The genetic and psychological factors involved in food maintenance and 
body size
Stephaney M. Cox

	There is much debate about the influence of genetics and that of 
environment on the behavior of an individual.  One topic that has been 
the focus of study is that of food maintenance and body size.  I will 
examine the effects of genetics, psychological factors, and proteins on 
eating behavior, as well as monogenetic and polygenetic effects on 
appetite and weight gain.
	
Overview of the Causes of Hunger and Satiety
	In order to stay alive, we must feed our living body with 
nutrients.  These nutrients come from the foods we eat.  Our body gives 
us signals when we are hungry and when we are full.  We are equipped 
with short and long term storage reservoirs in our body; the short-term 
reserves (carbohydrates) are stored in our liver and in our muscles, 
and the long-term reserves (fats) are stored in adipose tissue 
(Carlson, 2000).  When we have strained our reserves, our body sends us 
signals to ingest more food, thereby giving it the energy it needs.  
The carbohydrate glucose that we ingest with our food is present 
in the digestive tract when it is plentiful in the body, as it is after 
a meal.  It is converted into glycogen by the liver when stimulated by 
the presence of insulin in the blood.  The glycogen can then be 
converted to glucose by glucagon for use by the body when the immediate 
supplies have dwindled.  Glucagon and insulin are both produced by the 
pancreas.  The short-term reserve of carbohydrates is responsible for 
keeping the central nervous system (CNS) and the rest of the body 
functioning between meals.  
When there is a decrease in the amount of glucose in the blood, 
as there is between meals, metabolism is in a "fasting phase."  During 
this phase, the pancreas stops secreting insulin and starts secreting 
glucagon, prompting the liver to convert glycogen to glucose.  The 
presence of glucagon also triggers the breaking down of triglycerides 
in the long-term storage. If the short-term supply of carbohydrates is 
left to dwindle, the CNS has to depend on glucose derived from 
glycerol, which resides in long-term storage in fats in the form of 
triglycerides.  The other body cells are meanwhile being fueled by 
fatty acids derived from the triglycerides.  
A feeling of hunger can be generated by both physiological and 
psychological means.  Both modes contribute to our everyday eating 
habits.
The feeling of hunger arises physiologically when we begin to use 
up energy from our long-term triglyceride storage.  When the long-term 
reserves are plentiful, a peptide hormone is released which reduces the 
feeling of hunger.  However when long-term reserves diminish, the 
peptide hormone secretion lessens, causing the areas of the brain that 
control eating to signal hunger.  A feeling of satiety, or fullness, 
comes about when receptors in the stomach detect an adequate amount of 
nutrients; the duodenum in the small intestine detects sufficient 
levels of glucose, amino acids, and fatty acids; and when the liver, 
after receiving nutrients, reinforces these signals with its own.
Psychological stimuli that cause a feeling of hunger are 
plentiful and widely studied.  The presence of other people at a meal 
setting, meal schedule customs, the smell or sight of food, and past 
eating habits can all stimulate a feeling of hunger.

The "nurture" aspect of hunger and satiety
A major psychological cause of food intake regulation is our 
daily schedule.  If we have a daily eating schedule then we will become 
accustomed to eating at a particular time, whether or not our bodies 
actually call for food intake.
If we smell food or sometimes even if we see food, our bodies 
begin to prepare for the intake of nutrients.  Generally this is first 
apparent by the increase of saliva in the mouth, readying its enzymes 
to break down food.  The reaction is carried on all the way down in the 
stomach as well, where hydrochloric acid is produced in preparation for 
food intake.
There is also a correlation between the number of people we share 
a meal with and how much we eat.  If there are more people, we will 
ingest more during the course of the meal.  In this way, our 
psychological reaction to social factors can regulate our food intake.
The fact that high-flavor, inexpensive foods are readily 
available to our society also affects our intake of food (Hill & 
Peters, 1998).  The fast foods that millions of Americans eat every day 
come in portions that are getting increasingly large, especially with 
big selling gimmicks like "super-sizing."  This can lead to a 
subconscious increase in the amount of food taken in.
Studies completed on obesity and other eating disorders have been 
instrumental in giving us some clue as to the genetic and psychological 
influences on eating habits.  I will draw on evidence from these 
studies to examine the effect of our psychological makeup on the way 
that we eat and how those habits affect our body size.
Eating can be a psychologically regulated activity, as previously 
mentioned.  It can also be a learned behavior.  Birch et al. (1987) 
showed that hunger and satiety could be conditioned by rewarding a 
child for finishing a plate of food, regardless of the necessity of the 
nutrient intake.  This conditioned manner of food intake regulation can 
affect the psychological hunger and satiety signals that the child will 
feel for the rest of its life, setting up psychological eating 
patterns.  In the future, it is thought that the child will not be able 
to estimate the caloric intake of meal portions, leading to a tendency 
to overeat, and therefore leading to an accumulation of fat.

The "nature" aspect of hunger and satiety
	Given the extensive research on genetics and hunger, it is 
impossible to deny that genes have a direct role in determining our 
eating lifestyles and proclivities toward certain body sizes.
	A person who has obese relatives is more likely to become obese 
himself (Hill & Peters, 1998).  Twin studies have shown that there is a 
greater resemblance in the degree of obesity between monozygotic twins 
as between dizygotic twins, suggesting that a genetic link for hunger 
and body size may be shared (Sorensen & Echwald, 2001).  It has also 
been shown that adopted children's body size is more closely related to 
their biological parents than their adoptive parents (Maes, Neale, & 
Eaves, 1997).  
	Leptin is a protein secreted by fat cells and stimulated into 
production by the so-called "ob" gene (Carlson, 2000).  It seems that 
leptin sensitizes the brain to satiety signals from the stomach, 
causing a cessation of food intake.  Mutations to the ob gene cause an 
inability of the body to produce leptin, leading to the eating of much 
larger amounts of food.   Montague et al. (1997) studied two cousins 
with extreme childhood obesity and suggested that their congenital 
leptin deficiency led to the obesity.  Such cases of obvious connection 
between leptin deficiency and obesity are rare, and so cannot be 
credited with all cases of obesity.  The correlation does however lend 
support to the idea of hunger and satiety having some genetic 
influence.

Monogenetic and polygenetic influences on food intake
Sorensen (2001) suggests that "the pattern of inheritance of 
obesity strongly suggests that the effect is polygenetic, with each 
variant of many genes making a small difference in effect."  There have 
been a few genes, however, such as the ob gene, that cause a 
monogenetic form of obesity in humans (Comuzzie & Allison, 1998).  

Conclusion
	The psychology and genetics of food intake and body size are 
being widely studied, especially with the increase in technology 
available to analyze the human genome.  Everyone seems to agree that 
our rate of food intake and our body size are caused by a combination 
of environmental and genetic influences, although there is yet to be 
found exact evidence for the specific interactions between the two.


References

Birch, L.L., McPhee, L., Shoba, B.C., Steinberg, L., & Krehbiel, R. 
(1987).  "Clean up your plate": Effects of child feeding practices on 
the conditioning of meal size.  Learning and Motivation (18:301-317).

Carlson, N.R.  (2000).  Physiology of behavior.  Boston: Allyn and 
Bacon.

Comuzzie, A.G., & Allison, D.B.  (1998).  The search for human obesity 
genes.  Nature (280: 1374-1377).

Hill, J.O., & Peters, J.C.  (1998).  Environmental contributions to the 
obesity epidemic.  Science (280: 1371-1374).

Maes, H., Neale, M.C., & Eaves, L.J.  (1997).  Genetic and 
environmental factors in relative body weight and human obesity.  
Behavioral Genetics (27: 325-351).

Montague, C.T., et al.  (1997).  Congenital leptin deficiency is 
associated with severe early-onset obesity in humans.  Nature (387: 
903-908).

Sorensen, T.I.A., & Echwald, S.E.  (2001).  Identifying single genes in 
polygenic inheritance is not easy.  British Medical Journal (322: 630-
633).

Copyright © 2001, Dr. John M. Morgan, All rights reserved - This page last edited 8 May, 2001
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