Unemployment and health impairments: Longitudinal analyses for the Federal Republic of Germany

In recent years many studies of unemployment and health haveshown that unemployed persons are in poorer health. However,one question remained unanswered: is the poorer health of theunemployed caused by unemployment Itself (causation hypotheses)or is it a result of selection processes, whereby people inpoor health are more likely to lose their job and less likelyto be re-employed (selection hypothesis)? Findings from a studybased on the longitudinal data of the German Socio-economicPanel (1984–1988, N=5, 516 persons, 18–64 years)are presented. All health indicators (health satisfaction, chronicillness, handicaps in fulfilling daily life tasks, disability)showed poorer outcomes for the unemployed persons, even aftercontrolling for the possible confounding effects of sodo-demographicvariables. Unemployed persons also consulted a physician morefrequently and were hospitalized more often. But longitudinalanalyses (of becoming unemployed and of re-employment) did notlend much support to the causation hypothesis. Instead, a constantlevel of health satisfaction for persons losing their job andfor the re-employed compared to their initial ratings supportedthe selection hypotheses. This means that in the Federal Republicof Germany persons in poorer health are more likely to losetheir jobs and persons in better health are more likely to bere-employed.     

THE SECRETION OF THYROTROPHIN WITH IMPAIRED BIOLOGICAL ACTIVITY IN PATIENTS WITH HYPOTHALAMIC–PITUITARY DISEASE

We describe here two patients with hypothyroidism due to pituitary-hypothalamic disease in whom basal thyrotrophin (TSH) levels measured by radioimmunoassay (RIA) were elevated yet when measured by a cytochemical bioassay (CBA) were found to be normal. This finding and the absence of the normal rise of thyroid hormones in response to thyrotrophin-releasing hormone (TRH) mediated release of TSH confirms for the first time the secretion of TSH with impaired biological activity. Primary thyroid disease as a cause for the elevated immunoreactive TSH was excluded by the absence of circulating thyroid antibodies and by a normal thyroidal radioiodine uptake response to exogenous TSH.     

Necrobiosis lipoidica in two diabetic sisters

Two sisters with diabetes mellitus have developed necrobiosis lipoidica within an interval of 14 years. Evidence is presented to suggest that inherited factors are involved in the aetiology of this uncommon skin disorder.     

The response of hepatic lipase and serum lipoproteins to acute hyperinsulinaemia in type 2 diabetes

Hepatic lipase has a putative role in the catabolism of HDL particles and, while its activity is dependent upon insulin in the rat, no such insulin responsiveness has been demonstrated in man. We studied 21 patients with type 2 diabetes to examine whether hepatic lipase activity was influenced by hyperinsulinaemia during a 2-4 h isoglycaemic clamp study. Acute changes in lipids, lipoproteins and apolipoproteins were also documented in pre- and post-clamp serum. Hepatic lipase activity during hyperinsulinaemia was compared with activity measured after an equivalent period without insulin. For comparison, nine non-diabetic subjects (matched for age and body mass index) underwent similar clamp studies. In the control experiment without insulin, hepatic lipase activity did not change significantly (mean 9.7 (range 2.3-22.3) in the morning and 9.9 (3.0-22.5) mmol h-1 l-1 in the afternoon, NS). In contrast, after the hyperinsulinaemic clamp, hepatic lipase activity fell significantly in diabetic subjects from 12.8 (4.4-30.6) to 10.4 (3.3-31.3) mmol h-1 l-1, P less than 0.0002 along with serum triglycerides and total and LDL cholesterol. The change in hepatic lipase activity was positively related to the fasting apoprotein B concentration (Spearman r = 0.54, P = 0.016). In the normal subjects, a similar decline in hepatic lipase activity was observed during hyperinsulinaemia (from 15.1 (9.8-32.7) to 12.6 (6.3-28.3) mmol h-1 l-1, P less than 0.01) along with decreases in total, HDL and LDL cholesterol, triglycerides and apoproteins A1 and B.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormalities of Glucose Tolerance Following Gestational Diabetes

Glucose tolerance and insulin secretion were studied in 56 women6–12 years following a pregnancy complicated by gestationaldiabetes, and in 23 matched controls. At recall 14 women wereknown to have diabetes and five were again pregnant with recurrentgestational diabetes. The early development of diabetes wasassociated with a fasting plasma glucose >6 mmol/l duringpregnancy and with a high plasma glucose response to oral glucosewhich persisted after delivery. Obesity was predictive of non-insulin-dependentdiabetes whereas those that later required insulin were notobese. At recall, seven of the remaining 37 women were foundto have unrecognized diabetes, 13 had impaired glucose tolerance(IGT) and 17 were normal by WHO criteria using a 75 g oral glucosetolerance test. In these 37 women, fasting plasma glucose andthe glucose response to oral glucose in pregnancy were not predictiveof subsequent diabetes or impaired glucose tolerance. Obesityin pregnancy and subsequent weight gain were associated withnon-insulin-dependent diabetes and impaired glucose toleranceat recall. Insulin deficiency was observed during the oral glucosetolerance test in the diabeties (the mean±SEM ratio insulinarea: glucose area 4.1±1.3 diabetics, 10.7±1.8controls, p<0.05), whereas in the group with impaired glucosetolerance insulin levels were high and in proportion to theirhyperglycaemia (insulin area: glucose area 10.9±1.4 1GT,9.4±1.4 controls). Women with normal glucose toleranceand previous gestational diabetes had significantly lower insulinresponses than their controls, despite mild hyperglycaemia (insulinarea: glucose area 4.0±0.7 normal glucose tolerance,7.6±1.1 controls, p<0.02). Abnormalities of glucosetolerance and insulin secretion are present following a gestationaldiabetic pregnancy. Gestational diabetes identifies women atrisk for developing diabetes and impaired glucose tolerance,both of which are risk factors for premature vascular disease.