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Weight Cardiovascular Heart
In 1989, Dr. David Barker and his colleagues, working in University of Southampton, suggested that lower weight of an infant at birth and during infancy had a direct correlation with a higher risk of cardiovascular disease later in life. Later studies conformed to the idea that poor nutritional conditions of the mother resulted in low birth weight, which was associated with subsequent development of coronary heart disease, hypertension and diabetes type II. He compiled his findings and postulated ‘Barker’s Hypothesis’, now renamed as ‘Fetal Origins Hypothesis’.
‘Fetal Origins Hypothesis proposes that coronary heart disease originates through responses to under nutrition during fetal life and infancy, which permanently changes the body’s structure, physiology, and metabolism.’(1)
It was suggested that low birth weight, at full term, indicated malnourishment. Therefore, it was implied that the fetus made physiological adjustments to prepare itself for life. Consequently, changes in the fetus’ physiology and metabolism, made it more prone to chronic diseases in adulthood. Further, it shed light on the dramatic consequences of increases in weight after the age of two years. It proposed that the risk of developing coronary heart disease and diabetes type II rapidly increases due to weight gain after the age of two years.(1)
The prenatal period is divided into an embryonic period and a fetal period. After conception, the embryonic period lasts for 8 weeks. During this period, all the body organs are formed and the embryo forms a distinctly human appearance. Further, morphogenesis starts after the third week of development. The end of the embryonic period marks the beginning of the fetal period. Anatomically, the fetal period manifests by the vascular penetration of the humerus. The fetus is not as prone to damage as the embryo was to environmental exposures during the embryonic period. This phase is marked by growth and development of major structures already formed in the fetus.
Genes play a vital role in the development of necessary organs of the body. Environmental influences can disrupt the functioning of ‘imprinted genes’ resulting in inhibited growth, thus affecting the birth weight. Consequently, there is a higher risk of chronic diseases developing in later life. These imprinted genes are prone to alterations as they are functionally haploid and have different controlling mechanisms than the rest of the genome. (2)
Malnourishment can disrupt the fetus’ cell cycles and slow down their cellular division. Therefore, the fetus physiologically adapts by favoring development of vital organs, such as the brain, over the growth of non essential organs such as kidney (nephron mass) and the pancreas (beta cell mass).Consequently, these developmental adaptations, in response to deficient maternal-placental nutrient supply, may be the root of future chronic diseases later in life.(3)
Birth Mass and Diabetes Mellitus
A number of studies have showed the correlation with low birth weight and insulin resistance. Preston studies show the direct relationship between low birth weight and insulin resistance, measured using the ponderal index. (4) Table 1 shows the relationship between reduced birth weight and diabetes type II. (5)
Maternal malnourishment results in a decrease in insulin production and increase in peripheral insulin resistance. Subsequently, more glucose is diverted towards the brain and heart and less towards tissues, such as skeletal muscle, which are more insulin dependant.(6)Therefore, muscles become resistant to insulin. Consequently, later in life, when adequate nutrients are available, peripheral insulin resistance can cause glucose intolerance and diabetes. (6) The Preston studies conform to the idea that undernourished babies have muscles which become resistant to insulin. (4)
On average, there are one million nephrons in a normal kidney. (7) However, maternal under nutrition can change the progamme of development. According to Widdowson and Mccance, malnourishment can result in decreased number of cells. (4) Further, studies show that low birth weight result in a decreased number of nephrons and associated increase in glomerular volume. (7)
Fetal growth restriction has adverse effects on kidney development. According to Brenner and Mackenzie, such restrictions result in decrease in number of nephrons. In addition to that they proposed that there is an associated increase in glomerular filtration rate and hydrostatic pressure. Consequently, there is an increase in the risk of developing glomerular sclerosis.(8) In order to maintain adequate kidney function, the reduced number of glomeruli undergo hypertrophy and hyperfiltration. Subsequently, intraglomerular hypertension is compromised, further damaging the kidney and increasing nephron loss. (7) Moreover, Keijzer-Veen and colleagues recognized an inverse relationship between birth weight and serum creatinine implying that low birth weight was associated with a higher risk of developing progressive renal failure. (8) Diagram 1 shows a summary of events leading to kidney failure. (7)
Link between Birth Weight and Hypertension
Kidney is a vital organ in controlling blood pressure. The association of intrauterine events with kidney development imply there effect on development of hypertension. Initially described by Guyton, the kidney’s role in the rennin-angiostatin-aldosterone system and its homeostatic functions are well accepted.(7) In addition to that, number of studies have showed a direct association of low birth weight and development of hypertension in adult life. The link between birth weight and hypertension was first demonstrated by Barker and Osmond in a cohort of 46 to 64 year olds. (7) According to the Helsinki studies, there was inverse correlation between birth weight and blood pressure.
Brenner and Chertow postulated that decreasednephron number associated with retarted fetal growth could increaserisk of hypertension and chronic renal disease/failure. (9)They also hypothesized about a concept known as ‘nephron dosing.’ They suggested that reduced number of nephrons for a constant body mass resulted in an imbalance between the load to be excreted and capacity of the nephron. As a result, the infant is prone to hypertension later in life. Further, experimental work has shown how decreased numbers of nephrons activate renin-angiotensin system to maintain glomerular filtration rate. Therefore, sodium and water retention increases resulting in increase in blood pressure. (9) In addition to that, lack of stretchiness in vessel walls and excess glucocorticoids, which induce expression of angiotensin related molecules, make the infant more prone to hypertension later in life.(4,8) Diagram 2 summarizes the effect of reduced number of nephrons. (9)
Birth Mass and Cardiovascular Disease
Diabetes type II, kidney disease and hypertension are potential causal agents of cardiovascular disease. As illustrated above, the relationship between low birth weight and the diseases mentioned, there is an indirect link to cardiovascular disease. Furthermore, a small number of studies have shown the inverse association between mass at birth with cardiovascular disease in later life. (10) Scarcities of food supply to mothers results in the fetal programme to adapt to a situation where undernourishment is the norm. However, when these individuals turn obese in later years, they have an increased risk of cardiovascular disease.
Prevalence of cardiovascular disease (CVD) risk factorclustering (percentage of individuals with at least 3 of systolic blood pressure, glucose and triglycerides in the highest sex-specific tertile,and HDL cholesterol in the lowest tertile) within joint tertiles of birthweight and adult body mass index (BMI) among men and women born during the Institute of Nutrition of Central America and Panama (INCAP) supplementation study in one of 4 study villages in Guatemala; 1969–1976, and examined in 1997–1999.
All hypotheses need thorough measures of refutation. A number of criticisms have been raised with regard to the Fetal Origins Hypothesis. It has been suggested that coronary heart disease in later life is associated with one or more confounding factors including parental features, such as low socioeconomic status, genetic and environmental factors resulting in coronary heart disease. Hübinette and colleagues concluded from their research that low birth mass and development of coronary heart disease later in life is resultant from the combination of genetic factors and unmeasured maternal influences that function independently of birth weight. (12)
Moreover, studies conducted in Southampton have certain inconsistencies. In those studies, measures of actual nutrition were not recorded. ‘Early nutrition isinferred indirectly from fetal and infant growth, and fetalgrowth especially is a doubtful surrogate measure. Thus evenif we take the findings as valid we still must ask whether nutritionor some other effect is being measured.’(13) In short, maternal nutrition is not equivalent to fetal nutrition. Additionally according to Kramer & Joseph (1996), there is significant selection bias in the retrospective studies conducted. (14)
Furthermore, most of the studies done till now take into account two points in time to measure the weight- one at birth and one later in life. Without another transitional measuring point, it is hard to differentiate whether cardiovascular diseases are linked to fetal and postnatal exposures or are merely elements of postnatal growth. (15)
Recent systematic overviews show strong inverse associations between birth weight and cardiovascular disease, diabetes type II, hypertension and kidney disease. (15) Taking into account its criticisms, it would be safe to conclude that retarded fetal growth is linked with increase in risk of developing the above mentioned diseases in later life. Barker’s hypothesis has created awareness on a large scale level defining the importance of maternal nourishment and its effects on causing subsequent disease in future. In addition to that, explanations regarding genetic and environmental influences, and confounding factors such as socioeconomic status cannot be excluded with regard to their effect on the development of chronic disease later life. On the whole, the fetal origins hypothesis has been a discovery and a very important one leading to a whole new explanation of the development of chronic diseases in adult life.
In short, fetal development is dramatically influenced by environmental factors including chemical, physical and biological factors. Consequently, fetal programming results in physiological adaptations affecting fetal growth and birth weight. Moreover, compensatory effects result in disturbances in normal growth of crucial organs. As a result birth weight is reduced. Furthermore, post natal increase in weight as an attempt to rectify the low birth weight is harmful to the child in the later years as it further increases the risk of cardiovascular disease. Lastly, these influences can be passed on from generation to generation. (16)
(1) The Science - The Barker Theory. Available at: http://thebarkertheory.org/science.html. Accessed 3/22/2008, 2008.
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(10) Lawlor DA, Ronalds G, Clark H, Smith GD, Leon DA. Birth weight is inversely associated with incident coronary heart disease and stroke among individuals born in the 1950s: findings from the Aberdeen Children of the 1950s prospective cohort study. Circulation 2005 Sep 6;112(10):1414-1418.
(11) Stein AD, Conlisk A, Torun B, Schroeder DG, Grajeda R, Martorell R. Cardiovascular disease risk factors are related to adult adiposity but not birth weight in young guatemalan adults. J.Nutr. 2002 Aug;132(8):2208-2214.
(12) Poulter NR. Birthweights, maternal cardiovascular events, and Barker hypothesis. The Lancet, 2001 6/23;357(9273):1990-1991.
(13) Paneth N, Susser M. Early origin of coronary heart disease (the "Barker hypothesis"). BMJ 1995 Feb 18;310(6977):411-412.
(14) Langley-Evans SC. Fetal programming of cardiovascular function through exposure to maternal undernutrition. Proc.Nutr.Soc. 2001 Nov;60(4):505-513.
(15) Gillman MW. Epidemiological challenges in studying the fetal origins of adult chronic disease. Int.J.Epidemiol. 2002 Apr;31(2):294-299.
(16) Sobsey D. Fetal Programming: Implications for Development and Developmental Disability. Available at: http://22.214.171.124/search?q=cache:2dpttiNsV2YJ:www.ualberta.ca/~jpdasddc/ARTICLES/2000(2)/pp71-75SobseyFetal.pdf+Fetal+Programming:+Implications+for+Development+and+Developmental+Disability&hl=en&ct=clnk&cd=1&gl=uk. Accessed 4/14/2008, 2008.