Here is a commentary by yours truly, Dr. Kirschenbaum, discussing the food addiction hypothesis that so many people believe.

On a Potential Challenge to My Perspective about the Food Addiction Hypothesis (Food Addiction Causes Obesity and Prevents Weight Loss)

New findings from science can change what we do and how we think about the concept of food addiction.  After all, we changed our policy about self-weighing when the data came in that this practice seems quite helpful for LTWCs.  In my clinical work with obese people in the 1970s, I did not focus on a low fat or a very low fat diet.  Science taught me and most others in the 1990s, that this was the way to go.  Does this study with rats and cheesecake suggest considering an alternative way of thinking about obesity?  That’s a very reasonable question.

The results of this study seem to suggest that foods have drug-like properties.  Therefore, perhaps people can become addicted to certain foods just like people become addicted to drugs – and that addiction can cause obesity/prevent successful weight loss.  Many findings and factors argue against this hypothesis.  On the other hand, Dr. Phil, Dr. Oz and Dr. Oprah (oops…) believe in this notion whole heartedly.  It becomes difficult in this culture, especially when reading a study like this, to believe otherwise.  To see why this hypothesis does not work, I’ll describe more about the food addiction model, present an example of a true addiction in contrast (smoking), and argue, once again, in favor of the healthy obsession model (with the athletic metaphor prominently featured).

Food Addiction Model of Obesity

Science has proven repeatedly that under some conditions various foods have drug-like properties in animals.  Almost all of the studies on sugar and fat, like this one, seriously overdose animals and show some drug-like effects occasionally (including distraction, analgesic and even opiate-like effects).  Did you know that a high enough dose of carrots has a drug-like effect: death? Vitamin A toxicity can indeed kill you – as it killed dozens of people in Australia who went on a carrot-based diet. (Their skin even turned orange before they died.) High doses of sugar can reduce perception of pain in animals (e.g., tail pinching experiments with rats).  Have you ever met an obese person who seemed addicted to carrots?

The So-What Question.  What do these drug-like properties that occur in animals tell us about human obesity?  Not much.  Consider what happens to campers and students in our programs when they switch to a Wellspring Plan diet.  Has anyone seen symptoms of withdrawal (high fever, night sweats, hallucinations, reports of monstrously powerful cravings for cheesecake or doughnuts)?  Nope – not a bit.  Homesickness, yes, but withdrawal due to reduction in their “addiction to food?” Nope.  In fact, usually they start feeling better right away – more energetic and happier – and in some cases fewer GI symptoms, also right away.

What about tolerance?  Addictions, by definition, require withdrawal symptoms and tolerance.  Tolerance means that more of the substance is required to produce the same effect with continued use.  Addicts take higher and higher doses to produce the same effects over time: alcohol, heroine, cocaine, vicodin, etc.  The study described below seemed to show some type of dose related effect, but do obese people or those becoming obese show this?  If they did, then almost all obese people would be binge eaters.  They’d eat more and more of that cheesecake over time to feel OK, just like those crazed rats – totally preoccupied with their food.  So, do 95% of obese people binge eat or have a strong history of binge eating?  Nope.  80%? Nope.  50%? Nope.  About 10% of obese people binge eat consistently; a higher % of obese people who seek treatment binge eat – maybe 30% or so, but that’s about it.  So, what caused the obesity in the case of the 90% of obese people who do not binge eat?  Certainly not an addiction to cheesecake or any other type of food.

Smoking

Consider what we know about true addictions.  Smoking, for example, clearly comes closer to meeting the classic definition of an addiction.  Most smokers gradually increase the numbers of cigarettes per day (despite the inherent toxicity of smoking) until certain levels (e.g., at least a pack a day) are craved and smoked regularly.  Reduction of numbers of cigarettes per day or even time between cigarettes produces strong and immediate cravings – which have obvious biological bases.  When smokers switch to lower nicotine cigarettes, they smoke more of them and inhale more deeply; they regulate their nicotine levels that way.  Nicotine patches help smokers lower the number of cigarettes they require, although that will only happen if the smoker really makes a commitment to quit.  Studies in which smokers took pills that raised the acid level of their urine (Vitamin C or Acidulin), resulted in smokers increasing their smoking.  Acidic urine will result in excreting nicotine.  When nicotine gets excreted at a higher than usual level, we’d expect smokers to increase smoking to get that nicotine level back to what they’re addicted to consuming.  That’s exactly what happens.  Behavioral and environmental factors also influence smoking tremendously, but obviously this addiction has powerful and immediate physiological elements that affect it.

In what way does smoking resemble obesity?  Smoking involves one substance.  Obesity involves both eating (and eating thousands of different types of foods potentially) and activity levels + biological predispositions to gain weight + knowledge and skills to manage it.  People do not have biological predispositions to smoke (based on genetic studies).  Quitting smoking involves minimizing the physiological cravings and making changes in one’s environment (e.g., not hanging out with smokers) and learning alternative ways of doing things to avoid triggers, etc.  After many months of this, sometimes a year or more, smoking can become especially aversive to many smokers.  They find they can live full and happy lives without smoking and have relatively few cravings – sometimes absolutely no cravings, just revulsion, after years of abstinence.  Formerly obese people continue to eat food every single day.  Yet, thousands remain slim and do not become crazed or stay crazed.  They often feel much better as they modify their habits and attitudes and environments.

Healthy Obsession Model

Powerful biological forces combine with an obesogenic culture, lack of knowledge, and perhaps some personal tendencies to produce obesity.  Overcoming these consistently antagonistic forces, requires the development of an athlete’s mindset about goals, plans, focusing and commitment.  The athlete develops super-normal self-regulatory skills to overcome his/her body’s resistance to high levels of consistent performance.  The LTWC does the same thing.  They do not have to go cold turkey or wear patches to minimize consumption of doughnuts and cheesecake or cotton candy or white bread. They do not suffer withdrawal symptoms because they can no longer rely on food to make them feel good.  They use principles of science to minimize their appetites (very low fat diet; low calorie density diet, etc.) and to avoid metabolic reductions while maximize fat metabolism (i.e., by getting a good dose of activity every day).  They can still use food to make themselves feel good – just not the high fat kind and not without considering quantity altogether – at least most of the time.  They develop healthy obsessions via CBT (or in some other way) to help them stay focused consistently, manage themselves effectively, and stay committed when the inevitable lapses occur.

The food addiction model just does not work.  It does not explain what we know about the causes of obesity or the approach that seems best to lose weight and keep it off.

FATTY FOODS – ADDICTIVE???

(Health.com) — Scientists have finally confirmed what the rest of us have suspected for years: Bacon, cheesecake, and other delicious yet fattening foods may be addictive.

A new study in rats suggests that high-fat, high-calorie foods affect the brain in much the same way as cocaine and heroin. When rats consume these foods in great enough quantities, it leads to compulsive eating habits that resemble drug addiction, the study found.

Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, Ph.D., an associate professor of molecular therapeutics at the Scripps Research Institute, in Jupiter, Florida. Eventually the pleasure centers “crash,” and achieving the same pleasure–or even just feeling normal–requires increasing amounts of the drug or food, says Kenny, the lead author of the study.

“People know intuitively that there’s more to [overeating] than just willpower,” he says. “There’s a system in the brain that’s been turned on or over-activated, and that’s driving [overeating] at some subconscious level.”

In the study, published in the journal Nature Neuroscience, Kenny and his co-author studied three groups of lab rats for 40 days. One of the groups was fed regular rat food. A second was fed bacon, sausage, cheesecake, frosting, and other fattening, high-calorie foods–but only for one hour each day. The third group was allowed to pig out on the unhealthy foods for up to 23 hours a day.

Not surprisingly, the rats that gorged themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats in the third group gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high.

They began to eat compulsively, to the point where they continued to do so in the face of pain. When the researchers applied an electric shock to the rats’ feet in the presence of the food, the rats in the first two groups were frightened away from eating. But the obese rats were not. “Their attention was solely focused on consuming food,” says Kenny.

In previous studies, rats have exhibited similar brain changes when given unlimited access to cocaine or heroin. And rats have similarly ignored punishment to continue consuming cocaine, the researchers note.

The fact that junk food could provoke this response isn’t entirely surprising, says Dr.Gene-Jack Wang, M.D., the chair of the medical department at the U.S. Department of Energy’s Brookhaven National Laboratory, in Upton, New York.

“We make our food very similar to cocaine now,” he says.

Coca leaves have been used since ancient times, he points out, but people learned to purify or alter cocaine to deliver it more efficiently to their brains (by injecting or smoking it, for instance). This made the drug more addictive.

According to Wang, food has evolved in a similar way. “We purify our food,” he says. “Our ancestors ate whole grains, but we’re eating white bread. American Indians ate corn; we eat corn syrup.”

The ingredients in purified modern food cause people to “eat unconsciously and unnecessarily,” and will also prompt an animal to “eat like a drug abuser [uses drugs],” says Wang.

The neurotransmitter dopamine appears to be responsible for the behavior of the overeating rats, according to the study. Dopamine is involved in the brain’s pleasure (or reward) centers, and it also plays a role in reinforcing behavior. “It tells the brain something has happened and you should learn from what just happened,” says Kenny.

Overeating caused the levels of a certain dopamine receptor in the brains of the obese rats to drop, the study found. In humans, low levels of the same receptors have been associated with drug addiction and obesity, and may be genetic, Kenny says.

However, that doesn’t mean that everyone born with lower dopamine receptor levels is destined to become an addict or to overeat. As Wang points out, environmental factors, and not just genes, are involved in both behaviors.

Wang also cautions that applying the results of animal studies to humans can be tricky. For instance, he says, in studies of weight-loss drugs, rats have lost as much as 30 percent of their weight, but humans on the same drug have lost less than 5 percent of their weight. “You can’t mimic completely human behavior, but [animal studies] can give you a clue about what can happen in humans,” Wang says.

Although he acknowledges that his research may not directly translate to humans, Kenny says the findings shed light on the brain mechanisms that drive overeating and could even lead to new treatments for obesity.

“If we could develop therapeutics for drug addiction, those same drugs may be good for obesity as well,” he says.