Gram Negative Bacteria and Obesity – 180 Degree Health

By Andrew Kim 

Introduction

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 AND THE INTESTINAL FLORA

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.

RECOMMENDATIONS

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 www.andrewkimblog.com

 REFERENCES

  1. Overweight and Obesity. Centers for Disease Control and Prevention (2013). at http://www.cdc.gov/obesity/data/adult.html
  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).

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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If my selling things on the blog makes you uncomfortable, you might want to check out this post.  Thanks for reading! ~Ragen

'Healthy Obese' Is Possible, But Maybe Not Forever

As many as a third of obese adults are considered metabolically healthy, meaning they have normal cholesterol and blood pressure levels and show no signs of developing diabetes. Still, they’re considered a medical mystery, but new research has shed some light on why some people can be healthy at any size, while others cannot.

It has to do with fat cells, according to a new study in the journal of Diabetologia. Compared to obese people who are healthy, those who are metabolically unhealthy have “impaired mitochondria” and a “reduced ability to generate new fat cells.”

What researchers found was that in a healthy obese person, new cells are generated to help store fat as it accumulates, whereas the cells of an unhealthy obese person “swell to their breaking point,” making their fat cells larger than any other group.

They were swollen and riddled with inflammation. The breakdown and mobilization of their fat stores was suppressed, and a closer look showed that their mitochondria were malfunctioning. Their ability to burn fuel and produce adenosine triphosphate, or ATP, the body’s energy currency, was reduced.

It leads to ectopic fat accumulation, meaning that fat gets into organs like the heart and liver. (A fatty liver is linked to Type 2 diabetes.)

However, for a healthy obese person, the fat doesn’t travel throughout the body, and remains just beneath the skin, where it doesn’t seem to cause any physical harm.

A study that appeared in the journal Diabetes Care in August found that metabolically healthy obesity is more frequently found in younger adults, but it may be a transition state, and that “some, if not many, people in this category will eventually develop the expected metabolic disturbances.”

Dr. Jussi Naukkarinen, the lead researcher in the fat cell study, said that anti-inflammatory drugs have been shown to “protect mitochondrial function and improve diabetic symptoms and glucose metabolism.” He also suggests that high glycemic foods (like sugar and white flour) play a role in spiking blood glucose and insulin levels.

But ultimately, he believes that studying healthy obese people will help those that are unhealthy.

“People haven’t really paid that much attention to metabolically healthy obesity, but I think it can teach us a lot about usual obesity,” he said. “It’s only recently that people studying depression have done happiness studies showing what goes right, and I’m thinking about the metabolically healthy obese phenomenon in the same way.”

Image via xrender/Shutterstock

The ‘Healthy Obese’ and Their Healthy Fat Cells [NYT]

Whole Health Source: Sleep and Genetic Obesity Risk

Evidence is steadily accumulating that insufficient sleep increases the risk of obesity and undermines fat loss efforts.  Short sleep duration is one of the most significant risk factors for obesity (1), and several potential mechanisms have been identified, including increased hunger, increased interest in calorie-dense highly palatable food, reduced drive to exercise, and alterations in hormones that influence appetite and body fatness.  Dan Pardi presented his research at AHS13 showing that sleep restriction reduces willpower to make healthy choices about food.

We also know that genetics has an outsized influence on obesity risk, accounting for about 70 percent of the variability in body fatness between people in affluent nations (2).  I have argued that “fat genes” don’t directly lead to obesity, but they do determine who is susceptible to a fattening environment and who isn’t (3).  I recently revisited a 2010 paper published in the journal Sleep by University of Washington researchers that supports this idea (4).


Dr. Nathaniel Watson and colleagues used twins to tease apart what proportion of obesity risk is due to genes vs. environment, and if sleep duration influences that relationship.  Consistent with other studies, genetics explained 60 percent of the variability in body fatness between participants.  Also consistent with other studies, people who slept less tended to be fatter.  However, what sets this study apart is that they determined how sleep duration influences the relationship between genetics and body fatness.

What they found is nothing short of remarkable.  In people sleeping less than 7 hours per night, genetics determined 70 percent of body fatness, while the environment (lifestyle/diet and ‘random’ effects) explained only 30 percent.  In people sleeping more than 9 hours per night, genetics only explained 32 percent of body fatness, while environment explained 68 percent.  In other words, in people who sleep more than 9 hours, the environment and not genes was the primary determinant of body fatness.

The result was summarized in the following graph:



According to the authors, short sleep duration appears to favor the expression of genetic risk factors for obesity:

Our work suggests latent genetic variability in susceptibility to obesity requires activation by sleep curtailment.

In other words, in an obesity-promoting (low-sleep) environment, people who are genetically susceptible to obesity gain fat, while in a non-obesity-promoting (high-sleep) environment, genetic risk factors are less relevant and don’t influence body fatness as much.  “Obesity genes” act primarily in an obesity-promoting environment.

As a whole, I find the sleep-obesity research quite compelling.  This is one of the reasons why the Ideal Weight Program focuses on improving sleep quantity and quality, a strategy that sets it apart from nearly every other fat loss program.  We combine a tracking system that provides consistent objective feedback on sleep habits, with sleep guidance that helps overcome barriers to restorative sleep.

There's an Obesity Epidemic Among America's Dogs

It’s only natural that, being a nation of fatties, our lifestyle is directly reflected on our pets. More than half of American dogs are overweight, according to the Association for Pet Obesity Prevention, and while it might be kind of cute, it’s definitely not healthy.

Just like with humans, canine obesity puts dogs at a heightened risk for diabetes, high blood pressure, arthritis, and respiratory diseases, so vets are advising that their patients be put on strict diet and exercise regimens. After all, dogs tend to be overweight because of “lazy owners who confuse food with affection and attention.”

“Dogs today have butlers and maids,” Cesar Millan said. “They don’t hunt for their food anymore, but they should work for food.”

It also has to do with a carb-heavy diet. Dogs apparently don’t really possess a need for carbs unless they are pregnant or nursing. Ideally, they should be on a raw-foods diet, which actually means “a whole rabbit…or a whole squirrel for a fox terrier” which is completely disgusting.

What’s sad is that fat dogs have less of a chance of being adopted.

Indigo Ranch in Vernonia, Ore., is a kennel that offers what it calls a doggy fat camp. The camp began about two years ago, shortly after a county shelter contacted Indigo Rescue, the nonprofit rescue organization financed by Indigo Ranch, about a 3-year-old Lab aptly named Butters. At 142 pounds, he was considered unadoptable and was about to be euthanized, said Heather Hines, the director of Indigo Ranch…

…About five months after he arrived, he had slimmed to 84 pounds.

“He didn’t know he could run or jump until he lost the weight,” Ms. Reed said.

Poor Butters.

Image via WilleeCole/Shutterstock

Roll Over? Fat Chance [NYT]

Preventing Childhood Obesity: Tips for Parents and Caretakers

Balance is key in helping your child maintain a healthy weight. Balance the calories your child eats and drinks with the calories used through physical activity and normal growth.

Overweight and obese children and teens should reduce the rate of weight gain while allowing normal growth and development. Don’t put your child on a weight-reduction diet without talking to your health care provider.

Balancing calories: Help Kids Develop Healthy Eating Habits
Offer your kids nutritious meals and snacks with an appropriate number of calories. You can help them develop healthy eating habits by making favorite dishes healthier and by reducing calorie-rich temptations.

  1. Encourage healthy eating habits. Small changes can lead to a recipe for success!
    • Provide plenty of vegetables, fruits and whole-grain products.
    • Include low-fat or non-fat milk or dairy products.
    • Choose lean meats, poultry, fish, lentils and beans for protein.
    • Serve reasonably sized portions.
    • Encourage your family to drink lots of water.
    • Limit sugar-sweetened beverages, sugar, sodium and saturated fat.
       
  2. Make favorite dishes healthier. Some of your favorite recipes can be healthier with a few changes. You can alsotry some new healthy dishes that might just become favorites too!
     
  3. Remove calorie-rich temptations. Treats are OK in moderation, but limiting high-fat and high-sugar or salty snacks can also help your children develop healthy eating habits. Here are examples of easy-to-prepare, low-fat and low-sugar treats that are 100 calories or less:
    • A medium-size apple
    • A medium-size banana
    • 1 cup blueberries
    • 1 cup grapes
    • 1 cup carrots, broccoli, or bell peppers with 2 tbsp. hummus
       
  4. Help your kids understand the benefits of being physically active. Teach them that physical activity has great health benefits like:
    • Strengthening bone
    • Decreasing blood pressure
    • Reducing stress and anxiety
    • Increasing self-esteem
    • Helping with weight management
       
  5. Help kids stay active.
    Children and teens should participate in at least 60 minutes of moderate-intensity physical activity most days of the week, and every day if possible. You can set a great example! Start adding physical activity to your own daily routine and encourage your child to join you. Some examples of moderate-intensity physical activity include:
    • Brisk walking
    • Playing tag
    • Jumping rope
    • Playing soccer
    • Swimming
    • Dancing
       
  6. Reduce sedentary time. Although quiet time for reading and homework is fine, limit “screen time” (TV, video games, Internet) to no more than two hours a day. The American Academy of Pediatrics doesn’t recommend TV for kids age 2 or younger.12 Encourage your children to find fun activities to do with family members or on their own that simply involve more activity.

Learn more:

  • Childhood Obesity
  • BMI in Children
  • Making a Healthy Home

The whys of rising obesity | Harvard Gazette

Harvard nutrition expert Walter Willett compared the marketing of junk food to kids with an earlier era’s child labor practices, saying that young people have been “exploited” by both systems. He said such food marketing is an important factor in America’s obesity epidemic.

“Children are being exploited, same as sweatshops,” Willett said. “This is a natural consequence of a capitalist food supply.”

Willett, speaking today at a Forum at Harvard School of Public Health (HSPH), said that much of the blame for the obesity epidemic should go to food industry researchers who have done their jobs all too well. Under pressure from the ever-competitive food industry, the researchers perfected not just the preferred tastes of prepared foods, but also their packaging and advertising.

Marketing strategies aimed at children influence a population this is not only vulnerable to such messages, but is also establishing long-lasting dietary habits.

Panelists on the forum webcast included Willett, who chairs the HSPH’s Nutrition Department; Michael Rich, an associate professor at HSPH and Harvard Medical School (HMS) and director of the Center on Media and Child Health at Harvard-affiliated Children’s Hospital Boston; Dariush Mozaffarian, associate professor of epidemiology at HSPH and associate professor of medicine; and former Food and Drug Administration Commissioner David Kessler, now a professor at the University of California at San Francisco. The hour-long panel, called “Why We Overeat: The Toxic Food Environment and Obesity,” took place before a small studio audience in the Kresge Building and drew Internet viewers from as far away as Australia.

The discussion cast a strong light on America’s children, 17 percent of whom are obese and 5 percent of whom are in a new category called “severely obese,” according to panel moderator Meredith Melnick of the Huffington Post, which co-sponsored the event.

While food industry marketing plays an important role in the obesity epidemic, panelists described several other important factors that are increasingly causing experts to view the epidemic not as a collective failure of personal willpower but as the offshoot of an unhealthy food environment. Among the concerns are changing eating habits, where people no longer eat just at mealtimes, and the tendency to eat while watching television.

Television is a factor in the fattening of America, the panelists said, displaying what public health officials call a “dose-response” relationship with obesity — meaning the more television we watch, the fatter we get. The amount of time children spend interacting with screens on televisions, computers, cellphones, and other devices has risen dramatically, Rich said, to more than seven hours a day. But it is television time — with focused attention, exposure to advertising, and “mindless eating” — that has proven a key obesity factor, Rich said.

Although sedentary lifestyles often share part of the blame for the epidemic, Mozaffarian said that is largely unwarranted. People today, he said, are no less active than they were in the 1970s, before the epidemic began to take hold. Rather, he said, the blame lies squarely on changes to the American diet since the early 1980s.

In that time, portion sizes have increased, and consumption of sugary drinks has soared. One important factor in the changes, he said, was well-intended. The anti-fat messages of the ’80s drove many people concerned about their health to avoid fat in foods, and instead to increase their carbohydrate intake. The problem, Mozaffarian said, was that much of those carbohydrates were in the form of highly processed starches that in the body behave in much the same way as sugar.

Willett and Mozaffarian rejected the idea that genetics plays a role in the epidemic. Though some experts have pointed to the body’s ability to hold onto calories as an ancient defense against famine, the two pointed out that the current crisis is a new development, one largely not suffered in our grandparents and great-grandparents’ time, when obesity rates were a third what they are today. Genes, they said, don’t change that quickly.

Panelists disagreed about the significance of America’s high-sugar diet, with Kessler saying that sugar combines with too much salt and fat in irresistible products that amount to a food “carnival.” Mozaffarian, however, said the focus on any particular component of food can be misleading. Instead, he said, people should focus on eating whole foods like fruits, vegetables, nuts, and grains.

“It’s really the kinds of food that’s important,” Mozaffarain said. “We focus a lot on what not to eat; we need to focus on what’s good to eat.”

Willett suggested something akin to the Mediterranean diet, which Mozaffarian pointed out has more fat in it than the typical American diet. Without some sort of regulation to force a change, however, Willett was pessimistic that a solution is near.

“If we have no restraints, the problem isn’t going away. It’s only going to get worse,” Willett said.

Can Bacteria Fight Obesity? Gut Bacteria From Thin Humans Can …

fat-mouse-bannerfat-mouse-banner

Why are some people fat? It’s not just a question that fat people ask themselves, but also one that drives much medical research because obesity increases the risk of serious illnesses including heart disease and diabetes.

A study recently published in Science adds gut bacteria to the list of possible causes of obesity.

The intestine is home to trillions of microbes that help the body break down and use food. The particulars of the mix have been found to vary significantly from person to person, even among identical twins.

Gordon-RidauraGordon-RidauraIn an effort to isolate the contribution of gut bacteria to weight, researchers led by Jeffrey Gordon, of Washington University in St. Louis took the bacteria from pairs of identical and fraternal twins, each with one obese twin and one lean, and put it in previously germ-free cloned mice. (We glossed tastefully over the matter of the fecal transplant.)

The results indicate that bacteria does in fact play a powerful role: The mouse that got the obese twin’s bacteria grew fat and developed metabolic problems linked to insulin resistance, even when fed only low-fat mouse chow.

The researchers then housed the fat and thin mice together, allowing their gut bacteria to mix. (Mice housed in the same cage typically eat each other’s droppings.) The thin bacteria beat out the fat bacteria in the obese mice, and they became thin again.

So is obesity purely a question of gut bacteria? No such luck. The “thin” bacteria, specifically a group called Bacteroidetes, was only able to triumph when the fat mice were eating low-fat mouse chow. When they were fed a higher-fat food meant to mimic a typical American diet, obese mice kept the obese twin’s gut bacteria — and the excess weight.

Bacteroides biacutisBacteroides biacutis

Bacteroides biacutis

“Eating a healthy diet encourages microbes associated with leanness to quickly become incorporated into the gut. But a diet high in saturated fat and low in fruits and vegetables thwarts the invasion of microbes associated with leanness. This is important as we look to develop next-generation probiotics as a treatment for obesity,” said Gordon.

It can’t be long before we see Bacteroidetes and other potentially thinning “probiotics” for sale in the supermarket next to green tea.

But, buyer beware, the mouse studies are far from conclusive. The next step for Gordon and his team will be growing microbes in the lab and mixing them to nail down which combinations have which metabolic effects.

“There’s intense interest in identifying microbes that could be used to treat diseases,” he said.

Especially diseases that make us fat.

Photos: Lexicon Genetics Incorporated via Wikimedia Commons; Gordon with graduate student and co-author Vanessa Ridaura, E. Holland Durando, Washington University of St. Louis; CDC via Wikimedia Commons

The Obesity Conspiracy | In Their Own Words | Big Think

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I think we’re facing, unfortunately, a loosely organized conspiracy to promote disease and obesity.  By default or by design, one-third of our economy profits from people being sick and fat. So big food, which is industrial food, big farming, which is agribusiness, and big pharma all profit from making people sicker and fatter. 

It’s hard to fight that battle.  We see, for example, the Robert Wood Johnson Foundation spends $100 million fighting childhood obesity in this country.  The food industry spends that in four days to promote junk food and processed food, and the worse the food is for you the more they advertise and promote it. 

It’s hard to fight that when government subsidies are supporting high fructose corn syrup production and trans fats, when you’re standing at the fast food restaurant and the government is standing there with you buying your cheeseburger or French fries and soda but they’re not standing with you at the produce aisle because there are no subsidies for fruits and vegetables. 

So we’re providing an obesogenic environment and we need to think about how we can change that by changing some of our policies, by changing how we market foods.  The government requested, the FTC requested, that the food industry change its marketing around food and basically restrict marketing for foods that had high salt, fat and sugar.  But this was only a recommendation to change.  It wasn’t a demand or a regulation.  And they only suggested they do it in five years, so that’s like saying to tobacco let’s stop marketing cigarettes to kids in five years, and, by the way, you only have to do it if you really want to.  That’s not how we’re going to create change in America.  

In Their Own Words is recorded in Big Think’s studio.

Image courtesy of Shutterstock

 

Fat But Fit: Metabolically Healthy Obesity


Photo:
Suzanne Tucker/Shutterstock

Can you be fat and healthy at the same time? Apparently so, according to a new study by University of Pennsylvania physicians and obesity researchers who say that there are people with “metabolically healthy obesity.”

Many obese people are classified as such when their body mass index or BMI reaches a certain value. BMI, a formula based on a person’s weight and height, was invented by Belgian mathematician Adolphe Quetelet in the early 19 century and has garnered wide acceptance as a simple way to measure “fatness.” It’s quick and easy to administer – requiring only a scale and a ruler – and allows for comparison for broad populations, taking in age and country-by-country variations. Indeed, BMI is a good statistical measure of the obesity of a whole population of people.

Doctors have noted, however, that some people with BMI in the obese range are actually quite healthy and that in many cases, fat people fare better than thin ones with the same ailments. In the “obesity paradox,” researchers noted that diabetic patient of normal weight are twice as likely to die than those who are obese. Others have pointed out that thin dialysis patients are more likely to die than heavier ones.

In recent years, the medical field has began to accept that BMI is not a reliable measure of health in individuals, and that some people who are obese do not have nor are they in any danger of developing obesity-related diseases.

But how many people are actually “fat but fit” and “not fat but not fit”? The answer may surprise you. For 1 in 5 Americans, BMI may actually tell the wrong story:

– 8% of normal-weight adults in the United States are actually metabolically unhealthy
This translates to 19.2 million people whom doctors may not currently worry about but should.

– 10% of obese adults
are actually metabolically healthy
This means that 24 million chubby Americans are not in any danger of dying because of obesity-related illnesses, but are probably badgered by their family, friends and employers to lose weight.