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  • richardmitnick 10:23 am on January 13, 2017 Permalink | Reply
    Tags: , , , , Obesity, Sugar stands accused   

    From Harvard: “Sugar stands accused” This Is Important for All 

    Harvard University

    Harvard University

    Sugar was in the dock at Harvard Law School this week, accused of a prime role in the twin epidemics of obesity and diabetes sweeping the country.

    1
    Gary Taubes signs copies of his book “The Case Against Sugar” following his talk for the Food Law and Policy Clinic. The acclaimed science writer hypothesizes that sugar “has deleterious effects on the human body that lead to obesity and diabetes, and that it should be considered a prime suspect [in the national dietary epidemic].” Stephanie Mitchell/Harvard Staff Photographer

    Science journalist and author Gary Taubes ’77 made his case that sugar consumption — which has risen dramatically over the last century — drives metabolic dysfunction that makes people sick. The hour-long talk was sponsored by the Food Law and Policy Clinic and drawn from Taubes’ new book, The Case Against Sugar.

    A reputation for “empty calories” — devoid of vitamins and nutrients but otherwise no different from other foods containing an equal number of calories — has allowed sugar to maintain a prominent place in the U.S. diet. Taubes is dubious. First, all calories are not equal because the body metabolizes different foods in different ways. More specifically, there may be something about eating too much sugar — in particular fructose, which is metabolized in the liver — that implicates it in metabolic disease.

    “I’m making an argument that sugar is uniquely toxic,” said Taubes. “It has deleterious effects on the human body that lead to obesity and diabetes.”

    Taubes laid out a case that he admitted was “largely circumstantial,” though one he considers compelling enough that it would gain at least an indictment from an impartial jury. The problem with the evidence, he said, is that public health researchers haven’t focused enough attention on sugar.

    “The research doesn’t exist beyond reasonable doubt that sugar is to blame,” Taubes said.

    Diabetes, Taubes noted, was once a rare disease. He traced its rise through the 1800s and 1900s from just a fraction of 1 percent of the cases seen at Massachusetts General Hospital to a condition that afflicts nearly 10 percent of the U.S. population, according to the Centers for Disease Control and Prevention. That increase, he said, coincides with an increase in sugar in the American diet.

    He tied today’s problems to both the sugar industry and some of the scientists responsible for informing the public about diet. Two researchers prominent in Harvard’s history didn’t escape blame: Elliott Joslin, the founder of the Harvard-affiliated Joslin Diabetes Center, and Frederick Stare, the founder of the Harvard T.H. Chan School of Public Health’s Nutrition Department.

    See the full article here .

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    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 9:15 am on January 2, 2015 Permalink | Reply
    Tags: , , Obesity   

    From NYT: “Gene Linked to Obesity Hasn’t Always Been a Problem, Study Finds” 

    New York Times

    The New York Times

    DEC. 31, 2014
    Carl Zimmer

    Among scientists who study how our DNA affects our weight, a gene called FTO stands out. “It’s the poster child for the genetics of obesity,” said Struan F. Grant, an associate professor of pediatrics at the University of Pennsylvania School of Medicine.

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    Decades ago, physical activity may have protected people like this lumber worker from genes that promote obesity, a new study suggests. Credit Hulton Archive/Getty Images

    In 2007, researchers discovered that people with a common variant of FTO tend to be heavier than those without it. Since then, studies have repeatedly confirmed the link. On average, one copy of the risky variant adds up to 3.5 extra pounds of weight. Two copies of the gene bring 7 extra pounds — and increase a person’s risk of becoming obese by 50 percent.

    But the gene doesn’t seem to have always been a problem. If scientists had studied FTO just a few decades ago, they would have found no link to weight whatsoever. A new study shows that FTO became a risk only in people born after World War II.

    The research, published this week in the Proceedings of the National Academy of Sciences, raises questions that extend far beyond obesity. Genes clearly influence our health in many ways, but so does our environment; often, it is the interplay between them that makes the difference in whether we develop obesity or cancer or another ailment.

    But the relative importance of certain genes may shift over the years, the new study suggests, as our environment changes.

    James Niels Rosenquist of Massachusetts General Hospital and his colleagues were inspired to conduct the study by recent research documenting how people’s experiences alter the effects of their genes. A variant of a gene called AKT1, for example, can raise the risk of psychosisbut only if the carrier smokes a lot of marijuana. If e avoids smoking, the AKT1 variant doesn’t cause a problem.

    To document genetic links to disease, scientists have compared people only at a single moment in history, Dr. Rosenquist noted. “They weren’t thinking in the dimension of time, because they didn’t have the data for it,” he said.

    Yet our environment has changed drastically over the past century. We eat different kinds of food today, we have different jobs, and we use different chemicals and technology. Dr. Rosenquist and his colleagues wondered if our genes have had different influences on health at different times in history.

    The scientists decided to focus on FTO, because its effects are so clear. To reconstruct its history, they took advantage of a remarkable study that has been running for over 60 years.

    In 1948, researchers enlisted over 5,000 people in Framingham, Mass., and began to follow their health. In 1971, the so-called Framingham Heart Study also recruited many of the children of original subjects, and in 2002, the grandchildren joined in. In addition to such data as body mass index, the researchers have been gathering information on the genes of their subjects.

    The scientists compared Framingham subjects with the risky variant of FTO to those with the healthy variant. Over all, the scientists confirmed the longstanding finding that people with the risky FTO variant got heavier.

    But when they compared subjects born in different eras, the data told a surprising story.

    People born before the early 1940s were not at additional risk of putting on weight if they had the risky variant of FTO. Only subjects born in later years had a greater risk. And the more recently they were born, the scientists found, the greater the gene’s effect.

    Some change in the way people lived in the late 20th century may have transformed FTO into a gene with a big impact on the risk of obesity, the researchers theorized. Giles S.H. Yeo, a geneticist at the University of Cambridge who wasn’t involved in the study, said he suspected that physical activity had something to do with the change.

    It is possible that before World War II, people were so physically active that they were shielded from FTO’s obesity risks. As people became sedentary, they lost that protection and the gene emerged as a danger.

    Timothy M. Frayling, a geneticist at the University of Exeter Medical School who was not involved in the study, suspects that modern diets also may have increased FTO’s impact.

    He points to recent studies that find that FTO increases appetite. Dr. Frayling also notes that people who eat fried foods or drink sugary beverages gain more weight if they have the FTO variant, compared to those who do not.

    “You could imagine any gene that affects appetite would have a bigger effect in today’s environment, where we all have lots of access to food,” Dr. Frayling said.

    While Dr. Frayling said he thought the new study made sense, he cautioned that it needed to be replicated in bigger groups of people — a difficult task.

    Dr. Nicholas A. Christakis, a sociologist and physician at Yale University and a co-author of the new study, suggested that the influence of many other genes on health had waxed and waned over the past century. Reconstructing this history could drastically influence the way doctors predict disease risk. What might look like a safe version of a gene today could someday become a risk factor.

    “The thing we think is fixed may not be fixed at all,” said Dr. Christakis.

    See the full article here.

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