This narrative mini- review summarizes current knowledge of the role of polyphenols in health outcomes—and non-communicable diseases specifically—and discusses the implications of this evidence for public health, and for future directions for public health practice, policy, and research. The publications cited originate mainly from animal models and feeding experiments, as well as human cohort and case-control studies. Hypothesized protective effects of polyphenols in acute and chronic diseases, including obesity, neurodegenerative diseases, type 2 diabetes, and cardiovascular diseases, are evaluated. Potential harmful effects of some polyphenols are also considered, counterbalanced with the limited evidence of harm in the research literature. Recent international governmental regulations are discussed, as the safety and health claims of only a few specific polyphenolic compounds have been officially sanctioned. The implications of food processing on the bioavailability of polyphenols are also assessed, in addition to the health claims and marketing of polyphenols as a functional food. Finally, this mini-review asserts the need for increased regulation and guidelines for polyphenol consumption and supplementation in order to ensure consumers remain safe and informed about polyphenols.

Few studies have evaluated the relationship between changes in diet quality over time and the risk of death. We used Cox proportional-hazards models to calculate adjusted hazard ratios for total and cause-specific mortality among 47,994 women in the Nurses’ Health Study and 25,745 men in the Health Professionals Follow-up Study from 1998 through 2010. Changes in diet quality over the preceding 12 years (1986–1998) were assessed with the use of the Alternate Healthy Eating Index–2010 score, the Alternate Mediterranean Diet score, and the Dietary Approaches to Stop Hypertension (DASH) diet score. The pooled hazard ratios for all-cause mortality among participants who had the greatest improvement in diet quality (13 to 33% improvement), as compared with those who had a relatively stable diet quality (0 to 3% improvement), in the 12-year period were the following: 0.91 (95% confidence interval [CI], 0.85 to 0.97) according to changes in the Alternate Healthy Eating Index score, 0.84 (95 CI%, 0.78 to 0.91) according to changes in the Alternate Mediterranean Diet score, and 0.89 (95% CI, 0.84 to 0.95) according to changes in the DASH score. A 20-percentile increase in diet scores (indicating an improved quality of diet) was significantly associated with a reduction in total mortality of 8 to 17% with the use of the three diet indexes and a 7 to 15% reduction in the risk of death from cardiovascular disease with the use of the Alternate Healthy Eating Index and Alternate Mediterranean Diet. Among participants who maintained a high-quality diet over a 12-year period, the risk of death from any cause was significantly lower — by 14% (95% CI, 8 to 19) when assessed with the Alternate Healthy Eating Index score, 11% (95% CI, 5 to 18) when assessed with the Alternate Mediterranean Diet score, and 9% (95% CI, 2 to 15) when assessed with the DASH score — than the risk among participants with consistently low diet scores over time. Improved diet quality over 12 years was consistently associated with a decreased risk of death. (Funded by the National Institutes of Health.)

The Boston Puerto Rican Health Study is an ongoing longitudinal cohort study designed to examine the role of psychosocial stress on presence and development of allostatic load and health outcomes in Puerto Ricans, and potential modification by nutritional status, genetic variation, and social support.

Background—: Adherence to several diet quality scores, including the Alternative Healthy Eating Index, Alternative Mediterranean Diet score, and Dietary Approach to Stop Hypertension, has been associated with lower risk of cardiovascular disease (CVD), but little is known about how changes in these scores over time influence subsequent CVD risk. Methods and Results—: We analyzed the association between 4-year changes in the 3 diet quality scores (Alternative Healthy Eating Index, Alternative Mediterranean Diet score, and Dietary Approach to Stop Hypertension) and subsequent cardiovascular disease (CVD) risk among 29 343 men in the Health Professionals Follow-up Study and 51 195 women in the Nurses’ Health Study (1986–2010). During 1 394 702 person-years of follow-up, we documented 11 793 CVD cases. Compared with participants whose diet quality remained relatively stable in each 4-year period, those with the greatest improvement in diet quality scores had a 7% to 8% lower CVD risk in the subsequent 4-year period (pooled hazard ratio, 0.92 [95% confidence interval (CI), 0.87–0.99] for the Alternative Healthy Eating Index; 0.93 [95% CI, 0.85–1.02] for the Alternative Mediterranean Diet score; and 0.93 [95% CI, 0.87–0.99] for the Dietary Approach to Stop Hypertension; all P for trend <0.05). In the long term, increasing the diet scores from baseline to the first 4-year follow-up was associated with lower CVD risk during the next 20 years (7% [95% CI, 1–12] for the Alternative Healthy Eating Index, and 9% [95% CI, 3–14] for the Alternative Mediterranean Diet score). A decrease in diet quality scores was associated with significantly elevated risk of CVD in subsequent time periods. Conclusions—: Improving adherence to diet quality scores over time is associated with significantly lower CVD risk in both the short term and long term.

Leptin promotes satiety and modulates energy balance and weight. Diet-induced obesity leads to leptin resistance, exacerbating overeating. We reviewed the literature on the relationship between diet and leptin, which suggests that addressing leptin resistance through dietary interventions can contribute counteracting obesity. Albeit some limitations (e.g., limited rigor, small samples sizes), studies in animals and humans show that diets high in fat, carbohydrates, fructose, and sucrose, and low in protein are drivers of leptin resistance. Despite methodological heterogeneity pertaining to this body of literature, experimental studies show that energy-restricted diets can reduce leptinemia both in the short and long term and potentially reverse leptin resistance in humans. We also discuss limitations of this evidence, future lines of research, and implications for clinical and public health translations. Main limitations include the lack of a single universally-accepted definition of leptin resistance, and of adequate ways to accurately measure it in humans. The use of leptin sensitizers (drugs) and genetically individualized diets are alternatives against leptin resistance that should be further researched in humans. The tested very-low-energy intervention diets are challenging to translate into wide clinical or population recommendations. In conclusion, the link between nutritional components and leptin resistance, as well as research indicating that this condition is reversible, emphasizes the potential of diet to recover sensitivity to this hormone. A harmonized definition of leptin resistance, reliable methods to measure it, and large-scale, translational, clinical, and precision nutrition research involving rigorous methods are needed to benefit populations through these approaches.