Early nutritional origins of vascular disease: a hypothesis still lacking support

Paneth, N.; Stein, Adam C.

doi:10.1016/s0143-4004(96)90082-x

Cited by 23 publications

(33 citation statements)

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“…However, if we adjusted for BMI at age 58 years the association between birth weight and blood pressure at age 58 years was statistically significant (data not shown). This approach, and the finding of an increased association after adjustment for current weight or BMI, is common in studies of the late effect of low birth weight and has been criticized on methodological grounds as an example of inappropriately treating a mediating variable as a confounder [30].…”

Section: Discussionmentioning

confidence: 99%

Low birth weight in combination with catch‐up growth predicts the occurrence of the metabolic syndrome in men at late middle age: the Atherosclerosis and Insulin Resistance study

Fagerberg

Bondjers

Nilsson

2004

Journal of Internal Medicine

125

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Abstract. Fagerberg B, Bondjers L, Nilsson P (Institute of Internal Medicine and Sahlgrenska University Hospital, Göteborg; and Malmö University Hospital, Lund University, Lund; Sweden). Low birth weight in combination with catch-up growth predicts the occurrence of the metabolic syndrome in men at late middle age: the Atherosclerosis and Insulin Resistance study. Objectives. To study the combined effects of a low birth weight and a pronounced weight increase up to early adulthood on the presence of cardiovascular risk factors constituting the metabolic syndrome in late middle age. Design and setting. A structured sample of 396 men, 58 years old from the general population. Birth weight and weight at 18 years were obtained from medical records and registers. Main outcome measures. Body mass index (BMI), waist : hip ratio (WHR), blood pressure, serum concentrations of insulin, triglycerides, HDL cholesterol and LDL particle size at age 58 years. Results. The ratio between weight at age 18 years and birth weight correlated with a number of characteristics at age 58 years: BMI (r ¼ 0.24, P < 0.001), WHR (r ¼ 0.24, P < 0.001), diastolic blood pressure (r ¼ 0.13, P < 0.05), insulin (r ¼ 0.14, P < 0.01), triglycerides (r ¼ 0.10, P < 0.05), HDL cholesterol (r ¼ )0.13, P < 0.01) and LDL particle size (r ¼ )0.17, P < 0.05). The metabolic syndrome, according to current definitions, were more common at the age of 58 years in the third tertile of the weight at 18/birth ratio, than in the other tertiles (P ¼ 0.008). Conclusions. The interaction between a low birth weight and an accelerated catch-up growth to early adulthood is associated with the occurrence of the metabolic syndrome in the late middle age. These findings are in accord with the concept that the effects of genes are conditioned by fetal growth, and that the effects of a small body size at birth are conditioned by growth during childhood and by environmental factors in childhood and adult life.

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Section: Discussionmentioning

confidence: 99%

Low birth weight in combination with catch‐up growth predicts the occurrence of the metabolic syndrome in men at late middle age: the Atherosclerosis and Insulin Resistance study

Fagerberg

Bondjers

Nilsson

2004

Journal of Internal Medicine

125

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“…This lifestyle possibly goes along with intrauterine growth retardation. Despite criticisms about the validity of their observations (2), the association between low birth weight and adult diseases is now further supported by several studies with similar findings (3)(4)(5)(6). Moreover, the understanding of the mechanisms of this association represents a challenge for investigators in this area.…”

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confidence: 99%

Perinatal Salt Restriction: A New Pathway to Programming Insulin Resistance and Dyslipidemia in Adult Wistar Rats

et al. 2004

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Several studies support the hypothesis that chronic diseases in adulthood might be triggered by events that occur during fetal development. This study examined the consequences of perinatal salt intake on blood pressure (BP) and carbohydrate and lipid metabolism in adult offspring of dams on high-salt [HSD; 8% (HSD2) or 4% (HSD1)], normal-salt (NSD; 1.3%), or low-salt (LSD; 0.15% NaCl) diet during pregnancy and lactation. At 12 wk of age, female Wistar rats were matched with adult male rats that were fed NSD. Weekly tail-cuff BP measurements were performed before, during, and after pregnancy. After weaning, the offspring received only NSD and were housed in metabolic cages for 24-h urine collection for sodium and potassium and nitrate and nitrite excretion measurements. At 12 wk of age, intra-arterial mean BP was measured, a euglycemic-hyperinsulinemic clamp was performed, and plasma lipids and nitrate and nitrite concentrations were determined. Tail-cuff BP was higher during pregnancy in HSD2 and HSD1 than in NSD and LSD dams. Mean BP (mm Hg) was also higher in the offspring of HSD2 (110 Ϯ 5) and HSD1 (107 Ϯ 5) compared with NSD (100 Ϯ 2) and LSD (92 Ϯ 2). Lower glucose uptake and higher plasma cholesterol and triacylglycerols were observed in male offspring from LSD dams (glucose uptake: HSD2 17 Ϯ 4, HSD1 15 Ϯ 3, NSD 11 Ϯ 3, LSD 4 Ϯ 1 mg · kg Ϫ1 · min Ϫ1 ; cholesterol: HSD2 62 Ϯ 6, HSD1 82 Ϯ 11, NSD 68 Ϯ 10, LSD 98 Ϯ 17 mg/dL; triacylglycerols: HSD2 47 Ϯ 15, HSD1 49 Ϯ 12, NSD 56 Ϯ 19, LSD 83 Ϯ 11 mg/dL). In conclusion, maternal salt intake during pregnancy and lactation has long-term influences on arterial pressure, insulin sensitivity, and plasma lipids of the adult offspring. (Pediatr Res 56: 842-848, 2004) Abbreviations BP, blood pressure HSD, high-salt diet HR, heart rate LSD, low-salt diet MBP, mean blood pressure NSD, normal-salt diet NOx, nitrate plus nitrite RAS, renin-angiotensin system tcBP, tail-cuff blood pressure Almost two decades ago, Barker and Osmond (1) proposed that ischemic heart disease could be triggered by events that occur during fetal life and early childhood (1). They showed an association between poor living standard during the perinatal period and ischemic heart disease in adulthood. This lifestyle possibly goes along with intrauterine growth retardation. Despite criticisms about the validity of their observations (2), the association between low birth weight and adult diseases is now further supported by several studies with similar findings (3-6). Moreover, the understanding of the mechanisms of this association represents a challenge for investigators in this area.Intrauterine growth is controlled by a complex interplay of maternal and fetal factors, including circulatory, endocrine, and metabolic systems (7). An increasing number of studies have shown that small modifications in fetal growth may have profound consequences in later life (8 -10).

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“…3,4 However, there has been criticism of the epidemiological evidence supporting this link between fetal undernutrition and hypertension in human populations. 5 In their critical review, Paneth et al 6 concluded that "the inverse relationship of birthweight to blood pressure is found inconsistently and, when present, is not strong." Moreover, the findings are potentially confounded by variables such as social class, which generally have not been taken into account.…”

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confidence: 99%

Prenatal Malnutrition-Induced Changes in Blood Pressure

et al. 1998

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Abstract-A link between prenatal malnutrition and hypertension in human populations has recently been proposed. Rat models of prenatal malnutrition have provided major support for this theory on the basis of tail-cuff measurements. However, this technique requires restraint and elevated temperature, both potential sources of stress. To determine the effect of prenatal protein malnutrition on blood pressure under nonstress conditions, 24-hour radiotelemetric measurements were taken in the home cage. Male rats born to dams fed a 6% casein diet for 5 weeks before mating and throughout pregnancy were studied in early adulthood (from 96 days of age). During the waking phase of their cycle but not the sleep phase, prenatal malnutrition gave rise to small but significant elevations of diastolic blood pressure and heart rate compared with well-nourished controls. Direct effects of stress on blood pressure responses were determined in a second experiment using an olfactory stressor. Prenatally malnourished rats showed a greater increase in both systolic and diastolic pressures compared with well-nourished controls during the first exposure to ammonia. A different pattern of change of cardiovascular responses was also observed during subsequent presentations of the stressor. These findings of a small baseline increase in diastolic pressure consequent to prenatal malnutrition, but an augmented elevation of both systolic and diastolic pressures after first exposure to stress, suggest the need to reevaluate interpretation of the large elevations in blood pressure previously observed in malnourished animals using the stressful tail-cuff procedure. (Hypertension. 1998;32:108-114.)

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Early nutritional origins of vascular disease: a hypothesis still lacking support

Cited by 23 publications

References 0 publications

Low birth weight in combination with catch‐up growth predicts the occurrence of the metabolic syndrome in men at late middle age: the Atherosclerosis and Insulin Resistance study

Low birth weight in combination with catch‐up growth predicts the occurrence of the metabolic syndrome in men at late middle age: the Atherosclerosis and Insulin Resistance study

Perinatal Salt Restriction: A New Pathway to Programming Insulin Resistance and Dyslipidemia in Adult Wistar Rats

Prenatal Malnutrition-Induced Changes in Blood Pressure

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