The Problems of Chronic Disease in Old Age Start in Infancy
Introduction
The rapid increase in the number and types of chronic diseases is now an issue of public concern for the global health care system. Nearly 79% of deaths as a result of chronic diseases are being reported in developing countries, with middle-aged men being the main culprits (World Health Organization, 2002). At the same time, a growing body of evidence from the available literature on nutrition indicate that the risk factors associated with chronic diseases start as early as the foetal stage of human life, and then continue through childhood, adulthood, and into old age (Barker et al., 2001). Indeed, old age is a period when one is most vulnerable to developing one or more chronic diseases, including cardiovascular heart disease (CHD), stroke, diabetes, and high blood pressure. While both an individual’s lifestyle and genetics play a major role in the causation of such chronic diseases, there is now compelling evidence to show that the problems of chronic disease in old age start in infancy. Therefore, chronic diseases evident in adulthood, is evidence of a cumulative lifetime exposure of an individual to social and physical environments that can be traced as far back as the infancy period.
Foetal development process and maternal environment
Four relevant aspects of foetal life have identified. These are: IUGR (intra-uterine growth retardation), prematurely-delivered foetus, utero-overnutrition, and intergenerational factors. Considerable evidence from literature on foetal development, mainly from developed nations, indicate an association between IUGR and increased risk of developing strike, heart diseases, high blood pressure, and diabetes (World Health Organization, 2002; Aboderin et al., 2002; Godfrey & Barker, 2000; Forsen et al., 2000; Ericksson et al., 1999; Forsen et al., 1999; Rich-Edwards et al., 1999; Leon et al., 1998; McKeigue, 1997; Lithel et al., 1996; Martyn et al., 1996); Martyn et al., 1994). In this case, the underlying disease pathways has been linked to restricted foetal growth and the subsequent rapid catch-up growth often experienced at the postnatal stage of infant development.
However, other studies have pointed at macrosomia (a phenomenon in which infants are large-sized at birth) as being linked to an increased risk for the development of cardiovascular disease and diabetes (Leon et al., 1998; McCance et al., 1994). For example, a study conducted in India among the adult population revealed an association between fatness (as signified by high ponderal index) at birth, and impaired glucose tolerance (Fall et al., 1998). On the other hand, a similar study administered among Mexican Americans failed to reveal such a relationship (Valdez et al., 1994). Elsewhere, a relationship between a higher weight at birth and increased risk of developing breast cancer, among other forms of cancers, has also been reported (Kuh & Ben-Shlomo, 1992).
Stunted growth
During infancy, stunted growth is best exemplified by the the inability of an infant to gain the desired height and weight, compared to other infants of his age. In this case, stunted growth and excessive height or weight gain have been recognised as formidable factors for the development of chronic diseases later in life. Towards this end, retarded growth during early infancy (that is, an infant whose weight is comparatively low at 1 year of age), has been identified as a potential risk factor for the development of CHD (coronary heart diseases), regardless of the size of the infant at birth (Barker et al., 1989; Ericksson et al., 2001). It is important to note that infants with the highest weight gain during infancy, as well as those characterised by stunted growth, have been found to be at a higher risk of developing high blood pressure (Walker et al., 2001).
Stunted growth is often used as an indicator of a childhood characterised by socio-economic deprivation (Gunnell et al., 1998). In addition, it is also linked to an elevated risk for stroke and CHD, and to a certain extent, diabetes (Aboderin et al., 2002; Rich-Edwards et al., 1999). At the same time, where shorter children demonstrate rapid growth in height, this has been associated with an increased cancer mortality (including uterus, colon, and breast cancer), as well as the risk of stroke (Walker et al., 1998).
Considerable evidence from existing literature on infant nutrition points at a strong link between IUGR and an elevated risk for the development of CHD (coronary heart disease), diabetes, and stroke (Barket et al., 2000; Barker et al., 2001). Most of these studies have been conducted in the developed countries. Available evidence from retrospective studies or historical cohorts reveal clear link between the risk of developing diabetes (Kuh & Ben-Shlomo, 1992), CHD (Valdez et al., 1994), and stroke (McCance et al., 1994), and retarded foetal growth (signified by small sized infant at birth).
Famine Studies
Additional evidence of a link between the development of chronic diseases later in life and IUGR during infancy has been revealed by ‘famine studies’ conducted on various populations, such as the Dutch famine that occurred between 1944 and 1945 (McCarronPet et al., 20000), as well as the Russian famine of between 1941 and 1944 that was a culmination of the Leningrad siege (Wannamethee et al., 1998) during the Second World War. The Dutch study showed an association between an elevated risk for developing heart disease and exposure to famine in the early stages of gestation. On the other hand, no such effect was revealed by the Russian study. In the case of the developing countries, so far, we have only had a few studies conducted on this relationship, such as the one that took place in India (Marmot et al., 1997) In one of the studies, a link was found between CHD and low birth weight (Ericksson et al., 2000) while in the other, subsequent diabetes was linked to obesity (as evidenced by higher ponderal index), as opposed to low birth weight (Must & Lipman, 1999).
Low birth weight
The association between blood pressure and low birth weight has also been found in cohort studies conducted in both the developing and the developed countries, including China, India, the UK, Chile, Jamaica, Zimbabwe, DR Congo, South Africa, and Guatemala (Barker et al., 2000). Only a limited number of studies have failed to find this association. A study conducted in Hong Kong showed an association between higher blood pressure and greater length at birth (Singhal, Cole & Lucas, 2001). Indeed, the link between childhood blood pressure and low birth weight could be determined by the type of growth impairment or retardation experienced in utero. There seems to be good, albeit non conclusive, evidence of a relationships between elevated risk for developing metabolic syndrome in middle life on the one hand, and reduced foetal growth, on the other hand (Wilson et al., 1998).
However, the link between impaired glucose tolerance (IGT) and foetal growth still remains unclear (Barker et al., 2000), with different studies reporting conflicting results. For example, the Dutch famine study revealed a strong link between a broader lipid profile and famine exposure in utero (Ravelli et al., 2000). However, neither the Russian nor the Dutch studies revealed any significant link between adverse TG or HDL levels and exposure to famine in utero (Wannamethee et al., 1998).
There is strong and consistent association in historical cohort studies between IGT in adulthood and IUGR, and small size at birth in India, South Africa, as well as China (Barker et al., 2000). Also, retarded foetal growth is linked to high systolic blood pressure as demonstrated in adulthood (Roberts, 2001). However, there is no indication as to whether this relationships acts as a mediator of the relationship between cardio vascular disease (CVD) and IUGR (Barker et al., 2001). This apparent association has been the point of focus of a recent meta-analysis, which has cited methodological problems as the possible cause (Davis, 2001).
Also, the meta-analysis has also summed up that birth weight plays a very minor role in determining an individual’s blood pressure levels later in life. On the other hand, the association has been supported by evidence from both developing and developed countries, such as South Africa (Barker et al., 2001), and China (Gillman et al., 2001). Moreover, an interacting impact between gained weight or obesity and the increased risk of diabetes or CHD has been linked to impaired foetal; growth, as well as a possible impact on blood pressure. The Swedish study indicated enhanced blood pressure in low birth weight infants, that appears to rise with an increase in their BMI (body mass index) as adults.
Breastfeeding
A growing body of evidence shows as association between breastfeeding among pre-term and term infants and significantly reduced levels of blood pressure in childhood (Wilson et al., 1998). In addition, infants who consume formula as opposed to breast milk have also been shown to be at an increased risk of mean and diastolic arterial blood pressure as adults. On the other hand, such an association has not been reported by cohort studies conducted among adults (Fall et al., 1998) as well as the Dutch study of famine (Ravelli et al., 2000). Moreover, strong evidence suggest that exclusive breastfeeding is linked to reduced risk of developing obesity (Gillman et al., 2001). While this association depends on the duration of breastfeeding, it only becomes apparent in late childhood (Roberts, 2001). Maternal education and socio-economic factors can best explain a number of the discrepancies that often accompany such findings.
Data obtained from majority of the observational studies on term infants suggest that formula consumption by infants could lead to adverse effects on risk factor for the development of high blood pressure and cardiovascular diseases. However, controlled clinical trials that have thus far been conducted on this issue have offered limited information in support of such findings (Roberts, 2001). On the other hand, the weight of current evidence point to the fact that formula milk has some adverse effects on the risk factor for developing cardiovascular diseases as evidenced by the high mortality among older adults who as infants, were formula-fed, in comparison to those who were exclusively breastfed (Roberts, 2001). Besides, short-term breastfeeding and the use of breast-milk substitutes have also been linked to an increased risk for the development of a number of chronic diseases in childhood and adolescence, including coelic diseases, type 1 diabetes, inflammatory bowel diseases, and several forms of childhood cancers.
High-cholesterol feeding of infants
The potential impact of high-cholesterol feeding of infants in early life has attracted a lot of interest among researchers. When infants are introduced to high cholesterol feeding early in their lives, this could help to control their lipoprotein and cholesterol metabolism later in life. There is limited animal data that seems to support this theory, although the hypothesis by Reiser et al (1979) has triggered the conduction of a number of prospective and retrospective studies whereby the researchers compared lipoprotein and cholesterol metabolism in infants fed on formula compared to those who were fed breast milk.
Research findings of studies conducted in suckling rats indicate that the introduction of cholesterol in an infant’s early diet could aid in identifying a metabolic pattern for plasma cholesterol and lipoproteins that could prove advantageous in later life. On the other hand, the study carried out by Mott, Lewis and McGill (1991) involving differential diets in infant baboons, failed to reveal any such benefits later in life. However, this research motivated other scientists to conduct observatory studies involving modified responses of bile cholesterol saturation indices, rate of bile production among adults, and bile acid turnover, based on whether the baboons had been fed formula or breast milk. These observations revealed that elevated dietary cholesterol in the infant baboon’s early life was associated with elevated levels of total plasma in cholesterol, as evidenced by increased atherosclerosis lesions. It is important however to mention that so far, no long-term data on human mortality and morbidity has been reported regarding this idea.
Conclusion
The infancy period and maternal environment are important parameters as they play a huge role in enhancing the risk factors for developing chronic diseases such as various forms of cancers, CHD, high blood pressure, stroke, and diabetes, among other chronic diseases, in old age. This is based on various forms of evidence revealed by different famine studies, meta-analyses and retrospective studies carried out in both the developing and developed countries that have revealed a strong association between an increase in the risk factors for the development of the aforementioned chronic diseases and certain conditions prevailing during infancy. For example, restarted growth, elevated cholesterol feeding, breastfeeding, milk formulas, excessive height or weight, and low birth weight are some of the parameters that have been linked to an increased risk for development of chronic diseases in old age. Based on these findings, it appears that good maternal practices by pregnant mothers such as access to a balanced diet and exclusive breastfeeding of the infant can go a long way in reducing the probability of the child getting afflicted by one or more of the chronic diseases later in life.
Reference List
Aboderin, I et al. (2002). Life course perspectives on coronary heart disease, stroke and
diabetes: the evidence and implications for policy and research. Geneva: World Health
Organization.
Barker D.J.P. et al. (1989). Weight gain in infancy and death from ischaemic heart disease.
Lancet, 2, 577-580.
Barker, D.J.P. et al. (1993). Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced foetal growth. Diabetologia, 36, 62- 67.
Barker, D.J.P. et al. (1993). Growth in utero and serum cholesterol concentrations in adult life.
British Medical Journal, 307, 1524-1527.
Barker, D.J.P. (1995). Foetal origins of coronary heart disease. British Medical Journal, 311,171
Barker, D.J.P. et al. (2000). Growth in utero and blood pressure levels in the next generation.
Journal of Hypertension,18, 843-846.
Barker, D.J.P. et al. (2001). Size at birth and resilience to effects of poor living conditions in
adult life: longitudinal study. British Medical Journal, 323,1273-1276.
Davis, M. K. (2001). Breastfeeding and chronic disease in childhood and adolescence. Paediatric Clinics of North America, 2001, 48, 125-141.
Dietz, W.H. (2001). Breastfeeding may help prevent childhood overweight. Journal of the American Medical Association, 285, 2506-2507.
Eriksson, J. G. et al. (1999). Catch-up growth in childhood and death from coronary heart
disease: a longitudinal study. British Medical Journal, 318, 427-431.
Eriksson J.G. et al. (2000). Early growth, adult income, and risk of stroke. Stroke, 2000, 31:869
874.
Eriksson, J. G. et al. (2001). Early growth and coronary heart disease in later life: longitudinal study. British Medical Journal, 322, 949-953.
Fall, C.H.D. et al. (1998). Size at birth, maternal weight, and type II diabetes in South India. Diabetic Medicine, 15, 220-227.
Forsén, T et al. (1999). Growth in utero and during childhood in women who develop coronary
heart disease: a longitudinal study. British Medical Journal, 319,1403-1407.
Forsén, T et al. (2000). The fetal and childhood growth of persons who develop type II diabetes.
Annals of Internal Medicine, vol. 33, pp. 176-182.
Gillman, M.W. et al. (2001). Risk of overweight among adolescents who were breastfed as
infants. Journal of the American Medical Association, 285, 2461-2467.
Godfrey, K.M., & Barker, D. J. (2000). Fetal nutrition and adult disease. American Journal of
Clinical Nutrition, 71(5), S1344-S1352.
Gunnell, D. J. et al. (1998). Socio-economic and dietary influences on leg length and trunk length in childhood: a reanalysis of the Carnegie (Boyd Orr) survey of diet and health in prewar Britain (1937-39). Pediatric and Perinatal Epidemiology, 12(1), 96-113.
Kuh, D., & Ben-Shlomo, Y. (1997). A life course approach to chronic disease epidemiology. Oxford: Oxford University Press.