Smart Economy

Longevity and Healthy Aging

Aging Gracefully without Chronic Human Diseases

Time Magazine and National Geographic both recently ran cover stories with a baby on the cover. The tagline reads: This baby could live to be 142 years old. So the question that immediately comes to mind  is: Is this possible  and can everyone age gracefully without chronic human diseases? And can we do it with today’s technology ?

To explore this question we first need to compare the mortality in 1900 versus today. In 1900, half of the deaths were caused by pneumonia, influenza, tuberculosis, gastrointestinal infections.  These diseases were cured largely with antibiotics and antivirals after world war two. Cancer, diabetes, coronary  heart disease, and Alzheimer’s were present but  not near the rates we see today.  Now, the top causes of death today, according to US statistics are heart disease, lung cancer, lung disease (asthma) , stroke, Alzheimer’s,  diabetes  and hypertension. An interesting question to ask would be: Do all these new, twenty first century diseases all have something in common, just like the top causes of death  in 1900 where from bacterial or viral sources?  A review of the medical literature shows two primary causes. In turns out that most chronic human diseases are 1) triggered by excess free radicals or oxidative stress and 2) are the result of a lack of essential minerals and trace minerals and cofactors in our diets.

Oxidative Stress

Free radicals or oxidative stress is the result of our cells metabolizing or breathing oxygen. Free radical are the “waste” products of life, and they are very destructive to cell membranes, proteins and DNA.  Our body has a natural protective system-antioxidant enzymes that neutralize excess free radicals. If this delicate balance is  disrupted,  this then leads to an inflammation response in the body and eventually, chronic diseases could ensue. As we age, our natural antioxidant protective systems decline and we are told to supplement with natural botanical antioxidants, such as blueberries , green tea or cinnamon or antioxidant supplements such as Vitamin E or coenzyme Q10. But then we run into the “antioxidant paradox”. All these food antioxidants  work great as antioxidants in a test tube in the lab, but in human clinical trials, the beneficial effects are either inconclusive or negative. This is because saliva and gut bacteria metabolise many these botanical antioxidants, before they have a chance to act beneficially.

Ukrainian scientists discovered the world’s highest antioxidant called Carbon 60 hydrated fullerenes, which is stable and inert and not metabolised by bacteria. Carbon 60, a natural product,  was discovered in 1985 and a Nobel prize in Chemistry was awarded for this discovery in 1996.  Scientists and doctors were calling it the panacea or silver bullet in medicine, but because it’s not naturally water soluble, just like diamonds, charcoal or activated charcoal, this frustrated scientists. Ukrainian scientist in Kharkiv the first to discovered how to dissolve Carbon 60 in water in 1994. After 20 years of preclinical, safety and clinical studies,  Carbon 60 hydrated fullerenes  were approved as a  “dietary supplement” by the Ukrainian Ministry of Health and has been on the Ukrainian market since 2010. There is now a US patent pending. Scientists are now claiming that most chronic human diseases are triggered by excess free radicals. Just do a search on PUBMED with the key words “oxidative stress” and your own disease and you will find a link. (http://www.ncbi.nlm.nih.gov/pubmed ). Reduce excess free radicals and reduce your disease symptoms. A study at the University of Paris in 2010 showed that rats feed a diet supplemented  with Carbon 60 in olive oil, increased the lifespan of rats by 90% from an average of 25-30 months to over 55 months.

Essential minerals and trace minerals.

The National Post ran a story on May 1- “Obese Canadians should be granted legal protection from discrimination, professor says.”  The obesity debate is totally missing the point. Most Doctors are ignoring their own medical research. The cause of the 400% increase in obesity in last 3 decades in Canada and sharp rise in most other chronic human diseases since the 1930’ is due to a chronic lack of essential minerals and trace minerals in our diet (plants, fruits and vegetables) that are needed as co-factors in the body for our biochemical pathways to work efficiently.

The soil minerals concentrations have been dropping  worldwide for the last 100 years, so less and less minerals are  absorbed in fruits, vegetables and other plants. This is due primarily to the fact that  we no longer cook and heat our homes with wood and throw away the ashes (95% minerals) back into the garden to replenish the soil with the 60 essential and trace minerals that our bodies need. Fertilizer only has 3 minerals. Even the nutritional supplements commonly found in most health food stores don't carry the full complement of 90  essential nutrients, which should include 60 essential minerals, 15 essential vitamins, 12 essential amino acids and 3 fatty acids and  the right doses of each and the correct easily absorbable mineral salts.

How do we know that we need 90 essential nutrients? Just talk to any veterinarian. Vets have cured over 600 chronic human diseases in farm animals and in zoo animals by supplementing their food with nutritional pellets. When was the last time you saw a cow with arthritis and a pig with Alzheimer’s?  Vets have to cure an animal after the first time otherwise beef would cost over $500 a pound or eggs $50 a dozen.  Why? Because animals don’t have health insurance. Doctors are quite content to treat your disease symptoms for the rest of your life, billing health insurance and not curing your disease after a few visits. Human  clinical studies in the past 40 years have shown that most chronic human diseases are also caused by essential mineral deficiencies and can be controlled with the proper essential and trace minerals. Diabetes has been controlled with the right amount of chromium and vanadium and other essential cofactors. Arthritis is a lack of proper calcium absorption and cofactors such as Vitamin D and magnesium. Greying hair is a copper deficiency in the diet.

So can we live to be 100 or over without chronic human diseases? Yes by reducing excess oxidative stress or free radicals in our body and ensuring that we get the right daily balance of 90 essential nutrients including 60 minerals and trace minerals.

If you would like more information on the above or a copy of my presentation on Aging Gracefully without Chronic Human Diseases that  I gave at Ukrainian Canadian Social Services last week, send me an email  [email protected] or call (416) 819-9667 or download it from this link  http://bit.ly/1KzZvm8  For Ukrainian listeners,  catch  my Ukrainian radio interview on Radio KONTAKT archives from Saturday April 25, 2015 http://www.kontaktglobal.com/radio-saturday.html

 

Walter Derzko is the president of the startup C60 Water North America

Do Gut Bacteria Rule Our Minds?

 

 In an Ecosystem Within Us, Microbes Evolved to Sway Food Choices       

 

          By Jeffrey Norris on August 15, 2014

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It sounds like science fiction, but it seems that bacteria within us – which outnumber our own cells about 100-fold – may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.

In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.

A Power Struggle Inside the Gut

Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem – our digestive tracts – they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.

Are we at the mercy of our gut bacteria? The above image illustrates how microbes can "pull our strings," driving us to crave foods that give them the nutrients they need, including fat and sugar.

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”

Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.

“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”

There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.

The Connection Between Digestive Tract and Brain

Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

Athena Aktipis, PhD

Carlo Maley, PhD

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.

Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?

The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.

“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.

Implications for Obesity, Diabetes and even Cancer

The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago.

Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.

In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.

“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.

The co-authors’ BioEssays study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation and the Institute for Advanced Study, in Berlin.

UC San Francisco (UCSF), now celebrating the 150^th anniversary of its founding, is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

NIH study uncovers probable mechanism underlying resveratrol activity

Public release date: 2-Feb-2012

Findings may settle scientific debate surrounding this chemical found in red wine and other foods

National Institutes of Health researchers and their colleagues have identified how resveratrol, a naturally occurring chemical found in red wine and other plant products, may confer its health benefits. The authors present evidence that resveratrol does not directly activate sirtuin 1, a protein associated with aging. Rather, the authors found that resveratrol inhibits certain types of proteins known as phosphodiesterases (PDEs), enzymes that help regulate cell energy.

These findings may help settle the debate regarding resveratrol's biochemistry and pave the way for resveratrol-based medicines. The chemical has received significant interest from pharmaceutical companies for its potential to combat diabetes, inflammation, and cancer. The study appears in the Feb. 3 issue of Cell.

"Resveratrol has potential as a therapy for diverse diseases such as type 2 diabetes, Alzheimer's disease, and heart disease," said lead study author Jay H. Chung, M.D., Ph.D., chief of the Laboratory of Obesity and Aging Research at the NIH's National Heart, Lung, and Blood Institute. "However, before researchers can transform resveratrol into a safe and effective medicine, they need to know exactly what it targets in cells."

Several previous studies suggested that resveratrol's primary target is sirtuin 1. Chung and colleagues suspected otherwise when they found that resveratrol activity required another protein called AMPK. This would not be the case if resveratrol directly interacted with sirtuin 1.

In this study, the researchers methodically traced out the metabolic activity in cells treated with resveratrol and identified PDE4 in the skeletal muscle as the principal target for the health benefits of resveratrol. By inhibiting PDE4, resveratrol triggers a series of events in a cell, one of which indirectly activates sirtuin 1.

To confirm that resveratrol attaches to and inhibits PDE proteins, Chung's group gave mice rolipram, a drug known to inhibit PDE4. Rolipram reproduced all of the biochemical effects and health benefits of resveratrol, such as preventing diet-induced obesity, improving glucose tolerance, and increasing physical endurance.

Chung noted that because resveratrol in its natural form interacts with many proteins, not just PDEs, it may cause not-yet-known toxicities as a medicine, particularly with long-term use.   He added that the levels of resveratrol found in wine or foods are likely not high enough to produce significant health benefits or problems. Convincing clinical studies in humans have used about 1 gm of resveratrol per day, roughly equal to the amount found in 667 bottles of red wine. 

The study results also suggest that inhibitors of PDE4 may offer the benefits of resveratrol without the potential toxicities arising from resveratrol's interactions with other proteins.  One PDE4 inhibitor called roflumilast has already been approved by the FDA for the treatment of COPD (chronic obstructive pulmonary disease).

"This result underscores the need for careful, well-controlled studies to illuminate how these natural products operate," said Robert Balaban, Ph.D., director of the NHLBI Division of Intramural Research. "As Dr. Chung's work suggests, the effects of resveratrol seem to be more complicated than originally thought. However, this new insight into the phosphodiesterases might prove an interesting avenue to pursue."

In addition to Dr. Chung's lab at the NHLBI, other contributors to this study included collaborators in the Cardiovascular Pulmonary Branch of the NHLBI; the University of California, Davis; the University of North Carolina, Chapel Hill; University of Texas Southwestern Medical Center, Dallas; Sun Yat-sen University, Guangzhou, China; University Medical Center, Utrecht, The Netherlands; and Emerald BioStructures, Bainbridge Island, Wash.

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To schedule an interview with Dr. Chung or another NHLBI spokesperson, contact the NHLBI Office of Communications at 301-496-4236 or [email protected].

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders.  The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics.  NHLBI press releases and other materials are available online at www.nhlbi.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services.  NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases.  For more information about NIH and its programs, visit www.nih.gov.

NIH...Turning Discovery Into Health

Diets rich in antioxidant resveratrol fail to reduce deaths, heart disease or cancer

But don't put down the Chianti yet: As-yet-unknown compounds in such foods may still be conferring health benefits, researchers say

A study of Italians who consume a diet rich in resveratrol — the compound found in red wine, dark chocolate and berries — finds they live no longer than and are just as likely to develop cardiovascular disease or cancer as those who eat or drink smaller amounts of the antioxidant.

"The story of resveratrol turns out to be another case where you get a lot of hype about health benefits that doesn't stand the test of time," says Richard D. Semba, M.D., M.P.H., a professor of ophthalmology at the Johns Hopkins University School of Medicine and leader of the study described May 12 in JAMA Internal Medicine. "The thinking was that certain foods are good for you because they contain resveratrol. We didn't find that at all."

Despite the negative results, Semba says, studies have shown that consumption of red wine, dark chocolate and berries does reduce inflammation in some people and still appears to protect the heart. "It's just that the benefits, if they are there, must come from other polyphenols or substances found in those foodstuffs," he says. "These are complex foods, and all we really know from our study is that the benefits are probably not due to resveratrol."

The new study did not include people taking resveratrol supplements, though few studies thus far have found benefits associated with them.

Semba is part of an international team of researchers that for 15 years has studied the effects of aging in a group of people who live in the Chianti region of Italy. For the current study, the researchers analyzed 24 hours of urine samples from 783 people over the age of 65 for metabolites of resveratrol. After accounting for such factors as age and gender, the people with the highest concentration of resveratrol metabolites were no less likely to have died of any cause than those with no resveratrol found in their urine. The concentration of resveratrol was not associated with inflammatory markers, cardiovascular disease or cancer rates.

Semba and his colleagues used advanced mass spectrometry to analyze the urine samples.

The study participants make up a random group of people living in Tuscany where supplement use is uncommon and consumption of red wine — a specialty of the region — is the norm. The study participants were not on any prescribed diet.

Resveratrol is also found in relatively large amounts in grapes, peanuts and certain Asiatic plant roots. Excitement over its health benefits followed studies documenting anti-inflammatory effects in lower organisms and increased lifespan in mice fed a high-calorie diet rich in the compound.

The so-called "French paradox," in which a low incidence of coronary heart disease occurs in the presence of a high dietary intake of cholesterol and saturated fat in France, has been attributed to the regular consumption of resveratrol and other polyphenols found in red wine.

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Kai Sun, M.S., a Johns Hopkins statistician, worked on the research. Researchers from the National Institutes of Health's National Institute on Aging (NIA), the New England Research Institutes, the University of Barcelona in Spain, the Catalan Institute of Oncology in Spain, Azienda Sanitaria in Italy and the Instituto Nazionale di Ripose e Cura per Anziani V.E.II.-Instituto di Recovero e Cura a Carattere Scientifico in Italy also contributed to the study.

The work was supported by grants from the NIA (R01 AG027012), the National Institutes of Health's National Heart, Lung and Blood Institute (R01 HL094507), the Italian Ministry of Health, the Spanish government and the NIA Intramural Research Program.

Johns Hopkins Medicine (JHM), headquartered in Baltimore, Maryland, is a $6.7 billion integrated global health enterprise and one of the leading health care systems in the United States. JHM unites physicians and scientists of the Johns Hopkins University School of Medicine with the organizations, health professionals and facilities of The Johns Hopkins Hospital and Health System. JHM's vision, "Together, we will deliver the promise of medicine," is supported by its mission to improve the health of the community and the world by setting the standard of excellence in medical education, research and clinical care. Diverse and inclusive, JHM educates medical students, scientists, health care professionals and the public; conducts biomedical research; and provides patient-centered medicine to prevent, diagnose and treat human illness. JHM operates six academic and community hospitals, four suburban health care and surgery centers, and more than 30 primary health care outpatient sites. The Johns Hopkins Hospital, opened in 1889, was ranked number one in the nation for 21 years in a row by U.S. News & World Report.

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Johns Hopkins Medicine Media Relations and Public Affairs Media Contacts:

Contact: Stephanie Desmon [email protected] 410-955-8665 Johns Hopkins Medicine

Lauren Nelson 410-955-8725; [email protected]

Does a junk food diet make you lazy? UCLA psychology study offers answer

 

 

A new UCLA psychology study provides evidence that being overweight makes people tired and sedentary — not the other way around. 

Life scientists led by UCLA's Aaron Blaisdell placed 32 female rats on one of two diets for six months. The first, a standard rat's diet, consisted of relatively unprocessed foods like ground corn and fish meal. The ingredients in the second were highly processed, of lower quality and included substantially more sugar — a proxy for a junk food diet. 

After just three months, the researchers observed a significant difference in the amount of weight the rats had gained, with the 16 on the junk food diet having become noticeably fatter.       

"One diet led to obesity, the other didn't," said Blaisdell, a professor of psychology in the UCLA College of Letters and Science and a member of UCLA's Brain Research Institute.    

The experiments the researchers performed, Blaisdell said, also suggest that fatigue may result from a junk food diet.   

As part of the study, the rats were given a task in which they were required to press a lever to receive a food or water reward. The rats on the junk food diet demonstrated impaired performance, taking substantially longer breaks than the lean rats before returning to the task. In a 30-minute session, the overweight rats took breaks that were nearly twice as long as the lean ones. 

The research is currently online and is scheduled for publication in the April 10 print edition of the journal Physiology and Behavior.

After six months, the rats' diets were switched, and the overweight rats were given the more nutritious diet for nine days. This change, however, didn't help reduce their weight or improve their lever responses.   

The reverse was also true: Placing the lean rats on the junk food diet for nine days didn't increase their weight noticeably or result in any reduction in their motivation on the lever task. These findings suggest that a pattern of consuming junk food, not just the occasional binge, is responsible for obesity and cognitive impairments, Blaisdell said. 

"There's no quick fix," he noted.     

What are the implications for humans? Do people who are overweight become less healthy or do less healthy people become overweight? 

"Overweight people often get stigmatized as lazy and lacking discipline," Blaisdell said. "We interpret our results as suggesting that the idea commonly portrayed in the media that people become fat because they are lazy is wrong. Our data suggest that diet-induced obesity is a cause, rather than an effect, of laziness. Either the highly processed diet causes fatigue or the diet causes obesity, which causes fatigue." 

Blaisdell believes the findings are very likely to apply to humans, whose physiological systems are similar to rats'. Junk food diets make humans — and rats — hungrier, he said.       

In addition, the researchers found that the rats on the junk food diet grew large numbers of tumors throughout their bodies by the end of the study. Those on the more nutritious diet had fewer and small tumors that were not as widespread. 

Blaisdell, 45, changed his diet more than five years ago to eat "what our human ancestors ate." He avoids processed food, bread, pasta, grains and food with added sugar. He eats meats, seafood, eggs, vegetables and fruits, and he has seen dramatic improvements in his health, both physically and mentally. 

"I've noticed a big improvement in my cognition," he said. "I'm full of energy throughout the day, and my thoughts are clear and focused." 

An expert in animal cognition, Blaisdell conducts research that addresses the relationship between health and lifestyle (diet and exercise) and the relationship between a junk food diet and cognitive impairments it may induce. 

"We are living in an environment with sedentary lifestyles, poor-quality diet and highly processed foods that is very different from the one we are adapted to through human evolution," he said. "It is that difference that leads to many of the chronic diseases that we see today, such as obesity and diabetes."

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Co-authors of the research are Yan Lam Matthew Lau, Ekatherina Telminova and Boyang Fan, UCLA undergraduate students in Blaisdell's laboratory; Hwee Cheei Lim, the manger of Blaisdell's lab; Cynthia D. Fast, a UCLA graduate student in the lab; Dennis Garlick, a postdoctoral scholar in the lab; and David Pendergrass, a biology professor at the University of Kansas. 

The research was funded by the National Science Foundation and by entrepreneur Cameron Smith.

 

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Monkeys that eat omega-3 rich diet show more developed brain networks

 

02/05/14  Portland, Ore.

Study gives new insight into similarity of complex brain networks in monkeys, humans

Monkeys that ate a diet rich in omega-3 fatty acids had brains with highly connected and well organized neural networks — in some ways akin to the neural networks in healthy humans — while monkeys that ate a diet deficient in the fatty acids had much more limited brain networking, according to an Oregon Health & Science University study.

The study, published today in the Journal of Neuroscience, provides further evidence for the importance of omega-3 fatty acids in healthy brain development. It also represents the first time scientists have been able to use functional brain imaging in live animals to see the large-scale interaction of multiple brain networks in a monkey. These patterns are remarkably similar to the networks found in humans using the same imaging techniques.

"The data shows the benefits in how the monkeys' brains organize over their lifetime if in the setting of a diet high in omega-3 fatty acids," said Damien Fair, PA-C, Ph.D., assistant professor of behavioral neuroscience and assistant professor of psychiatry in the OHSU School of Medicine and senior author on the paper. "The data also shows in detail how similar the networks in a monkey brain are to networks in a human brain, but only in the context of a diet rich in omega-3-fatty acids."

Omega-3 fatty acids are considered essential fatty acids for the human body. But while they are needed for human health, the body can't make them — it has to get them through food.

The study measured a kind of omega-3 fatty acid called docosahexaenoic acid, or DHA, which is a primary component of the human brain and important in development of the brain and vision. DHA is especially found in fatty fish and oils from those fish — including salmon, mackerel and tuna. Research by a co-author on the paper, Martha Neuringer, Ph.D., an associate scientist in the Division of Neuroscience at OHSU’s Oregon National Primate Research Center, previously showed the importance of DHA for infants’ visual development — a finding that led to the addition of DHA to infant formulas.

The scientists studied a group of older rhesus macaque monkeys — 17 to 19 years of age — from ONPRC that had been fed all of their lives either a diet low or high in omega-3 fatty acids, including DHA. The study found that the monkeys that had the high-DHA diet had strong connectivity of early visual pathways in their brains. It also found that monkeys with the high-DHA diet showed greater connections within various brain networks similar to the human brain — including networks for higher-level processing and cognition, said David Grayson, a former research assistant in Fair's lab and first author on the paper. Grayson is now studying at the Center for Neuroscience, University of California-Davis.

"For example, we could see activity and connections within areas of the macaque brain that are important in the human brain for attention," said Fair.

Now that those measurements and monitoring are possible, Fair said, the next step will be to analyze whether the monkeys with deficits in certain networks have behavioral patterns that are similar to behavioral patterns in humans with certain neurological or psychiatric conditions — including Attention Deficit Hyperactivity Disorder and autism.

Fair, who was among the 102 people given the 2013 Presidential Early Career Award for Scientists and Engineers by President Barack Obama, is a leader in using the same kind of brain imaging to explore brain networks in children with ADHD and autism. He said he hopes to use these non-invasive brain imaging techniques to provide an important link between research in humans and animals in order to better characterize, treat, and prevent these types of developmental mental health issues.

Fair added that another longer-term goal would be to study brain development in the monkeys fed various diets from birth into maturity.

"It would be important to see how a diet high in omega-3s might affect brain development early on in their lives, and across their lifespan," Fair said.

The study was funded by the Oregon Clinical and Translational Research Institute (through National Institutes of Health grant UL1TR000128), several other NIH grants (grants UL1 RR024140, P510D011092, K99/R00 MH091238, R01 MH096773, EY13199, and DK29930) and the Foundation Fighting Blindness.

About OHSU Brain Institute

The Oregon Health & Science University Brain Institute is a national neuroscience leader in patient care, research and education. With more than 1,000 brain scientists and specialists, OHSU is home to one of the largest communities of brain and central nervous system experts in the nation. OHSU Brain Institute scientists have won national recognition for breaking new ground in understanding Alzheimer’s disease and for discoveries that have led to new treatments for Parkinson’s disease, multiple sclerosis, stroke and other brain disorders and diseases.

About OHSU

Oregon Health & Science University is a nationally prominent research university and Oregon’s only public academic health center. It serves patients throughout the region with a Level 1 trauma center and nationally recognized Doernbecher Children’s Hospital. OHSU operates dental, medical, nursing and pharmacy schools that rank high both in research funding and in meeting the university’s social mission. OHSU’s Knight Cancer Institute helped pioneer personalized medicine through a discovery that identified how to shut down cells that enable cancer to grow without harming healthy ones. OHSU Brain Institute scientists are nationally recognized for discoveries that have led to a better understanding of Alzheimer’s disease and new treatments for Parkinson’s disease, multiple sclerosis and stroke. OHSU’s Casey Eye Institute is a global leader in ophthalmic imaging, and in clinical trials related to eye disease.

Timing-changing meal times could have a significant effect on the levels of triglycerides in the liver.

Time is of the Essence

05Feb 2014

Biochemistry

        

New findings in mice suggest that merely changing meal times could have a significant effect on the levels of triglycerides in the liver. The results of this Weizmann Institute of Science study, recently published in Cell Metabolism, not only have important implications for the potential treatment of metabolic diseases, they may also have broader implications for most research areas in the life sciences.

Many biological processes follow a set timetable, with levels of activity rising and dipping at certain times of the day. Such fluctuations, known as circadian rhythms, are driven by internal “body clocks” based on an approximately 24-hour period – synchronized to light-dark cycles and other cues in an organism’s environment. Disruption to this optimum timing system in both animal models and in humans can cause imbalances, leading to such diseases as obesity, metabolic syndrome and fatty liver. Night-shift workers, for example, have been shown to have higher incidence of these diseases. 

Image: Thinkstock

In studying the role of circadian rhythm in the accumulation of lipids in the liver, postdoctoral fellow Yaarit Adamovich and the team in the lab of Dr. Gad Asher of the Weizmann Institute’s Biological Chemistry Department, together with scientists from Dr. Xianlin Han’s lab in the Sanford-Burnham Medical Research Institute, Orlando, US, quantified hundreds of different lipids present in the mouse liver. They discovered that a certain group of lipids, namely the triglycerides (TAG), exhibit circadian behavior, with levels peaking about eight hours after sunrise. The scientists were astonished to find, however, that daily fluctuations in this group of lipids persist even in mice lacking a functional biological clock, albeit with levels cresting at a completely different time – 12 hours later than the natural schedule. “These results came as a complete surprise: One would expect that if the inherent clock mechanism is ‘dead,’ TAG could not accumulate in a time-dependent fashion,” says Adamovich. So what was making the fluctuating lipid levels “tick” if not the clocks? “One thing that came to mind was that, since food is a major source of lipids – particularly TAG – the eating habits of these mice might play a role.” Usually, mice consume 20% of their food during the day and 80% at night. However, in mice lacking a functional clock, the team noted that they ingest food constantly throughout the day. This observation excluded the possibility that food is responsible for the fluctuating patterns seen in TAG levels in these mice. 

When the scientists proceeded to check the effect of an imposed feeding regimen upon wild type mice, however, they were in for another surprise: After they provided the same amount of food – but restricted 100% of the feeding to nighttime hours – the team observed a dramatic 50% decrease in overall liver TAG levels. 

These results suggest that the time at which TAG accumulation occurs, as well as its levels, are determined by the clocks together with timing of meals. The details of the mechanism that drives the actual fluctuating behavior are yet to be discovered. 

Asher: “The striking outcome of restricted nighttime feeding – lowering liver TAG levels in the very short time period of 10 days in the mice – is of clinical importance. Hyperlipidemia and hypertriglyceridemia are common diseases characterized by abnormally elevated levels of lipids in blood and liver cells, which lead to fatty liver and other metabolic diseases. Yet no currently available drugs have been shown to change lipid accumulation as efficiently and drastically as simply adjusting meal time – not to mention the possible side effects that may be associated with such drugs.” Of course, mice are nocturnal animals, so in order to construe these results for humans, the timetable would need to be reversed. 

Time is a crucial element in all biological systems, so these findings are likely to impact biological research in general: Circadian clock mechanisms function even in cultured cells, so research results could vary depending on the time at which samples are analyzed, or, with animals, their feeding regimen might significantly affect the experimental outcomes. In other words, when it comes to designing experiments, scientists should be aware that “timing is everything.”

 

 

Dr. Gad Asher’s research is supported by the Willner Family Leadership Institute; the Yeda-Sela Center for Basic Research; the Adelis Foundation; the Abisch Frenkel Foundation for the Promotion of Life Sciences; the Samuel M. Soref & Helene K. Soref Foundation; the late Rudolfine Steindling; and the Estate of Dorothy Geller.

 

Popular blood type diet (Eat Right for Your Type) debunked

 

Researchers from the University of Toronto (U of T) have found that the theory behind the popular blood type diet--which claims an individual's nutritional needs vary by blood type--is not valid. The findings are published this week in PLoS One.

"Based on the data of 1,455 study participants, we found no evidence to support the 'blood-type' diet theory," said the senior author of the study, Dr. Ahmed El-Sohemy, Associate Professor and Canada Research Chair in Nutrigenomics at the U of T.

"The way an individual responds to any one of these diets has absolutely nothing to do with their blood type and has everything to do with their ability to stick to a sensible vegetarian or low-carbohydrate diet," said El-Sohemy.

Researchers found that the associations they observed between each of the four blood-type (A, B, AB, O) diets and the markers of health are independent of the person's blood type.

The 'blood-type' diet was popularized in the book Eat Right for Your Type, written by naturopath Peter D'Adamo. The theory behind the diet is that the ABO blood type should match the dietary habits of our ancestors and people with different blood types process food differently. According to the theory, individuals adhering to a diet specific to one's blood type can improve health and decrease risk of chronic illness such as cardiovascular disease. The book was a New York Times best-seller that has been translated into 52 languages and sold over 7 million copies.

The U of T researchers took an existing population of mostly young and healthy adults who provided detailed information about their usual diets and provided fasting blood that was used to isolate DNA to determine their ABO blood type and the level of cardiometabolic risk factors, such as insulin, cholesterol and triglycerides. Diet scores were calculated based on the food items listed in Eat Right for Your Type to determine relative adherence to each of the four 'blood-type' diets.

El-Sohemy says that a previous lack of scientific evidence doesn't mean the diets didn't work. "There was just no evidence, one way or the other. It was an intriguing hypothesis so we felt we should put it to the test. We can now be confident in saying that the blood type diet hypothesis is false." Last year, a comprehensive review published in the American Journal of Clinical Nutrition found no evidence to support the 'blood-type' diet and called for properly designed scientific studies to address it.

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How fiber prevents diabetes and obesity

           

Scientists have known for the past twenty years that a fiber-rich diet protects the organism against obesity and diabetes but the mechanisms involved have so far eluded them. A French-Swedish team including researchers from CNRS, Inserm and the Université Claude Bernard Lyon 1 (Unité Inserm 855 “Nutrition et Cerveau”) has succeeded in elucidating this mechanism, which involves the intestinal flora and the ability of the intestine to produce glucose between meals. These results, published in the journal Cell on 9 January 2014, also clarify the role of the intestine and its associated microorganisms in maintaining glycaemia. They will give rise to new dietary recommendations to prevent diabetes and obesity.   

© Inserm / MITHIEUX G. & BESNARD P The enzyme responsible for the final reaction in intestinal glucose production is highlighted by immunofluorescence (red) using confocal microscopy. 

Most sweet fruit and many vegetables such as salsify, cabbage or beans are rich in so-called fermentable fibers. Such fibers cannot be digested directly by the intestine but are instead fermented by intestinal bacteria into short-chain fatty acids such as propionate and butyrate, which can in fact be assimilated by our bodies. The protective effect of these fibers is well known to researchers: animals fed a fiber-rich diet become less fat and are less likely to develop diabetes than animals fed a fiber-free diet. Nevertheless, the mechanism behind this effect has until now remained a mystery.

The team headed by Gilles Mithieux, CNRS researcher in the “Nutrition et Cerveau” unit (Inserm / Université Claude Bernard Lyon 1), wondered whether this mechanism could be linked to the capacity of the intestine to produce glucose. The intestine is in fact capable of synthesizing this sugar and releasing it into the blood stream between meals and at night. However, glucose has particular properties: it is detected by the nerves in the walls of the portal vein (which collects the blood coming from the intestine), which in turn sends a nerve signal to the brain. In response, the brain triggers a range of protective effects against diabetes and obesity: the sensation of hunger fades, energy expenditure at rest is enhanced and, last but not least, the liver produces less glucose.

In order to make the connection between fermentable fibers and the production of glucose by the intestine, the researchers subjected rats and mice to diets enriched with fermentable fibers, or with propionate or butyrate. They then observed a strong induction of the expression of genes and enzymes responsible for the synthesis of glucose in the intestine. They showed that the intestine of these animals used propionate as precursor to increase the production of glucose. Mice fed a fat- and sugar-rich diet, but supplemented with fibers, became less fat than control mice and were also protected against the development of diabetes thanks to significantly increased sensitivity to insulin.

The researchers repeated the experiment with mice whose intestine’s ability to produce glucose had been suppressed by genetic engineering. No protective effect was then observed: these mice became fat and developed diabetes like those fed a fiber-free diet. It is therefore the production of glucose by the intestine from propionate and butyrate that is behind the positive effects of fermentable fibers on the organism.

Apart from this previously unknown mechanism, this work sheds light on the role of the intestinal flora which, by fermenting dietary fiber, provides the intestine with precursors to produce glucose. It also demonstrates the importance of the intestine in the regulation of glucose in the body. Finally, these findings should make it possible to propose nutritional guidelines and to highlight new therapeutic targets for preventing or treating diabetes and obesity.

TO CITE THIS PAGE : Press release –   Inserm press room – How fiber prevents diabetes and obesity
Link : http://presse-inserm.fr/en/how-fiber-prevents-diabetes-and-obesity/10631/

New compounds discovered that are hundreds of times more mutagenic

New      

       

CORVALLIS, Ore. – Researchers at Oregon State University have discovered novel compounds produced by certain types of chemical reactions – such as those found in vehicle exhaust or grilling meat - that are hundreds of times more mutagenic than their parent compounds which are known carcinogens.

These compounds were not previously known to exist, and raise additional concerns about the health impacts of heavily-polluted urban air or dietary exposure. It’s not yet been determined in what level the compounds might be present, and no health standards now exist for them.

The findings were published in December in Environmental Science and Technology, a professional journal.

The compounds were identified in laboratory experiments that mimic the type of conditions which might be found from the combustion and exhaust in cars and trucks, or the grilling of meat over a flame.

“Some of the compounds that we’ve discovered are far more mutagenic than we previously understood, and may exist in the environment as a result of heavy air pollution from vehicles or some types of food preparation,” said Staci Simonich, a professor of chemistry and toxicology in the OSU College of Agricultural Sciences.

“We don’t know at this point what levels may be present, and will explore that in continued research,” she said.

The parent compounds involved in this research are polycyclic aromatic hydrocarbons, or PAHs, formed naturally as the result of almost any type of combustion, from a wood stove to an automobile engine, cigarette or a coal-fired power plant. Many PAHs, such as benzopyrene, are known to be carcinogenic, believed to be more of a health concern that has been appreciated in the past, and are the subject of extensive research at OSU and elsewhere around the world.

The PAHs can become even more of a problem when they chemically interact with nitrogen to become “nitrated,” or NPAHs, scientists say. The newly-discovered compounds are NPAHs that were unknown to this point.

This study found that the direct mutagenicity of the NPAHs with one nitrogen group can increase 6 to 432 times more than the parent compound. NPAHs based on two nitrogen groups can be 272 to 467 times more mutagenic. Mutagens are chemicals that can cause DNA damage in cells that in turn can cause cancer.

For technical reasons based on how the mutagenic assays are conducted, the researchers said these numbers may actually understate the increase in toxicity – it could be even higher.

These discoveries are an outgrowth of research on PAHs that was done by Simonich at the Beijing Summer Olympic Games in 2008, when extensive studies of urban air quality were conducted, in part, based on concerns about impacts on athletes and visitors to the games.

Beijing, like some other cities in Asia, has significant problems with air quality, and may be 10-50 times more polluted than some major urban areas in the U.S. with air concerns, such as the Los Angeles basin.

An agency of the World Health Organization announced last fall that it now considers outdoor air pollution, especially particulate matter, to be carcinogenic, and cause other health problems as well. PAHs are one of the types of pollutants found on particulate matter in air pollution that are of special concern.

Concerns about the heavy levels of air pollution from some Asian cities are sufficient that Simonich is doing monitoring on Oregon’s Mount Bachelor, a 9,065-foot mountain in the central Oregon Cascade Range. Researchers want to determine what levels of air pollution may be found there after traveling thousands of miles across the Pacific Ocean.

This work was supported by the National Institute of Environmental Health Sciences and the National Science Foundation. It’s also an outgrowth of the Superfund Research Program at OSU, funded by the NIEHS, that focuses efforts on PAH pollution. Researchers from the OSU College of Science, the University of California-Riverside, Texas A&M University, and Peking University collaborated on the study.