Metabolism, Nutrition, & Health Decision Making

In Chapter 4, Sapolsky (2004) yet again explains a complicated process in the simplest way. Specifically, he uses an analogy to describe how our bodies work throughout the chapter, but what I liked most from this read was his discussion of both juvenile and adult diabetes. As an undergraduate, I worked in a behavioral neuroscience laboratory where we focused on understanding the neural mechanisms that mediate addiction to drugs of abuse, such as nicotine. We wanted to uncover why close to 20% of diabetic individuals continue to smoke and have a harder time staying smoke-free when trying to stop. To answer this question, we injected rats with a drug called Streptozotocin (STZ). In humans, this drug is used to treat pancreatic cancer, but in rats, can destroy the insulin-producing beta cells in the pancreas to stop the production of insulin altogether. While I was reading the chapter, it reminded me that when we would explain our research in posters/publications we would always state that using STZ to induce diabetes was modeling Type 1 diabetes or an advanced form of Type 2 diabetes. As an undergrad, I just nodded my head in agreement, but it was not until reading Sapolsky’s article (sadly, I guess) that I understood what this phrase meant. Type 1 insulin-dependent diabetes is pretty easy to understand. Your body attacks the insulin-producing cells in the pancreas, which is pretty much what STZ does, but what I did not know was that in an individual with type 2 diabetes can go on to develop Type 1 diabetes because of all the damage they put their pancreas through. In the end, our study found that diabetic rats showed enhanced rewarding effects from nicotine and enhanced withdrawal effects from the drug. Thus, it may be that humans who are diabetic and who smoke are finding cigarettes more rewarding and when trying to quit smoking, have enhanced withdrawal effects to the drug as well. While this information was rewarding because we may have found the underlying mechanisms mediating diabetic smokers behaviors, we still need to find a way to encourage these individuals to quit smoking. The review article by Magnan, Shorey Fennell, and Brady (2017) may help us in doing so. In their article, they describe different social cognitive models of health behaviors and introduce cognitive-based models that describe how different individuals would react in certain situations. I wonder whether one of these models would be better than the other in deterring diabetic smokers to change their smoking behavior. My gut is leaning me towards the Social Cognitive Theory proposed by Bandura because it emphasizes an interaction between the individual and the environment (Magnan, Shorey Fennell, & Brady, 2017). Back in the 1950’s everyone smoked. They smoked in buildings including schools, offices, you name it. Today, because of the damaging effects of smoking cigarettes, no one smokes. I’ve heard some people say even smelling smoke is revolting to them. Additionally, many places do not let you smoke even close to their building. Because of these perceived personal, social, and environmental obstacles, I feel as though this model would push such individuals to change their smoking habits.

Additionally, continuing with the theme of addiction, Finch & Tomiyama (2014) make the point to emphasize how stress-induced eating can activate the neural reward circuitry just as other addictions such as smoking can. Unfortunately, as outlined in their paper, repeatedly indulging in stress-induced eating leads to the accumulation of visceral fat brought on by the increase in glucocorticoids and insulin (Finch & Tomiyama, 2014). I would definitely say that I experienced this during my first year of graduate school when I put on close to 20 lbs. of fat because, without noticing, I would eat when not hungry and eat when stressfully preparing for my stats quizzes/finals. Furthermore, the meals that I decided to indulge in during these stressful times were high in fats. Kecolt-Glaser et al. (2015) sought to understand the impact daily stressors and previous history of depression had on the metabolic responses to different high-fat diets. They found that individuals who experience a greater amount of stressors the day before eating a high-fat meal had decreased energy after consuming the meal. Furthermore, greater stressors were also associated with lower fat oxidation and higher insulin production which enhances fat storage (Kecolt-Glaser et al., 2015). Thus, there should be many things we think about before we make the decision to eat a high-fat meal. Sure, eating some high-fat diet meals aren’t going to kill us (immediately), but it is definitely all about variety.

Finch, L.E., & Tomiyama, A.J. (2014). Stress-induced eating dampens physiological and behavioral stress responses. Nutrition in the Prevention and Treatment of Abdominal Obesity. Elsevier Inc.

Kiecolt-Glaser, J.K., Habash, D.L., Fagundes, C.., Andridge, R., Peng, J., Malarkey, W.B., and Belury, M.A. (2015). Daily stressors, past depression, and metabolic responses to high-fat meals: a novel path to obesity. Biological Psychiatry, 77, 653-660.

Magnan, R.E., Shorey Fennell, B.R., Brady, J.M. (2017). Health decision making and behavior: the role of affect-laden constructs. Soc Personal Psychol Compass, 11, e12333.

Sapolsky, R.M. (2004) Why zebras don’t get ulcers: A guide to stress, stress related diseases, and coping. New York: W.H. Freeman.

1 Comment

  1. It was very interesting learning about your previous research on smoking cessation in diabetic rats, Ceci! I would imagine with both food reward and nicotine reward there would be both hormonal imbalance, as well as activation in neural reward pathways. Since you study the brain, do you have a thought as to which specific brain areas might either both or independently increase/decrease in activation in response to nicotine and/or food?

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