Association of adiposity with pulse pressure amongst gujarati Indian adolescents.

Sir,

I read Dr. Shaikh's paper, “Association of Adiposity with Pulse Pressure Amongst Gujarati Indian Adolescents,” with interest. Dr. Shaikh and colleagues must be applauded for investigating such a worthy concept; one which does not receive the same glitz as other research fields.

I do suggest a few concepts, however. While the study shows a correlation between adiposity and vascular distensibility in boys, I suggest that it may be informative to establish why this relationship occurs.

The hormone leptin is produced by adipocytes and plays a key role in both the regulation of appetite and body weight.(12) It is well-established that leptin concentrations show exponential increases with rising percentage body fat; obese individuals also have markedly increased leptin concentrations, perhaps as a result of resistance to its actions. Interestingly, leptin receptors are widespread on vascular cells, suggesting that leptin also plays a role in vascular physiology.(34)

Colleagues at University College London have investigated the link between leptin and arterial distensibility. They have shown that there was a strong inverse association between arterial distension and leptin concentration (regression coefficient, 1.3% change in arterial distension per 10% increase in leptin concentration; 95% CI, 1.9%–0.8%; P< 0.001), and this was independent of potential confounding factors (including gender).(5)

The association of arterial distensibility with leptin was independent of fat mass and metabolic and inflammatory markers. Although earlier studies have shown a relation between body fatness and C-reactive protein concentration or insulin resistance, the influence of leptin on arterial distensibility was not dependent on these variables. Insulin resistance has been suggested to explain the link between arterial distensibility and obesity.(67) These studies, however, did not usually assess healthy children with a low risk of insulin resistance(89) and often used body mass index (BMI) as a relatively inaccurate proxy for adiposity.

As a word of advice, I would suggest that future researchers omit BMI as a measure of establishing obesity. BMI is a measure of both lean and fat mass,(1011) and therefore, inaccuracies in predicting fat mass from BMI could explain the many inconsistent associations between arterial distensibility and BMI.(81012)

Shaikh presciently suggests that estrogen plays a protective role in protecting the vasculature from atherosclerosis, thereby explaining the differences found in his study. I agree with this finding. Investigators have hypothesized that gender differences in vascular function are entirely due to differences in sex hormones. This hypothesis is supported by the demonstration of BP-independent improvement in pulse wave velocity with estrogen replacement therapy in a postmenopausal cohort,(13) the correlation between changes in serum estrogen compounds and progression of carotid atherosclerosis,(14) and improvement in carotid stiffness with administration of estrogen.(15) In addition, data in children support the estrogen hypothesis in that gender differences in large artery stiffness occurred only after puberty was complete.(16)

In summary, I thoroughly enjoyed reading Dr. Shaikh's work and would encourage other Indians to pursue such important research questions.