4. Diet, nutrition and chronic diseases in context:
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Retarded growth in infancy can be a reflected in a failure to gain weight and a failure to gain height. Both retarded growth and excessive weight or height gain (“crossing the centiles”) can be factors in later incidence of chronic disease. An association between low growth in early infancy (low weight at 1 year) and an increased risk of coronary heart disease (CHD) has been described, irrespective of size at birth (3, 25). Blood pressure has been found to be highest in those with retarded fetal growth and greater weight gain in infancy (26). Short stature, a reflection of socioeconomic deprivation in childhood (27), is also associated with an increased risk of CHD and stroke, and to some extent, diabetes (10, 15, 28-34). The risk of stroke, and also of cancer mortality at several sites, including breast, uterus and colon, is increased if shorter children display an accelerated growth in height (35, 36).
There is increasing evidence that among term and pre-term infants, breastfeeding is associated with significantly lower blood pressure levels in childhood (37, 38). Consumption of formula instead of breast milk in infancy has also been shown to increase diastolic and mean arterial blood pressure in later life (37). Nevertheless, studies with older cohorts (22) and the Dutch study of famine (39) have not identified such associations. There is increasingly strong evidence suggesting that a lower risk of developing obesity (40-43) may be directly related to length of exclusive breastfeeding although it may not become evident until later in childhood (44). Some of the discrepancy may be explained by socioeconomic and maternal education factors confounding the findings.
Data from most, but not all, observational studies of term infants have generally suggested adverse effects of formula consumption on the other risk factors for cardiovascular disease (as well as blood pressure), but little information to support this finding is available from controlled clinical trials (45). Nevertheless, the weight of current evidence indicates adverse effects of formula milk on cardiovascular disease risk factors; this is consistent with the observations of increased mortality among older adults who were fed formula as infants (45-47). The risk for several chronic diseases of childhood and adolescence (e.g. type 1 diabetes, coeliac disease, some childhood cancers, inflammatory bowel disease) have also been associated with infant feeding on breast-milk substitutes and short-term breastfeeding (48).
There has been great interest in the possible effect of high-cholesterol feeding in early life. Reiser et al. (49) proposed the hypothesis that high cholesterol feeding in early life may serve to regulate cholesterol and lipoprotein metabolism in later life. Animal data in support of this hypothesis are limited, but the idea of a possible metabolic imprinting served to trigger several retrospective and prospective studies in which cholesterol and lipoprotein metabolism in infants fed human milk were compared with those fed formula. Studies in suckling rats have suggested that the presence of cholesterol in the early diet may serve to define a metabolic pattern for lipoproteins and plasma cholesterol that could be of benefit later in life. The study by Mott, Lewis & McGill (50) on differential diets in infant baboons, however, provided evidence to the contrary in terms of benefit. Nevertheless, the observation of modified responses of adult cholesterol production rates, bile cholesterol saturation indices, and bile acid turnover, depending on whether the baboons were fed breast milk or formula, served to attract further interest. It was noted that increased atherosclerotic lesions associated with increased levels of plasma total cholesterol were related to increased dietary cholesterol in early life. No long-term human morbidity and mortality data supporting this notion have been reported.
Short-term human studies have been in part confounded by diversity in solid food weaning regimens, as well as by the varied composition of fatty acid components of the early diet. The latter are now known to have an impact on circulating lipoprotein cholesterol species (51). Mean plasma total cholesterol by age 4 months in infants fed breast milk reached 180 mg/dl or greater, while cholesterol values in infants fed formula tended to remain under 150 mg/dl. In a study by Carlson, DeVoe & Barness (52), infants receiving predominantly a linoleic acidenriched oil blend exhibited a mean cholesterol concentration of approximately 110 mg/dl. A separate group of infants in that study who received predominantly oleic acid had a mean cholesterol concentration of 133 mg/dl. Moreover, infants who were fed breast milk and oleic acid-enriched formula had higher high-density lipoprotein (HDL) cholesterol and apoproteins A-I and A-II than the predominantly linoleic acid-enriched oil diet group. The ratio of low density lipoprotein (LDL) cholesterol plus very low-density lipoprotein (VLDL) cholesterol to HDL cholesterol was lowest for infants receiving the formula in which oleic acid was predominant. Using a similar oleic acid predominant formula, Darmady, Fosbrooke & Lloyd (53) reported a mean value of 149 mg/dl at age 4 months, compared with 196 mg/dl in a parallel breast-fed group. Most of those infants then received an uncontrolled mixed diet and cow’s milk, with no evident differences in plasma cholesterol levels by 12 months, independent of the type of early feeding they had received. A more recent controlled study (54) suggests that the specific fatty acid intake plays a predominant role in determining total and LDL cholesterol. The significance of high dietary cholesterol associated with exclusive human milk feeding during the first 4 months of life has no demonstrated adverse effect. Measurements of serum lipoprotein concentrations and LDL receptor activity in infants suggests that it is the fatty acid content rather than the cholesterol in the diet which regulates cholesterol homeostasis. The regulation of endogenous cholesterol synthesis in infants appears to be regulated in a similar manner to that of adults (55, 56).
4.2.3 Childhood and adolescence
An association between low growth in childhood and an increased risk of CHD has been described, irrespective of size at birth (3, 25). Although based only on developed country research at this point, this finding gives credence to the importance that is currently attached to the role of immediate postnatal factors in shaping disease risk. Growth rates in infants in Bangladesh, most of whom had chronic intrauterine undernourishment and were breastfed, were similar to growth rates of breastfed infants in industrialized countries, but catch-up growth was limited and weight at 12 months was largely a function of weight at birth (57).
In a study of 11-12 year-old Jamaican children (26), blood pressure levels were found to be highest in those with retarded fetal growth and greater weight gain between the ages of 7 and 11 years. Similar results were found in India (58). Low birth weight Indian babies have been described as having a characteristic poor muscle but high fat preservation, so-called “thin-fat” babies. This phenotype persists throughout the postnatal period and is associated with an increased central adiposity in childhood that is linked to the highest risk of raised blood pressure and disease (59-61). In most studies, the association between low birth weight and high blood pressure has been found to be particularly strong if adjusted to current body size - body mass index (BMI) - suggesting the importance of weight gain after birth (62).
4. Diet, nutrition and chronic diseases in context:
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