Q. What are some factors involved with Genetics and Body Composition? And what does some of the research show?
A. Heritability
Early
research suggests heritability and body fat content ranged from 0-90%
(6). Interestingly, heritability estimates in twin studies are
generally high (60-80%) whereas adoption studies (10) or general family
studies (11) give lower results (30-60%). However, a large share of
this heritability could be due to non-additive factors. Maes et al.
(12) summarized and confirmed through familial studies that even at the
lowest heritability estimate (30%), genetic factors are involved in
body weight variation. Although this research confirms our
understanding of a genetic contribution, there are still some
discrepancies concerning the importance of genetic factors in the
familiar resemblance observed for body fat (6). Due to the increased
cost of direct body fat measurements, most studies have used BMI or
skinfold techniques at a few sites as approximates of body composition.
Due to this limitation, it is difficult to assess the validity and
legitimacy of the research for heritability and of body fat content.
A
recent twin study (13) based on a sample of children born after the
onset of obesity, provides results in agreement with previous research.
In an obesity producing environment, genetic impact on body weight is
very large. Wardle (13) also explains the thrifty genotype hypothesis,
whereas genes that predispose individuals to obesity would have had a
selective nature, and initiate an obesity epidemic, in association with
the altered environmental setting.
Overall, the heritability of obesity is estimated at 40% to 70%,
as previously indicated, although higher values have been reported. A
more thorough insight of the genetic regulation in body composition
demands detection of key genes and their mutations, along with specific
proteins, that play a role in body composition.
Hormones
Insulin and leptin are known as important adiposity signals involved in the neuroendocrine regulation of food intake. Leptin,
a crucial hormone produced by the adipoctye and released into
circulation, acts on the hypothalamus to regulate body weight.
Circulating levels of leptin reflect the adipose tissue mass as well as
current nutritional status and thus forms a long-term and short-term
energy balance signal (14). Normally, leptin blunts the urge to eat when caloric intake maintains ideal fat stores.
Nonetheless, Leptin may effect certain neurons in the arcuate nucleus
(located inside the hypothalamus) to stimulate production of chemicals
that control appetite and/or reduce the levels of brain chemicals that
stimulate appetite (15). An individual with a gene defect for either
adipoctye leptin production and/or hypothalamic leptin sensitivity, the
brain inadequately assesses the body's adipose tissue status; thus the
need to eat continues. However, Leptin alone does not determine obesity
or explain why some people eat whatever they want while weight gain is
minimal, and others gain weight with the same caloric diet.
Notwithstanding, obesity syndromes associated with leptin deficiency
and leptin receptor mutations have been reported in humans (14). The
majority of obese humans, however, have increased serum leptin
concentrations, implicating leptin resistance may be important in human
obesity.
Insulin
is the chief hormone controlling blood glucose levels, and its
secretion by the pancreatic ß-cells is partly determined by the
neighboring glucose concentration. Woods and Seeley (8) state the
responsiveness of pancreatic ß-cells to glucose is a function of
fatness, with fatter individuals secreting additional insulin for a
given increase in blood glucose. Therefore, insulin concentrations reflect both fat stores and current metabolic requirements.
Cholecystokinin,
is the prototypical hormone produced by the cells in the duodenum and
jejunum. The secretion response is to existing nutrients within the gut
lumen, specifically fat and protein. Although there are two receptor
subsets, CCK-1 (located mainly in the GI tract), and CCK-2 (located
mainly in the brain), cholecystokinin inhibits food intake by decreasing meal size and duration
(16). The satiety effect is regulated by the CCK-1 receptors on the
ends of the sensory fibers of the vagus nerve (17). In turn, CCK-1
receptor antagonists increase caloric intake and reduce satiety, thus
suggesting an effect on appetite and food intake regulation (16,18).
However, taken alone, chronic administration of cholecystokinin does
not result in weight loss, but a combination of peripheral
cholecystokinin and leptin has been shown to stimulate greater body
loss than leptin alone (19).
Biochemical Signals
Many
biochemical signals have been directly associated with human body
composition and the regulation of food intake (9,20,21). One such gut
hormone is peptide tyrosine-tyrosine also known as Peptide YY-36,
where Y depicts the abbreviation for tyrosine. PYY is a 36 amino acid
hormone that has been suggested as a potential therapeutic agent for
obesity (9). PYY is released by the intestinal cells in
proportion to the caloric content of a meal. PYY travels to the
hypothalamus to initiate the urge to eat. Interestingly, obese
individuals normally make less of this satiety signal than normal body
weight individuals. Furthermore, a recent study reported that obese
persons have lower fasting and postprandial circulating PYY than lean
individuals and require a much greater caloric load to produce an
equivalent stimulation of PYY (22). Regardless if the decrease
signaling of PYY in the obese has a critical part in the functioning of
obesity, it represents an attractive target for human body composition.
The newly discovered endocannabinoid system
has been shown to contribute to physiologic regulation of energy
metabolism, food intake, and fat and glucose metabolism (21). Although
human trials have not been established and confirmed, it is likely the
CB-1 and CB-2 receptors will be an important regulator of human energy
balance, body weight and body composition.
References
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~Jonathan Mike, CSCS, USAW, NSCA-CPT
Doctoral Student, Assistant Editor | 
