Cardiologists are increasingly checking patients’ unique genetic profiles as a first step in caring for them. This may partly explain why the American Heart Association last year elected a UAB genetic epidemiologist as its president in Donna Arnett, Ph.D. As her term ends this week, we thought to talk to her about her year in office and what's next in the treatment of massive, global health problems like high blood pressure.
Within the UAB School of Public Health, Dr. Arnett is chair of the Department of Epidemiology, the science that examines patterns in populations, including who is at risk for major diseases and why. She leads several nationwide studies looking at whether genetic variations in each person make them more at risk for heart diseases – or less likely to respond to commonly used anti-cholesterol or anti-inflammatory drugs.
What came across is her passion for scientific inquiry and determination to find better treatments for the families at higher risk for heart disease thanks to their genes. At the same time, she is the first to recommend that Americans get some exercise and eat better, rather than depend on genetics to eventually yield cures.
Show notes for the podcast:
1:40 Dr. Arnett began her career as a clinical research nurse working in a veterans hospital, and proceeded to become a leading genetic epidemiologist in cardiology and AHA president. Much of her inspiration has come from her strong curiosity, a need to ask questions. Early in her career at the veterans hospital, she wanted to know, for instance, why African Americans with the same level of high blood pressure as whites often had more serious kidney damage. Why were African Americans also more likely to have left ventricular hypertrophy. It's a thickening of the muscle in the left ventricle, one of the heart's chambers, that comes with fibrosis (scarring) and increased risk for heart attack and stroke. Why did people have different responses to the same doses of the same drug?
2.04 Unanswered questions drove her forward into the field of genetic epidemiology just as it was being founded. She said it was just good luck that she got into a field just as it was taking off.
3:00 She worked as a research nurse in general cardiovascular studies, but her office at the time was down the hall from the hospital's dialysis center. She got to know some of the veterans, and was struck by how many of the dialysis patients with severe kidney damage were African Americans. The experience brought home the human cost of the genetic contribution to disease.
4:15 Dr. Arnett said cardiology as a field is behind neurology and oncology, not only in genetic epidemiology, but also in pharmacogenomics, the study of the effect of each person's genetic variations on their response to drug treatments.
5:25 In her speech last year as began her term as AHA president, Dr. Arnett spoke about on the theme of “transforming cardiovascular health through genes and environment.” As a genetic epidemiologist she has a passionate interest in searching for genetic clues that may influence each person's disease risk. Some families with no traditional risk factors (not overweight; don't smoke) have struggled with tremendous disease burden and premature deaths. So learning how genes contribute to that is a must. That said, the thing that could save most lives from heart disease in America today would be a focus on environmental factors like the obesity epidemic. Our lifestyle is dominated by processed foods and sedentary inactivity, so Dr. Arnett believes we need to be "battling at both ends."
6:50 A focus of Dr. Arnett's tenure as AHA president has been hypertension or high blood pressure. It affects more than a billion people in the world, and does tremendous damage. On the bright side, nations and international institutions are starting to pay attention. The United Nations has held summits in recent years on diseases like hypertension that are caused by diet and lifestyle, where past efforts focused on infectious diseases. The World Health Organization has launched a campaign meant to reduce non-communicable diseases by 25 percent by 2025, with hypertension as a major focus.
7:25 In the U.S., the American Heart Association this year has partnered with the Million Hearts Initiative led by the Department of Health and Human Services, in an effort to prevent one million heart attacks in the next four years. The partnership will seek to achieve this goal through a combination of awareness campaigns, better access to care, new monitoring programs and initiatives that help people to take their medicine. Dr. Arnett said only a multi-pronged approach that include individuals, physicians, pharmacists, employers, companies and government agencies, combined with culture change, has a chance of making a difference. New technologies may help the cause, including smart phone apps that monitor blood pressure and upload it directly to a patient's electronic medical record.
9:45 The field of genetics within cardiology continues its high-speed evolution, she said. It's moving toward analysis of each person's entire gene code, or genome, to look for small differences that contribute to that person's risk for heart disease. Past approaches that tried to find a few genetic differences that placed large numbers of people at risk across populations are giving way to the study of individuals. Technologies have evolved to the point that whole genome sequencing of individuals is becoming affordable. It is being used around the country, said Dr. Arnett, to help diagnose diseases that seemingly have no cause. She and her colleagues are also using it to search for rare genetic variations that cause higher risk for left ventricular hypertrophy in some families.
11:45 Dr. Arnett has focused on left ventricular hypertrophy in her work because it is one of the four basic causes of heart disease -- along with smoking, high blood pressure and high cholesterol -- first identified by the landmark Framingham Heart Study in 1967. It is also the only one of the four that still has no known treatment for it (apart from lowering blood pressure).
12:38 The modern day life of the human body has changed drastically from the one in which it evolved, said Dr. Arnett. We went from running constantly to hunt and eating mostly plants during the first 8,000 generations of human existence, to sitting on the couch eating a steady diet of fatty, heavily salted food for the last four generations. Looking back even further, Dr. Arnett said, we evolved from saltwater fish, and with fine-tuned bodily mechanisms for regulating salt. The refrigeration and processing of food came about after World War II, drastically changing the way we eat. Heavily salted foods have changed the fluid balance in our bodies, which is regulated by the kidneys, to result in pandemic high blood pressure. Our genes may be slowly evolving to better handle salt but it will take many generations. .
Showing posts with label obesity. Show all posts
Showing posts with label obesity. Show all posts
Thursday, June 27, 2013
Thursday, February 14, 2013
Obesity, exercise and epigenetics: no excuses
No excuses. It's the mantra of many a fitness boot camp and weight room. But what if your genes make you more likely to store fat on your body or less likely to lose weight when you exercise?
In the experience of Molly Bray, Ph.D., professor of epidemiology and genetics at UAB, the many obese people she has worked with do not see genetic barriers to weight loss as excuses. To the contrary, learning that their genes are making it harder to lose weight is empowering. New enthusiasm and harder workouts replace the frustration of doing everything your doctor tells you and getting nowhere.
Along with counseling people about genetic components of obesity risk, Bray leads a research effort to understand the mechanisms behind them. As she explained in her presentation at a recent UAB Epigenetics Symposium, some people have versions of genes that contribute to obesity. Risk may be influenced further by epigenetic chemical reactions that determine when genes that control energy use are turned on or off.
To recap for this third podcast in our epigenetics series, the human genetic system is composed of more than genes, the long stretches of DNA that encode instructions for the building of proteins. Proteins are the workhorse molecules that comprise the body's structures and carry its signals. We inherit genes and proteins from our parents largely unchanged, because changes often cause disease or death, even though they are necessary if we are to evolve.
While genes form the basic instructions for human life, they are not very good at changing quickly as our surroundings change. In fact, you and many like you may have to die (say during a plague) before the gene pool gets around to favoring those who happen to have the mutations (slow, random changes in genes) that make some better adapted to survive.
That may explain why we have epigenetic mechanisms: quick, reversible chemical reactions that turn genes on and off, often in response to environmental cues. Research has revealed that many genes are turned on and off epigenetically based on whether or not we eat good food, breathe clean air and exercise, and these changes have consequences for our risk of developing many diseases, including obesity.
Show notes for the podcast:
1:50 Epigenetic changes proceed very rapidly, some believe within 24 hours, said Bray.
2:23 The Human Genome Project, for all it has revealed about the DNA sequence of our genes, could not account for the variation in risk for many diseases going from person to person. Differences in the mechanisms that regulate genes may explain more about this disease risk variability than differences in genes themselves.
3:29 Methylation, the attachment of a methyl group (one carbon plus three hydrogens) to certain spots in the DNA chain, is recognized as a major epigenetic mechanism. It enables other proteins to assemble there in a way that silences or turns off the surrounding gene. Researchers once thought that such methylation marks were made in the womb and persisted throughout life, an idea which gave rise to theories about the fetal origins of adult disease. Then came the discovery of enzymes called demethylases, which remove methyl groups. The field now understands that methylation is an active process, with epigenetic changes occurring throughout life, some of them in response to our diet and excercise patterns.
4:18 One reason that epigenetic changes may be important for each person's obesity risk has to do with a gene called FTO (fat mass and obesity related transcript), said Bray. Certain versions of this gene are more closely associated with obesity risk than any other gene, with the effect consistently shown in several studies across multiple populations and in people of all ages.
4:55 Researchers theorize that the protein built according to the instructions encoded in the FTO gene may act as a demethylase. Its not known why FTO continues to be associated with obesity, but it could be that an FTO demethylase is turning on or off genes that govern energy balance (e.g. how we burn calories in response to exercise).
5:40 Importantly, regular exercise largely erases the increased risk for obesity associated with the versions of the FTO gene. No one then is doomed by their genes, said Bray, because behavior can change them. A recent, small study showed that a single exercise session changes the methylation status of many genes.
7:24 Bray's lab is currently studying how people respond to exercise. Lack of response to an exercise program can be extremely frustrating, but the answer may be straightforward: work out harder. Her data shows that clinicians can safely increase exercise intensity for many of these patients, and that current treatment guidelines in this regard may need to change. People can tolerate harder workouts if that's what it takes, said Bray.
8:06 Genes may influence several aspects of a person's response to exercise, including the tough combination of making you need higher intensity workouts to get results and less able to tolerate them. Exercise for some may not "feel good."
8:22 Generally when people find out that a genetic or epigenetic variation may be affecting their response to exercise, they don't see it as an excuse. They benefit greatly from the insight, and realize they're not "just lazy," Bray said.
9:55 Obesity is associated with inflammation, the out-of-place triggering of the immune response. Inflammation has been established as one link between obesity and several complex diseases, including cardiovascular disease, diabetes and cancer. Excercise has been shown to counter inflammation. At the intersection of these processes, many of the methylation changes related to exercise and obesity are happening on genes that govern immune responses and inflammation.
Along with counseling people about genetic components of obesity risk, Bray leads a research effort to understand the mechanisms behind them. As she explained in her presentation at a recent UAB Epigenetics Symposium, some people have versions of genes that contribute to obesity. Risk may be influenced further by epigenetic chemical reactions that determine when genes that control energy use are turned on or off.
To recap for this third podcast in our epigenetics series, the human genetic system is composed of more than genes, the long stretches of DNA that encode instructions for the building of proteins. Proteins are the workhorse molecules that comprise the body's structures and carry its signals. We inherit genes and proteins from our parents largely unchanged, because changes often cause disease or death, even though they are necessary if we are to evolve.
While genes form the basic instructions for human life, they are not very good at changing quickly as our surroundings change. In fact, you and many like you may have to die (say during a plague) before the gene pool gets around to favoring those who happen to have the mutations (slow, random changes in genes) that make some better adapted to survive.
That may explain why we have epigenetic mechanisms: quick, reversible chemical reactions that turn genes on and off, often in response to environmental cues. Research has revealed that many genes are turned on and off epigenetically based on whether or not we eat good food, breathe clean air and exercise, and these changes have consequences for our risk of developing many diseases, including obesity.
Show notes for the podcast:
1:50 Epigenetic changes proceed very rapidly, some believe within 24 hours, said Bray.
2:23 The Human Genome Project, for all it has revealed about the DNA sequence of our genes, could not account for the variation in risk for many diseases going from person to person. Differences in the mechanisms that regulate genes may explain more about this disease risk variability than differences in genes themselves.
3:29 Methylation, the attachment of a methyl group (one carbon plus three hydrogens) to certain spots in the DNA chain, is recognized as a major epigenetic mechanism. It enables other proteins to assemble there in a way that silences or turns off the surrounding gene. Researchers once thought that such methylation marks were made in the womb and persisted throughout life, an idea which gave rise to theories about the fetal origins of adult disease. Then came the discovery of enzymes called demethylases, which remove methyl groups. The field now understands that methylation is an active process, with epigenetic changes occurring throughout life, some of them in response to our diet and excercise patterns.
4:18 One reason that epigenetic changes may be important for each person's obesity risk has to do with a gene called FTO (fat mass and obesity related transcript), said Bray. Certain versions of this gene are more closely associated with obesity risk than any other gene, with the effect consistently shown in several studies across multiple populations and in people of all ages.
4:55 Researchers theorize that the protein built according to the instructions encoded in the FTO gene may act as a demethylase. Its not known why FTO continues to be associated with obesity, but it could be that an FTO demethylase is turning on or off genes that govern energy balance (e.g. how we burn calories in response to exercise).
5:40 Importantly, regular exercise largely erases the increased risk for obesity associated with the versions of the FTO gene. No one then is doomed by their genes, said Bray, because behavior can change them. A recent, small study showed that a single exercise session changes the methylation status of many genes.
7:24 Bray's lab is currently studying how people respond to exercise. Lack of response to an exercise program can be extremely frustrating, but the answer may be straightforward: work out harder. Her data shows that clinicians can safely increase exercise intensity for many of these patients, and that current treatment guidelines in this regard may need to change. People can tolerate harder workouts if that's what it takes, said Bray.
8:06 Genes may influence several aspects of a person's response to exercise, including the tough combination of making you need higher intensity workouts to get results and less able to tolerate them. Exercise for some may not "feel good."
8:22 Generally when people find out that a genetic or epigenetic variation may be affecting their response to exercise, they don't see it as an excuse. They benefit greatly from the insight, and realize they're not "just lazy," Bray said.
9:55 Obesity is associated with inflammation, the out-of-place triggering of the immune response. Inflammation has been established as one link between obesity and several complex diseases, including cardiovascular disease, diabetes and cancer. Excercise has been shown to counter inflammation. At the intersection of these processes, many of the methylation changes related to exercise and obesity are happening on genes that govern immune responses and inflammation.
Wednesday, January 30, 2013
Top Seven Obesity Myths
We “just know” that having sex burns enough calories to make a difference, breastfeeding protects a baby against future obesity and gym classes keep kids thin.
It turns out these are among many popular obesity myths; widespread beliefs held dearly despite evidence to the contrary. That is the conclusion of an article just published in the New England Journal of Medicine. Such inaccurate beliefs, the authors argue, are leading to inaccurate public health recommendations, wasted resources and a less healthy America.
David Allison, Ph.D., associate dean for science in the UAB School of Public Health, led a research team that analyzed articles published in the scientific and popular press to separate myths from evidence-supported facts.
The authors also defined six “presumptions” – beliefs held to be true even though more studies are needed. For instance, some have presented as fact the idea that regularly eating versus skipping breakfast contributes to weight loss, but the few studies that have been done have found no effect.
The team identified research-proven facts as well. Weight-loss programs for overweight children that involve parents and the child’s home, for instance, achieve better results than programs that take place in schools. Also, many studies show that while genetic factors play a large role in obesity, “heritability is not destiny.” Big enough changes to lifestyle and environment can bring about as much weight loss as the most effective weight-loss drugs. This is the kind of information that should be shaping public policy, Allison said. The most valuable message is an old, unpopular one: eat less in general and use up more energy than you take in.
For more on the top myths, presumptions and facts, please see the UAB press release and the NEJM article it covers.
Dr. Allison added that the field should conduct more randomized, controlled clinical trials to answer key obesity questions as it advises the public. This type of study rules out chance effects and counters researcher bias. Public health advocates, says Allison, need to be clear with the public about what has and has not been proven. Mixing seemingly good ideas in with proven ideas does not serve the public good.
Allison said the widespread acceptance of obesity myths and presumptions raises the larger question of why we so often believe things that are not so. The authors identified several factors that seem to contribute to this. One is the “mere exposure effect,” where repeating an idea often enough makes people more likely to believe it. Another factor is that people may like certain ideas so much that they hesitate to let them go despite evidence to the contrary. Then there is the phenomenon of “confirmation bias,” where we tend to systematically seek out only the sources of information that confirm our opinions.
Given this whirlwind of effects, it is a wonder we know anything at all.
It turns out these are among many popular obesity myths; widespread beliefs held dearly despite evidence to the contrary. That is the conclusion of an article just published in the New England Journal of Medicine. Such inaccurate beliefs, the authors argue, are leading to inaccurate public health recommendations, wasted resources and a less healthy America.
The authors also defined six “presumptions” – beliefs held to be true even though more studies are needed. For instance, some have presented as fact the idea that regularly eating versus skipping breakfast contributes to weight loss, but the few studies that have been done have found no effect.
The team identified research-proven facts as well. Weight-loss programs for overweight children that involve parents and the child’s home, for instance, achieve better results than programs that take place in schools. Also, many studies show that while genetic factors play a large role in obesity, “heritability is not destiny.” Big enough changes to lifestyle and environment can bring about as much weight loss as the most effective weight-loss drugs. This is the kind of information that should be shaping public policy, Allison said. The most valuable message is an old, unpopular one: eat less in general and use up more energy than you take in.
For more on the top myths, presumptions and facts, please see the UAB press release and the NEJM article it covers.
Dr. Allison added that the field should conduct more randomized, controlled clinical trials to answer key obesity questions as it advises the public. This type of study rules out chance effects and counters researcher bias. Public health advocates, says Allison, need to be clear with the public about what has and has not been proven. Mixing seemingly good ideas in with proven ideas does not serve the public good.
Allison said the widespread acceptance of obesity myths and presumptions raises the larger question of why we so often believe things that are not so. The authors identified several factors that seem to contribute to this. One is the “mere exposure effect,” where repeating an idea often enough makes people more likely to believe it. Another factor is that people may like certain ideas so much that they hesitate to let them go despite evidence to the contrary. Then there is the phenomenon of “confirmation bias,” where we tend to systematically seek out only the sources of information that confirm our opinions.
Given this whirlwind of effects, it is a wonder we know anything at all.
Monday, November 12, 2012
Do gut bugs drive cancer risk?
So far, 2012 has been the year of the human microbiome. That's the set of bacteria, viruses and fungi living on our skin, up our noses and in our mouths and guts. The subject made national news in June when the Human Microbiome Project, a massive, NIH-funded effort to catalog the mix of bugs living on and in Americans, reported its first results.
Our ancestors first “invited in” gut bugs, for instance, 450 million years ago because doing so let them harness bacterial enzymes to get more energy from more kinds of food. Today, microbes contribute 360 times as many genes responsible for the human ability to convert food into energy as human genes themselves. Humans and their bugs may now represent a single super-organism.
With the typical set of bugs now outlined, researchers are searching for the bug profiles that correlate with diseases. New understanding of our complex microbial communities is laying the foundation for advances in the treatment of infectious, autoimmune and inflammatory diseases, including the process by which inflammation contributes to cancer. The work could even make possible prescription fecal transplants that replace disease-causing microbiomes.
Against this backdrop, the UAB Comprehensive Cancer Center chose "cancer and the microbiome" as the theme for its recent research retreat. The Mix interviewed several retreat presenters, each a nationally recognized expert in the area, and will feature the chats as a podcast series over the next few weeks.
Our guest today is Casey Morrow, Ph.D., professor in the UAB Department of Cell, Developmental and Integrative Biology and the retreat’s organizer.
Show notes from the podcast:
0:45 We would be unable to digest most of our food without our microbiome — and it may have helped to establish our immune system. The wrong bugs, though — or our immune system’s reaction to them — also help to drive many infectious and inflammatory diseases, possibly including heart disease and cancer.
1:25 The microbiome is a name for the complex communities of microbes found on and in the various habitats around the body. Over the last 10 years, the field has found that a person's mix of bugs can be extremely helpful or dangerous to them.
2:24 Human microbes have become a subject of greater interest with the realization that we exist in symbiosis with them; that they are a part of us.
2:57 Along with aiding in the digestion of food, these bacteria, viruses and fungi have a complex and ancient relationship with our immune system. In one sense, they teach our immune system how to tell the difference between helpful and destructive bugs, and whether or not to ramp up an immune response. The latter is a crucial decision, because immune responses fight disease in the right context, but they also cause unwanted inflammation when they misfire.
3:12 The field has come to recognize that inflammation caused by an overactive immune system, sometimes in reaction to helpful gut bacteria, contributes to a variety of diseases, including cancer. Beyond triggering immune responses out of turn, some bugs may also release compounds themselves that damage DNA and contribute to cancer risk.
4:16 The team organized this retreat based on the UAB Cancer Center's strategic plan, which reflects work in many labs showing that a person's bug profile not only contributes to inflammation, cancer and obesity, but that all of them influence each other.
5:19 Dr. Morrow and colleagues established a UAB Microbiome Core within the Cancer Center with the help of Cancer Center director Edward Partridge, M.D., but the core is in the process of expanding into a university-wide effort.
6:42 The core is set up such that UAB researchers can easily add microbiome analysis to their ongoing studies of many diseases with a "one-stop shopping" approach. Researchers can bring in samples of microbes from mouths, guts or other habitats in patients or study animals, and the team will analyze the microbiomes. After core scientists prepare the DNA for the client, they hand it off to Michael Crowley, Ph.D., and his team at UAB's Heflin Center for Genomic Science. These researchers determine the sequences of the DNA chains in the bug genetic material, and then send the vast amounts of genetic data they generate through high-speed sequencing techniques to Eliott Lefkowitz, Ph.D., who leads UAB's Molecular and Genetic Bioinformatics Facilty. His team then provides the client with the identities of the bugs in the sample.
8:19 As they conduct clinical trials, researchers interested in diabetes, cancer and obesity can collect samples, store them for later analysis with the microbiome core, and look for associations between microbiomes and pathology. Such analyses promise to help track microbial communities in a given person as he or she goes from health to any given disease state.
9:43 The consensus now is that microbial communities are actively driving health and disease. We even have currently available cultures, yogurts and pills that change the microbiome in the mouth or gut to improve health, part of a billion-dollar industry.
11:25 Presenters at the UAB symposium were among the pioneers that showed the differences between the gut microbiomes of obese and thin people. The UAB microbiome core works closely with UAB's Gnotobiotic and Genetically Engineered Mouse Core, led by Casey Weaver, M.D. Gnotobiotic mice are genetically engineered and raised to have no gut microbiome, and fascinatingly, can be made to gain significant weight if the microbial gut community from an obese human is transplanted into them.
12:29 The gnotobiotic facility offers a system for studying how you can transplant microbiomes from healthy individuals to obese ones, which becomes vital when the goal is to perform such transplants in humans a few years down the road.
With the typical set of bugs now outlined, researchers are searching for the bug profiles that correlate with diseases. New understanding of our complex microbial communities is laying the foundation for advances in the treatment of infectious, autoimmune and inflammatory diseases, including the process by which inflammation contributes to cancer. The work could even make possible prescription fecal transplants that replace disease-causing microbiomes.
Against this backdrop, the UAB Comprehensive Cancer Center chose "cancer and the microbiome" as the theme for its recent research retreat. The Mix interviewed several retreat presenters, each a nationally recognized expert in the area, and will feature the chats as a podcast series over the next few weeks.
Our guest today is Casey Morrow, Ph.D., professor in the UAB Department of Cell, Developmental and Integrative Biology and the retreat’s organizer.
Show notes from the podcast:
0:45 We would be unable to digest most of our food without our microbiome — and it may have helped to establish our immune system. The wrong bugs, though — or our immune system’s reaction to them — also help to drive many infectious and inflammatory diseases, possibly including heart disease and cancer.
1:25 The microbiome is a name for the complex communities of microbes found on and in the various habitats around the body. Over the last 10 years, the field has found that a person's mix of bugs can be extremely helpful or dangerous to them.
2:24 Human microbes have become a subject of greater interest with the realization that we exist in symbiosis with them; that they are a part of us.
2:57 Along with aiding in the digestion of food, these bacteria, viruses and fungi have a complex and ancient relationship with our immune system. In one sense, they teach our immune system how to tell the difference between helpful and destructive bugs, and whether or not to ramp up an immune response. The latter is a crucial decision, because immune responses fight disease in the right context, but they also cause unwanted inflammation when they misfire.
3:12 The field has come to recognize that inflammation caused by an overactive immune system, sometimes in reaction to helpful gut bacteria, contributes to a variety of diseases, including cancer. Beyond triggering immune responses out of turn, some bugs may also release compounds themselves that damage DNA and contribute to cancer risk.
4:16 The team organized this retreat based on the UAB Cancer Center's strategic plan, which reflects work in many labs showing that a person's bug profile not only contributes to inflammation, cancer and obesity, but that all of them influence each other.
5:19 Dr. Morrow and colleagues established a UAB Microbiome Core within the Cancer Center with the help of Cancer Center director Edward Partridge, M.D., but the core is in the process of expanding into a university-wide effort.
6:42 The core is set up such that UAB researchers can easily add microbiome analysis to their ongoing studies of many diseases with a "one-stop shopping" approach. Researchers can bring in samples of microbes from mouths, guts or other habitats in patients or study animals, and the team will analyze the microbiomes. After core scientists prepare the DNA for the client, they hand it off to Michael Crowley, Ph.D., and his team at UAB's Heflin Center for Genomic Science. These researchers determine the sequences of the DNA chains in the bug genetic material, and then send the vast amounts of genetic data they generate through high-speed sequencing techniques to Eliott Lefkowitz, Ph.D., who leads UAB's Molecular and Genetic Bioinformatics Facilty. His team then provides the client with the identities of the bugs in the sample.
8:19 As they conduct clinical trials, researchers interested in diabetes, cancer and obesity can collect samples, store them for later analysis with the microbiome core, and look for associations between microbiomes and pathology. Such analyses promise to help track microbial communities in a given person as he or she goes from health to any given disease state.
9:43 The consensus now is that microbial communities are actively driving health and disease. We even have currently available cultures, yogurts and pills that change the microbiome in the mouth or gut to improve health, part of a billion-dollar industry.
11:25 Presenters at the UAB symposium were among the pioneers that showed the differences between the gut microbiomes of obese and thin people. The UAB microbiome core works closely with UAB's Gnotobiotic and Genetically Engineered Mouse Core, led by Casey Weaver, M.D. Gnotobiotic mice are genetically engineered and raised to have no gut microbiome, and fascinatingly, can be made to gain significant weight if the microbial gut community from an obese human is transplanted into them.
12:29 The gnotobiotic facility offers a system for studying how you can transplant microbiomes from healthy individuals to obese ones, which becomes vital when the goal is to perform such transplants in humans a few years down the road.
Friday, September 21, 2012
Do sugar-sweetened drinks drive obesity?
The Obesity Society opened its annual meeting, Obesity 2012, this week in San Antonio with a debate on that very subject.
In the debate, David Allison, Ph.D., associate dean for science within the UAB School of Public Health and director of the NIH-funded UAB Nutrition Obesity Research Center, faced off against Frank Hu, M.D., Ph.D., professor of Nutrition and Epidemiology at Harvard School of Public Health.
Allison sat down with The Mix to comment on the debate and on related studies just published in the New England Journal of Medicine.
Show notes on the interview
1:25 Sugar-sweetened beverages have figured centrally in public health discussions about obesity for more than a decade. Some evidence has suggested that such drinks may play a unique role. What’s needed now, says Allison, are rigorous studies to prove (or disprove) that reducing consumption of these beverages actually increases weight loss or slows weight gain.
2:02 Public health as a field changed over the last decade as the obesity epidemic became more evident. Advocacy has wrestled with purely scientific discussion, and emotions are running high.
3:44 Valid, scientific study results are a must when deciding whether or not any one factor contributes to, or reduces, obesity, and the standard for that validity is a randomized clinical trial.
4:38 Up until the meeting, the evidence has not been there to demonstrate that reducing sugar-sweetened beverage intake would reduce obesity, according to Allison. In six of the six randomized clinical trials to date, he argues, the primary analysis of all patients studied showed no statistically significant difference in weight gain, weight loss or BMI between those who kept drinking sugary drinks and those who cut back.
5:26 On top of the six clinical trials mentioned, however, a series of papers were just this minute published in the New England Journal of Medicine. Two of the studies — one in children, one in adolescents — did indeed represent the kind of randomized clinical trials Allison has been calling for. The authors of both studies offer valid evidence, Allison says, that reducing consumption of sugar-sweetened beverages reduced weight gain in specific groups under certain conditions, but more studies are needed to confirm that the patterns apply to everyone.
9:23 While sugar-sweetened beverages remain an important area of inquiry, Allison says he thinks other emerging thrusts in obesity research warrant attention as well. These include the roles of sleep, daily weigh-ins and eating vs. skipping breakfast.
10:32 UAB’s Nutrition Obesity Research Center has joined with six other NORCS and a center in Denmark to organize a randomized clinical trial in 300 patients to generate evidence that having or skipping breakfast in the morning affects body weight.
11:36 UAB meeting highlights beyond the presidential debate included a presentation by Nefertiti Durant, M.D., assistant professor in the UAB School of Medicine's Division of General Pediatrics and Adolescent Medicine, as part of a symposium on adjusting obesity prevention approaches to account for a person’s age. Her talk, titled “Freshman 15 and Beyond,” discussed contributing factors and potential solutions. In addition, James Rimmer, Ph.D., Lakeshore Foundation Endowed Chair in Health Promotion and Rehabilitation Sciences in the UAB School of Health Professions, will be talking about how people with intellectual disabilities have higher rates of obesity than the general public based on several factors, including their living arrangements.
13:10 For good information on obesity, Allison recommends the Weight-control Information Network organized by the National Institute of Diabetes and Digestive and Kidney Diseases. He also points to the U.S. Agriculture Department’s Dietary Health page. For researchers, Allison offers the UAB NORC’s seminar series, which is available to all online, goes back 12 years and discusses a great many aspects of nutrition theory and related scientific evidence.
Also important is a recent editorial in the Journal of the American Medical Association by the director of the National Institutes of Health, Francis Collins, M.D., Ph.D. Of the editorial, which argues that public policy must be founded on valid science, Dr. Allison says he couldn’t agree more.
14:22 End podcast
About the podcaster
Greg Williams @gregscience @themixuab is research editor within Media Relations at the University of Alabama at Birmingham.
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