Gram Negative Bacteria and Obesity – 180 Degree Health

By Andrew Kim 


As the research evolves, the matter of diet and nutrition is being forced to be recognized as not only the most poorly understood of all the sciences but also one of the most complex, outranking all the others.

Weight loss is a recurrent theme on this site and this should be expected, as obesity is the most common “disease” in the United States.1 But herein lies a wrinkle that adds to the complexity of this matter: What constitutes a healthy weight is not an objective, uniformly agreed upon standard.

Suffice it to say here, we know that having excess body fat is strongly linked to cardiovascular disease, kidney disease, diabetes, and hypertension.  It also aggravates arthritis, gout, gallbladder disease, and blood lipid disorders.  And, it appears to aggravate certain cancers.2 

The interplay among the fat tissue, organs, muscles, and immune system is, to me, highly complex – even after drawing out all the ways in which they do in great detail.  However, up until doing researching for this post, I hadn’t fully appreciated the dimension added to this interplay by the intestinal flora and biome.

In light of the extreme claims made on behalf of (expensive) probiotic and prebiotic supplements, such as in the video below…

…my inaugural post for this site will present, in my estimation, the most important experiments that have added clarity about the connection among intestinal flora, metabolism, and weight loss.  What will be clear is that:

  1. There are observed differences between the intestinal flora of lean and the intestinal flora of obese individuals.
  2.   The interaction between the host and the intestinal flora is intricate and entails changes in the host gene expression involved in nutrient – particularly carbohydrate – processing and appetite regulation, which are not fully understood.
  3.   High-fat diets promote the passage of a bacterial poison called endotoxin into the body, potentially leading to endotoxemia (arbitrarily defined as when endotoxin levels rise by 2- to 3-fold above normal levels).
  4.  Weight loss is probably the great equalizer in that weight loss, in and of itself, reverts the intestinal flora and biome of obese individuals to that of lean individuals.


Obesity changes the gut flora, and these changes have been directly correlated with a host of metabolic imbalances and diseases in animals.  This fact should not be a surprise anymore, as the intestinal flora is now known to play an indispensable role in the nutrient metabolism – particularly carbohydrate metabolism – of its host.  It was shown, for instance, that in the rectum, over 100 genes are regulated differentially by intestinal flora; and in the jejunum, over 200 genes.3

But test tube studies like the one described above are obviously limited in what we can take away from them.  Luckily, many of the assumptions and hypotheses about the intestinal flora are testable in living organisms.

In one now classic experiment, despite eating 30 percent less food than germ-free mice, normal mice were 40 percent fatter than germ-free mice.  In a follow up experiment, upon inoculating germ-free mice with the flora from normal mice, the germ-free mice became about 60 percent fatter and developed insulin resistance after 2 weeks, despite eating less food than normal.4 Leptin levels increased, too, and though the authors merely correlated the increase in leptin to the increase in fatness, it was probably also driving the insulin resistance that had developed.

Since living in a germ-free environment isn’t possible and since wiping out the flora in our intestines entirely would lead to serious deficiencies and malnutrition, we could, next, investigate dietary interventions that alter the microbial biome in a way that matches that of healthy and lean individuals.

Generally, mice fed on high-fat diets have a significant increase in endotoxin levels – indicating either a greater ratio of gram-negative bacteria to gram-positive bacteria in the intestines, as only gram-negative bacteria have coats that bear endotoxin.  Endotoxin is quite toxic to the human body5 and large exposures to it can be quickly life threatening and fatal.

In short, endotoxin creates a state of shock in the human body – known as septic shock.  Lucky for us, to get to this point, very large bacterial invasions into the body are needed by way of breaks in the skin – including the “skin” of the intestines.

However, at relatively lower, chronic doses, endotoxin:

  • Favors wide spread blood clotting
  • Leads to fatty liver conditions
  • Promotes oxidative stress and metabolic disorders (including glucose intolerance and insulin resistance)
  • Initiates an immune response (however, I’m open to the possibility that this effect, though the mechanisms are less clear to me, may actually serve the host favorably in the big picture)5

Further, mice fed on high-fat diets, compared to high-carbohydrate diets, have reduced concentrations of Bifidobacterium species – a major type of gram-positive bacteria normally present in the intestines of mammals.  A lower concentration of Bifidobacterium species creates a vacuum in which more virulent, endotoxin-bearing gram-negative bacteria could seed and proliferate. (Because of the presence of endotoxin in their coats, gram-negative bacteria are not only more virulent than gram-positive bacteria, but they are also more resistant to antibiotics, as antibiotics have difficulty penetrating this outer coat.)  In fact, Bifidobacterium species reduce the intestinal endotoxin load, and at the same time, strengthens the intestinal barrier.6

I mention this fact to point out how a simple dietary change could, by altering the intestinal biome, bring about marked changes in a person’s metabolism and health – regardless of the amount of calories consumed.

Further, the introduction of Bifidobacterium species has been shown to reduce the intestinal endotoxin load, improve the barrier functioning of the intestinal wall, and protect against obesity and endotoxemia brought about by a high-fat diet.7

Although the majority of studies showing an increase an endotoxin levels caused by high-fat diets were performed in rodents, I think, considering the major way in which endotoxin moves into the body, it’s reasonable to assume that the same result would be seen in humans.

Endotoxin is continuously generated and released into the intestines by bacteria upon their destruction or death.  From there, endotoxin is transported into the capillaries, which surround the intestines, via newly made lipoproteins called chylomicrons, whose formation is stimulated by the presence of dietary fat.  So following a high-fat meal, a rise, albeit a usually modest rise, of endotoxin would be seen in the blood.

Before I leave this train of thought and move cautiously along to my recommendations, we need to consider one additional seminal experiment, which was carried out in humans.  In said experiment, weight loss – via a low-fat diet or a calorie restricted low-carbohydrate diet – resulted in a shift in the intestinal microbial ecology in obese subjects, more closely matching that of lean controls.4 In other words, weight loss, in and of itself, altered the intestinal microbial biome favorably.


I’ve always been skeptical about the use of probiotics and prebiotics, and up until doing research for this post saw little evidence to justify their use for any condition – the evidence was so thin.

However, evidence from clinical trials in humans is emerging on the use of prebiotics and probiotics – particularly for the reduction in heart disease risk.

But whether an altered intestinal biome through the use of probiotics or prebiotics could accelerate fat lass and eradicate obesity in humans is unclear to me at this point and I seriously have my doubts about the effectiveness of orally administered probiotic and prebiotic supplements and foods.

From my own experiments and observations, I have been an advocate for, foremost, maximizing and expanding the capacity of oxidative energy generation to promote weight loss and health at the same time – cliché as this is. (At least until fecal probiotic transplants are properly tested for safely reducing body fat and become easily available to us all).  Fundamentally, this entails the following:

  • Increasing oxygen delivery to cells.
  • Supplying adequate amounts of B vitamins, as many of the coenzymes and carrier molecules that operate (as cardinal adsorbents) in the mitochondrial respiratory chain are made from thiamine, riboflavin, niacin, etc.  Ubiquinone, also known as CoQ10, is also important, and the more cholesterol we produce, the more ubiquinone will be made in the amounts needed by cells. Sucrose, namely its fructose half, is a potent stimulator of cholesterol synthesis.8
  • Maintaining the optimal rate of secretion, blood levels, and conversion of thyroid hormone, as thyroid hormone is the main regulator of a person’s metabolic rate and stimulates all reactions in the mitochondria involved in oxidative metabolism.

Regarding the first point, suffice it to say here, putting a brake on the excessive release and oxidation of fatty acids enhances the delivery of oxygen to cells and prevents tissue hypoxia.  Ditching high-fat low-carbohydrate diets serve this purpose.  In addition, “fast-moving” blood is essential, so platelet aggregation and fibrin production must be kept under control.

Because absorbed endotoxin stimulates fibrin production (and interferes with oxidative metabolism), its entry into the body must be minimized (or its removal from the body must be cranked up).

Vitamins K1 and K2, for instance, by enhancing the activity of an intestinal enzyme, minimizes the errant passage of endotoxin (and other harmful substances) into the body.  Vitamin K can be gotten from green vegetables and smaller amounts from fermented dairy and soy products.

Salicylates block the production of a certain prostaglandin that causes platelets to clump and blood vessels to constrict.  Aspirin and other non-steroidal antiinflammatory drugs (NSAIDs) are end products of salicylates, which occur abundantly in plants – especially in fruits.  Gotten from plants – namely fruits – salicylates are delivered to the body at a safer rate and concentration than drugs.  Salicylates also happen to prevent some of the inflammatory responses initiated by endotoxin.

Stress should be kept as low as possible.  Space does not permit me to go further into what I mean here except to say that cravings – namely for salt, sugar, and more food – should not be ignored or suppressed.  This act of defiance imposes undue stress on the body, further enhancing fibrin production.  Listen closely to your body, not diet gurus or Jenny Craig, please.

Of obvious note yet still worth bringing to your attention, one should avoid smoking and excessive alcohol consumption to promote efficient oxidative metabolism because smoking increases the exposure to carbon monoxide, a metabolic poison, and alcohol increases the permeability of the intestinal barrier.

And finally, although the research and evidence for this last recommendation is relatively scant, I would try to eat smaller meals spaced equally throughout the day, instead of large, infrequent meals.  Compared to large meals, I think small meals place less burden on the liver, keep blood sugar levels more steady, reduce endotoxin levels, and decrease the likelihood of storing the food you eat as fat, rather than to generate energy.

Andrew KimAndrew Kim is a graduate of the University of Maryland with degrees in Microbiology and Japanese. His blog has garnered much attention since its release earlier this year. Read more of Kim’s work at


  1. Overweight and Obesity. Centers for Disease Control and Prevention (2013). at
  2. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults–The Evidence Report. National Institutes of Health. Obesity research 6 Suppl 2, 51S–209S (1998).
  3. Mutch, D. M. et al. Impact of commensal microbiota on murine gastrointestinal tract gene ontologies. Physiological genomics 19, 22–31 (2004).
  4. Ley, R. E. et al. Obesity alters gut microbial ecology. Proceedings of the National Academy of Sciences of the United States of America 102, 11070–5 (2005).
  5. Rang, H. P., Dale, M. M., Ritter, J. M., Flower, R. J. Henderson, G. Rang Dale’s Pharmacology. 792 (2011).
  6. Griffiths, E. A. et al. In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice. Digestive diseases and sciences 49, 579–89 (2004).
  7. Cani, P. D. et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia 50, 2374–83 (2007).
  8. Silbernagel, G. et al. Cholesterol synthesis is associated with hepatic lipid content and dependent on fructose/glucose intake in healthy humans. Experimental diabetes research 2012, 361863 (2012).

New Drug May Someday Battle Obesity and Diabetes – WebMD

New Drug May Someday Battle Obesity and Diabetes

Researchers find slim evidence to support many

By Dennis Thompson

HealthDay Reporter

WEDNESDAY, Oct. 30 (HealthDay News) — A new diabetes drug may one day perform double duty for patients, controlling both their blood sugar levels and helping them lose weight, researchers report.

In mouse trials, doctors found the drug prompted weight loss, in addition to managing blood sugar levels.

“That [weight loss] is not what this drug was designed to do, but it’s a very attractive additional benefit,” said study co-author Richard DiMarchi, a research chemist at Indiana University in whose lab the drug was created.

The injectable medication is based on a single molecule that combines the properties of two hormones that send chemical signals to the pancreas, said DiMarchi.

“They signal to the pancreas that you are taking a meal,” DiMarchi said. “The pancreas then responds by secreting insulin and to synthesize additional amounts of insulin for subsequent use.”

People with type 2 diabetes have lower levels of these pancreas-signaling hormones, which are known as incretins, explained Dr. John Anderson, president of medicine and science at the American Diabetes Association.

“The incretin defect in type 2 diabetes is well known, and it’s only within the last few years we have had agents to treat it,” Anderson said.

Human and primate trials revealed that the new drug controls blood sugar with fewer side effects than other diabetes medications. Those side effects can include nausea, vomiting and stomach pain.

“In this study, the degree of gastrointestinal discomfort is much more modest than is experienced in conventional drugs,” DiMarchi said. “We get beneficial glycemic control with this combination drug, and it seems to be with less adverse drug effect.”

The medication combines the action of the hormones GLP-1 and GIP. Current diabetes medications of this sort target GLP-1 receptors in the body; studies involving GIP have produced mixed results.

GLP is known to suppress appetite, and DiMarchi said the weight loss observed in mice might be occurring because the second hormone, GIP, is somehow “turbo-charging” that appetite suppression.

In the mouse trials, a drug based on GLP-1 alone decreased body weight by an average 15 percent. But the new drug combining GLP-1 and GIP decreased body weight by nearly 21 percent, as well as controlling blood glucose and decreasing appetite.

A six-week human trial involving 53 patients with type 2 diabetes found that the medication effectively controlled their blood sugar levels. However, the researchers did not note any change in weight during the relatively short study period.

The higher potency of the combined molecule suggests it could be administered at lower doses than other incretin-based medications, reducing side effects and making the drug easier to take.

“Currently approved drugs are quite effective,” DiMarchi said, “but they are insufficient in normalizing glucose, and they certainly don’t cause much loss of body weight.”

Childhood obesity drops in Chicago kindergarteners

As thousands of Chicago Public School kids sit anxiously waiting for trick or treat time, the city offers some good news and some bad news.

First the good news: New figures released today by the Chicago Department of Public Health suggest that childhood obesity among CPS kindergarteners has dropped by five percentage points, from 24 percent in 2003 to 19.1 percent in 2012.

Yay, right?

Well, don’t break out the king size Snickers yet. That figure still puts their obesity levels well above the national average (12 percent) for kids their age, and even the average (14 percent) for low-income kids.

Additionally, the latest figures don’t show any statistically significant improvements among older students who are measured at 6th and 9th grade.  Instead, those levels seem to be hitting a plateau, which mirrors overall obesity figures in the U.S. during the last decade.

Despite these qualifiers, the news was greeted with some optimism by local folks who have been working on this issue for years.

“I think the new numbers are promising,” said Adam Becker, who heads the Consortium to Lower Obesity in Chicago Children. “For decades we’ve seen major increases in the rates and so to see the rates going down, even in small increments at a time, is an indication that we are moving in the right direction.”

The improvement among CPS kindergarteners follows modest progress in 21 states across the country among very young children, and improvements in other big cities including New York and Los Angeles. But Chicago still posts higher childhood obesity numbers than those big cities for reasons researchers are not quite able to explain.

“I think we are starting to see what we all hope will be an ongoing national decline in obesity levels for all kids,” Becker said. “And this should just encourage us to step it up.” 

Most researchers agree that tripling of childhood obesity in the U.S. over the last 35 years was a result of several converging factors.

To combat them, the city has recently taken a multifaceted approach that has included adding more fruits and vegetables to school lunches and ditching the daily nachos. Other initiatives have involved offering grocers incentives to open in underserved neighborhoods, supporting fresh produce cart vendors, restoring recess to schools and finally gathering and calculating these CPS obesity figures to begin with.

“Obviously I’m really excited about seeing these numbers headed in the right direction,” said Health Commissioner Bechara Choucair. “But we’ve still got a lot of work to do.” 

New Obesity Panacea Feature: Participants Needed

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Every so often here on Obesity Panacea I have posted details about studies looking for participants (thanks to everyone who has decided to participate!).

I’ve recently had requests from a few colleagues asking if I would be willing to post details about their studies, and I’ve decided to make it a semi-regular feature on the blog. Once each month, I will put up a post with short descriptions of studies requiring human subjects.

I have two basic requirements. To be included, a study must:

  1. Have received institutional ethics approval.
  2. Be related in some way to physical activity, sedentary behaviour, diet, or obesity.

If I feel a study is inappropriate for some reason, then I won’t post it. But otherwise I’m happy to promote studies in any geographic location, and on any specific population. Research can’t happen without participants, and I’m happy to help people find out about studies that might be of interest to them.

Today we have two studies, both looking for participants in the Ottawa region. Although I am ineligible for Study 1 (sadly, I am neither female nor perimenopausal), I just finished participating in Study 2 and it was a pretty interesting study.  If you are interested in learning more about either study, please contact the researchers directly.  And if you would like to have your own study featured here on Obesity Panacea, email me the study details at saunders (dot) travis (at) gmail (dot) com.

Study 1: Menopause and Body Composition

Joseph StudyLocation: Ottawa

Participant Population: Females aged 40-60 years

Study Outcomes: The effects of exercise on body composition changes at different menopausal statuses

Contact: Joseph Abdulnour at 613-562-5800 ext. 7361 or by email at

Study 2: Body Morphology and Sweating Response

Matt poster

Location: Ottawa

Participant Population: Males aged 18-40 years

Study Outcomes: The impact of body morphology (e.g. size) on sweating response to exercise

Contact: Matthew Cramer at 613-562-5800 x2655 or by email et

Travis’ Note: I just finished participating in this study myself, and it mainly involved watching movies while cycling at a light-moderate intensity.  And you get a VO2max test, so not a bad deal if you’d like to quantify your fitness.



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Is DDT a time-bomb behind the obesity epidemic? | Grist

ddt_adMichael Skinner didn’t start the experiment with the hypothesis that he’d find a connection between the insecticide DDT and obesity.

“We didn’t expect to find that,” he said. “In fact, the frequency of obesity really came as a surprise.”

Skinner, a scientist at Washington State University, wanted to take a close look at the way DDT affected inheritance. So his team injected DDT into pregnant rats and watched first their children, and then their grandchildren (or is it grandrats?). It was only in the third generation, the great-grand-rat, that they saw it: Fully half of these rats were obese. The implication is that the same thing could be happening with humans.

Michael Skinner
Michael Skinner.

“Is there a correlation between the fact that we were all exposed to DDT in the 1950s for 10 years, and the fact that we are now seeing high levels of obesity?” Skinner asked. His work suggests that there could be.

Of course, the more immediate cause of obesity is too many calories. But there may be more going on here than too much food. Humans are getting fat, so are our pets, so are wild animals. There’s a trend toward obesity in nearly every species scientists have studied.

Of course it’s too early to lay the blame on DDT. This study simply raised the possibility. But the findings are plausible.

“I do believe that the observed obesity is real,” emailed Andrea Gore, a professor of pharmacology and toxicology at the University of Texas Austin. Other experiments have already shown that endocrine-disrupting chemicals can cause obesity generations after exposure, Gore said.

Skinner had already seen that he could trigger the inheritance of disease with various chemicals. There’s a narrow window during the gestation, where an exposure to lots of things can cause heritable epigenetic changes.

“The majority of things we’ve tested came up positive,” he said.

So the obvious question: Is this a problem specific to DDT, or would we have seen similar results if Skinner’s team had decided to inject the rats with vitamin C? In other words, is this about the chemical, or just the timing of the exposure?

If the DDT had caused kidney disease, Skinner said, he would have been reassured. A lot of things seem to have epigenetic effects that lead to kidney disease. But obesity is unusual — that suggests a problem with DDT itself, Skinner said.

Skinner started this experiment after the World Health Organization lifted the ban on DDT to help fight malaria. That was a good decision based on the available information, Skinner said, but no one had looked to see if DDT had an effect on subsequent generations. “On the one hand, there are 2 million deaths per year in Africa from malaria. On the other hand, we’re looking at the possibility of metabolic disease in every generation to come,” Skinner said.

The word “possibility” there is key. This wasn’t a risk assessment study, and we don’t know if we’d see something similar in humans from environmental exposure to DDT, as opposed to direct injection. But this study should give pause to the people arguing to reintroduce DDT to places even without a malaria problem, Skinner said. It’s now being used in France, among other places. And once you spray DDT, it’s out there for a long time.

“If you go to any river in the U.S., and push your finger down into the mud one or two inches, the primary contaminant you will find there is DDT,” Skinner said. The stuff just takes a really long time to break down, and Skinner’s research suggests that its effects could last much longer.

Battle of the bulge: US food corporations fueling obesity epidemic …

Reuters/Lucas Jackson

By 2030, more than half of Americans could be obese, taxing the nation’s health while costing the country $500 billion in lost economic productivity. The food industry, however, is doing its best to keep the public hooked – no matter what the price.

With one out of three adults clinically obese and 40 percent of
children officially overweight, the US is the fattest country in
the developed world. The burgeoning public health crisis will see
instances of diabetes, heart disease, stroke and cancer skyrocket
over the next two decades, taking an already strained healthcare
system to breaking point.

But with food manufacturers keen on keeping customers loyal while
maximizing their profits, public health concerns are likely to be
dwarfed by the bottom line.

“What these food scientists have done is that they’ve gone to a
lab and they’ve created these chemical concoctions that are very
sweet, very fatty and very salty. And they call that the bliss
point. Meaning they’ve created addictive foods that are going to
get consumers hooked and they’re going to keep wanting to come
back for more and more foods,”
Elizabeth Kucinich, of
Physicians Committee For Responsible Medicine, told RT.


And while critics might also point toward issues of self-control,
the foods which are least healthy are also the cheapest, although
this reality is more a failure of government policy than an

In 1980, no one had even heard of high-fructose corn syrup. But
agricultural subsidies highly distorted market prices, bringing
about the rise of cheap corn, which is a staple of highly
processed foods like soft drinks and much of what one finds on
the supermarket shelves.

Between 1985 and 2010, the price of beverages sweetened with
high-fructose corn syrup fell 24 percent in real terms, with
American children consuming on average an extra 130 calories
daily from soft drinks.

If that wasn’t bad enough, a 2010 Princeton University study
found that rats with access to high-fructose corn syrup gained
substantially more weight than those with access to table sugar,
even if their overall caloric intake was equal.  

However, a plan by New York City Mayor Michael Bloomberg to limit
soda drinking cups to 16 ounces, for example, was met with
derision, even when the public health benefits of such a ban were

And it’s not just corn. Casein, a milk protein commonly used in
processed foods, also has addictive qualities that lead to

“Milk protein… casein, when it breaks down in our digestive
system, turns into casomorphin, [which] is relative to morphine –
the drug,”
Kenneth Kendrick, a whistleblower and food safety
advocate, told RT. “It gives us a little stimulation in our
brain and gives us a little bit of pleasure.”

Kendrik said the reason why food in the US is both addictive and
laden with fat, sugar and salt is simple.  

“In one word, I would say: greed. We obviously are putting
money above public health,” he said. “Just like with cigarettes,
we want to keep people addicted. I equate it to what the
cigarette industry did. They deliberately wanted to put things in
that were addictive because that drives sales and will continue
to drive generations of sales.”

But as savvy and unrestrained marketing campaigns allow
corporations full rein to market their products to the US public,
the defeat of California’s Proposition 37, which would have
required the labeling of all food products containing genetically
modified organisms, proves that they want full control over the
narrative about what US consumers are putting into their bodies.

“While European countries require genetically modified foods
to be labelled, in the US the biotech industry and corporations
like Pepsi Co. and Coca Cola spent millions last year to defeat
the California ballot initiative for GMO genetically modified
organism labeling,”
Kucinich said.

It is this perfect storm of labeling control, addictive food
additives and shockingly effective marketing that has America on
course for an epidemic of monumental proportions.

Dispute over data rights forces retraction of obesity paper …

bmcresnotesA group of researchers in South Africa has lost their 2012 article in BMC Research Notes after one of the author’s institutions evidently pulled rank and sought to claim the data as its own.

The article, “Association of body weight and physical activity with blood pressure in a rural population in the Dikgale village of Limpopo Province in South Africa,” appeared last February. Its first author was Seth Mkhonto, who listed two affiliations, the Human Sciences Research Council, in Pretoria, and the University of the Limpopo.

But the latter institution seems not to have given Mkhonto approval to publish the data — a rather strange state of affairs given the whole “publish or perish” ethos of academia.

According to the retraction notice:

This article has been retracted by the Editor because the authors do not have ownership of the data they report. A formal investigation conducted by the University of Limpopo, South Africa, has concluded that the data reported in this article are the sole property of the University of Limpopo.

The abstract of the paper doesn’t shed any light on why it might have been controversial:

Africa is faced with an increasing burden of hypertension attributed mainly to physical inactivity and obesity. Paucity of population based evidence in the African continent hinders the implementation effective preventive and control strategies. The aim of this study was to determine the association of body weight and physical activity with blood pressure in a rural black population in the Limpopo Province of South Africa.


A convenient sample of 532 subjects (396 women and 136 men) between the ages 20-95 years participated in the study. Standard anthropometric measurements, blood pressure, and physical activity were recorded by trained field workers.

The paper has been cited once, according to Thomson Scientific’s Web of Knowledge.

Child obesity: Families 'in denial' over dangers of overweight …

Families in denial over dangers of child obesity
Families ‘need to recognise that obese children are in trouble’ (Picture: PA)

Obese children are having their chances of fighting the flab scuppered by relatives in denial, a report reveals.

Overweight youngsters face serious health problems in later life and need family members to recognise they are in trouble, the study states.

And with about 30 per cent of two to 15-year-olds in England classified as overweight or obese, the National Institute for Health and Care Excellence is calling for urgent action. ‘Efforts to manage a child or young person’s weight are not always supported, and are sometimes undermined, by members of the wider family,’ the Nice report says.

‘A lack of recognition or denial that the child is overweight can hinder uptake and adherence to a lifestyle weight management programme.’ Children with at least one obese parent are more likely to follow suit themselves, the Nice report added.

Meanwhile, 79 per cent of overweight early teens are likely to be so as adults, raising the risk of cancer, heart disease and type 2 diabetes.

Although critical of families who refuse to admit their children have a problem, Nice said local authorities should step in to help battle the bulge. Prof Mike Kelly said: ‘Parents should not have to face the challenge of obesity on their own.

We are recommending family-based lifestyle programmes are provided which give tailored advice.’

However, Tam Fry, of the National Obesity Forum, said councils have been handed a ‘poisoned chalice’ of dealing with it without proper funding.

Suffering from Obesity | Dances With Fat

Belly Bump with one of my heroes - Marilyn Wann

Belly Bump with one of my heroes – Marilyn Wann

I decided to repost this blog based on a few conversations I had and saw in the last few days.  I see people talk a lot about how we need to “do something,” and how abusive and exploitative things like The Biggest Loser are justified  because so many people are “suffering from obesity”.  I won’t presume to speak for everyone but I will say that while I sometimes do suffer because I’m obese, I’ve never suffered from obesity.

I’m suffering from living in a society where I’m shamed, stigmatized and humiliated because of the way I look. Where I’m oppressed by people who choose to believe that I could be thin if I tried (even though there’s no evidence for that), and that I am, in fact, obligated to try to be thin because that’s what they want me to do – as if personal responsibility means that I’m personally responsible for doing what they think I should do and looking like they think I should look (though this does not seem to be a two way street as none of these people has ever invited by commentary and suggestions on their life and choices.)

I’m suffering from doctors who have bought into a weight=health paradigm so deeply that they are incapable of giving me appropriate evidence-based healthcare.  I’m not just talking about diagnosing me as fat and giving me a treatment plan of weight loss (which is using a completely unreliable diagnostic and then prescribing a treatment that has the opposite result 95% of the time).  I’m also talking about the two doctors who tried to prescribe me blood pressure medication without taking my blood pressure or looking at my chart to see that it is always 117/70 (which means that taking blood pressure medication would have been dangerous).  I’m talking about a doctor trying to get me to lose weight to treat me for Type 2 Diabetes when I actually had anemia.  I’m talking about a doctor telling me that my strep throat was due to my weight. I’m talking about people who are supposed to be scientists abandoning science and research in a way that strongly resembles the time when the Catholic church told Galileo to sit down and shut up.

I’m suffering from a societal witch hunt where instead of putting me in a river they put me on a scale.  People look at my body and feel comfortable blaming me for everything from global warming to healthcare costs despite a lack of evidence for either. People send me ridiculous hate mail, say nasty things to me at the gym (although making fun of a fat person at the gym is something I will never understand).  People who are drenched in thin privilege try to use that position of privilege to make me feel bad about myself.

I’m suffering from the misinformation campaign that is led by the diet industry, weight loss pharmaceutical industry and surgeons who profit from mutilating people who look like me, none of whom are willing to be honest about the risks or horrible success rates of their interventions long term, and some of whom just don’t seem to care.

I am suffering from living in a society that tells me that the cure for social stigma, shame, humiliation and incompetent healthcare is for me to lose weight, when the truth is that the cure for social stigma is ending social stigma.

What has lessened my suffering is that I now realize that this isn’t my fault – although it becomes my problem. One of the reasons that I choose to pursue a life of social justice work is that nothing makes me feel better than knowing that I am doing what I can to fight this and making some kind of difference – whether it’s in the lives of individuals or in society, or just in my own life.  I deserve better and so does everyone else and I and lots of others are fighting for it and we’re going to win.  But to be clear, we shouldn’t have to.  Nobody should have to fight to be treated with basic human respect.   And that’s what I find so sad – all of this suffering of fat people could end right this second and nobody needs to lose a pound – society just needs to stop trying to shame, stigmatize, humiliate and hate people healthy.  We can work on access to healthy foods, we can work on access to safe movement options that people enjoy, we can work on making sure that people have access to appropriate, evidence-based healthcare.  If we give up being a horribly failed example for making people thin, we could be a successful example for giving people options for health.

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Safe foods – Lets take on childhood obesity | Grovelands Childcare

Parents are being urged to make practical changes to everyday lifestyle habits such as portion sizes, drinks and screen time to make a big difference to the health and wellbeing of children and combat the island’s high levels of childhood overweight and obesity. That was the message from safefood with the launch today of a new public health campaign to help parents take on childhood obesity. The campaign will feature on television, radio, poster and point of sale advertising and includes a free booklet for parents that will be available nationwide in crèches, health centres, GP surgeries, and from public health nurses and local libraries.

Launching the campaign, Minister for Health Dr James Reilly TD said: “Obesity presents a real clinical, social and financial challenge which will have a detrimental legacy lasting decades and which will undoubtedly lead Ireland to an unhealthy and extremely costly, if not unaffordable, future if action is not taken now. I want to encourage everybody to help create generations of healthy children who can enjoy their lives to the full and reach their full potential as they develop into adults by making healthier food choices, by being more active and taking the first steps towards reducing overweight and obesity.”

Speaking at the campaign launch, Minister for Children and Youth Affairs Frances Fitzgerald TD said “Childhood obesity has reached epidemic proportions in Europe and Ireland is one of the countries worst affected. The Growing Up in Ireland survey, 2011 which is funded by my Department found that 1 in 4 children as young as 3 years of age are overweight or obese. I particularly welcome this new campaign as it seeks to help parents with very practical tips and ideas for actions they can take. We know from research that tackling obesity in childhood requires a family-centred approach, that is part of a wide ranging multi-agency set of initiatives.

The safefood campaign emphasises the importance of taking on practical changes for the whole family which are sustainable for the long term. Dr Cliodhna Foley-Nolan, Director of Human Health and Nutrition, safefood said: “We have based our campaign on strong feedback from parents that they wanted a solutions-based approach. For this phase we’re focusing on reducing portion sizes for children, replacing sugary drinks with water and being realistic about foods that ‘should be’ treat foods. While parents may be somewhat aware of the sugar levels in fizzy drinks, they may not be as aware of the sugar content in juice drinks and cordials, and research tells us they are regularly given to children at mealtimes. The sugar content of these drinks varies enormously and parents need to consider replacing these drinks with water instead”, added Dr. Foley-Nolan.

The three year, all island campaign by safefood in partnership with the HSE and Healthy Ireland Framework in the Republic of Ireland and the ‘Fitter Futures for All’ Implementation Plan in Northern Ireland also reminds parents about the negative health impacts of excess weight in childhood and how this can impact on a child’s quality of life.

Dr Cate Hartigan, Head of Health Promotion and Improvement, HSE said “Parents want what is best for their children, however tackling overweight and obesity is a sensitive and difficult task. A fundamental goal of Healthy Ireland is supporting people to enjoy a healthy and active life. This campaign helps make this a reality by motivating and supporting parents to make healthier choices for their children, and by raising awareness and knowledge among health professionals.

Chair of the safefood Advisory Board, Ms Lynn Ní Bhaoighealláin said “We all want children to have a bright future and we get them into all sorts of healthy habits, like brushing their teeth or crossing the road safely. This campaign is about supporting parents in making small changes in their everyday family lives.” At present, approximately 1 in 4 primary¹ school children are overweight or obese. The prevalence of excess weight is also beginning earlier in childhood², with currently 6% of 3 year olds being obese. Speaking at the campaign launch, Consultant Paediatrician and Clinical Lead for the W82GO Healthy Lifestyles programme at Temple Street Children’s Hospital, Dr Sinead Murphy said “With a quarter of children overweight or obese, we need to tackle the issue of childhood obesity head on or our next generation will be beset with significant health problems later in life. Evidence shows that once obesity is established, it is both difficult to reverse and can track into adulthood”. “Sadly, children who are overweight are at serious risk of becoming adults who are obese. This increases the risk manifold of developing serious illnesses such as type 2 diabetes, heart disease, stroke, certain types of cancers and shortened life-expectancy”, she continued.

Welcoming this initiative by safefood, Dr Darach O’Ciardha, ICGP Spokesperson said “Obesity is one of the conditions where prevention is certainly better than cure. Any move to educate parents about the need to monitor and prevent bad dietary habits which will last a lifetime, from developing is welcome. This initiative is a first step in tackling the ticking time bomb that is rising obesity levels particularly amongst the young.”

The safefood campaign will also be supported on the safefood website and on social media, including Facebook and Twitter. To find out more about the campaign including how-to videos from health experts and practical advice and guides for parents, visit:  – See more at: