Sunday, May 6, 2018

Food Addiction

I want to make sure that people who read this post don't think I'm suggesting anything about weight or diet. I'm not. I feel like I should put that in bold red lettering. I'm presenting information and don't necessarily have an opinion one way or another; I'm just interested in the ongoing research on addiction, especially regarding the brain. When discussing obesity, eating disorders, addiction, and diet in this post, I'm only drawing on information I've found that I feel is credible, so rest assured that I'm not promoting anything or suggesting anything about anyone. Take what is useful to you and leave the rest.

My writing here is done entirely without judgment. To make it clear, I support your right to choose how you want to live your life and make no assumptions about you based on appearance or lifestyle. I am absolutely not suggesting anything about anyone's willpower in this post and am not implying anything about what people should or shouldn't eat. 

In my previous post on low carb diets, I may not have been clear enough that I don't deny the evolving research on obesity and insulin sensitivity, just like I don't deny the research (that also needs further testing) that shows a Keto diet adversely affects test results that require a higher order of mental processing and flexibility, however, the one thing in common is that all of these studies address specifics, not overall wellbeing. In one two-week study, for example, it was determined that a ketogenic diet MAY substantially increase insulin sensitivity in obese subjects with type 2 diabetes. I don't dispute this.  

My main point is that research in nutrition science is more often than not flawed, and, more importantly, a diet is basically ineffective if people can't stick to it. My caution to anyone who claims there's "all this research" around a certain issue is to look at as many studies as you can find and decide for yourself whether or not the sample size in each was large enough, the duration of the study was sufficient, the research conducted was controlled as much as possible, and the results were presented accurately without any speculation or false correlations. Additionally, as was the case in several sugar and obesity studies, animal models don't always accurately predict what happens in humans. In the words of Gary Taubes:


 Anecdotes are often the basis of quackery – but not always. Much of reliable medical knowledge emerged initially from anecdotal observations. Medical science can be thought of as a process that begins with such observations and, through relentless testing of hypotheses, eventually generates truth.


There's no doubt that anyone can have a predisposition to either drug use or eating disorders or both, but having a predisposition doesn't guarantee a specific outcome. There are other factors involved. When it comes to addiction, there are slight physiological differences between dependence on a substance and what people call an addiction to food. From a genetic standpoint, the allele that's most often present and considered a risk factor in cases of addiction is rarely present in those who are obese or have eating disorders. Looking at the central nervous system, it's not surprising that people oversimplify the effects of addiction because incredibly complex systems are involved. It's important to understand that neurotransmitters aren't limited to one area of the brain. There are billions of neurons and trillions (yes, that's with a "t") of connections in our brains.

In the case of dopamine, the neurotransmitter most associated with addiction, there are several dopaminergic pathways (dopamine is also found outside of the central nervous system), but most people focus only on the one associated with reward-seeking behavior. Specifically, the mesolimbic tract is associated with drug use rather than the mesocortical tract that's associated with eating disorders. The mesocortical tract connects the ventral tegmentum (sort of like the brain's superhighway) to the prefrontal cortex and plays a role in planning, cognitive function, and emotional response, among other things. Dopamine elsewhere in the central nervous system is involved with much more than reward-seeking, including but not limited to motor control, sexual gratification, and motivation. In other words, it can't be targeted in isolation. In addition, dopamine isn't the only neurotransmitter involved with addiction or addiction-like behavior, and the dopamine pathway isn't the only pathway involved, either. Depending on the type of drug, mu-opioids, GABA, acetylcholine, and others can play a role.

It may be that the outcome is similar in terms of potential interference with life, but food addiction is largely considered a behavioral addiction rather than a literal substance addiction. When it comes to food addiction, it's more the act of eating that's addicting, at least from a neurological standpoint. That's not to say that foods don't affect the brain's chemistry. All foods do to some extent, but the way people eat and eating disorders, in particular, affect hormone levels (leptin, insulin, ghrelin) that can eventually affect the brain's chemistry. Drugs, on the other hand, act directly on either neurotransmitters or on the cells that regulate neurotransmitters. The difference is subtle but important.

According to the 2014 Behavioral and Neuroscience Review that addressed the hypothesis that sugar is addicting:

Addiction-related behaviors in sugar consumption (such as tolerance and a withdrawal syndrome) have not been observed in humans (Benton, 2010). Instead, most observational and mechanistic evidence for addiction to sugar comes from rat models pioneered in Bart Hoebel's laboratory.


This means that addiction to sugar was not seen in humans, only in rats though observational and mechanistic evidence. These findings support the idea that in humans, sugar addiction is more of a behavioral addiction and not a substance addiction. The same was found to be true of other palatable foods. When people talk about coffee or chocolate withdrawal, a headache, feeling low or emotionally wrecked isn't the same as your body's cells not functioning without the substance on which you have become physically dependent. True withdrawal is extremely painful and can be life-threatening. It's not just feeling meh or a little bit cranky. (I hear that last part being said in the voice of Patton Oswalt for some reason.)

Like with autism and many other illnesses and disorders, our definition of addiction is ever-changing and expanding. It used to be that behaviors were not considered addictions, but they are included in the DSM-5 now, which some people claim has moved away from evidence-based, strict definitions in favor of subjective, broad criteria. It's likely that this is for diagnostic purposes, probably so doctors can prescribe medications or therapy. This isn't to suggest that a psychological addiction isn't potentially dangerous to some, more to illustrate that there are different types of addiction. A psychological addiction can cause a person to feel dependent on a substance such as weed or coffee, but if he or she goes without it, the withdrawal itself won't be deadly. This basically addresses the disease model vs the psychological or medical model of addiction, too. The latter can include just about anything, while the former is considered more of a disease with a source or sources of origin. 

What does this all mean? It depends. For the average person, all this research and speculation mean very little. For someone struggling with addiction or an eating disorder, perhaps it might provide a better understanding of the mechanisms involved in both substance abuse and eating disorders. It probably won't solve problems directly, but it might eventually lead to improved methods of addiction and eating disorder treatment. 

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