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Biomedical subjects

Clive Osmond

Publications and source records attributed to Clive Osmond.

At least 37 records · Page 2Linked to original sources
PubMed2005

Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood in the New Delhi birth cohort.

BACKGROUND: South Asians have a muscle-thin but adipose body phenotype and high rates of obesity-related disease. Adult body composition may be predictable in early life. OBJECTIVE: Anthropometric indexes of adult body composition were examined in relation to birth size and body mass index (BMI) during childhood. DESIGN: A population-based cohort of 1526 men and women aged 26-32 y in Delhi, India, who were measured sequentially from birth until 21 y of age were followed up. Adult weight, height, skinfold thicknesses, and waist and hip circumferences were measured. BMI and indexes of adiposity (sum of skinfold thicknesses), central adiposity (waist-hip ratio), and lean mass (residual values after adjustment of BMI for skinfold thicknesses and height) were derived. RESULTS: Mean birth weight was 2851 g. As children, many subjects were underweight-for-age (>2 SDs below the National Center for Health Statistics mean; 53% at 2 y), but as adults, 47% were overweight, 11% were obese, and 51% were centrally obese (according to World Health Organization criteria). Birth weight was positively related to adult lean mass (P < 0.001) and, in women only, to adiposity (P = 0.006) but was unrelated to central adiposity. BMI from birth to age 21 y was increasingly strongly positively correlated with all outcomes. BMI and BMI gain in infancy and early childhood were correlated more strongly with adult lean mass than with adiposity or central adiposity. Higher BMI and greater BMI gain in late childhood and adolescence were associated with increased adult adiposity and central adiposity. CONCLUSIONS: Birth weight and BMI gain during infancy and early childhood predict adult lean mass more strongly than adult adiposity. Greater BMI gain in late childhood and adolescence predicts increased adult adiposity.

Adipose Tissue↗
PubMed2005

Maternal body composition, offspring blood pressure and the hypothalamic-pituitary-adrenal axis.

We tested the hypothesis that women who are thin or have poor pregnancy weight gain have offspring with higher blood pressure and examined whether this link is mediated by increased secretion of cortisol. We studied a cohort of 388 children born in Kingston, Jamaica. From hospital records we obtained information about their mother's body mass index (BMI) and weight gain during pregnancy. At age 8.5 years we measured the children's fasting plasma cortisol concentrations and blood pressure and assessed their mother's anthropometry. There were no relationships between the mother's BMI or weight gain during pregnancy and offspring blood pressure. However, mothers with a greater subscapular to triceps skinfold thickness ratio (SSTR) had offspring with higher blood pressure (5.6 mmHg systolic and 3.7 mmHg diastolic increase per unit change in SSTR, P = 0.002 and P = 0.008 respectively). Fasting plasma cortisol concentrations correlated with the children's systolic (r = 0.33, P < 0.0001) and diastolic pressures (r = 0.12, P = 0.02) independently of age, gender, weight or socio-economic status and were also predicted by the mother's SSTR. These findings suggest that maternal truncal obesity rather than thinness is associated with raised blood pressure in the offspring, and that this link may be mediated by increased cortisol secretion.

Analysis of Variance↗
PubMed2005

Association of HLA class I and class II polymorphisms with age-related macular degeneration.

PURPOSE: To evaluate whether HLA genotypes are associated with age-related macular degeneration (AMD). METHODS: HLA class I-A, -B, and -Cw and class II DRB1 and DQB1 principal allele groups were genotyped in two stages: initially for principal allele groups in a cohort of 100 AMD cases and 92 control subjects, and then, in the next 100 cases and controls from the same cohort, for alleles or allele groups with P < 0.1 on initial typing. Genotype frequencies were compared by 2 x 2 contingency tables. The strongest associations for individual HLA alleles were calculated with two-locus stratification analysis and logistic regression for all possible pair-wise HLA combinations. Bonferroni corrections were applied for multiple measurements (P(c)). Each HLA allele was subjected to logistic regression for known AMD covariates. HLA immunohistochemistry for class I antigens was performed on elderly donor eyes. RESULTS: Allele Cw*0701 (P = 0.004, P(c) = 0.036) correlated positively with AMD, whereas alleles B*4001 (P = 0.003, P(c) = 0.027) and DRB1*1301(P = 0.001, P(c) = 0.009) were negatively associated. These HLA associations were independent of any linkage disequilibrium. Immunohistochemistry demonstrated differential HLA class I expression in choriocapillary endothelial cells. CONCLUSIONS: Significant positive and negative associations exist between HLA alleles and AMD. HLA polymorphisms influence the development of AMD, possibly via modulating choroidal immune function.

Aged↗
PubMed2004

Microalbuminuria in adults after prenatal exposure to the Dutch famine.

Maternal undernutrition during gestation is associated with an increase in cardiovascular risk factors in the offspring in adult life. The effect of famine exposure during different stages of gestation on adult microalbuminuria (MA) was studied. MA was measured in 724 people, aged 48 to 53, who were born as term singletons in a university hospital in Amsterdam, the Netherlands, around the time of the Dutch famine 1944 to 1945. Twelve percent of people who were exposed to famine in mid gestation had MA (defined as albumin/creatinine ratio >/=2.5) compared with 7% of those who were not prenatally exposed to famine (odds ratio 2.1; 95% confidence interval 1.0 to 4.3). Correcting for BP, diabetes, and other influences that affect MA did not attenuate this association (adjusted odds ratio 3.2; 95% confidence interval 1.4 to 7.7). The effect of famine was independent of size at birth. Midgestation is a period of rapid increase in nephron number, which is critical in determining nephron endowment at birth. Fetal undernutrition may lead to lower nephron endowment with consequent MA in adult life.

Albuminuria↗
PubMed2004

Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood.

BACKGROUND: The risk of type 2 diabetes mellitus is increased in people who have low birth weights and who subsequently become obese as adults. Whether their obesity originates in childhood and, if so, at what age are unknown. Understanding the origin of obesity may be especially important in developing countries, where type 2 diabetes is rapidly increasing yet public health messages still focus on reducing childhood "undernutrition." METHODS: We evaluated glucose tolerance and plasma insulin concentrations in 1492 men and women 26 to 32 years of age who had been measured at birth and at intervals of three to six months throughout infancy, childhood, and adolescence in a prospective, population-based study. RESULTS: The prevalence of impaired glucose tolerance was 10.8 percent, and that of diabetes was 4.4 percent. Subjects with impaired glucose tolerance or diabetes typically had a low body-mass index up to the age of two years, followed by an early adiposity rebound (the age after infancy when body mass starts to rise) and an accelerated increase in body-mass index until adulthood. However, despite an increase in body-mass index between the ages of 2 and 12 years, none of these subjects were obese at the age of 12 years. The odds ratio for disease associated with an increase in the body-mass index of 1 SD from 2 to 12 years of age was 1.36 (95 percent confidence interval, 1.18 to 1.57; P<0.001). CONCLUSIONS: There is an association between thinness in infancy and the presence of impaired glucose tolerance or diabetes in young adulthood. Crossing into higher categories of body-mass index after the age of two years is also associated with these disorders.

Adult↗
PubMed2004

Exercise protects against glucose intolerance in individuals with a small body size at birth.

BACKGROUND: Small body size at birth is a risk factor for Type 2 diabetes. We investigated whether regular exercise is related to lower rates of glucose intolerance in individuals with a small body size at birth and whether birth size affects exercise habits in adulthood. METHODS: Five hundred subjects aged 65-75 years with data on birth measurements underwent an oral glucose tolerance test. They reported their weekly exercise frequency and intensity and yearly physical leisure time activity. RESULTS: Frequent (> or = 3/week) or moderate weekly exercise and yearly physical activity were all related to lower rates of glucose intolerance. This effect was, however, dependent on birth size, being strongest among subjects with a small body size at birth (birth weight < or = 3000 g and/or ponderal index < or = 26 kg/m3). Among men, frequency (P = 0.033) and intensity (P = 0.030) of exercise as well as yearly physical activity (P = 0.005) correlated inversely with birth size. CONCLUSIONS: Subjects predisposed to Type 2 diabetes due to a small birth size are strongly protected from glucose intolerance by regular exercise. Although a small body size at birth is related to a smaller muscle mass in adulthood, men born thin exercised more in adulthood than those not born thin. In these elderly subjects this might indicate the survival of the fittest.

Aged↗
PubMed2004

Size at birth, the metabolic syndrome and 24-h salivary cortisol profile.

OBJECTIVE: Individual variation in hypothalamic-pituitary-adrenal axis (HPAA) function has been suggested to be important in linking small size at birth with adult cardiovascular disease and its risk factors, in particular the metabolic syndrome. Human studies have, however, so far only been performed in clinic settings, and their results have not been consistent. Our aim was to assess whether HPAA activity in everyday living circumstances is related to the metabolic syndrome and size at birth. DESIGN: Clinical birth cohort study. SUBJECTS: A total of 151 women born between 1924 and 1933 in Helsinki, Finland, with measurements at birth recorded. The subjects had previously undergone detailed clinical examinations including fasting cortisol measurement and 1 micro g ACTH1-24 and overnight 0.25 mg dexamethasone tests. MEASUREMENTS: Salivary cortisol concentration was measured during a normal 24-h period: at awakening, 15 and 30 min thereafter, at 12.00 h, 17.00 h and 22.00 h and the following morning. In addition, the following summary variables were calculated: awakening response (mean of the three awakening measurements), mean of all individual measurements, and mean, SD and contrast (a measure of blunted diurnal variability, calculated as mean of morning minus mean of 1200, 1700 and 2200) of all individual z scores. RESULTS: Salivary cortisol awakening response was correlated with serum fasting (r = 0.17; P = 0.04), ACTH1-24-stimulated (r = 0.32; P < 0.0001), and dexamethasone-suppressed (r = 0.29; P = 0.0004) cortisol concentrations. However, no salivary cortisol measurement was associated with any component of the metabolic syndrome (waist circumference, serum triglyceride, HDL cholesterol or glucose concentration, or blood pressure). Moreover, no correlation was observed between salivary cortisol and weight, length, ponderal index, or gestational age at birth. CONCLUSIONS: In elderly women, cortisol concentrations in an everyday environment do not appear to be associated with the metabolic syndrome or size at birth. We propose that detecting relationships between HPAA function, prenatal events and adult disease might require a test involving HPAA stimulation.

Aged↗
PubMed2004

The infant growth of boys who later develop coronary heart disease.

BACKGROUND: The association between low birth-weight and coronary heart disease has been repeatedly shown. Only two previous studies have examined the effects of weight gain during infancy and later coronary heart disease. AIM: The aim of this study was to assess the association between infant growth and coronary heart disease in adult life. METHODS: 2345 men born at the Helsinki City Maternity Hospital during 1934-44 with information on birth size and growth during infancy and childhood were included in the study cohort. RESULTS: There was a 3-fold fall in hazard ratios for coronary heart disease between men who weighed < or = 8 kg at 1 year and those who weighed > 12 kg (P < 0.00001). The fall was steeper among men whose placental weight at birth was below average. Men born into families with low socio-economic status had lower weight gain during infancy and higher rates of coronary heart disease. The increased risk of coronary heart disease in men who grew slowly during infancy was greatest in those who had low placental weight at birth. CONCLUSIONS: Poor infant growth and small body size at one year predict coronary heart disease more strongly than low birth-weight.

Adult↗
PubMed2004

Interactions between peroxisome proliferator-activated receptor-gamma 2 gene polymorphisms and size at birth on blood pressure and the use of antihypertensive medication.

OBJECTIVE: The combination of small birth size and the Pro12Pro variant of the peroxisome proliferator-activated receptor-gamma 2 (PPAR-gamma 2) gene has been shown to be associated with insulin resistance, which is linked to hypertension. We examined whether the association between small body size at birth and adult blood pressure is modulated by PPAR-gamma 2 gene polymorphism, and whether the use of any class of antihypertensive medication is related to birth size. DESIGN AND METHODS: A total of 500 subjects from an original epidemiological cohort of 7086 men and women aged 65-75 years attended a clinical study. Two hundred and eight of them (73 men and 135 women) were taking antihypertensive medication and are included in this study. The Pro12Ala polymorphism of the PPAR-gamma 2 gene was determined using the polymerase chain reaction single-strand conformation polymorphism method. RESULTS AND CONCLUSIONS: Hypertensive subjects with low birth weight or short length at birth and the Pro12Pro variant had raised systolic blood pressure. We suggest that insulin resistance enhances the regulatory responses of the renin-angiotensin system, leading to raised blood pressure levels. Those hypertensive subjects who had small birth size and the Pro12Pro variant tended to use angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers (ACEI/ARB). This could be because insulin resistance interacts with the renin-angiotensin system in ways that make ACEI/ARB an effective therapy. Alternative explanations include more severe and treatment resistant hypertension, leading to application of ACEI/ARB, or co-morbid conditions, such as myocardial infarction and type 2 diabetes, known to be linked to low birth weight.

Aged↗
PubMed2004

The association of the K121Q polymorphism of the plasma cell glycoprotein-1 gene with type 2 diabetes and hypertension depends on size at birth.

Birth weight and length serve as indicators of the intrauterine environment, and a small body size at birth is a predictor of type 2 diabetes and hypertension. Insulin is one of the growth factors regulating fetal growth. The plasma cell glycoprotein 1 (PC-1) gene impairs insulin signaling at the insulin receptor level. Therefore, we investigated whether the K121Q polymorphism of the PC-1 gene association with insulin sensitivity, insulin levels, and the prevalence of diabetes and hypertension in adult life depends on size at birth in 489 subjects born in Helsinki during 1924-1933. We found that the effect of the PC-1 gene polymorphism on insulin levels and insulin sensitivity, measured as the homeostasis model assessment for insulin resistance, depended on birth length because fasting insulin levels and insulin resistance were highest in subjects carrying the 121Q allele who were small at birth (P for interaction = 0.04 and 0.05). Additionally, in those whose birth length was up to 49 cm, the K121Q polymorphism of the PC-1 gene was associated with a 2-fold higher incidence of type 2 diabetes. Moreover, subjects who were short at birth and who had the 121Q allele had the highest incidence (31.6%) of type 2 diabetes together with hypertension. We conclude that the interaction between the K121Q polymorphism of the PC-1 gene and birth length affects insulin sensitivity and increases susceptibility to type 2 diabetes and hypertension in adulthood.

Aged↗
PubMed2004

The effects of the ACE gene insertion/deletion polymorphism on glucose tolerance and insulin secretion in elderly people are modified by birth weight.

The I allele of an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme gene (ACE) appears to be protective against the complications of type 2 diabetes. Low birth weight, a marker of an adverse intrauterine environment, is associated with higher rates of type 2 diabetes. We examined whether the ACE I/D polymorphism could explain or modify the association between low birth weight and adulthood glucose tolerance. We measured plasma glucose and insulin concentrations after an oral glucose challenge in a group of 423 men and women, ages 65-75 yr, with measurements at birth recorded. The presence of the I allele was associated with shorter duration of gestation (P = 0.006) and, relative to gestational age, higher birth weight (P = 0.008) and length (P = 0.02). The I allele was associated with lower glucose at 120 min (P = 0.04) and a greater insulin response (P = 0.03 for insulin at 30 min and P = 0.06 for insulin area under the curve) to a standard oral glucose tolerance test. However, the associations between the ACE genotype and adulthood insulin secretion were only present in people with low birth weight (P for interaction birth weight * ACE genotype on insulin at 30 min = 0.003 and on insulin area under the curve = 0.05). The ACE I allele is associated with shorter duration of gestation and higher birth weight. The association between the presence of the ACE I allele and increased indices of adult insulin secretion is confined to subjects with low birth weight. We suggest that these findings reflect interactions between genotype and intrauterine environment with resulting changes in gene expression.

Birth Weight↗
PubMed2003

Self-perpetuating effects of birth size on blood pressure levels in elderly people.

It has been suggested that essential hypertension is determined by 2 separate mechanisms: a growth-promoting process in childhood and a self-perpetuating mechanism in adult life. We report a clinical study of 500 people taken from a cohort of 7086 men and women who were born in Helsinki from 1924 to 1933, and whose body size at birth was recorded. As expected, blood pressure levels were inversely related to birthweight and birth length. These associations, however, were confined to the 213 people who had previously been diagnosed as having hypertension. In them, a 1-kg increase in birthweight was associated with a 6.4-mm Hg (95% confidence interval, 1.0 to 11.9) decrease in systolic blood pressure recorded at the clinic, and with a 9.3-mm Hg (95% confidence interval, 2.1 to 16.5) decrease recorded by ambulatory measurement. We conclude that pathological processes initiated in utero become self-perpetuating in adult life and lead to hypertension. Among elderly people with established hypertension, these processes have a strong effect on blood pressure levels, because they are processes that do not respond well to treatment.

Aged↗
PubMed2003

Perceived health of adults after prenatal exposure to the Dutch famine.

People who were undernourished in early gestation are more obese, have a more atherogenic lipid profile, and altered blood coagulation and seem to have an increased risk of coronary heart disease. We now report on whether they also feel less healthy. We therefore assessed the perceived health of 50-year-old-men and women born alive as singletons around the time of the Dutch famine in the Wilhelmina Gasthuis in Amsterdam. People who had been exposed to famine in early gestation, but not those exposed in mid- or late gestation, more often rated their health as poor (10.3% vs. to 4.9% in the unexposed, odds ratio (OR) 2.2 [1.0, 4.8]). The effect of exposure to famine in early gestation on perceived health could only partly be explained by an increased prevalence of coronary heart disease, respiratory diseases, hypertension, type 2 diabetes, hypercholesterolaemia or cancer (adjusted OR 2.2 [0.9, 5.2]). Adjustment for adult risk factors (BMI, LDL/HDL cholesterol ratio, blood pressure, smoking, lung function) also attenuated the results to some extent (adjusted OR 1.9 [0.6, 5.5]). People who were exposed to famine in early gestation were not only less healthy in terms of objective measures of health but they also felt less healthy. Because poor perceived health is a strong predictor of mortality, we may expect increased mortality in people who were exposed to famine in early gestation in the future.

Adult↗
PubMed2003

The relationship among circulating insulin-like growth factor (IGF)-I, IGF-binding proteins-1 and -2, and birth anthropometry: a prospective study.

Fetal IGF-I is a determinant of birth weight, but whether maternal IGF-I plays a significant role is controversial. We sought to examine the relationships among maternal IGF-I, IGF-binding protein (IGFBP)-1, and IGFBP-2, with maternal and newborn anthropometry, in a cohort of 325 nondiabetic pregnant women of African origin. Blood was collected for IGF-I, IGFBP-1, and IGFBP-2 at 9, 25, and 35 wk gestation and in cord blood at delivery. In the second and third trimesters, maternal IGF-I was significantly correlated (P < 0.005) with maternal body mass index and triceps skinfold thickness. Maternal IGFBP-1 and -2 had an inverse correlation (P < 0.0001), with maternal anthropometry. Maternal IGF-I at 35 wk, and fetal IGF-I by cord blood were significantly correlated with birth weight (P = 0.001 and 0.048, respectively). IGFBP-1 in the third trimester and cord blood were negatively correlated with birth weight (P = 0.012 and 0.002). In multiple regression analyses, maternal IGF-I at 35 wk, fetal IGF-I, maternal weight at the first antenatal visit, gender, and gestational age were significant independent factors in the determination of birth weight. In conclusion, maternal IGF-I levels, especially during late pregnancy, positively influence birth weight.

Adolescent↗
PubMed2003

Serum insulin-like growth factor (IGF)-I and IGF-binding protein-1 in elderly people: relationships with cardiovascular risk factors, body composition, size at birth, and childhood growth.

The IGF system is important in regulation of fetal and childhood growth. In later life, IGF-I and IGF-binding protein-1 (IGFBP-1) have been implicated in the pathogenesis of arteriosclerosis. They are, thus, potential candidates in explaining the link between early growth and adult cardiovascular disease. We measured fasting serum IGF-I and IGFBP-1 concentrations in 394 men and women from a cohort of 7086 individuals, born between 1924 and 1933 in Helsinki, Finland, whose weight and height were recorded at birth and from 7 to 15 yr of age. They also underwent clinical examination, including measurement of body fat using bioimpedance, blood pressure, glucose tolerance, and plasma insulin and fibrinogen concentrations. Serum IGF-I was positively correlated with fasting glucose (r = 0.10, P = 0.06) and fibrinogen (r = 0.19, P = 0.0001) concentrations and blood pressure (systolic and diastolic r = 0.10, P </= 0.05) and inversely with percentage body fat (r = -0.13, P = 0.01) and waist circumference (r = -0.11, P = 0.03). IGFBP-1 was inversely correlated with adult body mass index (BMI) (r = -0.46, P < 0.0001), fasting glucose and insulin concentrations, and blood pressure. There were correlations between the adult level of IGFBP-1 and birth weight (r = 0.11, P = 0.03) and ponderal index (weight/length(3)) at birth (r = 0.13, P = 0.01), but IGF-I was not related to birth measurements. There were interactive effects between childhood height or BMI and adult BMI on IGF-I and IGFBP-1 in adulthood. Tall height and high BMI at 7 yr were associated with low IGF-I (P = 0.03 for height and P = 0.003 for BMI) and high IGFBP-1 (P = 0.02 and P = 0.06) in adulthood but only in those subjects whose current BMI was below median. On further analysis these interactive effects were particularly strong for height in childhood and adult lean BMI (lean body mass/height(2)). Among men and women of below-average lean BMI, tall height at 7 yr was associated with low adult IGF-I (P = 0.007) and high IGFBP-1 (P = 0.0004) concentrations [interaction (7-yr height x adult lean BMI); P = 0.008 for IGF-I and 0.001 for IGFBP-1]. There is no evidence that reduced fetal growth programs IGF-I concentrations in old age. An association between small size at birth and low IGFBP-1 concentrations may in part reflect fetal programming effects on insulin resistance. Given the anabolic effects of the GH-IGF-I axis, subjects with tall height in childhood but low adult lean body mass may be at risk of late-life GH-IGF-I axis dysfunction. Prospective studies should address whether this group is susceptible to type 2 diabetes, coronary heart disease, and osteoporosis.

Adolescent↗
PubMed2003

Birthsize, gestational age and adrenal function in adult life: studies of dexamethasone suppression and ACTH1-24 stimulation.

OBJECTIVE: Several studies show that low birthweight is associated with long-term alterations in the function of the hypothalamic-pituitary-adrenal axis (HPAA). We recently reported that the relationship between birthweight and fasting serum cortisol concentrations differed according to the gestational age of the babies, suggesting that both hypercortisolism and hypocortisolism could be a consequence of impaired fetal growth. We have now extended these findings by examining the relationship between birthweight, gestational age and tests of adrenal suppression and stimulation. DESIGN: Prospective birth cohort study. SUBJECTS AND METHODS: We studied 165 women (mean age 71.3 Years) born at term in Helsinki, Finland, between 1924 and 1933, whose body size and gestational age at birth were recorded. These women underwent an overnight 0.25 mg dexamethasone suppression test followed by a 1 microg ACTH(1-24) stimulation test. RESULTS: In all women combined, low birthweight was associated with lower total (P=0.03) and free (P=0.02) cortisol concentrations following dexamethasone. However, these relationships were dependent on gestational age at birth, interactions between the effects of birth size and gestational age on dexamethasone responsiveness being statistically significant. To demonstrate these interactions, we divided the study population into two groups according to gestational age. In subjects born at 40 weeks of gestation or more, low birthweight was strongly associated with enhanced dexamethasone suppression (P=0.003 for total and P=0.0004 for free cortisol), while in subjects born before 40 weeks of gestation there was no association. There was, however, no correlation between birth size and the adrenal response to ACTH(1-24). CONCLUSIONS: These findings reinforce our suggestions that events during prenatal life may lead to both up-regulation and down-regulation of the HPAA.

Adrenal Cortex↗
PubMed2003

Pathways of infant and childhood growth that lead to type 2 diabetes.

OBJECTIVE: Although a link between small body size at birth and later type 2 diabetes has been repeatedly documented, less is known about the associations between the disease and growth during infancy. The aim of this study was to explore the pathways of infant and early growth that lead to type 2 diabetes in adult life. RESEARCH DESIGN AND METHODS: We carried out a longitudinal study of 8760 subjects born in Helsinki from 1934 to 1944. On average, they had 8 measurements of height and weight between birth and 1 year of age and another 10 measurements between 1 and 12 years of age. We identified people with type 2 diabetes using a national register. RESULTS: Among babies whose birth weights were 3.5 kg, slow growth in length between birth and 3 months of age predicted later disease. Rapid gain in BMI after age 2 years increased the risk of later disease in both groups of babies, but this effect was greatest among children who had slow growth in length between birth and 3 months of age. In children whose Z-scores for length decreased, an SD increase in BMI at age 12 years was associated with an odds ratio (OR) for type 2 diabetes of 1.77 (95% CI 1.50-2.09). The corresponding OR in subjects whose Z-scores for length increased was 1.42 (95% CI 1.20-1.69). Rapid gain in childhood BMI was associated with high maternal BMI and socioeconomic factors (fewer people in the home and lower social class). CONCLUSIONS: Babies with above-average birth weights may develop type 2 diabetes later in life if poor living conditions lead to faltering growth in length in the first few months after birth. We speculate that growth faltering at this time is associated with lifelong impairment of insulin metabolism and inability to meet the challenge of rapid childhood increase in BMI.

Aged↗