Pursuant to my previous post about stress fucking with your head, here’s some stuff on how stress fucks with your body — and how susceptible folks may respond.
I’ll be devoting a section in my upcoming book to appetite and eating behaviour regulation — in other words, what makes us want food? Why do we want the kinds of foods we want?
One of the arguments I’ll make is that appetite, hunger, and satiety are complex phenomena, which are strongly affected by our stress responses. Overweight and obesity can be viewed as the consequence of eating behaviour that is, in part, a coping mechanism. My own experiences, experience with hundreds of nutrition clients, and the clinical literature seems to support this argument.
Folks who tend towards overweight/obese (which, in North America, is the majority) are not necessarily “metabolically” different in the way that is commonly understood (i.e. that fatter folks have “slower metabolisms”). In fact, arguably they are metabolically normal — but responding to abnormal circumstances, whether that’s increased stress, emotional dysregulation, environmental stress (such as the speed and pace of life, or screwed-up light-dark cycles from shift work, etc.), or simply the abundance of tasty foodlike substances.
We can thus understand overweight/obesity (along with a host of disordered eating behaviours that don’t necessarily result in excess body fat, but are still not healthy food relationships) as the consequence of a coping mechanism. Humans and many animals use food and eating in some way to deal with pain, discomfort, and distress.
The coping mechanism operates through several pathways, but basically you can understand eating behaviour as a potential mode of self-medication and self-soothing. Here’s a recent article from Neuropsychopharmacology about one of the ways in which this can occur.
Similar to alcohol and other drugs, highly caloric and palatable foods activate brain stress and motivational pathways that likely evolved to respond and adapt to challenging environments and primary rewards necessary for survival. Chronic substance use and high BMI states are associated with alterations in stress pathways which in turn are associated with stress-related consummatory behaviors. [Krista’s note: Not sure this is the best word choice, LOL! Kinda sounds like increased stress-related humping.]
A central component of the stress/reward motivational neurocircuitry involves the ventral striatum (VS), a structure implicated in reward processing (including reward-based learning and expectation, valuation, or anticipation of rewards) and stress responsiveness. Stress, food, and drugs all increase neurotransmission in the VS.
A reduction in striatal dopamine 2/3 (DA D2) receptors in obese individuals similar in magnitude to those observed in drug-addicted individuals has been reported, suggesting alterations in striatal function in obese individuals in stress/reward neurocircuitry. Furthermore, DA D2 receptor measures correlate inversely with BMI, suggesting that individuals with the lowest levels of striatal DA D2 receptors have the highest BMIs.
Together, these data suggest that similar aspects of striatal dysfunction may contribute to drug addiction, obesity, and stress vulnerability.
So basically, what we have here is a situation in which obesity is correlated with some malfunction (or perhaps over-function) of the reward and stress-response systems.
We can understand obesity/overweight as a consequence of this malfunction. If you’re prone to overweight, it likely means that in some way, you are hyper-responsive to stress or discomfort; you seek self-soothing via eating; and you may need a bigger “hit” of eating/palatable food in order to soothe yourself enough.
The dopamine reward system is also trainable — in other words, the more a person opts for a self-soothing choice, the more that choice becomes ingrained as an optimal one. The more you do, the more you want. And the more it seems like that choice is the only option.
OW/OB [overweight/obese] individuals have increased responses in motivation/reward neurocircuitry that are related to peripheral metabolic factors linked to non-homeostatic feeding [aka overeating] in individuals with elevated BMIs. The finding of altered VS activation in the neutral relaxing and stress conditions suggests that treatments targeting stress management or anxiety reductions may prove to be beneficial through their influences on central motivation/reward neural pathways.
Next time you attack that buffet, announce, “I’m doing non-homeostatic feeding!”
Anyway, this study suggests what I have long felt as a nutrition coach: Telling people what to eat is largely useless — we must retrain ourselves in how to eat and understand why we eat. And maybe time spent lecturing people about eating broccoli would be better invested in helping them chill out.