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Less Acute MI, More HF: European Task Force Shifts Support for ‘Overhyped’ Cell Therapy Research – TCTMD

The decade-old excitement surrounding the potential for autologous cell therapy to treat cardiovascular disease may have fizzled into futility for many clinicians. But according to a new European consensus document, its possible this technology will yet find a way into future practice .

One of the problems the field has faced is that people got super excited 10 years ago because it was overhyped, and essentially . . . it led to the expectation that every time we presented [something] at clinical meetings, the field would move forward. And of course that wasnt the case, chair of the European Society of Cardiology stem cell task force and lead author Anthony Mathur, MD (St Bartholomews Hospital West Smithfield, London, England), told TCTMD.

The reason why I think people have run out of steam on this one is that theyve shared the 10-year journey with us. Anthony Mathur

Mathur contrasted the story of cell therapy to that of drug or device development, which is usually kept private until promising phase III data are available to support its routine use. What we’ve done is weve exposed the clinical and scientific community to a journey that in pharma we just wouldn’t see as clinicians, he said. The reason why I think people have run out of steam on this one is that theyve shared the 10-year journey with us.

The document, which appeared online February 15, 2017, ahead of print in the European Heart Journal, was written as an update to a slightly more optimistic statement from the same task force published in 2006.

Of all of the recommendations that the original document made, very few have borne fruit. For example, the task force suggested the completion of a randomized trial for the use of autologous stem cells to treat acute MI patients presenting after more than 12 hours or who fail to respond to therapy. A trial such as this has not been undertaken and likely wont happen, given that primary angioplasty practice in Europe and the United States has revolutionized the treatment of acute MI and drastically lowered mortality, Mathur said. Any new method of treating acute MI will find it really tough to demonstrate an improvement unless its a complete game changer.

Since these patients may well develop heart failure, for which chronic cell therapy strategies are under development, research efforts should refocus there for now, the task force writes.

However, they stand by one 2006 recommendation for a randomized trial of autologous cells in acute MI patients presenting within 12 hours and treated with immediate revascularization. The ongoing phase III BAMI trial, undertaken by members of this task force including Mathur, will study just that but results are not expected for several years. Once these results are available, it will be time to either draw a line under it or ask for regulatory approval, but it’s sort of pointless to keep rehashing the whole thing and going back asking the same question, Mathur said.

Careful But Hopeful

Looking back, Mathur said that the trajectory of cell therapy in cardiology has taught him to be self-critical and very careful about what we say, and to understand that it is okay to stop doing certain things that were once thought to be appropriate. Also, because those involved in translational research lack the tools that give us an evidence or an idea of the signal that we should expect in larger clinical trials, [a] lot of what weve come across is potentially unexpected. Unfortunately, it also means . . . weve probably disregarded areas of research based on the signals we haven’t seen in smaller studies simply because, in a way, the tools we have arent sensitive enough to pick it up, he said.

If there is any biological signal found in a phase II study, Mathur stressed the importance of trying to complete a phase III study in order to unlock these unexpected kernels.

Far from being defeated, he said he is hopeful that cell therapy will pan out in some way for cardiac patients. Whether cell therapy worked or not, it’s all about the amazing stories and how it changed people’s lives seemingly for the better. So thats something thats difficult to drop, Mathur said. We have seen a signal for patients in heart failure in which there seems to be some sort of benefit. And some might say its purely psychological. Fine, but these people who were told there was nothing else that could be done got better.

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Less Acute MI, More HF: European Task Force Shifts Support for ‘Overhyped’ Cell Therapy Research – TCTMD

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Research on repair of broken hearts hints at possibility of new designer cardiovascular therapies – News-Medical.net

February 22, 2017 at 3:02 AM

Unlike the self-repair abilities of our skin, bone and other tissues, which can readily heal and rebuild themselves after injury, evolution has left the mammalian heart with relatively little regenerative capacity.

More than one million Americans have heart attacks each year. Although many will survive, damage to heart muscle is permanent, causing heart attack survivors to be at an increased risk of a repeated attack or other problems later in life, including congestive heart failure. During a heart attack, blocked arteries cause the heart muscle to become starved for oxygen, and eventually some muscle cells die. Finding new ways to repair and protect a broken heart is the core of labs like those of physician-scientists Jon Epstein, MD, executive vice dean and chief science officer at Penn Medicine, and Rajan Jain, MD an assistant professor of Cardiovascular Medicine.

Their labs are working on a suite of angles for future therapies for failing hearts that include immune cells involved in protecting heart muscle after an attack, stem-like cells and associated growth factors that may one day be able to regenerate heart muscle, and better understanding mutations that lead to heart failure.

Harnessing Immune Cells

Jain and Epstein are looking at how immune cells respond to the damage caused by a heart attack to begin the repair process, which can sometimes result in too much scar tissue. This over-reaction turns the heart into a stiff fibrous organ that can’t pump efficiently. Their work suggests that medicines that act on the immune system might be used to improve outcomes in some patients after a heart attack.

“We are hoping to harness the immune system, just as other research teams at Penn are doing to fight cancer, in order to improve the balance between scar formation and regeneration after a heart attack,” said Epstein. Jain’s work with Epstein on the heart’s interaction with the immune system in post-heart-attack responses hints at the possibility of developing designer cardiovascular therapies.

Inspiration from Stem Cells

After a heart attack, cardiac muscle cells are sometimes injured beyond complete repair and having a way to regenerate or replace compromised tissue might extend or enhance the life of a person with heart disease. Studying the development from the stage of an embryo, when the heart forms from stem-like cardiac progenitor cells, is giving cardiologists new ideas for therapies. In particular, scientists want to identify progenitor cells that have matured just beyond the stem-cell stage when they become committed to making only one type of cardiac cell. “We want to one day produce progenitor cells that can be locally delivered or fabricated into transplantable tissue patches – like skin grafts – for heart patients,” Jain said.

In 2015, Jain and Epstein thought that the protein HopX would label a multipotent progenitor cell, but they were surprised to learn that it was marking only cells destined to make heart muscle. A Penn and Stanford group collaborated with many others a year later to describe a roadmap on how to steer one type of human embryo cell population – including those marked by HopX — down a series of choices to make specific types of cells. This is the first step of many to make the transplantable heart cells that Jain would like to have for heart patients.

Genome Organization Jain’s ideas for new ways to look at cardiovascular therapies is also informed by the time he has worked in the clinical arena with Anjali Owens, MD, an assistant professor of Cardiovascular Medicine who directs the Penn Center for Inherited Cardiovascular Disease. They were puzzled by the observation that some patients with heart failure had mutations in their lamin proteins — support proteins that make up an architectural network of struts in a cell’s nucleus.

Researchers think lamins play an important role in organizing a cell’s genetic material and thereby which parts of the genome are available for translating into the collection of proteins that make one cell different from another. Certain lamin mutations that Jain and Owens observed translated into a particularly aggressive type of heart failure in young patients. “My lab’s mission is to better understand how genome organization establishes and maintains cellular identity – and what happens when that finely tuned system goes awry — in order to guide the development of new therapeutics,” Jain said.

By delving into the unique biology of heart muscle cells, Jain and Epstein have myriad new places to find potential therapies for many Heart Months to come.

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Nanostraws Sample Cells Without Damage – R & D Magazine

Tiny nanostraws may offer a glimpse into a cells contents without causing any damage to the cell.

The nanostraws were developed by researchers at Stanford University, who devised a method of sampling cell contents without disrupting its natural processes, which is a staple of current cell sampling methods.

The new method relies on tiny tubes 600 times smaller than a stand of hair that allow researchers to sample a single cell at a time. The nanostraws are able to penetrate a cells outer membrane without damaging it and draw out proteins and genetic material from the cells salty interior.

It’s like a blood draw for the cell, Nicholas Melosh, an associate professor of materials science and engineering and senior author on a paper, said in a statement.

According to Melosh, this technique will significantly impact the understanding of cell development and could yield much safer and effective medical therapies because it allows for long term, non-destructive monitoring.

What we hope to do, using this technology, is to watch as these cells change over time and be able to infer how different environmental conditions and ‘chemical cocktails’ influence their developmentto help optimize the therapy process, he said.

If researchers gain a better grasp on how a cell works they can address those processes directly.

For stem cells, we know that they can turn into many other cell types but we do not know the evolutionhow do they go from stem cells to, say, cardiac cells? Yuhong Cao, a graduate student and first author on the paper, said in a statement. This sampling technique will give us a clearer idea of how it’s done.

A benefit of the sampling method is it could inform cancer treatments and answer questions about why some cancer cells are resistant to chemotherapy while others are not.

With chemotherapy, there are always cells that are resistant, Cao said. If we can follow the intercellular mechanism of the surviving cells, we can know, genetically, its response to the drug.

The nanostraws are grown in a small sampling platform designed to mimic biology called the Nanostraw Extraction (NEX) sampling system.

Cells divide and change over time, with thousands of chemical reactions occurring within each cell every day, which makes it difficult to truly understand the inner workings of cells.

Currently, scientists use a method of cell sampling called lysing, which ruptures the cell. However, once a cell is destroyed it cannot be sampled from again.

Cells in our bodies are connected by a system of gates through which they send each other nutrients and molecules.

Melosh was inspired to develop the new system when he observed the intercellular gates after he was trying to determine a non-destructive way of delivering substances, including DNA or medicines, inside cells.

The new sampling system is the reverse of that process, as scientists are able to observe whats happening within a cell.

When the research team compared their cells samples from the NEX with cell samples taken by breaking the cells open, they found that 95 percent of the samples were congruous.

The team also found that when they sampled from a group of cells day after day, certain molecules that should be present at constant levels remained the same, which indicated that their sampling accurately reflected the cells interior.

The team not only sampled generic cell lines but also with human heart tissue and brain cells grown from stem cells and in each case the nanostraw sampling reflected the same cellular contents as lysing the cells.

The study was published in the Proceedings of the National Academy of Sciences of the United States of America.

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Nanostraws Sample Cells Without Damage – R & D Magazine

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Study: Changing the environment within bone marrow alters blood cell development – ScienceBlog.com (blog)

Researchers at the University of Illinois report they can alter blood cell development through the use of biomaterials designed to mimic characteristics of the bone marrow.

The findings, reported in the journal Science Advances, are a first step toward developing more effective bone marrow treatments for diseases like leukemia and lymphoma.

Blood cells flow throughout the body delivering life-supporting oxygen and nutrients. As these cells are used and recycled they are regenerated by bone marrow, the soft tissue inside the bodys long and hollow bones.

Certain regions of bone marrow contain hematopoietic stem cells, the precursors of all blood and immune cells, said University of Illinois chemical and biomolecular engineering professor Brendan Harley, who led the research with postdoctoral researcher Ji Sun Choi.

The tissue environment that surrounds these cells in the bone marrow provides a wealth of signals that can alter how these precursor cells behave. This paper looked at the signals provided by the tissue matrix itself, said Harley, who also is affiliated with the Carl R. Woese Institute for Genomic Biology at Illinois.

One of the major tools that oncologists use to treat leukemia and lymphoma involves transplanting HSCs. The donor stem cells must locate marrow cavities and start producing blood and immune cells. However, there is a limited quantity of available donor HSCs and the success rate of transplantation is low.

Were interested in this problem from an engineering standpoint, Harley said. The goal is to create better tools to both expand the number of donor HSCs and improve their capacity to repopulate the bone marrow after transplantation.

Like cells throughout the body, HSCs are contained in a three-dimensional tissue environment known as the extracellular matrix. Harley and Choi gathered samples of HSCs from mice and then grew them in the laboratory using biomaterials engineered to mimic some of the extracellular matrix properties of the native bone marrow. Their goal was to examine how these engineered systems could alter the HSCs capacity to proliferate and differentiate to become blood cells.

The researchers examined two main elements of the matrix that regularly interact with HSCs: collagen and fibronectin. They found that the HSCs that were exposed to collagen proliferated more rapidly but that they had differentiated, meaning they were no longer stem cells. When exposed to fibronectin, the stem cells proliferated less rapidly, but were able to maintain their stem cell-like nature.

With the collagen substrates, we got more cells but not useful cells, Harley said. With the right combination of stiffness in the matrix and the presence of fibronectin, we identified a class of biomaterials that show promise for being able to maintain and eventually expand these stem cells outside of the body. An engineered bone marrow will be of enormous value for treating hematopoietic cancers such as leukemia, but also for understanding the process of bone marrow failure and other hematopoietic diseases.

This project is only the first step in controlling the signals from the matrix that influence HSCs, Harley said. He and other researchers in his lab are currently investigating other features of the matrix that can be manipulated to increase the number of stem cells and make them more effective in transplantation.

The paper, Marrow-inspired matrix cues rapidly affect early fate decisions of hematopoietic stem and progenitor cells, is available online. The National Science Foundation, National Institutes of Health and the American Cancer Society of Illinois supported this research. _____________

Photo by L. Brian Stauffer.

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BONE MARROW/STEM CELL DONOR DRIVE – Rayne Acadian-Tribune

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Stem Cell Treatments Could Be The Next Frontier In Fixing Broken Pitchers – Deadspin

In an interesting dispatch from spring training, Yahoos Jeff Passan reports on Los Angeles Angels pitcher Garrett Richardss recovery from a May 2016 elbow injury that shut him down for the season.

Instead of electing to undergo standard Tommy John surgery, Richards decided to try to heal his injury by getting an injection of stem cells directly into his elbow. Passan, whose 2016 book The Arm showed hes not afraid to make his readers feel queasy, described the procedure as such: Richards was fortunate to only suffer a partial tear, which is naturally easier to repair than a full tear.

A doctor guided a needle into the iliac crest of his pelvic bone and began to extract bone marrow.

[…]

Within a few minutes, the harvested marrow was hurried to a centrifuge, spun to separate the good stuff, mixed into a slurry of platelet-rich plasma and readied to inject into Richards damaged right elbow.

Gross, but it apparently worked. Passan reports Richards is feeling great and throwing 98 mph at spring training. Richards is clearly pleased with the tentatively positive outcome: Science, bro. Im a believer now, Richards told Passan.

Dr. Neal ElAttrache, sports premiere orthopedic surgeon, says he is looking forward to seeing where the research on the efficacy of orthobiologics goes, but he also has a theory that the simple resting of the muscle could be the impetus for muscle repair. Or, at least, that the two factors combined can be effective.

A stem cell procedure is less invasive than UCL surgery, of course, and right now it looks like the healing process could be much shorter than that of Tommy John surgery, at least for pitchers with partial UCL tears. Standard TJ recovery time is 14 monthsnearly long enough to inspire an oh yeah, that guy reaction when the player eventually returns. Richards underwent his stem cell procedure in May 2016 and Passan reports that he was throwing by August and was ready to go by October.

Richards will, of course, be kept on a short leash this season as he and the Angels look to avoid a setback or worse, but the potential for an expedited return from partial UCL tears is a major development for the science of pitching.

If stem cell treatments can get electric pitchers like Richards healed and back on the field quicker than surgery can, thats obviously a good thing for baseball. Still, its hard to read Passans story and not come away from it asking, Whats a PED again? Heres Richards talking about his stem cell treatment in the Los Angeles Timesback in 2016:

Stem cells are a remarkable thing. The body heals itself, so thats awesome. Were not out of the woods yet, but todays a good day.

HGH doesnt exactly work the same way this stem cell treatment appears to, but their essential benefits are the same. While the term performance enhancing drugs is still commonly associated with the mega-roids 1990s, HGH is of value to athletes largely for its ability to quicken injury recovery and extend careers. Doctors pushing orthobiologics experiments on their patients are free of the whiff of impropriety, but it seems that has less to do with their virtue than it does their good fortune at being on the right side of baseballs arbitrary PED laws.

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Stem Cell Treatments Could Be The Next Frontier In Fixing Broken Pitchers – Deadspin

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Super Foods In Skin Care – FOX31 Denver

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The essential oils, vitamins and extracts from foods contain some of the most bioactive natural ingredients out there — and they are superior options for our skin to soothe, give a spectacular glow, hydrate and renew. theHAUTEbar shares these hot new product launches.

Avocado Oil is one of the most penetrative of all natural plant oils. This results in extremely soft and hydrated facial skin. And, due to its humectant properties that prevent drying out, this moisturizing effect is long-lasting.

Devenir Light Bright Light Organic Facial Oil is perfect for all skin types who wants brighter luminous glow to their skin.

Caffeine as an ingredient in skin care reduces swelling and puffiness through its powerful antioxidant properties. Onomie Bright Concealing Elixir is a silky-smooth blend that instantly corrects under eye circles as a concealer, and clinically reduces the appearance of dark circles over time.

Fruit Stem Cells are advanced high potency juices that take the place of petroleum by-products and fillers for boosted beauty benefits.

Apple Juice, a.k.a. Malic Acid is rich in vitamins, potent malic alpha-hydroxy acids, phytonutrients, flavonoids, phenols; and provides powerful antioxidant activity to help promote beautiful skin.

Grape Juice, a.k.a. Resveratrol is rich in vitamins; potent tartaric alpha-hydroxy acid and resveratrol antioxidants.

Lemon is rich in vitamins, lycopene, phytonutrients, flavonoids, and alpha-hydroxy citric acids; powerful antioxidant benefits to help clarify and improve skin tone and texture.

Juice Beautys Stem Cellular Exfoliating Peel Spray instantly exfoliates to uncover smoother, younger looking skin after just one use. Formulated with a unique, gentle, plant-derived exfoliant that resurfaces skin within seconds on contact, to visibly loosen and lift away old skin cells.

Green tea is packed with some of the most powerful antioxidants going around thanks to its high levels of oligomeric proanthocyanidins. Because of this, green tea has healing properties which protect the skin from being punished by harmful free radicals. Its anti-inflammatory properties can help protect your skin from sunburn, and green tea has been attributed to increasing elasticity to help reduce the appearance of wrinkles. Babe Green Tea Body Scrub detoxes, purifies and beautifies the body to give skin its best glow and tone. H2O+ Aquadefense protective matcha facial moisturizer is whipped and the matcha green tea helps prevent environmental pollutants from negatively affecting skin.

Coconut oil for the all around skin {and hair} win. Coconut oil makes skin everything you want it to beglowy, healthy, hydrated, young, supple and smooth. Thats because its made mostly of fatty acids. Coconut oil also makes hair healthy, strong, glossy, and even moisturizes the scalp. Coconut is full of restorative proteins and vitamin E and helps increase body and shine of your hair.

Koparis Organic Coconut Melt is the mother of all multitaskers is the ultimate all-over skin moisturizing, under eye rescuing, hair deep-conditioning, belly-balming, baby skin soothing, beauty in a bottle for your whole bod. Vapurs Lux Organic Lip Conditioner is a blissfully restorative formula for healthy, luscious lips. R + Co Palm Springs pre-shampoo treatment mask taps coconut oil as one of its key ingredient oils providing deep hydration to hair and intense conditioning to seal in moisture.

Wild Watermelon Seed Oil, also known as Kalahari Melon seed oil moisturises, regenerates and restructures the skin, and is rich in essential fatty acids, especially linoleic, oleic and palmitic fatty acids.

Treets Traditions Nourishing Spirits Foaming Shower Gel is a rich shower gel that transforms into a soft foam with just a splash of water — and contains Baobab oil and Kalahari melon to nourish and protect skin.

Cucumber Seed Oil is loaded with antioxidants and is super soothing, calming and smoothes the skin. MNs Akwi Purifying Cleanser is a gentle, oil-based cleanser that sweeps away impurities and unclogs pores without stripping the skin.

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Super Foods In Skin Care – FOX31 Denver

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Why Spark’s CEO says 2017 may be a ‘historic year’ for his gene therapy company – Philadelphia Business Journal


Philadelphia Business Journal
Why Spark's CEO says 2017 may be a 'historic year' for his gene therapy company
Philadelphia Business Journal
We look forward to continued innovation, execution and growth in 2017, which may be a historic year for Spark Therapeutics and for patients as we potentially deliver what has been unimaginable before the first gene therapy in the United States for a
Spark Therapeutics Reports 2016 Financial Results and Business HighlightsGlobeNewswire (press release)

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Why Spark’s CEO says 2017 may be a ‘historic year’ for his gene therapy company – Philadelphia Business Journal

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Genetic basis for male baldness identified in large-scale study – Medical News Today

Although common, male baldness can have negative psychological effects and some studies have even linked it to a handful of serious illnesses. New research identifies the genetic variants involved in the condition, which could eventually enable researchers to predict a person’s chances of hair loss.

Male baldness – also referred to as androgenetic alopecia or male pattern baldness (MPB) – affects a significant number of people in the United States, as the condition accounts for over 95 percent of all hair loss in men.

According to the American Hair Loss Association, two thirds of U.S. adults will be affected by MPB to a certain degree by the age of 35, and around 85 percent of men will have experienced significant hair loss by the age of 50.

A lot of these men are seriously affected by the condition, which can have a negative effect on a person’s self-image, as well as on their interpersonal relationships.

Additionally, some genetic studies have even associated MPB with negative clinical outcomes such as prostate cancer and cardiovascular disease.

A new study – led by Saskia Hagenaars and David Hill of the University of Edinburgh in the United Kingdom – explores the genetic basis for the condition. The findings were published in the journal PLOS Genetics.

Scientists analyzed the genomic and health data of more than 52,000 men enrolled in the UK Biobank – an international health resource offering health information on more than 500,000 individuals.

The team located more than 250 independent genetic regions linked to severe hair loss.

The researchers split the 52,000 participants into two groups: a so-called discovery sample of 40,000 people and a target sample of 12,000 individuals. Based on the genetic variants that separated those with no hair loss from those with severe hair loss, the team designed an algorithm aimed to predict who would develop MPB.

The algorithmic baldness predictor is based on a genetic score, and although accurate predictions are still a long way off, the results of this study might soon enable researchers to identify subgroups of the population that are particularly prone to hair loss.

In the present study, researchers found that 14 percent of the participants with a submedian genetic score had severe MPB, and 39 percent had no hair loss. By contrast, 58 percent of those scoring in the top 10 percent on the polygenic score had moderate to severe MPB.

Co-lead author Saskia Hagenaars – a Ph.D. student at the University of Edinburgh’s Centre for Cognitive Aging and Cognitive Epidemiology – comments on the findings:

“We identified hundreds of new genetic signals,” Hagenaars says. “It was interesting to find that many of the genetics signals for male pattern baldness came from the X chromosome, which men inherit from their mothers.”

The study’s other lead author, Dr. David Hill, notes that the study did not collect data on the age of baldness onset, but only on hair loss pattern. However, he adds that, “we would expect to see an even stronger genetic signal if we were able to identify those with early-onset hair loss.”

To the authors’ knowledge, this is the largest genetic study of MPB to date.

The study’s principal investigator, Dr. Riccardo Marioni, from the University of Edinburgh’s Centre for Genomic and Experimental Medicine, explains the significance of the findings:

“We are still a long way from making an accurate prediction for an individual’s hair loss pattern. However, these results take us one step closer. The findings pave the way for an improved understanding of the genetic causes of hair loss.”

Learn how a drug promises robust new hair growth.

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Genetic basis for male baldness identified in large-scale study – Medical News Today

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Genetic data show mainly men migrated from the Pontic steppe to Europe 5000 years ago – Phys.Org

February 21, 2017

A new study, looking at the sex-specifically inherited X chromosome of prehistoric human remains, shows that hardly any women took part in the extensive migration from the Pontic-Caspian Steppe approximately 5,000 years ago. The great migration that brought farming practices to Europe 4,000 years earlier, on the other hand, consisted of both women and men. The difference in sex bias suggests that different social and cultural processes drove the two migrations.

Genetic data suggest that modern European ancestry represents a mosaic of ancestral contributions from multiple waves of prehistoric migration events. Recent studies of genomic variation in prehistoric human remains have demonstrated that two mass migration events are particularly important to understanding European prehistory: the Neolithic spread of agriculture from Anatolia starting around 9,000 years ago, and migration from the Pontic-Caspian Steppe around 5,000 years ago. These migrations are coincident with large social, cultural, and linguistic changes, and each has been inferred to have replaced more than half of the contemporaneous gene pool of resident Central Europeans.

Dramatic events in human prehistory can be investigated using patterns of genetic variation among the people that lived in those times. In particular, studies of differing female and male demographic histories on the basis of ancient genomes can provide information about complexities of social structures and cultural interactions in prehistoric populations.

Researchers from Uppsala and Stanford University investigated the genetic ancestry on the sex-specifically inherited X chromosome and the autosomes in 20 early Neolithic and 16 Late Neolithic/Bronze Age human remains. Contrary to previous hypotheses suggesting patrilocality (social system in which a family resides near the man’s parents) of many agricultural populations, they found no evidence of sex-biased admixture during the migration that spread farming across Europe during the early Neolithic.

For later migrations from the Pontic steppe during the early Bronze Age, however, we find a dramatic male bias. There are simply too few X-chromosomes from the migrants, which points to around ten migrating males for every migrating female, says Mattias Jakobsson, professor of Genetics at the Department of Organismal Biology, Uppsala University.

The research group found evidence of ongoing, primarily male, migration from the steppe to central Europe over a period of multiple generations, with a level of sex bias that excludes a pulse migration during a single generation.

The contrasting patterns of sex-specific migration during these two migrations suggest a view of differing cultural histories in which the Neolithic transition was driven by mass migration of both males and females in roughly equal numbersperhaps whole familieswhereas the later Bronze Age migration and cultural shift were instead driven by male migration.

Explore further: Baltic hunter-gatherers began farming without influence of migration, ancient DNA suggests

More information: “Ancient X chromosomes reveal contrasting sex bias in Neolithic and Bronze Age Eurasian migrations,” PNAS, DOI: 10.1073/pnas.1616392114 , http://www.pnas.org/content/early/2017/02/17/1616392114.abstract

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A new study, looking at the sex-specifically inherited X chromosome of prehistoric human remains, shows that hardly any women took part in the extensive migration from the Pontic-Caspian Steppe approximately 5,000 years ago. …

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Genetic data show mainly men migrated from the Pontic steppe to Europe 5000 years ago – Phys.Org

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Men inherit male pattern baldness from their mum’s side of the family … – Metro

It all comes from your X chromosome (Picture: Getty)

Getting a bit smooth up top? Judging on how you feel about it, your mum is the one you should be blaming /thanking.

Researchers at the University of Edinburgh have found that men inherit most of their baldness genes from their mums side of the family.

For what is the largest ever analysis of hair loss, scientists looked at the DNA of 52,000 men.

They identified almost 300 genes that could contribute to male pattern baldness most of which come from the X chromosome.

Saskia Hagenaars, who jointly led the research, said: We identified hundreds of new genetic signals.

It was interesting to find that many of the genetics signals for male pattern baldness came from the X chromosome, which men inherit from their mothers.

Before this research, published in PLOS Genetics, scientists had only identified a handful of genes related to baldness.

The studys principle investigator, Dr Riccardo Marioni, added: We are still a long way from making an accurate prediction for an individuals hair loss pattern.

However, these results take us one step closer.

The findings pave the way for an improved understanding of the genetic causes of hair loss.

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Men inherit male pattern baldness from their mum’s side of the family … – Metro

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Experts Are One Step Closer To Predicting A Man’s Risk For Hair Loss – Huffington Post

More than 200 new genetic markers linked with male pattern baldness have been identified, according to a new study from the United Kingdom.

The findings greatly increase the number of known genetic markers linked with baldness in men; a previous large study identified just eight such markers.

The researchers in the new study were also able to use their set of genetic markers to predict mens chances of severe hair loss, although the scientists noted that their results apply more to large populations of people than to any given individual.

We are still a long way from making an accurate prediction for an individuals hair-loss pattern. However, these results take us one step closer, study co-author Riccardo Marioni, of the University of Edinburghs Centre for Genomic and Experimental Medicine, said in a statement. The findings pave the way for an improved understanding of the genetic causes of hair loss, Marioni said. [5 Myths About the Male Body]

In the study, the researchers analyzed information from more than 52,000 men ages 40 to 69 years in the United Kingdom. Of these men, about 32 percent said they had no hair loss, 23 percent said they had slight hair loss, 27 percent said they had moderate hair loss and 18 percent said they had severe hair loss

The researchers then analyzed participants genomes, looking for genetic variations, known as single-nucleotide polymorphisms, or SNPs, that were linked with severe hair loss. That search revealed 287 genetic variations, located on more than 100 genes, that were linked with severe hair loss.

Many of the genetic variations were located on or near genes that have previously been linked with hair growth, hair graying or the biological structures involved in making hair, the researchers said.

Forty of the genetic variations were located on the X chromosome, which men inherit from their mothers, the researchers said. One of the genes on the X chromosome the gene for the androgen receptor, which binds to the hormone testosterone was strongly linked with severe hair loss. Previous studies have also pinpointed this gene as tied to male pattern baldness.

The researchers then created a formula, which resulted in a genetic risk score, to try to predict the chances of severe hair loss in the men. Among those men with a below-average score, 39 percent had no hair loss and 14 percent had severe hair loss. In contrast, among those with a high score that put them in the top 10 percent of those in the study, 58 percent had moderate-to-severe hair loss.

The researchers noted that in the study, they did not collect information on the age at which the men started losing their hair. The scientists said they would expect to see even stronger genetic associations with hair loss if they were able to include information about which men experienced early onset hair loss.

As more information from these participants becomes available, the researchers may be able to further refine their predictions, they said.

The study was published today (Feb. 14) in the journal PLOS Genetics.

Original article on Live Science.

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Baldness linked to over 280 genes – BioNews

A new study has found over 280 genes associated with male-pattern baldness.

These genes could be used to predict a man’s chance of hair loss or possibly provide targets for drug development in the future.

The research, published in PLOS Genetics, is the largest genomic study of baldness to date. Researchers studied the DNA of more than 52,000 men aged between 4069 years old enrolled in the UK Biobank, looking for genes associated with baldness.

‘We identified hundreds of new genetic signals,’ Saskia Hagenaars, a PhD student at the University of Edinburgh and co-lead author, said. ‘It was interesting to find that many of the genetics signals for male-pattern baldness came from the X chromosome, which men inherit from their mothers.’

Many of the 287 genes linked with hair loss were related to hair growth and development. The researchers used these genes to try to predict the chance that a man will go bald, and found that almost 60 percent of those with the most number of hair loss genes showed signs of moderate to serious balding. However, the authors state that predictions for individuals are still ‘relatively crude’.

‘Data were collected on hair-loss pattern but not age of onset; we would expect to see an even stronger genetic signal if we were able to identify those with early-onset hair loss,’ said Dr David Hill, University of Edinburgh, who co-led the research.

Male-pattern baldness affects around half of all men by the age of 50. The condition is hereditary and thought to be linked to levels of a certain male sex hormone. Previous genetic studies have also associated male-pattern baldness with prostate cancer and heart disease.

The study’s principal investigator, Dr Riccardo Marioniof theUniversity of Edinburgh, said: ‘We are still a long way from making an accurate prediction for an individual’s hair-loss pattern. However, these results take us one step closer. The findings pave the way for an improved understanding of the genetic causes of hair loss.’

The study was based on information from the first release of data from the UK Biobank in 2015. The authors say that the release of data from the full cohort will enable them to further refine their predictions of male-pattern baldness and investigate its genetic basis.

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More Than 200 Baldness-Linked Genetic Markers Found – Yahoo News

More than 200 new genetic markers linked with male pattern baldness have been identified, according to a new study from the United Kingdom.

The findings greatly increase the number of known genetic markers linked with baldness in men; a previous large study identified just eight such markers.

The researchers in the new study were also able to use their set of genetic markers to predict men’s chances of severe hair loss, although the scientists noted that their results apply more to large populations of people than to any given individual.

“We are still a long way from making an accurate prediction for an individual’s hair-loss pattern. However, these results take us one step closer,” study co-author Riccardo Marioni, of the University of Edinburgh’s Centre for Genomic and Experimental Medicine, said in a statement. “The findings pave the way for an improved understanding of the genetic causes of hair loss,” Marioni said. [5 Myths About the Male Body]

In the study, the researchers analyzed information from more than 52,000 men ages 40 to 69 years in the United Kingdom. Of these men, about 32 percent said they had no hair loss, 23 percent said they had slight hair loss, 27 percent said they had moderate hair loss and 18 percent said they had severe hair loss

The researchers then analyzed participants’ genomes, looking for genetic variations, known as single-nucleotide polymorphisms, or SNPs, that were linked with severe hair loss. That search revealed 287 genetic variations, located on more than 100 genes, that were linked with severe hair loss.

Many of the genetic variations were located on or near genes that have previously been linked with hair growth, hair graying or the biological structures involved in making hair, the researchers said.

Forty of the genetic variations were located on the X chromosome, which men inherit from their mothers, the researchers said. One of the genes on the X chromosome the gene for the androgen receptor, which binds to the hormone testosterone was strongly linked with severe hair loss. Previous studies have also pinpointed this gene as tied to male pattern baldness.

The researchers then created a formula, which resulted in a genetic “risk score,” to try to predict the chances of severe hair loss in the men. Among those men with a below-average score, 39 percent had no hair loss and 14 percent had severe hair loss. In contrast, among those with a high score that put them in the top 10 percent of those in the study, 58 percent had moderate-to-severe hair loss.

The researchers noted that in the study, they did not collect information on the age at which the men started losing their hair. The scientists said they would expect to see even stronger genetic associations with hair loss if they were able to include information about which men experienced early onset hair loss.

As more information from these participants becomes available, the researchers may be able to further refine their predictions, they said.

The study was published today (Feb. 14) in the journal PLOS Genetics.

Original article on Live Science.

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More Than 200 Baldness-Linked Genetic Markers Found – Yahoo News

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Can Your Anxiety Impact How Long You Last In Bed? – Men’s Health


Men’s Health
Can Your Anxiety Impact How Long You Last In Bed?
Men’s Health
To rule out the influence of genetics, the researchers only studied male twins and brothers of twins. After analyzing their responses, the researchers found no link between anxiety symptoms reported in 2006 with later reports of premature ejaculation

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A UO lab digs into worms in the quest to lengthen human life – AroundtheO

In a collaborative project, the UOs Patrick Phillips tackles a problem of reproducibility while studying potential anti-aging compounds

Worms. Might they help us live a healthier and longer life?

Extending human life in ways that keep people both healthy and productive is a goal of many scientists, including the UO’s Patrick Phillips.

His latest project, which he leads in collaboration with two other U.S. institutions, may not immediately move us closer to extending human life beyond the national average of 79. It has, however, opened a window on how basic research that which seeks fundamental knowledge about how something works should be done to harness robust results that speed progress toward medical advances.

In a new paper published Feb. 21 in the high-profile journal Nature Communications, Phillips and 33 collaborators got right to the heart of the challenge: Too many laboratory findings are not reproducible, and the genetic makeup of model organisms often responds differently to compounds thought to offer promise.

“Aging is universal. It is complex. Individuals die for many different reasons, so there is a lot of noise in the system,” said Phillips, a professor of biology and acting executive director of the Phil and Penny Knight Campus for Accelerating Scientific Impact. “It is a challenge to figure out the elements necessary to change the process. To do this you have to approach the question at a scale that has never been done before. That’s what our paper is about.”

In their study, Phillips nine-member UO team and researchers from the Buck Institute for Research on Aging in California and Rutgers University in New Jersey carefully carried out experiments using identical protocols. They simultaneously tested the effects of 10 different compounds on life extension across 22 diverse genetic backgrounds drawn from three species of roundworms.

“This is the largest aging study that has ever been done on an animal hundreds of thousands of individuals have been tested,” Phillips said.

Our study indicates that even when following the same methods, insufficient replication of trials could account for failures to reproduce previous studies, the research team noted in the paper. Our focus on rigorously adhering to defined methods to reduce variability between sites necessitated making choices about specific methodologies for which there was no standard across the field.

Locations of worm strains

Across the labs, the researchers identified six compounds that extended the lifespan in one strain of worms. Overall, two compounds had positive results across the various strains, with an amyloid dye, Thioflavin T, being the most effective; two other compounds offered promise under specific conditions. Genetic differences among the species are comparable to those found in mice and humans, the researchers noted.

More details about the science and Thioflavin T are covered in a news release issued by the Buck Institute.

Future experiments, Phillips said, will test these and other promising compounds in genetically diverse strains of roundworm species to see how they perform. Eventually, the most widely acting compounds could advance into testing in other animal models and, eventually, in human clinical trials.

The research emerged from three-year grants to each of the three collaborating institutions from the National Institutes of Health. It is part of an extension of the National Institute on Agings decade-old Intervention Testing Program that has targeted aging studies using mice at three other institutions. The roundworm project is known as the Caenorhabditis Intervention Testing Program.

Roundworms, which have a lifespan of two to three weeks, have a simple genetic makeup that is similar to mice, which in laboratories can live up to three years. Thus, Phillips noted, more individual worms can be used more cheaply in the course of experiments that span the life cycle.

Compounds that have been found to extend life in worms and mice have proved so far to be limited to organisms with a particular genetic background.

Roundworms

This is a dark side of studying a model organism, Phillips said. You have genetic uniformity in worms and mice, but humans are not genetically uniform. We know that different individuals respond differently to drugs and that the cause of disease is often different in each individual. Overcoming those limitations is a big part of the push toward personalized medicine.

From the outset, he said, the roundworm project has been about reproducibility in a way that mirrors the approaches used by the institutions studying mice.

We’ve had to invest a lot of time in coordinating activities, Phillips said. That’s often an unstated part of the difficulty of doing science. For this, we’ve written hundreds of pages of standard operating procedures to try to normalize the research process.

There is a history in aging studies where one lab finds a result but another lab cannot reproduce it,” he said. “Cancer studies are the same. Only about 25 percent of studies can be reproduced with similar results. This is a big emerging issue in science now, so we feel like our study is one of the best on reproducibility that has ever been produced.

For the project, the leaders of the three labs brought different specialties of nematode biology to the table: Phillips is an expert in evolutionary genetics; Gordon J. Lithgow of the Buck Institute is a specialist on chemical interventions; and Rutgers Monica Driscoll is an aging and health expert.

Can we expect to see extended human lifespans soon?

What we find in this worm may or may not work in mice or humans, Phillips said. We’re looking at things that affect fundamental cellular processes that are conserved genetically across all animals.

Carrying basic research forward is a goal of the Knight Campus, a $1 billion initiative designed to accelerate the cycle of generating impact from discoveries. The Knight Campus, which has seen some recent behind-the-scences progress on staffing and the selection of architects and general contractors, will foster exchanges of ideas among basic-science researchers with applied scientists and entrepreneurs to foster that translational process.

With this research, you are seeing the classic impact cycle, Phillips said. You have a guy working in a most esoteric part of evolutionary biology something that you’d generally think could have no general impacts just to gain understanding about something about the world. It is important, but in terms of affecting human health, who knows? Understanding genetic variation is being recognized as being more important each day. And so what once seemed esoteric is now important for understanding translational medicine.

As scientists expand into studying stress and aging in terms of natural genetic variation in different species, then my area’s unique contributions fit into a broader scale. We’re looking at compounds in a way thats never been done before. We are identifying compounds that can affect health and aging, he said. What do we do with that?

The point is not to make worms live a long time. It’s how we use the information. How might this translate a decade from now into something that could go into human clinical trials to try to help people to live longer healthier lives? Can we turn this basic research into something that is relevant? Are there potential drugs that could?

That could be a Knight Campus story, Phillips said.

By Jim Barlow, University Communications

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A UO lab digs into worms in the quest to lengthen human life – AroundtheO

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Major study finds testosterone therapy is no fountain of youth – Philly.com

Testosterone supplements have grown into a $2 billion market, with millions of men of a certain age taking it for low energy, low libido, low mood what marketers call “low T” even though that’s not an approved use.

Now, the first study to rigorously test whether the quintessential male hormone can fight the toll of aging shows it isn’t much of a youth elixir.

A year of testosterone treatment was no better than a placebo for memory and thinking, and it increased fatty plaque in coronary arteries, a risk factor for heart disease. The hormone helped anemia and low bone density in the minority of men with those conditions, which can be treated with other, proven therapies.

The results, published Tuesday in the Journal of the American Medical Association and JAMA Internal Medicine, add to findings from a year ago: Testosterone did not improve fatigue or walking speed, and its modest benefits on sexual function faded by the end of the study.

“The hopes for testosterone-led rejuvenation for older men are dimmed and disappointed if not yet finally dashed,” University of Sydney professor of medicine David J. Handelsman concluded in an editorial accompanying the latest results.

University of Pennsylvania endocrinologist Peter Snyder, who led the complicated, government-funded clinical trials involving 788 senior men at 12 medical centers, disagreed.

“It shows for the first time that treatment of older men with low testosterone has certain benefits, including bone density and anemia,” Snyder said. “I would say the effects on bone and anemia were striking.”

He added a caveat. Even though the $50 million “T Trials” are the most conclusive studies ever done on the hormone, researchers didn’t follow enough men long enough to tell whether testosterone increases risks such as heart attacks, stroke, or prostate cancer.

AbbVie, which donated its leading brand, Androgel, to the trials, said in a statement that the company is “committed to our patients and is proud of our continuous support of research that advances science for the benefit of hypogonadism patients.”

Actually, hypogonadism occurs when the body doesn’t produce enough of the hormone due to disease, injury, or chemotherapy.It’s the condition for which testosterone-replacement therapy is approved.

Prescribing testosterone for age-related deficiency which is only vaguely defined took off in 2000. The trend was driven not by solid scientific evidence, but by the introduction of convenient, rub-on testosterone products, the first being Androgel. Many men are put on testosterone with no tests of their levels or despite tests showing normal levels, a study of Medicare claims found.

Two years ago, the U.S. Food and Drug Administration cracked down on this overprescribing. It ordered drugmakers to revise product labeling to stress the approved use, and to warn that the drug may increase the risk of heart attacks and stroke. Another order that manufacturers conduct a clinical trial to clarify the heart risks is “under discussion,” the FDA said Friday.

Concerns about testosterone use also led the National Institute on Aging to fund the T Trials, which began enrolling men over age 64 in 2009.

T Trials researchers had to screen more than 50,000 men to find 788 with confirmed abnormally low testosterone levels along with one or more age-related symptom that the hormone might help. More than 60 percent of the men were also obese, a condition that can depress testosterone levels.

Now, with a clearer scorecard on benefits, Snyder would like to see the government fund a study to tease out the risks an effort that would take 5,000 men, five years of treatment, and $500 million.

Other experts see no point in defining the downsides of a therapy with weak upsides.

“The improvements in outcomes in the T Trials were minimal,” said Deborah Grady, a professor of medicine at the University of California, San Francisco, and an editor of JAMA Internal Medicine.

Grady was a leader of the Women’s Health Initiative, the mammoth government study that in 2002 shattered the deeply held belief that menopausal hormone therapy protected women’s hearts. The National Institutes of Health agreed to fund the initiative because estrogen, unlike testosterone, had decades of circumstantial evidence of cardiac benefits.

Testosterone’s cardiac effects are still unsettled. Some studies that mine medical records including one in Tuesday’s JAMA Internal Medicine have found men taking it have fewer heart problems.

The T Trials’ anemia findings add to the complexity.

Testosterone is known to increase production of red blood cells, which carry hemoglobin, a protein that ferries oxygen. In 126 men with mild anemia a deficiency of red blood cells or hemoglobin that can cause fatigue testosterone was better than a placebo at boosting hemoglobin. The hormone corrected anemia that had no apparent cause, as well as anemia caused by iron deficiency or inflammation.

However, in six men, the hormone triggered an oversupply of red blood cells. Testosterone labeling warns about this because the blood can become too thick, a risk for dangerous blood clots or stroke.

Like all participants in the trials, the six men were closely monitored, so the problem was detected, their testosterone dose was reduced, and their red blood cell counts returned to normal, Snyder said.

“The results illustrate that decisions about testosterone treatment need to be individualized,” said Evan Hadley , director of the National Institute on Aging’s geriatrics division.

Physician Michael Carome, director of health research at the consumer advocacy organization Public Citizen, drew a different bottom line: “This body of research indicates that testosterone is not the fountain of youth that some patients, doctors, and industry have hoped, or represented it as being.”

Published: February 21, 2017 11:03 AM EST The Philadelphia Inquirer

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Healthy eating, the Hyman way – Durham Herald Sun

Twenty years ago if you wanted to be laughed out of town, you would have written a book titled: “Eat Lots of Fat and Lose Weight.” If you were a doctor and the author of that book you would have risked professional ridicule.

At the end of 2016, Mark Hyman, MD’s “Eat Fat, Get Thin,” was published by Little, Brown and Company and it became a New York Times best seller. The only chuckle heard was the IRS giggling all the way to the U.S. Treasury.

Hyman is the director of the Cleveland Clinic Center for Functional Medicine.

In his new book, Hyman explores the biggest myth: When it comes to weight gain or loss, it’s a calories-in, calories-out world. He says that’s simply not true. The key to weight loss or gain is how different calorie sources are metabolized. Essentially, eating Hyman’s way, you can stop counting calories.

Hyman makes it clear, backing it up with studies, that our bodies process sugars or highly processed carbohydrate calories differently from a protein calorie or a fat calorie.

He writes: “When taken as a whole, the science shows us a clear pattern of evidence that carbs make you fat, while fat makes you thin.” The complete opposite of the decades-long mantra we’ve all been chanting.

Hyman’s book, “Eat Fat, Get Thin,” explains that all that science backs up what he believes is a food plan that can lead to healthy weight loss and maintenance. He is not just the living example of that truth; he’s treated more than 20,000 patients who also appear to be true believers.

Hyman’s a huge coconut oil fan thanks to its medium-chain triglycerides and explains why some of the saturated fats that make up coconut oil can and do promote health.

He also likes olive oil; not so much for cooking, more for salad dressings and for making homemade mayonnaise (yes, he’s got a recipe for that).

Hyman’s no fan of trans fat (partially hydrogenated oil). For reasons too long to list here, his best advice: stay as far away from trans fats as possible.

Hyman recommends a blend of the best of vegan and Paleo that he (unfortunately) calls Pegan.

Here’s an abridged list of what Hyman likes in his food plan: organic, local, fresh whole foods (high in vegetables and fruits); low or no pesticides, antibiotics, or hormones; very few or no chemicals; higher in quality fats (like olive oil and avocados). The plan is low in refined, processed vegetable oils (say goodbye to canola and soybean oils); moderate amounts of protein; animal food (from humanely and sustainably raised, antibiotic and hormone free sources); fish (of course low-toxin, like sardines or anchovies).

Hyman shuns dairy, but, no surprise, he’s big on veggies. He lists 43 vegetables to eat in virtually unlimited quantities, such as artichokes, asparagus, bell peppers, broccoli, cabbage, carrots, eggplant, fennel, green beans, kale, lettuce, mushrooms, onions, snap peas, summer squash and tomatoes. Potatoes aren’t on that list.

Select fruits work; Hyman’s favorites are the berries (except for strawberries) like frozen blackberries, wild blueberries and raspberries, along with kiwi, pomegranate and watermelon. Oranges, bananas or grapes, all of which are high in natural sugars, are absent from that list.

There’s a lot to learn about Hyman’s food plan. Read all about it in “Eat Fat, Get Thin” book. If you buy into his weight-loss plan, then you’ll also want to get his “Eat Fat, Get Thin Cookbook.”

It may take a while to get used to how it all works, but I believe it’ll turn out to be worth the effort.

Here’ one of Hyman’s recipe’s from his cookbook to try.

Chicken and Arugula Salad with Roasted Red Pepper Vinaigrette

4 (6-ounce) boneless, skinless chicken breasts

1/4 teaspoon freshly ground black pepper

1 teaspoon sea salt

2 tablespoons avocado oil

2 jarred roasted red peppers, patted dry

1/4 cup extra-virgin olive oil

2 tablespoons sherry vinegar

2 garlic cloves

1/2 teaspoon dried thyme

4 cups baby arugula

1 small red onion, thinly sliced

1 cup pitted Kalamata olives

2 hard-cooked eggs, peeled and quartered

Preheat the oven to 350 degrees.

Season the chicken breasts on both sides with teaspoon of salt and the pepper.

In a large oven-safe skillet, warm the avocado oil over medium-high heat until shimmering. Add the chicken breasts to the pan in a single layer and cook for 5 minutes. Flip the breasts, transfer the pan to the oven, and cook until the meat is opaque throughout and the internal temperature reaches 165 degrees on an instant-read thermometer, about 6 to 7 minutes. Transfer the chicken breasts to a cutting board and let rest for 2 to 3 minutes while you make the vinaigrette.

Combine the roasted red peppers, olive oil, vinegar, garlic, thyme and the remaining salt in a blender. Blend on high speed until smooth, about 30 seconds.

Cut the chicken breasts crosswise into -inch slices. Divide the arugula among 4 plates and top with the onion slices, olives, hard-cooked eggs, and chicken, evenly distributing the ingredients. Drizzle vinaigrette over each salad and serve.

Nutrition values per serving: 507 calories (41.4 percent from fat), 30 g fat (4 g saturated fat), 8 g carbohydrates, 2 g fiber, 32 g protein, 171 mg cholesterol, 1122 mg sodium.

— Used with permission from “The Eat Fat, Get Thin Cookbook” by Mark Hyman, MD (Little Brown, 2016).

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Studies show testosterone offers little benefits to aging men – Ars Technica

The testosterone gel used in a series of trials assessing health effects.

In decades of research, scientists have found only one medical condition thats clearly and effectively treated with testosterone supplements: pathological hypogonadismthats low testosterone levels due to disease of the hypothalamus, pituitary gland, or testes.

But that hasnt stopped drug makers and the supplement industry from convincing men that jacking their testosterone will stave off the effects of aging. Getting old naturally lowers testosterone in the body. In efforts to combat Low T, testosterone sales sprung 10-fold in the US between 2000 and 2011.

In light of that trend, researchers are trying to get a handle on the health benefits of that beefed-up hormone consumption. So far, it looks wimpy.

In a series of placebo-controlled, randomized trials, researchers tracked the effect of testosterone on the cognition, bone health, anemia, and cardiovascular health of 788 men for a year. All the men were aged 65 or older and had low testosterone levels that couldnt be explained by anything other than age.

The results, reported Tuesday in JAMA and JAMA Internal Medicine, offer mixed results.

Among the 493 in the trial who also had age-related memory declines, testosterone didnt have any effect on memory or cognitive abilities. In the study, 247 got testosterone and 246 got a placebo.

But for cardiovascular health, there was an effecta bad one. Over the year,plaque buildup in the coronary arterywhich is a risk factor for heart diseaseincreased in 73 men on testosterone compared with 65 on placebo. However, other studies have found mixed results on this. Longer, bigger trials will be needed to sort out the risks.

In the anemia study, testosterone did seem to improve iron levels in men with mild anemia. The bone health study also showed that testosterone could improve bone density.

However, its unclear if those benefits outweigh the possible cardiovascular risks. And other drugs may be more effective at treating anemia and improving bone mass than testosterone.

In anaccompanying editorial, Dr. David Handelsman of the University of Sydney and Concord Hospital in Australia concluded that the overall findings do not materially change the unfavorable balance of safety and efficacy to initiate testosterone treatment for age-related hypogonadism. Thus, he added, the hopes for testosterone-led rejuvenation for older men are dimmed and disappointed if not yet finally dashed. But health experts and medical societies should revise guidelines and recommendation to best inform patients, he argued.

Testosterone misuse will not simply disappear for lack of logic or evidence as none was needed to get it startedrejuvenation fantasies thrive on hope without needing factsand educational efforts are essential.

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CardioBrief: After Yet Another Failure, Stem Cell Leaders Double Down – MedPage Today

Despite an unrelieved history of negative trials, stem cell leaders continue to defend their field.

In response to the failure of yet another cardiac stem clinical trial, Roberto Bolli, a prominent leader in the field, argued that it’s time for a “paradigm shift” in the field. We need more stem cell therapy, not less, he argued, perhaps counterintuitively, in an article in Circulation Research. Bolli, who is also the editor-in-chief of the journal, proposed the novel position that the single dose of cells used in virtually all previous stem cell therapy trials should be replaced down the road with repeated doses of stem cells.

It is an understatement to say that cardiac stem cell therapy has not lived up to earlier expectations and hype. As Bolli himself wrote in his article, “a rising tide of skepticism has bedeviled the field” and “enthusiasm for cell therapy has been dampened by the inconsistent, modest, borderline, or undetectable benefits reported in clinical trials.” He noted that “no cell-based therapy is close to being approved for heart disease” and “leading some critics even to question whether clinical studies should continue.”

Bolli rejected this grim view of the field. His response was to double down on stem cells, writing that “just as most pharmacologic agents are ineffective when given once but can be highly effective when given repeatedly, so a cell product may be ineffective, or modestly effective, when given as a single treatment, but may turn out to be quite efficacious if given repeatedly. This concept constitutes a major paradigm shift, with potentially vast implications for the entire field of reparative medicine.”

Bolli wrote that the single-dose model was based on the initial hope that “transplanted cells would engraft and differentiate into cardiac cells.” As it turns out, “we now know that the vast majority of transplanted cells disappear quickly, regardless of the number that is administered.”

The new concept is that “transplanted cells impart their salubrious effects not by engrafting, but by releasing EVs [extracellular vesicle](or other paracrine factors) into the surrounding tissue.” However, as critics have pointed out, there is no consensus on the existence of this “salubrious effect,” since these have only emerged in secondary or post hoc analyses. Further, there is no agreement or detailed elucidation of a biologically-plausible mechanism for this effect.

One reason multiple dosing hasn’t been attempted in the past, even in rodents, is “because the stress of repeated thoracotomies is associated with prohibitively high mortality and because most Animal Committees would not approve such protocols,” Bolli stated. Now that cells can be delivered percutaneously, Bolli argued, it may be feasible to study multiple doses in animals and in humans.

Bolli didn’t dwell on it, but one implication here is that human trials would require patients to undergo multiple percutaneous procedures. But this would almost certainly raise a whole host of new issues. What are the ethical issues of performing multiple invasive procedures on patients of an entirely unproven therapy? Further, even if it proved successful, what would be the cost of multiple invasive procedures requiring expensive cell isolation and preparation techniques?

Circling The Wagons

Bolli’s paper accompanied the publication in Circulation Research of PreSERVE-AMI, a highly anticipated (in the stem cell field, at least) trial “to evaluate the safety and bioactivity of autologous CD34+ cell (CLBS10) intracoronary infusion in patients with left ventricular dysfunction post STEMI.” To cut to the chase, no safety issues emerged but there was no difference in the primary endpoint of the trial, which was change in resting myocardial perfusion over 6 months.

But, like Bolli, the trial investigators managed to find a ray of hope. There were three deaths in the trial, all in the control arm. And, in a secondary analysis, “when adjusted for time of ischemia, a consistently favorable cell dosedependent effect was observed in the change in left ventricular ejection fraction and infarct size, and the duration of time subjects was alive and out of hospital (P=0.05).”

These findings led the investigators to conclude that the trial “provides evidence supporting safety and potential efficacy.” This rosy view of the trial gained support in a second editorial about the trial, written by a group of stem cell researchers at the University of Miami led by another prominent leader in the field, Joshua Hare. Despite the main results, “the positive post hoc analyses from this trial will undoubtedly lead to important new hypotheses to be tested in future trials,” they wrote.

Searching For The Pony

Bolli’s proposal can be viewed as a desperate Hail Mary effort to salvage a dying — or, some would say, already dead — field of research. But if all the failures are due to single dosing then the entire fields gets a do-over.

“If one dose is not sufficient to evaluate efficacy, then the conclusions of these studies, particularly those that have reported ‘negative’ results, could be questioned because the benefits of the treatment may have been underestimated or even completely overlooked,” he wrote. “Disquietingly, an entire body of literature (almost all studies conducted to date) may have to be reconsidered.” But, of course, there’s no concrete evidence that repeated doses will result in a different outcome.

Bolli wondered if the negative results were “because the product did not work or because the treatment protocol was inadequate?” But Bolli, along with the trial investigators and the other editorialists, failed to seriously consider the more plausible explanation that the repeated and consistent failures indicate that stem cell therapy is just not ready for prime time. These researchers are like the boy in the proverbial stable, frantically shovelling out an enormous pile of manure. When asked why he’s working so hard he explains, “There must be a pony here somewhere!”

Perhaps it’s about time for cardiac stem cell researchers to admit there’s no pony.

Previous Stem Cell Stories:

2017-02-20T16:00:00-0500

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CardioBrief: After Yet Another Failure, Stem Cell Leaders Double Down – MedPage Today

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Minuscule nanostraws sample a cell’s contents without damage … – Stanford University News

Cells within our bodies divide and change over time, with thousands of chemical reactions occurring within each cell daily. This makes it difficult for scientists to understand whats happening inside. Now, tiny nanostraws developed by Stanford researchers offer a method of sampling cell contents without disrupting its natural processes.

Nicholas Melosh, associate professor of materials science and engineering, developed a new, non-destructive system for sampling cells with nanoscale straws. The system could help uncover mysteries about how cells function. (Image credit: L.A. Cicero)

A problem with the current method of cell sampling, called lysing, is that it ruptures the cell. Once the cell is destroyed, it cant be sampled from again. This new sampling system relies on tiny tubes 600 times smaller than a strand of hair that allow researchers to sample a single cell at a time. The nanostraws penetrate a cells outer membrane, without damaging it, and draw out proteins and genetic material from the cells salty interior.

Its like a blood draw for the cell, said Nicholas Melosh, an associate professor of materials science and engineering and senior author on a paper describing the work published recently in Proceedings of the National Academy of Sciences.

The nanostraw sampling technique, according to Melosh, will significantly impact our understanding of cell development and could lead to much safer and effective medical therapies because the technique allows for long term, non-destructive monitoring.

What we hope to do, using this technology, is to watch as these cells change over time and be able to infer how different environmental conditions and chemical cocktails influence their development to help optimize the therapy process, Melosh said.

If researchers can fully understand how a cell works, then they can develop treatments that will address those processes directly. For example, in the case of stem cells, researchers are uncovering ways of growing entire, patient-specific organs. The trick is, scientists dont really know how stem cells develop.

For stem cells, we know that they can turn into many other cell types, but we do not know the evolution how do they go from stem cells to, say, cardiac cells? There is always a mystery. This sampling technique will give us a clearer idea of how its done, said Yuhong Cao, a graduate student and first author on the paper.

The sampling technique could also inform cancer treatments and answer questions about why some cancer cells are resistant to chemotherapy while others are not.

With chemotherapy, there are always cells that are resistant, said Cao. If we can follow the intercellular mechanism of the surviving cells, we can know, genetically, its response to the drug.

The sampling platform on which the nanostraws are grown is tiny about the size of a gumball. Its called the Nanostraw Extraction (NEX) sampling system, and it was designed to mimic biology itself.

In our bodies, cells are connected by a system of gates through which they send each other nutrients and molecules, like rooms in a house connected by doorways. These intercellular gates, called gap junctions, are what inspired Melosh six years ago, when he was trying to determine a non-destructive way of delivering substances, like DNA or medicines, inside cells. The new NEX sampling system is the reverse, observing whats happening within rather than delivering something new.

Its a super exciting time for nanotechnology, Melosh said. Were really getting to a scale where what we can make controllably is the same size as biological systems.

Building the NEX sampling system took years to perfect. Not only did Melosh and his team need to ensure cell sampling with this method was possible, they needed to see that the samples were actually a reliable measure of the cell content, and that samples, when taken over time, remained consistent.

When the team compared their cell samples from the NEX with cell samples taken by breaking the cells open, they found that 90 percent of the samples were congruous. Meloshs team also found that when they sampled from a group of cells day after day, certain molecules that should be present at constant levels remained the same, indicating that their sampling accurately reflected the cells interior.

With help from collaborators Sergiu P. Pasca, assistant professor of psychiatry and behavioral sciences, and Joseph Wu, professor of radiology, Melosh and co-workers tested the NEX sampling method not only with generic cell lines, but also with human heart tissue and brain cells grown from stem cells. In each case, the nanostraw sampling reflected the same cellular contents as lysing the cells.

The goal of developing this technology, according to Melosh, was to make an impact in medical biology by providing a platform that any lab could build. Only a few labs across the globe, so far, are employing nanostraws in cellular research, but Melosh expects that number to grow dramatically.

We want as many people to use this technology as possible, he said. Were trying to help advance science and technology to benefit mankind.

Melosh is also a professor in the photon science directorate at SLAC National Accelerator Laboratory, a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute, Stanford ChEM-H and the Precourt Institute for Energy. Wu is also the Simon H. Stertzer, MD, Professor; he is director of the Stanford Cardiovascular Institute and a member of Stanford Bio-X, the Child Health Research Institute, Stanford ChEM-H and the Stanford Cancer Institute. Pasca is also a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute and Stanford ChEM-H.

The work was funded by the National Institute of Standards and Technology, the Knut and Alice Wallenberg Foundation, the National Institutes of Health, Stanford Bio-X, the Progenitor Cell Biology Consortium, the National Institute of Mental Health, an MQ Fellow award, the Donald E. and Delia B. Baxter Foundation and the Child Health Research Institute.

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Minuscule nanostraws sample a cell’s contents without damage … – Stanford University News

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Researchers implicate suspect in heart disease linked to diabetes – Medical Xpress

February 21, 2017 by Mark Derewicz Top Row: Heart arteries in normal mice, diabetic mice, and normal mice with deleted IRS-1 gene. Bottom row: when artery is wounded, diabetic mice with less IRS-1 and normal mice with deleted IRS-1 gene show much greater blockage due to over-proliferation of smooth muscle cells. Credit: Clemmons Lab, UNC School of Medicine

People with diabetes are at high risk of developing heart disease. Despite knowing this, scientists have struggled to trace the specific biology behind that risk or find ways to intervene. Now, UNC School of Medicine researchers have hunted down a possible culprit – a protein called IRS-1, which is crucial for the smooth muscle cells that make up veins and arteries.

According to a study published in the Journal of Biological Chemistry, too little of IRS-1 causes cells to revert to a “dedifferentiated” or stem-cell like state, and this may contribute to the buildup of plaque in the heart’s arteries, a condition known as atherosclerosis, which increases the risk of heart attack, stroke, and other forms of heart disease.

“When diabetes is poorly managed, your blood sugar goes up and the amount of this protein goes down, so the cells become subject to abnormal proliferation,” said senior author David R. Clemmons, MD, Sarah Graham Kenan Professor of Medicine at the UNC School of Medicine. “We need to conduct more studies, but we think this cell pathway may have significant implications for how high blood glucose leads to atherosclerosis in humans.”

The research could bring scientists one step closer to finding drugs to help stave off heart disease in people with diabetes, who are twice as likely to have heart disease or experience a stroke, as compared to people without diabetes. People with diabetes also tend to experience major cardiac events at a younger age.

The study focused on the cells that form the walls of veins and arteries, known as vascular smooth muscle cells. The main function of these cells is to contract whenever the heart beats, helping to push oxygen-rich blood to the body’s tissues. When plaque builds up along the arterial walls, these cells gradually lose their ability to contract.

In their previous work, Clemmons and colleagues discovered that diabetes can trigger an abnormal cell signaling pathway that causes vascular smooth muscle cells to proliferate, which contributes to atherosclerosis. But their attempts to correct the abnormal signaling pathway didn’t seem to completely solve the problem, leading them to suspect another factor.

In the new study, the team found that IRS-1 acts as an inhibitor of the abnormal signaling pathway thereby keeping the vascular smooth muscle cells differentiated, or specialized. In the absence of IRS-1, the cells revert to a stem-cell like state, which in turn activates the abnormal signaling pathway and promotes cell proliferation.

In people with diabetes, the presence of IRS-1 is strongly influenced by how well – or how poorly – blood sugar is kept in check. Previous studies have shown that patients who frequently or consistently have high blood sugar show dramatic reductions in IRS-1. The new study is the first to link this reduction with a predisposition for heart disease.

“The study suggests that you can’t just inhibit the abnormal signaling, which we’ve already figured out how to do,” Clemmons said. “Our work suggests you probably have to restore the normal signaling pathway, at least to some extent, in order to completely restore the cells to normal cell health, differentiation, and functioning.”

As a next step, the Clemmons lab will look for things that might stimulate the synthesis of this protein even in the presence of high blood glucose.

To prove that IRS-1 acts as a brake on the abnormal signaling pathway that leads to cell proliferation, the team conducted experiments in three different types of mice: healthy mice, diabetic mice, and nondiabetic mice that were genetically engineered to produce no IRS-1. The scientists made a small incision in the blood vessels of the animals and then watched to see how the vascular smooth muscle cells reacted. In healthy mice, the incision stimulated wound healing but little cellular proliferation. In both the diabetic animals and the nondiabetic IRS-1 deficient animals, the researchers observed a marked increase in abnormal cellular proliferation.

The findings suggest that it may be possible to counteract the deleterious effects of high blood sugar on atherosclerosis by developing drugs that boost IRS-1.

Clemmons said the activities of IRS-1 might also play a role in other diabetes complications, such as eye and kidney disease. The researchers plan to study those potential links.

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Why do some people get Type 2 diabetes, while others who live the same lifestyle never do?

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I was diagnosed with type 2 Diabetes and put on Metformin on June 26th, 2016. I started the ADA diet and followed it 100% for a few weeks and could not get my blood sugar to go below 140. Finally i began to panic and called my doctor, he told me to get used to it. He said I would be on metformin my whole life and eventually insulin. At that point i knew something wasn’t right and began to do a lot of research. On August 13th I found Lisa’s diabetes story (google ” HOW EVER I FREED MYSELF FROM THE DIABETES ” ) I read that article from end to end because everything the writer was saying made absolute sense. I started the diet that day and the next morning my blood sugar was down to 100 and now i have a fasting blood sugar between Mid 70’s and the 80’s. My doctor took me off the metformin after just three week of being on this lifestyle change. I have lost over 30 pounds and 6+ inches around my waist in a month

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Researchers implicate suspect in heart disease linked to diabetes – Medical Xpress

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Right to try, right to buy, right to test – Washington Post

By Sally Satel By Sally Satel February 21 at 8:04 PM

(Dr. Sally Satel, who has guest-blogged here before, was kind enough to write up this item on a topic that has long interested me; Im delighted to pass it along: -EV)

In 2007, Eugene Volokh, the host of this site, published an essay in the Harvard Law Reviewtitled Medical Self-Defense, Prohibited Experimental Therapies, and Payment for Organs in which he argued that the government should need a very good reason to prevent sick people from saving their own lives.

That insight impels the Right to Try movement, which seeks to give terminally ill patients the right to try drugs that show promise but not have received FDA approval and which has received sympathetic hearings from President Trump and Vice President Pence. One of the leaders of Right to Try reform, the libertarian Goldwater Institute, said it best: We just fundamentally do not believe that you should have to apply to the government for permission to try to save your own life.

That principle has vital implications for patients needing bone marrow and kidney transplants.

Each year, 2,000 to 3,000 individuals with leukemia and other forms of bone marrow disease die while waiting to receive another persons bone marrow cells. Its not that strangers are indifferent to their plight, but that suitable biological matches are hard to find. And even when a match is found, there is a 1-in-2 chance that the needle-in-a-haystack donor either cant be located by registry personnel or, incomprehensibly, refuses to donate even though he had earlier volunteered to be tested.

We can enlarge the pool of potential donors while increasing the likelihood that compatible donors will follow through if they are paid or if sick patients (or charities acting on their behalf) have the Right to Buy, as I call it.

But there is an obstacle to buying. The 1984 National Organ Transplant Act, or NOTA, bans exchange of valuable consideration that is, anything of material worth for solid organs, such as kidneys and livers, as well as for bone marrow.

The Institute for Justice, a libertarian public-interest law firm, fought the prohibition. It sued the Justice Department on behalf of families afraid their ill loved ones would die because they couldnt get a bone marrow transplant.

In a unanimous 2012 ruling, a three-judge panel of the U.S. Court of Appeals for the 9th Circuit rejected the federal governments argument that obtaining bone-marrow stem cells through a needle in a donors arm violates NOTA. The judges based their decision on the fact that modern bone-marrow procurement, a process known as apheresis, is akin to drawing blood. Indeed, filtered stem cells, they held, are merely components of blood, no different from blood-derived plasma, platelets and clotting factors, all of which are replenished by the body within weeks of a donation. Because its legal to compensate blood donors, its also legal to pay bone marrow donors, the court ruled.

Unfortunately, the Department of Health and Human Services rejected the courts ruling. In 2013, it proposed a rule that would extend the NOTA prohibition to bone marrow stem cells. Under the proposed regulation, anyone who accepted material gain for giving bone-marrow stem cells would be subject to NOTAs penalties, facing imprisonment for up to five years. According to HHS, compensation runs afoul of NOTAs intent to ban commodification of human stem cells and to curb opportunities for coercion and exploitation, encourage altruistic donation and decrease the likelihood of disease transmission.

The solicitor general could have asked the Supreme Court to review the 9th Circuits bone-marrow decision, but he declined. Perhaps he grasped the central folly of HHSs position: How could the agency justify its worry about opportunities for coercion and exploitation and the likelihood of disease transmission when it came to bone marrow cells, yet not apply those same concerns to plasma?

For three years, HHS has been silent on its proposed rule. Meanwhile, people are dying because nonprofits that want to begin paying donors on behalf of needy patients cant move forward until they are assured that the agency cant shut them down. The Institute for Justice is considering a legal challenge over the HHS delay, which is causing needless deaths.

But perhaps the lawsuit can wait. With a new administration that is skeptical of overregulation, HHS Secretary Tom Price could withdraw the proposed rule. Ideally, Congress would thwart future regulatory blockades by amending NOTA to stipulate that marrow stem cells are not organs covered by the act.

Changes to NOTA should also be made for other organs. I feel strongly about this on fundamental grounds of liberty but also because, in 2005, I needed to save my own life. I developed kidney failure but could not find a donor. Thank goodness, an angel, or as some readers know her, Virginia Postrel, heard about my predicament and gave me a kidney. And this summer another living saint, Kimberly Hendrickson, who saw how desperate I was many years ago, offered me one of hers when the first transplant began to fail. Every day, 12 people die because no one wasable to come to their rescue and, had a patient offered money for an organ, both the patient and the donor who accepted the money would face felony charges.

Congress could take the bold step of revising NOTA to permit donors who are willing to save the life of a stranger through kidney donation to receive valuable consideration from governments or nonprofit organizations. Or, lawmakers could take the intermediate step of creating a pilot program allowing doctors to study the effect of such measures, as proposed last May by Rep. Matthew Cartwright (D-Pa.), who introduced the Organ Donor Clarification Act of 2016.

Rather than large sums of cash, potential rewards could include a contribution to the donors retirement fund, an income tax credit or a tuition voucher, lifetime health insurance, a contribution to a charity of the donors choice, or loan forgiveness. Only the government, or a government-designated charity, would be allowed to disburse the rewards. Consequently, all patients, not just those with financial means, could benefit. The funds could potentially come from the savings from stopping dialysis, which costs roughly $80,000 a year per person.

The pilot programs, to be designed by individual medical centers, could also impose a waiting period on prospective donors, thereby cooling any impulsivity. Prospective donors would be fully informed about the risks of surgery and carefully screened for physical and emotional health, as all non-compensated kidney donors are now.

The idea of the government standing between a dying person and his salvation is deeply troubling. I know. We need to at least test better ways to recruit more marrow and kidney donors.

Dr. Sally Satelis a resident scholar at the American Enterprise Institute and editor ofWhen Altruism isnt Enough: The Case for Compensating Kidney Donors.

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Right to try, right to buy, right to test – Washington Post

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Opinion: Oregon patients should beware of stem cell therapy fraud – Portland Business Journal

Opinion: Oregon patients should beware of stem cell therapy fraud
Portland Business Journal
… to help us understand and treat a range of diseases, injuries and other health-related conditions. For example, one long-established use of blood stem cells is to treat diseases of the blood and regrow bone marrow after certain kinds of cancer

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Opinion: Oregon patients should beware of stem cell therapy fraud – Portland Business Journal

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How baseball players are trying stem cells to avoid Tommy John – Yahoo Sports

TEMPE, Ariz. On the day he hoped would save his elbow, Garrett Richards laid face down on a table with his back exposed. A doctor guided a needle into the iliac crest of his pelvic bone and began to extract bone marrow. Richards was wide awake, the blessing of local anesthesia saving him from physical pain but not the anxiety that crept into his head: Is this really going to work?

Within a few minutes, the harvested marrow was hurried to a centrifuge, spun to separate the good stuff, mixed into a slurry of platelet-rich plasma and readied to inject into Richards damaged right elbow. Rather than the standard tear across his ulnar collateral ligament, Richards ran lengthwise along the middle of his UCL, a rare manifestation of an increasingly commonplace injury that almost always ends with Tommy John surgery. Not in this case. While he could have chosen that route, he wanted to explore first the efficacy of the aforementioned good stuff: stem cells.

Today, Garrett Richards is darting 98-mph fastballs again. I feel as good as I ever have throwing a baseball, he said Monday from Tempe Diablo Stadium, where the Los Angeles Angels, perhaps the most Tommy John-addled team in baseball, expect to break camp with Richards as their opening day starter. The 28-year-old is the latest player to turn to orthobiologics, the class of treatments that includes stem cells and PRP, in hopes of healing an injury. While clinical studies have shown great success with those who use orthobiologics, they are not yet a panacea for the pervasive elbow injuries in baseball for two reasons: They work only on partial ligament tears, like Richards, and medical studies have yet to validate their efficacy independent of other treatments run concurrently.

The lack of knowledge as to how orthobiologics work inside the body while the proteins in stem cells and platelets are believed to regrow damaged tissue, doctors have yet to isolate best practices for particular injuries speaks to the difficulties in true medical advances. Still, the desire of Richards and others to avoid surgery lends orthobiologics enough credence to warrant further studies.

I truly think this kind of treatment has significant potential, said Dr. Neal ElAttrache, a longtime orthopedic surgeon at the Kerlan-Jobe clinic in Los Angeles who introduced orthobiologics to Major League Baseball when he injected PRP into the elbow of Dodgers reliever Takashi Saito in 2008. Theres no question biologics are here to stay and biologic manipulation is the frontier of treatment in what were doing. The problem, as I see it, is that the marketing and clinical use has far exceeded the science behind it.

Translation: Once the use of PRP and stem cells found traction in the media, pro athletes and weekend warriors alike sought their use, even if the success stories skewed anecdotal. Bartolo Colon resurrected his career after a stem cell injection in 2010 and is still pitching today at 43. Others did so without the fanfare or publicity. Richards faced a choice after being diagnosed with a partially torn UCL last May: Undergo Tommy John surgery and, at earliest, return following the 2017 All-Star break or follow the advice of Dr. Steve Yoon, a partner of ElAttraches at Kerlan-Jobe, and try to salvage the ligament with stem cells.

Science, bro, Richards said. Im a believer now.

Two weeks before Richards began his treatment, teammate Andrew Heaney had looked to avoid Tommy John via stem cells. Richards figured theyd rehab together every step of the way and be back in time for the fall instructional league. Then at the end of June, a scan showed Heaneys elbow wasnt healing, and he would need reconstructive surgery. Already Tyler Skaggs had taken nearly two years to return from his 2014 surgery, and six weeks after Heaneys, starter Nick Tropeano went down. Like Heaney, he is expected to miss the 2017 season.

It made Richards recovery that much more imperative. His first checkup, six weeks in, showed regrowth in the torn area via ultrasound. By August, he started throwing, and come October, when instructional league was in full bloom, so too was Richards. He didnt hesitate to pump his fastball and rip off one of his spin-heavy breaking balls. As far as pure, raw stuff goes, few in baseball can match Richards.

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He was convinced science was working, bro, though the skepticism about orthobiologics generally remains, and understandably so, in the medical community. In May 2013, a paper published in the American Journal of Sports Medicine found 30 of 34 overhand throwers with partial UCL tears who used PRP had returned to their previous level of competition. This was reason for celebration. If a player could avoid the 14-month-plus recovery from the surgery, better for him as well as the team.

Another study arrived in 2016 that didnt cast doubt on the value of orthobiologics so much as offer a different avenue: rest. The 28 players used everything from electrical stimulation, ultrasound, laser therapy, massage and other soft-tissue work. And when paired with rest, their return to previous level came in at 84 percent. It was almost exactly as effective as PRP.

This reinforced ElAttraches concern: Neither of those studies had a control group against which to measure, so the numbers, while impressive, could not isolate what helped and what didnt. This chicken-or-egg question struck ElAttrache just the same when Saito returned and went on to pitch five seasons.

Maybe it was the injection, ElAttrache said. Or maybe it was that we shut him down and let him heal.

Garrett Richards is darting 98-mph fastballs again after turning to orthobiologics. (Getty Images)

He doesnt know, and thats an important distinction as orthobiologics grows exponentially. In 2004, voters in California pledged to provide $3 billion for stem-cell research and create the California Institute of Regenerative Medicine. It remains a benefactor for an industry trying to find its place in the United States.

Across the world, stem cells have far greater potency. U.S. law prevents doctors from manipulating the cells in any way. They are extracted and put back into patients bodies as is. In Switzerland, for example, doctors will harvest stem cells, manipulate them to promote greater healing capacity and then inject them. At least one star pitcher this offseason sought a stem cell injection in the United States, according to sources, while another veteran traveled halfway across the world to Zurich, seeking the comparative lack of regulations just as Peyton Manning did in 2011 to help heal a neck injury that eventually needed surgery.

The future of orthobiologics domestically doesnt end with the FDA loosening rules on stem cell usage. Doctors see significant promise in stem cells from a babys umbilical cord or a mothers placenta, both of which can be frozen. Already theyre capable of harvesting stem cells from old patients and engineering the cells into an immature state. The possibilities going forward are endless.

For right now, theyre going to play themselves out in Anaheim. The danger zone for re-injury after using orthobiologics tends to fall between April and June, though Richards cant imagine falling prey again. In addition to the 13-week break from throwing he took over the summer, Richards spent 10 more weeks in the offseason letting it heal further.

During his down time, Richards studied his own delivery to find even the slightest inefficiencies. He had three numbers in mind. The first was 85. Thats the percent at which he said hell throw his fastball, though because of improved mechanics he expects it wont hinder his velocity. The second is 100. Thats the pitch limit the Angels will foist on Richards, and hes not one to fight. The third is 200. Thats the number of innings Richards wants to pitch this season. He did it in 2015 and sees no reason he cant again.

If he can throw 85 percent, keep his pitch count below 100 and get those 200 innings, it will play publicly as another validation of orthobiologics. Just the same, if Richards elbow gives out eventually, his association with stem cells could perhaps give those considering it pause. Richards pays no mind to this. He just wants to be great.

So much so, in fact, that its going to cost him. Inside the Angels clubhouse, a chart, labeled 1 through 13, is taped to the side of a locker. Its a list of shame with the price buying lunch for the entire team. Players, coaches, P.R. directors, even manager Mike Scioscia are on there. Next to No. 6, it read: G. Rich Ace. He had made the mistake of saying aloud what he believed to be true: that hes the ace of the Angels.

Fulfilling that depends on plenty of things, none as important as his elbow, and Richards knows that. Hell do everything he can to take care of it, to nurture it, to fight against its natural gift of velocity that puts him at such risk. To make sure that next time hes on a table in the doctors office, its not with his elbow opened up and another season lost.

More on Yahoo Sports: Tom Bradys missing jersey is worth a small fortune Bob Huggins says he fell to his knees because his defibrillator activated Kings GM Vlade Divac says he turned down abetter deal for DeMarcus Cousins Yoenis Cespedes is back with his amazing cars

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How baseball players are trying stem cells to avoid Tommy John – Yahoo Sports

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