Wednesday, June 11, 2014

Has Obesity Research Failed?

I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates.  According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.

Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*.  What gives?  Maybe if we just scrapped the whole endeavor we'd be better off.

Let's take a closer look at this argument and see how it holds up.

Why Do Research?

There are two fundamental reasons why we do research:
  1. To gather accurate information about the natural world.  This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
  2. Practical applications.  We want to solve problems and improve our lives.
If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.

Has Obesity Research Gathered Accurate Information?

By this metric, there can be no question that obesity research has been a smashing success.  Starting as far back as the 1700s**, and accelerating rapidly until today, researchers have uncovered a tremendous amount of information about the human body that relates to obesity-- from digestion, to the thermodynamics of energy balance, to the physiology and endocrinology of energy regulation by the body, to the neurobiology of appetite and body fat regulation, to the psychology of eating behavior.  

We understand many of the hormones and neural signals that regulate the body's use and storage of fats, carbohydrates, and proteins.  We understand many (probably most) of the primary pathways that regulate appetite.  Researchers like Scott Sternson, Brad Lowell, and Richard Palmiter are dissecting the neural circuits of appetite down to the cellular and molecular level-- a feat that would have been inconceivable 50 years ago.  

We understand the impact of a number of food properties on food selection and intake.  We understand how the food environment impacts eating.  We've identified countless differences between obese and lean people, including in genetics, neurobiology, energetics, metabolism, endocrinology, and behavior.

Collectively, the information we've gathered forms a massive, highly buttressed body of knowledge that meshes seamlessly with related fields of science.  Some of the details are probably wrong, but the likelihood that there's something fundamentally wrong with the whole edifice, is, in my opinion, approximately nil.  

The current literature contains more than enough evidence to form a reasonable working model that explains the obesity epidemic.  But explaining isn't the same as doing something about it.

Has Obesity Research Delivered Practical Value?

In an ideal world, obesity researchers would have discovered techniques for easily preventing and reversing obesity.  Similar to how researchers identified the nutritional cause of pellagra (niacin deficiency) and virtually eliminated the epidemic with vitamin fortification in the early 20th century, perhaps we might have identified some agricultural chemical that's behind it all, and eliminated it.  Case closed, great work, high five, let's call it a day.

Clearly, that hasn't happened.  Despite the mountains of information we've accumulated, we still have an obesity epidemic, and no easy cures.

On the other hand, researchers have actually identified a number of effective techniques for preventing and reversing obesity.  The simplest of these is calorie restriction.  A number of tightly controlled studies show that calorie intake has a powerful influence on body fatness.  The problem with restricting calories isn't that it's ineffective-- in fact, it's 100 percent effective.  The problem is that it's difficult to implement and maintain.  The unconscious energy-regulating parts of the brain fight back by increasing hunger and reducing the number of calories expended, and ingrained preferences and habits undermine long-term adherence to the restriction.  Increasing calorie expenditure via exercise has similar effects.

A large proportion of obesity research has been dedicated to trying to figure out ways to get people to eat fewer calories.  Countless diets and behavioral strategies have been tested in randomized controlled trials.  If there's one consistent finding that has emerged from these studies, it's that it's exceedingly difficult to get people to change their behavior sustainably, particularly when the change involves a diet.  We know people lose fat when they eat less, but it's difficult to get them to do so, regardless of the strategy.  That being said, some strategies are clearly more effective than others.

Another effective technique is bariatric (weight loss) surgery.  The Roux-en-Y and sleeve gastrectomy procedures cause remarkable fat loss and resolution of type 2 diabetes-- far superior to any other method that has ever been tested in free-living people.  This isn't because people can't fit as much food in their stomachs, and it also isn't because more calories end up in the toilet.  It seems to relate to (poorly understood) alterations in the communication lines between the gut and the brain.  The problem with bariatric surgery isn't that it doesn't work, and it isn't that it's unsafe***-- the problem is that most people don't want to have major surgery on their digestive tract, and it's only available for extreme cases.  Researchers are currently trying to understand the mechanisms of bariatric surgery so we can mimic it without surgery, and they've made some encouraging progress.

Research has also uncovered a number of effective anti-obesity drugs.  One of the earliest was 2,4-dinitrophenol, which causes the mitochondria to pump out heat instead of chemical energy, wasting calories.  It's effective drug but it caused too many deaths due to overheating.  Apparently some bodybuilders still use it, illegally.

In recent decades, a number of drugs were developed that act on the brain pathways that regulate appetite.  You may have heard of fen-phen (fenfluramine/phentermine), an effective weight loss combo that increases monoamine neurotransmitter (dopamine, serotonin, norepinephrine) levels in the brain.  Fen-phen was taken off the US market in 1997 due to negative side effects-- primarily its ability to promote heart valve disease.

Rimonabant is basically "reverse marijuana", acting to block the same receptor that gives people the marijuana munchies.  This pathway regulates appetite and pleasure.  It was an effective weight loss drug, but perhaps unsurprisingly, it had adverse psychological effects including increased suicide rates.

Currently, we have three obesity drugs approved for the US market, and more in the pipeline.  Lorcaserin acts on an appetite circuit in the brain, and seems fairly innocuous, but its effect is pretty modest.  Phentermine/topiramate (Qsymia) acts on appetite and reward centers and is a fairly effective drug, but it has significant negative side effects.  Orlistat blocks about 1/3 of fat digestion so that some of it ends up in the toilet.  It's relatively safe but the results are modest.

Liraglutide is a drug that has done well in clinical trials of obesity treatment.  Novo Nordisk has filed for FDA approval of the drug for obesity treatment purposes.  It's already approved for the treatment of type 2 diabetes.  It mimics a natural satiety (and insulin-secretion) factor called GLP-1.  It's relatively safe as far as we know, and some of its known side effects are actually positive, but unfortunately it's expensive and it has to be injected daily.  It may be available for obesity therapy relatively soon.

Contrave (bupropion/naltrexone) is another drug that may gain FDA approval soon.  It acts on appetite and reward centers in the brain, and its effectiveness seems to be somewhere between lorcaserin and phentermine/topiramate.

It's clear that obesity research has uncovered a number of effective obesity therapies.  At a minimum, the effectiveness of these treatments demonstrates that our current scientific models of obesity are correct.  Yet all of them have major drawbacks, either related to limited effectiveness or negative side effects.  None are the super easy, 100 percent effective magic bullet we would like.  Why not?

The reason we don't have a magic bullet is that obesity is a difficult problem.  Preventing and treating obesity means fighting the natural tendency of the human body and mind in the context of our current culture.  You can tell people to eat less sugar, white flour, added fats, and processed foods in general, but only a minority of people will actually alter their behavior significantly as a result.  This is because people don't eat junk food for its health benefits-- they eat it because they like it, it's cheap, and it's readily available (obesity isn't caused by eating junk food in all individuals, but it is a major cause on a population level).  Obesity is much more challenging than a simple infectious agent or nutritional deficiency that can be readily treated.

Since obesity is largely related to brain activity, we typically attempt to treat it using drugs targeted to the brain.  These approaches work, but they're limited by the fact that the brain is extremely complex, it's protected by the blood-brain barrier, and drugs are typically not specific enough to hit the relevant circuits without collateral damage.  Bathing the entire brain in a drug is a sledgehammer approach that tends to be too non-specific for therapeutic purposes, although there are occasional exceptions****.

Personally I think it's inevitable that we'll develop better obesity therapies, but these will have to swim upstream against our increasingly fattening culture.

Has Obesity Research Failed?

I hope it's clear that obesity research has not failed-- it has produced huge amounts of scientifically robust information, and a number of effective therapies.  None of these therapies are the magic bullet we wish they were, yet there's no reason to believe this is because our understanding of obesity is fundamentally flawed.

The reason we don't have a magic bullet is that obesity is a tough problem to solve.  Researchers can identify causes, but they can't force people to change their lives.  They can develop effective treatments, but these tend to cost a lot of money and/or have serious drawbacks.

Measuring the success of obesity research in terms of its ability to prevent or reverse the obesity epidemic is setting an impossibly high standard.  In a sense, I believe this is the point of the argument.  By setting an impossibly high standard and rejecting the field as a whole, this allows people to excuse themselves from the time and effort required to understand the subject.


* Although NIH funding in general, including for obesity research, has dropped in recent years.  Hopefully that trend will reverse as the economy bounces back.

** Antoine de Lavoisier was one of the first researchers to contribute meaningfully to the modern understanding of obesity.

*** There is a significant risk of surgical complications and death from bariatric surgery, however the complications and death risk of remaining extremely obese are much higher.  Therefore, relative to remaining extremely obese, bariatric surgery is very safe.

**** There are many therapeutic drugs that act successfully in the brain.  I use the word "occasionally" because for every drug that is currently in therapeutic use in humans, there are probably hundreds that didn't make the cut.  Among those that work, most are blunt tools.

37 comments:

Robert said...

Thank you for the excellent article, Dr. G.

I believe research funding will increase substantially as modern societies start to feel the full economic cost of prediabetes/diabetes complications. Especially now that we know how common prediabetes is among the UK (link below), US, and China, how most of the CVD damage associated with CHD mortality likely occurs during this metabolic phase, and how obesity itself is likely a primary cause of the metabolic complications of pre-DM. A Manhattan-project mentality should seep into the health policy budget in the next 20 years. And hopefully a serious, society-wide anti-obesity focus will follow a la smoking.

http://bmjopen.bmj.com/content/4/6/e005002

The Ancestral Chemist said...

What about metformin? It seems to be fairly effective and safe as a weight-loss drug, especially in pre-diabetic or insulin-resistant people.
http://www.ncbi.nlm.nih.gov/pubmed/23147210

Ken Adkins said...

Hi Stephan,

I don't mean to sound rude, but when considering the effectiveness of research as a whole, ought you not also consider potential harms caused by research?

Certainly, physicists can't only consider the implications of improved aerodynamics in vehicles, and engineers can't only consider improved labor-saving machines. They must also consider the potential harm caused by inventions such as weapons or explosives, or the exploitation of laborers (to be fair, you'd also have to consider the pros of such inventions, too).

Obesity researcher have to consider the misery they have condemned many obese people to by telling them to move more and eat less, then following failure to do so with character insults. While the advice may well work, it has extremely debilitating side-effects; most choose to give in to their hunger rather than live with them. After all, you can't hold a gun to their heads to make them do things.

I tend to lean toward humility in areas of my expertise, so take that as you may, but it would make me consider that maybe the treatment is ineffective.

Deirdre said...
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OldTech said...

Thanks. This looks like it is good summary of your views. However, so far I find the arguments presented by Taubes and many others more persuasive.

My own personal experience also fits better with Taubes and others. In other words their recommendations are working for me.

I am, however, willing to admit that it may be more complex than just carbohydrates and insulin. It seems clear that they are both involved once metabolic disease is triggered. It is not so clear what triggers it.

Stephan Guyenet said...

Hi Ancestral Chemist,

Metformin seems pretty safe and does promote weight loss, however it's not specifically approved as a weight loss therapy in the US. The study you cited reported a clinically meaningful degree of weight loss. I don't know if that study is representative of the literature as a whole though. I also don't know what metformin's mechanism of action on weight is.


Hi Ken,

I think it's fair to consider the potential harm caused by obesity researchers, physicians, and public policy experts. There has certainly been a kernel of moral superiority in some of their behavior. Thin people like to think of reasons why they're thin that make them feel morally superior. In fact, the main fundamental difference between lean and obese people in the US is genetics.

Ken Adkins said...

Hi Stephan,

I honestly can't tell if you're being sarcastic or not. The brevity of your reply makes me lean toward the sarcasm.

I apologize that the medium makes this difficult for me to understand.

Michele said...

Metformin seems to also work on the gut-brain axis. Probably also ties into bile acid metabolism implicated in the FXR KO model you reference.

http://www.ncbi.nlm.nih.gov.proxygw.wrlc.org/pubmed/?term=Shin+NR%2C+Lee+JC%2C+Lee+HY%2C

http://www.ncbi.nlm.nih.gov.proxygw.wrlc.org/pubmed/23840042

Stephan Guyenet said...

Hi Deirdre,

There have been a number of studies on ketogenic diets in humans and animal models, and the research is ongoing. We still have a lot to learn about it, but give the researchers a little bit of time to do their research, OK?

Hi Ken,

No sarcasm intended.

Hi Michele,

Thanks, I'll have a look.

raphi said...

SG says: "[...] effective techniques for preventing and reversing obesity. The simplest of these is calorie restriction"

How is this any different than saying "engineers have found an effective technique to reduce excessive fuel use per km driven: driving slower..."?

There may well be people who drive "too fast" - the question is then Why? How do we get them to slow down?

Animals & humans have never needed to know about calories to maintain health/weight.
You might say the new food environment requires this of us now? OK - say it does (for the sake of argument). This still only tells us about 1 important variable in the equation to look out for.

The next question is what affects that variable, how & why?

You're correct Stephan, a significant number of people who identify as part of low-carb/paleo community have made outlandish claims. Nothing crazier than usual though...I would urge you to distinguish those claims from the actual science behind it.

Wout Mertens said...

I think you're painting a picture with too broad a brush.

I have no doubt that our current diet is obesity-inducing (on a population level), and no doubt that a Paleo-ish diet reduces obesity (on an individual level).

I'm pretty sure that you can get fat on a Paleo-type diet if you try hard enough.

Our current diet is the end result of (questionable) recommendations based on (bad) research and the interaction with the free market and civilization.

All that doesn't add up to what you're saying though. I'm sure that if dietary recommendations are shifted towards the Paleo-esque, the industry will follow suit, as will the population.

The industry would still invent hyper-palatable foods, but they would at least not actively damage us as they do now, just provide an overabundance of calories... (which is damage enough)

We would still have obesity, but of a lesser magnitude both in severity and count, with less diet-related health issues.

Beth@WeightMaven said...

Deidre, what is the longer term success (5 years plus) of your 800kcal patients? What percentage of your patients provide this kind of data?

Ken Adkins said...

Hi Stephan,

I read your blog with some regularity, I had no idea that you leaned toward the genetic argument as an explanation for obesity.

I generally don't believe that argument, but I also have to admit that I really haven't read up on it very much.

Could I ask you to direct me to some of your posts that cover the topic?

Robert said...

Once someone's body fat set(tling) point is raised from normal to obese, is it stuck forever? I know some people lose weight and transition form obese to normal body fat levels, but most obese individuals will remain obese their entire lives despite constant dietary efforts. RCTs show this over and over again.

Therefore, I'm wondering if the key goal is preventing the body fat set point rise in kids, so that they never get "stuck" in obesity. This means older, more obese people are basically screwed but this seems to be a reality based on the current evidence.

Anecdotally, ~90% of my older relatives (aunts, uncles, grandparents) are overweight if not obese. Every single one has tried to lose weight for decades to no avail. This is 30-odd people intelligent people, all of whom were rail thin as youths, attempting dozens of diets over decades and failing. Many have lost weight, some a lot of weight, and gained it all back despite hating being fat, suffering strokes, cancer, etc. due to their obesity, and having huge amounts of will power.

This is a depressing situation.

Brian O'Connell said...

Drugs or surgery will never be the cure for the obesity epidemic. That any of the solutions mentioned in this post can be called effective strikes me as scientific reductionism gone wild.

The problem is environmental, and as Wout said above, the change in the environment came about due to bad science backed by our government and ratified by industry. Between the three of them, along with a compliant media that endorses whatever the government says, we've created a food environment where an obesity epidemic is inevitable. And drugs with nasty side effects and surgery, which of course has inherent dangers, are presented as possibly effective responses- this is insane.

This article focuses on a few trees and misses the forest entirely. Our knowledge of appetite and diet on a biochemical level should lead us to change wrong-headed government policies about food production and markets- and not to create horrible new chemicals to alter our biochemistry so that it can thrive in this politically induced environment.

IcedCoffee said...

I always wonder why DNP hasn't made a resurgence in one form or another. It seems to me the most realistic long term weight loss drug will be a metabolic-rate booster. That way big-food can keep their profits up, and people can eat as much as they want. Not to mention the money we would save on indoor heating.
And while this sounds sarcastic, I genuinely think this is the only realistic solution. Dieting is miserable, eating less is bad for business, and a drug to fix our problems is the American way.

As a side note, you forgot to mention liposuction, arguably the most obvious form of weight loss. A bit crude, but worth mentioning.

Nate said...

I agree that obesity research has learned a tremendous amount about the human body and mind. I also think that the research in other fields for diabetes, physiology, lipids, etc have added to the obesity research. In fact, the role of insulin, the fat storage hormone, is a prime example. I'm guessing that the fat storage hormone was never mentioned in this article because it was found thru research on diabetics. However, as you know, insulin is necessary to get fat into storage and to turn carbohydrates into fat. Also, importantly for me as a Type 1 diabetic, the extreme hunger caused by too much insulin in the blood in relation to glucose should also have been discussed. If I eat a meal and accidentally take too much insulin, my hunger can get so great in an hour that I can absolutely only think about food and of course eat it. To control that hunger on a daily basis, as I understand many obese people do, is beyond the possible. Lowering insulin levels should be an important tool for the obese. So, yes eating a low carb/ high fat diet should be an option if not the first option.

Stephan Guyenet said...

Hi Nate,

Insulin-induced hypoglycemia is a well-known cause of hunger and increased food intake, but it's rarely associated with common obesity. Usually it only occurs in people who are injecting insulin, who have insulin-secreting tumors in the pancreas, or who have rare genetic mutations that affect insulin secretion.

I feel that "fat storage hormone" is a misnomer for insulin. The most accurate description would be the "fuel selection hormone" due to its role in switching between fat and carbohydrate metabolism in response to what's consumed.

Deirdre said...
This comment has been removed by the author.
aaron blaisdell said...

I think we as a society have learned quite a bit about the causes of obesity. If we didn't, we couldn't manipulate those causes to construct obesogenic "foods" and "food"-marketing. :) But, this makes it difficult to find effective, sustainable "treatments" for obesity for the majority of the population living in an obesogenic environment. Seth Robert's Shangri La diet (based on a Pavlovian conditioning theoretical framework for understanding the relationship between body-fat set point and hunger, and how to manipulate body-fat set point to reduce hunger and drive weight loss) seems to have the most traction from what I can tell (including for myself).

aluchko said...

Deirdre,

"When my dieters reduce their daily intake of carbohydrates and fat, and consume adequate protein - not high protein, but enough to spare their lean body tissue in gluconeogenesis - they experience rapid fat loss (which we monitor through weekly body composition analysis). In essence, my dieters appear to be “living off their fat stores” – which I logically assume is how our bodies evolved over millions of years to accommodate unpredictable food environments and leaner times. "

I'm not sure I buy this argument. The mechanism may work, but in evolutionary terms I'd expect low food environments to be associated with a reduction in fat and protein, not carbs and fat. Animal based food sources are a lot more inconsistent than plant based (maybe this works different post-agriculture).

Deirdre said...
This comment has been removed by the author.
Grinch said...

I think the obesity epidemic is largely an effect of capitalism combined with having personal freedom mixed with our genetics. The food industry is intentionally creating foods that are highly palatable in order to expand their market share. They are also funding studies that show their food isn't harmful, at least not directly. When we eat these foods our homeostatic system of body fat is overriden and so we end up with an imbalance of calories, leading to obesity when we are genetically susceptible.

I'm not convinced most of the country even understands this, especially the policymakers. Most of the time I hear that obesity is an issue of personal responsibility, that people are unwilling to life a healthy lifestyle. Well the problem with that is you don't have millions of people in a population spontaneously decide they want to be unhealthy. There needs to be an environmental explanation as to why such a large population would slowly kill themselves with their lifestyle. In my opinion the only way to stop obesity are either with some breakthrough miracle drug, or to enact a lot of legislation to make it very inconvenient to live an unhealthy lifestyle. But as long as humans are wired the way we are and based on our track record, just telling people they the responsibility is on them to become healthy will never, ever solve the obesity problem. The tools that people have today to help them are woefully inadequate while living in this environment.

Stephan Guyenet said...

Hi Deirdre,

Impatience and science don't mix well. Have you ever tried looking up "ketogenic" in PubMed or Google Scholar?

Deirdre said...
This comment has been removed by the author.
Beth@WeightMaven said...

Deidre, I was actually wondering if you saw better longer term success with your approach than other similar very low cal approaches like the HCG diet. Do you know how many of your patients have maintained their weight loss after 5 years?

ProfessorEd said...

there is another big reason for researching ketogenic diets

I just finished reading Seyfried's (2012) "Cancer as a Metabolic Disease," which is a technical biochemistry book aimed primarily at cancer researchers. He makes a very convincing case for cancer being a metabolic disease in which the cancer cells are forced to rely on fermentation of glucose and glutamine as their primary source of energy. If deprived of these by drugs (such as 3BP) or a diet, they can be starved.

I have not seen reference to this book among those interest in nutrition, but it should be read by those with a professional interest, or a very serious interest (and suitable background medical knowledge).

Such diets would be ketogenic (apparently cancer cells cannot use ketone bodies), such as are now used for children with epileptic seizures. Near the end of the book (chapters 17 -18) he discusses such diets for treatment, which would require very high fat diets (60% to 80%), and calorie restriction to the minimum required to maintain life (he suggests a scheduled loss of 2 lbs. per week in most patients, not yet below normal weights).

There has been success in brain cancers. Obviously, such diets are very hard to maintain, even for those diagnosed with terminal cancer for which this may be their only hope.

In Chapter 19 he discusses prevention using ketogenic diets. The argument of the books suggests that cancer rates would be reduce by lowering blood sugar, which calls for both calorie restriction and reducing carbohydrates (at the expense of fat).

I have not seen this discussed much in the arguments over desired proportions of macronutrients.

Galina L. said...

@aluchko,
" Animal based food sources are a lot more inconsistent than plant based (maybe this works different post-agriculture)."
Do you have a natural preserve near by? What would you eat there year round? Plant sources in nature are not consistent as well, humans don't eat grass(animals do), fruits, nuts and tubers are very seasonal. Animals are not as seasonal as plants are. I live now in Florida, insects here are abandon and animals which eat insects abandon too, there are a lot of fish and shell-fish. If I had nothing to eat due to a cataclysmic event of some sort here, I would be gathering oysters from tide estuaries because I know there is nothing to eat in a forest here. We still have hills in our parks created by shells discarded by Native People after eating oysters. Not many plants in a warm climate store starch. In a temperate climate you perhaps could find more starchy plants, but you will need a storage place and planning to make sure it would last you during a cold season.

Deirdre said...
This comment has been removed by the author.
Galina L. said...

@Beth, not long time ago we already witnessed another "miracle" 800 calories diet which is now known as a Kimkins Fraud.

The aftermath for the victims besides a class-action law-suit:

moderate-to-severe hair loss
dizziness
nausea
muscle-fatigue
joint pain
irregular heartbeat
irregular menstruation
irritability and mood disorders

So, we know already how sustainable such diet is, I wonder what Deirdre knows when she doesn't answer your questions. Stephan is right to recommend her to do some basic reading.

Deirdre said...
This comment has been removed by the author.
Stephan Guyenet said...

Hi Galina and Deirdre,

This discussion is becoming increasingly acrimonious so I'm not going to publish further comments.

Unknown said...

With the existing plethora of research on obesity from every aspect it seems that more is really not needed. Rather, understanding how the primary chronic diseases like heart disease, diabetes II, cancer are affected by diet is far more important. Obesity is not complicated from the overeating and reduced physical activity aspect but the how it messes up metabolism. It is not a disease in itself, but a risk factor.

Then there are still a large number of folks who developed chronic diseases who are not obese but yet diet is still a root cause.

Lastly, Dr. Terry Wahls has developed it not the, the closed to the optimal human diet.

Reversing her own secondary progressive multiple sclerosis has given us all a way to eat for optimal human health.

This is the diet that should be studied intensively. Now, she has to limit research because her diet does not conform to the USDA recommendations nor obviously drug companies aren't interested.

So this diet based on Paleo Principles and Functional Medicine may reverse many chronic diseases. But many,many folks would not give up their sugar, refined grains and corn oil and start eating way more vegetables. What to do? We do have a crisis in health care costs and sick people because of the Standard American Diet.

The only answer is to use the tobacco model and make vegetables and fruits less expensive than Junk. Not one but many Congressional actions.

Dr Bob said...

Hello Stephan, I cited references in my comment on your last post. Those references support a carbohydrate restricted approach to treating obesity. So far drugs have failed and as a clinician I witness the complications of bariatric surgery(death, malabsorption, sepsis, renal failure, ARDS, multiple recurrent hernias, loss of abdominal wall structures from infections, chronic pain and weight gain within a few years to name a few). I have not seen convincing long term morbidity and mortality data comparing bariatric surgery to an intensive program of carb-restriction (let alone carb restriction plus ancestral foods.) We will probably never see such a study because of the biases held by funding agencies. But I would suggest that if we spent as much money as the cost of bariatric surgery and applied it to an individualized intensive nutritional/exercise/meditative/social support program that involved teaching cooking, food selection, shopping, meditation, exercise instruction, supervised very regularly by a clinical practitioner with social support systems and group therapy (like Dean Ornish's program without the vegan low fat diet) we would find better results with a non-invasive non-surgical approach. I make my living in the operating room but I advocate for a treatment without surgery.
Ultimately our culture of junk food must change to prevent obesity. But as long as the "low fat is healthy" message pervades our society there is low probability for cultural change.

john doe said...

One thing you're forgetting Stephan is Money. It's all about money. If a truth is benign to elites, then it will freely rise to the top. The science of, say, human prosthetics,or the study of moths can go on undisturbed. Unfortunately, obesity research is on the wrong side of the fence. When rich people or corporations stand to lose money, that truth will be blocked. Red meat (especially CAFO raised) is clearly linked to disease, but the Meat industry uses its power, and allies like the Atkins foundation, to convince people that its ok. I won't get into the saturated fat debate, but you have to admit the Chowdhury meta analysis was a steaming pile of B.S. Cola products are clearly bad, but Coke and Pepsi do a good job of spreading confusion, and keeping their products in schools. I could go on and on, but you get the idea. The media also exacerbates things, as someone already mentioned, because they whore themselves for clicks and views, and will print anything. (e.g. TIME's "eat butter" article...)The end result is public confusion, and no clear answer to the question: "so, how do i lose weight?"

Todd said...

Hey Steve, I'm sorry you aren't commenting on this thread because I have a few points I think are worth adding.

Fen/Phen was pulled from the market, but a physician named Mike Anchors found that combining phentermine with an SSRI (like prozac) had the same beneficial weight loss effect without the heart valve defect issue (which was due to the fenfluramine). Google terms like 'phen-pro' to read more about Anchors work.

Also on the subject of drugs, cimetidine (an OTC heartburn drug) has shown some promise as a weight loss drug, possibly due to its effects on CCK.

http://www.ncbi.nlm.nih.gov/pubmed/11208394

The article about bile and FXR being a factor in obesity surgery was interesting. Do you know if there is any research on bile acid sequesterants as a potential treatment for obesity, or would that even work along the same pathway as the one described in the article about gastric sleeve obesity surgery and FXR.

tomR said...

@Unknown - about Terry Wahls diet. What is clear is that the entire dietary research has no good reference diets. No good point to test a tested approach against. The average diet is no good, "official" government diet is far from optimal. "Mediterrenean" is nice, but heavily undefined.

But we have very good candidates for reference diets; they are new from 2012-2014. I'd argue that both Perfect Health Diet and Wahls Paleo are great choices as references. They are: real world diets, well defined by detailed large books, they are specifically designed to avoid deficiencies, they tend to work well: no ethical problems putting control people on such diets, and a valuable result of comparing a new thing to something good.

My bet is that it would result in a great clarification effect; as most research would end up with something like "compared to the reference this new diet is not good" - a great filtering out of unnecessary spam of diets. Using average Western diets as references is not going to produce such result - no filtring of diets that are better than modern average, but no good overall.