Position specific physical performance and running intensity fluctuations in elite women's football.

The purpose of the present study was to investigate the physical performance of elite female football players during match play along with transient alterations in running performance following 1- and 5-min univariate peak periods. 54 elite female players from four top-level Norwegian teams were monitored for one season (n = 393 match observations), and physical performance data collected using STATSport GPS APEX. Results revealed significant differences in physical performance between the positions during full match play, particularly between wide and central players. Both full backs (FBs) and wide midfielders (WMs) covered more total distance (TD), high-speed running distance (HSRD), and sprint distance (SpD) than center backs (CBs) (p < 0.05-0.001), while WMs also covered more HSRD than both central midfielders (CMs) (p < 0.01) and forwards (FWs) (p < 0.05), and more acceleration -and deceleration distance (Accdist and Decdist ) than both CBs and CMs (p < 0.01-0.001). A similar pattern was observed for the peak period analysis, with FBs and WMs covering more SpD in peak 1 min than CBs and CM (p < 0.001) and more SpD in peak 5-min than CBs, CMs, and FWs (p < 0.001). Irrespective of the variable analyzed, greater distances were covered during the peak 5-min period than in the next-5 and mean 5-min periods (p < 0.001). Significant (p < 0.001), but small to trivial (Cohen's Dz : 0.07-0.20), decreases in distance covered were also observed for each variable following each univariate peak 5-min period. In conclusion, practitioners should account for differences in physical performance when developing training programs for female football players and be aware of transient reductions in physical performance following univariate peak 1- and 5-min periods. Specifically, the very high intensity in 1-min peak periods adds support to the principal of executing speed endurance activities during training to mirror and be prepared for the physical demands of match play.

Global Matrix 3.0 physical activity report card for children and youth: a comparison across Europe.

OBJECTIVES: The Global Matrix of report card grades on physical activity serves as a public health awareness tool by summarising the status of child and youth physical activity prevalence and action. The objectives were to: (1) provide a detailed examination of the evidence informing the 'School' and 'Community and Environment' indicators across all participating European Global Matrix 3.0 countries; (2) explore the comparability of the grades for these two indicators across Europe; (3) detail any limitations or issues with the methods used to assign grades; and (4) provide suggestions on how future grading of the indicators could be improved. STUDY DESIGN: A comparative review of published methods on the grading of Global Matrix 3.0 indicators across European countries. METHODS: Key documents relating to the European countries involved in the 2018 Global Matrix 3.0 were collated and a template used to extract data for both the 'School' and 'Community and Environment' indicators. RESULTS: Seventeen of the 20 European Report Card countries (85%) had a grade for schools, and 15 countries (75%) had a grade for community and environment. All countries considered between one and five factors when assigning the grade for these indicators. There were wide disparities in the number and sources of evidence used to assign the grades for both indicators, limiting the comparability of the evidence between different countries. CONCLUSION: To enable comparability, the authors recommend moving towards an agreed standardised set of metrics for grading each indicator. Furthermore, it would be useful to develop and share common tools, methods and instruments to collect data in a uniform way across countries, where possible. Such action will ultimately make the Global Matrix a more robust and useful tool for the future.

Glycemic index, glycemic load, dietary carbohydrate, and dietary fiber intake and risk of liver and biliary tract cancers in Western Europeans.

BACKGROUND: The type and quantity of dietary carbohydrate as quantified by glycemic index (GI) and glycemic load (GL), and dietary fiber may influence the risk of liver and biliary tract cancers, but convincing evidence is lacking. PATIENTS AND METHODS: The association between dietary GI/GL and carbohydrate intake with hepatocellular carcinoma (HCC; N = 191), intrahepatic bile duct (IBD; N = 66), and biliary tract (N = 236) cancer risk was investigated in 477 206 participants of the European Prospective Investigation into Cancer and Nutrition cohort. Dietary intake was assessed by country-specific, validated dietary questionnaires. Hazard ratios and 95% confidence intervals were estimated from proportional hazard models. HBV/HCV status was measured in a nested case-control subset. RESULTS: Higher dietary GI, GL, or increased intake of total carbohydrate was not associated with liver or biliary tract cancer risk. For HCC, divergent risk estimates were observed for total sugar = 1.43 (1.17-1.74) per 50 g/day, total starch = 0.70 (0.55-0.90) per 50 g/day, and total dietary fiber = 0.70 (0.52-0.93) per 10 g/day. The findings for dietary fiber were confirmed among HBV/HCV-free participants [0.48 (0.23-1.01)]. Similar associations were observed for IBD [dietary fiber = 0.59 (0.37-0.99) per 10 g/day], but not biliary tract cancer. CONCLUSIONS: Findings suggest that higher consumption of dietary fiber and lower consumption of total sugars are associated with lower HCC risk. In addition, high dietary fiber intake could be associated with lower IBD cancer risk.

Concentrations of IGF-I and IGFBP-3 and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition.

BACKGROUND: Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. METHODS: Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables. RESULTS: Neither circulating levels of IGF-I (OR=1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR=1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR=1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR=1.72, 95% CI 1.05-2.83; P-interaction=0.154). CONCLUSION: On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk.

Inflammation marker and risk of pancreatic cancer: a nested case-control study within the EPIC cohort.

BACKGROUND: Established risk factors for pancreatic cancer include smoking, long-standing diabetes, high body fatness, and chronic pancreatitis, all of which can be characterised by aspects of inflammatory processes. However, prospective studies investigating the relation between inflammatory markers and pancreatic cancer risk are scarce. METHODS: We conducted a nested case-control study within the European Prospective Investigation into Cancer and Nutrition, measuring prediagnostic blood levels of C-reactive protein (CRP), interleukin-6 (IL-6), and soluble receptors of tumour necrosis factor-α (sTNF-R1, R2) in 455 pancreatic cancer cases and 455 matched controls. Odds ratios (ORs) were estimated using conditional logistic regression models. RESULTS: None of the inflammatory markers were significantly associated with risk of pancreatic cancer overall, although a borderline significant association was observed for higher circulating sTNF-R2 (crude OR=1.52 (95% confidence interval (CI) 0.97-2.39), highest vs lowest quartile). In women, however, higher sTNF-R1 levels were significantly associated with risk of pancreatic cancer (crude OR=1.97 (95% CI 1.02-3.79)). For sTNF-R2, risk associations seemed to be stronger for diabetic individuals and those with a higher BMI. CONCLUSION: Prospectively, CRP and IL-6 do not seem to have a role in our study with respect to risk of pancreatic cancer, whereas sTNF-R1 seemed to be a risk factor in women and sTNF-R2 might be a mediator in the risk relationship between overweight and diabetes with pancreatic cancer. Further large prospective studies are needed to clarify the role of proinflammatory proteins and cytokines in the pathogenesis of exocrine pancreatic cancer.

Metabolic risk factors and skin cancer in the Metabolic Syndrome and Cancer Project (Me-Can).

BACKGROUND: Little is known about the associations of metabolic aberrations with malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). OBJECTIVES: To assess the associations between metabolic factors (both individually and combined) and the risk of skin cancer in the large prospective Metabolic Syndrome and Cancer Project (Me-Can). METHODS: During a mean follow-up of 12 years of the Me-Can cohort, 1728 (41% women) incident MM, 230 (23% women) fatal MM and 1145 (33% women) NMSC were identified. Most NMSC cases (76%) were squamous cell carcinoma (SCC) (873, 33% women). Hazard ratios (HRs) were estimated by Cox proportional hazards regression for quintiles and standardized z-scores (with a mean of 0 and SD of 1) of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and for a combined metabolic syndrome score. Risk estimates were corrected for random error in the measurements. RESULTS: Blood pressure per unit increase of z-score was associated with an increased risk of incident MM cases in men and women [HR 1·17, 95% confidence interval (CI) 1·04-1·31 and HR 1·18, 95% CI 1·03-1·36, respectively] and fatal MM cases among women (HR 2·39, 95% CI 1·58-3·64). In men, all quintiles for BMI above the reference were associated with a higher risk of incident MM. In women, SCC NMSC risk increased across quintiles for glucose levels (P-trend 0·02) and there was a trend with triglyceride concentration (P-trend 0·09). CONCLUSION: These findings suggest that mechanisms linked to blood pressure may be involved in the pathogenesis of MM. SCC NMSC in women could be related to glucose and lipid metabolism.

Diabetes mellitus, glycated haemoglobin and C-peptide levels in relation to pancreatic cancer risk: a study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

AIMS/HYPOTHESIS: There has been long-standing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development. Prospective epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism, overall and as a function of lag times between marker measurements (blood donation) and date of tumour diagnosis. METHODS: Pre-diagnostic levels of HbA(1c) and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospective Investigation into Cancer and Nutrition. Conditional logistic regression models were used to estimate ORs for pancreatic cancer. RESULTS: Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA(1c) levels up to an OR of 2.42 (95% CI 1.33, 4.39 highest [≥ 6.5%, 48 mmol/mol] vs lowest [≤ 5.4%, 36 mmol/mol] category), even for individuals with HbA(1c) levels within the non-diabetic range. C-peptide levels showed no significant relationship with pancreatic cancer risk, irrespective of fasting status. Analyses showed no clear trends towards increasing hyperglycaemia (as marked by HbA(1c) levels) or reduced pancreatic beta cell responsiveness (as marked by C-peptide levels) with decreasing time intervals from blood donation to cancer diagnosis. CONCLUSIONS/INTERPRETATION: Our data on HbA(1c) show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA(1c) levels, relatively independently of obesity and insulin resistance-the classic and major risk factors for type 2 diabetes. While there is no strong difference by lag time, more data are needed on this in order to reach a firm conclusion.

PIN diode driver for NMR and MRI.

Designing custom coils for magnetic resonance systems, such as nuclear magnetic resonance (NMR) spectrometers and magnetic resonance imaging (MRI) scanners, often entails using non-standard configurations of the transmit-receive (T/R) switch and Q-spoiling circuits. The built-in drivers of commercial NMR and MRI systems are, typically, only reconfigurable within a narrow application range (if at all). Thus, the built-in driver may not be able to properly control the custom T/R switches and Q-spoiling circuits when using custom built coils. We present a PIN diode driver which functions in both an MRI scanner and NMR spectrometer. The PIN diode driver is based on readily available discrete components and achieves switching times for the reverse and forward bias states (transmit on and off) of 2 µs and 0.4 µs respectively. Hence, this work enables a higher degree of customization of the RF switching circuits in an MR system and is potentially of interest for designers of custom coils for both NMR spectrometers and MRI scanners.

Drinking pattern and mortality in Danish nurses.

BACKGROUND/OBJECTIVE: Moderate alcohol consumption has beneficial effects on survival. Sex differences, however, have been suggested implying less beneficial effect among women. We examined the impact of alcohol consumed on weekdays and at weekends, respectively, on risk of death among women. SUBJECTS AND METHODS: At baseline in 1993, a total of 17 772 female members of the Danish Nurse Association completed questionnaires on alcohol intake and other lifestyle factors. The influence of alcohol intake on risk of death was analyzed using Cox proportional hazard model. RESULTS: Alcohol intake of 1-3 drinks per week was associated with the lowest risk of death. Intake above six drinks per weekend (Friday through Sunday) increased risk of death from all causes by 3% for each additional drink consumed per weekend (corresponding to an increased risk by 9% per drink per weekend day). Consumption of one or more drinks per weekday (Monday, Tuesday, Wednesday or Thursday) increased risk by 4% for each additional drink consumed per day. CONCLUSIONS: The results indicated an increasing risk of death for intake above six drinks per weekend and of one or more drinks per weekday.

Intake of wine, beer and spirits and risk of gastric cancer.

The objective was to study prospectively the relation between quantity and type of alcohol and risk of gastric cancer. In a pooled database from three population studies conducted in 1964-1992, a total of 15,236 men and 13,227 women were followed for a total of 389,051 person-years. During follow-up 122 incident cases of gastric cancer were identified. Total alcohol intake itself was not associated with gastric cancer, but type of alcohol seemed to influence risk. Compared with non-wine drinkers, participants who drank 1-6 glasses of wine had a relative risk ratio of 0.76 (95% confidence interval (CI) 0.50-1.16), whereas those who drank >13 glasses of wine per week had a relative risk ratio of 0.16 (95% CI 0.02-1.18). Linear trend test showed a significant association with a relative risk ratio of 0.60 (95% CI 0.39-0.93) per glass of wine drunk per day. These relations persisted after adjustment for age, gender, educational level, body mass index, smoking habits, inhalation and physical activity. There was no association between beer or spirits drinking and gastric cancer. In conclusion, the present study suggests that a daily intake of wine may prevent development of gastric cancer.

Type of alcohol and drinking pattern in 56, 970 Danish men and women.

OBJECTIVE: To describe drinking patterns among individuals who prefer drinking wine, beer or spirits. DESIGN: Cross-sectional study obtaining detailed information on intake of wine, beer and spirits and on frequency of alcohol intake. Adjustment for gender, age, smoking habits, educational attainment and body mass index. SETTING: Denmark. SUBJECTS: 27, 151 men and 29, 819 women, randomly selected from Copenhagen and Aarhus, Denmark. MAIN OUTCOME MEASURES: Drinking pattern-steady or binge drinking. RESULTS: A vast majority (71%) of both men and women preferred wine or beer. At all levels of total alcohol intake, beer drinkers were most likely to be frequent drinkers. Thus, light drinkers of beer had an odds ratio for being frequent drinkers of 1.97 (95% confidence limits 1.50-2.58) as compared to light drinkers of wine (total alcohol intake 3-30 drinks per month), while people who preferred beer had an odds ratio of 1. 29 (1.19-1.40) compared with wine drinkers in the moderate drinking category (31-134 drinks per month). There were no significant differences in total alcohol intake between individuals preferring different alcoholic beverages. CONCLUSION: If binge drinking is less healthy than steady drinking, the relation between wine intake and coronary heart disease mortality could be subject to negative confounding, since beer drinkers seem to have the most sensible drinking pattern. SPONSORSHIP: Danish Cancer Society and the Danish National Board of Health. European Journal of Clinical Nutrition (2000) 54, 174-176

Avian mycoplasma identification using polymerase chain reaction amplicon and restriction fragment length polymorphism analysis.

A general mycoplasma polymerase chain reaction (PCR) was used to generate amplicon (DNA amplification product) from nine avian mycoplasma species. The PCR amplicons were reacted with 24 restriction enzymes, and the electrophoretic patterns of restriction fragment length polymorphism (RFLP) were evaluated for differences between species of mycoplasms. Four (DraI, MseI, RsaI, Tsp5091) of the 24 restriction enzymes cut the PCR amplicon of all nine mycoplasma species. The nine avian mycoplasma species could be distinctly differentiated using the RFLP analysis of the PCR amplicon.

Stereospecific pharmacokinetics of free and protein-bound ketoprofen in serum and synovial fluid of horses after intravenous and intramuscular administration.

OBJECTIVE: To determine intravascular and intrasynovial pharmacokinetics of the R and S enantiomers of ketoprofen after i.v. and i.m. administration to horses. ANIMALS: 6 healthy adult mares. PROCEDURE: Horses were weighed and ketoprofen (2.2 mg/kg of body weight) was administered i.v. Blood and synovial fluid samples were obtained and analyzed for concentrations of the R and S enantiomers by means of a modified reverse-phase stereospecific high-pressure liquid chromatographic method. Three weeks later, the procedure was repeated, except that ketoprofen was given IM. Protein binding of ketoprofen enantiomers was determined by means of ultrafiltration. Nonlinear least squares methods were used to calculate pharmacokinetic parameters. RESULTS: Data obtained after i.v. administration best fit an open, two-compartment model. Mean +/- SD S-to-R serum concentration ratios after i.v. and i.m. administration were 1.36 +/- 0.214 and 1.34 +/- 0.245, respectively. Intrasynovial concentrations of the R and S enantiomers of ketoprofen could be measured for only the first 3 hours after i.v. administration; concentrations were less than the limit of quantification by 4 hours after i.v. administration and at all times after i.m. administration. Extent of protein binding of the R enantiomer was not significantly different from extent of protein binding of the S enantiomer; extent of protein binding did not appear to be concentration dependent. Mean free S-to-free R serum concentration ratios, adjusted for protein binding, after i.v. and i.m. administration were 1.58 and 1.56, respectively. CONCLUSIONS: The R and S enantiomers of ketoprofen are rapidly absorbed and eliminated, have low volumes of distribution, and are highly protein bound.

Population based cohort study of the association between alcohol intake and cancer of the upper digestive tract.

OBJECTIVE: To examine the relation between different types of alcoholic drinks and upper digestive tract cancers (oropharyngeal and oesophageal). DESIGN: Population based study with baseline assessment of intake of beer, wine, and spirits, smoking habits, educational level, and 2-19 years' follow up on risk of upper digestive tract cancer. SETTING: Denmark. SUBJECTS: 15 117 men and 13 063 women aged 20 to 98 years. MAIN OUTCOME MEASURE: Number and time of identification of incident upper digestive tract cancer during follow up. RESULTS: During a mean follow up of 13.5 years, 156 subjects developed upper digestive tract cancer. Compared with non-drinkers (drinkers of <1 drink/week), subjects who drank 7-21 beers or spirits a week but no wine were at a risk of 3.0 (95% confidence interval 1.5 to 6.1), whereas those who had the same total alcohol intake but with wine as >=30% of their intake had a risk of 0.5 (0.2 to 1.4). Drinkers of >21 beers and spirits but no wine had a relative risk of 5.2 (2.7 to 10.2) compared with non-drinkers, whereas those who drank the same amount, but included wine in their alcohol intake, had a relative risk of 1.7 (0.6 to 4. 4). CONCLUSION: A moderate intake of wine probably does not increase the risk of upper digestive tract cancer, whereas a moderate intake of beer or spirits increases the risk considerably.

[Beer, wine, spirits and mortality]. / Øl, vin, spiritus og dØdelighed.

A population based cohort study investigates the association between alcohol intake and mortality from all causes, coronary heart disease and cancer. The design is prospective with baseline assessment of intake of beer, wine and spirits, smoking habits, educational level, physical activity, and body mass index and a total of 257,859 person-years follow-up on mortality. A total of 4,833 participants died, of these 1,075 from coronary heart disease and 1,552 of cancer. Compared with non-drinkers, light drinkers who avoided wine, had a relative risk of death from all causes of 0.90 (0.82-0.99) and those who drank wine had a relative risk of 0.66 (0.55-0.77). Heavy drinkers who avoided wine were at higher risk of death from all causes than were heavy drinkers who included wine in their alcohol intake. Wine drinkers had significantly lower mortality from both coronary heart disease and cancer than did non-wine drinkers (p = 0.007 and p = 0.004, respectively). In conclusion, wine intake may have a beneficial effect on all cause mortality that is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer.

[Smoking cessation in patients with severe irreversible chronic obstructive pulmonary disease, "smoker's lung"]. / Rygestop hos patienter med svaer grad af irreversibel kronisk obstruktiv lungesygdom, "rygerlunger".

A one year prospectively recorded material of 80 patients with severe chronic obstructive pulmonary disease (COPD) (FEV-1 < 40% predicted), only one never smoker and 26 ex-smokers, were included in the study. The 53 smokers were offered a smoking cessation program. Fifty-three of the total were alive after one year, including 16 of the ex-smokers. Twenty-one (57%) of the 37 surviving smokers had quit smoking (carbon monooxide in expired air < 10 ppm), whereas 16 (43%) still were smoking. FEV-1 increased by median 100 ml among both the quitters (p < 0.01), and the ex-smokers (p < 0.02), whereas FEV-1 declined by 50 ml (p > 0.05) among those who continued to smoke. There were more deaths among the sustainers than among the quitters (p < 0.05). Taking into consideration the many sources of bias in this small, uncontrolled study it seems as if smoking cessation prevents loss of lung function and perhaps even death among patients with advanced degree of smoker's lung.

[Beer, wine, spirits and mortality. Results from a prospective population study]. / Øl, vin, spiritus og dødelighed. Resultater fra Hovedstadens Center for Prospektive Befolkningsstudier.

INTRODUCTION: The aim of the present population-based cohort study was to examine the association between alcohol intake and mortality from all causes, coronary heart disease, and cancer. METHODS: A prospective population study with baseline assessment of beer, wine and spirit consumption, smoking habits, educational level, physical activity, and body mass index in a total of 257,859 person-years follow-up on mortality. RESULTS: A total of 4833 participants died, 1075 of these from coronary heart disease and 1552 of cancer. Compared with non-drinkers, light drinkers, who avoided wine, had a relative risk of death from all causes of 0.90 (0.82-0.99) and those who drank wine had a relative risk of 0.66 (0.55-0.77). Heavy drinkers, who avoided wine, were at higher risk of death from all causes than were heavy drinkers, who included wine in their alcohol consumption. Wine drinkers had a significantly lower mortality from both coronary heart disease and cancer than had non-wine drinkers (p = 0.007 and p = 0.004, respectively). CONCLUSION: A moderate consumption of wine may have a beneficial effect on all causes of mortality, which is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer.

Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts.

AIM: To investigate mechanisms behind heptanol (Hp)-induced infarct size reduction and in particular if protection by pre-treatment with Hp is triggered through mitochondrial mechanisms. METHODS: Langendorff perfused rat hearts, isolated mitochondria and isolated myocytes were used. Infarct size, mitochondrial respiration, time to mitochondrial permeability transition pore (MPTP) opening and AKT and glycogen synthase kinase 3 beta (GSK-3ß) phosphorylation were examined. RESULTS: Pre-treatment with Hp reduced infarct size from 29.7 ± 3.4% to 12.6 ± 2.1%. Mitochondrial potassium channel blockers 5-hydroxy decanoic acid (5HD) blocking mitoK(ATP) and paxilline (PAX) blocking mitoK(Ca) abolished cardioprotective effect of Hp (Hp + 5HD 36.7 ± 2.9% and Hp + PAX 40.2 ± 2.8%). Hp significantly reduced respiratory control ratio in both subsarcolemmal and interfibrillar mitochondria in a dose-dependent manner (0.5-5.0 mm). The ADP oxygen ratio was also significantly reduced by Hp (2 mm). Laser scanning confocal microscopy of tetramethylrhodamine-loaded isolated rat myocytes using line scan mode showed that Hp increased time to MPTP opening. Western blot analysis showed that pre-treatment with Hp increased phosphorylation of AKT and GSK-3ß before ischaemia and after 30 min of global ischaemia. CONCLUSION: Pre-treatment with Hp protects the heart against ischaemia-reperfusion injury. This protection is most likely mediated via mitochondrial mechanisms which initiate a signalling cascade that converges on inhibition of opening of MPTP.

Type of alcohol consumed and mortality from all causes, coronary heart disease, and cancer.

BACKGROUND: Although the J-shaped relation between alcohol intake and mortality has been reproduced in many large cohort studies, the question of whether the effects of beer, wine, and spirits differ remains controversial. OBJECTIVE: To examine the relation between intake of different types of alcohol and death from all causes, coronary heart disease, and cancer. DESIGN: Pooled cohort studies in which intake of beer, wine, and spirits; smoking status; educational level; physical activity; and body mass index were assessed at baseline. SETTING: Copenhagen, Denmark. PARTICIPANTS: 13 064 men and 11 459 women 20 to 98 years of age. MEASUREMENTS: Number of deaths and time to death from all causes, coronary heart disease, and cancer during follow-up. RESULTS: During 257 859 person-years of follow-up, 4833 participants died. J-shaped relations were found between total alcohol intake and mortality at various levels of wine intake. Compared with nondrinkers, light drinkers who avoided wine had a relative risk for death from all causes of 0.90 (95% CI, 0.82 to 0.99) and those who drank wine had a relative risk of 0.66 (CI, 0. 55 to 0.77). Heavy drinkers who avoided wine were at higher risk for death from all causes than were heavy drinkers who included wine in their alcohol intake. Wine drinkers had significantly lower mortality from both coronary heart disease and cancer than did non-wine drinkers (P = 0.007 and P = 0.004, respectively). CONCLUSION: Wine intake may have a beneficial effect on all-cause mortality that is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer.