etabolic syndrome, often used synonymously with
Syndrome X or Insulin resistance syndrome, is a constellation of risk
factors that predisposes to an enhanced risk of Type 2 diabetes and
cardiovascular disease [1]. The clustering of atleast three of five risk
factors – elevated blood pressure, elevated fasting plasma glucose, high
triglycerides, low HDL-cholesterol and increased waist circumference –
have been variously described to constitute the metabolic syndrome. The
International Diabetes Federation [2], revised National Cholesterol
Education Program (NCEP-ATP III) [3] and WHO [4] have different
diagnostic criteria, and this necessitated guidelines for a harmonized
definition, accounting for ethnic differences in adiposity and metabolic
risk [5].
The pathways to developing metabolic syndrome have
been researched over the last few decades in different populations
[6–9]. The role of size at birth and later disease proposed by Prof.
David Barker stimulated research that has now established this link for
a number of adult diseases and risk factors, including those that
constitute the metabolic syndrome [10]. However, increasingly, birth
weight was seen as a proxy measure, as the earlier intrauterine growth
trajectory and the factors that influence this were seen as important
factors too. Maternal pre-pregnancy nutrition and nutrition during
pregnancy can cause significant changes in fetal structure, growth and
metabolism that set the stage for future disease risk. Classical studies
like the Dutch Hunger Winter have established the role of even the time
during gestation when maternal nutrition has differing and lasting
impacts on later life disease in their offspring [11]. Again, other
studies have focused on gestational diabetes mellitus and greater
maternal pre-pregnancy body mass index (BMI), both alone or in
combination interacting to result in fetal macrosomia [12]. More recent
studies both in animals and humans show that maternal nutritional status
affects pancreatic beta-cell size and function which causes early
changes that predispose to altered glucose and fat metabolism in the
next generation [13].
Subsequent years saw the progress from use of birth
size measurements to postnatal size and growth patterns during infancy
and childhood as implicating factors in predisposition to adult
cardiometabolic disease. Studies from both developed and developing
countries established that a small size at birth, lower infant
anthropometric measurements and consequent accelerated growth patterns
in childhood, were in combination most predictive of a poor
cardiometabolic risk profile in adulthood. In particular, studies that
had serial measurements of length/height, weight and BMI from birth,
through childhood, adolescence and adulthood were able to clearly
exemplify that lower birth size, thinner infants, early age of peaking
BMI and adiposity rebound (earliest age at which the BMI starts to climb
in childhood) were important predictors of adult disease risk [14].
Those in the lowest category of size at birth and highest category of
childhood BMI were more likely to be overweight/obese, have increased
adiposity measures (whether measured by traditional methods of waist
circumference or skinfold measurements or sophisticated methods of fat
measurement using DEXA scans and MRI), impaired glucose tolerance,
higher blood pressure and abnormal lipid measurements.
The study by Chaudhari, et al. [15], published
in this issue of Indian Pediatrics, has prospectively followed
low birth weight (LBW) infants to young adulthood and assessed their
cardiometabolic risk profile at 22 years in comparison with children of
normal birth weight. They used the IDF criteria to establish that the
LBW group had greater prevalence of two risk factors as compared to
normal weight infants, with hypertension being the first risk factor to
appear. There was not enough evidence pointing to the presence of a
minimum of three risk factors to define greater metabolic syndrome
amongst the low birth weight group. However, the findings corroborate
earlier evidence that being born small and gaining rapidly in weight to
fall in the higher weight categories in adulthood portends serious
adverse disease risk, including the components of the metabolic
syndrome.
What emerges from the above discussion is a clear
need to move from only a developmental origins perspective to a
life-course perspective in tackling the rising epidemic of "metabisity."
Early life origins school of researchers had emphasized the importance
of focusing on the prenatal and maternal pregnancy nutrition and
socio-demographic factors to ensure delivery of healthy newborns. This
stimulated policy changes and programs in different settings that
included nutritional supplementation of the girl child and pregnant
women to ensure that the health of future generations was protected.
India’s own flagship program of Integrated Child Development Services
(ICDS) rolled out in the late 80’s was a step in the right direction
given the poor maternal nutrition and consequent infant morbidity and
mortality statistics. Back then, it was crucial to arrest the vicious
cycle of mothers with adverse nutritional environments giving birth to
babies of lower birth weight, in turn vulnerable to a host of early
childhood infections and higher childhood morbidity. However the
epidemiological transition, coupled with a significant nutritional and
environmental transition in recent decades, has led to the rapid
emergence of lifestyle disorders including hypertension, diabetes,
overweight and obesity with a significant proportion of younger
individuals displaying a tendency to develop one or more risk factors.
This calls for using a different lens to look at the programs and
interventions that will encourage, enable and sensitize individuals to
adopt a healthy lifestyle across their lifespan. This necessarily means
presenting to policy makers the substantial evidence that we now have to
push for effective and impactful programs that will help arrest the
growing epidemic of metabolic risk and lifestyle-related disorders in
India.
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Lenfant C. Definition of metabolic syndrome: report of the National
Heart, Lung, and Blood Institute/American Heart Association conference
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2. Alberti KGM, Zimmet P, Shaw J, IDF Epidemiology
Task Force Consensus Group. The metabolic syndrome—a new worldwide
definition. Lancet. 2005;366:1059-62.
3. Third Report of the National Cholesterol Education
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