Breast feeding and obesity in childhood: cross sectional study
BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7420.904 (Published 16 October 2003) Cite this as: BMJ 2003;327:904All rapid responses
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The "Obesity Epidemic in Children" and the world
Testosterone reduces leptin. Leptin reduces appetite. Therefore,
children of higher testosterone have less appetite suppression. It is my
hypothesis that the percentage of individuals of higher testosterone is
increasing. Therefore, overeating is increasing. This may account for the
obesity "epidemic" in the U.S.
(Copyright 2003, James Michael Howard, 1037 North Woolsey Avenue,
Fayetteville, Arkansas 72701-2046, U.S.A.)
"Relation of race, age, and sex hormone differences to serum leptin
concentrations in children and adolescents.
We explored the effects of race, age, and sex hormones on the serum
leptin concentrations in 203 white and 88 black children and adolescents
(ages 9.3-20.5 years). A significant sex by race interaction on serum
leptin levels (p = 0.0301) was observed with lower serum leptin
concentrations, adjusted for subscapular thickness and age, in black boys
than in white boys. Girls had serum leptin levels that were on average
2.15 times those of boys (p < 0.0001). There was an age by sex
interaction (p < 0.0001) with serum leptin concentrations decreasing in
boys but not in girls with age. A strongly inverse relationship of serum
testosterone levels with serum leptin levels in boys (p = 0.0067) appeared
to explain this effect of age. In conclusion, the serum leptin
concentration is slightly lower in black boys. A higher testosterone level
in boys appears to account for an age-related decline in serum leptin in
boys and the overall lower levels in boys than in girls." (Horm Res.
1998;49(5):240-6)"
Competing interests:
None declared
Competing interests: No competing interests
This study does not seem to have been concerned with the effects of
other things in the study population's diets in early infancy. It is
unfortunate that the reader cannot determine the number of babies who were
exclusively breastfed nor the duration of such exclusive breastfeeding,
but it could be that these data were not recorded.
Breastmilk is not a magical substance imparting protection against
all ills for the rest of a person's life, requiring only the presence of
minute amounts to work its charms. Breastmilk alone, without supplements
or complements, appears to be the optimal food for humans for about the
first 6 months. Infant growth is a function of everything the infant
takes in, and the widespread use of artificial baby milks and early
introduction of semisolid foods in combination with breastfeeding would
make it hard to see distinct differences between 'breastfed' and 'not
breastfed' groups.
It remains to be seen whether there are differing rates of obesity in
later life, dependent on the duration of exclusive breastfeeding in the
first year. I would like to register a plea for researchers to
distinguish between the periods of exclusive, predominant, and symbolic
breastfeeding, as well as to specify the foods that replaced breastmilk in
the diet of the subjects, in all future studies about the effects of
breastfeeding on later health.
Competing interests:
None declared
Competing interests: No competing interests
Persons conducting cross sectional studies should
keep in mind that a cross sectional study of the
population of the state of Florida invariably shows that
everyone there is born Cuban and dies Jewish.
Competing interests:
None declared
Competing interests: No competing interests
Re: Obesity epidemic may be due to increasing testosterone
Testosterone also works the other side of this "coin." That is, the
appetite stimulant, ghrelin, is stimulated by testosterone. So,
testosterone reduces the appetite suppressant, leptin, and increases the
appetite stimulant, ghrelin. A strong combination to produce an "obesity
epidemic."
"Testosterone replacement therapy restores normal ghrelin in
hypogonadal men.
We recently described a connection between androgens and ghrelin in
women affected by the polycystic ovary syndrome. To further investigate
the interaction between sex steroids and ghrelin, we investigated
circulating ghrelin levels in a group of hypogonadal men before and after
therapeutic intervention aiming at normalization low testosterone (T)
concentrations. Seven hypogonadal men were compared with nine
overweight/moderately obese men matched for body mass index and body fat
distribution parameters, as well as with 10 normal weight controls. Total
and free T and plasma ghrelin levels were significantly lower in the
hypogonadal men than in the control groups. Hypogonadal men also had a
significantly higher insulin resistance state. Ghrelin levels were
positively correlated with both total and free T concentrations. A
significant correlation was also found between ghrelin and the
anthropometric parameters and the insulin resistance indexes. However, in
a multiple regression analysis in which a correction for all covariants
was performed, only the relationship with total and free T persisted.
After the 6-month replacement T therapy, ghrelin levels of hypogonadal
patients increased and did not differ significantly in comparison with
both control groups. The positive correlation between ghrelin and
androgens still persisted after T replacement therapy, after adjusting for
confounding variables. These data further indicate that sex hormones
modulate circulating ghrelin concentrations in humans. This may be
consistent with the concept that ghrelin may exert a relevant role in the
endocrine network connecting the control of the reproductive system with
the regulation of energy balance." ( Clin Endocrinol Metab. 2003
Sep;88(9):4139-43)
Competing interests:
None declared
Competing interests: No competing interests