1,721,020 research outputs found
Birth weight and the future development of diabetes a review of the evidence
No full textRecent studies in Europe, North America, and the developing world have shown that low birth weight and other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of glucose intolerance and NIDDM in adult life. Reduced fetal growth is also associated with a higher prevalence of the metabolic syndrome (in particular, hypertension and vascular disease) and with insulin resistance in adult life. Because birth size is determined largely by nongenetic factors, these findings have led to the 'fetal origins' hypothesis, which proposes that fetal adaptations to an adverse intrauterine environment that reduces fetal growth program lifelong physiological changes. These changes in turn predispose to diabetes and the metabolic syndrome. The mechanisms are unknown, but evidence from animal studies and preliminary human evidence suggests that adverse events in early life may influence the neuroendocrine development of the fetus. This results in long-term alterations in the setpoint of several major hormonal axes, including an increase in adrenal glucocorticoid secretion. These hormonal alterations may contribute to the predisposition to diabetes and the metabolic syndrome in people who were small at birth.</p
Iodine, milk, and the elimination of endemic goitre in Britain: the story of an accidental public health triumph
No full textOBJECTIVE: To determine how iodine deficiency and endemic goitre disappeared in Britain.DESIGN: Review of surveys of endemic goitre and iodine nutrition.MAIN RESULTS: Endemic goitre was widespread in Britain but has declined, most notably since the 1960's. Its disappearance was probably due to changes in farming practice, especially iodine supplementation in dairy herds which has resulted in iodine contamination of milk and dairy produce.CONCLUSIONS: Although iodization of dairy herds offers an indirect method of counteracting iodine deficiency, it is haphazard and there should be careful and continuous monitoring of iodine intakes in the population.</p
Relation of Fetal Growth to Adult Muscle Mass and Glucose Tolerance
No full textRecent studies show reduced fetal growth is associated with insulin resistance and a raised prevalence of glucose intolerance in adult life. Because early growth retardation in animal models leads to permanent changes in body composition and a reduction in the mass of muscle, a major insulin sensitive tissue, reduced adult muscle mass could explain the link between impaired fetal growth and glucose intolerance. To investigate this hypothesis, muscle mass has been determined in a group of men and women aged around 50 who were born in Preston, Lancashire and compared with their birthweight or body size at birth and their current insulin resistance and glucose tolerance. Subjects who had lower birthweights were shorter and lighter but their weight adjusted for height (BMI) was similar to that of other subjects. Much of the difference in weight was accounted for by a reduction in muscle mass. Muscle mass as estimated by the urinary creatinine excretion rose from 18.8% of body weight in women who had birthweights of 2.5 kg or less to 24.7% of bodyweight in those with birthweights of 3.4 kg or more. Trends in men were similar. Regression analysis showed that adult muscle mass was predicted by low birthweight (p = 0.004), low placental weight (p = 0.02), and small head circumference (p = 0.02) but not, however, by thinness at birth, the birth measurement most predictive of insulin resistance. In addition there were no significant relationships between muscle mass and insulin resistance or glucose tolerance in either men or women.(ABSTRACT TRUNCATED AT 250 WORDS)</p
Twins and the fetal origins hypothesis. Many variables differ between twins and singleton infants
No full textSeasonal variations in dietary iodine intake and thyrotoxicosis
No full textFood composition tables were used to estimate the iodine intake of 105 men and 112 women living in Cambridge who completed 7-day semi-weighed records of food consumption. Intakes in men ranged from 195 micrograms per day in summer to 306 micrograms in winter, and in women from 126 micrograms to 236 micrograms. Seasonal variations in intake were mainly due to seasonal differences in the iodine content of milk which varies directly in relation to farming practices. The authors speculate that a spring-summer peak in thyrotoxicosis incidence in Britain may be causally related to the high milk iodine levels in winter.</p
Iodine intake and excretion in two British towns: aspects of questionnaire validation
No full textOne hundred and eighty-nine women aged 25-64 years living in Preston and Southampton completed a postal questionnaire on their usual consumption of the major dietary sources of iodine. A subsample of 56 women collected 24-h urine specimens. Median iodine intakes based on the questionnaire responses and food consumption tables were 99 micrograms and 97 micrograms per day, respectively, but these figures rose to 105 micrograms and 118 micrograms when the women were given the opportunity to revise their original responses and analysed values for milk iodine were used. Median urinary iodine excretion (determined by the dry-ashing method) was 70 micrograms/day in Preston and 76 micrograms/day in Southampton. Although positive associations between intake and excretion were observed, the study lacked sufficient statistical power to validate the questionnaire as a measure of iodine intake. Some problems of questionnaire validation are discussed.</p
Current incidence of thyrotoxicosis and past prevalence of goitre in 12 British towns
No full textThe incidence of thyrotoxicosis was determined in a collaborative study in 12 towns in England and Wales. Cases were ascertained prospectively through biochemistry laboratories carrying out routine thyroid function tests. The annual incidence varied from 9.7 to 49.2 per 100 000. Reassay of sera at a reference laboratory showed that this variation did not result from inter-laboratory differences in the techniques for measuring thyroid function. The incidence of thyrotoxicosis was strongly correlated with the previous prevalence of endemic goitre in the towns. Current high dietary intakes of iodine--largely the result of milk contamination--may cause toxic nodular goitre in people made susceptible by a lack of iodine early in life. They may also contribute to the occurrence of Graves' disease.</p
Association between low birthweight and high resting pulse in adult life: is the sympathetic nervous system involved in programming the insulin resistance syndrome?
No full textTo test the hypothesis that elevated sympathetic nervous system (SNS) activity could be determined in utero and be one of the processes mediating the link between size at birth and insulin resistance and raised blood pressure in adult life, we have studied the resting pulse rate of 449 men and women aged 46 to 54 (mean 50) years born in Preston, Lancashire, England whose birth size was recorded in detail. The subjects were visited at home by trained fieldworkers who measured resting pulse rate and blood pressure using an automated recorder. The resting pulse rate ranged from 44 to 108 (mean 73) beats min(-1). It rose with increasing body mass index (r = 0.14, p = 0.003) and waist to hip ratio (adjusted for sex r = 0.10, p = 0.003) and correlated significantly with systolic and diastolic blood pressures (p = 0.001), fasting glucose (p = 0.02), split proinsulin (p = 0.001), and triglyceride concentrations (p = 0.02). The pulse rate fell progressively from 76 beats min(-1) among subjects who weighed 5.5 lb (2.5 kg) or less at birth to 71 beats min(-1) among those who weighed 7.5 lb (3.3 kg) or more (decline in pulse rate per kg increase in birthweight = 2.7, 95 % CI 0.6 to 4.8 beats min(-1). The association was independent of current body mass index, waist to hip ratio and of potential confounding variables including smoking, alcohol consumption, and social class. Although the resting pulse rate is an imperfect index of SNS activity, these findings are consistent with the hypothesis that elevated SNS activity established in utero is one mechanism linking small size at birth with the insulin resistance syndrome in adult life.</p
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