Home > Nutrition > The Psychology of Semi-Starvation

The Psychology of Semi-Starvation

In my last post regarding the concept of energy balance I talked about a case of internal starvation that would result from the body partitioning incoming calories into fat as opposed to energy.  If this were to happen the person would be starving despite intaking a large amount of calories.  In such a case, fat tissue would be a parasite of sorts, stealing away calories from other biological activities.

It runs against the grain of popular culture and common medical advice to suggest that someone who is overweight is starving in any way.  If they were starving, then prescribing fewer net calories would be bad advice would it not?  In addition to misguided advice is the fault in common thought that ones eating habits are a purely logical behavior and that the overweight are but those with substandard willpower.

What I present in the following is not conclusive evidence of causation; sadly I don’t have those data.  What I looked for was the psychological impacts of starvation and obesity.  If obesity is starvation, then they could have similar psychological effects.

The first experiment I want to discuss is the Minnesota Starvation Experiment, which was conducted during World War II.  This experiment included a 6-month semi-starvation period.  A standardized test (MMPI) was used to assess the psychological affects of the experimentation.  The psychological affects were summarized as follows:

The psychologic changes, although more complicated and more difficult to measure, are just as characteristic as are the physical changes. The chief psychologic manifestations which were found characteristically in all subjects are intense preoccupation with thoughts of food, emotional change tending toward irritability and depression, decrease in self-initiated activity, loss of sexual drive, and social introversion.  …  The elevation of the neurotic end of the profile (Hs, D, and Hy) during semistarvation gives a quantitative and graphic indication of the personality changes observed clinically.  In rehabilitation these changes were reversed, although the profile obtained at the end of controlled rehabilitation is still above the normal. In this connection it may be pointed out that the first twelve weeks of rehabilitation were in reality a continuation of the stress. This was especially true of the first six weeks and of the men in the lower caloric groups. It was only some time after release from the controlled diet that complete rehabilitation was effected. Profiles on 20 subjects obtained after thirty-three weeks of refeeding had returned to the
“normal,” semistarvation level.  The average score on the Pd scale was initially low and there was little change during semistarvation.  This indicates an absence of a tendency to devolop aggressive, antisocial reactions or “character neuroses.” It is of interest that 3 of the 4 subjects who failed to complete the experiment (and were not included in the group profile) did show significant elevation in Pd score. The moderate elevation of the scores on the Pa, Pt, Sc, and Ma scales was entirely within “normal” limits and is further evidence of the absence of “psychotic” types of reaction in the average subject. This was not true of a few individuals who showed more severe or unusual symptomatology. (Source)
A little interpretation; the MMPI scores showed increased prevalence of  Hypochondria (Hs), Depression (D), and Hysteria (Hy) during the starvation period and this was reversed afterward.   This study indicates elevation in the same MMPI categories in the obese (Hs, D, Hy).
This study goes a step further and shows similar trending; supranormal Hs, D, and psychopathic deviate (Pd) in the morbidly obese AND those who suffer from anorexia and bulimia.  The study examined the three groups; hospitalized anorexia patients, hospitalized bulimia patients and morbidly obese outpatients.  From the abstract:

The results indicated that there was no significant difference in the overall profiles of the three experimental groups, but that all differed from the control group.

As previously noted one cannot assign a causative link with these sort of data but I believe that a hypothesis that claims that obesity, like anorexia and bulimia, is a form of starvation is not unreasonable, even if incomplete.

To bolster such a hypothesis I ask you to consider this, which discusses the connections between brain chemistry and food intake and the resultant cravings and possible obesity.  In addition to the effects of carbohydrates in general, the specific affects of exorphins which result from the digestion of wheat gluten and milk may be players.

In summary, what and how much we eat can affect our brain chemistry to such a degree that it can change what we eat and/or how much.  In the same way that I argued that it’s not as simple as calories in calories out, it’s also not as simple as just controlling food quantity and quality in a logical way due to the psychological affects of food on our decisions.

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Categories: Nutrition
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