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Year : 2012  |  Volume : 37  |  Issue : 2  |  Page : 133-134

Association of adiposity with pulse pressure amongst Gujarati Indian adolescents

Department of Dermatology, Western General Hospital, Edinburgh, United Kingdom

Date of Web Publication12-May-2012

Correspondence Address:
Sreedhar Krishna
Department of Dermatology, Western General Hospital, Edinburgh
United Kingdom
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-0218.96107

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How to cite this article:
Krishna S. Association of adiposity with pulse pressure amongst Gujarati Indian adolescents. Indian J Community Med 2012;37:133-4

How to cite this URL:
Krishna S. Association of adiposity with pulse pressure amongst Gujarati Indian adolescents. Indian J Community Med [serial online] 2012 [cited 2022 May 21];37:133-4. Available from: https://www.ijcm.org.in/text.asp?2012/37/2/133/96107


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. [1],[2] 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. [3],[4]

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. [6],[7] These studies, however, did not usually assess healthy children with a low risk of insulin resistance [8],[9] 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, [10],[11] and therefore, inaccuracies in predicting fat mass from BMI could explain the many inconsistent associations between arterial distensibility and BMI. [8],[10],[12]

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.

   References Top

1.Hamilton BS, Paglia D, Kwan AYM, Deitel M. Increased obese mRNA expression in omental fat cells from massively obese humans. Nat Med 1995;1:953-6.  Back to cited text no. 1
2.Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. Serum immunoreactiveleptin concentrations in normal-weight and obese humans. N Engl J Med 1996;334:292-5.  Back to cited text no. 2
3.Sierra-Honigmann MR, Nath AK, Murakami C, García-Cardeña G, Papapetropoulos A, Sessa WC, et al. Biological action of leptin as an angiogenic factor. Science 1998;281:1683-6.  Back to cited text no. 3
4.Bouloumie A, Drexler HC, Lafontan M, Busse R. Leptin, the product of the ob gene, promotes angiogenesis. Circ Res 1998;83:1059-66.  Back to cited text no. 4
5.Singhal A, Farooqi IS, Cole TJ, O'Rahilly S, Fewtrell M, Kattenhorn M, et al. Influence of leptin on arterial distensibility: A novel link between obesity and cardiovascular disease? Circulation 2002;106:1919-24.  Back to cited text no. 5
6.van Popele NM, Westendorp IC, Bots ML, Reneman RS, Hoeks AP, Hofman A, et al. Variables of the insulin resistance syndrome are associated with reduced arterial distensibility in healthy non-diabetic middle-aged women. Diabetologia 2000;43:665-72.  Back to cited text no. 6
7.Giltay EJ, Lambert J, Elbers JM, Gooren LJ, Asscheman H, Stehouwer CD. Arterial compliance and distensibility are modulated by body composition in both men and women but by insulin sensitivity only in women. Diabetologia 1999;42:214-21.  Back to cited text no. 7
8.Toto-Moukouo JJ, Achimastos A, Asmar RG, Hugues CJ, Safar ME. Pulse wave velocity in patients with obesity and hypertension. Am Heart J 1986;112:136-40.  Back to cited text no. 8
9.Balkestein EJ, van Aggel-Leijssen DP, van Baak MA, Struijker-Boudier HA, van Bortel LM. The effect of weight loss with or without exercise training on large artery compliance in healthy obese men. J Hypertens 1999;17:1831-5.  Back to cited text no. 9
10.van Popele NM, Westendorp IC, Bots ML, Reneman RS, Hoeks AP, Hofman A, et al. Variables of the insulin resistance syndrome are associated with reduced arterial distensibility in healthy non-diabetic middle-aged women. Diabetologia 2000;43:665-72.  Back to cited text no. 10
11.Wells JC. A Hattori chart analysis of body mass index in infancy and childhood. Int J Obes Relat Metab Disord 2000;24:325-9.  Back to cited text no. 11
12.Yamashita T, Sasahara T, Pomeroy SE, Collier G, Nestel PJ. Arterial compliance, blood pressure, plasma leptin, and plasma lipids in women are improved with weight reduction equally with a meat-based diet and a plant-based diet. Metabolism 1998;47:1308-14.  Back to cited text no. 12
13.Kawecka-Jaszcz K, Czarnecka D, Olszanecka A, Rajzer M, Jankowski P. The effect of hormone replacement therapy on arterial blood pressure and vascular compliance in postmenopausal women with arterial hypertension. J Hum Hypertens 2002;16:509-16.  Back to cited text no. 13
14.Karim R, Hodis HN, Stanczyk FZ, Lobo RA, Mack WJ. Relationship between serum levels of sex hormones and progression of subclinical atherosclerosis in postmenopausal women. J Clin Endocrinol Metab 2008;93:131-8.  Back to cited text no. 14
15.Kallikazaros I, Tsioufis C, Zambaras P, Stefanadis C, Toutouzas P. Conjugated estrogen administration improves common carotid artery elastic properties in normotensive postmenopausal women. Clin Cardiol 2002;25:167-72.  Back to cited text no. 15
16.Ahimastos AA, Formosa M, Dart AM, Kingwell BA. Gender differences in large artery stiffness pre- and post-puberty. J Clin Endocrinol Metab 2003;88:5375-80.  Back to cited text no. 16


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