Inability to Cope with Stress May Increase Risk of Diabetes Among Men

Low resistance to stress in men at age 18 years can increase the risk of type 2 diabetes in adulthood by up to 50%, revealed a new study.

 The study published in Diabetologywas by Dr Casey Crump, Department of Medicine, Stanford University, Stanford, CA, USA, and colleagues in Sweden and the USA. It examined the cohort of all 1,534,425 military conscripts in Sweden during 1969-1997, the men did not have diabetes.

‘Low stress resilience earlier in life is associated with a higher risk of type 2 diabetes, possibly mediated by behavioral and physiological factors.’

They assessed them for their stress resilience through a standardized psychological assessment, rating it based on a scale of one to nine. Next, the team followed up the development of type 2 diabetes in these men by looking at outpatient and inpatient diagnoses from 1987 through 2012.

The results revealed that 20 percent of the men who scored stress resilience from one to three were 51 percent more prone to developing type 2 diabetes than the ones who scored 7 to 9 in the scale. The researchers found out that low-stress resilience increased the chances of developing the disease.

The authors conclude, "These findings suggest that psychosocial function and ability to cope with stress may play an important long-term role in etiological pathways for type 2 diabetes. Additional studies will be needed to elucidate the specific underlying causal factors, which may help inform more effective preventive interventions across the lifespan." 

 

Positive and Negative Aspects of Aging

 We age because over the years the cells in our bodies begin to malfunction. This is the general view that scientists hold of the aging process. For example, in older people the cells' internal quality control breaks down.

 This control function usually eliminates proteins that have become unstable and lost their normal three-dimensional structure. These deformed proteins accumulate in the cells in a number of diseases, such as Parkinson's and Alzheimer's. 

‘American scientists demonstrated that mice with accumulations in their nerve cells exhibit a more stable long-term memory.’

For Yves Barral, Professor of Biochemistry at ETH Zurich, the view of the aging process as a consequence of flawed cell function and disease is too narrow. It ignores the fact that the mentioned so-called prion-like protein accumulations could have a positive effect, too, and therefore should not be referred to as cellular malfunction, he says. 

Old cells cope better with stress Barral drew this conclusion based on his research on yeast cells. He and his colleagues recently found in these cells a new type of protein aggregate, which appears as the cells get older. As the scientists were able to show, these protein aggregates do not arise as the result of a cell's malfunctioning internal quality control. On the contrary: in yeast cells with such aggregates, quality control functions even better. "It certainly seems that these aggregates help yeast cells to cope with the physiological changes caused by aging," says Juha Saarikangas, a postdoc in Barral's group and first author of the recent study in the journal eLife. "We are very exited to learn what type of information is stored in these structures." 

The scientists assume that these age-associated aggregates are formed by several different proteins. The researchers have already identified one prion-like protein that is part of the accumulations. What other proteins are involved and why the aggregates remain in the parent cells during cell division are subjects of further research. 

Aggregates improve memory Only in recent years have scientists speculated that aggregating proteins in the cells can generally play a positive role. Barral and his research group showed back in 2013 that yeast cells memorise experiences related to unsuccessful sexual reproduction attempts in the form of aggregated proteins. These aggregates - which are not identical to the newly discovered age-associated accumulations - thus serve as molecular memory for yeast cells. Even in mice there is a positive relationship between prion-like aggregates and memory. A few months ago, American scientists demonstrated that mice with such accumulations in their nerve cells exhibit a more stable long-term memory. 

"Bad end to a good thing" Whether such age-associated protein accumulations are primarily a malfunction or a normal function of healthy cells is for Barral a scientific question - one in which philosophy also plays a role: "Our western society understands aging as something that is predominantly negative, a disease that has to be combated," he says. "This thinking is reflected in the work of many scientists, whose research on aging focuses on finding defects in cells." Other societies, however, place more value on the positive effects of aging, such as increased experience and knowledge - a view that corresponds with the newly discovered role of aggregates as information storage or memory for cells. 

"We're still a fairly small group of scientists who say: aggregate proteins are not pathological - they are neither an accident nor a defect," says Barral. Rather, these proteins aggregate because it is their normal function. Diseases such as Parkinson's and Alzheimer's only arise when the system becomes imbalanced and too many prion-like proteins accumulate in the wrong place in the cells. Barral continues: "There are two aspects to aging. Yes, you die at the end of the process, and this is negative. But you die wise. And Alzheimer's is perhaps a bad end to a good thing." 

Source: Eurekalert
 
 

Study Explains Why Eating Fish During Pregnancy Improves Child's Brain

Researchers from Tohoku University in Japan have identified the link between eating fish during pregnancy and the health of the baby's brain.

he study revealed that omega-6 and omega-3 balance is important for future brain function and reinforced earlier suggestions that maternal intake of fish during pregnancy boosts the health of the baby's brain. 

‘A balanced intake of lipids by pregnant women is necessary for the normal brain formation of the unborn child.’

"Dietary lipid contains fatty acids such as omega-6 and omega-3 that are essential nutrients for many animals and humans," she added.

In an animal study, the researchers noticed that when female mice were fed an omega-6-rich/omega-3-poor diet, their offsprings were born with a smaller brain and showed abnormal emotional behaviour in adulthood.

According to Osumi, the brain abnormality found in the offsprings of mice, was caused by a premature aging of fetal neural stem cells that produce brain cells.

The premature aging was promoted by an imbalance of oxides of omega-6 and omega-3 fatty acids, Osumi said.

Source: IANS

   

Low-fiber diet may cause irreversible depletion of gut bacteria over generations

A study by Stanford University School of Medicine investigators raises concerns that the lower-fiber diets typical in industrialized societies may produce internal deficiencies that get passed along to future generations.

The study, conducted in mice, indicates that low-fiber diets not only deplete the complex microbial ecosystems residing in every mammalian gut, but can cause an irreversible loss of diversity within those ecosystems in as few as three or four generations.

Once an entire population has experienced the extinction of key bacterial species, simply "eating right" may no longer be enough to restore these lost species to the guts of individuals in that population, the study suggests. Those of us who live in advanced industrial societies may already be heading down that path.

The proliferation of nearly fiber-free, processed convenience foods since the mid-20th century has resulted in average per capita fiber consumption in industrialized societies of about 15 grams per day. That's as little as one-tenth of the intake among the world's dwindling hunter-gatherer and rural agrarian populations, whose living conditions and dietary intake presumably most closely resemble those of our common human ancestors, said Justin Sonnenburg, PhD, associate professor of microbiology and immunology and senior author of the study, to be published Jan. 13 in Nature.

Suboptimal diets

Virtually all health experts agree that low-fiber diets are suboptimal. Probably the chief reason for this is that fiber, which can't be digested by human enzymes, is the main food source for the commensal bacteria that colonize our colons, Sonnenburg said.

Thousands of distinct bacterial species inhabit every healthy individual's large intestine. "We would have difficulty living without them," he said. "They fend off pathogens, train our immune systems and even guide the development of our tissues." While we pick up these microscopic passengers in the course of routine exposures throughout our lifetimes, one of the most significant sources of our intestinal bacterial populations is our immediate family, especially our mothers during childbirth and infancy.

Surveys of humans' gut-dwelling microbes have shown that the diversity of bacterial species inhabiting the intestines of individual members of hunter-gatherer and rural agrarian populations greatly exceeds that of individuals living in modern industrialized societies, Sonnenburg said. In fact, these studies indicate the complete absence, throughout industrialized populations, of numerous bacterial species that are shared among many of the hunter-gatherer and rural agrarian populations surveyed, despite those groups' being dispersed across vast geographic expanses ranging from Africa to South America to Papua New Guinea.

High- versus low-fiber diet

"Numerous factors including widespread antibiotic use, more-frequent cesarean sections and less-frequent breastfeeding have been proposed for why we see this depletion in industrialized populations," said the study's lead author, Erica Sonnenburg, PhD, a senior research scientist at Stanford (she and Justin Sonnenburg are married). "We asked ourselves whether the huge difference in dietary fiber intake between traditional and modern populations could, alone, account for it."

The Stanford researchers employed young laboratory mice that had been specially bred and raised in aseptic environments so that, unlike ordinary mice (and ordinary humans), their intestines were devoid of any microbial inhabitants. After populating the mice's guts with microbes from a human donor, the scientists divided them into two groups. One group was fed a diet rich in plant-derived fiber. The other group's diet, equivalent to the first with respect to protein, fat and calories, was practically devoid of fiber content.

During the experimentation that followed, the researchers analyzed fecal samples from the animals. The two groups' gut-bacteria profiles were initially indistinguishable but soon diverged. "Within a couple of weeks, we saw a massive change," said Justin Sonnenburg. "The low-fiber-intake mice harbored fewer bacterial species in their gut." More than half of these bacterial species' numbers had dwindled by over 75 percent, and many species seemed to have disappeared altogether.

After seven weeks, the mice that had consumed a low-fiber diet were switched back to a high-fiber diet for four weeks. The mice's gut-bacteria profiles partly recovered -- probably due to an uptick in abundance of some bacteria whose ranks had declined to undetectable levels during the low-fiber-intake period. Still, this restoration was only partial: One-third of the original species never fully recovered despite their return to a high-fiber diet.

No such changes were seen in the control mice consistently fed a high-fiber diet.

Generational effects

The real surprise came after mice had been bred and maintained on low-fiber diets for a few generations. In their experimental confines, these mice were exposed to microbes only through contact with their parents. Each successive generation's gut-bacterial ecosystem declined in diversity. By generation four, the depletion had reached a point where nearly three-quarters of the bacterial species resident in their great-grandparents' guts appeared absent in their own. Even after these mice were put back on a high-fiber diet, more than two-thirds of the bacterial species identified in the guts of their first-generation ancestors proved irretrievable, indicating extinction of those species by the fourth generation of fiber deprivation.

On the other hand, a somewhat more aggressive measure -- fecal transplantation -- did result in these lost species' retrieval, the study found. Introducing fecal contents of fourth-generation high-fiber-diet mice into the intestines of fourth-generation low-fiber mice, together with putting them on the high-fiber diet for two weeks, fully restored their bacterial profiles. Within 10 days of the procedure, the composition and diversity of the bacteria in the intestines of this group were indistinguishable from those of control mice.

These findings hold major implications for humans, said Erica Sonnenburg. "There are very few ecosystems where low species diversity is a good thing. There's no reason to think our gut is any exception," she said.

Possible fixes

"The extremely low-fiber intake in industrialized countries has occurred relatively recently," noted Justin Sonnenburg. "Is it possible that over the next few generations we'll lose even more species in our gut? And what will the ramifications be for our health?"

Simple tweaks in our cultural practices -- for example, not washing our hands after gardening or petting our dogs -- could be a step in the right direction, and steering away from overuse of antibiotics certainly is, he said. More extreme measures, such as mass fecal transplants, would require large-scale testing to make sure they are both necessary and safe.

Source:STANFORD UNIVERSITY MEDICAL CENTER

Reduce Sugar, Salt - New Dietary Guidelines by US Department of Agriculture

Red meat and processed foods contribute to cholesterol, plaque, and atherosclerosis, which can result in heart attack and stroke. Less sugar and salt, more fruits, vegetables, nuts, and whole grains; those are the recommendations in the new dietary guidelines put out every five years by the United States Department of Agriculture.
Sahil Parikh, interventional cardiologist at University Hospitals Case Medical Center, said, "The guidelines are a little bit less clear when it comes to saying red meat and processed foods should be restricted. They say you should reduce saturated fat without saying expressly you should reduce red meat and processed food, which frequently contain high levels of saturated fat."  Dr. Parikh agrees with reducing hypertension-causing sodium and said, "The new measure of also reducing sugar to 10% of daily caloric intake (50 grams or one can of soda in a 2000 calorie-a-day diet) is another good measure. Clearly there is a diabetes epidemic in this country and dietary sugar and caloric intake specifically contribute to obesity and subsequently Type 2 diabetes." The guidelines also say it's okay to consume alcohol moderately (one drink for women daily and two drinks for men), with wine showing some benefit to the heart. Additionally, moderate coffee drinking (three to five cups a day) is alright as well, because it's shown to reduce Type 2 diabetes, cardiovascular disease, and possibly Parkinson's disease. Source: Newswise

Low-Sugar Diet Helps Reverse Liver Damage Faster

Liver damage caused by a diet high in fat, sugar and cholesterol may be difficult to reverse even if diet is generally improved, says a new study.

This study, done with laboratory animals, showed that diets low in fat and cholesterol could in fact aid with weight loss, improved metabolism and health. But even then, if the diet was still high in sugar there was much less liver recovery, the scientists concluded. 

The findings are significant, scientists say, because liver problems such as nonalcoholic fatty liver disease are surging in the U.S., affecting 10-35 percent of adults and an increasing number of children. The incidence of this problem can reach more than 60 percent in obese and type-2 diabetic populations. 

"Many people eating a common American diet are developing extensive hepatic fibrosis, or scarring of their liver, which can reduce its capacity to function, and sometimes lead to cancer," said Donald Jump, a professor in the OSU College of Public Health and Human Sciences, principal investigator with the Linus Pauling Institute, and corresponding author on this research. 

"There's a lot of interest in finding ways to help the liver recover from this damage, but this research suggests that diets lower in fat and cholesterol, even if they help you lose weight, are not enough," Jump said. "For more significant liver recovery, the intake of sugar has to come down, probably along with other improvements in diet and exercise." 

The issues are both serious and complex, the researchers said. 

"Everyone recognizes this is a serious problem," said Kelli Lytle, an OSU doctoral candidate and lead author on this study. "We're trying to find out if some of the types of dietary manipulation that people use, such as weight loss based on a low fat diet, will help address it. However, a common concern is that many 'low-fat' food products have higher levels of sugar to help make them taste better." 

Weight loss does appear to help address some of the problems associated with the Western diet, the research shows. But according to this study, a diet with continued high levels of sugar will significantly slow recovery of liver damage that has already been done. 

Complications related to liver inflammation, scarring and damage are projected to be the leading cause of liver transplants by 2020, the researchers noted in their study. Such scarring was once thought to be irreversible, but more recent research has shown it can be at least partially reversed with optimal diet and when the stimulus for liver injury is removed. 

In this report, scientists studied two groups of laboratory mice that had been fed a "Western diet" and then switched to different, healthier diets, low in fat and cholesterol. 

Both of the improved diets caused health improvements and weight loss. But one group that was fed a diet still fairly high in sugar - an amount of sugar comparable to the Western diet - had significantly higher levels of inflammation, oxidative stress and liver fibrosis. 

More research is still needed to determine whether a comprehensive program of diet, weight maintenance, exercise and targeted drug therapies can fully resolve liver fibrosis, the study concluded. 



Source: Eurekalert

 

Blueberries, citrus fruits and red wine associated with reduced erectile dysfunction

Flavonoid-rich foods are associated with a reduced risk of erectile dysfunction - according to a new collaborative study from the University of East Anglia (UEA) and Harvard University.

Research published today in The American Journal of Clinical Nutrition reveals that eating foods rich in certain flavonoids is associated with a reduced risk of erectile dysfunction in men, with the greatest benefit in those under 70.

Of all the different flavonoids, Anthocyanins (found in blueberries, cherries, blackberries, radishes and blackcurrant), flavanones and flavones (found in citrus fruits) were found to offer the greatest benefits in preventing the condition.

It is already known that increased exercise can improve erectile function, but this research shows that eating a flavonoid-rich diet is as good for erectile function as briskly walking for up to five hours a week.

The study also showed that a higher total fruit intake was associated with a 14 per cent reduction in the risk of erectile dysfunction. And that a combination of consuming flavonoid-rich foods with exercise can reduce the risk by 21 per cent.

The study was carried out by nutrition departments at the Harvard TH Chan School of Public Health and UEA's Norwich Medical School.

Lead researcher Prof Aedin Cassidy from UEA said: "We already knew that intake of certain foods high in flavonoids may reduce the risk of conditions including diabetes and cardiovascular disease. This is the first study to look at the association between flavonoids and erectile dysfunction, which affects up to half of all middle-aged and older men.

"Flavonoids are present in many plant-based foods and drinks including fruits, vegetables, tea, herbs and wine. We examined six main types of commonly consumed flavonoids and found that three in particular - anthocyanins, flavanones and flavones - are beneficial.

"Men who regularly consumed foods high in these flavonoids were 10 per cent less likely to suffer erectile dysfunction. In terms of quantities, we're talking just a few portions a week."

More than 50,000 middle aged men were included in this large population based study. They were asked about their ability to have and maintain an erection sufficient for intercourse - dating back to 1986. Data on dietary intake was also collected every four years.

The research team took into account a range of factors such as body weight, physical activity, amount of caffeine consumed, and whether the participants smoked. The research was also restricted to men who were otherwise in good health.

More than one third of the men surveyed reported suffering new onset erectile dysfunction. But those who consumed a diet rich in anthocyanins, flavones and flavanones were less likely to suffer the condition.

Prof Cassidy said: "The top sources of anthocyanins, flavones and flavanones consumed in the US are strawberries, blueberries, red wine, apples, pears, and citrus products."

"We also found that the benefits were strongest among younger men," she added.

The team also looked at other lifestyle factors and found that men who consumed a high intake of anthocyanins and flavanones and who were also physically active had the lowest risk of erectile dysfunction.

Dr Eric Rimm, senior author on the study and a Professor of Epidemiology and Nutrition at the Harvard TH Chan School of Public Health, said: "As well as improving sexual health for middle-aged men, there is another important benefit linked to heart health. Erectile dysfunction is often an early barometer of poor vascular function and offers a critical opportunity to intervene and prevent cardiovascular disease, heart attack and even death.

"Men with erectile dysfunction are likely to be highly motivated to make healthier lifestyle choices, such as exercising more and eating the right foods - which would greatly benefit their long-term cardiovascular health as well."

Source:UNIVERSITY OF EAST ANGLIA

Link between obesity and increased risk of colorectal cancer revealed

 Obesity has long been associated with increased risk of colorectal cancer, but the link has never been understood. Now, a research team led by investigators at Thomas Jefferson University has revealed the biological connection, and in the process, has identified an approved drug that might prevent development of the cancer. Their study is published in Cancer Research.

In mice, investigators found that a high caloric diet turned off expression of a key hormone in the intestine, which led to deactivation of a tumor suppressor pathway. Genetic replacement of that hormone turned the tumor suppressor back on and prevented cancer development -- even when mice continued to eat excess calories.

These findings position the use of the pill linaclotide (Linzess), which is structurally related to the lost hormone, as a therapeutic approach to preventing colorectal cancer in obese patients, says the study's senior author, Scott Waldman, M.D. Ph.D., Chair of Pharmacology & Experimental Therapeutics at Sidney Kimmel Medical College of Thomas Jefferson University.

The U.S. Food and Drug Administration approved linaclotide in 2012 to treat irritable bowel syndrome with constipation as well as chronic idiopathic constipation (chronic constipation from unknown causes).

"Our study suggests that colorectal cancer can be prevented in obese individuals with use of hormone replacement therapy -- much as other diseases associated with hormone deficiency, such as loss of insulin in diabetes, can be treated," Dr. Waldman says.

"These findings came as a surprise -- we and many other researchers worldwide have been trying to disentangle obesity from development of colorectal cancer," he says. "Calories sit in the middle of these two conditions, but the question of what they were doing has been one of the most perplexing and provocative questions in cancer research.

"Now we finally have a big clue as to the origin of colorectal cancer in obese individuals and perhaps in other people as well," says Dr. Waldman, who is also the Samuel MV Hamilton Professor.

The risk of developing colorectal cancer in obese persons is about 50 percent greater, compared to risk in lean people. Scientists had thought the issue was one based on the amount of fat tissue and the associated unknown metabolic processes -- excess calories that fuel cell energy and growth -- but that did not turn out to be the case here, Dr. Waldman says.

Dr. Waldman is already involved in a multisite clinical study testing dose and side effects of linaclotide use in healthy volunteers. Investigators from the National Cancer Institute, Mayo Clinic, and Fox Chase Cancer Center are participating.

In the present study, the research team -- which includes investigators from Harvard and Duke Medical Schools -- used genetically engineered mice on different diets to conduct their investigation.

They found that obesity (either from excess fat or carbohydrate consumption, or both) is associated with loss of the hormone guanylin, which is produced in the intestine's epithelium -- the cells lining the organ. The hormone turns on its receptor, guanylyl cyclase C (GUCY2C), which regulates processes underlying regeneration of the intestinal epithelium. "The lining of the intestines is very dynamic and continuously being replaced, and GUCY2C contributes to the choreography of the key processes needed for this regeneration," Dr. Waldman says.

Deactivation of the guanylin gene is common in colorectal cancers in both humans and animals, he says. In that regard, morbidly obese patients exhibit an 80 percent decrease in guanylin gene expression compared to lean people, he says.

But in this study, the researchers discovered the consequences of that loss. They found that the guanylin hormone receptor acts as a growth-controlling tumor suppressor, and without the hormone, the receptor is silenced. "This happens extremely early in development of the cancer," Dr. Waldman says. "When the receptor is silenced, the epithelium becomes dysfunctional, setting up the conditions for cancer development."

The scientists checked their findings by creating mice that carried a transgene that won't allow the guanylin gene to be shut off. "Even in the setting of excess calories, from any diet source, tumors don't develop," he says.

Their experiments demonstrated that obese mice, compared to lean mice, were much more likely to silence the hormone and its receptor. "We believe that if colorectal cancer is going to develop, it will be through this silencing mechanism -- and that it will happen much more frequently in the obese," Dr. Waldman says. Even so, investigators don't yet know the precise molecular mechanism that turns off hormone production.

"The beauty of our findings is that while we know the hormone is lost in the obese mice, its receptors are just sitting there waiting to be switched on. And this study demonstrates that if you can prevent hormone loss, you can also prevent tumor development. These findings suggest that a drug like linaclotide, which acts like guanylin, can activate GUCY2C tumor-suppressing receptors to prevent cancer in obese patients," he says.

The researchers also showed that the effect of excess calorie consumption can be reversed via calorie restriction, even in obese mice. "The challenges of lifestyle modification notwithstanding, our observations suggest that calorie restriction can reconstitute guanylin expression," Dr. Waldman says. "This may be an effective strategy to prevent colon cancer in the obese."

Source:THOMAS JEFFERSON UNIVERSITY