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:

  • Leigh Gibson
  • Roehampton University, London, UK

Presiding Chair: Harry R. Kissileff, Ph.D.

Rapporteur: Kathleen L. Keller, Ph.D.

Attendees and their Affiliation:

Kathleen KellerColumbia/Obesity Research Center
Harry KissileffObesity Research Center
Diane KleinNYSPI/CU
Janet SchebendachNYSPI/CU
Maria Bernalls-KounsNY ORC
Eva ConceicaORC
Eugene DinkevichSUNY-Downstate
John G. KralDownstate
Richard W. FoltinCU/NYSPI
Z. WangColumbia
BT WalshColumbia/PI
JA GrinkerUniversity of MI
Eva KovacsUnilever
Allan GeliebterORC
Susan CarnellORC

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?
A. They probably aren¡¯t specific to chocolate, but chocolate does have some sensory properties that are unique.

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?
A. One mechanism is that these foods probably release brain dopamine.
Comment: Chocolate also contains a substance called theobromine that has pharmacological effects.
A. Yes, there is some data on that from Smit, Gaffan, and Rogers (2004)

Q. The cocoa powder that you used didn¡¯t have caffeine in it, right? Why does the caffeine + theobromine group show larger effects?
A. I¡¯m not sure that the effect you are looking at is statistically significant.

Q. Was there any control for BMI in the Ward & Mann (2000) study you cited?
A. I can¡¯t remember the particulars of that study.

Q. What was the stress question that you used?
A. Under stress, do you have the tendency to eat much less, the same, or much more (something like that).

Q. What about actual BMI? Did you measure that?
A. We collected BMI by self-report.

Q. These types of findings look to be common among undergrads. What about adults?
A. I have some data from working adult men coming up.

Q. What about salty foods? Do people eat those when they are stressed?
A. They are not typically the foods that people report eating under stress.

Q. Did you have an independent measure of the physiological intensity of stress?
A. Yes, we looked at blood pressure and heart rate.

Q. Did you look at the strength of perceived stress and intake of sweets under stress?
A. We probably did, but likely didn¡¯t find anything.

Q. Were these binge eaters? Were they bulimic or obese?
A. They weren¡¯t necessarily bulimic, but likely had binge eating behaviors.

Q. The serotonin hypothesis ignores the fact that other people find ¡°fat¡± an important nutrient in comfort foods.
A. I agree, but I¡¯m not sure that fat matters for the serotonin story.

Q. What would be the mechanism for serotonin¡¯s ability to reduce stress?
A. I think that humans who have low serotonin levels might get a boost in mood and that this may result in a decrease in perceived stress.

Q. How was the stress prone group determined?
A. We used a neuroticism scale that was originally written in Dutch, but we had it translated.

Q. Do people move in and out of these categories of stress, for example, when they lose their job?
A. That¡¯s a brilliant question, but I think that these traits are not easily changed.

Q. Do you think it¡¯s realistic that energy flow to the brain would actually be changed during times of stress?
A. In Peters et al (2007) they argue that it would. There are a number of systems that can increase glucose supplies to the brain.

Q. Is exercise stressful?
A. In some cases, yes, but it depends on the intensity level of the exercise.

Q. Why isn¡¯t leptin included on your summary figure (chronic stress model)?
A. I haven¡¯t found much evidence that leptin is involved in this model. We have not seen acute changes in leptin levels with stress.

Q. How do you get an r=0.032 with a p-value of 0.006?
A. By having a very large (n). These are from meta-analyses and when you do that, you combine the (n) across studies.

Q. Is it possible to go back and check those that are ¡°stress-reactive¡± in past studies?
A. Maybe, but some of the studies use crude measures.

Q. Do you think there is any application for these data for studying eating disorders?
A. It¡¯s possible. With anorexia, there is definitely a stress component. Early experiences may create a more vulnerable or sensitive stress system. Comment: Since anorexics may sometimes exercise to extremes, it might be interesting to look at the link between cortisol and physical activity.

Q. Have you tried testing artificial sweeteners to see if they play a role on stress levels?
A. I think you could fool the system in the short-term, but in the long-run, it would be interesting to see how the body responds.