their environment, blocking various cell signalling molecules that normally provide the sperm with a sense of direction. Although the t haplotype sperm cells were more motile as a result of this competitive edge, the researchers did not test their ability to fertilise an egg.

The team also found a link between sperm success and an important protein in the body called RAC1, which plays a role in general cell movement and directs the sperm cell towards the egg. The levels of RAC1 in the body have to be just right too high or too low and the sperm cells wont move straight.

Sperm immotility is a big deal in male infertility, says Herrmann. Investigating the levels of this protein in human samples could help to develop treatments for infertility in men, he says.

Journal reference: PLOS Genetics, DOI: 10.1371/journal.pgen.1009308

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Some mouse sperm try to sabotage rivals in race to fertilise the egg - New Scientist News

BERLIN, Germany The biological race between sperm to reach an egg is a fierce and competitive process. Now, researchers in Germany say they have discovered which protein gives sperm the winning edge. Their study finds a molecular switch in sperm could also allow men to turn their fertility on and off.

Experiments on mice find the winner carries a set of toxic mutations that poison rival sperm. Researchers say a genetic factor called t-haplotype promotes the success of the sperm carrying it. They are also fueled by a protein called RAC1, the molecular switch that propels sperm forward.

Sperm with this protein move faster than their peers, establishing an advantage in who reaches the egg first. The findings are expected to apply to humans as well. It could lead to a pill that boosts fertility in men, or a male oral contraceptive.

It would target this chemical, boosting or lowering levels. However, too much may cause male infertility. On average a man produces between 80 and 300 million sperm each time he ejaculates. Despite that, more than 60 percent of fertility issues are related to poor sperm, so its important to keep them healthy.

Sperm with the t-haplotype manage to disable sperm without it, says corresponding author Bernhard Herrmann of the Max Planck Institute for Molecular Genetics in a university release.

The trick is that the thaplotype poisons all sperm, but at the same time produces an antidote, which acts only in t-sperm and protects them. Imagine a marathon, in which all participants get poisoned drinking water, but some runners also take an antidote.

The study finds some of the genes carry mutations that distort regulatory signals, which then get distributed to all the sperm. These are the poison that disturbs progressive movement. The antidote comes into action after the set of chromosomes are split evenly between sperm during maturation, with each cell now containing only half.

Only those with the t-haplotype produce an additional factor that reverses the negative effect. Optimal amounts of RAC1 improve the competitiveness of individual sperm, offering fresh hope of combating male infertility.

It is literally a race for life when millions of sperm swim towards egg cells to fertilize them. Herrmann and colleagues described t-haplotype as a selfish and naturally occurring segment of DNA. It breaks the standard rules of genetic inheritance and awards a success rate of up to 99 percent to sperm cells containing it.

Analysis of individual sperm revealed most made only little progress on their paths and were genetically normal. On the other hand, straight moving sperm contained the t-haplotype. Crucially, RAC1 was identified as the key to differences in motility. It transmits signals from outside the cell to the inside by activating other proteins. RAC1 also directs sperm cells towards the egg, sniffing their way to the target.

The competitiveness of individual sperm seems to depend on an optimal level of active RAC1; both reduced or excessive RAC1 activity interferes with effective forward movement, first author Alexandra Amaral adds.

When the researchers treated the mixed population of sperm with a substance that inhibits RAC1, genetically normal sperm could now swim progressively. The advantage of t-sperm disappeared. The results explain why mice with two copies of the t-haplotype, one on each of the two chromosomes 17, are sterile.

They produce only sperm that carry the t-haplotype. These cells have much higher levels of active RAC1 than sperm from genetically normal mice. However, sperm from normal mice treated with the RAC1 inhibitor also lost their ability to move progressively. In other words, too little RAC1 activity is also disadvantageous. The researchers believe abnormal RAC1 activity might also be the underlying problem in forms of human infertility among men.

Our data highlight the fact that sperm cells are ruthless competitors, Herrmann says.

Furthermore, the example of the t-haplotype demonstrates how some genes use somewhat dirty tricks to get passed on.

Genetic differences can give individual sperm an advantage in the race for life, thus promoting the transmission of particular gene variants to the next generation.

The groundbreaking study appears in the journal PLoS Genetics.

SWNS writer Mark Waghorn contributed to this report.

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Sperm switch would allow men to turn their fertility on and off - Study Finds

A former friend once told me that she would never date a Black man because she finds dark skin unattractive. She is white. While I was not surprised by her statement, I nonetheless felt uncomfortable and frustrated. This was not the first time I encountered blatantly racist ideas about attractiveness, nor are such beliefs novel to many Black people and people of color, more broadly.

Racism is oddly tolerated in the dating realm, allowing racist beliefs to be passed off as innocuous preferences. However, such preferences mandate myopically believing in white-centric standards of beauty and lumping together people of color based on racist stereotypes.

Take the trend shown in the Tiktok video below as a microcosmic representation of this problem. The video starts with a white man pointing to the camera with the caption, Look its the dude who think black girls attractive. Seven other men (including Black men) responded to the video by recording themselves turning and looking over their shoulder, indicating that they do not find Black women attractive. This particular version ends with a different white man, @btcm_abbc, crossing his arms and leaning back against a table, indicating that he does think Black women are attractive. He says, What about it?

(Note that @btcm_abbc does not objectify or hypersexualize Black women. This would have been fetishization, which I talk about later.)

Not degrading Black women should be the bare minimum, yet here we are. Although users declare their preferences very casually, racism ultimately drives the belief that Black women are unattractive.

Race is a social construct not grounded in genetics. When early racial theorists/white supremacists invented race and used it to justify slavery and colonialism, they lauded whiteness as exceptionally attractive.

Building the myth of white supremacy also mandated the fabrication of stereotypes about appearance. However, no physical trait or set of traits is unique to or accurately describes an entire racial group.

While American beauty standards have somewhat evolved to be more inclusive, colorism is still rampant inside and outside of Black, Latinx, and Asian American communities; natural hairstyles are still widely regarded as unprofessional or dirty (unless the wearer is not Black); and representation of people of color in mainstream media is seriously lacking. This all stems, in part, from Western societies mobilizing a racialized definition of beauty and framing whiteness as a default state of being.

Blind adherence to the idea that proximity to whiteness equates to beauty fails to acknowledge that standards of beauty have to be created and sold, just like the racist beliefs that shape them. Therefore, racial preferences based on physical attributes are neither harmless or arbitrary: they are racist. Such beliefs ultimately result from internalizing, and thus perpetuating, overt or covert messaging that whiteness is superior.

This messaging also contributes to beliefs about personality based on race. If someone arrives at the conclusion that x group of people is un/attractive because they lack/possess y personality trait, they are dehumanizing and racially stereotyping members of that group. This includes stereotypes frequently used to justify not preferring members of certain racial groups (such as the stereotypes that Black women are too loud and Asian men are effeminate), as well as stereotypes that lead to preferring members of certain groups.

Stereotypes that rely on exoticizing and hypersexualizing people of color lead to fetishization, a sexual obsession fueled by objectification. Fetishization of Black men and women represents one example. The medias obsession with the Spicy Latina represents another. Still one more is yellow fever, the fetishization of Asian people.

Yellow fever originates from popular Western portrayals of Asian women as submissive, passive, and exotic that proliferated during the 19th century. These stereotypes have persisted and since merged with the model minority myth, contributing to the fetishization of Asian women among the white supremacists of the alt-right. Obsession with male K-pop idols and their soft masculinity has contributed to the fetishization of Asian men as well.

@_itsjing lists real messages she has received from men who have yellow fever.

Fetishizing someone is not a compliment. Yellow fever fails to recognize the individuality, personality, and humanity of Asian people, instead reducing them down into the same monolithic caricature on the basis of their race.

@sourandnasty talks about a related problem: the idea that someone would only be attracted to Asian people if they have yellow fever.

Think about which traits are attractive to you. Do you want a partner who has a good sense of humor? Someone who is kind and compassionate? Flirty? Thoughtful? Loyal? Would you avoid someone who is rude? Dishonest? A bad listener? These are human traits that have nothing to do with race. Someone saying that they do/do not prefer members of a certain race based on their having/lacking those traits is simply absurd.

The video below demonstrates this: in it, @mmdvg40 acts as himself and a potential romantic interest (played by him with a paper towel on his head). The romantic interest describes various traits she finds attractive, such as a sense of humor and a taste for indie music, all of which @mmdvg40 possesses. However, he eventually figures out that she has a bias against Black men, despite claiming to be not racist.

Across the political spectrum, those who pride themselves on being anti-racist (or at least emphatically claim that they are not racist) sometimes fail to engage with how their beliefs have been shaped by systems and messaging intended to perpetuate racial inequality.

In the video below, @ambermorman46 and a co-TikToker say, Were we really ugly, or did we just go to a predominantly white school? Anyways. The point is that whiteness is not the pinnacle of beauty despite the racist spaces and beliefs that promote it as such.

Too often at institutions like Princeton and beyond, the euphemizing language of preference is used to conceal beliefs that result from failure to question and willingness to embrace the tenets of white supremacy deeply embedded into Western societies. An ignorant conception of beauty centered on whiteness and characterized by stereotypes perpetuates racism, regardless of how insistently someone maintains that their preferences are not racist.

Brittani Telfair is a junior from Richmond, Va. majoring in SPIA and pursuing a certificate in African American Studies. She can be reached at btelfair@princeton.edu.

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Decolonize dating: a Tiktok essay - The Princetonian - The Daily Princetonian

It is important to recognize the signs of a heart attack, which can vary by person. Sometimes a person may have a heart attack without realizing it and not seek the emergency medical care they need. That could lead to lasting heart damage.

The medical name for a heart attack is a myocardial infarction (MI).

A heart attack usually happens because a coronary artery becomes blocked, reducing or stopping the nourishing blood supply to the heart muscle.

Chest pain is the most recognized sign of a heart attack, but the symptoms someone experiences can depend on their gender and age.

It is essential to identify a heart attack as early as possible and seek prompt medical attention. Treatment can minimize damage and increase the chances of a full recovery.

This article looks at the various symptoms of heart attacks, how these may vary in females and older adults, and when to seek medical attention. It also looks at risk factors, treatment, and prevention.

Most people know that chest pain is a typical heart attack symptom. However, a heart attack can affect the entire body, not just the heart.

Individuals of different ages and sexes may experiences heart attack symptoms differently.

Most heart attacks do have several defining symptoms, which according to the Centers for Disease Control and Prevention (CDC), are:

Heart attacks typically involve some level of pain or discomfort in the chests middle or left side. It may feel like sharper pain, or more like squeezing, fullness, or uncomfortable pressure.

Usually, this accompanies chest pain, but shortness of breath may also begin before any chest discomfort.

A person may feel pain or discomfort in one or both arms, which can radiate to the shoulders. There may also be pain in the neck, jaw, or back.

Someone may feel weak, faint, or break out into a cold sweat.

Heart attack symptoms may show up differently in females, and may seem less evident or unrelated to heart problems.

The following are common heart attack symptoms in females that can occur with or without chest pain:

Because heart attacks are commonly associated with chest pain, females often misread their symptoms and delay consulting a doctor.

It is crucial that everyone, especially females, recognize heart attack symptoms that may be atypical and seek immediate medical help when necessary.

Like females, older adults who experience heart attacks may have non-typical symptoms.

Asymptomatic or silent heart attacks are more common in older adults, and chest pain is an infrequent finding.

During a silent heart attack, someone may experience no symptoms and feel relatively well apart from feeling unusually tired or short of breath. They may also show one or more of the signs associated with heart attacks in females.

The National Heart, Lung, And Blood Institute state that acting quickly could save someones life in the case of a heart attack.

Even if an individual is not entirely certain they are experiencing a heart attack, it is best to seek emergency medical help to limit any potential damage to the heart.

The consequences of an untreated heart attack could be severe.

People should always seek medical attention if they suspect a heart attack.

If someone experiences heart attack symptoms for more than 15 minutes, the hearts muscle cells are at a high risk of damage.

From the onset of symptoms, an individual has less than 90 minutes before critical damage levels occur.

If the heart does not receive oxygenated blood, it cannot function normally, which can cause a heart attack. This can happen when a coronary artery is partially or fully blocked.

The most common cause of blocked coronary arteries is coronary heart disease.

When coronary heart disease occurs, fats and cholesterol can form deposits or plaques on the arterial walls, called atherosclerosis.

Over time, the plaques narrow the arteries, and eventually, this obstructs blood flow.

Use of recreational drugs, such as cocaine, can also cause heart attacks.

Several factors increase an individuals risk of a heart attack. These include being age 65 or over, being male, or having a family history of heart disease.

Race also plays a part, as people of African, Mexican, and American Indian descent are at higher risk.

There are also modifiable factors that increase the risk of heart attacks. These include:

The good news is that people can change, treat, or control the modifiable risk factors to reduce the chances of having a heart attack.

Anyone who thinks they are having a heart attack should immediately seek medical attention.

A doctor will diagnose heart attack based on symptoms, age, general health, and family history. They will also carry out tests including:

If the tests show that an individual has had a heart attack, doctors may recommend the following procedures:

A doctor may also treat a heart attack with medications to thin the blood, break up clots, relax the blood vessels, and help with pain relief.

Heart attacks can damage the heart muscle, leading to complications including:

The severity and duration of any complications often depend on how much damage the heart attack caused to the heart muscle.

Although people cannot control all the risk factors of heart attacks, such as gender, age, and genetics, habit changes could help with prevention. These include:

Fortunately, for most people, having a heart attack does not mean the end of a normal, healthy life. However, around 20% of people over age 45 will have further heart attacks in the 5 years following their first.

For this reason, it is important to focus on living a lifestyle that can help prevent heart problems in the future.

Although most people are familiar with a heart attacks common signs, such as chest pain and breathlessness, they may not realize that females and older adults can experience heart attacks differently.

In these groups, heart attack symptoms such as indigestion and extreme fatigue can seem unrelated.

If someone is experiencing any symptoms that may be related to heart problems, they should seek immediate medical attention.

Prompt treatment can save someones life and prevent permanent heart damage from occurring.

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How to recognize the signs of a heart attack and what to do - Medical News Today

The NutriNet-Sant study is an ongoing investigation into the relationship between nutrition and health. In this Special Feature, we look at some of the projects findings and speak with Principal Investigator Dr. Mathilde Touvier, who has been involved in the study since its inception.

A range of factors influences health, including genetics, lifestyle, environmental factors, and diet. Unraveling the complex relationships between these factors is a challenge.

For many reasons, it is incredibly difficult to investigate the role of nutrition in health and disease. For instance, no two people eat the exact same diet, and very few people eat the exact same food 2 days in a row.

As it is neither feasible nor ethical to ask thousands of people to follow a strict diet for 10 years to see what happens, researchers have to find other ways of unpicking the links between diet and disease.

The best way to tackle any difficult health-related question is to generate as much good quality data as possible, and this is the NutriNet-Sant studys raison detre.

Beginning in 2009, the NutriNet-Sant study was the first internet-based study of its kind. By the start of 2021, the team was regularly collecting data from 171,000 people aged 15 years and older, making it the largest ongoing nutrition study in the world.

Now running in France and Belgium, the team is also seeding similar projects in Canada, Mexico, and Brazil.

Specifically, the researchers set out with the following aims:

The researchers keep a biobank of serum, plasma, and urine from about 20,000 people. They also collect stool to monitor and analyze gut bacteria.

Alongside questions about food intake, the NutriNet-Sant team collects information about food packaging, cooking practices, mode of production, physical activity, tobacco, drugs, environmental factors, and domestic and professional exposures.

Importantly, data from the NutriNet-Sant study are linked with medical and insurance records to improve accuracy regarding medications, diagnoses, and long-term sick leave. The study is financed entirely by public institutions.

Article highlights:

In recent years, ultra-processed foods have become a nutritional pariah, and the NutriNet-Sant study has played no small part in this.

Over recent years, data from the NutriNet-Sant study have revealed associations between diets high in ultra-processed foods and an increased risk of cancer, cardiovascular disease, mortality, depressive symptoms, type 2 diabetes, obesity, and gastrointestinal disorders.

As an example, one paper based on data from the NutriNet-Sant cohort, which appeared in the BMJ in 2018, concluded:

In this large prospective study, a 10% increase in the proportion of ultra-processed foods in the diet was associated with a significant increase of greater than 10% in risks of overall and breast cancer.

Another study using their data, which also appeared in BMJ, concludes:

[H]igher consumption of ultra-processed foods was associated with higher risks of cardiovascular, coronary heart, and cerebrovascular diseases.

Yet more research, which appeared in BMC Medicine in 2019, investigated ultra-processed foods and their links with depression. The authors write:

Overall, [ultra-processed food] consumption was positively associated with the risk of incident depressive symptoms, suggesting that accounting for this non-nutritional aspect of the diet could be important for mental health promotion.

Next, the NutriNet-Sant researchers plan to investigate the causative aspects of this relationship. They will drill down into the specific compounds that might be responsible.

According to Dr. Touvier, thanks to the researchers wealth of nutrition data, they can now estimate the additive exposure for more than 330 additives authorized in Europe and also detect the mixtures of additives that are consumed by the population.

They have already identified these cocktails of additives and are now searching for relationships between particular mixtures of compounds and specific disease states.

Understanding which foods are associated with which health conditions is important, but the next step changing behavior can be even more challenging.

To address this, the NutriNet-Sant study focused on food labeling. Although product labels already provide information about levels of fat, sugar, and other ingredients, as Dr. Touvier pointed out, quickly gauging whether a product is healthful as you rush around a grocery store is not easy.

With this in mind, the NutriNet-Sant group designed Nutri-Score. This simple label gives each product a score from A to E, with A being the most healthful and E the least healthful.

The scoring system takes into account the amount of sugar, saturated fats, sodium, protein, fiber, fruits, vegetables, nuts, and legumes to provide a score.

The score has been validated against many health outcomes, using the NutriNet-Sant cohort [and other cohorts]. So we showed that people who ate foods with a better score had less risk of cancers, cardiovascular disease, obesity, and so on. We also validated it in other independent cohorts, explained Dr. Touvier.

We also used the NutriNet-Sant cohort to validate how the score is understood and used by participants to rate nutritional quality.

And, even more importantly, the research has shown that in a grocery setting, people with access to this type of labeling choose more healthful foods. As the authors of one paper explain:

The Nutri-Score was associated with a higher nutritional quality of purchases in experimental and large scale trials.

In France, some companies are already applying this label on a voluntary basis. To date, 520 firms, including a total of 690 brands, have registered to use the scoring system.

Dr. Touvier and the team are currently trying to convince the European Union to roll out the scoring system throughout the E.U. in 2022. However, they are facing stiff resistance from certain large food corporations and their lobbying groups.

More than 40 published studies back the benefits of the Nutri-Score. Dr. Touvier hopes that it will be adopted because, for the consumer, we really showed it will have a great impact.

Over the years, there has been a fair amount of controversy around the benefits of eating organic produce. As Dr. Touvier explained, until recently, there were simply not enough data to make connections between these products and health outcomes.

Once again, the NutriNet-Sant study has begun to fill these gaps. According to Dr. Touvier, the team found an association between higher concentrations of organic food and a lower risk of breast cancer and lymphoma. Similarly, the data showed a lower risk of obesity, overweight, and metabolic syndrome.

The researchers have also demonstrated that people who eat more organic foods have lower levels of pesticides in their urine. Next, they plan to quantify exposures to the various types of pesticides and identify cocktails of pesticide exposures. They are in the process of assessing whether certain pesticidal cocktails might be associated with specific health outcomes.

According to Dr. Touvier, one such study, which has just been accepted for publication in the International Journal of Epidemiology, found that:

People exposed to these cocktails of pesticides had a higher risk of postmenopausal breast cancer.

As the COVID-19 pandemic continues, so does NutriNet-Sants data collection. The scientists are tracking how diets have shifted during these unusual times.

One study, for instance, showed that the pandemic has affected people differently, with some eating less healthfully and others improving their diet significantly.

We saw a very diverse profile of participants. Some of them started to eat more sugary foods and to eat between meals because they were bored or stressed. Also, they lowered the level of physical activity. [] For these participants, we saw an increase in body weight, explained Dr. Touvier. But the pandemic has had different effects on other people, she noted:

Other participants began to cook more at home, so less processed foods and more homemade meals, and they increased their level of physical activity [] These participants lost weight.

The NutriNet-Sant scientists also found that there were people who had made no change to their diet or level of activity.

As the researchers have also collected dried blood spots from more than 20,000 participants, they are able to detect anti-SARS-CoV-2 antibodies.

They are currently working on a way to link infection to diet. This research could reveal whether any dietary patterns are associated with an increased risk of SARS-CoV-2 infection or, conversely, whether any nutritional profiles are associated with a protective effect.

Investigating nutrition is challenging. Every individual eats hundreds or thousands of ingredients each week, and no two diets are the same. Also, when scientists rely on self-reported dietary information, they are likely to get imprecise answers.

The NutriNet-Sant study was the first to use online questionnaires to collect data. As trailblazers for this methodology, the researchers spent a great deal of energy making sure that the data they were collecting were accurate and meaningful.

Medical News Today asked Dr. Touvier how the NutriNet-Sant study team went about this. She explained that early on in the study, the investigators ran a series of validation studies in which they checked participants self-reported food intake against their blood and urinary biomarkers and their phone interviews with trained dietitians.

They found a high correlation between the information coming from participants, blood markers, and interview data.

In some cases, the data they collected were more reliable than the phone interviews. Dr. Touvier explained that some participants were more likely to enter unhealthful food in the anonymous online form than they were to mention it when speaking with a dietitian. She said:

Its not perfect. Its still an observational study, but we have validated all of these methods, so they are reliable.

Another common issue that nutrition scientists face is that one brand of frozen pizza is not the same as another, and one bag of chips can harbor entirely different ingredients than another.

To help minimize this issue, the researchers designed a barcode reader that allows participants to scan their food items directly into the system. In this way, the scientists have direct access to the precise nutritional content of the food item.

Another significant issue with nutrition research is the role of industry bias. Studies that receive funding from interested parties are more likely to report the benefits of their produce. The NutriNet-Sant study, however, is publicly funded, and the data are not open access.

As Dr. Touvier explained, we have a moral agreement with the participants not to provide the data to the food industry. However, the team does share their data with other public researchers.

Correlation versus causation is the thorn in any observational studys heel. Finding an association is one thing, but proving that one factor directly causes another is a different challenge altogether. To ensure that the researchers chop away as many confounding factors as possible, they track a great number of variables.

For instance, they keep anthropometric data, such as height and weight; socioeconomic data; information about participants occupations so that they can track potential environmental exposures to chemicals, for instance; medical history; current and past medications; activity levels; and more.

The NutriNet-Sant scientists are beginning to dive even deeper into the complexities of nutrition and health. Beyond the nutritional makeup of foods, they are beginning to investigate how the packaging might interact with food items and influence health. Their innovative barcode system helps them collate this information.

These data will also help with investigating sustainability, which is another area on which the team is beginning to focus.

The wealth of data that the NutriNet-Sant team has collected and continues to collect will slowly allow scientists to answer increasingly complex questions.

As the number of participants in the study steadily grows, Dr. Touvier hopes that the NutriNet-Sant team can continue indefinitely. Undoubtedly, the insights that this team generates will have a beneficial effect on the health of future generations.

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What have we learned from the worlds largest nutrition study? - Medical News Today

Their eyes met across the rugged mountain landscape of prehistoric Romania.

He was a Neanderthal, and stark naked apart from a fur cape. He had good posture and pale skin, perhaps reddened slightly with sunburn. Around one of his thick, muscular biceps he wore bracelet of eagle-talons. She was an early modern human, clad in an animal-skin coat with a wolf-fur trim. She had dark skin, long legs, and her hair was worn in braids.

He cleared his throat, looked her up and down, and in an absurdly high-pitched, nasal voice deployed his best chat-up line. She stared back blankly. Luckily for him, they didnt speak the same language. They had an awkward laugh and, well, we can all guess what happened next.

Of course, it could have been far less like a scene from a steamy romance novel. Perhaps the woman was actually the Neanderthal and the man belonged to our own species. Maybe their relationship was of the casual, pragmatic kind, because there just werent many people around at the time. Its even been suggested, too, that such hook-ups werent consensual.

While we will never know what really happened in this encounter or others like it what we can be sure of is that such a couple did get together. Around 37,000-42,000 years later, in February 2002, two explorers made an extraordinary discovery in an underground cave system in the southwestern Carpathian mountains, near the Romanian town of Anina.

Even getting there was no easy task. First they waded neck-deep in an underground river for 200m (656ft). Then came a scuba dive for 30m (98ft) along an underwater passage, followed by a 300-metre (984ft) ascent up to the poarta, or mouse hole an opening through which they entered a previously unknown chamber.

Inside the Petera cu Oase, or "Cave with Bones", they found thousands of mammalian bones. Over its long history, its thought to have primarily been inhabited by male cave bears extinct relatives of the brown bear to which they largely belong. Resting on the surface among them was a human jawbone, which radiocarbon dating revealed to be from one of the oldest known early modern humans in Europe.

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Here's what we know sex with Neanderthals was like - BBC News

Odin, in Norse mythology, is an extremely powerful god whos also a trickster. He has only one eye, having sacrificed the other for wisdom. Among his many talents, he can wake the dead, calm storms, cure the sick, and blind his enemies. Not infrequently, he transforms himself into an animal; as a snake, he acquires the gift of poetry, which he transfers to people, inadvertently.

The Odin, in Oakland, California, is a company that sells genetic-engineering kits. The companys founder, Josiah Zayner, sports a side-swept undercut, multiple piercings, and a tattoo that urges: Create Something Beautiful. He holds a Ph.D. in biophysics and is a well-known provocateur. Among his many stunts, he has coaxed his skin to produce a fluorescent protein, ingested a friends poop in a D.I.Y. fecal-matter transplant, and attempted to deactivate one of his genes so that he could grow bigger muscles. (This last effort, he acknowledges, failed.) Zayner calls himself a genetic designer and has said that his goal is to give people access to the resources they need to modify life in their spare time.

The Odins offerings range from a Biohack the Planet shot glass, which costs three bucks, to a genetic engineering home lab kit, which runs almost two thousand dollars and includes a centrifuge, a polymerase-chain-reaction machine, and an electrophoresis gel box. I opted for something in between: the bacterial CRISPR and fluorescent yeast combo kit, which set me back two hundred and nine dollars. It came in a cardboard box decorated with the companys logo, a twisting tree circled by a double helix. The tree, I believe, is supposed to represent Yggdrasil, whose trunk, in Norse mythology, rises through the center of the cosmos.

Inside the box, I found an assortment of lab toolspipette tips, petri dishes, disposable glovesas well as several vials containing E. coli and all Id need to rearrange its genome. The E. coli went into the fridge, next to the butter. The other vials went into a bin in the freezer, with the ice cream.

Genetic engineering is, by now, middle-aged. The first genetically engineered bacterium was produced in 1973. This was soon followed by a genetically engineered mouse, in 1974, and a genetically engineered tobacco plant, in 1983. The first genetically engineered food approved for human consumption, the Flavr Savr tomato, was introduced in 1994; it proved such a disappointment that it went out of production a few years later. Genetically engineered varieties of corn and soy were developed around the same time; these, by contrast, have become more or less ubiquitous.

In the past decade or so, genetic engineering has undergone its own transformation, thanks to CRISPRshorthand for a suite of techniques, mostly borrowed from bacteria, that make it vastly easier for biohackers and researchers to manipulate DNA. (The acronym stands for clustered regularly interspaced short palindromic repeats.) CRISPR allows its users to snip a stretch of DNA and then either disable the affected sequence or replace it with a new one.

The possibilities that follow are pretty much endless. Jennifer Doudna, a professor at the University of California, Berkeley, and one of the developers of CRISPR, has put it like this: we now have a way to rewrite the very molecules of life any way we wish. With CRISPR, biologists have already createdamong many, many other living thingsants that cant smell, beagles that put on superhero-like brawn, pigs that resist swine fever, macaques that suffer from sleep disorders, coffee beans that contain no caffeine, salmon that dont lay eggs, mice that dont get fat, and bacteria whose genes contain, in code, Eadweard Muybridges famous series of photographs showing a horse in motion. Two years ago, a Chinese scientist, He Jiankui, announced that he had produced the worlds first CRISPR-edited humans, twin baby girls. According to He, the girls genes had been tweaked to confer resistance to H.I.V., though whether this is actually the case remains unclear. Following his announcement, He was fired from his academic post, in Shenzhen, and sentenced to three years in prison.

I have almost no experience in genetics and have not done hands-on lab work since high school. Still, by following the instructions that came in the box from the Odin, in the course of a weekend I was able to create a novel organism. First I grew a colony of E. coli in one of the petri dishes. Then I doused it with the various proteins and bits of designer DNA Id stored in the freezer. The process swapped out one letter of the bacterias genome, replacing an A (adenine) with a C (cytosine). Thanks to this emendation, my new and improved E. coli could, in effect, thumb its nose at streptomycin, a powerful antibiotic. Although it felt a little creepy engineering a drug-resistant strain of E. coli in my kitchen, there was also a definite sense of achievement, so much so that I decided to move on to the second project in the kit: inserting a jellyfish gene into yeast in order to make it glow.

The Australian Centre for Disease Preparedness, in the city of Geelong, is one of the most advanced high-containment laboratories in the world. It sits behind two sets of gates, the second of which is intended to foil truck bombers, and its poured-concrete walls are thick enough, I was told, to withstand a plane crash. There are five hundred and twenty air-lock doors at the facility and four levels of security. Its where youd want to be in the zombie apocalypse, a staff member told me. Until recently, the center was known as the Australian Animal Health Laboratory, and at the highest biosecurity levelBSL-4there are vials of some of the nastiest animal-borne pathogens on the planet, including Ebola. (The laboratory gets a shout-out in the movie Contagion.) Staff members who work in BSL-4 units cant wear their own clothes into the lab and have to shower for at least three minutes before heading home. The animals at the facility, for their part, cant leave at all. Their only way out is through the incinerator is how one employee put it to me.

About a year ago, not long before the pandemic began, I paid a visit to the center, which is an hour southwest of Melbourne. The draw was an experiment on a species of giant toad known familiarly as the cane toad. The toad was introduced to Australia as an agent of pest control, but it promptly got out of control itself, producing an ecological disaster. Researchers at the A.C.D.P. were hoping to put the toad back in the bottle, as it were, using CRISPR.

A molecular biologist named Mark Tizard, who was in charge of the project, had agreed to show me around. Tizard is a slight man with a fringe of white hair and twinkling blue eyes. Like many of the scientists I met in Australia, hes from somewhere elsein his case, England. Before getting into amphibians, Tizard worked mostly on poultry. Several years ago, he and some colleagues at the center inserted a jellyfish gene into a hen. This gene, similar to the one I was planning to plug into my yeast, encodes a fluorescent protein. A chicken in possession of it will, as a consequence, emit an eerie glow under UV light. Next, Tizard figured out a way to insert the fluorescence gene so that it would be passed down to male offspring only. The result is a hen whose chicks can be sexed while theyre still in their shells.

Tizard knows that many people are freaked out by genetically modified organisms. They find the idea of eating them repugnant, and of releasing them into the world anathema. Though hes no provocateur, he, like Zayner, believes that such people are looking at things all wrong. We have chickens that glow green, Tizard told me. And so we have school groups that come, and when they see the green chicken, you know, some of the kids go, Oh, thats really cool. Hey, if I eat that chicken, will I turn green? And Im, like, You eat chicken already, right? Have you grown feathers and a beak?

Anyway, according to Tizard, its too late to be worried about a few genes here and there. If you look at a native Australian environment, you see eucalyptus trees, koalas, kookaburras, whatever, he said. If I look at it, as a scientist, what Im seeing is multiple copies of the eucalyptus genome, multiple copies of the koala genome, and so on. And these genomes are interacting with each other. Then, all of a sudden, ploomph, you put an additional genome in therethe cane-toad genome. It was never there before, and its interaction with all these other genomes is catastrophic. It takes other genomes out completely. He went on, What people are not seeing is that this is already a genetically modified environment. Invasive species alter the environment by adding entire creatures that dont belong. Genetic engineers, by contrast, just alter a few stretches of DNA here and there.

What were doing is potentially adding maybe ten more genes onto the twenty thousand toad genes that shouldnt be there in the first place, and those ten will sabotage the rest and take them out of the system and so restore balance, Tizard said. The classic thing people say with molecular biology is: Are you playing God? Well, no. We are using our understanding of biological processes to see if we can benefit a system that is in trauma.

Formally known as Rhinella marina, cane toads are a splotchy brown, with thick limbs and bumpy skin. Descriptions inevitably emphasize their size. Rhinella marina is an enormous, warty bufonid (true toad), the U.S.Fish and Wildlife Service notes. The U.S.Geological Survey observes that large individuals sitting on roadways are easily mistaken for boulders. The biggest cane toad ever recorded was fifteen inches long and weighed six poundsas much as a chubby chihuahua. A toad named Big Bette, who lived at the Queensland Museum, in Brisbane, in the nineteen-eighties, was nine and a half inches long and almost as wideabout the size of a dinner plate. The toads will eat almost anything they can fit in their oversized mouths, including mice, dog food, and other cane toads.

Cane toads are native to South America, Central America, and the southernmost tip of Texas. In the mid-eighteen-hundreds, they were brought to the Caribbean. The idea was to enlist the toads in the battle against beetle grubs, which were plaguing the regions cash crop, sugar cane. (Sugar cane, too, is an import; it is native to New Guinea.) From the Caribbean, the toads were shipped to Hawaii. In 1935, a hundred and two toads were loaded onto a steamer in Honolulu, headed for Australia. A hundred and one survived the journey and ended up at a research station in sugar-cane country, in northeast Queensland. Within a year, theyd produced more than 1.5 million eggs. (A female cane toad can produce up to thirty thousand eggs at a go.) The resulting toadlets were intentionally released into the regions rivers and ponds.

Its doubtful that the toads ever did the sugar cane much good. Cane beetles perch too high off the ground for a boulder-size amphibian to reach. This didnt faze the toads. They found plenty else to eat, and continued to produce toadlets by the truckload. From a sliver of the Queensland coast, they pushed north, into the Cape York Peninsula, and south, into New South Wales. Sometime in the nineteen-eighties, they crossed into the Northern Territory. In 2005, they reached a spot known as Middle Point, in the western part of the Territory, not far from the city of Darwin.

Along the way, something curious happened. In the early phase of the invasion, the toads were advancing at the rate of about six miles a year. A few decades later, they were moving at the pace of twelve miles a year. By the time they hit Middle Point, theyd sped up to thirty miles a year. When researchers measured the individuals at the invasion front, they found out why. The toads had significantly longer legs than the toads back in Queensland, and this trait was heritable. The Northern Territory News played the story on its front page, under the headline SUPER TOAD. Accompanying the article was a doctored photo of a cane toad wearing a cape. It has invaded the Territory and now the hated cane toad is evolving, the newspaper gasped. Contra Darwin, it seemed, evolution could be observed in real time.

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CRISPR and the Splice to Survive - The New Yorker

Ten years ago, Tony Herbert developed a lump on the right side of his chest. The clump of tissue grew and became painful and he was tested for breast cancer. The result was positive.

I had surgery and chemotherapy and that worked, he said last week. But how had Herbert managed to develop a condition that is so rare in men? Only about 400 cases of male breast cancer are diagnosed every year in the UK compared with around 55,000 in women. A genetic test revealed the answer. Herbert had inherited a pathogenic version of a gene called BRCA2 and this mutation had triggered his condition.

The genetic link was a crucial revelation that not only played a key role in Herberts recovery and survival over the next decade, but which has also helped many women and men fight breast cancer as well as cancers of the ovary and prostate. All three cancers are now known to be linked to mutated versions of BRCA2 a gene whose existence was first revealed 25 years ago this month in a paper in Nature.

Today it is calculated that in the UK alone there are tens of thousands of people who carry pathogenic versions of the gene, which is known as Breast Cancer 2 or BRCA2. It can be inherited from either parent and can spread through lineages with devastating effect. Revealing its existence which was achieved by a research team led by Michael Stratton, who was then working at the Institute of Cancer Research in London has revolutionised the treatment of cancers for a great many individuals.

In the case of Herbert, his inheritance of the mutated gene meant he was susceptible not just to breast cancer but to prostate cancer as well, as doctors realised. I was monitored for prostate cancer and it was found to be at quite an advanced stage. I was given radiotherapy and to be honest I now feel fine, said Herbert who campaigns to raise awareness about breast cancer in men.

The crucial point is that his fight against both the cancers that have touched his life would not have been possible without the discovery of BRCA2. Pinpointing the mutated, pathogenic gene, which is passed through families leaving carriers prone to breast, ovary and prostate cancers, was a medical milestone that involved UK scientists in a desperate race against US companies who wanted to find the gene and patent it for private gain. For good measure Stratton who is now director of the Wellcome Sanger Institute in Cambridgeshire was told by some researchers that he was wasting time when he launched his project. One breast cancer gene, BRCA1, had already been found and it was unlikely there would be a second, I was told, Stratton told the Observer last week.

Nevertheless he and his colleagues persisted and began investigating several large UK and Irish families who were suffering grim numbers of cases of breast and ovary cancers. Was there an unknown mutant gene being passed from one generation of women to the next, one that was leaving them vulnerable to tumours? We looked at hundreds of genetic markers to see if we could find one that was carried only by women who got cancer. That would tell us where the new cancer gene was located.

Genetic markers are small pieces of DNA that are found stretched across the 46 chromosomes that make up the human genome. A first attempt was made using 250 of such markers but failed to produce a result. It was dispiriting, admitted Stratton.

But the team persisted and developed a second set of 300 different markers. I came into the laboratory one day and the results of our study were waiting. They clearly showed a piece of DNA on chromosome 13 that tracked women who went on to develop cancer. We had discovered a new breast cancer gene and, for good measure, we had found out where it lay on the human genome. It was a wonderful feeling, though we realised we still had to pinpoint the gene itself.

The breakthrough also came with a complication. Strattons team had been cooperating with several laboratories in their BRCA2 hunt, including one in the US. This group was backed by the company Myriad Genetics who had found the first breast cancer gene, BRCA1, and who had taken out a patent on it. We did not believe in patenting genes to make profits, however. So we decided to go our own way.

So the race to find BRCA2 began. Initially the prospects for Strattons team looked poor. Myriad Genetics had already found one such gene. It had the experience and also plenty of funds to back its search for another cancer gene. However, an unexpected ally stepped in when the newly opened Sanger Centre (later renamed the Wellcome Sanger Institute) offered to turn its DNA sequencing prowess to explore the region of chromosome 13 where BRCA2 was known to reside.

Sanger scientists provided precise details of the millions of units of DNA on that part of chromosome 13. One morning we went through the most recent data and found a tiny piece of a gene on the chromosome that was missing, a deletion of several DNA units that would have destroyed its function as the gene in which it lay, said Stratton.

Crucially women who inherited that deletion in the family they were studying usually went on to develop breast cancer. That was exactly the sort of thing that we had been looking for, said Stratton. We had landed right on BRCA2. It was an extremely humbling moment.

Over the next two months, the team discovered different abnormalities in this gene in different breast cancer families. It was incontrovertible evidence that this gene was BRCA2, added Stratton. In most families, BRCA2 plays a role in DNA repair and so helps to prevent the triggering of cancers. In families where the gene is damaged, that protection is lost. The discovery was published in Nature and had a dramatically speedy clinical impact. A woman in one of our families was very worried she would get breast cancer and was considering a double mastectomy. We tested her straightaway and found she had not inherited the mutated gene that ran in her family. That meant we were able to tell her she didnt need the operation, added Stratton.

Since then thousands of others have benefited from screening and treatments that have emerged in the wake of BRCA2s discovery, a point stressed by Clare Turnbull, professor of cancer genomics at the Institute of Cancer Research. If a woman gets breast cancer, and we find she is a gene carrier, we can treat her for that condition and also offer to operate to remove her ovaries if shes completed her family because we now know of BRCA2s link to ovarian cancer. Such an operation dramatically reduces the likelihood of women developing ovarian cancer.

In addition, siblings who might have also inherited a pathogenic gene from a mother or father can be tested. For those who test negative, that knowledge relieves anxiety, added Turnbull. For those who test positive, we can offer breast cancer screening while they are still in their 30s. They can also choose to have a mastectomy. In addition, drugs that can counter the effects of the pathogenic version of BRCA2 gene have also been developed, added Turnbull.

In the beginning, breast and ovary cancers formed the main targets of BRCA2 research. However, more recently, it was found that cases of prostate cancer in men were also linked to the gene, as was found in the case of Herbert.

If a man inherits a pathogenic mutation in BRCA2, then, when hes in his early 60s, we now know he will have a 20% chance of developing prostate cancer. That compares with the normal risk for that age of about 3%, said Professor Rosalind Eeles, at the Institute of Cancer Research. In addition, those cancers are a lot more aggressive than standard cases of prostate cancer.

As a result, new European medical guidelines have recently recommended that men over the age of 40 who have a pathogenic BRCA2 mutation should be offered annual screening for prostate cancer. We also hope it will become a UK guideline in the near future, added Eeles.

In addition, Eeles said research showed that prostate cancers in men with BRCA2 mutations are more likely to spread to surrounding tissue but would respond better to surgery to remove tumours as opposed to using radiotherapy alone. All this is a consequence of finding BRCA2 25 years ago, she added.

But testing for BRCA2 can also bring stress, a point made by Dee Gardner. In 2013, after being treated for ovarian cancer, she was urged to have a BRCA2 test. It was positive and I was completely sideswiped. I had three children all young adults then and I now knew each had a 50-50 risk of carrying a gene that could predispose them to cancer.

Gardners children have since had a BRCA2 test of their own. However, there was a further problem. I come from a very large family with lots of cousins and I realised it was up to me to tell them they could also be carrying the gene. It really weighed heavily on me. They needed to be told of the risks, said Gardner, a social worker who lives in Colchester, Essex, with her husband, Howard.

In the end, Gardner wrote to many of her cousins to pass on the troubling news, but it was a strain. It was tough. I knew my letter would cause pain. The trouble is that there is no emotional support for people who are put in this situation, and that lack needs to be addressed.

On the other hand, Gardners BRCA2 status picked up because she developed ovarian cancer led her to undergo investigations for signs of breast cancer. I was found to be in the early stages of a tumour and so elected to have double mastectomy, she added. So yes, finding I had the BRCA2 gene may also have saved my life.

Each of us has around 20,000 genes that direct the manufacture of the proteins from which our bodies are constructed. These genes are bundled together in chromosomes. We get 23 of these chromosomes from our mothers and 23 from our fathers. The genes that lie along these chromosomes are made of deoxyribonucleic acid, DNA, which is made up of twin chains of complex chemicals that coil around each other to form a double helix.

BRCA2 is found on chromosome 13. As we each have two chromosome 13s one inherited from our mother, one from our father if one parent has a mutant BRCA2 gene there will be a 50-50 chance they will pass it on to one of their children.

BRCA2 is involved in repairing damaged DNA and helps to keep cells in a healthy condition. When the gene mutates and becomes pathogenic, the gene no longer helps to keep DNA from becoming damaged and this raises the risk that a cell will become cancerous and grow uncontrollably. BRCA2 is said to be a tumour suppressor gene because it helps to stop cells from growing and dividing too rapidly or in an uncontrolled manner.

BRCA2 is not the only gene whose mutations are linked to increased risks of developing breast cancer. Pathogenic versions of BRCA1 have a similar effect while abnormal versions of another gene known as PALB2 has also been found to increase risk. The prospect of getting breast cancer over an average lifetime for a woman is 12%. However, if they carry mutated versions of BRCA1 or BRCA2 that risk rises to around 70%. An abnormal version of PALB2 raises that risk to around 50%.

In addition to increasing prospects of developing breast cancer, mutant forms of BRCA2 also raise risks of a carrier developing ovary, prostate and pancreatic cancer.

Read more:
How race to track mystery gene with links to three cancers saved millions - The Guardian