Kristian D. Lindsted

Effects of walnuts on serum lipid levels and blood pressure in normal men

BACKGROUND In a recent six-year follow-up study, we found that frequent consumption of nuts was associated with a reduced risk of ischemic heart disease. To explore possible explanations for this finding, we studied the effects of nut consumption on serum lipids and blood pressure. METHODS We randomly placed 18 healthy men on two mixed natural diets, each diet to be followed for four weeks. Both diets conformed to the National Cholesterol Education Program Step 1 diet and contained identical foods and macronutrients, except that 20 percent of the calories of one diet (the walnut diet) were derived from walnuts (offset by lesser amounts of fatty foods, meat, and visible fat [oils, margarine, and butter]). RESULTS With the reference diet, the mean (+/- SD) serum values for total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol were, respectively, 182 +/- 23, 112 +/- 16, and 47 +/- 11 mg per deciliter (4.71 +/- 0.59, 2.90 +/- 0.41, and 1.22 +/- 0.28 mmol per liter). With the walnut diet, the mean total cholesterol level was 22.4 mg per deciliter (0.58 mmol per liter) lower than the mean level with the reference diet (95 percent confidence interval, 28 to 17 mg per deciliter [0.72 to 0.44 mmol per liter]); the LDL and HDL cholesterol levels were, respectively, 18.2 mg per deciliter (0.47 mmol per liter) (P < 0.001) and 2.3 mg per deciliter (0.06 mmol per liter) (P = 0.01) lower. These lower values represented reductions of 12.4, 16.3, and 4.9 percent in the levels of total, LDL, and HDL cholesterol, respectively. The ratio of LDL cholesterol to HDL cholesterol was also lowered (P < 0.001) by the walnut diet. Mean blood-pressure values did not change during either dietary period. CONCLUSIONS Incorporating moderate quantities of walnuts into the recommended cholesterol-lowering diet while maintaining the intake of total dietary fat and calories decreases serum levels of total cholesterol and favorably modifies the lipoprotein profile in normal men. The long-term effects of walnut consumption and the extension of this finding to other population groups deserve further study.

Self-report of physical activity and patterns of mortality in Seventh-Day Adventist men.

The Adventist Mortality Study provides 26-year follow-up through 1985 for 9484 males who completed a lifestyle questionnaire in 1960. The relationship of self-reported physical activity and all cause and disease-specific mortality was examined by survival analysis and with the Cox proportional hazards model, controlling for demographic and lifestyle characteristics. Moderate activity was associated with a protective effect on cardiovascular and all cause mortality in both analyses. In the Cox model, age-specific estimates of relative risk (RR) were obtained for several endpoints due to a significant interaction between level of physical activity and attained age (age at death or end of follow-up). This model permits calculation of the age at which the RR = 1.0, or the age at crossover of risk. For moderate activity, this age was 95.6 years (95% confidence intervals, 81.7-109.4 years) for all cause mortality and 91.5 years (95% confidence intervals, 79.0-104.0 years) for cardiovascular mortality. While the protective effect on mortality associated with moderate activity decreased with increasing age, it remained significant to the verge of the present life span.

Healthy volunteer effect in a cohort study: Temporal resolution in the adventist health study☆

The healthy volunteer effect was studied by comparing 6 years of mortality data for 31,124 participants from the Adventist Health Study (AHS) who responded to both a relatively brief census questionnaire (CQ) in 1974 and a detailed life-style questionnaire (LQ) in 1976 (responders), to mortality data for 8,762 individuals who did not respond to the second questionnaire. The rate ratio (RR) comparing LQ nonresponders to responders for all cause mortality decreased from 2.5 (2.2-2.9) in 1977 to 1.4 (1.2-1.7) in 1982 (p for trend = 0.02); for ischemic heart disease mortality from 2.3 (1.8-3.0) to 1.3 (1.0-1.7); and for all sites cancer mortality from 1.8 (1.3-2.5) to 1.5 (1.1-2.0). The death rate decreased markedly among nonresponders and increased slightly among responders during the study. Similar results were seen for age and gender subgroups. Multivariate analysis controlling for confounding variables confirms these results, except that the apparent effect of education is probably due to effect modification by age. The RR decreased to about one after 3 years of follow-up in young subjects but remained elevated (> 2) in older subjects. Available sociodemographic information reveals that a higher proportion of responders are married, have college education, are SDA church members, and use medical services less than nonresponders during the previous year. Because the risk remains elevated at the end of the study in some but not all subgroups, it seems reasonable that the elevated risk in nonresponders may be due in part to a less healthy life style and in part to exclusion of individuals who did not feel well during enrollment. The results suggest that for internal comparisons no bias is likely to occur; but descriptive statistics for certain subgroup comparisons, and external comparisons, may be biased by the healthy volunteer effect.

Body Mass and 26-year Risk of Mortality from Specific Diseases among Women Who Never Smoked

We examined the relation between Quetelets body mass index (BMI) and age-adjusted mortality risk from specific diseases in a 26-year prospective cohort study of 12,576 non-Hispanic white women who had never smoked. To account for effects due to antecedent disease, we focused on women surviving 15–26 years after their report of body weight. High BMI (>27 kg per m2) decreased the risk of fatal respiratory disease (hazard ratios of 0.7 for ages 30–54 years and 0.6 for ages 55–74 years) but increased risk in all other disease categories. Low BMI (<21 kg per m2) increased the risk of fatal respiratory disease (hazard ratios of 2.0 for ages 30–54 years and 1.4 for ages 55–74 years). Among middle-aged women (ages 30–54 years), we found that low BMI also increased the risk of certain fatal cardiovascular diseases (hazard ratios of 1.5 for cerebrovascular death and 2.5 for hypertensive and other cardiovascular deaths), but the increase in the risk of fatal cerebrovascular disease did not remain (hazard ratio of 0.4) after exclusion of subarachnoid and intraparenchymal hemorrhage deaths from the endpoint. Although the inverse relation between BMI and risk of fatal respiratory disease was also evident in the subset who reported body weight 17 years after baseline, further restriction of this subset to stable-weight women reporting no history of respiratory disease resulted in a U-shaped relation. Data from this subset also indicated that weight loss substantially increased the risk of fatal respiratory disease. These findings implicate high and low BMI as risk factors for fatal respiratory disease but suggest that the risk due to high BMI was obscured by weight loss that followed the onset of disease. The overall findings support an association between obesity and a higher risk of fatal disease but also raise the possibility that apparently healthy, never-smoking women can experience a higher long-term risk of fatal cardiovascular and respiratory diseases due to a lower body weight. (Epidemiology 1998;9:246–254)

Long‐term (24‐year) recall reliability in cancer cases and controls using a 21‐item food frequency questionnaire

The following two questions concerning diet recall were addressed when studying 117 incident cancer cases and 99 controls from the Adventist Mortality Study. Are recalls of past dietary habits reliable? Does recall ability differ between cancer cases and controls? Two sets of dietary data were compared using the American Cancer Societys food frequency questionnaire--as reported in 1960 and recalled in 1984. Ability to recall 21 key food items was evaluated both for individual foods and a combination of all foods by comparing recall scores. The comparison revealed that among food groups, 24-year recall ability varied greatly. There was no significant difference in recall ability between cancer incident cases and controls after controlling for factors that may be related to recall ability (e.g., age, education, and sex). Also, there was no significant difference in recall ability among subjects with or without other chronic diseases likely to affect diet pattern. The results revealed no significant differences in recall ability by sex and body mass index; however, significant differences by vegetarian status and diet stability were found. Significant differences by educational level were found only in univariate analysis.

Comparison of Adipose Tissue Fatty Acids with Dietary Fatty Acids as Measured by 24-hour Recall and Food Frequency Questionnaire in Black and White Adventists: The Adventist Health Study

PURPOSE To calibrate and compare intake of different fats and individual fatty acids as assessed with a food frequency questionnaire (FFQ) against that estimated with (i) a series of dietary recalls and; (ii) the relative fat concentration in an adipose tissue biopsy. The FFQ was specially designed for use in a cohort of Seventh-day Adventists. In preparation for a large cohort study investigating the effect of diet on risk of colon, prostate and breast cancer. METHODS The association of adipose tissue fatty acids and dietary fat intake was assessed in 49 black and 72 white Seventh-day Adventists subjects using 8 different 24-hour recalls, a 200-item food frequency questionnaire (FFQ) and adipose tissue biopsies from each subject. RESULTS Pearson correlation between fatty acids in adipose tissue and dietary intake as assessed by multiple 24-hour recalls were as follows: Linoleic acid: 0.77 in black and 0.71 in white subjects, respectively; Linolenic acid: 0.68 (blacks) and 0.62 (whites); Total Polyunsaturated fat (PUFA): 0.78 (blacks) and 0.70 (whites); Total Monounsaturated fat (MUFA): 0.35 (blacks) and 0.03 (whites); Total Saturated fat (SFA): 0.46 (blacks) and 0.56 (whites). Correlations between fatty acids in adipose tissue and dietary intake as assessed by FFQ were: Linoleic acid: 0.61 (blacks) and 0.52 (whites), respectively; Linolenic acid: 0.29 (blacks) and 0.49 (whites); PUFA: 0.62 (blacks) and 0.53 (whites); MUFA: 0.07 (blacks) and 0.31 (whites), SFA: 0.21 (blacks) and 0.31 (whites). CONCLUSIONS Our study confirms findings of others that 24-hour recalls are valid for assessing dietary intake of different types of fat. The FFQ we developed and used in this study gave reasonably valid measures of fatty acid intake in our population and is thus suitable for use in large cohort studies. It had validity comparable to that observed for other FFQs.

Coffee consumption and cause-specific mortality. Association with age at death and compression of mortality.

The relationship between reported coffee consumption and specific causes of death was examined in 9484 males enrolled in the Adventist Mortality Study in 1960 and followed through 1985. Coffee consumption was divided into three levels: less than 1 cup per day, 1-2 cups per day, and greater than or equal to 3 cups per day. Approximately one third of the subjects did not drink coffee. Cause-specific mortality rates were compared using survival analysis including Coxs proportional hazard model, and controlling for potential confounders such as body mass index, heart disease and hypertension at baseline, race, physical activity, marital status, educational level, smoking history, and dietary pattern. Inclusion of interaction terms between coffee consumption and attained age as time-dependent covariates allowed the hazard ratio to vary with age. Univariate analyses showed a statistically significant association (p less than 0.05) for coffee consumption and mortality for most endpoints. Multivariate analyses showed a small but statistically significant association between coffee consumption and mortality from ischemic heart disease, other cardiovascular diseases, all cardiovascular diseases, and all causes of death. For the major causes of death, the hazard ratios decreased from about 2.5 at 30 years of age to 1.0 around 95 years of age. These results indicate that abstinence from coffee leads to compression of mortality rather than an increase in lifespan.

Reliability of eight-year diet recall in cancer cases and controls.

We addressed three questions concerning diet recall in a population of 181 incident cancer cases diagnosed between 1976 and 1984 in the Adventist Health Study, and 225 controls randomly selected from the same population after removing cancer cases: (1) Are recalls of past dietary habits reliable? (2) Does recall ability differ between cancer cases and controls? and (3) Are current or retrospectively recalled reports the best estimator of past dietary practices? Three sets of dietary data were compared using a 35-item nonquantitative food frequency questionnaire: initial reports in 1976, recalled reports obtained retrospectively in 1984, and current reports for 1984. Recall ability was evaluated for individual foods and for all foods combined by comparing recall error scores summing the absolute differences between initial and recalled frequencies. Means and medians for all three food groups were similar for cases and controls. The Spearman rank-order correlations between pairs of reports (initial/recalled, initial/current, and recalled/cunent) averaged 0.48, 0.41, and 0.62, respectively. A crude difference of 2.0 between cases and controls (p < 0.05) in the recall error score indicated that cases on the average recalled two foods one frequency category closer to the initial estimate compared with controls. The case-control difference decreased to a nonsignificant 0.4 (p = 0.7) in multivariate analysis that conditioned on dietary changes. On the average, recalled reports estimated initial reports one frequency category closer than did current reports for three foods (p < 0.001), primarily because of changes in dietary habits

Body mass and 26 y risk of mortality among men who never smoked: a re-analysis among men from the Adventist Mortality Study.

OBJECTIVE: To re-analyse the previously reported linear relation between Quetelet’s body mass index (BMI) and mortality, among men from the Adventist Mortality Study after accounting for effects due to age at measurement of BMI, smoking history and race.DESIGN: Prospective cohort study. To specifically account for effects due to age at measurement of BMI, smoking history and race, our methodology includes: 1, computing hazard ratios for BMI quintiles from a proportional hazard regression, with ‘time on study’ as the time variable, and age at baseline as a covariate; 2, conducting separate analyses of middle-aged (age 30–54 y) and older (age 55–74 y) men; and 3, restriction of the analyses to never-smoking, non-Hispanic white males.SUBJECTS: 5062 men (age: 30–74 y, BMI: 14–44 kg/m2) from the Adventist Mortality Study.MEASUREMENTS: Subjects reported data on anthropometric, demographic, medical, dietary and lifestyle characteristics at baseline and were enrolled in mortality surveillance during a 26 y study period (1960–1985).RESULTS: During the early years of follow-up (years 1–8, 9–14), we found some evidence of excess risk among the leanest men that was probably due to the effects of antecedent illness. During the later years of follow-up (years 15–26), effects due to antecedent illness were not apparent and a significant positive, linear relation between BMI and all-cause mortality was consistently found among middle-aged (30–54 y) and older (55–74 y) men. Disease-specific analyses of the later follow-up (years 15–26) revealed that the positive linear trends with all-cause mortality, were primarily due to excess risk of cardiovascular disease and cancer among the heavier men. Among older men, a significant inverse relation between BMI and respiratory disease mortality risk was identified during later follow-up (years 15–26), but this effect attenuated after restriction of the analyses to men with no baseline history of respiratory disease.CONCLUSIONS: The re-analysis confirms the findings of a positive, linear relation between BMI and all-cause mortality, reported in the original study.

Determinants of Eight-Year Diet Recall Ability

This study investigated how well people can recall their food habits of years ago and identified factors that predict recall ability. We examined the self-reported dietary intakes of 623 people, about one-third of whom were vegetarians. Subjects included cancer cases and controls who were selected as a representative sample of the Adventist Health Study population. We compared the initial (1976) dietary data with data recalled retrospectively in 1984. The initial and retrospective assessments made use of the same food frequency questionnaire for the same 35 food items. Recall ability was measured in two ways: exact recall and recall error. Persons with a stable diet had by far the best recall. Vegetarian status and level of education also were determinants of exact recall, whereas diet stability and education were the most significant determinants of recall error. These results indicate that some individuals, particularly those with a stable diet, those with a vegetarian diet, and those with more education, are able to recall their past dietary practices with reasonable reliability