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    Globesity and Tax in the Far North

    June 30th, 2015


    Childhood Obesity News has been looking back over debates about tax, in recent years, and some of the attempts to implement taxes on soda and junk food to offset the enormous costs of public health care. Around the world, various countries have tried to cope with the problem, experiencing varying degrees of success.

    Freakonomics authors Stephen J. Dubner and Steven D. Levitt attended a seminar, sponsored by the Robert Wood Johnson Foundation, on what to do about childhood obesity, and naturally the subject of a “fat tax” (an umbrella term for taxing various unhealthful goodies) was on the table. Dubner remarked:

    One objection that I was surprised no one raised: the simple fact that taxpayers might hate the tax and rebel against it to the point where it becomes politically and economically impossible.

    As luck would have it, it was during this conference that Denmark announced it was abandoning a brave and innovative fat tax (affecting oil, butter, sausage, cheese and cream) after only a year of implementation. A government assessment found that there had been a negative effect on the economy, and that the tax had been especially damaging to small businesses. In the wake of this decision, the Danish government also gave up on a planned sugar tax.

    In 2014, when Canada was considering a fat tax, people remembered how Jens Klarskov of the Danish Chamber of Commerce had compared the food tax notion to using nuclear weapons for rabbit-hunting—in other words, an unnecessary show of overkill. Journalist Jordan Bateman gave more details on Denmark’s short-lived experiment:

    It was an economic disaster: half of all Danes poured south to shop in cheaper Germany, more than 1,300 Danish jobs were lost, and merchants became snared in red tape.

    The discredited Danish effort set an unsavory precedent that food-tax opponents eagerly cited time after time. This echo came from Gary Dawson CEO of Australia’s Food and Grocery Council (read: industry lobbyists) who said of Denmark’s aborted fat tax:

    It raised food prices, hit the poorest the hardest and failed to bring about any measurable public health benefit—a shocking policy trifecta that no sensible government would want to emulate.

    Of the Nordic countries, Finland is the fattest, but when a poll was commissioned earlier this year to take the public temperature regarding a fat tax, the research company found little enthusiasm. Its news service reported:

    In the questionnaire about one thousand people were asked, among other things, if more tax money should be allocated for dealing with the problem. As many as 57 percent of respondents weren’t keen on this option. So should there be a fat tax—that is, a surcharge for overweight people using healthcare services? As many as 73 percent of respondents opposed such additional charges.

    The researcher also made the sensible point that in Finland, a great deal of the native obesity is attributable to alcohol consumption. Even if it were successfully passed, a fat tax on food would cause social uproar disproportionate to the amount of good effect it might possible have.

    Your responses and feedback are welcome!

    Source: “Fans of a “Fat Tax” Will Be Saddened by the News From Denmark,”, 11/13/12
    Source: “Opinion: Food taxes didn’t work in Denmark and won’t work here,”, 05/22/14
    Source: “Federal Government backed study into fat tax on fast foods,”, 05/21/13
    Source: “Survey: Finns are against fat tax,”, 05/05/15
    Image by Tom Woodward

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    Antibiotics, Babies, and Obesity

    June 29th, 2015

    Check out the curls!

    Childhood Obesity News continues to explore the complicated links between antibiotics, prematurity, ototoxicity, obesity, and epigenetics.

    A child born early is more likely to become obese than a full-term child. To prevent infection, it is likely that antibiotics will be administered to a premature baby, increasing the obesity risk. Antibiotics also increase the likelihood of hearing loss, and a deaf child is more likely than his hearing counterpart to be obese. At the present time, with regard to obesity issues, the deaf community is just beginning to be recognized as understudied and underserved. To confuse matters even more, every passing month brings more evidence that the effects of any and all of these conditions can influence future generations in ways we barely understand.

    In the 1990s in the United Kingdom, the Avon Longitudinal Study showed that children who had received antibiotics during their first half-year of life were more likely to become obese toddlers. In 2012, a study by the New York University School of Medicine confirmed a suspicious relationship between treating babies under six months of age with antibiotics and their tendency to beef up by the time they reach their third year. The researchers theorized that disruption (read: death) of healthy gut bacteria somehow led to over-absorption of calories. Dr. Charles Bailey, from Children’s Hospital of Philadelphia, agreed:

    One of the side effects of [prescribing a] broad-spectrum antibiotic is not just an upset stomach…not just a little bit of diarrhea that will go away in a week, but…an increased risk of being obese 3 years later.

    On the question of whether antibiotic overuse bears any blame for childhood obesity, the answer seems to be affirmative. The nutrients taken in by the body are processed by the intestinal fauna, and if those microorganisms are killed off by antibiotics, trouble ensues. A creature called H. Pylori, for instance, influences the production of the hormones leptin and ghrelin, both of which are connected with obesity.

    By now, it is no surprise that future generations are affected. When a girl grows up with an inadequate supply of beneficial fauna, she is unable to pass along the bacterial birthright to the fetus she gestates, who is born already handicapped by a deficient microbiome. Our intestinal tenants influence our size in other labyrinthine ways, and this problem is non-trivial. Michael Pollan wrote:

    Children in the West receive, on average, between 10 and 20 courses of antibiotics before they turn 18. And those prescribed drugs aren’t the only antimicrobials finding their way to the microbiota; scientists have found antibiotic residues in meat, milk and surface water as well.

    Many activists have tried to warn the public about the ubiquity of these substances. The meat industry accounts for about 70 percent of America’s antibiotic use, which is passed along to any meat-eaters. In a way, the causation of obesity by antibiotics is good news, because that can be changed. There seems to be a slow movement away from meat consumption. On the medical side, retirement is gradually reducing the number of physicians who saw broad-spectrum antibiotics as their go-to answer for everything.

    The awareness of doctors can be raised, and parents can be educated to not blindly demand antibiotics for every sniffle. Better yet, scientists can tweak the molecular structure of the medications themselves, tailoring them to cause less harm. It is difficult and very time-consuming, but do-able, as has been shown by Dr. Anthony Ricci and Dr. Alan Cheng. The exciting story of their quest for an aminoglycoside that does not cause deafness can be found at Stanford University’s website.

    Your responses and feedback are welcome!

    Source: “Early Antibiotic Use Linked to Childhood Obesity,”, 08/21/12
    Source: “Medscape Medical News,”, 11/19/13
    Source: “Some of My Best Friends Are Germs,”, 05/15/13
    Source: “New version of common antibiotic could eliminate risk of hearing loss, study finds,”, 01/02/15
    Image by Howard Lewis Ship


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    The Cheese Roundup

    June 26th, 2015

    eat block of cheese

    When obesity is the topic, cheese is destined to be a star. In Dr. Pretlow’s very useful booklet, “Addiction Model Intervention for Obesity in Young People” it holds a prominent place on the list of problem foods (see page 33).

    Since last discussing cheese, we have collected a few items of cheese trivia. According to Amy Terlisner, NMD, cheese contains the mycotoxin citrinin, a poisonous spore-based life form that may reduce testosterone production and contribute to kidney disease. In her book Life is Hard, Linda Spangle named cheese as one of the specific food types that appeal to a person who is trying to alleviate sadness, rather than some other kind of stress. Many nutrition professionals recommend niacin supplements to counteract cheese cravings.

    By the way, depending on its type, cheese just might contain gluten. It is also purported to contain BCM7, which is suspected of affecting the human body like an opiate, is potentially addictive and definitely hinders weight loss.

    Anti-cheese activists have a way of describing the stuff that can cause a listener to avoid it for days, if not weeks. The same illustration might look enticing or disgusting, either or both—like one titled “Close-up of Nathan’s Chili Cheese Fries.” The photo might also have been taken at the autopsy of a very obese person. The only indication that it was not is the section of decorated ceramic plate.

    How do the corporations and the government conspire to (their words) “trigger the cheese craving?” Why does the U.S. Department of Agriculture maintain a huge agency (with a staff of 160 or so) whose one job is to help fast food companies cram the maximum amount of cheese down the throats of Americans? The Dairy Council named cheese the nation’s #1 snack food. Why is it the prevalent ingredient in almost every fast food genre?

    Substance-Use Disorder in DSM-5” aims to help understand the categories and terminology of the Diagnostic and Statistical Manual. In this fanciful little drama, as the exemplar of an abused substance, cheese is the star. Another previous Childhood Obesity News post contains quotations from young visitors to Dr. Pretlow’s Weigh2Rock website, where many similar messages can be found. In his book, Overweight: What Kids Say, the most relevant and expressive messages have been curated, which provides a certain advantage.

    The same post also recalls words from Jen Kirkman. Indeed, cheese seems to hold a special place in the hearts of comedians. “See what I did there?” as the cheesy ones are fond of saying. Here are two more quotations from contemporary stand-up comedy artists:

    There’s almost no reason to ever eat cheese. It gives you nothing. It’s all only bad.
    —Ari Shaffir

    I think I’d give up sex before cheese.
    —Candice Thompson

    … which segues smoothly into the astonishing news that some people will quit chocolate sooner than renouncing cheese. That is a significant red flag, or ought to be.

    Your responses and feedback are welcome!

    Source: “Against the Grain: Mycotoxins in Our Food,”, October 2012
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    Antibiotics, Prematurity, Ototoxicity, Obesity, and Epigenetics

    June 25th, 2015

    Premie in incubatorAs Childhood Obesity News recently pointed out, deaf children are at greater risk of becoming obese, and that is only one aspect of a complicated five-way relationship between hearing loss, obesity, prematurity, antibiotics, and the passing along of somatic liabilities to descendents. One corner of the puzzle was described by Mathew Dearnaley for the New Zealand Herald:

    Children born prematurely not only risk becoming overweight adults, but they may also hand a legacy of obesity to their own offspring… And although early-born males are far more likely than premature females to pile on unhealthy fat in adulthood…a second generation of children is at greater risk of being overweight compared to other youngsters.

    Researchers from the University of Auckland found that a child whose parent (of either gender) had been born prematurely, would have 12 to 21 percent more body fat than a child of full-term parents. Quoted in the story, Associate Professor Paul Hofman noted:

    So an environmental insult has an impact in the next generation—it has a heritability about it which is quite scary.

    This observation harks back to another recent Childhood Obesity News post, which discussed the work done by Sr. Edward Archer, who realized that depriving pregnant mice of exercise wheels would cause their grandchildren to be fat.

    Returning to the topic at hand, there is a link between pre-term birth and obesity. There is also a link between pre-term birth and antibiotics. In 2009, Jeremy Laurance reported for The Independent:

    An estimated 20,000 premature babies are treated each year with the powerful antibiotics, called aminoglycosides… Genetic specialists at the Institute of Child Health, who reviewed blood samples from over 9,000 children, found one in 500 had a genetic mutation that made them vulnerable to aminoglycosides.

    Premature babies are given antibiotics to bolster their underdeveloped immune systems, but at a horrific price. Such miracle drugs as streptomycin have saved many lives, and have also proven to be ototoxic, poisoning to the ears. Otolaryngologist Anthony Ricci, Ph.D., explains how hearing functions correctly when…

    …sound waves open ion channels within the sensory hair cells of the inner ear, allowing their conversion to electrical signals that eventually reach the brain.

    But aminoglycosides kill those non-regenerating hair cells and cause deafness. Aminoglycoside use is incredibly widespread, since this type of antibiotic treats pneumonia, sepsis, peritonitis, mystifying infections of unknown origin, and bacterial diseases. It is used to prevent these disasters in kids who suffer from cancer, cystic fibrosis, and prematurity.

    Back in 2009, it was believed that only one person in 500 has a genetic mutation making them susceptible to the danger of rogue aminoglycosides. Now, it appears that “an estimated 20-60 percent of all patients who receive these antibiotics suffer partial or complete hearing loss.”

    To temporarily sum up: kids born premature already face increased obesity risk. If they are prophylactically dosed with antibiotics, that adds more obesity risk. The antibiotics might also cause deafness, and for a separate set of reasons, that disability adds more obesity risk. This is the simplest, straight-line scenario, but with so many variables and incidental factors, the landscape quickly becomes one of nightmarish confusion.

    Next time: more about antibiotics and babies

    Your responses and feedback are welcome!

    Source: “Premature birth links to obesity, say researchers,”, 11/23/13
    Source: “Antibiotics Blamed for Child Deafness,”, 02/05/09
    Source: “New version of common antibiotic could eliminate risk of hearing loss, study finds,”, 01/02/15
    Image by Mike Blyth


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    An Overlooked and Under-Served Obese Population: the Deaf

    June 24th, 2015

    Cheerleader in Air take #1

    We are familiar with the idea that in the United States, children of color are more susceptible to forces, including their own genetic makeup, that cause childhood obesity. There is another demographic whose vulnerability has nothing to do with race: the deaf. The conjunction of deafness and obesity is studied by an organization signified by a mouthful of letters: RPRC:NCDHR, which stands for Rochester Prevention Research Center: National Center for Deaf Health Research.

    RPRC is the world’s only research center that employs CBPR, or Community-Based Participatory Research. The Center’s webpage describes “Deaf Strong Hospital 2015,” a role-playing exercise in which deaf people pretend to be health care professionals and professionals, as part of their training, try to explain their medical needs to people who only speak American Sign Language. The results are probably hilarious, and also very revealing of exactly why it has been difficult for the hard-of-hearing population to make its problems understood.

    Studying the Health of the Deaf and Hearing Loss Communities

    RPRC sees two distinct “health disparity communities”—those who were born deaf and learned American Sign Language, and those who lost their hearing somewhere along the way. Both groups are characterized as overlooked, excluded, understudied, and underserved. Also, RPRC holds the belief that education and training are needed for researchers from all three sectors—the hearing, the Deaf, and the hearing loss communities.

    In 2008, RPRC:NCDHR designed a sign language survey and developed “generalizable measures and methods that can be used in research and health surveillance with Deaf populations in other locations.” It included questions from other established studies like the Youth Risk Behavior Survey and the National College Health Assessment. The result was a Deaf Health Survey covering 98 items. In the initial round, most of the respondents were either born deaf or had lost their hearing very early. In 2008:

    Deaf adults reported low rates of current smoking, and higher rates of overweight/obesity, recent suicide attempts and experiences of interpersonal violence.

    The researchers went on to survey adults at the 40th Reunion celebration of the National Technical Institute for the Deaf. The results were similar, and also confirmed that “health disparities exist in deaf groups with high educational attainment.”

    The Deaf Weight Wise Program

    More recently, the university published more information on its Deaf Weight Wise program, a core research project for deaf American Sign Language users designed to “establish the effectiveness of an intervention to reduce weight gain and obesity.” They say with pride:

    To our knowledge, this is the first randomized control trial of a healthy lifestyle intervention to be conducted in a Deaf population.

    Some of the reasons why deaf people would become obese are easy to understand. Hearing people have stimuli coming in all the time, whether intentional like listening to music, or accidental like the constant ongoing hum of ambient noise that accompanies life. A hearing person can listen to a radio show or podcast, or talk on the phone, or eavesdrop on other people’s interesting conversations, while doing any number of other things like peeling potatoes, mowing the lawn, driving, or catching some rays. A deaf person cannot multi-task in the same way.

    The lonely, profound boredom of deafness is difficult to imagine, but when assessing the impact, it helps to remember that sensory deprivation is used as a form of torture. Then there is the fact that when one sense is lost, the others become more acute. However much pleasure a hearing person gets from a piece of strawberry pie, it’s possible that a deaf person enjoys it even more.

    A brand new report from Padbury, Australia, (a suburb of Perth) describes the Active Deaf Kids program,designed to tackle the problem. Irena Farinacci of the basketball Deaflympians (and a Deaf Sports Australia development officer) told reporter Mark Donaldson that deaf children have significantly fewer opportunities to participate in sports than their hearing classmates. Last month, 60 kids attended when Farinacci presented an event, along with other deaf athletes from basketball, cricket, and soccer, designed to inspire younger children to participate more and become more fit.

    And then…there are the antibiotics, which can also be a factor, and which we will discuss next time.

    Your responses and feedback are welcome!

    Source: “About RPRC:NCDHR,”, undated
    Source: “Deaf Health Survey 2008: Determinants of Health Risk in the Deaf Population,”, 2008
    Source: “An Update on Deaf Weight Wise (2009-2014)”, 2014
    Source: “Active inspiration,”, 06/23/15
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    The Obesity Tax Landscape in 2012

    June 23rd, 2015

    Luxury Taxes for the Rich

    Childhood Obesity News has been looking back at how the anti-tobacco model has influenced the idea of taxing junk food and sugar-sweetened beverages.

    Alcohol and tobacco are heavily taxed, with the revenues supposedly going to help pay for the medical havoc wreaked by those substances. Sugar-sweetened drinks, or soda pop, or fizzy beverages—whatever we call them, the debate goes on about whether they should be taxed so the government can make some money that (in theory anyway) can be used to treat health conditions caused by obesity.

    All along, one of the big stories has been Michelle Obama’s determination to end childhood obesity. Another has been the administration’s strangely cozy relationship with giant food corporations in ways that seem in direct contradiction to her well-publicized Let’s Move! crusade. Bridget Huber is one critic who has questioned whether the First Lady’s anti-obesity campaign has been too tolerant of Big Food.

    Echoing Dr. Kelly Brownell’s sentiment that, “History is littered with unfulfilled industry promises to protect kids’ health,” Huber gave the example of the 2009 “Smart Choices” initiative dreamed up by 14 major food companies. Supposedly illustrating how well the industry could self-police, the program awarded little green “smart choice” checkmarks to the packaging of Lucky Charms, Fudgsicles, and other absurd products. Detractors have described these self-policing schemes as the fox guarding henhouse, or the lunatics running the asylum.

    Will Taxes Cure Obesity? What About Healthcare?

    Huber’s analysis of Michelle Obama’s vexed relationship with the industry included a look at the Partnership for a Healthier America, funded not only by seemingly neutral foundations, but by the food manufacturers themselves. The Healthy Weight Commitment Foundation, a consortium of 16 of the biggest food companies, made a pledge to remove 1.5 trillion calories from their products by 2015, which would take the number of calories they sold back to the 2007 baseline level, which was nothing to be proud of even then.

    According to the American Journal of Preventative Medicine, that goal has already been accomplished, the 16 companies having sold 6.4 trillion fewer calories by 2012 than in 2007. This supposedly reduced the average America’s calorie intake by 99 calories per day, but whether it has made any actual difference has yet to be evaluated. The CUNY School of Public Health has been chosen for the task.

    An agreement from Walmart to open more stores in “food deserts” was not exactly a major victory, considering all the problems that stem from that corporation, such as employees who are paid so little that they need to be on public assistance. The Affordable Care Act, or Obamacare, was touted as a measure that would do a lot toward ridding the nation of the childhood obesity plague, but not much has had a chance to happen on that front. Furthermore, the Supreme Court might strike down part of that program, the subsidies that help people afford health insurance (but only in the states using the federal health care exchanges). The projected results include:

    Fourteen million fewer people would be enrolled in Medicaid, and 18 million fewer people would have private insurance purchased on the open market or on public exchanges established under the health law… It would save $824 billion in Medicaid and the Children’s Health Insurance Program.

    Your responses and feedback are welcome!

    Source: “Michelle Obama’s Moves.”, 10/29/12
    Source: “The Healthy Weight Commitment Foundation Pledge.” October 2014
    Source: “Mixed Effects Are Seen on an Affordable Care Act Repeal.”, 06/19/15
    Image by Ken Teegardin


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    Thinking about Tax in 2012

    June 22nd, 2015

    coke truckChildhood Obesity News is looking back over the last 5 years, at how different factions in America think about taxation in the context of obesity prevention, and at various efforts that have been made both here and abroad. Probably, by the year 2030, no state will have an obesity rate under 44 percent, and in 13 states, the obesity rate will be 60 percent. These numbers are projected by the Centers for Disease Control and Prevention, and the dollar amounts that go with them are equally dismaying.

    By 2030, the annual cost of treating obesity-related medical conditions in the US is expected to be $210 billion per year, a substantial portion of which will be paid by the American taxpayer. It seems only fair that the people who will need medical care should start paying for it up front, at the point of sale. Some call it a “sin tax,” to punish people for the transgressions of eating candy, drinking soda pop, and becoming obese.

    Mark Bittman, New York Times columnist and author of “How to Cook Everything,” is no fan of sugar, which he characterizes as a dangerous substance of perfect legality and universal availability. He particularly resents the expenditure of billions of dollars to influence children. His words are:

    What choice do we have but to regulate it, just as we would—and do—regulate tobacco and alcohol and, for that matter, firearms?

    Sugar is not exactly an invading army, but it can be thought of as a hostile force, and the processed food industry has succeeded in getting us to eat way more of it than is good for us. Will power alone isn’t enough to stop that—we need national defense.

    The purpose of government, he says, is “to protect us from the things from which we cannot protect ourselves.” The counterargument to that, with regard to children, is that parents are the ones who buy the food, and it’s their job to supervise what their kids eat, and handing over such intimate matters to the government equals capitulation to tyranny.

    Usually, regulation takes the forms of licensing, taxation, and various sanctions tailored to particular situations such as hiring. Regulation always has unintended consequences. It can create black markets and crime, in place of the poor judgment and bad choices we already have now. These are some of the more familiar objections.

    It becomes more and more obvious that childhood obesity originates from many underlying causes that are like tributaries flowing into the mighty river of Addiction. The contributing factors are advertising, and availability, and economic status, and family dynamics, and cultural influences, and many more. They all join in the middle, where pretty much everybody seems addicted to something.

    While addiction can be treated, it is apparent that the healing might not be complete or permanent until the underlying causes of the psychological distress are addressed. No government could undertake such a monumental task, and a lot of Americans would not even want it to try. For, Greg Critser wrote a piece called “Close to markets or not, fat poor kids are different than fat rich kids.” He tackled the tax question:

    Building new supermarkets or farmer’s markets addresses none of these core causes, but building other kinds of institutions would. To get at the root of the problem, we need more maternal services in the inner city, from pre-natal care to nutrition education and early childhood monitoring of growth rates. Traditionally such clinics derive funding from universities and city governments, but what if we required big food sellers—the kind who reap huge profits by selling soft drinks—to underwrite such basic services as part of their business license fees? Think of the tobacco industry’s forced underwriting of smoking cessation programs.

    Your responses and feedback are welcome!

    Source: “Fat America – You Ain’t Seen Nothing Yet,”, 01/11/12
    Source: “Sugar: Public (health) enemy No. 1?,”, 03/01/12
    Source: “Close to markets or not, fat poor kids are different than fat rich kids,”, 05/07/12
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    The One Big Answer—Sedentary Women

    June 19th, 2015

    Pregnant - 33 weeks

    Edward Archer, Ph.D., works at the University of Alabama at Birmingham’s Nutrition and Obesity Research Center, where his bio says:

    He is an obesity theorist and computational physiologist, and has a broad interdisciplinary background with graduate degrees and training in physiology, psychology, nutrition, exercise science, and epidemiology. His research spans the continuum of human bioenergetics, from the physiology of nutrient energy partitioning to national nutrition surveillance and chronic non-communicable disease epidemiology.

    In the light of several recent news stories about obesity genes, we looked at Archer’s assertion that the search for obesity genes has failed. Their whereabouts was only one of several questions that came up as he studied discoveries in many different fields. Everyone is trying to figure out what really causes obesity, but if some of the other “answers” were true, he felt that everyone, without exception, would unavoidably be obese. Regarding the findings in the field of genetics, he is unimpressed, and says:

    Despite the recent fanfare over the identification of a suite of genes associated with obesity, they explain less than 2 percent of the variation in obesity between individuals. This leaves the other 98 percent—known as the missing heritability—still to be discovered.

    Dr. Archer tells how, as a student, he was intrigued by the size difference between mice where there should have been no difference, because they were genetically identical and all ate the same food. With the same nature (their DNA) and the same nurture (their diet) they were supposed to be the same weight. Looking into it, he realized that when pregnant mice were deprived of exercise wheels, their kids had bigger, fatter kids. He says:

    While the first and second generations weren’t much larger, subsequent generations certainly were. To me, this was an amazing observation: The activity levels of grandmothers and mothers during pregnancy determined the fatness of future generations.

    For anyone raised on the King James Bible, this is uncomfortably close to verses in the book of Exodus and elsewhere that speak of “visiting the iniquity of the fathers upon the children, and upon the children’s children, unto the third and to the fourth generation.” Except in this case, it’s the mothers who come in for some blame. At the same time, Dr. Archer exonerates them in language that is also biblical when he says “gluttony and sloth are not the primary determinants of obesity.” Those are, of course, the archaic words for eating too much and not exercising enough.

    Dr. Archer believes he has pinpointed the single most important cause of obesity: sedentary female ancestors. (This is a circumstance, of course, over which a person has no power. The knowledge is useless for self-interest, and only useful as a gift to bestow on future generations.) The theory was introduced in the November issue of the Mayo Clinic Proceedings, under the title, “The Childhood Obesity Epidemic As a Result of Non-Genetic Evolution: the Maternal Resources Hypothesis.”

    Exhaustive research convinced Dr. Archer that the “missing heritability” had been located in “a combination of a mother’s body composition and physical activity during pregnancy.” Here’s how it works:

    When pregnant women are physically active, the increased energy demands redirect nutrients to her muscles and away from her fetus. This competition between the mother’s muscles and the developing fetus’s fat cells produces leaner, healthier babies.

    To put it another way, the uterine environment permanently alters “the metabolic processes that predispose some fetuses to obesity and metabolic disease.” When a prospective mother is inert, this healthful and productive competition for resources does not take place. If the mother’s body isn’t grasping for energy from nutrients, those nutrients turn into bad news for the growing fetus. Filled with all those unneeded fat cells, millions of babies are on track for a high birth weight, and then probably for adult obesity and Type 2 diabetes and “Their genes and food intake are irrelevant to the process.”

    The big take-away here is not that pregnant women need to get more exercise (although they do). According to Archer, a sedentary lifestyle before pregnancy can affect the uterine environment and thus a woman’s children and grandchildren. To give future generations the best chance at avoiding obesity, women should lead healthy, active lives even before they get pregnant.

    Your responses and feedback are welcome!

    Source: “Novel Theory Connects Mothers to Childhood Obesity,”, 11/17/14
    Source: “The real reason that people are obese,” 06/15/15
    Image by Kelly Hunter

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    Where Are the Obesity Genes?

    June 18th, 2015

    Wooden Sculpture of Science Genetics

    Edward Archer, Ph.D., studies obesity at the Nutrition and Obesity Research Center at the University of Alabama at Birmingham. His fields of expertise are many—computational physiology, psychology, nutrition, exercise science, and epidemiology. Yet, in explaining his theory of non-genetic evolution as obesity villain, Archer asked, “If our genes cause us to be fat, why has the search for ‘obesity genes‘ failed?”

    It seems like obesity genes are called out on practically a daily basis. In 2008, Reuters reported the identification of six new gene mutations linked to obesity. All the variations were found to have some influence on how the brain and the nervous system control a person’s eating and metabolism. Researcher Dr. Kari Stefansson said:

    This study essentially doubles in one fell swoop the number of known and replicated genetic factors contributing to obesity as a public health problem.

    Then there is KSR2, which, if it suffers a mutation, can cause sluggish metabolism and increased appetite, and KLF14, which appears to be the “master switch” that controls the genes in fat tissue. This time last year, the FTO variant was making news, and no wonder. Previously it had been thought to affect one person in six. Another set of researchers said it was found in 45 percent of their study’s participants. The report says:

    A common genetic mutation linked to childhood obesity also increases the likelihood of becoming overweight in adulthood.. They found the genetic variation also increases impulsive eating as well as a person’s appetite for fatty foods.

    It causes higher blood levels of the “hunger hormone,” ghrelin, and increases the brain’s sensitivity to the molecule. While possession of this gene would increase a person’s likelihood of becoming obese, the study’s authors also noted that previous research showed, “exercise can still overcome the increased risk of obesity posed by the FTO variant.” Not long before that, a story about obesity prediction said:

    While the researchers were unable to accurately predict child obesity risk using a formula based on genetic variations, they say about one in 10 cases of obesity are caused by rare mutations that disrupt appetite regulation.

    When talking about millions and millions of obese people, one in 10 is a gigantic number. Then, there is a story about 2,500 pairs of British twins that starts by affirming that several genes that influence appetite and self-control had previously been discovered, and that size is explained “mostly by genetic factors.” Published in the journal Obesity, the twin study:

    …suggests that genes account for 82 per cent of the variation in body mass index in 10-year-olds. The influence of genes on weight appeared to increase substantially throughout childhood, which scientists put down to older children having more freedom to act on their urge to eat….

    According to epigenetics, the environment changes the expression of the genes. An example is a study from the Norwegian University of Science and Technology to examine how the macronutrient composition of food can affect gene expression. Dave Asprey wrote:

    The group that ate a “healthy” amount of carbohydrates…expressed genes that are directly involved in some of the worst modern diseases such as type 2 diabetes, cardiovascular disease, Alzheimer’s, and cancer. The high carbohydrate group expressed a cascade of genes that trigger inflammation. Since inflammation is a contributing factor to almost every disease, it’s safe to say a high-carb diet contributes to almost every known chronic disease.

    Despite all this, Dr. Archer believes that humankind will continue to be disappointed by attempts to find the genes that make us fat, because genes and food are not enough to explain the current obesity epidemic. He writes:

    Despite the recent fanfare over the identification of a suite of genes associated with obesity, they explain less than 2 percent of the variation in obesity between individuals.

    Has the search for “obesity genes” failed?

    Your responses and feedback are welcome!

    Source: “The real reason that people are obese,” 06/15/15
    Source: “Study finds six new gene mutations linked to obesity,”, 12/14/08
    Source: “’Fat gene’ linked to adult obesity and impulsive eating,” BioNews,org, 06/02/14
    Source: “Childhood obesity calculator may be most accurate predictor yet,”, 11/29/12
    Source: “Childhood obesity linked to genes,” Khaleej, 04/28/14
    Source: “Amazing New Study Shows You How to Feed Your Genes: Part 1,”, 07/30/12
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    Everything You Know About Lipocytes is Wrong

    June 17th, 2015

    Sweat is just fat crying

    Once upon a time, Ruben Meerman lost 15 kg (more than 30 pounds) and wondered where the weight had gone. The doctors he asked didn’t seem to know. He conducted a survey of 150 health professionals, of whom “more than half thought that fat was converted into heat or energy.” But as a physicist, he found this theory to be in conflict with the Law of Conservation of Mass.

    Meerman joined forces with the man who runs the School of Biotechnology and Biomolecular Sciences at the University of New South Wales. After arduous research, Andrew Brown found the game-changing clue—a formula in a 1949 scientific paper which stated that “oxygen atoms are shared between the carbon and hydrogen in fat at a ratio of 2:1.” The study authors say:

    People who wish to lose weight while maintaining their fat-free mass are, biochemically speaking, attempting to metabolise the triglycerides stored in their adipocytes…The complete oxidation of a single triglyceride molecule involves many enzymes and biochemical steps…

    After biomolecular reactions have divvied them up, some of the oxygen atoms will bond with different atoms to become water, and twice as many will end up as part of carbon dioxide. In other words, “The correct answer is that most of the mass is breathed out as carbon dioxide. It goes into thin air.” The other component, water, is disposed of in the ways usual for liquids. The bladder, sweat glands, and tear ducts are fat’s secondary organs of excretion. “The lungs are the primary excretory organ for fat.” So says the study, which was published in the British Medical Journal. Meerman and Brown wrote:

    To calculate these values, we traced every atom’s pathway out of the body.

    Stoichiometry shows that complete oxidation of 10 kg of human fat requires 29 kg of inhaled oxygen producing 28 kg of CO2 and 11 kg of H2O. This tells us the metabolic fate of fat but remains silent about the proportions of the mass stored in those 10 kg of fat that depart as carbon dioxide or water during weight loss.

    When people eat more than they need, proteins and carbohydrates get changed into triglycerides, which are then “stored in lipid droplets inside fat cells.” Until they are liberated, and their carbon set free, no weight is lost. But once the triglycerides have been broken down, the fat is no longer fat.

    When the broken-down fat can be induced to leave the body, it makes its departure in the form of H2O and CO2. For a person to “lose” 22 pounds, 64 pounds of inhaled oxygen have to be brought in, making a combined total of 86 pounds of stuff. For this alchemy to take place requires the expenditure of 94,000 calories, and the end product is 24 pounds of water and almost 62 pounds of carbon dioxide (also totaling 86 pounds.) All this can be more easily assimilated via Ruben Meerman’s TED talk on “The Mathematics of Weight Loss.”

    What about the widespread yet erroneous belief that fat is converted to energy or heat? The study authors say:

    We suspect this misconception is caused by the “energy in/energy out” mantra and the focus on energy production in university biochemistry courses. Other misconceptions were that the metabolites of fat are excreted in the faeces or converted to muscle.

    Losing weight requires unlocking the carbon stored in fat cells, thus reinforcing that often heard refrain of “eat less, move more.”…A single 100 g muffin represents about 20% of an average person’s total daily energy requirement. Physical activity as a weight loss strategy is, therefore, easily foiled by relatively small quantities of excess food.

    That last line is quite important for anyone who works out and then fills up on the “I deserve it” theory. Deserving or no, it takes only a small bit of nibbling to negate the good effects of what seemed like a monumental amount of exertion. Ignoring this amounts to self-sabotage.

    Your responses and feedback are welcome!

    Source: “This is where body fat ends up when you lose weight,”, 12/17/14
    Source: “When somebody loses weight, where does the fat go?,”,12/16/14
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