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C Osmond

Publications and source records attributed to C Osmond.

At least 37 records · Page 2Linked to original sources
PubMed2002

Fetal origins of adult disease: strength of effects and biological basis.

BACKGROUND: Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication. METHODS: Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented. RESULTS: The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension. CONCLUSIONS: Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.

Aged↗
PubMed2001

Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview.

Chronic diseases are the main public health problem in Western countries. There are indications that these diseases originate in the womb. It is thought that undernutrition of the fetus during critical periods of development would lead to adaptations in the structure and physiology of the fetal body, and thereby increase the risk of diseases in later life. The Dutch famine--though a historical disaster--provides a unique opportunity to study effects of undernutrition during gestation in humans. This thesis describes the effects of prenatal exposure to the Dutch famine on health in later life. We found indications that undernutrition during gestation affects health in later life. The effects on undernutrition, however, depend upon its timing during gestation and the organs and systems developing during that critical time window. Furthermore, our findings suggest that maternal malnutrition during gestation may permanently affect adult health without affecting the size of the baby at birth. This may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences of improved nutrition of pregnant women will be underestimated if these are solely based on the size of the baby at birth. Little is known about what an adequate diet for pregnant women might be. In general, women are especially receptive to advice about diet and lifestyle before and during a pregnancy. This should be exploited to improve the health of future generations.

Adaptation, Physiological↗
PubMed2001

Size at birth and resilience to effects of poor living conditions in adult life: longitudinal study.

OBJECTIVE: To determine whether men who grew slowly in utero or during infancy are more vulnerable to the later effects of poor living conditions on coronary heart disease. DESIGN: Follow up study of men for whom there were data on body size at birth and growth and social class during childhood, educational level, and social class and income in adult life. SETTING: Helsinki, Finland. PARTICIPANTS: 3676 men who were born during 1934-44, attended child welfare clinics in Helsinki, were still resident in Finland in 1971, and for whom data from the 1980 census were available. MAIN OUTCOME MEASURES: Hospital admission for or death from coronary heart disease. RESULTS: Men who had low social class or low household income in adult life had increased rates of coronary heart disease. The hazard ratio among men with the lowest annual income (<8400 pound sterling) was 1.71 (95% confidence interval 1.18 to 2.48) compared with 1.00 in men with incomes above 15, 700 pound sterling. These effects were stronger in men who were thin at birth (ponderal index <26 kg/m(3)): hazard ratio 2.58 (1.45 to 4.60) for men with lowest annual income. Among the men who were thin at birth the effects of low social class were greater in those who had accelerated weight gain between ages 1 and 12 years. Low social class in childhood further increased risk of disease, partly because it was associated with poor growth during infancy. Low educational attainment was associated with increased risk, and low income had no effect once this was taken into account. CONCLUSION: Men who grow slowly in utero remain biologically different to other men. They are more vulnerable to the effects of low socioeconomic status and low income on coronary heart disease.

Aged↗
PubMed2001

Tallness and overweight during childhood have opposing effects on breast cancer risk.

Using birth and school health records we studied how weight and height during childhood affect breast cancer risk among 3447 women born during 1924-33 at the University Hospital of Helsinki, Finland. Through linkages with the National Hospital Discharge Registry and the Cause of Death Registry we identified 177 women who during 1971-1995 had been admitted to hospital with breast cancer, of whom 49 had died from the disease. Of these, 135 (76%) were aged 50 years or more at the time of diagnosis, and therefore likely to have been post-menopausal. Hazard ratios for breast cancer rose with increasing weight and length at birth, though neither trend was statistically significant. At each age, from 7 to 15 years, the girls who later developed breast cancer were on average taller and had lower body mass than the other girls. Unadjusted hazard ratios rose across the range of height (P = 0.01 at age 7 years) and fell across the range of body mass index (P = 0.009 at age 7 years). In a simultaneous analysis the hazard ratio for breast cancer was 1.27 (95% CI 0.97-1.78, P = 0.08) for every kilogram increase in birth weight and 1.21 (95% CI 1.06-1.38, P = 0.004) for every kg/m(2) decrease in body mass index at 7. Our findings indicate that tallness in childhood is associated with increased risk of developing breast cancer. One possible explanation is persisting high plasma concentrations of insulin-like growth factors in tall women. In contrast, we found that being overweight in childhood reduces breast cancer risk. The increased adipose tissue-derived oestrogen levels in overweight children could induce early breast differentiation and eliminate some targets for malignant transformation.

Adolescent↗
PubMed2001

Early growth and coronary heart disease in later life: longitudinal study.

OBJECTIVE: To determine how growth during infancy and childhood modifies the increased risk of coronary heart disease associated with small body size at birth. DESIGN: Longitudinal study. SETTING: Helsinki, Finland. SUBJECTS: 4630 men who were born in the Helsinki University Hospital during 1934-44 and who attended child welfare clinics in the city. Each man had on average 18.0 (SD 9.5) measurements of height and weight between birth and age 12 years. MAIN OUTCOME MEASURES: Hospital admission or death from coronary heart disease. RESULTS: Low birth weight and low ponderal index (birth weight/length(3)) were associated with increased risk of coronary heart disease. Low height, weight, and body mass index (weight/height(2)) at age 1 year also increased the risk. Hazard ratios fell progressively from 1.83 (95% confidence interval 1.28 to 2.60) in men whose body mass index at age 1 year was below 16 kg/m(2) to 1.00 in those whose body mass index was >19 (P for trend=0.0004). After age 1 year, rapid gain in weight and body mass index increased the risk of coronary heart disease. This effect was confined, however, to men with a ponderal index <26 at birth. In these men the hazard ratio associated with a one unit increase in standard deviation score for body mass index between ages 1 and 12 years was 1.27 (1.10 to 1.47; P=0.001). CONCLUSION: Irrespective of size at birth, low weight gain during infancy is associated with increased risk of coronary heart disease. After age 1 year, rapid weight gain is associated with further increase in risk, but only among boys who were thin at birth. In these boys the adverse effects of rapid weight gain on later coronary heart disease are already apparent at age 3 years. Improvements in fetal, infant, and child growth could lead to substantial reductions in the incidence of coronary heart disease.

Aged↗
PubMed2001

Association of schizophrenia with low maternal body mass index, small size at birth, and thinness during childhood.

BACKGROUND: Nutritional factors in early life may contribute to the neurodevelopmental deficit in schizophrenia. This study explores the influence of maternal body size, size at birth, and childhood growth on future risk for schizophrenia. SUBJECTS AND METHODS: This population-based cohort study comprised births at Helsinki University Central Hospital in Helsinki, Finland, from 1924 to 1933. Prospective data from birth and school health records of 7086 individuals were collected and linked to the Finnish Hospital Discharge Register. RESULTS: Schizophrenia or schizoaffective disorder had been diagnosed in 114 individuals. A lower late-pregnancy maternal body mass index (BMI) increased the risk (odds ratio [OR], 1.09 per kilogram/meter(2); 95% confidence interval [CI], 1.02-1.17) for schizophrenia among the offspring. The risk of schizophrenia increased with low birth weight (OR, 1.48 per kilogram; 95% CI, 1.03-2.13), shortness at birth (OR, 1.12 per centimeter; 95% CI, 1.03-1.22), and low placental weight (OR, 1.22 per 100 g; 95% CI, 1.04-1.43). Schizophrenia cases were thinner than comparison subjects from 7 to 15 years of age. In a joint model comprising late-pregnancy maternal BMI, body size at birth, and childhood BMI, childhood BMI was an independent predictor of schizophrenia, whereas other factors exhibited attenuated effects. CONCLUSION: Indicators of intrauterine and childhood undernutrition are associated with an increased lifetime risk of schizophrenia.

Adolescent↗
PubMed2001

Testing the fetal origins hypothesis in twins: the Birmingham twin study.

AIMS/HYPOTHESIS: To test whether the link between birthsize and raised blood pressure or glucose tolerance is due to genetic or intrauterine factors, we studied whether differences in birthweight between pairs of monozygous and dizygous twins are associated with adult differences in blood pressure and glucose tolerance. METHODS: A sample of 58 monozygous and 140 dizygous twins were identified from a register of births in Birmingham, United Kingdom, between 1950 and 1954. The twins had their blood pressure measured and underwent an oral glucose tolerance test. RESULTS: There were no statistically significant associations between birthweight, length or ponderal index, and either blood pressure or glucose tolerance in the twins. Although there were substantial within-pair differences in birthweight between monozygous and dizygous twin pairs, these differences did not correlate with the adult outcomes. Monozygous correlations, however, for both blood pressure and glucose tolerance were statistically significantly higher than dizygous correlations and a quantitative genetic model suggested statistically significant heritability for these traits. In contrast correlations of birthsize were similar in monozygous and dizygous pairs suggesting only a small genetic component in determining fetal size. CONCLUSION/INTERPRETATION: Our results show that birthsize in twins does not predict adult blood pressure or glucose tolerance. We also suggest that shared genetic determinants for fetal growth and adult outcomes are not likely to be prevalent or powerful.

Adult↗
PubMed2001

Maternal height, childhood growth and risk of hip fracture in later life: a longitudinal study.

Although measures to enhance bone mineralization during childhood and adolescence are widely incorporated into preventive programmes against osteoporotic fracture, there are no published data directly linking growth rates in childhood with the risk of later hip fracture. We addressed this issue in a unique Finnish cohort in whom birth and childhood growth data were linked to later hospital discharge records. This permitted follow-up of 3639 men and 3447 women who were born in Helsinki University Central Hospital between 1924 and 1933, who went to school in Helsinki and still lived in Finland in 1971. Body size at birth was recorded and an average of 10 measurements were obtained of height and weight throughout childhood. We identified 112 subjects (55 men and 57 women) who sustained a hip fracture during 165 404 person-years of follow-up. After adjustment for age and sex in a proportional hazards model, we identified two major determinants of hip fracture risk: tall maternal height (p < 0.001) and a low rate of childhood growth (height, p = 0.006; weight, p = 0.01). The hazard ratio for hip fracture was 2.1 (95% CI 1.2-3.5) among men and women born to mothers taller than 1.61 m, when compared with those whose mothers were shorter than 1.54 m. The ratio was 1.9 (95% CI 1.1-3.2) among those whose rate of childhood height gain was below the lowest quartile for the cohort, compared with those whose growth rate was above the highest quartile. The effects of maternal height and childhood growth rate were statistically independent of each other, and remained after adjusting for socioeconomic status. The patterns of childhood growth that predicted future hip fracture differed between boys and girls. In boys, there was a constant deficit in height and weight between ages 7 and 15 years among those later sustaining fractures; in girls, there was a progressively increasing deficit in weight but a delayed height gain among those later sustaining fractures. This epidemiologic study provides the first direct evidence that a low rate of childhood growth is a risk factor for later hip fracture. Whether reduced growth rate is a consequence of childhood lifestyle, genetic background or intrauterine hormonal programming, the data support measures to optimize childhood growth as part of preventive strategies against osteoporotic fracture in future generations.

Adolescent↗
PubMed2001

Second-trimester placental volume and infant size at birth.

OBJECTIVE: To investigate the ability of second-trimester placental volume measured sonographically to predict birth size. METHODS: A total of 712 women were recruited from the antenatal clinic of the University Hospital of the West Indies; 561 fulfilled the study criteria and progressed to delivery. Placental volume and fetal anthropometry (biparietal diameter, head and abdominal circumferences, and femoral length) were measured sonographically at 14, 17, and 20 weeks. The main outcome measures were infant birth and placental weights, length, head, chest, and abdominal circumferences at birth. RESULTS: Placental volume in the second trimester was positively associated with all birth measurements. Of the fetal measurements at 14 and at 17 weeks, head circumference was the strongest predictor of birth weight (B [slope of the regression line] =.095, P =.014 at 14 weeks; B =.118, P =.012 at 17 weeks), but at 20 weeks, abdominal circumference was the strongest. However, at each age, placental volume was the strongest determinant of birth weight, and improved the prediction based only on fetal measurements. The odds ratio for low birth weight (under 2500 g) increased by 1.68 (95% confidence interval 1.05, 2.69, P = 0.03) for every standard deviation decrease in placental volume at 14 weeks' gestation. CONCLUSION: The present study suggests that low birth weight was often preceded by small placental volume in the second trimester. Placental volume may be a more reliable predictor of size at birth than fetal measurements, and may be useful in early identification of the fetus at risk in the perinatal period.

Adolescent↗
PubMed2001

Associations between childhood living circumstances and schizophrenia: a population-based cohort study.

OBJECTIVE: It has been suggested that household crowding may constitute an environmental risk factor for schizophrenia. The present population-based cohort study explores the associations of childhood family size and living conditions to schizophrenia. METHOD: The cohort comprised people born at Helsinki University Central Hospital from 1924 to 1933, who went to school in the city and were still living in Finland in 1971. Prospectively gathered data from birth and school health records of these 7086 individuals were collected and linked to the Finnish Hospital Discharge Register. RESULTS: Ninety-eight cases of schizophrenia were identified in the cohort. Number of siblings at school start was significantly associated with schizophrenia when adjusted for sex and age of mother. Number of siblings was negatively correlated with body mass index at age 7. Childhood household crowding, defined as number of people per room, and total number of rooms in household were not significantly associated with schizophrenia. CONCLUSION: Our study indicates that the total number siblings in household during childhood is of greater importance than childhood number of inhabitants per room. Subjects who originated from families with many children had been leaner, which may imply that childhood nutritional factors partly is the mediating factor between number of siblings and schizophrenia. Other possible underlying mechanisms of the associations found include infectious and psychological factors.

Adolescent↗
PubMed2001

Size at birth, childhood growth and obesity in adult life.

BACKGROUND: Several studies have shown tracking of obesity from childhood to adult life. People who develop obesity in adult life may therefore have had a particular path of growth from birth through childhood. OBJECTIVE: To examine the relationship of obesity to size at birth and childhood growth. DESIGN: Birth cohort study. PARTICIPANTS: A total of 5210 individuals alive and living in Finland in 1997, who were born at the Helsinki University Central Hospital between 1924 and 1933 and who went to school in Helsinki were sent a questionnaire in order to get information about adult weight and height. Detailed birth and school health records were available for all subjects. In all, 3847 responded and 3659 (1552 men and 2107 women) with adequate data are included in the present study. MEASUREMENTS: Incidence of obesity based upon lifetime maximum body mass index (BMI) ascertained from a postal questionnaire and defined as a BMI>30 kg/m(2). The main explanatory measurements were size at birth and childhood growth in height, weight and BMI. RESULTS: The cumulative incidence of obesity was 34.2% in men and 33.9% in women. The incidence rose with increasing birth weight and ponderal index (birthweight/length(3); P=0.01 and P=0.04, respectively). These associations were statistically significant only among males. By the age of 7 y the mean weights, heights and BMI of people who later became obese exceeded the average and remained above average at all ages from 7 to 15 y. In both men and women there was a 3-fold increase in obesity associated with a BMI>16 kg/m(2) at age 7 compared with a BMI<14.5 kg/m(2) (P<0.0001). Boys and girls whose mothers had a high BMI in pregnancy had more rapid childhood growth and an increased risk of becoming obese. This effect was stronger among boys (P=0.008). CONCLUSIONS: Obesity is initiated early in life. These results emphasise the importance of early preventive measures for its treatment.

Adolescent↗
PubMed2001

Adult survival after prenatal exposure to the Dutch famine 1944--45.

Early life events may affect adult survival. We studied the effect of prenatal exposure to the Dutch famine 1944--45 on survival among 2254 people born in Amsterdam. Mortality up to age 50 was highest among those born before the famine (15.2%) and among those exposed to famine in late gestation (14.6%). It was lower among those exposed in mid- (11.2%) or early gestation (11.5%), and was lowest among those conceived after the famine (7.2%). These differences were caused by effects on mortality in the first year after birth and were mainly related to nutrition and infections. There was no effect of exposure to famine on mortality after the age of 18. The hazard ratio was 1.4 [0.8, 2.3] for those born before the famine, 1.1 [0.5, 2.3] for those exposed in late gestation, 0.8 [0.3, 1.8] for those exposed in mid-gestation and 1.1 [0.5, 2.5] in those exposed in early gestation compared with those conceived after the famine. We could not demonstrate effects of prenatal exposure to famine on cause-specific mortality after the age of 18. Because prenatal exposure to famine is linked to cardiovascular risk factors and disease, increased cardiovascular mortality in the future may be expected.

Adult↗
PubMed2001

Maternal nutrition during gestation and blood pressure in later life.

OBJECTIVE: To assess the link between maternal diet during pregnancy and blood pressure of the offspring. DESIGN: Follow-up study. SETTING: A university hospital in Amsterdam, The Netherlands. PARTICIPANTS: People born at term as singletons between November 1943 and February 1947. MAIN OUTCOME MEASURE: Blood pressure at adult age. RESULTS: Adult blood pressure was not associated with protein, carbohydrate or fat intake during any period of gestation. We found, however, after adjustment for sex that the systolic blood pressure decreased by 0.6 mmHg (0.1-1.1) for every 1% increase in protein/carbohydrate ratio in the third trimester. This association was present both in people who had been exposed to the famine during gestation as well as in those who had not been exposed. The association between protein/carbohydrate ratio in the third trimester and adult blood pressure was furthermore independent of maternal weight gain and final weight, and birth weight [increase for every 1% increase in protein/carbohydrate ratio 0.6 mmHg (0.0-1.2)]. Adjustment for adult characteristics such as body mass index, smoking and socio-economic status did not affect the observed association appreciably [adjusted increase 0.5 mmHg (0.0-1.0)]. CONCLUSION: Adult blood pressure seems to be affected by small variations in the balance of macro-nutrients in the maternal diet during gestation rather than by relatively large variations in the absolute amounts.

Adult↗
PubMed2001

Birth weight and the risk of depressive disorder in late life.

BACKGROUND: Low birth weight is a risk factor for coronary heart disease, diabetes, stroke and hypertension. Depression is highly associated with these conditions. AIMS: To examine the association between birth weight and depression in late life. METHOD: A total of 882 singleton term births in the 1920s had contemporary records of birth weight and weight at 1 year. At 68 years all completed the Geriatric Depression Scale and 867 completed the Geriatric Mental State Examination. A logistic regression was used to analyse the associations between depression, birth weight and weight at 1 year while adjusting for known risk factors. RESULTS: Current social class, social class at birth, recent bereavement, social isolation and physical illness increased the risk of depression. After adjusting for these and weight at 1 year, the odds ratios for depression among men, but not women, rose incrementally with decreasing birth weight (1.0, 12.8; for continuous variable, P<0.007). CONCLUSIONS: Foetal undernutrition predisposes men to depression in late adult life. If replicated, these results would suggest a neurodevelopmental aetiology of depression, possibly mediated by programming of the hypothalamic-pituitary-adrenal axis.

Aged↗
PubMed2001

Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview.

People who were small at birth have been shown to have an increased risk of CHD and chronic bronchitis in later life. These findings have led to the fetal origins hypothesis that proposes that the fetus adapts to a limited supply of nutrients, and in doing so it permanently alters its physiology and metabolism, which could increase its risk of disease in later life. The Dutch famine--though a historical disaster--provides a unique opportunity to study effects of undernutrition during gestation in humans. People who had been exposed to famine in late or mid gestation had reduced glucose tolerance. Whereas people exposed to famine in early gestation had a more atherogenic lipid profile, somewhat higher fibrinogen concentrations and reduced plasma concentrations of factor VII, a higher BMI and they appeared to have a higher risk of CHD. Though the latter was based on small numbers, as could be expected from the relatively young age of the cohort. Nevertheless, this is the first evidence in humans that maternal undernutrition during gestation is linked with the risk of CHD in later life. Our findings broadly support the hypothesis that chronic diseases originate through adaptations made by the fetus in response to undernutrition. The long-term effects of intrauterine undernutrition, however, depend upon its timing during gestation and on the tissues and systems undergoing critical periods of development at that time. Furthermore, our findings suggest that maternal malnutrition during gestation may permanently affect adult health without affecting the size of the baby at birth. This gives the fetal origins hypothesis a new dimension. It may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences for health in later life. CHD may be viewed as the price paid for successful adaptations to an adverse intra-uterine environment. It also implies that the long-term consequences of improved nutrition of pregnant women will be underestimated if these are solely based on the size of the baby at birth. We need to know more about what an adequate diet for pregnant women might be. In general, women are especially receptive to advice about diet and lifestyle before and during a pregnancy. This should be exploited to improve the health of future generations.

Adult↗
PubMed2000

The fetal and childhood growth of persons who develop type 2 diabetes.

BACKGROUND: Type 2 diabetes is associated with low birthweight followed by obesity in adulthood. Persons who develop the disease may therefore have a particular pattern of growth from birth through childhood. OBJECTIVE: To examine the relation of type 2 diabetes to size at birth and childhood growth. DESIGN: Cohort study. SETTING: Helsinki, Finland. PARTICIPANTS: Men (n = 3,639) and women (n = 3,447) who were bom at the Helsinki University Central Hospital between 1924 and 1933, who went to school in Helsinki, and who still lived in Finland in 1971. Detailed birth and school health records were available for all 7,086 participants. We identified 471 men and women who developed type 2 diabetes by using the national Social Insurance Institution's register of all persons in Finland who are receiving long-term therapy with medication. MEASUREMENTS: Incidence of diabetes ascertained from a national register. The main explanatory measurements were size at birth and childhood growth in terms of height, weight, and body mass index. RESULTS: The cumulative incidence of type 2 diabetes was 7.9% (n = 286) in men and 5.4% (n = 185) in women. The incidence increased with decreasing birthweight, birth length, ponderal index (birthweight/length(3)), and placental weight The odds ratio for type 2 diabetes was 1.38 (95% CI, 1.15 to 1.66; P < 0.001) for each 1-kg decrease in birthweight. The mean weights and heights of the children at 7 years of age who later developed type 2 diabetes were about average. Thereafter, their growth in weight and height was accelerated until 15 years of age. The odds ratio for development of type 2 diabetes was 1.39 (CI, 1.21 to 1.61; P < 0.001) for each standard deviation increase in weight between 7 and 15 years of age. The odds ratio became 1.83 (CI, 1.37 to 2.45; P< 0.001) in an analysis restricted to persons whose birthweights were below 3,000 g. Children of both sexes whose mothers had a high body mass index in pregnancy had more rapid growth during childhood and an increased incidence of type 2 diabetes. CONCLUSIONS: These findings are consistent with the hypothesis that type 2 diabetes is programmed in utero in association with low rates of fetal growth. The increased risk for type 2 diabetes associated with small size at birth is further increased by high growth rates after 7 years of age.

Adolescent↗
PubMed2000

Low birth weights contribute to high rates of early-onset chronic renal failure in the Southeastern United States.

BACKGROUND: The southeastern United States is a region in which rates of cardiovascular and renal diseases are excessive. Within the Southeast, South Carolina has unusually high rates of end-stage renal disease (ESRD) in young people, with more than 70% of cases attributed to hypertension and diabetes. OBJECTIVE: To determine whether the increased vulnerability to early-onset ESRD might originate through impaired renal development in utero as measured by low birth weight. METHODS: Patients who were diagnosed with renal failure and undergoing dialysis from 1991 through 1996 were identified from the ESRD registry maintained by the Southeastern Kidney Council, Raleigh, NC. Birth weights reported on birth certificates were selected for the ESRD cases and non-ESRD controls who were born in South Carolina in 1950 and later. Birth weights were compared for 1230 cases and 2460 controls who were matched for age, sex, and race. RESULTS: Low birth weight was associated with ESRD among men and women as well as blacks and whites. Among people whose birth weight was less than 2.5 kg, the odds ratio for ESRD was 1.4 (95% confidence interval, 1.1-1.8) compared with people who weighed 3 to 3.5 kg. This association was present for renal failure resulting from diabetes, hypertension, and other causes. CONCLUSIONS: Low birth weights, which reflect adverse effects on development in utero, contribute to the early onset of ESRD in South Carolina. Since low birth weight increases the risk of ESRD from multiple causes, the data suggest that an adverse environment in utero impairs kidney development and makes it more vulnerable to damage from a range of pathological processes.

Adult↗