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. 2017 Mar 1;185(5):345-361.
doi: 10.1093/aje/kww124.

Milk, Fruit and Vegetable, and Total Antioxidant Intakes in Relation to Mortality Rates: Cohort Studies in Women and Men

Free PMC article

Milk, Fruit and Vegetable, and Total Antioxidant Intakes in Relation to Mortality Rates: Cohort Studies in Women and Men

Karl Michaëlsson et al. Am J Epidemiol. .
Free PMC article

Abstract

High milk consumption might shorten life span through increased oxidative stress. We aimed to determine whether higher mortality rates with high milk consumption are modified by fruit and vegetable intake or total antioxidant intake (oxygen radical absorbance capacity). We used information from food frequency questionnaires completed by 61,420 women in a Swedish cohort (22,391 deaths from the 1987-1990 baseline onward), 36,714 women from a second survey (1997) of this cohort, and 45,280 Swedish men (15,478 deaths from the 1998 baseline onward). Compared with low consumption of milk (<1 glass/day) and high consumption of fruits/vegetables (≥5 servings/day), time-updated information revealed an adjusted hazard ratio for death of 2.79 (95% confidence interval (CI): 2.42, 3.21) in women who consumed ≥3 glasses of milk/day and <1 serving/day of fruit/vegetables and a hazard ratio of 1.60 (95% CI: 1.40, 1.82) in women who consumed the same amount of milk but ≥5 servings/day of fruits/vegetables. The same comparisons in men, based on a single food frequency questionnaire, displayed hazard ratios of 1.31 (95% CI: 1.14, 1.51) and 1.07 (95% CI: 0.97, 1.18), respectively. Total antioxidant consumption showed similar patterns as fruit/vegetable intakes. Dietary antioxidant intake, especially in women, seems to modify the elevated death rate associated with high milk consumption.

Keywords: antioxidants; fruit; galactose; lactose; milk; mortality; oxidative stress; vegetables.

Figures

Figure 1.
Figure 1.
Sex-specific multivariable-adjusted spline curves illustrating the relationship of milk intake (A), fruit and vegetable intake (B), and oxygen radical absorbance capacity (ORAC; µmol/day) (C) with hazard ratios for death from all causes by the use of time-updated information in the whole Swedish Mammography Cohort (SMC; baseline 1987–1990) (solid line), in the SMC after administration of the second food frequency questionnaire (baseline 1997) (short-dashed line), and in the Cohort of Swedish Men (baseline 1998) (long-dashed line). The shaded areas illustrate 95% confidence intervals. One glass of milk corresponds to 200 mL. Covariates were age, body mass index (weight (kg)/height (m)2), height, energy intake, alcohol intake, intakes of yogurt, cheese, and red and processed meat, education, marital status (living alone vs. not), physical activity (metabolic equivalent-hours/day), smoking habits (never, former, or current smoker and, for baseline 1997, also pack-years of smoking), ever use of antioxidant-containing supplements, and weighted Charlson's comorbidity index. Associations with milk intake were further adjusted for intake of fruit and vegetables, and associations with fruit and vegetable intake and ORAC were adjusted for intake of milk.
Figure 2.
Figure 2.
Adjusted hazard ratios (HRs) and 95% confidence intervals (in parentheses) for all-cause mortality according to combined intakes of milk and fruit and vegetables, using persons with the lowest milk intake and the highest fruit and vegetable intake as the reference group. A) HRs based on time-updated information on the whole Swedish Mammography Cohort (SMC) (women, baseline 1987–1990); B) HRs based on the SMC after administration of the second food frequency questionnaire (women, baseline 1997); C) HRs based on the Cohort of Swedish Men (men, baseline 1997). The shading corresponds to the value of the HR; the darker the shading, the larger the HR. One glass of milk corresponds to 200 mL. Covariates were age, body mass index (weight (kg)/height (m)2), height, energy intake, alcohol intake, intakes of yogurt, cheese, and red and processed meat, education, marital status (living alone vs. not), physical activity (metabolic equivalent-hours/day), smoking habits (never, former, or current smoker and, for baseline 1997, also pack-years of smoking), ever use of antioxidant-containing supplements, and weighted Charlson's comorbidity index.
Figure 3.
Figure 3.
Adjusted hazard ratios (HRs) and 95% confidence intervals (in parentheses) for all-cause mortality according to combined daily intake of milk and oxygen radical absorbance capacity (ORAC; µmol/day), using persons with the lowest intake of milk and the highest quartile of ORAC as the reference group. A) HRs based on the Swedish Mammography Cohort after administration of the second food frequency questionnaire (women, baseline 1997); B) HRs based on the Cohort of Swedish Men (men, baseline 1997). The shading corresponds to the value of the HR; the darker the shading, the larger the HR. One glass of milk corresponds to 200 mL. Covariates were age, body mass index (weight (kg)/height (m)2), height, energy intake, alcohol intake, intakes of yogurt, cheese, and red and processed meat, education, marital status (living alone vs. not), physical activity (metabolic equivalent-hours/day), smoking habits (never, former, or current smoker and pack-years of smoking), ever use of antioxidant-containing supplements, and weighted Charlson's comorbidity index.
Figure 4.
Figure 4.
Overview of galactose metabolism. The major pathway of galactose metabolism (the Leloir pathway) operates via the enzymes galactokinase (GALK), galactose-1-phosphate uridylyltransferase (GALT), and uridine diphosphate (UDP) galactose 4-epimerase (GALE), resulting in UDP-glucose. The conversion to galactitol by aldose reductase via the polyol pathway results in decreased availability of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione, with increased production of free radicals (56). By way of a nonenzymatic reaction with amino groups in proteins, lipids, and nucleic acids, galactose is converted to advanced glycation end products (AGEs).

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References

    1. Michaëlsson K, Wolk A, Langenskiold S, et al. Milk intake and risk of mortality and fractures in women and men: cohort studies. BMJ. 2014;349:g6015. - PMC - PubMed
    1. Cui X, Zuo P, Zhang Q, et al. Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: protective effects of R-alpha-lipoic acid. J Neurosci Res. 2006;83(8):1584–1590. - PubMed
    1. Song X, Bao M, Li D, et al. Advanced glycation in D-galactose induced mouse aging model. Mech Ageing Dev. 1999;108(3):239–251. - PubMed
    1. Hao L, Huang H, Gao J, et al. The influence of gender, age and treatment time on brain oxidative stress and memory impairment induced by D-galactose in mice. Neurosci Lett. 2014;571C:45–49. - PubMed
    1. Cui X, Wang L, Zuo P, et al. D-galactose-caused life shortening in Drosophila melanogaster and Musca domestica is associated with oxidative stress. Biogerontology. 2004;5(5):317–325. - PubMed

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