Coca-Cola and the Presidential Candidate


This is a convoluted story of political machinations, so buckle up. Last November, as part of the big Hillary Clinton email scandal, it was revealed that the Coca-Cola Company had not only been working on her, but had also been haranguing various other public figures and journalists.

Coke wanted to sell the idea that the obesity epidemic is due solely to the lack of physical activity, especially among children. The corollary to the theory is that sugar-sweetened beverages bear absolutely no responsibility for obesity; and the other spinoff is that soft drinks have been falsely accused, and wrongfully and tragically maligned.

Also, it was whispered that Coke had donated somewhere around $10 million to Clinton’s campaign, and expected that the candidate would in turn stop supporting the Philadelphia soda tax and renounce it and every other attempt at such a tax. Coke executives assured each other that Clinton’s advisors were “working on how to walk this back” — in other words, on how to create such a graceful flip that the public would not even notice that she had reversed her position.

For more background, journalist Jill Ettinger added:

Earlier this year, University of California research found that over several decades the sugar industry paid researchers to help shift focus away from sugar and toward fat as the culprit in health issues including heart disease. The move helped to shape flawed decades-long dietary recommendations and a low-fat craze that led millions of Americans to avoid fats critical to health (such as omega-fatty-acids) and indulge in harmful trans fats instead.

The efforts to make Clinton change her policy turned out to be moot, as Donald Trump won the presidential election. During the past half-year, the changeover of personnel in Washington, D.C., has given Americans plenty to think about, to the point where a seemingly minor but potentially disruptive governmental appointment could go unnoticed. However, this one matters quite a lot.

Earlier this month, the federal department of Health and Human Services announced that the new chief of the Centers for Disease Control and Prevention will be Brenda Fitzgerald, who trained as an OB/GYN doctor and went on to be the Public Health Commissioner of Georgia. That unfortunate state ranks as one of the most obese, and also distinguished itself by wanting a ton of exemptions when the federal government made new rules about junk food vending in schools.

While in charge of Georgia’s health, Fitzgerald was instrumental in the formulation of SHAPE, a statewide effort to address childhood obesity through “physical activity before class, physical activity during class, and more structured recess,” which in practical terms, came out to about 30 minutes of extra activity per day.

Now, there is absolutely nothing wrong with either exercise or fitness, and kids have a particularly strong need to move around a lot. But critics point out that it all sounds like more of the victim-blaming habitually practiced by Big Food and Big Soda. Corporate executives enjoy promising their customers that the products are not at fault. If the consumer will just be reasonable and devote about 20 hours per day to working out, the weight gained can be easily lost.

(To be continued…)

Your responses and feedback are welcome!

Source: “The Soda Industry’s Panicked Downward Spiral,”, 11/08/16
Source: “Trump’s new CDC chief championed partnership with Coca-Cola to Solve Childhood Obesity,”, 07/08/17
Photo credit: Bill Wilson (okchomeseller) via Visualhunt/CC BY

The Food Addiction — Eating Addiction Quandary


We left off with Dr. Pretlow’s thoughts about food addiction versus eating addiction, and his observation that amount addiction appears to be a very powerful force. Dr. John Menzies of the University of Edinburgh also finds it “more appropriate to think about chronic overeating in terms of an eating addiction.”

He is not happy with the substance addiction paradigm because:

The National Institute on Drug Abuse defines it as a “chronic, relapsing brain disease” because longterm drug abuse can permanently change a brain’s wiring and how it works. Currently, Menzies argues, there’s just not enough evidence to show that certain nutrients or foods do the same thing.

But wait. Obesity, whatever its underlying cause, actually can be said to cause permanent changes in the body. For instance, a person can make new fat cells, but they never go away.

Apparently, obesity can also change the brain. Drs. S. Sharma and S. Fulton looked into the biological links between depression and metabolic disorders, with particular attention to diabetes and obesity.

Nutritional therapist Maria Zaretti framed the pertinent questions as follows:

Do you eat because you are depressed? Or are you depressed because of what you eat?

The Sharma/Fulton research had this objective:

To determine the impact of a palatable high-fat diet (HFD) on depressive-like behaviour and biochemical alterations in brain reward circuitry in order to understand the neural processes that may contribute to the development of depression in the context of diet-induced obesity (DIO).

As Zaretti explains the results, “excessive consumption of high-fat foods can cause chemical reactions in the brain ultimately leading to depression.” It’s all about dopamine, and changes in the brain’s reward and pleasure centers.

That actually sounds like the kind of permanent brain-changing that Dr. Menzies does not see happening. But as Zaretti again spells out:

Dr. Fulton draws a comparison with drug addiction whereby a vicious cycle sets in where “food-highs” are used as a way to combat depression. “In a similar way to illicit drugs” says Fulton “continually eating high-fat foods can lead to depression as the ‘come-downs’ take their toll”.

The report on the work of Drs. Sharma and Fulton, published by the International Journal of Obesity, concluded:

[…] that chronic consumption of high-fat food and obesity induce plasticity-related changes in reward circuitry that are associated with a depressive-like phenotype. As increases in striatal BDNF and CREB activity are well implicated in depressive behaviour and reward, we suggest these signalling molecules may mediate the effects of high-fat feeding and DIO to promote negative emotional states and depressive-like symptomology.

Zaretti further explains:

CREB is a molecule that activates genes involved in brain function including genes that dampen the reward-circuitry. Having high CREB may make the same-old dose of a “drug”, in this instance high-fat food, less rewarding and promote a negative mood state.

Here’s the thing. Striatal BDNF and CREB activity are things that happen in the brain. So to say there can’t be such a thing as food addiction, because food doesn’t make permanent marks on the brain, does not seem quite fitting.

Your responses and feedback are welcome!

Source: “Food Addiction vs. Eating Addiction: Why A Single Word Makes All The Difference,”, 09/23/14
Source: “Do you eat because you are depressed? Or are you depressed because of what you eat?,”, 08/23/16
Source: “Diet-induced obesity promotes depressive-like behaviour that is associated with neural adaptations in brain reward circuitry,”, March 2013
Photo credit: A Health Blog via Visualhunt/CC BY-SA

Addicted to What?


For The Huffington Post, journalist Anna Almendrala wrote the following:

Food addiction research is still in its infancy, but its appeal is obvious. The model paints a comprehensive picture of the “toxic food environment” we live in today and is a compelling way to link the rising processed food industry with growing rates of obesity…

Why is it useful to link the processed food industry with obesity statistics? Because many critics of the nutrition landscape have insisted for a long time that Big Food purposely engineers irresistible qualities into its products, thus making them literally addictive.

Childhood Obesity News has looked extensively at the omnipresent “manipulated” grocery items that fill supermarket shelves. We talked about Prof. Ashley Gearhardt, teacher of psychology at the University of Michigan and creator of the Yale Food Addiction Scale. Academics and clinicians who use the Food Addiction Scale have come to believe that “an estimated five to 10 percent of the general population may have some degree of food addiction.”

Granted, that sounds pretty vague. On the other hand, society does not need scientists to be making unwarranted overly-specific claims. At any rate, to Dr. Gearhardt, it seems obvious that some kinds of foods act very much like addictors, while others, such as cruciferous vegetables, do not inspire such fervor. Unless they do.

On the other hand, here is a vignette from Dr. Pretlow:

I recall a post from a mother on our site lamenting that she had removed all junk food from her house, yet her obese daughter then binged on apples!

Almendrala asked:

Is food addiction real, and should food industries be held accountable for engineering hyper-palatable sugar-salt-fat bombs that override feelings of fullness? Or is it more accurate to describe overeating as an eating addiction — a disordered relationship to all foods that can and should be brought to heel by the individual?

Just as we need to know how much of obesity originates in heredity and how much in the environment, we need to know how much stems from uncontrollable factors and how much from personal responsibility. And how much from a particular substance or class of substances, and how much from the simple and overwhelming desire to eat a lot.

Then, of course, we also need to discover what causes that desire to take in many times the amount of nourishment actually needed by the body, and how to quash that desire. Amount addiction, says Dr. Pretlow, depends not on specific foods or hyperpalatable foods, but basically on whatever happens to be around, as long as there is plenty of it.

Perhaps not all obesity is attributable to what he calls “the very powerful addiction of excessive food amounts,” but to whatever degree it holds sway. People who use eating as a coping mechanism against stress and change find that cutting down their amounts is extremely difficult.

Your responses and feedback are welcome!

Source: “Food Addiction vs. Eating Addiction: Why A Single Word Makes All The Difference,”, 09/23/14
Photo credit: Charles Smith (smith_cl9) via Visualhunt/CC BY-SA

Microbiome Revelations Continue


We left off with some of the questions that scientists were presented with in the course of learning more about the microbiome. Research showed that obese and lean people have different-size populations of various bacteria residing in their GI tracts, but right from the start it was also apparent that many other factors play a part.

For instance, the typical obese lab mouse has, overall, a paltry assortment of gut flora compared to the spectacularly diverse community that a lean mouse can boast of. Questions continued to arise. When the microbiome becomes altered, is it because of the inadequate diet? Or are the harmful changes indirect, caused by conditions created by obesity?

A team of Israeli scientists determined that microbes that thrive on artificial sweeteners are the same kind that other researchers had already found in excessive amounts, in the interiors of genetically obese mice. In recent years, many serious autoimmune conditions have been identified as emanating from chronic systemic inflammation, which originates in exactly one place, the gut.

Staphylococcus aureus and E. coli are both life forms that, for some reason, trigger human fat cells into producing inflammatory substances that irritate other cells and incidentally invite diabetes. Researchers have observed…

[…] a connection between certain types of bacteria and body fat that produces a heightened inflammatory response and drives the inflammatory process.

And then they found out about AD-36, the human adenovirus that apparently plays the dirty trick of changing adult stem cells into fat cells. More theories were proposed and more experiments designed.

At the University of Geneva, researchers kept mice very cold for as long as 10 days. Their inner bacterial universes adapted to the new reality. Some bug species prospered, while others failed to thrive.

When these hardy critters were transplanted into mice that had been intentionally engineered to have no microbiota of their own, the transplanted bugs helpfully facilitated the formation of more brown fat, and the recipient mice lost weight.

In the words of journalist Megan Thielking, the findings…

[…] suggested that harnessing the way cold changes the microbes in your body — and, consequently, the way you metabolize food — could be a potential avenue for fighting obesity.

Childhood Obesity News has mentioned Dr. Lara R. Dugas before. A physical activity epidemiologist, she has suggested redesigning the traditional school year because under the present system kids leave for the summer in relatively good shape and then slouch back to classes in the fall all bloated and misshapen.

The worst victims of this phenomenon are girls in the low-income and minority demographics. The website says of a study where Dr. Dugas was lead author:

A newly identified factor, the gut microbiota, which is a bacterial ecosystem residing within the gastrointestinal tract of humans, has now been implicated in the obesity epidemic. Importantly, this bacterial community is impacted by external environmental factors through a variety of undefined mechanisms.

In other words, just a year ago, the existence of our three or four pounds of bugs, constituting a separate and discrete organ, was still being referred to as a “newly identified factor.” And today, the microbiome’s mechanisms are not much better defined or understood than they were last July.

Your responses and feedback are welcome!

Source: “Regulation of Appetite, Satiation, and Body Weight by Enteroendocrine Cells,”, February 2015
Source: “Artificial Sweeteners May Change Our Gut Bacteria in Dangerous Ways,”, 03/17/15
Source: “Chronic Inflammation: How Majority Of Inflammatory Diseases Start In Your Gut,”, 11/21/15
Source: “The Truth about Freezing your Fat Off,”, 01/08/16
Source: “The obese gut microbiome across the epidemiologic transition,”, 01/11/16
Photo credit: Global Panorama via Visualhunt/CC BY-SA

The Microbiome Shares Its Secrets


Like Hansel and Gretel following a trail of bread crumbs through the forest, we are following some of the stages of microbiome awareness that could eventually lead to astonishing revelations and possibly even some ways to help people maintain normal weight without spending thousands of dollars on gym memberships, special food programs or debilitating operations.

A group of researchers from Massachusetts General Hospital and Harvard University looked at patients who had undergone Roux-en-Y gastric bypass surgery (familiarly known as RYGB) and found changes in their microbial ecology. These modifications were “due to gastrointestinal reconfiguration and not merely due to the associated changes in weight loss, diet, or intestinal transection.”

Their work showed that an altered microbiome could “trigger a reduction in host body weight and adiposity.” These colleagues were very interested in the properties of short-chain fatty acids (SCFAs), which are byproducts of microbial fermentation.

SCFAs feed the cells that line the colon, providing the energy for them to do what they need to do. They also affect the metabolic physiology of the host organism in various other ways. This is one reason why study of the microbiome does not harmonize with a one-size-fits-all paradigm.

Researchers did not know much at this point, but they knew enough to recognize the need for more studies, from several angles of approach, including “surgery, metagenomics, gnotobiotics, and genetic deletions for key metabolic signaling pathways.” Words like this were bandied about:

The human large intestine harbors a complex community of microorganisms (microbiota) that affect many aspects of our physiology and health… Numerous lines of evidence […] have suggested that the intestinal microbiota may play a role in the development of obesity.

Mouse experiments showed that when the microbiota from lean donors are introduced into the intestinal tracts of obese mice, in conjunction with an appropriate diet, weight gain can be reduced. This was a significant discovery, lending hope that similar interventions in humans could achieve the same result. Fecal transplants became a topic of conversation.

Researchers learned that the transplant material does not need to be introduced through the lower end of the intestinal tract, but can be delivered in pill form from above, into the duodenum. It was shown that such an intervention “significantly improves insulin sensitivity” in individuals with metabolic syndrome.

The term “obesogenic bacterial profile” became known as something to avoid, because particular species of microbes love a high-fat diet and use it to create intestinal inflammation and build insulin resistance.

Things got really interesting when it became clear that, bossy as they are, the gut bacteria do not always get their own way, because they are vulnerable to being acted on by the genetics of the host — that’s us.

A very heritable taxon, or group, of bugs, Christensenellaceae, are found in association with a non-obese body. These creatures are even called “the hub of a consortium of co-occurring heritable microbes that are associated with a lean BMI.”

Of course, every discovery brings a new set of questions:

Which specific taxa within the gut microbiome are heritable, and to what extent? Which predicted metagenomic functions are heritable? How do heritable microbes relate to host BMI?

Your responses and feedback are welcome!

Source: “Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity,”, March 2013
Source: “Fighting Obesity with Bacteria,”, Sept. 2013
Source: “Nutrient-Sensing Mechanisms in the Gut as Therapeutic Targets for Diabetes…,”, September 2013
Source: “Human Genetics Shape the Gut Microbiome,”, 11/06/14
Photo credit: sassypackratstudios via Visualhunt/CC BY-ND

Early Days of Microbiome Consciousness


The accumulated information about the microbiome grows every day. The bugs that colonize us have a lot going on, and figuring them out is tricky, because many of them can’t even be cultivated in a laboratory.

It is useful to compare our microbiome knowledge to an old-fashioned connect-the-dots puzzle. A lot of things seem to be in contact with each other, but it doesn’t make a whole lot of sense. Then, suddenly, with the last couple of lines drawn, everything falls into place and the picture is clear. We haven’t come to that part yet.

Study of the microbiome can also be compared to how, millennia ago, shepherds stared up at the night sky, connected the starry dots, and saw pictures. Sometimes, a person only needs to look at it from the correct angle, and it all clicks. Research hasn’t quite gotten there yet.

What we do know, is that the bugs have been implicated in everything from autism to chronic pain and obesity. Today we go back and pick up on some of the dots that may not yet be perfectly connected, but which show tantalizing promise.

The earlier microbiome research

In 2008, the idea that the microbiome could influence energy storage was not new. Researchers devised experiments to show that overweight is often preceded by “aberrant compositional development of the gut microbiota,” and they carefully considered the applicability of any discoveries to the child obesity problem in particular.

When an unwelcome intruder tries to gain power by creating artificial hunger, that is certainly obesity-related. A decade ago, many academics had already begun to wonder if our gut flora are secretly running our lives. The GI tract commonly contains both bacteria and yeast, and it is part of both their jobs to keep each other under control. When the candida organism reaches critical mass, everything goes haywire and anxiety becomes chronic.

Steven Kotler wrote:

This happens because, when the body is anxious it craves the fuel needed to react quickly to negative situations. Sugar breaks down fast, so sugar is what’s craved. But the reason the body is really craving sugar is because candida feeds on it. This means, at least under these circumstances, that your emotions are really just another’s hunger.

In 2012 a study came out with evidence that insufficient bacteria in the large intestine could slow down the burning of brown fat, and promote obesity, while other studies also suggested that the gut bacteria influence body weight in a number of other ways.

For instance, they digest complex carbohydrates for us, because we don’t have the right enzymes. The microbes transform these substances into fatty-acid molecules “whence they are fed into biochemical pathways that either liberate energy from them… or lay them down as fat.”

Your responses and feedback are welcome!

Source: “Early differences in fecal microbiota composition in children may predict overweight,”, 2008
Source: “You Are Not You: The Conundrum of the ‘Me’,”, 08/26/10
Source: “The gut microbiome: how does it affect our health?,”, 03/11/15
Source: “Me, myself, us,”, 08/18/12
Photo credit: whitney waller via Visualhunt/CC BY-SA

Valiant Anti-Obesity Efforts in the U.K.


In the U.S., childhood obesity is not the hot topic it was when Michelle Obama, as First Lady, continually drew attention to it. In the United Kingdom, interest in the subject apparently never ebbs, but just flows from one controversy to the next.

A study completed last year indicated that kids who eat breakfast, even if it’s a free breakfast provided by the government, are a lot better at reading, writing and math. Another study from University College London showed that skipping breakfast is sign that a child will likely become overweight or obese in future. In other words, breakfast is a good thing for growing kids.

In March, the British government announced that an additional 47,000 children would benefit from expanded breakfast/lunch programs. Naturally, critics who do not even want to understand the nuances will always ask, “If kids are too fat already, why should the taxpayers buy them breakfast?” But officials assured the public that early intervention in such matters truly pays off in the long run, and that children should all have an equal opportunity to fulfill their potential and break the cycle of disadvantage.

Meanwhile, other problems related to poor diet grow up hand in hand with the obesity crisis. The oral health of children in the U.K. is shocking. In the 5-9 year age group, there are 26,000 hospital admissions per year due to severely deteriorated teeth. Some kids wind up having every tooth in their mouth extracted at once.

Making a difference

As we have mentioned, Britain’s Obesity Health Alliance (OHA) is made up of 41 “medical groups, health charities and public health bodies” that banded together to produce a 10-point plan to which it hoped the warring political parties would pay attention. Many ordinary Brits felt that the fix was in, and that the administration had been bought off, or frightened off, by Big Food and Big Beverage. As candidates explicated their platforms in preparation for the June 8 elections, the OHA hoped to win hearts and minds.

What does this coalition want officialdom to do? A better job of informing consumers about the sugar present in foodstuffs, for starters. Also, even though Britain voted to leave the European Union, the obesity-conscious want to retain the “traffic light” food labeling system. And they want schools to serve lunches that comply with nutritional standards.

The OHA also subsidizes the flashy kind of research that makes startling headlines. The amount of public funds spent to treat obesity each year could pay the salaries of an additional 85,000 doctors or 165,000 nurses. For those who like their numbers expressed in operating-room terms, the costs of obesity could pay for 116,000 heart transplants or 730,000 hip replacements.

The combination of Britain’s slashed public health budgets and its universally cherished unhealthy lifestyle has caused dissent and despair. A politician named Norman Lamb blamed the Conservative government’s policies as disastrous and inexcusable, especially in regard to television advertising of junk food to children, and an impending sugar tax with too many loopholes.

Your responses and feedback are welcome!

Source: “47,000 more children to get school meals,”, 03/27/17
Source: “UK must get tough on childhood obesity, says top doctors,”, 05/04/17
Source: “Norman Lamb: BMA Report Shows Govt Failing to Tackle Childhood Obesity,”, 05/13/17
Photo credit: xavigm/123RF Stock Photo

How to Seriously Damage a Microbiome


Artificial sweeteners have been mentioned here before, but we haven’t gotten into how these substances affect our gut flora. The short answer is, not well.

For Scientific American, Ellen Ruppel Shell reported on the Israeli scientific team whose work with mice led them to describe a “cause-and-effect chain” leading from artificial sweeteners like saccharin to an adverse effect on our microbes, and then to obesity and diabetes in humans.

Shell wrote:

This study was not the first to note this link in animals, but it was the first to find evidence of a plausible cause: the sweeteners appear to change the population of intestinal bacteria that direct metabolism, the conversion of food to energy or stored fuel.

And that is the crux of the matter. The indications point to a need for people to be more cautious about messing around with the indwelling bugs, who are in a position to make our lives miserable. One thing these substances can do is cause a population explosion among “bacteria that make more calories available to us…” The relationship to obesity is obvious.

As always, others in the scientific community do not consider that a meaningful link has been proven. But more connections continue to appear.

Research scientist Meghan Azad, of the University of Manitoba, said:

Infants born to women who regularly consumed one or more artificially sweetened beverages during pregnancy were twice as likely to be overweight by 1 year of age.

Shell captured a pertinent quotation from New York University gastroenterologist Ilseung Cho:

A hormone is like a force multiplier — and if a change in our gut microbes has an impact on hormones that control eating, well, that would explain a lot.

Long “naughty” list

The microbiome has been found to detest many things: refined sugar, herbicides, pesticides, and genetically engineered foods. Statements like this one, from the Alliance for Natural Health, upset people:

The only published human feeding experiment revealed that genetic material inserted into GE soy transfers into the DNA of bacteria living inside our intestines and continues to function. Even after we stop eating GE foods, we may still have the GE proteins produced continuously inside us.

The microbiota also suffer from — and rebel against — the presence of gluten; antibiotics as medicine or secondhand from animal additives; non-steroidal anti-inflammatory drugs; chlorinated and fluoridated water; pollution; and stress. Again, there is a sizable overlap with the list of factors that are identified, to a greater or lesser extent, as obesity villains.

If Big Food is backing any gut flora research, in hopes of finding some foothold or advantage, the endeavor seems bound to disappoint. Studies of the microbiome, if honestly performed, could turn around and bite them, and they might wish they have left the subject alone. Because, so far, the evidence is strong that our friendly, helpful microbes don’t like junk food.

Your responses and feedback are welcome!

Source: “Artificial Sweeteners May Change Our Gut Bacteria in Dangerous Ways,”, 03/17/15
Source: “Artificial Sweeteners During Pregnancy May Make for Heavier Infants,”, 05/09/16
Source: “Get to Know Your Microbiome for Health & Wellness,”, 06/05/15
Source: “Genetically Engineered Food Alters Our Digestive Systems!,”, 05/31/11
Photo credit: frankieleon via Visualhunt/CC BY

Touring the Flaky Fringe


On the wilder frontiers of child obesity studies, there seems to be a lot of willingness to accuse parents of a particular gender for the entire problem. One headline, for example, purported to reveal the “untold story” which is that working mothers are to blame.

Truth be told, a lot of women would probably rather not work outside their homes. Also, whether they hold down jobs by choice or by necessity, they would rather not be blamed for childhood obesity.

But Nicole M. King seems to have done just that, in a article. As editor of what is billed as “the United States’ leading journal of family-policy research,” she is very familiar with the field, and opined that…

[…] the commentators bewailing the upsurge in childhood obesity have been keeping strangely quiet about an important backstory: namely, the role of maternal employment in incubating the problem.

Citing a study conducted by three universities in the United Kingdom, she points out “certain patterns” that line up with the presence of dangerously overweight children. Actually, it’s one pattern — a mother who works outside the home, and does not have enough time to cook healthful from-scratch meals, and fills her kids up with fast-food junk instead.

King writes:

In the current academic environment, it would take rare intellectual courage to challenge the cultural patterns that have taken mothers out of the home…

This is kind of hard to follow. What “cultural patterns”? Families can no longer afford to live on one income. In any state in the union, a full-time minimum wage employee does not make enough money to rent a one-bedroom apartment — forget about supporting a family.

Moms thanklessly bring home the bacon

A person can “challenge the cultural pattern” all day long, but since it is less a cultural pattern than a hardcore economic necessity, there isn’t much point, unless the critic is prepared to dismantle the entire system. Otherwise, there is little progress to be made by casting blame. This blaming implies that working mothers are acting out some kind of fairy-tale princess fantasy, to the children’s detriment, rather than working long hours for inadequate pay to house, feed and clothe those children.

The debate has another facet. To indict mothers who work outside the home is to frame the whole question in a very U.S.-centric way. In Mexico, the second most obese country after America, the culture tends more toward women doing their money-making activities at home, or taking their kids to work. In other words, a great many Mexican mothers are not separated from their kids all day, yet the result is childhood obesity — just like in America where moms leave the house and go alone to their workplaces.

Middle Eastern countries actively discourage women, especially mothers, from working outside the home. Yet obesity is a problem. In Samoa, the female workforce participation rate is only 26%, yet Samoans are known to be large people.

A change

Some time later, King reported again on the parental blame issue, this time in the course of reviewing a piece which attributed the problem to socioeconomic status. King, who is more a proponent of family environment as a causative factor, seems to now see the male parents as the bad guys. “Missing fathers, swelling waistlines” is the pertinent phrase.

But Childhood Obesity News has recently said a lot about fathers, so will leave it there for now.

Your responses and feedback are welcome!

Source: “The untold story behind child obesity,”, 11/22/13
Source: “Countries Where Women Are Least Likely To Be In The Labor Force,”, 03/13/17
Source: “Missing Fathers, Swelling Waistlines,”, 02/16/17
Photo credit: bialasiewicz/123RF Stock Photo

Tales From the Flaky Fringe


Childhood Obesity News looks at factors that may or may not impact the obesity epidemic. Today’s punchlines have a way of becoming tomorrow’s reality, and if there is an underlying macro-cause for the result that we call the obesity epidemic, it would be better to know about it.

At an international conference on Excellence in Pediatrics, professor of Human Nutrition from the University of Ulster Barbara Livingstone noted that science had identified more than 30 potential risk factors connected with childhood obesity, although admittedly only a few were at that point supported by solid evidence. Prof. Livingstone said that in many countries, the environment had become “obesogenic or obesity-causing.”

In 2014, University of Southern California researchers used data from a longitudinal (8 years) study of children living in proximity to freeways and other major roads, and of kids living with secondhand cigarette smoke. In either case, the children had a greater chance of becoming obese later. Some of the subjects fulfilled both categories, and they were “even more likely to experience weight gain than those who were exposed to only one — or to neither.”

Journalist Lecia Bushak reported for Medical Daily:

A recent study out of Brigham Young University, for example, found that secondhand smoke increased the risk for obesity. The researchers examined mice who were exposed to secondhand smoke, and found that tobacco caused the body to develop insulin resistance, which is of course the first step toward type 2 diabetes, a chronic disorder often linked to obesity.

In 2016, journalist Adele Peters looked into the notorious air pollution of China’s capital city, Beijing. It seems to have been accepted that modern progress brings along a certain amount of asthma, lung cancer, and heart disease, if people insist on breathing the air.

But air as obesity villain is a relatively new concept. Scientists established a lab about a mile from a 14-lane highway, let some rats breathe the polluted air, and provided others with HEPA-filtered environments. The polluted-air rats became as much as 18% heavier.

Peters wrote in an article for Fast Company:

At the beginning of the experiment, pregnant rats in both groups were basically all the same weight. Nineteen days in, those unlucky enough to live with air pollution were 15% fatter, with inflammation in their lungs and signs of insulin resistance. When their babies were born, they also gained weight quickly; the female babies were 10% heavier than the ones living in the filtered cage, and the male babies were 18% fatter.

This doesn’t sound good at all. Additionally, people often forget that the environment includes everything that isn’t us, including the stuff we put in our mouths.

No, not food this time, although food certainly counts. This is about Triclosan.

The Food and Drug Administration took four decades to think it over, and finally banned the chemical from being an ingredient in soap. But it can still be in toothpaste, including the biggest-selling brands. It has been shown that chemicals are absorbed more efficiently through the tissues of the mouth than through the skin, but, apparently, the FDA did not get the memo.

Why is this a problem? Nikita Mishra writes in The Quint:

Even if a trillionth per gramme of this seeps into your body, it can affect your normal thyroid function; damage your brain lining; cause infertility; and is co-related to a host of chronic health issues, like childhood obesity and diabetes, among others.

Maybe this is all true; maybe it is needlessly alarmist. But is it worth taking the chance?

Your responses and feedback are welcome!

Source: “Toxic environment causing obesity, says professor,”, 12/07/13
Source: “Children Exposed To Secondhand Smoke, Highway Air Pollution Are More Likely
To Gain Weight,”, 11/12/14
Source: “The Smog in Your City is Why You’re Fat,”, 03/08/16
Source: “Why Is a Banned Chemical Allowed in Leading Toothpastes?,”, 09/14/16
Photo credit: Nick Harris1 via Visualhunt/CC BY-ND

Childhood Obesity News | OVERWEIGHT: What Kids Say | Dr. Robert A. Pretlow
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