Minutes of the Columbia University Seminar on Appetitive Behavior(#529)Date: December 4th, 2008 Seminar Title: "Stress and obesity - are you eating comfortably?" Speaker's Name and Affiliation:
Presiding Chair: Harry R. Kissileff, Ph.D. Rapporteur: Kathleen L. Keller, Ph.D. Attendees and their Affiliation:
Summary: (Prepared by the Speaker) This brief narrative review considers recent evidence that addresses the question whether stress may be linked to obesity, and in particular whether ¡®comfort eating¡¯ may mediate any such link; and if so, by what mechanisms. Psychological stress is increasingly recognised as a barrier to healthy behaviour, as well as health per se, and is thus a potential factor underlying the current obesity epidemic. Comfort eating, i.e. eating to relieve stress and negative affect, is a culturally recognised phenomenon, and it is clear that particular sorts of food, typically sweet and/or fatty, and energy-dense snacks, are chosen in this context. Such foods may mediate stress relief via opioidergic systems. However, surveys indicate that comfort eating is not universal, and indeed some people report undereating during stress. It is becoming increasingly clear that comfort eaters are characterised by heightened stress reactivity, both perceived and expressed physiologically by increased activation of the limbic hypothalamic pituitary adrenal (LHPA) axis, for example. This stress proneness has also been linked to risk of central adiposity, as well as stress relief associated with dietary manipulation of serotonin function. Overactivation of the LHPA axis may promote binge eating of highly palatable energy-dense comfort foods, so in turn leading to weight gain, especially central adiposity. However, some data suggest this cycle may be self-limiting, as abdominal fat accumulation during chronic stress may in turn restrain the LHPA axis. This may be one reason why the epidemiological evidence for an association between stress and obesity is weak, although general life stress, such as occurs in a low socioeconomic environment, appears to be a significant risk factor for obesity. Discussion: Q. Why would these effects (opioid effects) be specific to chocolate?
Q. This is a fascinating phenomenon (tolerance to pain increased by
chocolate). Do we have any idea what the post-ingestive signals are that
cause the analgesic effects of these foods?
Q. The cocoa powder that you used didn¡¯t have caffeine in it, right? Why
does the caffeine + theobromine group show larger effects?
Q. Was there any control for BMI in the Ward & Mann (2000) study you cited?
Q. What was the stress question that you used?
Q. What about actual BMI? Did you measure that?
Q. These types of findings look to be common among undergrads. What
about adults?
Q. What about salty foods? Do people eat those when they are stressed?
Q. Did you have an independent measure of the physiological intensity of
stress?
Q. Did you look at the strength of perceived stress and intake of sweets
under stress?
Q. Were these binge eaters? Were they bulimic or obese?
Q. The serotonin hypothesis ignores the fact that other people find ¡°fat¡± an
important nutrient in comfort foods.
Q. What would be the mechanism for serotonin¡¯s ability to reduce stress?
Q. How was the stress prone group determined?
Q. Do people move in and out of these categories of stress, for example,
when they lose their job?
Q. Do you think it¡¯s realistic that energy flow to the brain would actually be
changed during times of stress?
Q. Is exercise stressful?
Q. Why isn¡¯t leptin included on your summary figure (chronic stress model)?
Q. How do you get an r=0.032 with a p-value of 0.006?
Q. Is it possible to go back and check those that are ¡°stress-reactive¡± in past
studies?
Q. Do you think there is any application for these data for studying eating
disorders?
Q. Have you tried testing artificial sweeteners to see if they play a role on
stress levels?
|