King Grub
2018-03-21, 11:59
Background
While low-grade chronic inflammation has been suggested as a major modulator of healthy aging (HA), no study has yet investigated the link between the inflammatory potential of the diet and multidimensional concepts of HA.
Objective
We aimed to evaluate the association between the inflammatory potential of the diet at midlife, as measured by the Dietary Inflammatory Index (DII), and HA assessed 13 y later.
Methods
We analyzed data from 2796 participants in the French Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) study aged 45–60 y at baseline (1994–1995) and initially free of diabetes, cardiovascular disease, and cancer. During the trial phase of the study (1994–2002), participants received either a placebo or a daily nutritional dose of antioxidant supplement (120 mg vitamin C, 6 mg β-carotene, 30 mg vitamin E, 100 μg Se, 20 mg Zn). HA was assessed in 2007–2009, and defined as having no major chronic disease, good physical and cognitive functioning, independence in daily activities, no depressive symptoms, good social health, good overall self-perceived health, and no function-limiting pain. The DII was calculated based on repeated baseline 24-h dietary records. Its association with HA was assessed by robust-error-variance Poisson regression, providing RR estimates.
Results
After adjustment for potential confounders, higher DII scores (reflecting a more proinflammatory diet), were associated with a decreased likelihood of HA: RRtertile 3/tertile 1 = 0.85 (95% CI: 0.74, 0.99); P-trend = 0.03. Secondary analyses revealed that this association was only significant among participants who had been in the placebo group during the trial phase: RRtertile 3/tertile 1 = 0.80 (95% CI: 0.64, 1.00); P-trend = 0.04.
Conclusions
This study suggests that a proinflammatory diet may lower the probability of overall HA.
The Inflammatory Potential of the Diet at Midlife Is Associated with Later Healthy Aging in French Adults. The Journal of Nutrition, Volume 148, Issue 3, 1 March 2018, Pages 437–444.
While low-grade chronic inflammation has been suggested as a major modulator of healthy aging (HA), no study has yet investigated the link between the inflammatory potential of the diet and multidimensional concepts of HA.
Objective
We aimed to evaluate the association between the inflammatory potential of the diet at midlife, as measured by the Dietary Inflammatory Index (DII), and HA assessed 13 y later.
Methods
We analyzed data from 2796 participants in the French Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) study aged 45–60 y at baseline (1994–1995) and initially free of diabetes, cardiovascular disease, and cancer. During the trial phase of the study (1994–2002), participants received either a placebo or a daily nutritional dose of antioxidant supplement (120 mg vitamin C, 6 mg β-carotene, 30 mg vitamin E, 100 μg Se, 20 mg Zn). HA was assessed in 2007–2009, and defined as having no major chronic disease, good physical and cognitive functioning, independence in daily activities, no depressive symptoms, good social health, good overall self-perceived health, and no function-limiting pain. The DII was calculated based on repeated baseline 24-h dietary records. Its association with HA was assessed by robust-error-variance Poisson regression, providing RR estimates.
Results
After adjustment for potential confounders, higher DII scores (reflecting a more proinflammatory diet), were associated with a decreased likelihood of HA: RRtertile 3/tertile 1 = 0.85 (95% CI: 0.74, 0.99); P-trend = 0.03. Secondary analyses revealed that this association was only significant among participants who had been in the placebo group during the trial phase: RRtertile 3/tertile 1 = 0.80 (95% CI: 0.64, 1.00); P-trend = 0.04.
Conclusions
This study suggests that a proinflammatory diet may lower the probability of overall HA.
The Inflammatory Potential of the Diet at Midlife Is Associated with Later Healthy Aging in French Adults. The Journal of Nutrition, Volume 148, Issue 3, 1 March 2018, Pages 437–444.