The human brain evolved to deal with a certain range of rewarding experiences. It didn't evolve to constructively manage strong drugs of abuse such as heroin and crack cocaine, which overstimulate reward pathways, leading to the pathological drug seeking behaviors that characterize addiction. These drugs are "superstimuli" that exceed our reward system's normal operating parameters. Over the next few posts, I'll try to convince you that in a similar manner, industrially processed food, which has been professionally crafted to maximize its rewarding properties, is a superstimulus that exceeds the brain's normal operating parameters, leading to an increase in body fatness and other negative consequences.In other words, when the brain perceives that a food is highly palatable or provides excessive food reward, a superstimulative effect will cause overall caloric intake to increase and will raise the bodyweight setpoint.
After a considerable back and forth between Stephan and his readers, he finally put up a summary post, Roadmap to Obesity. He concluded, "The basic idea is that in genetically susceptible people, excessive food reward/palatability/availability and inactivity cause overconsumption and an increase in the body fat setpoint, followed by the eventual accumulation of fat metabolites and inflammation in the hypothalamus, which exacerbate the problem and make it more difficult to treat. Other factors, such as micronutrients, gut flora, fiber, fat quality, polyphenols, sleep and stress, may also play a role."
The blog you are currently reading subscribes to the carbohydrate hypothesis of obesity. Here it is as described by Gary Taubes:
This alternative hypothesis of obesity constitutes three distinct propositions. First, as I've said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure. The second is that insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy. The third is that carbohydrates, and particularly refined carbohydrates-- and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed-- are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.Briefly summarized, the low-food-reward diet consists of simple foods such as gently cooked tubers, meats and vegetables. It minimizes added fats, added sugars, and added flavorings including salt, herbs and spices. The macronutrient breakdown is high carb, adequate protein and low fat. The low-carb diet consists of foods that are low in carbohydrate, moderate in protein and fairly high in fat. The use of salt is permitted and the use of herbs and spices is encouraged. Whole foods and natural foods are preferred, but many low-carbers also include low-carb food products such as protein shakes, protein bars and diet soda.
Okay, that's enough with the background. Superficially, if people are eating healthy whole foods, they should be healthy, right? So what's the problem? There are several of them.
Problem One--Cause and Effect
The low-food-reward diet assumes that food is similar to a drug. When palatable food is eaten, dopamine D2 receptors are stimulated and down-regulated in a manner similar to that seen in drug addiction. According to Johnson and Kenny in a 2010 rat study, "overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating."
While this may be true in rats, it seems a bit extreme in humans. One does not see addicted fatties mugging people or robbing houses to support a Twinkie habit. Indeed, a person who has just gorged on Twinkies does not present with the symptoms of, say a cocaine user. For 15-60 minutes after the ingestion of cocaine, a person will experience alertness, confidence, euphoria and high energy. A person who has overdosed on Twinkies will tend to experience quiet contentment and lethargy. While both drug-addicted people and people with obesity are observed to have lower than normal levels of the dopamine D2 receptor, it is possible that the causes of this condition are different. The real-world behaviors seen in drug addicts with low dopamine D2 receptors are certainly different from those in food-rewarded people with low dopamine D2 receptors.
The low-carb diet assumes that carbohydrate ingestion prompts a release of insulin by the pancreas in order to maximize storage and utilization of the glucose that will shortly be entering the circulation. Insulin is a hormone that acts through a transmembrane receptor on the surface of most cells. When insulin is present in high concentration and/or for long periods of time, insulin receptors are downregulated. This produces a condition called insulin resistance, meaning that a higher concentration of insulin will be required to effect insulin signaling in a particular cell. In the short term, insulin resistance is reversible. Just lower the blood insulin for several hours or days and eventually the usual number of insulin receptors will return to the cell surface. However, when insulin has been kept chronically high for years, the resilience of the system goes away. Eventually, insulin resistance becomes a constant feature. The liver resists turning off gluconeogenesis. Muscles resist taking up glucose. In most people, fat cells remain insulin responsive, but eventually they too bcome resistant to fat storage and will release free fatty acids from fat depots.
It is not certain that chronic high insulin alone produces insulin resistance. For instance, genetic susceptibility and inflammatory processes may also play a role. However, once the symptoms of insulin resistance are observed clinically, taking steps to reduce chronic high insulin will permit at least a partial recovery of insulin sensititivity. Not coincidentally, these actions will also cause the loss of fat while sparing the loss of lean muscle mass.
Problem Two--Scientific Training
In general, people with PhDs come to science in a way that differs from MDs. They are taught to break down large questions into small pieces and to look at differences between carefully controlled groups. They use dishes of cells, strains of rodents, and matched groups of human subjects. This makes it easier to see significant changes between groups that differ only (one hopes) because of the treatment variable. However, PhDs must always be careful to remember that their conclusions may not be valid outside the tissue type/rodent strain/particular human subjects they have studied. Scientific studies of this type are useful because they provide guidance about what might work to treat a particular condition or disease. They do not provide absolute truth about what must work to treat a particular condition or disease.
Unlike PhDs, MDs tend to be found in a clinical rather than an academic setting. While MDs are interested in scientific studies, they must also be aware that what works on paper may not be particularly successful when treating patients. The body has lots of counterregulatory systems, and what takes place in an isolated dish of cells may be prevented from happening the context of an entire organism. What is true for a particular type of rat may not follow the physiology of a human being. What happens in the short term in a controlled environment for a selected group of people may not be the case for a large number of free-range humans. MDs in active practice will tend to gravitate toward approaches that are successful for their patients, particularly if they are treating patients with similar conditions. Examples of this in the low-carb community are Robert Atkins in the treatment of obesity, the Drs. Eades in the treatment of obesity, Richard Bernstein in the treatment of diabetes and William Davis in the treatment of coronary heart disease.
Problem Three--Practical Experience
The idea of a low-food-reward diet has apparently been around at least since 1965 when Hashim and Van Itallie used a feeding machine that dispensed bland liquid food through a straw. They noted that morbidly obese volunteers lost a great deal of weight on that regimen. However, no follow-on studies were published. Many other diets have come and gone in the interim, including the standard low-fat diet promoted by much of the medical community, and none of these has been particulary successful.
A possible exception to this rule has been the low-carb diet. Starting with the publication of Dr. Atkins' Diet Revolution in 1972, the low-carb diet in one form or another has been found to be useful in weight loss and in the promotion of various aspects of good health such as decreased blood pressure, decreased blood glucose and improvement in other metabolic markers. (See here for a summary of three articles in top-tier scientific journals.) Judging by comments in health-related blogs, this has been the anedotal experience of many ordinary people who have tried the low-carb lifestyle. Nearly 40 years after Dr. Atkins wrote his book, there appears to be good evidence that low-carb eating provides lasting benefits with regard to weight loss and health.
Several commenters say that they have tried the low-food-reward approach to eating and have been successful with it. This may be true in the short term. In the long term, it remains to be seen whether following a low-food-reward diet will be of benefit in people who have eaten the standard American diet for 20 to 50 years, in people with type 2 diabetes, in people who have heart disease and/or in people who lose weight and then attempt to maintain the weight loss over many years. It might work in theory. We will need to wait several decades to see if it works in practice.
An excellent comparison of the food reward and the carbohydrate hypotheses of obesity can be found at Peter's Hyperlipid blog. Peter has much more training and experience in physiology than I do, and he presents several very important refutations of journal citations that seem to discredit the carbohydrate hypothesis. It may take a couple of readings to absorb his point-by-point analyses, but it will be very much worth the time invested.
I'm glad you came out of hibernation - for some reason I did too, and began to post on both Peter's and Stephan's blogs.
I think, at bottom, I'm getting sick and tired of those who have never even been overweight, much less obese, telling us this is right and that is wrong.
I don't doubt the science - I doubt the perceptibility and the attitude of the researcher looking at the data - because he or she has never lived it, that's all.
I'm a health educator, and as you pointed out, I need clinically effective programs. I don't necessarily care about the background biology, although i will change my slides as new research emerges.
I completely understand that we are all not a from a cookie-cutter mold (because I have seen it), but with some individual massaging, low-mod-carb works for most, if not all of my people, depending on their personal chemistry. Whether this is insulin, leptin, food reward, or Calorie reduction remains to be seen.
Thanks again for coming back online.
Very well stated, berto.
I wasn't really in hibernation, by the way. I just couldn't think of anything helpful that I wanted to write about. Then this controversy came up, but I couldn't crystallize my thoughts properly until Peter wrote what he did. He has both a humorous and an understandable way of expressing himself, and it finally clicked for me. Best wishes on your health education work!
Thank you so much for your post. I especially liked your contrast between researchers and clinicians. I tend to go with the clinicians first, since I am a big fan of N=1 data. Goodness knows, someone in a clinic has lots of access to data. That is why, even though I don't agree with all the data that someone like Dr. Davis shows, I have no doubt that his data from actual patients is priceless.
I went on over to hyperlipid to see the latest, and wow, the conversation sure had deteriorated! The arrogance, astounding! Let us be thankful that not only do we have a new obesity hypothesis, we have new definitions of accuracy and precision by the good doctors' homies and wannabees.
I am sure we will all sleep safely tonight sure that the knowledge is advancing. I feel thinner already.
LOL, Exceptionally Brash! The homies bother me, too. If an argument is valid, I like to hope that it will stand or fall of its own weight, not based on the loyal comments of a set of fans.
I hope that I am not a considered a homie ;)... (though it seems that I have been invited to be one).
I can't stand being talked down to by those who think their sh*t doesn't stink and when called on it, they either put the blame on another, or another's thought process. If you're gonna be brash, then be Brash!
I just found your blog this past weekend and have thoroughly enjoyed reading through the archives. I like the wit in your writing. Keep it up.
Thanks Berto, and I, or someone like me, was invited too. Not gonna get in the middle of that mess though! I am sure I will not qualify for internet pal status. (and no, you aren't a homie)
One thing that Dr. Harris and itsthewoo2 can heartily agree on is that some people really do need to get a life. Ha ha.
Another great post! I really enjoy your blog, keep up the good work!
People who are addicted to ciggies aren't likely to mug or murder for them. Are you really using that as a basis to define addiction?
It was hyperbole.
I am constantly amazed how the science of rodents and feeding somehow means anything to a neurobiologist writing a blog series on humans.
A paleo diet is macronutrient-agnostic, as is a low-reward diet. You could construct a 100% fat diet that is very low-reward.
Here's my problems with your problems:
1. If carbohydrate causes insulin resistance, why aren't Kitavans insulin resistant? If insulin resistance is a necessary condition for obesity, why aren't all obese people insulin resistant?
2. One's training should not be a consideration when assessing the quality of their ideas. Think Denise Minger.
3. The reward hypothesis explains how people can lose weight on low-fat diets, which the CHO can't explain at all. Also, a low-carb diet is often a lower-reward diet than the previous diet, so both hypotheses predict weight loss on a low-carb diet (in most cases).
I wanted to keep this comment separate so that if you choose to moderate out my link, the rest of my thoughts won't be moderated out as well. I wrote a blog post of my own - similar to this one, just advocating on the other side: http://www.engrevo.com/blog/food-reward-vs-carbohydrate-hypotheses-of-obesity/
Further support for the points in my other comment is provided there.
Regardless of which theory you ascribe to, the debate has certainly resulted in lots of interesting discussion.
I feel you on that idea.
But it's not that rodent experiments (or any non-human experiments, for that matter) should be meaningless, they should supplement rather than form the theories that seem to be defended with zest. The data derived from such studies need to support concepts that are applicable to humans, and not have paradigm shifts based off of them.
This is why I believe that an ex-obese researcher who has experienced weight loss/gain and the finally has their weight and hunger under control would take rodent studies with a grain of salt. A researcher not equipped with this experience simply follows the raw numbers, without trying to dovetail this acquired inner knowledge with the observations of rats.
Well put, glad to see you writing again. I really like your point about the role of researchers and how it shapes their perception. Brings to mind the tale of the blind men who find the elephant, and each thinks the part of the elephant they can feel IS the elephant.
@ Christopher, good points. I'll try to answer them briefly.
1. Regarding Kitavans, my hypothesis is that the main reason they are not obese is that their high carbohydrate diet is mostly tubers rather than flour and sugar. I have also heard a report that they typically only eat one meal a day. Both factors would mean that if their insulin went up as a result of carbs from tubers, the rise and fall would be slow and the peak would be relatively low. Once nutrients were stored, they would be able to return to a low basal insulin level and switch to efficient use of their endogenous fat stores (and occasionally glycogen) for energy.
2. Denise Minger is an excellent example of my belief that the truth of an idea should rise or fall on its own merits, not on the basis of the CV of the person who presents the idea. I presented the contrast between PhD and MD training because many of my readers have not experienced that training and don't understand that in a broad sense, these people tend to approach scientific problems in different ways. That may be why Stephan and Peter (who is a vet) seem to look at similar data in very different ways. Both approaches are valid, but both approaches also have their limitations.
3. I don't dispute that people can lose weight if they do low-fat/low-calorie diets. See here for a discussion. However, once insulin resistance sets in, particularly when people have a difficult time switching from burning carbs to burning fats, it becomes very difficult to control one's appetite. The drive to use carbs as fuel causes susceptible people to eat carbs about every two hours so they don't have to make the difficult metabolic switch to fat burning.
@Christopher, thanks for the link to your blog. Just a technical comment. The figure you show is from the article Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. What is not mentioned is that "The low-carbohydrate, non–restricted-calorie diet aimed to provide 20 g of carbohydrates per day for the 2-month induction phase and immediately after religious holidays, with a gradual increase to a maximum of 120 g per day to maintain the weight loss." (Bolding mine.) There was no comparable increase in calories with the Low-Fat Diet group or with the Mediterranean Diet group. It is not surprising therefore that the Low-Carb group gained weight after the first five months of the study. What does surprise me is that this lack of equivalent adjustments in the diets got past the referees.
Well, things keep getting more confusing rather than less the more I read up on low carb. And, ha, don't you see the joke? For a carb lover/addict a low carb diet IS a low-food-reward diet. Ha. Kind of funny but kind of not. In my experience low carb eating has done away with the overwhelming urge to eat carbs.... but society and traditions and plain old comfort food desires make carb foods high reward for me at times.
@stargazey, what the food reward hypothesis fails to take into account is when carb-burning becomes the norm, and appetite increases, people will eat all sorts of craptastic food to get the carbs out of it. So the idea of reducing that behavior by leaving off the salt and spices is simply ridiculous. Sure, it is easier to eat a box of donuts over a bag of flour, but only because donuts are easy and ubiquitous.
Exactly so, Exceptionally Brash.
By the way, I went over to your blog and enjoyed the visit. I tried to leave a comment but for some reason, over there Blogger has no idea who I am and won't accept my comments. The deep wisdom of Google at work, no doubt.
Also, berto, a belated thank you for your "translation" of my comment to Kurt G. Harris MD. I laughed out loud for quite a while when I read it.
Haha. But I do have to apologize for inserting words into your mouth, as it were.
That comment was brought over from Peter's comment section, where Dr. Harris continued to remind me that just because I highly respect his work, intelligence, and contributions, I can still despise the shit of the person. I don't like being looked at down one's nose, which he has done to me and other readers on many occasions.
But I again apologize, for bringing unnecessary baggage to your blog - nuff said about Dr. Harris.
And your welcome for the laugh ; )
Hej there, great article.
Your comparison with cocain isn't particularly valid. Its better to use marijuana as an example.
THC is xtremely potent binging agent. As it binds to CB1 in the brain the same as anandamide which promotes food intake apart from blissful state, and it binds with higher affinity to it, we can deduce from both observational and physiological points that its not good idea to use marijuana for weight loss. Marijuana addicted people, if such thing exists, will not raid the city for another dose.
Some foods probably upregulate endocanabionid system, PUFA is the primer suspect.
So, there is definitely something going on here. Is it dominant ? I don't know, it might be for some people. Would low carb help? Probably, for bunch of other reasons.
Good to see you back in cyberspace! I'd like to quibble with one observation, though:
"MDs in active practice will tend to gravitate toward approaches that are successful for their patients..."
How I wish that were true. In a few exceptional cases--like the individuals you list--it might be an accurate assessment, but it seems to me that most MDs keep recommending whatever the AHA or ADA or the Pharma companies have told them to recommend.
Most MDs seem to me to have lost their capacity for critical thought somewhere during medical school.
As to the low-food-reward vs low-carb issue, in a practical sense, if both worked, why would anyone prefer to live a live of low reward?
I believe the food-reward hypothesis is circular. (One of my friends gained a lot of his weight on pita bread dipped in unflavored hummus, which is about as bland as you can get. Ah, but the carbs themselves must have been "high-reward," then!)
The argument seems to take this form:
1) Obesity is caused by overeating, which is caused by high-reward foods.
2) Whatever foods are overeaten are high-reward foods for the obese person.
3) Overeating is whatever behavior is exhibited by those who are obese.
I don't find this stand to be terribly helpful. Or even testable.
David, your observations on physicians being led by the ADA, the AHA and pharmaceutical publications may be more true than I'd like to admit. My husband and his friends think as I've described, but that is certainly not true of every doctor. The constant threat of lawsuits also encourages physicians to adopt a more uniformitarian approach, to make it to easier to defend themselves (if necessary) in a court of law.
The rest of your comments also make very good points, particularly the circular argument idea. If you gain weight while eating a particular food, by definition it must be high reward. How convenient. It proves the theory and removes the need for high-cost scientific trials. On an individual level, it can account for every anecdotal experience that either contradicts or supports the theory. Brilliant!
I don't think that food reward is the chimera to be slain, but I do think that it plays a role. It simply adds a compulsion to eat to an already compulsion to eat lifestyle. Stephan may be stretching its role to have something to research about.
Think about alcohol and food reward: you eat more when drinking. The reward part of the brain gets short-circuited by alcohol (not including beer), and the binge may begin - hell, maybe not even a binge, but you will be "feeling" hunger, ie food reward. Sugar probably does the same thing, as does most carbs for those of us that are sensitive.
It (food reward) is just not the main thing to focus on, in my opinion.
Strong work Stargazey!
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