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Title: Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults

Authors: Ludwig DS, Pereira MA, et al.

Reference: JAMA 1999;282:1539-1546

Reviewer: Joaquin Barnoya

Location of study: USA

Problem addressed: Diet may affect insulin levels in 3 ways: by modulating insulin secretion, by affecting insulin action at peripheral sites, or by promoting obesity. There is evidence suggesting that dietary fiber, may play a role in regulating circulating insulin levels. Dietary fiber reduces insulin secretion by slowing the rate of nutrient absorption following a meal. The authors tested the hypothesis that fiber consumption is independently and inversely associated with insulin levels, weight gain, and other CVD risk factors among adults, and to compare the effect of fiber with fat and other major dietary components.

Purpose of study: This study examined the role of fiber consumption and its association with insulin levels, weight gain, and other CVD risk factors

Study design: multicenter population-based

Methods: Nearly equal number of black and whites, younger (18-24 years) and older (25-30 years) individuals, and those with more (>high school) and less (high school education) were included. A baseline examination was done in 1985-1986. The cohort has been followed for 10 years to date, with follow-up examinations at years 2, 5, 7, and 10. Individuals with extreme values of dietary intake were excluded, also excluded were women lactating at the baseline examinations or within 180 days of the year 10 examination; individuals having diabetes at examination years 0 or 10; individuals taking medication for blood pressure or lipid control; and those who had not fasted for at least 8 hours prior to clinic visit. As a result of these exclusions and missing data for covariates or dependent variables, the final sample size available for analysis varied from 1801 (2-hour insulin) to 2909 (body weight).

CARDIA diet history involved an interviewer-administered quantitative food frequency questionnaire including approximately 700 foods. Validity correlations between mean daily nutrient intakes from the CARDIA diet history and means from 7 randomly schedules 24-hour recalls ranged from 0.50 to 0.86 in white men and to 0.04 to 0.53 in black women. Prior to each examination, participants were asked to fast for 12 hrs. and to avoid smoking and heavy physical activity for 2 hrs.

Race-specific general linear models were computed to adjust least square means of CVD risk factors (dependent variables) according to quintiles of dietary factors (independent variables). Quintile cut points for dietary factors were based on distributions of the entire cohort, resulting in similar levels of intake between blacks and whites within each quintile. Dependent variables were body weight; WHR; systolic and diastolic blood pressure; HDL-C; LDL-C; fibrinogen; and the natural logarithms (to generate a near normal distribution) of fasting insulin, 2-hr. insulin, and triglycerides. Covariates included in the model as potential confounders were age, sex, CARDIA field center, education, energy intake, vitamin supplementation use, cigarette smoking, alcohol intake, and total physical activity. Since obesity causes insulin resistance and hyperinsulinemia, the associations between dietary components and insulin levels for BMI were also adjusted. To examine whether the associations between dietary components and risk factors may be mediated by insulin level, the authors adjusted for fasting insulin in additional models.

Results: Associations with age were positive for fiber, inverse for carbohydrate, weak for fat, and null for protein. Women consumed more fiber and carbohydrate but less protein and fat (whites only) than men. Cigarette smoking was inversely associated with carbohydrate and fiber intake and positively associated with fat intake (whites only). Physical activity was inversely associated with dietary fat, but positively associated with fiber, carbohydrate, and protein. Alcohol intake showed inverse associations with dietary carbohydrate and dietary fat. Finally, vitamin supplementation use was positively associated with dietary fiber, carbohydrate (whites only), and protein, and inversely associated with dietary fat. Body weight was inversely associated with fiber and carbohydrate and positively associated with protein intake in whites. Neither total nor saturated fat intake was associated with body weight in whites. In blacks, dietary fiber was also strongly associated with body weight, while total fat and carbohydrate were more modestly associated.

At all the levels of fat intake, individuals eating the most fiber gained less weight than those eating the least fiber. After adjusting for BMI and other confounding variables, both dietary fiber (mean difference of -5.6 mmol/L from lowest to highest quintiles, P=.007) and saturated fat (+4.2 mmol/L, P=.05) were associated with fasting insulin in whites. In blacks, fiber was the only dietary factor associated witfasting insulin level. Fiber, but neither total nor saturated fat, was associated with 2-hr. insulin in both races (whites: -26.4 mmol/L, P=.03; blacks: -110.4 pmol/L, P<.001).

In white men and women, fiber was associated with systolic blood pressure (mean difference from lowest to highest quintiles: (-2.2 mmHg, P=.01), diastolic blood pressure (-2.7 mmHg, P<.001), tryglicerides (-0.09 mmol/L, P=.05), HDL-C (+0.06 mmol/L, P=.005), LDL-C (-0.12 mmol/L, P=.06) and fibrinogen (-0.46 (mol/L, P=.005). With the exception of diastolic blood pressure, these associations were substantially attenuated after adjustment for fasting insulin. In contrast, no form of dietary fat was significantly associated with any of these CVD risk factors.

Comments: These findings underscores the potential importance of dietary fiber to CVD risk and are consistent with the Health Professionals' Follow-up Study in which the modest associations between dietary fat and myocardial infarction incidence were largely attenuated by adjustment for dietary fiber.

The authors believe that the strong inverse associations between dietary fiber and multiple CVD risk factors (e.g. excessive weight, central adiposity) are mediated, at least in part, by insulin levels. Dietary fiber exerts a major effect on the glycemic, and therefore the insulinemic, response to carbohydrate meal. A low-fiber diet would tend to stimulate relatively more insulin secretion than a high-fiber diet. The findings in this study confirm such assumption, as the highest insulin levels, after adjustment for BMI, were found among individuals with the lowest fiber intake.

The relation between dietary fiber and weight gain is of particular interest. The high insulin levels associated with low-fiber diets may promote excessive weight gain. This may operate by one of several mechanisms, alterations in adipose tissue physiology, by shunting of metabolic fuels form oxidation storage, and by increased appetite. Indeed, hyperinsulinemia has been associated with excessive weight gain in some, but not all, prospective epidemiological studies.

Several methodological issues need emphasis. As this study is observational, no causality can be proven. However, the conclusions reached appear robust: the data have been adjusted for all commonly, potential variables; dietary fiber is related to CVD risk by a plausible physiological mechanism; and these results are consistent with numerous studies demonstrating improvements in CVD risk factors on either high-fiber or low glycemic index diets. Another methodological issue is that a relatively large spread was observed in dietary fiber intake among individuals and these findings would not necessarily apply to other populations with different patterns of dietary fiber consumption. This study did not examine the effects of fiber type, source, or form, which may affect the insulin response as well as CVD risk.

In summary, dietary fiber was inversely associated with insulin levels, weight gain, and other risk factors for CVD in young adults. This findings add up to current evidence that fiber may play a greater role in determining CVD risk than total or saturated fat intake.