Low-Food-Reward versus Low-Carb

It appears that low-carb research is currently in the doldrums, but low-carb arguments are keeping everybody interested, especially the one going right now at Whole Health Source. The blog owner, Stephan Guyenet, has a PhD in neurobiology and studies the neurobiology of body fat regulation. His blog was thought of as one that advocated the Paleo diet, which is broadly similar to a low-carb type of diet. Then in April of 2011 Stephan wrote a blogpost entitled Food Reward: a Dominant Factor in Obesity, Part I, and everything seemed to change. Stephan stated,

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.

Post Script
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.