Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial.

BACKGROUND: Epidemiologic studies have suggested that vitamin E and beta-carotene may each influence the development of prostate cancer. In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, a controlled trial, we studied the effect of alpha-tocopherol (a form of vitamin E) and beta-carotene supplementation, separately or together, on prostate cancer in male smokers. METHODS: A total of 29133 male smokers aged 50-69 years from southwestern Finland were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), both agents, or placebo daily for 5-8 years (median, 6.1 years). The supplementation effects were estimated by a proportional hazards model, and two-sided P values were calculated. RESULTS: We found 246 new cases of and 62 deaths from prostate cancer during the follow-up period. A 32% decrease (95% confidence interval [CI] = -47% to -12%) in the incidence of prostate cancer was observed among the subjects receiving alpha-tocopherol (n = 14564) compared with those not receiving it (n = 14569). The reduction was evident in clinical prostate cancer but not in latent cancer. Mortality from prostate cancer was 41% lower (95% CI = -65% to -1%) among men receiving alpha-tocopherol. Among subjects receiving beta-carotene (n = 14560), prostate cancer incidence was 23% higher (95% CI = -4%-59%) and mortality was 15% higher (95% CI = -30%-89%) compared with those not receiving it (n = 14573). Neither agent had any effect on the time interval between diagnosis and death. CONCLUSIONS: Long-term supplementation with alpha-tocopherol substantially reduced prostate cancer incidence and mortality in male smokers. Other controlled trials are required to confirm the findings.

Alpha-Tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance.

BACKGROUND: Experimental and epidemiologic investigations suggest that alpha-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and beta-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received beta-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of beta-carotene and vitamin A. PURPOSE: We examined the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. METHODS: A total of 29,133 men aged 50-69 years who smoked five or more cigarettes daily were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), alpha-tocopherol and beta-carotene, or a placebo daily for 5-8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of alpha-tocopherol and beta-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. RESULTS: No overall effect was observed for lung cancer from alpha-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87-1.13; P = .86, logrank test). beta-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02-1.33; P = .02, logrank test). The beta-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07-1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76-1.23) and in those with a higher alcohol intake (> or = 11 g of ethanol/day [just under one drink per day]; RR = 1.35; 95% CI = 1.01-1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85-1.24). CONCLUSIONS: Supplementation with alpha-tocopherol or beta-carotene does not prevent lung cancer in older men who smoke. beta-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. IMPLICATIONS: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose beta-carotene supplementation.

Properties of purified bovine milk lipoprotein lipase.

Lipoprotein lipase has been purified from bovine milk by affinity chromatography on Sepharose containing covalently linked heparin. In addition to an enzyme eluted by salt, further activity could be eluted with detergent. Rechromatography experiments suggested that the two activities were due to the same enzyme. This assumption was further verified by several other criteria as follows: (a) both require a serum activator, (b) their apparent molecular weights (55 000), their amino acid compositions and amino sugar contents were similar and (c) they had identical immunological reactivities. Thus, the enzyme appears to be bound to the heparin-Sepharose matrix by both salt-reversed and detergent-reversed interactions. Sodium deoxycholate stimulated the activity eluted by high salt, but had no effect on the detergent-eluted enzyme.

Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism.

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.

Effect of vitamin E and beta carotene on the incidence of primary nonfatal myocardial infarction and fatal coronary heart disease.

BACKGROUND: Oxidized low-density lipoprotein is involved in the pathogenesis of atherosclerosis. In epidemiological studies antioxidants have been inversely related with coronary heart disease. Findings from controlled trials are inconclusive. METHODS: We studied the primary preventive effect of vitamin E (alpha tocopherol) and beta carotene supplementation on major coronary events in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, a controlled trial undertaken primarily to examine the effects of these agents on cancer. A total of 27 271 Finnish male smokers aged 50 to 69 years with no history of myocardial infarction were randomly assigned to receive vitamin E (50 mg), beta carotene (20 mg), both agents, or placebo daily for 5 to 8 years (median, 6.1 years). The end point was the first major coronary event, either nonfatal myocardial infarction (surviving at least 28 days; n = 1204) or fatal coronary heart disease (n = 907). RESULTS: The incidence of primary major coronary events decreased 4% (95% confidence interval, -12% to 4%) among recipients of vitamin E and increased 1% (95% confidence interval, -7% to 10%) among recipients of beta carotene compared with the respective nonrecipients. Neither agent affected the incidence of nonfatal myocardial infarction. Supplementation with vitamin E decreased the incidence of fatal coronary heart disease by 8% (95% confidence interval, -19% to 5%), but beta carotene had no effect on this end point. CONCLUSIONS: Supplementation with a small dose of vitamin E has only marginal effect on the incidence of fatal coronary heart disease in male smokers with no history of myocardial infarction, but no influence on nonfatal myocardial infarction. Supplementation with beta carotene has no primary preventive effect on major coronary events.

Coronary heart disease incidence in NIDDM patients in the Helsinki Heart Study.

OBJECTIVE: To determine coronary heart disease (CHD) incidence among dyslipidemic subjects with non-insulin-dependent diabetes mellitus (NIDDM) and to assess the effect of lipid-modifying treatment on serum and lipoprotein lipids and the CHD incidence in these patients. RESEARCH DESIGN AND METHODS: Of the 4081 men participating in the Helsinki Heart Study, a coronary primary prevention trial with gemfibrozil in middle-aged men with high non-high-density lipoprotein (HDL) cholesterol (greater than 5.2 mM; 200 mg/dL), 135 had NIDDM at entry. The incidence of definite myocardial infarction and cardiac death and changes in serum and lipoprotein lipids were determined during the 5-yr trial in the NIDDM patients and compared with those observed in nondiabetic trial participants. RESULTS: Compared with nondiabetic subjects, NIDDM patients had lower HDL cholesterol (P less than 0.001), higher triglyceride concentration (P less than 0.0001), and greater body mass index (P less than 0.001), there were more hypertensive patients (P less than 0.001) among them. The incidence of myocardial infarction and cardiac death was significantly higher among diabetic than nondiabetic participants (7.4 vs. 3.3%, respectively, P less than 0.02). CHD incidence in the gemfibrozil-treated diabetic men (n = 59) was 3.4% compared with 10.5% in the placebo group (NS). In multivariate analysis, diabetes (P less than 0.05), age (P less than 0.0001), smoking (P less than 0.0001), low HDL cholesterol (P less than 0.05), and high low-density lipoprotein cholesterol (P less than 0.005) were independently related to CHD incidence. Gemfibrozil-induced serum and lipoprotein lipid changes in diabetic patients were similar to those observed in nondiabetic subjects. CONCLUSIONS: Compared with similarly dyslipidemic nondiabetic subjects, patients with NIDDM are at markedly increased risk of CHD. This elevated risk can be somewhat reduced by gemfibrozil.

A controlled trial on the effects of patient education in the treatment of insulin-dependent diabetes.

The effect of patient education on diabetic control in insulin-treated diabetic adults was studied in 77 subjects randomized into two groups: intensive patient education (group A) and control (group B). The subjects in group A received intensive patient instruction, both individually and in small groups, from a team of physicians, teaching nurses, and a dietitian. The patients in group B received a short instruction course consisting mainly of printed material. A highly significant improvement in diabetic control was observed in both groups immediately after the education programs, with gradual return to the original level during the following 3-6 mo. No difference was observed between the two groups in any of the measured parameters during the 18-mo investigation. Factors related to good control during the study included the length of school education, the quality of the control at the beginning of the study, and the high degree of self-confidence and lack of signs of anxiety in the psychological tests. The results demonstrate that the effects of educational programs are of limited value if they do not lead to permanent changes in attitudes and motivation, which are critical factors affecting long-term diabetic control.

Lack of correlation between serum dopamine-beta-hydroxylase activity and blood pressure in middle-aged men.

The activity of serum dopamine-beta-hydroxylase (DBH) was measured in 1194 asymptomatic middle-aged men with diastolic blood pressure ranging from 75 to 125 mm Hg during the baseline examination of a multifactorial intervention program for primary prevention of coronary heart disease. No correlation was present between serum DBH activity and systolic (r = -0.01, NS) or diastolic (r = +0.02, NS) blood pressure. No significant differences in serum DBH activity was observed between individuals with blood pressure in the lower, middle or upper deciles. Serum DBH activity was similar in subjects with normal blood pressure, in individuals with widely fluctuating blood pressure and in patients with fixed hypertension. The results suggest that serum DBH activity cannot be used as an aid in the diagnosis of essential hypertension of middle-aged men.

High-density lipoprotein cholesterol elevation with gemfibrozil: effects of baseline level and modifying factors.

The effects of baseline level and modifying factors on gemfibrozil-induced high-density lipoprotein (HDL) cholesterol elevation were studied in 1028 participants with good compliance in the Helsinki Heart Study. The absolute (mmol/L) increment in HDL cholesterol was independent of baseline when the change in the placebo group (regression toward the mean) was considered. In contrast, absolute reductions in low-density lipoprotein (LDL) cholesterol and triglycerides correlated with their baselines, relative percentage changes being constant. Statistically, this could indicate differences in the mode of action of gemfibrozil: an independent and additive effect on HDL cholesterol and a multiplicative effect on LDL cholesterol and triglycerides. These differences may have a physiologic background because the main effect of gemfibrozil is in the stable HDL3 subfraction, rather than in the variable HDL2. Only 13% of the variation in gemfibrozil-induced HDL cholesterol changes were explained by modifying factors. The basic assumptions in the uses of absolute or relative changes as a measure of treatment effect are discussed.

Selenium metabolism and platelet glutathione peroxidase activity in healthy Finnish men: effects of selenium yeast, selenite, and selenate.

The mean dietary selenium intake in Finland increased from 40 to 100 micrograms/d in 1987 because of the addition in 1985 of selenium to fertilizers. A selenium-supplementation study was performed in 1987 on the same men as were followed in a 1981 study that had a similar design (200 micrograms Se/d). Selenite and selenate, but not selenium yeast increased platelet glutathione peroxidase (GSHPx) activity by 30% compared with placebo, much less than the 70% found in the previous study. Selenium yeast and selenite increased plasma selenium after 11 wk from 1.39 mumol/L to peak values of 2.15 and 1.58 mumol/L, respectively. Only yeast selenium was incorporated into red cells. From a regression plot based on present and literature data, it was estimated that the plasma selenium concentration needed to achieve maximal platelet GSHPx activity was 1.25-1.45 mumol/L. At the present selenium intake in Finland, 100 micrograms/d, GSHPx activity is saturated in plasma and red cells and almost saturated in platelets.

Bioavailability of selenium to Finnish men as assessed by platelet glutathione peroxidase activity and other blood parameters.

Three groups of 10 men of low selenium status were given 200 micrograms Se/day as Serich wheat, Se-rich yeast, or sodium selenate for 11 wk. Twenty unsupplemented subjects served as controls. Plasma Se levels increased steadily in the wheat and yeast groups for 11 wk without plateauing, whereas in the selenate group, plasma Se plateaued around 110 ng/ml after 4 wk. Platelet glutathione peroxidase (GSH-Px) activities increased rapidly in the wheat and selenate groups for 4 wk and then plateaued. Platelet GSH-Px increased more slowly in the yeast group. Ten weeks after the supplements were discontinued, platelet GSH-Px was higher in the wheat and yeast groups than in the selenate group. Assessment of Se bioavailability requires a short-term platelet GSH-Px measurement to determine immediate availability, a medium-term plasma Se measurement to estimate retention, and a long-term platelet GSH-Px measurement after supplements are discontinued to determine the covertibility of tissue Se stores to biologically active Se.

Effects of alpha-tocopherol and beta-carotene supplements on cancer incidence in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study.

The Alpha-Tocopherol Beta-Carotene (ATBC) Cancer Prevention Study was a placebo-controlled, randomized intervention trial testing the hypothesis that beta-carotene and alpha-tocopherol (vitamin E) supplements prevent lung and other cancers. The study is predicated on a substantial body of evidence supporting a role in cancer prevention for these micronutrients. Based on the 2 x 2 factorial study design, 29,133 eligible male cigarette smokers aged 50-69 y were randomly assigned to receive beta-carotene (20 mg), alpha-tocopherol (50 mg), beta-carotene and alpha-tocopherol, or placebo daily for 5-8 y. Capsule compliance was high (median = 99%). beta-Carotene treatment did not result in a decrease in cancer at any of the major sites but rather in an increase at several sites, most notably lung, prostate, and stomach (number of cases 474 compared with 402, 138 compared with 112, and 70 compared with 56, respectively). The vitamin E group had fewer incident cancers of the prostate and colorectum compared with the group not receiving vitamin E (number of cases 99 compared with 151 and 68 compared with 81, respectively), but more cancers of the stomach (70 compared with 56). In contrast to these intervention-based findings for beta-carotene and vitamin E supplements, we observed lower lung cancer rates in men with higher amounts of both serum and dietary beta-carotene and vitamin E at baseline.

Toenail selenium as an indicator of selenium intake among middle-aged men in an area with low soil selenium.

Toenail selenium concentration has been proposed as a long-term (6-12 mo) indicator of human selenium status. This study investigated the association between toenail selenium concentration and selenium intake and other dietary factors among 166 urban men aged 55-69 y. The dietary information was collected by food records covering a 6-mo period. Toenail clippings were collected by mail 9-10 mo after food recording. The mean selenium intake from food was 42.5 micrograms/d and the dietary intake was equal to that of users and nonusers of selenium supplements. The mean toenail selenium concentration was 0.47 mg/kg. The mean selenium intake from supplements was 29.7 micrograms/d among supplement users. In the analysis of covariance the best predictors of toenail selenium concentration were selenium intake from supplements and food, and among supplement users dietary beta-carotene also.

Tissue stores of individual monounsaturated fatty acids and breast cancer: the EURAMIC study. European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast Cancer.

The strongest evidence that monunsaturated fat may influence breast cancer risk comes from studies of southern European populations, in whom intake of oleic acid sources, particularly olive oil, appears protective. No previous study has examined the relation of adipose tissue fatty acid content to breast cancer in such a population. We used adipose biopsies with diverse fat intake patterns gathered in 5 European centers, including southern Europe (Malaga, Spain), to test the hypothesis that stores of oleic acid or other monounsaturates are inversely associated with breast cancer. Gluteal fat aspirates were obtained from 291 postmenopausal incident breast cancer patients and 351 control subjects, frequency-matched for age and catchment area. Logistic regression was used to model breast cancer by monounsaturates, with established risk factors controlled for. Oleic acid showed a strong inverse association with breast cancer in the Spanish center. The odds ratio for the difference between 75th and 25th percentiles was 0.40 (95% CI: 0.28, 0.58) in Malaga and 1.27 (0.88, 1.85) in all other centers pooled, with a peak at 2.36 (1.01, 5.50) for Zeist. Palmitoleic and myristoleic acids showed evidence of an inverse association outside Spain, and cis-vaccenic acid showed a positive association in 3 centers. These data do not support the hypothesis that increasing tissue stores of oleic acid are protective against breast cancer in non-Spanish populations. This finding implies that the strong protective associations reported for olive oil intake in dietary studies may be due to some other protective components of the oil and not to the direct effect of oleic acid uptake. Alternatively, high olive oil intake may indicate some other protective aspect of the lifestyle of these women.

The effect of alpha-tocopherol and beta-carotene supplementation on colorectal adenomas in middle-aged male smokers.

Epidemiological and experimental studies have indicated that dietary factors such as vitamin C, vitamin E, and beta-carotene are associated with the risk of colorectal cancer. This study was carried out within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study), whose participants were randomly assigned to four supplementation groups: (a) alpha-tocopherol (AT), 50 mg/day; (b) beta-carotene (BC), 20 mg/day; (c) both AT and BC; and (d) placebo. We included the 15,538 ATBC Study participants who had been randomized within the areas of three major cities in southern Finland. Cases of colorectal adenoma (n = 146) were identified by the pathology laboratories in the study areas, and these participants' medical records were collected and reviewed. Alpha-tocopherol supplementation increased the risk for adenomas (relative risk, 1.66; 95% confidence interval, 1.19-2.32), whereas beta-carotene supplementation had no effect on the risk (relative risk, 0.98; 95% confidence interval, 0.71-1.35). Slightly more prediagnosis rectal bleeding and intestinal pain occurred in those adenoma cases who received alpha-tocopherol supplements than in those who did not. Thus, some bias may have resulted, with alpha-tocopherol supplementation leading to more colonoscopies and, thus, to an increased detection of incident polyps in this group. This is further supported by the trial finding that alpha-tocopherol supplementation did not increase the risk of colorectal cancer.

Tissue antioxidants and postmenopausal breast cancer: the European Community Multicentre Study on Antioxidants, Myocardial Infarction, and Cancer of the Breast (EURAMIC).

Antioxidants may protect against free radical mediated carcinogenesis. Epidemiological studies have not confirmed this hypothesis for breast cancer, possibly because of methodological limitations. Time-integrated exposure of alpha-tocopherol and beta-carotene in adipose tissue, and selenium in toenails was investigated in a case-control study among postmenopausal women, ages 50-74 years, from five European countries. The study group comprised 347 incident breast cancer cases and 374 controls. Mean antioxidant levels, adjusted for age and center, did not significantly differ for alpha-tocopherol (cases were 4.5% higher than controls), beta-carotene (3.0% lower), or selenium (1.8% lower). Odds ratios for highest versus lowest tertiles of exposure, adjusted for potential confounders, were 1.15 (95% confidence interval, 0.75-1.77), 0.74 (0.45-1.23), and 0.96 (0.63-1.47), respectively, without evidence for a decreasing trend. No statistically significant interactions were observed. Moreover, a provisional antioxidant score, indicating whether concentrations were above the median for zero, one, two, or all three antioxidants, yielded odds ratios of 1.00 (reference; all below median), 1.58, 1.58, and 1.21, respectively (chi2 for association = 4.00; P = 0.26). These results do not support the hypothesis that antioxidants are important determinants of this hormone-related malignancy among postmenopausal women.

Adipose tissue trans fatty acids and breast cancer in the European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast Cancer.

To investigate the relationship between trans fatty acids and postmenopausal breast cancer in European populations differing greatly in their dietary fat intakes, a case control study using adipose tissue stores of trans fatty acids as a biomarker of exposure was conducted. Subjects included 698 postmenopausal incident cases of primary breast cancer and controls randomly drawn from local population and patient registries, ages 50-74 Concentrations of individual trans fatty acids in gluteal fat biopsies were measured in these women. The adipose concentration of trans fatty acids showed a positive association with breast cancer. The covariate-adjusted association with breast cancer. The covariate-adjusted OR was 1.40 (95% confidence interval: 1.02, 1.93) for the difference between the 75th and 25th percentiles of total adipose trans. The adjusted OR for trans in the lowest tertile of polyunsaturated fatty acid reached 3.6 (2.2, 6.1). These associations were not attributable to differences in age, body mass index, exogenous hormone use, or socioeconomic status. These findings suggest an association of adipose stores of trans fatty acids with postmenopausal breast cancer in European women. They require confirmation in other populations, with concomitant consideration of the potential roles of dietary saturated and monounsaturated fats.

Fat composition of the infant diet does not influence subsequent serum lipid levels in man.

The serum lipid concentrations have been followed until 5 years of age in children fed for between 1 and 6 months with breast milk (n = 35), a home-prepared cow's milk formula (n = 17) or proprietary formula with a low content of cholesterol and high content of linoleic acid (n = 32). The serum cholesterol concentrations were significantly lower in the proprietary formula-fed infants than in the infants fed with breast milk or cow's milk formula between 2 and 6 months of age, i.e. during the period of formula feeding. No differences were observed between the 3 groups in serum lipid values after 9 months of age. A statistically significant correlation was observed between cholesterol concentrations recorded before 6 months and after 3 years of age in children fed initially with the proprietary low-cholesterol formula, but not in the two other groups. It is concluded that the fat composition of the infant diet commonly used in the developed countries affects the contemporary serum cholesterol concentration, but does not influence the serum lipid or lipoprotein levels later in life.

Lifestyle determinants of HDL2- and HDL3-cholesterol levels in a hypercholesterolemic male population.

In this cross-sectional study we investigated the role of lifestyle and other factors in determining serum HDL2- and HDL3-cholesterol levels among 82 dyslipidemic (total cholesterol minus HDL-cholesterol greater than or equal to 5.2 mmol/l) middle-aged participants of the Helsinki Heart Study. Alcohol consumption correlated positively with both subfractions of HDL-cholesterol, while leisure time physical activity had a significant correlation with the HDL3-subfraction only. HDL levels were lower in smokers than in non-smokers but the differences were not statistically significant. Using the multiple linear regression model, alcohol consumption emerged as the only significant factor influencing both HDL cholesterol subfraction levels. Leisure time physical activity had an independent contribution to HDL3-level, but lifestyle variables other than alcohol consumption did not contribute significantly to HDL2-cholesterol level. The model incorporating alcohol consumption, physical activity, smoking and relative body weight explained 13.4% of the variation in HDL2 and 17.5% in HDL3-cholesterol.

Effects of coffee and tea on lipoproteins and prostanoids.

The effects of coffee and tea on serum lipoproteins, plasma and urinary prostanoids and thromboxane production by platelets were studied in 12 healthy volunteers aged 33-45 years. They consumed daily, during 3 successive periods of 3 weeks, 8 cups of either instant coffee (16 g/d), instant tea (2.8 g/d) or rosehip 'tea'. The daily dose of coffee yielded 520 mg caffeine, that of tea 200 mg caffeine, while no caffeine was detected in the rosehip 'tea'. No differences were observed between the study periods in the total serum or serum lipoprotein (VLDL, LDL, HDL2, HDL3) cholesterol or triglyceride concentrations. Plasma and serum concentrations and urinary excretion of prostanoids (plasma and urinary TXB2, PGE2 and 6-keto-PGF1 alpha and serum TXB2) remained constant during the three study periods. These results suggest that coffee or caffeine do not exert any detectable effects on serum lipids in healthy normolipidaemic individuals.