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The authors examine the cross-sectional and longitudinal relation of smoking habits and current alcohol intake to cognitive status and decline over a 3-year period as well as the extent to which these relations are modified by the presence of clinical conditions indicating atherosclerosis (cardiovascular disease (CVD)/diabetes). Data are from the cohort of men followed in the longitudinal Zutphen Elderly Study in 1990 (n = 489) and 1993 (n = 333). Cognitive function was measured in 1990 and 1993 with the 30-point Mini-Mental State Examination (MMSE). After adjustment for age, education, and alcohol intake, current smokers made 20% more errors on the MMSE than never smokers in the cross-sectional analyses. Cognitive decline was greatest in those with CVD/diabetes who currently smoked and never smoked (-1.9 and -1.3 points, respectively). After adjustment for age, education, and smoking status, men with CVD/diabetes and low-to-moderate alcohol intake had a significantly lower risk for poor cognitive function (MMSE < or = 25) than abstainers (odds ratios of 0.3 for less than one drink and 0.2 for one to two drinks per day). Alcohol intake was not associated with cognitive decline. These findings do not support the hypothesis of a protective effect of smoking on cognitive function; they suggest that smoking may be harmful among those with CVD/diabetes. Alcohol may result in an acute beneficial effect on cognitive function among those with CVD/diabetes. However, selection bias and unmeasured confounding should be of concern when evaluating these results.
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PMID:Smoking, drinking, and thinking. The Zutphen Elderly Study. 856 Nov 55

Cognitive impairment is highly prevalent among the elderly. Subjects with disturbed glucose metabolism may be at risk of impaired cognitive function, as these disturbances can influence cognition through atherosclerosis, thrombosis and hypertension. We therefore studied the cross-sectional association of cognitive function with hyperinsulinaemia, impaired glucose tolerance and diabetes mellitus in a population-based cohort of 462 men aged 69 to 89 years. Cognitive function was measured by the 30-point Mini-Mental State Examination. Results were expressed as the rate ratio (95% confidence interval) of the number of erroneous answers given on the Mini-Mental State Examination by the index compared to the reference group. Compared to subjects with normal glucose tolerance, known diabetic patients had a rate ratio of 1.23 (1.04-1.46), newly-diagnosed diabetic patients of 1.16 (0.91-1.48) and subjects with impaired glucose tolerance of 1.18 (0.98-1.41), after adjustment for confounding due to age, occupation and cigarette smoking (p-trend = 0.01). Non-diabetic subjects in the highest compared to the lowest quartile of the area under the insulin curve had a rate ratio of 1.24 (1.03-1.50), after adjustment for confounding (p-trend = 0.02). The results did not change appreciably when potentially mediating factors, including cardiovascular diseases and risk factors associated with the insulin resistance syndrome, were taken into account. These results suggest that diabetes, as well as impaired glucose tolerance and hyperinsulinaemia in non-diabetic subjects are associated with cognitive impairment.
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PMID:Glucose intolerance, hyperinsulinaemia and cognitive function in a general population of elderly men. 859 25

Hypoglycaemia may cause transient cognitive impairment and neurological deficits that are frequently unilateral. The effect of mild hypoglycaemia (serum glucose level 3.4 +/- 0.1 mmol/l; mean +/- SEM) on regional cerebral blood flow and cerebrovascular resistance was studied in eight right-handed children with insulin-dependent diabetes mellitus (age 14.9 +/- 0.7 years; diabetes duration 7.4 +/- 1.1 years; six males) using the intravenous xenon-133 clearance method. Global mean cerebral grey and white matter blood flow, adjusted to mean pCO2 of cohort, showed a trend towards an increase from 54.7 +/- 3.5 ml.100 g-1.min-1 at baseline euglycaemia to 58.0 +/- 4.1 ml.100 g-1.min-1 during hypoglycaemia (p = 0.075). Statistically significant changes were seen in global mean cerebral grey matter blood flow, as indexed by initial slope, which increased from 88.0 +/- 6.5 min-1 before hypoglycaemia to 96.3 +/- 7.2 min-1 during hypoglycaemia (p < 0.05). Cerebral grey matter blood flow was significantly higher in the right hemisphere compared to the left during hypoglycaemia (p < 0.01) but not at baseline euglycaemia. Measurements of global cerebrovascular resistance showed a borderline decrease from 1.64 +/- 0.11 to 1.54 +/- 0.11 mm Hg.ml-1.100 g-1.min-1 (p < 0.09). In conclusion, mild hypoglycaemia is associated with increases in cerebral blood flow which are greater in grey matter flow indices and in the right hemisphere. We speculate that asymmetrical cerebral blood flow changes may explain the frequent laterality of neurological deficits during severe hypoglycaemia.
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PMID:Regional cerebral blood flow during hypoglycaemia in children with IDDM. 859 24

To ascertain whether diabetes in elderly people is associated with cognitive impairment, we offered all residents of Melton Mowbray aged 75, 80 and 85 years both a modified glucose tolerance test (1985 WHO criteria) and Folstein mental state examination (MMSE, 23/24 cut-off). Analysis of the results, stratified by age, revealed that subjects with known diabetes were more likely than normal subjects to have low MMSE [odds ratio 3.30 (95% CI 1.3 to 8.5)], whilst newly found diabetic subjects were less likely to have low MMSE [odds ratio 5(-14) (95% CI 9(-25) to 0.003)]. The difference between known and newly found diabetic subjects might relate to duration of diabetes. The increased frequency of cognitive impairment in known diabetic subjects may be pertinent to the safe use of hypoglycaemic agents.
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PMID:Diabetes and cognitive impairment: a community-based study of elderly subjects. 866 47

To test the hypothesis that glycemic thresholds for hypoglycemic cognitive dysfunction, like those for neuroendocrine responses to and symptoms of hypoglycemia, shift to lower plasma glucose concentrations after recent antecedent hypoglycemia, 16 healthy young adult subjects (7 women and 9 men) were studied on two separate occasions in random sequence, once with hyperinsulinemic hypoglycemia (2.6 +/- 0.1 mmol/l, 47 +/- 1 mg/dl) and once with otherwise identical hyperinsulinemic euglycemia (4.8 +/- 0.1 mmol/l, 86 +/- 5 mg/dl) between 1430 and 1630. Neuroendocrine, symptomatic, and cognitive responses to hyperinsulinemic stepped hypoglycemic (4.7, 4.2, 3.6, 3.0, 2.8, 2.5, and 2.2 mmol/l; 85, 75, 65, 55, 50, 45, and 40 mg/dl) clamps were quantitated the following morning on both occasions. Cognitive function tests included measures of information processing (Serial Addition), attention (Stroop Arrow Word), pattern recognition and memory (Delayed Non-Match to Sample), and declarative memory (Paragraph Recall). As expected, plasma glucagon (P = 0.0094), epinephrine (P = 0.0063), and pancreatic polypeptide (P = 0.0046) responses to stepped hypoglycemia were reduced significantly, and symptomatic responses tended to be reduced after afternoon hypoglycemia. Performance on the cognitive function tests deteriorated (P < 0.0001) during stepped hypoglycemic clamps, but there were no significant overall effects of antecedent hypoglycemia on hypoglycemic cognitive dysfunction. Although deterioration was reduced (P < 0.05) from the 2.8 mmol/l (50 mg/dl) to the 2.5 mmol/l (45 mg/dl) steps on the Serial Addition and Delayed Non-Match to Sample tasks after afternoon hypoglycemia, comparable differences were not found on the Stroop Arrow Word or Paragraph Recall tasks. Thus, glycemic thresholds for hypoglycemic cognitive dysfunction, unlike those for neuroendocrine responses to and symptoms of hypoglycemia, do not seem to shift to substantially lower plasma glucose concentrations after recent antecedent hypoglycemia in nondiabetic humans.
Diabetes 1996 Aug
PMID:Impact of recent antecedent hypoglycemia on hypoglycemic cognitive dysfunction in nondiabetic humans. 869 Jan 48

Severe hypoglycaemia with cognitive dysfunction is 3 times more common in intensively, rather than conventionally, treated insulin-dependent diabetes mellitus (IDDM). To investigate the effect of diabetes control on higher brain function during acute hypoglycaemia, we studied one of the earliest detectable changes in cognitive function, i.e. the four-choice reaction time, and symptomatic and hormonal responses during euglycaemic and hypoglycaemic clamping in human subjects. There were no changes in symptoms or counterregulatory hormones and four-choice reaction time was stable during 220 min of euglycaemic insulin clamping in five men with IDDM, with a coefficient of variation of less than 2.2% (1% for accuracy) for the cognitive function test. During stepped hypoglycaemic clamping however, hormonal responses and subjective awareness of hypoglycaemia occurred in all groups but started at much lower blood glucose concentrations in eight intensively-treated diabetic subjects (Group 1) than in ten conventionally-treated (Group 2) or in eight non-diabetic subjects (Group 3). For example, for adrenaline, plasma glucose thresholds were 2.7 +/- 0.2 vs 3.4 +/- 0.2 and 3.2 +/- 0.1 mmol/l, respectively, p < 0.05, Group 1 vs Groups 2 or 3 and for subjective awareness of hypoglycaemia 2.3 +/- 0.2 vs 3.0 +/- 0.1 and 3.2 +/- 0.1 mmol/l, p < or = 0.003), as in previous studies. In contrast, deterioration in reaction time occurred at 3.2 +/- 0.3, 3.2 +/- 0.2 and 3.0 +/- 0.2 mmol/l, respectively (p = NS), thus occurring at higher glucose levels than subjective awareness in the intensively-treated subjects only. The altered hierarchy of responses to hypoglycaemia in well-controlled intensively-treated diabetes explains the increased risk of severe hypoglycaemia without warning seen in such patients.
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PMID:Lack of preservation of higher brain function during hypoglycaemia in patients with intensively-treated IDDM. 878 14

Considering the nervous system as a unit, it might be expected that diabetic patients with autonomic neuropathy could have a central abnormality expressed as cognitive dysfunction. To determine whether autonomic neuropathy is independently associated with cognitive dysfunction, we studied a cross-section of 20 non-insulin-dependent diabetic patients with autonomic neuropathy (14 males and six females; age (mean) = 60 + or - 1 years); 29 non-insulin-dependent diabetic patients without autonomic neuropathy (14 males and 15 females; age = 59 + or - 1 years) and 34 non-diabetic patients (10 males and 24 females; age = 58 + or - 1 years), matched by age, education and duration of disease. Cognitive function was evaluated by tests of immediate, recent and remote memory: verbal (digit span; word span) and visual (recognition of towers and famous faces). Diabetic patients with autonomic neuropathy scored (median) lower in visual memory tests than diabetic patients without autonomic neuropathy and controls (towers immediate = 5 versus 7 and 6; towers recent = 4 versus 6 and 6; faces = 16 versus 18 and 18; respectively; Kruskal-Wallis; P < 0.05). There was no difference in verbal memory performance (Kruskal-Wallis; P > 0.05). Entering age, education, duration of disease and fasting plasma glucose in a stepwise multiple regression, the performance in these tests remained associated with autonomic neuropathy (towers immediate, P = 0.0054, partial r2 = 0.166; towers recent, P = 0.0076, partial r2 = 0.163). Scores in visual tests correlated negatively with the number of abnormal cardiovascular tests (faces, r = -0.25; towers recent, r = -0.24; Spearman; P < 0.05). Decreased visual cognitive function in non-insulin-dependent diabetic patients is associated with the presence and degree of autonomic neuropathy.
Diabetes Res Clin Pract 1995 Nov
PMID:Memory dysfunction and autonomic neuropathy in non-insulin-dependent (type 2) diabetic patients. 883 30

The risk of hypoglycaemia and the resulting impairment in brain function are major factors preventing those with diabetes achieving normoglycaemia. The need to define these risks more precisely has prompted an increasing research effort to identify which aspects of cerebral function are particularly vulnerable and at which glucose level. Much of the evidence is inconsistent, reflecting not only the wide range of methods for measuring cognitive function and inducing hypoglycaemia, but also the inherent variability of the response. Nevertheless, the data suggest that those mental activities which are relatively undemanding are often unaffected at all levels of experimental hypoglycaemia while the performance of more complex tasks deteriorates at glucose concentrations of around 3 mmol l-1. The relative imprecision of cognitive testing is reflected in the debate which surrounds the pathogenesis of hypoglycaemia unawareness. There is some evidence that the glycaemic threshold for autonomic activation and symptoms can vary while the threshold for cognitive impairment is fixed. This has led to the hypothesis that hypoglycaemia unawareness arises when the autonomic response develops at a blood glucose below that for impaired cognition, thus preventing patients from recognizing or responding to their usual symptoms. However, contradictory data suggest that the threshold for cognitive impairment can alter in line with the autonomic response, a conclusion which falls to fit either the above hypothesis or the clinical description of hypoglycaemia unawareness. These differences may be methodological or relate to the relative imprecision of measurements of cognitive function. Resolution of these discrepancies may have to await the development of advanced technology such as high resolution MRI or PET scanning. In the meantime, progress could be made if all groups agreed on a limited range of cognitive function tests and used them in a standardized manner.
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PMID:The measurement of cognitive function during acute hypoglycaemia: experimental limitations and their effect on the study of hypoglycaemia unawareness. 884 93

Carer-assisted clean intermittent urethral catheterisation is an effective and safe treatment option for persistent urinary retention in a study of 56 elderly female patients (aged 65 years and above) with cognitive impairment and other disabilities. With this method of treatment, 54% of the patients were able to void spontaneously and were continent after a median period of 6 weeks with a range of 1 to 40 weeks. Twenty-seven per cent had significant improvement in the symptoms of urinary incontinence and the residual urine volumes became progressively smaller. However, 19% failed the programme. The recovery of spontaneous voiding was found to be significantly influenced by the age of the patient, the carer performing the intermittent catheterisation and the development of catheter-related urinary tract infection. Twenty-five per cent of the study patients developed symptomatic urinary tract infection which was associated with a delay in the recovery of spontaneous voiding. Its development was also found to be significantly associated with the presence of pre-existing diabetes mellitus, the person doing the catheterisation, the presence of dementia and with more predisposing common medical conditions.
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PMID:Carer-assisted intermittent urethral catheterisation in the management of persistent retention of urine in elderly women. 889 31

Dehydroepiandrosterone (DHEA; prasterone) is a major adrenal hormone with no well accepted function. In both animals and humans, low DHEA levels occur with the development of a number of the problems of aging: immunosenesence, increased mortality, increased incidence of several cancers, loss of sleep, decreased feelings of well-being, osteoporosis and atherosclerosis. DHEA replacement in aged mice significantly normalised immunosenescence, suggesting that this hormone plays a key role in aging and immune regulation in mice. Similarly, osteoclasts and lymphoid cells were stimulated by DHEA replacement, an effect that may delay osteoporosis. Recent studies do not support the original suggestion that low serum DHEA levels are associated with Alzheimer's disease and other forms of cognitive dysfunction in the elderly. As DHEA modulates energy metabolism, low levels should affect lipogenesis and gluconeogenesis, increasing the risk of diabetes mellitus and heart disease. Most of the effects of DHEA replacement have been extrapolated from epidemiological or animal model studies, and need to be tested in human trials. Studies that have been conducted in humans show essentially no toxicity of DHEA treatment at dosages that restore serum levels, with evidence of normalisation in some aging physiological systems. Thus, DHEA deficiency may expedite the development of some diseases that are common in the elderly.
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PMID:Dehydroepiandrosterone and diseases of aging. 889 25


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