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Correspondence
133 (
5
); 557-559
pmid:
21623047

Need for better anthropometric markers for prediction of cardiovascular risk in nutritionally stunted populations

Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695 011, India
Child Development Centre, Medical College, Thiruvananthapuram 695 011, India
Department of Pediatric Cardiology, Sree Avittom Thirunal Hospitals, Medical College, Thiruvananthapuram 695 011, India

*For correspondence: sivasct@hotmail.com

Licence

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Disclaimer:
This article was originally published by Medknow Publications and was migrated to Scientific Scholar after the change of Publisher.

Sir,

The article by Thakappan and colleagues in the January 2010 issue of the Journal, defines the enormous threat of non communicable diseases which the State of Kerala faces1. The results are aptly projected as the harbinger of what is going to happen in India and rest of the developing world. The study is all the more important for its finding that the anthropometric measures like body mass index (BMI) and waist circumference (WC) were only modest in predicting biochemical risk factors in this population. In this context, we would like to highlight the contribution of developmental origin of adult onset diseases and to project calf anthropometry as a marker to define the early life growth perturbation in this nutritionally stunted population. Though genetics and ethnic factors play role in the development of conventional risk factors, current literature is reassuring that lifestyle interventions can postpone the onset of adult onset diseases as a public health initiative2.

The National Family Health Survey (NFHS) -3 data on malnutrition and stunting in Kerala done in 1992 and 2005-2006 show (Table) a significant nutritional stunting irrespective of the improvement in per-capita calorie intake (up to 400 Kcals/day)34. Obesity in adults in the NFHS-3 and the reported study is also around 30 per cent, reflecting the double burden of nutritional diseases13.

Table Selected parameters of nutritional status in NFHS13

In the absence of childhood health records and basic birth weights, the markers of nutritional stunting in adult life could reflect the developmental origin of adult onset diseases in them5. Persistence of nutritional stunting in children is unlikely to be due to failure of the supplementary programmes to reach the deserving, given the social equity and health awareness in Kerala6. The alternate possibility is that the nutritionally stunted children are failing to respond to the nutritional supplementation with adequate catch up growth or a newer pool of low birth weight babies are being born7. It is very likely that this trend will persist for at least for a few more generations because of the vicious cycle of childhood undernutrition and maternal health status8. Child development centre at Thiruvananthapuram, Kerala, has been following a cohort of low birth weight children, and normal weight children for 16 years9. At the age of 16, 15 per cent had BMI of more than 22 and low density lipoprotein cholesterol level of more than 130 mg/dl. More than 55 per cent had high density lipoprotein cholesterol levels less than 45 mg/dl concurring with the younger age onset of risk factors as noted in this study1. The lower birth weight predicted higher triglyceride levels, though their adolescent BMI levels were lower.

BMI and waist circumference are the anthropometric measures utilized as per the WHO non-communicable disease surveillance and both the parameters were just modest in predicting the step 3 risk factors in this study1. Large population survey done in Kerala has observed better body mass indices not to be associated with adult onset disease mortality10. Eighteen year follow up of the Monica cohort which adopted a variety of lifestyle modification also showed that increase in BMI was not associated with increasing diabetes or cardiovascular diseases11. For a similar change in body composition, nutritionally stunted population will have a higher BMI, given the lower values in denominator. But it is well known that Asians develop the risk factors at a lower BMI12. This is a clear indication that metabolic abnormalities are developing in Keralites at normal weight, which is referred to as the “metabolically obese normal weight individuals”13. Sarcopenic adiposity, i.e., less muscle and more fat, is the common denominator for both nutritionally stunted adults, and thin fat Indian babies and is characterized by abnormal distribution of upper body and visceral fat14. For recognizing the visceral obesity in adults, waist circumference was used as a surrogate15. In study by Thankappan et al1 the predictive utility of the waist circumference to the biochemical risk factors was modest, suggesting that by the time the adult cut-off values are reached the risk factors are already established. Similarly the recent registry for acute coronary syndrome created in Kerala registered 25,000 patients and 2/3rd had a waist circumference less than 90 cm, the cut-off value currently recommended for males of Asian origin (personal communication, Dr PP Mohanan for the Kerala ACS registry).Waist circumference may fare better if lower cut-off values or indexing to height is attempted16. The alternative surrogate is the fat free muscle mass for which calf muscle circumference or urinary creatinine can be used as surrogate markers17. Calf circumference has shown good correlation with carotid intima media thickness in adult life18. Fat free muscle mass measured by calf circumference and skin fold thickness at maximal calf circumference could be a good anthropometric marker to understand sarcopenia in adults. The subcutaneous fat at the calf also is a negative predictor of adult onset diseases, and by measuring the same we may be able to define the calf muscle mass better1819.

Waist circumference is low cost non laboratory marker for cardiovascular risk reduction15. As a self measured marker it's now a popular public health strategy in Japan15. Unlike body mass index, measures of abdominal obesity takes the risk factor assessment to early life experiences14. But by the time the recommended cut-off value is reached, the risk factors are well established in this traditionally stunted population. The other alternative marker of growth perturbation in early life is adult height which is a good indicator of cardiovascular and body weight scaling5. It will be interesting to see the data analyzed with height alone as a variable in these multivariate models. But studies done at Framingham have failed to demonstrate the utility of adult height alone as a risk predictor, given the time trends in increasing height of the population and the age related decline in vertebral height20. During the last three decades Kerala children also have shown a trend in increasing height21.

Cohort studies done in the developed world and a few studies in the developing world have recognized short leg as a useful marker of early life growth perturbation, with adult onset cardiovascular diseases and risk factors2223. Growth of the human newborn, proceeds in the cephalocaudal direction, in early infancy24. Both calf length and calf circumference are simple measurements which can be done in early adult life. If substantiated in epidemiologic studies, calf anthropometry, could turn out to be the non laboratory marker for adult cardiovascular risk reduction in populations suffering nutritional stunting. The calf measures could be the indirect markers of the contribution of early life growth perturbations to adult onset diseases in adult life. Essentially calf anthropometry defines the best possible growth for the most affected segment in growth perturbation and can be ascertained in early adulthood.

Dr S. Sivasankaran (corresponding author) was supported by a Fogarty NIH D 43 grant to develop the concepts discussed in this letter (Grant No: 1D43HD065249-01).

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