Search

The hormone gastrin plays an important role in the regulation of acid secretion in the stomach which, in turn, stimulates the digestion of food. Previous studies reported that administration of beer and wine but not ethanol and spirits increases gastrin secretion in fasting volunteers. It is not known whether alcoholic beverages combined with a normal meal have an additional effect on the postprandial gastrin response. We therefore measured the gastrin response in eight volunteers who received either alcoholic beverages (40 g alcohol) in the form of beer, red wine or spirits, or mineral water as control in combination with a dinner. Two glasses were drunk before the meal, two glasses during the meal. Plasma gastrin concentrations were twofold increased at one hour after the dinner as compared to predinner values. However, no additional effect of beer, wine or spirits on this postprandial response was seen. The present study does not support the hypothesis that the consumption of beer or wine during a meal has a positive effect on the release of gastrin and therefore most probably does not contribute to an improved digestion of food by stimulation of acid secretion.

In a double-blind trial, the effect on blood pressure of supplementation of normal milk (1180 mg Ca2+, 1650 mg K+ and 110 mg Mg2+ d-1) vs. 'mineral-poor' milk (95 mg Ca2+, 580 mg K+ and 10 mg Mg2+ d-1) was studied. Young healthy normotensive female students consumed one of the two supplements while on a low calcium diet (less than 500 mg Ca2+ d-1) for a period of 6 weeks. In both the normal milk- and 'mineral-poor' milk-supplemented groups systolic blood pressure decreased slightly. However, this decrease was persistently greater in the milk-supplemented group. The individual mean systolic blood pressure change during normal milk treatment (-4.1%) was significantly greater (P = 0.03) than that during 'mineral-poor' milk treatment (-1.3%). An effect of normal milk supplementation on diastolic blood pressure could not be demonstrated. The results of the present study indicate a small hypotensive effect of milk consumption, which is attributable to its content of essential minerals.

Changes in platelet aggregation have often been proposed as an explanation for the protective effect of moderate alcohol consumption on the development of coronary heart disease, observed in epidemiological studies. To test the tenability of this assumption, the acute effect of moderate alcohol consumption on platelet aggregation was studied in eight healthy middle-aged men in a controlled study. The intake of alcohol consisted of two glasses of red wine at dinner and two glasses of distilled liquor (Hollands gin), combined with a snack, before bedtime. No acute effects of moderate alcohol consumption on platelet aggregation were observed.

Short-term effects of moderate alcohol consumption on platelet function, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were studied in two age groups of volunteers (20-30 and 45-55 years), each consisting of eight healthy males. The alcohol (30 g in red port and wine) was consumed during a standard dinner. Two blood samples were drawn: one in the postprandial phase, and one the next morning after fasting overnight. Alcohol consumption tended to increase platelet aggregation and production of hydroxy fatty acids, reduced plasma t-PA activity and increased PAI activity in the postprandial phase. After the overnight fast the effects on t-PA and PAI had disappeared whereas at that time alcohol consumption tended to decrease platelet function. The effects of alcohol on t-PA and PAI activity appeared mainly in the older age group, whereas the t-PA activity in this group was already much lower, irrespective of alcohol consumption.

Effects of a moderate dose of alcohol on blood lipids and lipoproteins were studied in volunteers of two age groups (20-30 and 45-55 years), each consisting of eight healthy men. The alcohol (30 g in red port and wine) was consumed during a standard dinner. Two blood samples were drawn: one in the postprandial phase, and one the next morning after fasting overnight. In the postprandial phase, one hour after intake, alcohol increased high-density lipoprotein cholesterol (HDL-C) by 11.5%, triglycerides (TG) by 15.3% and apolipoprotein A2 (Apo-A2) by 7.3% (P = 0.002, P = 0.044 and P = 0.024, respectively). The increase in HDL-C appeared to be mainly attributed to the HDL2-C subfraction which increased by 15.3% (P = 0.066). Furthermore, the increases in HDL-C, HDL2-C and TG were more pronounced in the middle-aged men then in the young men. After fasting overnight the effects of alcohol had disappeared.

The present report begins by comparing data on bone mineralization communicated in the literature to date with the authors' own previously published concept of the "three-phase model". The age-dependent accumulation of minerals in the femurs of Wistar rats was also chemically-analytically investigated. The results suggest that the mineral first formed is octacalcium phosphate. It is followed by sodium- and magnesium-containing phases. Maturation of octacalcium phosphate only occurs after this; it is converted into a highly carbon-deficient hydroxyapatite. During this conversion the molar Ca/P ratio rises from 1.33 to 2. However, the final value of 2 is not fully attained: this is attributable to the "turnover" activity of bone-metabolic processes. The paper concludes with a discussion of how the newly developed chemical method of determining bone turnover can be used to determine its vitality.