Half the planet will need glasses by 2050 because of screens

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Half of the world’s population could be short-sighted by 2050, research shows.

That’s a surge from the current 34 per cent that currently struggles with seeing distances.

The reason for the sudden decline in eyesight abilities is too much time spent looking at computer and smartphone screens and not enough time spent outside, according to the research published in the Opthalmology journal.

It predicts that 4.8 billion people – or 49.8 per cent of the world’s population – will require glasses by 2050. In 2010, 28.3 per cent of the global populus – or 2 billion people – suffered from short-sightedness, also known as myopia. So technology is nearly doubling the myopic population.

The changes “are widely considered to be driven by environmental factors,” said the researchers. “Principally lifestyle changes resulting from a combination of decreased time outdoors and increased near-work activities,” the term for time spent looking at screens.


The study shows that people living in high income countries, such as North America, Europe and parts of Asia, are more likely to be short sighted – as they spend more time looking at screens.

A separate study recently found that British children are twice as likely to be short-sighted now than 50 years ago. The research from Ulster University found 16.4 per cent of British children now suffer with short-sightedness compared with 7.2 per cent in the 1960s.

But the jury is still out on whether screen time is actually making our eyesight worse. Researchers at Ohio State University found staring at a computer screen for hours “does not cause short-sightedness”. The two decades study, which concluded last April, found “no association” between screen time and eyesight in 4,500 children.

“Near work has been thought to be a cause of myopia, or at least a risk factor, for more than 100 years,” said Karla Zadnik, dean of the College of Optometry at Ohio State University and lead author of the April study. “In this large dataset from an ethnically representative sample of children, we found no association.”

The two contradictory studies both agreed that children who spend more time outside are less likely to be short-sighted, but it is unknown what causes the protective effect, or if it’s related to screen time.

What is Myopia?

Short- or near-sightedness is a common eye condition that causes distant objects to appear blurred, while close objects can be seen clearly

  • Up to one in three people in the UK are affected
  •  The condition can range from mild, where treatment may not be required, to severe, where a person’s vision is significantly affected
  • Short-sightedness can develop in very young children but it usually starts around puberty and gets gradually worse
Signs that your child may be short-sighted can include:
  • Sitting too close to the TV
  • Complaining of headaches or tired eyes
  • Regularly rubbing their eyes
  • Needing to sit near the front of the class at school because they find it difficult to read the whiteboard

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Article Source: http://www.telegraph.co.uk/technology/2016/02/22/half-the-planet-will-need-glasses-by-2050-because-of-screens/

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Test Your Genes to Find Your Best Diet

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Your genes can help tell you what to eat and influence how diet affects your health.

Variants in some of our genes determine how we metabolize and utilize nutrients, a field of study known as nutrigenomics. Nutritional genetic testing is offered by a handful of companies and clinics, though it is currently expensive and generally not covered by insurance, limiting its usage.

People who have an impaired ability to metabolize iron, for instance, might have an iron deficiency, even if they eat the same diet as others who process the mineral more efficiently. Similarly, some people don’t adequately absorb calcium, and they might benefit from a bone-density test and specialized nutritional advice.

Gene variants also can help explain why people choose the foods they do—a greater propensity for sweets or salt, for instance. And the tests also can show how our bodies respond to different types of exercise.

Genetic testing has gained widespread use in other areas, especially in helping to determine our risk for developing various diseases, from cancer to cardiovascular conditions. Another, more recent use for genetic testing is known as pharmacogenomics, which can help doctors predict which of various medications are most likely to benefit individual patients.

CAFFEINE: People with certain variants on gene CYP1A2 are slow metabolizers of coffee, putting them at greater risk for high blood pressure or a heart attack when caffeine intake is high. 1 in 2 people is at risk. SPINACH: Deficiency in folate, found in greens, is linked to greater risk of heart disease and stroke. It can result from variants on gene MTHFR that slow the conversion of dietary folate into an active form of the nutrient. 2 in 3 people are at risk. PHOTO: GETTY IMAGES (2)

Some experts say genetic science is too young to be able to provide nutritional advice. “We still have a long way to go in the development of practical tools,” says José M. Ordovás, director of nutrition and genomics at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University and a leading researcher in nutrigenomics.

Dr. Ordovás says most nutritional genetic tests look at just a handful of genes, which isn’t enough to guide dietary decisions. His own research is aimed at evaluating the entire human genome, which consists of 20,000 to 25,000 genes.

The Academy of Nutrition and Dietetics—a professional organization of nutrition professionals—published a position statement in 2014 in the group’s journal saying it was too early to use nutritional genomics to manage chronic disease or provide dietary advice.

Nutrigenomix Inc., started by scientists at the University of Toronto, offers a test of seven genes, which provides insight into some basic nutritional properties, and another, more comprehensive test of 45 genes. The tests are offered through various clinical partners, including the Wellness Institute at the Cleveland Clinic. Dietitians and others buy the 45-gene test from the company for $300 and usually charge another $100 to $200 for a follow-up consultation.

“We’re talking about nutrition advice. We’re not talking about predicting disease,” saysAhmed El-Sohemy, chief scientific officer of Nutrigenomix. “This is about healthy eating and how you metabolize.”

The company only provides testing, which can be ordered online, if done through a health professional, says Dr. El-Sohemy, who is also a professor and research chair in nutrigenomics at the University of Toronto. For people who already eat a healthy diet, nutritional genetic testing might not be that useful, he says.

SALT: Gene ACE produces an enzyme to help regulate the body’s response to sodium intake. People with certain variants are at greater risk for high blood pressure when eating lots of salt. 7 in 10 people are at risk. SUGAR: Gene GLUT2 helps regulate glucose, or sugar. People with certain variants prefer sweet foods and drinks, putting them at greater risk for being overweight and developing cardiometabolic disease. 1 in 5 people is at risk. PHOTO: FROM LEFT: GETTY IMAGES; ISTOCK

Other companies that offer similar tests are 23andMe, Interleukin Genetics and Vitagene, among others. Some companies such as DNAFit also focus on genes related to exercise.

Mary Pipino ordered tests by Nutrigenomix through her nutritionist at the Cleveland Clinic’s Wellness Institute. Ms. Pipino, chief executive of an insurance-risk management firm, says she eats a healthy diet and is an avid exerciser and a certified group and personal trainer. She got the seven-gene test initially and recently also did the 45-gene test.

Ms. Pipino’s nutritionist helped her interpret the results. She says she learned her body doesn’t digest dairy or absorb iron well, and that she’s a slow metabolizer of caffeine. She also learned she is genetically predisposed to strength and endurance training, which she gravitates to anyway.

The 58-year-old says she eliminated yogurt from her diet, which made her feel less bloated. She also changed some of the vitamin supplements she takes, adding more iron but reducing B-12, which she absorbs adequately from her food.

“It’s much easier to put together your personal lifestyle plan after you have this information because it gives you the blueprint of your body,” she says.

“I don’t think it leads to a change in behavior in every single aspect of your diet,” saysKristin Kirkpatrick, manager of wellness nutrition services at the Wellness Institute, and Ms. Pipino’s nutritionist. “But it definitely changes behavior in more specific areas.”

Dr. Ahmed El-Sohemy, research chair in nutrigenomics at the University of Toronto, is also chief scientific officer of Nutrigenomix Inc., which offers nutritional genetic testing through various clinical partners. ‘This is about healthy eating and how you metabolize,’ he says. PHOTO: JAMES BRYLOWSKI

Genetic testing can also reveal, for example, how quickly people metabolize caffeine by examining a gene known as CYP1A2. Heavy coffee drinkers who are slow caffeine metabolizers retain more of the stimulant in the body, putting them at increased risk of having a heart attack and developing diabetes and hypertension, studies have found.

People who metabolize caffeine quickly receive a protective effect from moderate consumption of coffee, some studies have found. One theory is that because those people eliminate the bad parts of coffee faster they may be able to benefit from the good ingredients, such as polyphenols.

Another gene, GLUT2, can show how well the body regulates sugar, or glucose. People with certain variants of the gene could have a greater preference for sweet foods and drinks—a sweet tooth—which could put them at increased risk of being overweight.

Nutrition scientists have looked at whether genetic testing ends up improving eating behaviors. The evidence is mixed. A recent large randomized controlled study found there was little apparent benefit.

The six-month study, funded by the European Union, followed 1,269 people in seven countries. Three groups of participants were given personalized dietary advice, with variations based on their regular diet; their phenotype, including blood biomarkers such as cholesterol; and genetic variants. A control group was given conventional dietary advice.

“This was built on the idea that if you personalize advice and support for people they will pay more attention and be more likely to act on that in a sustained way,” says John Mathers, director of the Human Nutrition Research Centre at Newcastle University in England and senior author of the study, which was published in August in the International Journal of Epidemiology.

At the end of the study, the three groups that received personalized nutrition advice had all improved their eating habits, compared with the control group. But the improvements in each of the three groups were about the same. “It didn’t seem to matter whether you personalized based on current diet, phenotype or genotype,” Dr. Mathers says.

J. Bruce German, a professor and director of the Foods for Health Institute at the University of California, Davis, believes some people can benefit from nutritional genetic testing.

For example, some genetic variants on the MTHFR gene result in reduced activity of an enzyme that converts dietary folate into an active form of the nutrient. People with these genetic variants could have a folate deficiency, which has been linked to a greater risk for heart disease and stroke.

Dr. German is a slow folate absorber, he says, so he has increased the amount of greens in his diet. “Most people know that they should eat more green matter but they don’t anyway,” he says. “Being told you are genuinely at risk makes green vegetables a more convincing food choice,” says Dr. German, who is on a Nutrigenomix advisory board, a voluntary position.

Written by Sumathi Reddy Article Source: http://www.wsj.com/articles/test-your-genes-to-find-your-best-diet-1471887390

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Researchers Propose New Treatment to Prevent Kidney Stones

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Researchers have found evidence that a natural fruit extract is capable of dissolving calcium oxalate crystals, the most common component of human kidney stones. This finding could lead to the first advance in the treatment of calcium oxalate stones in 30 years.

Jeffrey Rimer, associate professor of chemical engineering at the University of Houston, was lead author of the study, published Aug. 8 in the online edition of Nature. The work offers the first evidence that the compound hydroxycitrate (HCA) is an effective inhibitor of calcium oxalate crystal growth that, under certain conditions, is actually able to dissolve these crystals. Researchers also explain how it works.

The findings are the result of a combination of experimental studies, computational studies and human studies, Rimer said.

Kidney stones are small, hard mineral deposits that form inside the kidneys, affecting up to 12 percent of men and seven percent of women. High blood pressure, diabetes and obesity can increase the risk, and the reported incidence is on the rise.

Preventive treatment has not changed much over the last three decades. Doctors tell patients who are at risk of developing stones to drink lots of water and avoid foods rich in oxalate, such as rhubarb, okra, spinach and almonds. They often recommend taking citrate (CA), in the form of potassium citrate, a supplement that can slow crystal growth, but some people are unable to tolerate the side effects.

The project grew out of preliminary work done by collaborator John Asplin, a nephrologist at Litholink Corporation, who suggested HCA as a possible treatment. HCA is chemically similar to CA and is also available as a dietary supplement.

“HCA shows promise as a potential therapy to prevent kidney stones,” the researchers wrote. “HCA may be preferred as a therapy over CA (potassium citrate).”

In addition to Rimer and Asplin, authors on the paper include Giannis Mpourmpakis and his graduate student, Michael G. Taylor, of the University of Pittsburgh; Ignacio Granja of Litholink Corporation, and Jihae Chung, a UH graduate student working in Rimer’s lab.

The head-to-head studies of CA and HCA determined that while both compounds inhibit the growth of calcium oxalate crystals, HCA was more potent and displayed unique qualities that are advantageous for the development of new therapies.

The team of researchers then used atomic force microscopy, or AFM, to study interactions between the crystals, CA and HCA under realistic growth conditions. According to Rimer, the technique allowed them to record crystal growth in real time with near-molecular resolution.

Chung noted that the AFM images recorded the crystal actually shrinking when exposed to specific concentrations of HCA. Rimer suspected the initial finding was an abnormality, as it is rare to see a crystal actually dissolve in highly supersaturated growth solutions. The most effective inhibitors reported in the literature simply stop the crystal from growing.

It turned out that Chung’s initial finding was correct. Once they confirmed it is possible to dissolve crystals in supersaturated solutions, researchers then looked at reasons to explain why that happened.

Mpourmpakis and Taylor applied density functional theory (DFT) – a highly accurate computational method used to study the structure and properties of materials – to address how HCA and CA bind to calcium and to calcium oxalate crystals. They discovered HCA formed a stronger bond with crystal surfaces, inducing a strain that is seemingly relieved by the release of calcium and oxalate, leading to crystal dissolution.

HCA was also tested in human subjects, as seven people took the supplement for three days, allowing researchers to determine that HCA is excreted through urine, a requirement for the supplement to work as a treatment.

While Rimer said the research established the groundwork to design an effective drug, questions remain. Long-term safety, dosage and additional human trials are needed, he said.

“But our initial findings are very promising,” he said. “If it works in vivo, similar to our trials in the laboratory, HCA has the potential to reduce the incidence rate of people with chronic kidney stone disease.”

More information: Molecular modifiers reveal a mechanism of pathological crystal growth inhibition, Nature, DOI: 10.1038/nature19062

Journal reference: Nature


Article Source: http://www.worldhealth.net/forum/thread/102570/researchers-propose-new-treatment-to-pre/

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Scientists challenge recommendation that men with more muscle need more protein

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Sports nutrition recommendations may undergo a significant shift after research from the University of Stirling has found individuals with more muscle mass do not need more protein after resistance exercise.

Health and exercise scientists from Scotland’s University for Sporting Excellence found no difference in the muscle growth response to protein after a full body workout between larger and smaller participants.

Kevin Tipton, Professor of Sport, Health and Exercise Science in the Faculty of Health Sciences and Sport, said: “There is a widely-held assumption that larger athletes need more protein, with nutrition recommendations often given in direct relation to body mass.

“In our study, participants completed a bout of whole-body resistance exercise, where earlier studies — on which protein recommendations are based — examined the response to leg-only exercise. This difference suggests the amount of muscle worked in a single session has a bigger impact on the amount of protein needed afterwards, than the amount of muscle in the body.”

Experts also found participants’ muscles were able to grow and recover from exercise better after a higher dose of protein.

Consuming 40 grams of protein after exercise was more effective at stimulating muscle growth than 20 grams. This increase occurred irrespective of the size of the participants.

Professor Tipton continued: “Until now the consensus among leading sports nutritionists, including the American College of Sports Medicine and the British Nutrition Foundation, is that weightlifters do not need more than around 25 grams of protein after exercise to maximally stimulate the muscle’s ability to grow.

“In order for nutritionists to recommend the correct amount of protein we first need to consider specific demands of the workout, regardless of athletes’ size. This throws commonly held recommendations into question and suggests the amount of protein our muscles need after exercise may be dependent on the type of workout performed. These results are limited to younger, trained men so we may see different results with other groups, such as older individuals or females digesting different amounts of protein.”

Young, resistance-trained males were recruited for the study and divided into two groups, one with lower lean body mass of less than 65 kilograms and one with higher lean body mass of more than 70 kilograms.

Each volunteer participated in two trials where they consumed protein after resistance exercise. In one trial participants consumed 20 grams of whey protein and in the second, they consumed 40 grams of whey protein after exercise. Scientists measured the muscle’s ability to grow at an increased rate with metabolic tracers and muscle biopsies.

Article Source: http://www.eurekalert.org/pub_releases/2016-08/uos-scr082216.php

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Lighter weights just as effective as heavier weights to gain muscle, build strength

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New research from McMaster University is challenging traditional workout wisdom, suggesting that lifting lighter weights many times is as efficient as lifting heavy weights for fewer repetitions.

It is the latest in a series of studies that started in 2010, contradicting the decades-old message that the best way to build muscle is to lift heavy weights.

“Fatigue is the great equalizer here,” says Stuart Phillips, senior author on the study and professor in the Department of Kinesiology. “Lift to the point of exhaustion and it doesn’t matter whether the weights are heavy or light.”

Researchers recruited two groups of men for the study—all of them experienced weight lifters—who followed a 12-week, whole-body protocol. One group lifted lighter weights (up to 50 per cent of maximum strength) for sets ranging from 20 to 25 repetitions. The other group lifted heavier weights (up to 90 per cent of maximum strength) for eight to 12 repetitions. Both groups lifted to the point of failure.

Researchers analyzed muscle and blood samples and found gains in muscle mass and muscle fibre size, a key measure of strength, were virtually identical.

“At the point of fatigue, both groups would have been trying to maximally activate their muscle fibres to generate force,” says Phillips, who conducted the work with graduate students and co-authors Rob Morton and Sara Oikawa.

While researchers stress that elite athletes are unlikely to adopt this training regime, it is an effective way to get stronger, put on muscle and generally improve health.

“For the ‘mere mortal’ who wants to get stronger, we’ve shown that you can take a break from lifting heavy weights and not compromise any gains,” says Phillips. “It’s also a new choice which could appeal to the masses and get people to take up something they should be doing for their health.”

Another key finding was that none of the strength or muscle growth were related to testosterone or growth hormone, which many believe are responsible for such gains.

“It’s a complete falsehood that the short-lived rise in testosterone or growth hormone is a driver of muscle growth,” says Morton. “It’s just time to end that kind of thinking.”

Researchers suggest, however, that more work remains to be done in this area, including what underlying mechanisms are at work and in what populations does this sort of program work.

The findings are published online in the Journal of Applied Physiology.

More information: Robert W. Morton et al, Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men, Journal of Applied Physiology (2016).DOI: 10.1152/japplphysiol.00154.2016

Journal reference: Journal of Applied Physiology search and more infowebsite

Provided by: McMaster University

Article Source: http://medicalxpress.com/news/2016-07-lighter-weights-effective-heavier-gain.html

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Adding ages

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MICHAEL RAE eats 1,900 calories a day, 600 fewer than recommended. Breakfast is a large salad, yogurt and a “precisely engineered” muffin. In a mere 100 calories this miracle of modern gastronomy delivers 10% of Mr Rae’s essential nutrients. Lunch is a legume-based stew and another muffin. Dinner varies. Today he is looking forward to Portobello mushroom with aubergine and sage. There will be a small glass of red wine. He has been constraining his diet this way for 15 years.

In some animals calorie restriction (CR) of this kind seems to lessen the risk of cancer and heart disease, to slow the degeneration of nerves and to lengthen life. Mr Rae, who works at an anti-ageing foundation in California, thinks that if what holds for rodents holds for humans CR could offer him an extra seven to 15 years of healthy life. No clinical trials have yet proved this to be the case. But Mr Rae says CR dieters have the blood pressure of ten-year-olds and arteries that are clean as a whistle.

The “profound sense of well-being” Mr Rae reports might seem reward enough for his privations. But his diet, and the life extension he thinks it might bring, are also a means to an end. Mr Rae, who is 45, thinks radical medical advances that might not merely slow but stop, or reverse, ageing will be available in the not-too-distant future. If CR gets him far enough to benefit from these marvels then a few decades of deprivation might translate into additional centuries of life. He might even reach what Dave Gobel, boss of the Methuselah Foundation, an ageing-research charity, calls “longevity escape velocity”, the point where life expectancy increases by more than a year every year. This, he thinks, is the way to immortality, or a reasonable approximation thereof.

That all remains wildly speculative. But CR is more than just an as-yet-unproven road to longer human life. Its effects in animals, along with evidence from genetics and pharmacology, suggest that ageing may not be simply an accumulation of defects but a phenomenon in its own right. In a state of nature this phenomenon would be under the control of genes and the environment. But in a scientific world it might in principle be manipulated, either through changes to the environment (which is what CR amounts to) or by getting in among those genes, and the metabolic pathways that they are responsible for, with drugs.

A treatment based on such manipulation might improve the prospects of longer and healthier life in ways that drugs aimed at specific diseases cannot match. Eileen Crimmins, a researcher at the University of Southern California in Los Angeles, points to calculations which show that the complete elimination of cardiovascular disease would add only 5.5 years to overall life expectancy in America, and removing deaths from cancer would add just 3.2 years. This is because diseases compete to kill people as they age; if one does not get you the next will. According to Dr Crimmins, increasing life expectancies much beyond 95 would require an approach that held the whole pack at bay, not just one particular predator.

Something which slowed ageing down across the board might fit the bill. And if it delays the onset of a range of diseases it might also go some way to reducing the disability that comes with age. An ongoing long-term study at Newcastle University has been looking at the health and ageing of nearly 1,000 subjects now aged 85. At this point they have an average of four to five health problems. None of them is free from disease. Most researchers in the field scoff at talk of escape velocities and immortality. But they take seriously the prospect of healthier 85 year olds and lifespans lengthened by a decade or so, and that is boon enough.

Indications of immortality

Before discovering whether anti-ageing drugs might be able to deliver such things, though, researchers need to solve a daunting regulatory conundrum. At the moment the agencies that allow drugs to be sold do not consider ageing per se to be an “indication” that merits therapy. It is, after all, something that happens to everyone, which makes it hard to think of as a disease in search of a cure, or even a condition in need of treatment. Unless ageing is treated as an indication, anti-ageing drugs can’t get regulatory approval. And there’s little incentive to work on drugs you can’t sell.

If regulators were to change their stance, though, the interest would be immense. A condition that affects everyone is as big a potential market as can be imagined. And there are hints that the stance may indeed be changing. Two existing drugs approved for other purposes—metformin, widely used and well tolerated as a treatment for diabetes, and rapamycin, which reduces the risk of organ transplants being rejected—look to some researchers as though they might have broad anti-ageing effects not unlike those claimed for CR. In 2014 a study of 90,000 elderly patients with type 2 diabetes found that those receiving metformin had higher survival rates than matched non-diabetic controls. Other work has shown its use is associated with a decreased risk of cancer.

Scientists at the Institute for Ageing Research at the Albert Einstein College of Medicine, in New York, want to mount a trial of metformin in elderly subjects to see whether it delays various maladies (and also death). If that turns out to be the case, it will go a long way to showing that there is a generalised ageing process that can be modulated with drugs. Nir Barzilai, one of the researchers involved, says an important reason to do the trial is to have an indication against which next-generation ageing drugs can be assessed by regulators.

This sort of interest seems to be triggering a change of tone at America’s Food and Drug Administration over whether it might approve an anti-ageing drug. The regulator is thinking about when a broad, and so far unprecedented, claim of anti-ageing might be considered to be supported by the evidence; it is “looking forward to seeing this area of science evolve”. In the dry language of a government agency these are encouraging words.

If an unregulated diet can do the trick, why does the world need drugs? Three reasons. One is that taking a few pills a day will be easier for most than subsisting on low-calorie muffins and salad. A second is that companies can make money making pills and will compete to create them. A third is that pills may work better than diets. Dr Barzilai, who is in the pill camp, points out that CR works less well in primates than other mammals, and that people with low body-mass indices, a natural condition for those restricting their calories, are in general more likely to die. Those who do well on CR, he says, are likely to be a subset benefiting from the right genetic make-up. His hope is that a range of targeted therapies might allow everyone to get the benefits.

If they do, it will be by inducing changes in metabolism. It has been known for 20 years that altering the gene daf-2 in roundworms slows their ageing and doubles their lifespans; another gene, daf-16, is now known to be required for this to work. Equivalent genes in humans are in charge of the cell-surface receptors for insulin and insulin-like growth factor 1, hormones with key metabolic roles. The human equivalent of daf-2 seems to be turned on by CR. Very long-lived people have been found to share particular variants of the human version of daf-16.

Another effect of CR is that it deactivates mTOR, a protein that helps pass signals from growth hormones to the parts of the cell involved in protein synthesis. It plays a role in regulating the cell’s metabolism, division and growth, and prevents the breakdown of damaged cells. When food is abundant mTOR stimulates cell division and growth.

Throwing the switch

These lines of research suggest that in the animals where CR works well it switches cells from a regime where they concentrate on growing to one where they concentrate on their own repair. In that second mode damage to cells accumulates more slowly, which means they age less. Drugs that seem to have an effect on ageing achieve some of the same shift. Metformin acts on a number of hormone receptors which are also affected by CR (see chart); rapamycin works on a pathway that gets its name from a protein that is the “target of rapamycin”: mTOR. Reducing the function of mTOR extends life in yeast, worms and flies. In 2009, work in a number of laboratories showed that rapamycin can extend the lifespan of middle-aged mice by 14%.

Alexander Zhavoronkov, the boss of Insilico Medicine, a longevity firm, says he is testing rapamycin on himself (self experimentation does not seem uncommon in the field). But he warns it is necessary to have a significant knowledge of biomedicine to do so safely. The drug has serious side effects; rodents treated with it suffer from insulin resistance and it suppresses the immune system. That’s good when preventing the rejection of organ transplants—the drug’s current medical use—but not so good in otherwise healthy people. One idea is that low doses might preserve the drug’s benefits while limiting its side-effects.

There are other drugs, though, that target the same pathway with fewer downsides. One of these, resveratrol, caused a great deal of excitement among longevity researchers a few years ago because it kept mice on rich diets youthful. A lot of the initial interest has waned since it was discovered to be less helpful in mice that are not overweight, but it is still being investigated as an Alzheimer’s treatment.

David Sinclair of the Harvard Medical School, who was part of the initial enthusiasm, describes it as a “dirty” drug, in that it has a number of targets within the cell. Among them are a set of proteins known as sirtuins which appear to be activated by resveratrol. Dr Sinclair created a company, Sirtris Pharmaceuticals, to investigate the potential of drugs aimed at these targets. GSK, a British pharma company which bought Sirtris in 2008, continues this work, though to date it has not yielded as much as was once hoped.

Sirtuins may act as metabolic sensors, and a number are found exclusively in the mitochondria, the structures in cells that look after respiration and which are central to the evolving concept of cellular ageing. Thomas von Zglinicki of Newcastle University says ageing cells are characterised by mitochondrial damage and have difficulty recycling damaged or broken cell machinery. They produce pro-inflammatory factors called cytokines which move neighbouring cells to senescence; chronic progressive inflammation of this sort drives various age-related diseases.

João Passos, also at Newcastle University, says cells from which mitochondria are removed start to look more like young cells and stop secreting cytokines. Other work has shown that killing off mitochondria can mimic some of the effects of drugs that activate mitochondrial renewal—such as rapamycin. Faster turnover of mitochondria seems to improve their functioning.

Data against death

Such discoveries in cell and molecular biology have perked up commercial interest in longevity. So too has data from the hundreds of thousands of human genome sequences. Dr Zhavoronkov’s Insilico Medicine, based in Baltimore, is using machine learning on vast piles of published genomic data to work out the differences between the tissues of young and old people and to look at how patterns of gene expression evolve as people age. It then looks in drug databases for molecules that might block the effects of the genes it thinks matter.

The force to be reckoned with in this field, though, is Craig Venter, a pioneer in gene sequencing. In 2013 he founded Human Longevity Inc (HLI), based in San Diego. Like Insilico, HLI wants to sift through genomic data; but it does so on a vastly larger scale, generating the genomic data itself and matching them with details of physiology and appearance. Dr Venter hopes this will allow the company to unpick the genetics of longevity and predict how long people will live. Research at HLI has already found that some genetic variations are absent in older people, a finding that implies they might be tied to shorter lifespans. Companies such as Celgene and AstraZeneca that work in drug discovery have made deals to collaborate with HLI. Dr Venter says HLI may eventually move into the drug business itself.

For those who cannot wait for drugs, HLI has a high-end “wellness” service called the Health Nucleus. At prices starting from $25,000 it will give a customer a constellation of cutting-edge tests, including a full sequence of both his genome and a battery of tests for the signs of cancer, Alzheimer’s and heart disease. Lots of tests means lots of possibilities for “false-positive” results; but the affluent clients of Health Nucleus may worry less about follow-ups that reveal false alarms than other people do.

In 2013 Google (now Alphabet) started a venture called the California Life Company, or Calico, to take a “moonshot” approach to anti-ageing; the company has said it will invest up to $750m in the venture. Calico is a drug-development company much more willing to talk about its world-leading scientists, such as Cynthia Kenyon, a worm biologist, and the track record of its boss, Arthur Levinson, who used to run Genentech, a biotech giant, than about what it is actually doing. But it has announced a series of collaborations, the most significant of which is a ten-year R&D deal with AbbVie, a pharma company based in Chicago, focused on cancers and degenerative nerve conditions.

Degeneration leads to thoughts of regeneration. Even the most enthusiastic adherents of slowing down ageing by means of diet or pharmacology have to admit that it will not keep people going forever. At best it might allow them to age as slowly as the slowest-ageing people do naturally. And that makes it unlikely, even at its most effective, to increase lifespans beyond 120, because that seems to be more or less the natural upper limit to a human lifespan. Improvements in medicine and welfare mean that there are many more people in their 90s and 100s round the world today than there used to be. The number of people in their 130s, though, remains stubbornly at zero.

To do something about this means not just slowing ageing but stopping or reversing it, either by causing bits of the body to rejuvenate themselves or by removing and replacing them. This is where stem cells come in. They play an important role in the repair and regeneration of tissue; they can be induced to differentiate into a range of specialised cells, and thus to replace cells that are worn out or used up. Regenerative therapies seek to supplement this repair using stems cells from elsewhere. They might be taken from frozen samples of placentas; they might be created from existing body cells.

Many stem-cell therapies are moving rapidly towards clinical trials under the rubric of “regenerative medicine”. Both Calico and HLI are active in the field. Research has shown that nerve cells grown from human embryonic stem cells and transplanted into rats with the equivalent of Parkinson’s disease proliferate and start to release dopamine, which is what such rats and people lack. Roger Barker of the University of Cambridge recently treated a man with Parkinson’s this way. ReNeuron, based in Bridgend in Wales, is in trials designed to discover the efficacy of stem cells as a treatment for disabilities brough on by stroke. Despite the risks of unregulated therapies, hundreds of clinics around the world are already rushing to offer “treatments” for the diseases of age. This is unsurprising. It is historically an area rich in hope, hype and quackery, and it will take some time for well-founded research to clean the stables—if, indeed, it can.

Another regenerative possibility flows from studies which find signs of rejuvenation in elderly animals exposed to the blood of younger animals. Infusions of young people’s blood plasma are being tried out on some Alzheimer’s patients in California. A startup called Ambrosia, based in Monterey, recently began “trials” of such a therapy with healthy participants who pay $8,000 to take part; critics say they are so lacking in controls that they are unlikely to generate any useful information. If particular genes are beneficial then gene therapy, or gene editing, could prove to be fertile ground; work to this end has begun in mice. And some won’t wait. Elizabeth Parrish, the boss of a biotech company called BioViva, claims she has already given herself an anti-ageing gene therapy.

Beyond this horizon

The extent to which any of this technology will help will depend on how old those it is used on are when it comes into its own. The scope for radically changing the lifespan of a 65-year-old is much smaller than that of a 20-year-old, let alone an embryo. But the amount that is lost by getting things wrong goes up in exactly the same way.

The idea that radical biotechnology can lead to longer lifespans than that of Jeanne Calment, a French woman whose recorded lifespan of 122 years has never been bettered, seems at best a plausible speculation. To say—as Aubrey de Grey, a noted cheerleader for immortality, has done—that the first person to live to 1,000 has probably already been born seems utterly outlandish. But thinking through Calment’s life might give you pause. When she was born, in 1875, the germ theory of disease was still a novelty and no one had ever uttered the word “gene”. When she died in 1997 the human genome was almost sequenced. All of modern medicine and psychiatry, barring general-purpose anaesthesia, was developed during her lifetime. If a little girl born today were to live as long—and why should she not?—she would see the world of 2138. The capabilities of medicine at that point will surely still be limited. But no one can guess what those limits will be.

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Today’s men are not nearly as strong as their dads were

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You’re dad might have told you about his younger days when men were men. And he might not be wrong.

A new study suggests millennial men may have significantly weaker hands and arms than men the same age did 30 years ago.

The study was published in the Journal of Hand Therapy.

Researchers measured the grip strength (how strongly you can squeeze something) and pinch strength — between two fingers — of 237 healthy full-time students aged 20 to 34 at universities in North Carolina. And especially among males, the reduction in strength compared to 30 years ago was striking.

The average 20-to-34-year-old today, for instance, was able to apply 98 lbs of force when gripping something with his right hand. In 1985, the average man could squeeze with 117 lbs of force.

Grip strength isn’t quite the same thing as benching 200 lbs or doing a set of squats. But researchers have found it to be a great predictor of a lot of other strength and health related outcomes. So it’s a useful proxy for overall muscular strength.

The participants in the North Carolina study were recruited only from college and university settings, so they’re not representative of the population as a whole.

But it matches the findings of other similar studies.

A 2013 study found that American children today are less physically fit than they were 30 years ago.

– with files from The Washington Post

Article Source: http://www.calgarysun.com/2016/08/15/todays-men-are-not-nearly-as-strong-as-their-dads-were?utm_source=facebook&utm_medium=recommend-button&utm_campaign=Today%27s+men+are+not+nearly+as+strong+as+their+dads+were

“The Greatest Health of Your Life”℠

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National Testosterone Restoration for Men
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