Prospective study of selenium levels in toenails and risk of coronary heart disease in men

Selenium is a trace mineral that plays a role in antioxidant defenses as a component of glutathione peroxidase. Epidemiologic findings on the relation of selenium status to risk of heart disease are inconsistent. Therefore, the authors investigated prospectively the association between toenail selenium levels and risk of coronary heart disease (CHD) in a case-control study nested within the Health Professionals Follow-up Study. Between 1987 and 1992, 470 CHD cases were newly diagnosed. A control matched to each case on age, smoking status, and date of toenail return was chosen. Toenail selenium levels analyzed by neutron activation were not associated with risk of total CHD after adjustment for age and smoking and other CHD risk factors (highest quintile vs. lowest: odds ratio (OR) = 0.86, 95% confidence interval (CI): 0.55, 1.32; p-trend = 0.75). Selenium level was inversely associated with risk of nonfatal myocardial infarction for extreme quintiles (OR = 0.54, 95% CI: 0.31, 0.93; p-trend = 0.07), was less so for fatal CHD (OR = 0.79, 95% CI: 0.39, 1.60; p-trend = 0.61), and was directly associated with coronary revascularization procedures (OR = 2.38, 95% CI: 1.11, 5.09; p-trend = 0.02). Although these findings suggest no overall relation between selenium status and CHD, a specific protective role for myocardial infarction cannot be excluded.     

Toenail nicotine levels as predictors of coronary heart disease among women

The authors assess the ability of toenail nicotine levels as a biomarker to predict incident coronary heart disease (CHD). A nested case-control study was carried out among 62,641 women aged 36-61 years in the Nurses' Health Study cohort who provided toenail clippings in 1982. Between 1984 and 1998, 905 incident CHD cases were diagnosed and matched with two controls by age and date of toenail collection. Using multivariate logistic regression analyses, the authors found a statistically significant dose-response association between increasing toenail nicotine levels and risk of CHD (p(trend) < 0.0001); women in the highest quintile had a relative risk of 3.44 (95% confidence interval (CI): 2.56, 4.62) compared with women in the lowest quintile. With each increase in the log-transformed unit of continuous toenail nicotine levels, there was a 42% increase in the risk of CHD (relative risk = 1.42, 95% CI: 1.33, 1.52). The association remained significant when the number of cigarettes smoked and passive smoking were included as covariates (relative risk = 1.12, 95% CI: 1.01, 1.24). In conclusion, toenail nicotine levels are predictive of CHD among women independent of other risk factors and remained significant even after adjustment for history of cigarette smoking.     

Myocardial infarction risk in relation to zinc concentration in toenails

Zn is an essential mineral. The role of Zn in atherosclerosis is not clear. Epidemiological studies, which have reported contradictory results, are limited by the use of serum Zn levels as a marker of intake. We assessed the association of toenail Zn, which integrates dietary Zn intake over 3 to 12 months, with the risk of a first myocardial infarction. Toenail Zn concentrations were determined by neutron activation analysis in the European multi-centre case-control study on antioxidants, myocardial infarction and breast cancer. This multi-centre case-control study included 684 cases and 724 controls from eight European countries and Israel. Toenail Zn levels of controls (adjusted for age and study centre) were positively associated with age, alpha-tocopherol and Se, but not with additional dietary variables or with classical risk factors for CHD. Average toenail Zn was 106.0 mg/kg in cases (95 % CI 103.1, 108.9) and 107.5 mg/kg in controls (95 % CI 104.5, 110.7). After controlling for cardiovascular risk factors and for centre, the adjusted odds ratios of myocardial infarction for quintiles 2-5 of toenail Zn with respect to the first quintile were 0.97 (95 % CI 0.59, 1.58), 1.15 (95 % CI 0.72, 1.85), 0.91 (95 % CI 0.56, 1.50), and 0.85 (95 % CI 0.52, 1.39). The P for trend was 0.45. In conclusion toenail Zn levels (reflecting long-term dietary intake) were not significantly associated with acute myocardial infarction.     

Phylloquinone intake as a marker for coronary heart disease risk but not stroke in women

OBJECTIVE: To examine the feasibility of using phylloquinone intake as a marker for coronary heart disease (CHD) and stroke risk in women. DESIGN AND SETTING: Nurses' Health Study, a prospective cohort study during 1984-2000. Dietary data were collected in 1984, 1986, 1990, and 1994 using a validated semiquantitative food frequency questionnaire. SUBJECTS: A total of 72 874 female nurses, aged 38-65 y, without previously diagnosed angina, myocardial infarction (MI), stroke, or cancer at baseline. MAIN OUTCOME MEASURES: Incidence of nonfatal MI, CHD deaths, total CHD events, ischemic, and total strokes. RESULTS: There were 1679 CHD events (1201 nonfatal) and 1009 strokes (567 ischemic). After adjustment for age and lifestyle factors associated with cardiovascular disease risk, the multivariate relative risks (RR) (95% CI) of total CHD from the lowest to the highest quintile category of phylloquinone intake were 1 (reference), 0.80 (0.69-0.94), 0.86 (0.74-1.00), 0.77 (0.66-0.99), and 0.79 (0.68-0.92), P for trend=0.01. Further adjustment for dietary intakes of saturated fat, polyunsaturated fat, trans fatty acids, eicosapentaenoic, and docosahexaenoic acids, cereal fiber, and folate attenuated the association (RR comparing extreme quintiles 0.84 [0.71-1.00], P for trend=0.12). Incidence rates of total or ischemic strokes were not associated with phylloquinone intake. CONCLUSION: The data suggest that high phylloquinone intake may be a marker for low CHD risk. Dietary and lifestyle patterns associated with phylloquinone intakes, rather than intake of the nutrient itself, might account for all or part of the weak association. .     

Measurement of low levels of arsenic exposure: a comparison of water and toenail concentrations

A study was conducted to evaluate toenail arsenic concentrations as a biologic marker of drinking water arsenic exposure. Study subjects were controls in a US population-based case-control study of nonmelanoma skin cancer, randomly selected from drivers' license records (those < 65 years of age) and Medicare enrollment files (those > or = 65 years of age). Between 1994 and 1997, a total of 540 controls were interviewed and toenail samples of sufficient weight were collected from 506 (93.7%) of these. Beginning in 1995, a sample of tap water was taken from the participants' homes; a total of 217 (98.6%) water samples were obtained from the 220 subjects interviewed. Arsenic determinations were made from toenail samples using neutron activation analysis. Water samples were analyzed using hydride-generation magnet sector inductively coupled mass spectrometry. Among 208 subjects with both toenail and water measurements, the correlation (r) between water and nail arsenic was 0.65 (p < 0.001) among those with water arsenic concentrations of 1 microg/liter or higher and 0.08 (p = 0.31) among those with concentrations below 1 microg/liter (overall r = 0.46, p < 0.001). Our data suggest that toenail samples provide a useful biologic marker for quantifying low-level arsenic exposure.     

Markers of low level arsenic exposure for evaluating human cancer risks in a US population

Epidemiologic studies conducted in the US have not previously detected an association between regional drinking water arsenic concentrations and corresponding cancer occurrence or mortality rates. To improve our estimation of cancer risk and arsenic exposure in the USA, we have investigated the reliability of several exposure markers. In the current study, we specifically evaluated the long-term reproducibility of tap water and toenail concentrations of arsenic, and the relation between water, toenail, and urinary measurement. Subjects included 99 controls in our case-control study on whom we requested a household tap water sample and toenail clipping three to five years apart. Additionally, participants were asked to provide a first morning void sample at the second interview. Tap water arsenic concentrations ranged from undetectable (<0.01 microg/L) to 66.6 microg/L. We found a significant correlation between both replicate water and toenail samples (intraclass correlation coefficient = 0.85, 95% confidence interval = 0.79-0.89 for water, and intraclass correlation coefficient = 0.60, 95% confidence interval = 0.48-0.70 for toenails). The inter-method correlations for water, urinary and toenail arsenic were all statistically significant (r = 0.35, p = 0.0024 for urine vs water; r = 0.33, p = 0.0016 for toenail vs water and r = 0.36, p = 0.0012 for urine vs toenails). Thus, we found both toenail and water measurements of arsenic reproducible over a three- to five-year period. Our data suggest that biologic markers may provide reliable estimates of internal dose of low level arsenic exposure that can be used to assess cancer risk.     

Correlates of serum lycopene in older women

Experimental and epidemiological evidence suggests that lycopene, a predominant carotenoid found in human serum, may reduce the risk of certain cancers. We examined the association of dietary, physiological, and other factors with serum lycopene concentrations in a subsample of 946 postmenopausal women participating in the Women's Health Initiative. Pearson partial correlation coefficients and linear regression coefficients were calculated after adjustment for age, ethnicity, and serum low-density-lipoprotein (LDL) cholesterol. Serum lycopene was correlated with serum LDL cholesterol (r = 0.23) and dietary lycopene (r = 0.17, both p < 0.001). Individual food items found to be correlated with serum lycopene after adjustment included fresh tomatoes or tomato juice (r = 0.11), cooked tomatoes, tomato sauce, or salsa (r = 0.17), and spaghetti with meat sauce (r = 0.19, all p < 0.01). Age and body mass index were negatively associated with serum lycopene levels (both p < 0.001). Serum lycopene levels were highest in the summer and highest for those living in the northeastern United States. If we postulate that high serum lycopene levels reduce cancer risk, it becomes apparent that we have limited ability to detect this association from studies of lycopene intake. An understanding of factors associated with serum lycopene levels can be useful for the interpretation of studies of dietary lycopene and disease risk.     

Lipid-related genes and myocardial infarction in 4685 cases and 3460 controls: discrepancies between genotype, blood lipid concentrations, and coronary disease risk

BACKGROUND: Blood lipid concentrations are causally related to the risk of coronary heart disease (CHD). Various associations between CHD risk and genes that moderately affect plasma lipid levels have been described, but previous studies have typically involved too few 'cases' to assess these associations reliably. METHODS: The present study involves 4685 cases of myocardial infarction (MI) and 3460 unrelated controls without diagnosed cardiovascular disease. Six polymorphisms of four 'lipid-related' genes were genotyped. RESULTS: For the apolipoprotein E epsilon2/epsilon3/epsilon4 polymorphism, the average increase in the plasma ratio of apolipoprotein B to apolipoprotein A(1) (apoB/apoA(1) ratio) among controls was 0.082 (s.e. 0.007) per stepwise change from epsilon3/epsilon2 to epsilon3/epsilon3 to epsilon3/epsilon4 genotype (trend P < 0.0001). The case-control comparison yielded a risk ratio for MI of 1.16 (95% CI: 1.06, 1.27; P = 0.001) per stepwise change in these genotypes. But, this risk ratio was not as extreme as would have been expected from the corresponding differences in plasma apoB/apoA(1) ratio between genotypes. Hence, following adjustment for the measured level of the plasma apoB/apoA(1) ratio, the direction of the risk ratio per stepwise change reversed to 0.83 (95% CI: 0.74, 0.92; P < 0.001). Similarly, for the apolipoprotein B Asn4311Ser and Thr71Ile polymorphisms, genotypes associated with more adverse plasma apolipoprotein concentrations were associated with significantly lower risk of MI after adjustment for the apoB/apoA(1) ratio. The B2 allele of the cholesteryl ester transfer protein TaqIb polymorphism was associated with a significantly lower plasma apoB/apoA(1) ratio, but with no significant difference in the risk of MI. Finally, the lipoprotein lipase Asn291Ser and T4509C (PvuII) polymorphisms did not produce clear effects on either the plasma apoB/apoA(1) ratio or the risk of MI. CONCLUSIONS: It remains unresolved why some of these genetic factors that produce lifelong effects on plasma lipid concentrations have significantly less than the correspondingly expected effects on CHD rates in adult life.     

Dietary patterns are associated with disease risk among participants in the Women's Health Initiative Observational Study

Coronary heart disease (CHD) is the leading cause of death in women. A nested case-control study tested whether dietary patterns predicted CHD events among 1224 participants in the Women's Health Initiative-Observational Study (WHI-OS) with centrally confirmed CHD, fatal or nonfatal myocardial infarct compared to 1224 WHI-OS controls matched for age, enrollment date, race/ethnicity, and absence of CHD at baseline or follow-up. The first six principal components explained >75% of variation in dietary intakes and K-mean analysis based on these six components produced three clusters. Diet cluster 1 was rich in carbohydrate, vegetable protein, fiber, dietary vitamin K, folate, carotenoids, α-linolenic acid [18:3(n-3)], linoleic acid [18:2(n-6)], and supplemental calcium and vitamin D. Diet cluster 2 was rich in total and animal protein, arachidonic acid [20:4(n-6)], DHA [22:6(n-3)], vitamin D, and calcium. Diet cluster 3 was rich in energy, total fat, and trans fatty acids (all P < 0.01). Conditional logistic regression analysis demonstrated diet cluster 1 was associated with lower CHD risk than diet cluster 2 (reference group) adjusted for smoking, education, and physical activity [OR = 0.79 (95% CI = 0.64, 0.99); P = 0.038]. This difference was not significant after adjustment for BMI and systolic blood pressure. Diet cluster 3 was associated with higher CHD risk than diet cluster 2 [OR = 1.28 (95% CI = 1.04, 1.57); P = 0.019], but this difference did not remain significant after adjustment for smoking, education, and physical activity. Within this WHI-OS cohort, distinct dietary patterns may be associated with subsequent CHD outcomes.     

Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas

Carotenoids possess antioxidant properties and thus may protect against prostate cancer. Epidemiological studies of dietary carotenoids and this malignancy were inconsistent, partially due to dietary assessment error. In this study, we aimed to investigate the relation between plasma concentrations of carotenoids and the risk of prostate cancer in a population-based case-control study in Arkansas. Cases (n = 193) were men with prostate cancer diagnosed in 3 major hospitals, and controls (n = 197) were matched to cases by age, race, and county of residence. After adjustment for confounders, plasma levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin were inversely associated with prostate cancer risk. Subjects in the highest quartile of plasma lycopene (513.7 microg/l) had a 55% lower risk of prostate cancer than those in the lowest quartile (140.5 microg/l; P trend = 0.042). No apparent association was observed for plasma alpha-carotene and beta-carotene. Further adjustment for the other 4 carotenoids did not materially alter the risk estimates for plasma lycopene, lutein/zeaxanthin, and beta-cryptoxanthin but appeared to result in an elevated risk with high levels of plasma alpha-carotene and beta-carotene. The results of all analyses did not vary substantially by age, race, and smoking status. This study added to the emerging evidence that high circulating levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin are associated with a low risk of prostate cancer.     

Whole-grain consumption and risk of coronary heart disease: results from the Nurses' Health Study.

BACKGROUND: Although current dietary guidelines for Americans recommend increased intake of grain products to prevent coronary heart disease (CHD), epidemiologic data relating whole-grain intake to the risk of CHD are sparse. OBJECTIVE: Our objective was to evaluate whether high whole-grain intake reduces risk of CHD in women. DESIGN: In 1984, 75521 women aged 38-63 y with no previous history of cardiovascular disease or diabetes completed a detailed, semiquantitative food-frequency questionnaire (SFFQ) and were followed for 10 y, completing SFFQs in 1986 and 1990. We used pooled logistic regression with 2-y intervals to model the incidence of CHD in relation to the cumulative average diet from all 3 cycles of SFFQs. RESULTS: During 729472 person-years of follow-up, we documented 761 cases of CHD (208 of fatal CHD and 553 of nonfatal myocardial infarction). After adjustment for age and smoking, increased whole-grain intake was associated with decreased risk of CHD. For increasing quintiles of intake, the corresponding relative risks (RRs) were 1.0 (reference), 0.86, 0.82, 0.72, and 0.67 (95% CI comparing 2 extreme quintiles: 0.54, 0.84; P for trend < 0.001). After additional adjustment for body mass index, postmenopausal hormone use, alcohol intake, multivitamin use, vitamin E supplement use, aspirin use, physical activity, and types of fat intake, these RRs were 1.0, 0.92, 0.93, 0.83, and 0.75 (95% CI: 0.59, 0.95; P for trend = 0.01). The inverse relation between whole-grain intake and CHD risk was even stronger in the subgroup of never smokers (RR = 0. 49 for extreme quintiles; 95% CI: 0.30, 0.79; P for trend = 0.003). The lower risk associated with higher whole-grain intake was not fully explained by its contribution to intakes of dietary fiber, folate, vitamin B-6, and vitamin E. CONCLUSIONS: Increased intake of whole grains may protect against CHD.     

Toenail mercury and dietary fish consumption

New England is one of three areas in the United States with the highest annual deposition of mercury, an established environmental pollutant with a variety of health effects. We measured the mercury content in toenails of 27 individuals in New Hampshire who participated as controls in a health study in 1994-95. The mean total toenail mercury concentration was 0.27 mcg/g (median 0.16; SD 0.27; range 0.04-1.15 mcg/g). The best predictor of toenail mercury levels was the mean combined fish and shellfish consumption measured using four simple questions from a validated food frequency questionnaire. Toenail total mercury content was significantly correlated with the mean average weekly consumption of finfish and shellfish (Spearman correlation coefficient 0.48, P=0.012). Multivariate models confirmed that toenail total mercury concentration was best predicted by total finfish and shellfish consumption.     

Predictors of subsequent coronary events,stroke, and death among survivors of first hospitalized myocardial infarction

We identified predictors of prognosis among n = 2,677 health maintenance organization enrollees 30 to 79 years old who survived a first hospitalized myocardial infarction (MI) during 1986-1996 (mean follow-up 3.4 years). Independent risk factors for reinfarction/fatal coronary heart disease (CHD) (incidence = 49.0/1,000 person-years, 445 events) were age, diabetes, chronic congestive heart failure (CHF), angina, high body mass index (BMI), low diastolic blood pressure (DBP), high serum creatinine, and low/high-density lipoprotein (HDL) cholesterol. Independent risk factors for stroke (incidence = 13.0/1,000 person-years, 124 events) were age, diabetes, CHF, high DBP, and high creatinine. Independent predictors of death (incidence = 44.2/1,000 person-years, 431 events) were age, diabetes, CHF, continued smoking after MI, low DBP, high pulse rate, high creatinine, and low HDL cholesterol, while BMI had a significant U-shaped association with death (elevated risk at low and high BMI). The occurrence of study end points did not differ significantly between men and women after adjustment for other risk factors and use of preventive medical therapies, although men tended to have higher rates of reinfarction/CHD than women among older subjects. In summary, we demonstrated that the major cardiovascular risk factors age, diabetes, CHF, smoking, and dyslipidemia are important prognostic factors in the years after nonfatal MI. Elevated BMI was associated with increased risk of reinfarction/CHD and death and elevated DBP with increased risk of stroke, but we also observed high mortality among those with low BMI and high risk of recurrent coronary disease and death among those with low DBP. Finally, high creatinine was a strong, independent predictor of a variety of adverse outcomes after first MI.     

Plasma Carotenoids and Prostate Cancer: A Population-Based Case-Control Study in Arkansas

Carotenoids possess antioxidant properties and thus may protect against prostate cancer. Epidemiological studies of dietary carotenoids and this malignancy were inconsistent, partially due to dietary assessment error. In this study, we aimed to investigate the relation between plasma concentrations of carotenoids and the risk of prostate cancer in a population-based case-control study in Arkansas. Cases (n = 193) were men with prostate cancer diagnosed in 3 major hospitals, and controls (n = 197) were matched to cases by age, race, and county of residence. After adjustment for confounders, plasma levels of lycopene, lutein/zeaxanthin, and β -cryptoxanthin were inversely associated with prostate cancer risk. Subjects in the highest quartile of plasma lycopene (513.7 μ g/l) had a 55% lower risk of prostate cancer than those in the lowest quartile (140.5 μ g/l; P trend = 0.042). No apparent association was observed for plasma α -carotene and β -carotene. Further adjustment for the other 4 carotenoids did not materially alter the risk estimates for plasma lycopene, lutein/zeaxanthin, and β -cryptoxanthin but appeared to result in an elevated risk with high levels of plasma α -carotene and β -carotene. The results of all analyses did not vary substantially by age, race, and smoking status. This study added to the emerging evidence that high circulating levels of lycopene, lutein/zeaxanthin, and β -cryptoxanthin are associated with a low risk of prostate cancer.     

Magnesium intake and risk of coronary heart disease among men

OBJECTIVE: Our aim in this study was to assess the relationship between magnesium intake and risk of coronary heart disease (CHD) among men. METHODS: A total of 39,633 men in the Health Professionals Follow-up Study who returned a dietary questionnaire in 1986 were followed up for 12 years. Intakes of magnesium, zinc and potassium and other nutrients were assessed in 1986, 1990 and 1994. Total CHD incidence (nonfatal myocardial infarction (MI) and fatal CHD) was ascertained by biennial questionnaire and mortality surveillance confirmed by medical record review. Standard CHD risk factors were recorded biennially. RESULTS: During 12 years of follow-up (414,285 person-years), we documented 1,449 cases of total CHD (1,021 non-fatal MI cases, and 428 fatal CHD). The age-adjusted relative risk (RR) of developing CHD in the highest quintile (median intake = 457 mg/day) compared with the lowest quintile (median intake = 269 mg/day) was 0.73 (95% CI 0.62-0.87, p for trend <0.0001). After controlling for standard CHD risk factors and dietary factors, the RR for developing CHD among men in the highest total magnesium intake quintile compared with those in the lowest was 0.82 (95% CI 0.65-1.05, p for trend = 0.08). For supplemental magnesium intake, the RR comparing the highest quintile to non-supplement users was 0.77 (95% CI 0.56-1.06, p for trend = 0.14). CONCLUSIONS: These results suggest that intake of magnesium may have a modest inverse association with risk of CHD among men.     

Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in men

BACKGROUND: Emerging evidence suggests a possible role of lycopene in the primary prevention of cardiovascular disease (CVD). OBJECTIVE: We examined whether plasma lycopene concentrations in the Physicians' Health Study were associated with CVD in a prospective, nested, case-control design. DESIGN: Baseline blood samples were collected starting in 1996. During a mean follow-up of 2.1 y, we identified 499 cases of CVD (confirmed myocardial infarction, stroke, CVD death, or revascularization procedures) and an equal number of men free of CVD and matched for age (x: 69.7 y), follow-up time, and smoking status. We collected self-reported coronary disease risk factors and measured plasma carotenoids, retinol, lipids, and C-reactive protein. RESULTS: In matched analyses with additional adjustment for plasma total cholesterol and randomized treatment, the relative risks (RRs) of CVD for men in the lowest to highest quartiles of plasma lycopene were 1.00 (reference), 0.92, 1.04, and 0.95 (P for linear trend = 0.93). With multivariate adjustment, the RRs of total CVD were 1.00 (reference), 1.08, 0.94, and 1.03 (P for linear trend = 0.98). For important vascular events (241 cases), excluding revascularization procedures, the multivariate RRs remained nonsignificant (P for linear trend = 0.50). Adding plasma carotenoids, lipids, or C-reactive protein to multivariate models had a minimal effect on the RRs of total CVD for plasma lycopene. Compared with lycopene, higher concentrations of plasma lutein/zeaxanthin and retinol suggested a moderate increase in CVD risk, whereas no association was found for beta-cryptoxanthin, alpha-carotene, and beta-carotene. CONCLUSIONS: Higher plasma lycopene concentrations were not associated with the risk of CVD in this study of older men. Further evaluation in diverse populations is necessary.     

Plasma levels of lipophilic antioxidant vitamins in acute ischemic stroke patients: correlation to inflammation markers and neurological deficits

OBJECTIVES: Acute ischemic stroke is a clinical condition accompanied by inflammation and oxidative stress. In this study, we compared levels of plasma lipophilic antioxidants and inflammation markers between patients with stroke and healthy controls and assessed the associations of antioxidants, inflammation markers, and neurologic deficits among patients with stroke. METHODS: We measured plasma levels of lipophilic antioxidant vitamins (retinol, lycopene, alpha-carotene, beta-carotene, alpha-tocopherol, and gamma-tocopherol), inflammation markers (high-sensitivity C-reactive protein [hs-CRP], fibrinogen, erythrocyte sedimentation rate, and white blood cell count), and neurologic deficits (indicated by the score of the National Institute of Health Stroke Scale) in 68 patients with acute ischemic stroke within 48 h after stroke onset in comparison with 41 normal controls. RESULTS: Plasma alpha- and beta-carotene concentrations were lower and levels of inflammation markers were higher among patients with acute ischemic stroke compared with normal controls. Levels of alpha- and beta-carotene in patients with stroke were negatively associated with hs-CRP level (R = -0.29 and -0.41, respectively, P < 0.01) and with neurologic deficits (R = -0.28 and -0.27, respectively, P < 0.05). The negative association between neurologic deficits and combined plasma levels of alpha- and beta-carotene remained after adjustment for age and sex (P = 0.04). However, the magnitude of association decreased after adjustment of hs-CRP (P = 0.08). CONCLUSION: Plasma concentrations of alpha- and beta-carotene are lower in patients with acute ischemic stroke than in healthy controls and are negatively correlated with hs-CRP level and neurologic deficits. The negative association between neurologic deficits and combined plasma alpha- and beta-carotene levels is confounded by hs-CRP.     

Vegetables, fruits, related dietary antioxidants, and risk of squamous cell carcinoma of the esophagus: a case-control study in Uruguay

In 1998-1999, a case-control study on esophageal cancer was conducted in Uruguay. For this purpose, 111 cases with squamous cell carcinoma of the esophagus and 444 controls with conditions unrelated to tobacco smoking, alcohol drinking, or recent changes in the diet were frequency matched on age, gender, residence, and urban/rural status. Vegetables and, more markedly, fruits were associated with strong reductions in risk. On the other hand, 12 of 15 dietary antioxidants displayed significant inverse associations with esophageal cancer risk. The strongest effect was observed for high intake of beta-cryptoxanthin (odds ratio = 0.16, 95% confidence interval = 0.08-0.36). Also, alpha-carotene, lycopene, and beta-sitosterol were associated with significant reductions in risk. Most antioxidants lost their effect when they were further adjusted for a term for all vegetables and fruits. beta-Carotene showed an increased risk with high intakes. On the other hand, vegetables and fruits remained as significant variables after adjustment for each antioxidant, suggesting that other substances or other mechanisms could explain this effect.     

Plasma lycopene concentrations in humans are determined by lycopene intake, plasma cholesterol concentrations and selected demographic factors

Higher plasma lycopene concentrations have been associated with a reduced risk of several chronic diseases. Determinants of lycopene concentrations in humans have received limited attention. We had blood lycopene concentrations and lycopene consumption data available from 111 participants in a two-center cancer prevention trial involving beta-carotene and examined determinants of plasma lycopene levels cross-sectionally. The median plasma lycopene level was 0.59 micromol/L (range 0.07-1.79). Low plasma concentrations of lycopene were associated with the following variables in univariate analyses: study site (Florida lower than Connecticut, P = 0.001), being nonmarried (P = 0.02), having lower income (P = 0.003), being nonwhite race/ethnicity (P = 0.03), having lower dietary lycopene intake (r = 0.29, P = 0.002), having lower plasma cholesterol (r = 0. 43, P = 0.0001) and triglyceride levels (r = 0.26, P = 0.005), and consuming less vitamin C (r = 0.20, P = 0.03). Women had slightly higher plasma lycopene levels than men (0.65 vs. 0.58 micromol/L; P = 0.31), despite lower dietary intake of lycopene (1,040 vs. 1,320 microg/d; P = 0.50). Plasma lycopene levels did not differ in smokers and nonsmokers. In stepwise regression analyses, the determinants of plasma lycopene were plasma cholesterol, dietary lycopene, and marital status; these three variables explained 26% of the variance in plasma lycopene. Relatively few lifestyle and demographic factors were important determinants of plasma lycopene levels, with plasma cholesterol, marital status, and lycopene intake being of greatest importance.     

Prospective study of job insecurity and coronary heart disease in US women

PURPOSE: To examine prospectively the relationship between job insecurity and incidence of coronary heart disease (CHD) among women. METHODS: We conducted the study in 36,910 women from the Nurses' Health Study, a prospective cohort of female registered nurses residing in 11 US states. These women were 46 to 71 years old, and did not have diagnosed CHD, stroke, or cancer at baseline (1992). We collected information on job insecurity in 1992 and coronary heart disease incidence between baseline (June 1, 1992) and return of the 1996 questionnaire. RESULTS: During 4 years of follow-up, we documented 154 incident cases of CHD (113 non-fatal cases of myocardial infarction (MI) and 41 CHD deaths). After adjustment for a wide array of potential confounders, the relative risk (RR) of total CHD over 2-year follow-up was 1.35 (95% CI, 0.78-2.34) and 1.04 (95% CI, 0.69-1.57) over 4-year follow-up. Job insecurity appeared to significantly increase the risk of non-fatal MI in the short term (2-year follow-up: RR=1.89, 95% CI, 1.03-3.50), though not over a longer follow-up period (RR=1.28, 95% CI, 0.82-2.00), nor fatal CHD in the short term (RR=0.49, 95% CI, 0.22-2.08). CONCLUSIONS: These data suggest that job insecurity may increase the short-term risk of non-fatal MI in women.