Annual Review of Nutrition - Early Publication

Dietary guidelines have been placed under unprecedented scrutiny in the past decade, as the “obesity epidemic” enters its fifth decade with limited evidence of public health progress. In the era of successful obesity pharmacotherapy, there is a heightened sense of urgency to make progress on dietary prevention of obesity and related chronic diseases, contributing to both diverse criticism of guidelines and low degrees of trust in nutritional sciences. In this review, I view nutritional guidance through a historical lens, tracking its development from its genesis through the modern focus on obesity and chronic diseases and consider criticisms of past and existing dietary guidance. I reflect on themes that emerge from this history and consider potential paths forward to improve the quality of nutritional guidance and actualize its goals of improving population health.

Dietary bioactive compounds such as omega-3 polyunsaturated fatty acids and phytochemicals have numerous health benefits, which include alleviating obesity-associated inflammation and metabolic dysfunction. While mechanistic studies have focused thus far on how these compounds or their metabolites affect whole-animal physiology or exert tissue-specific effects, detailed reports are lacking about how these bioactives specifically affect gut microbiota and mitochondrial function, two important processes impacted by metabolic diseases. Gut microbiota, through their composition and metabolites, play a significant role in overall health and mediating the effects of diet. Therefore, understanding how dietary bioactive compounds modulate gut microbiota is crucial for elucidating their contributions to metabolic health. Conversely, gut microbiota may also alter the metabolism of bioactives, especially phytochemicals, and impact their bioavailability and function. Mitochondria, particularly in adipose tissue, play a central role in energy metabolism and are implicated in the development of obesity-associated metabolic dysfunction. Thus, investigating the effects of dietary bioactive compounds on mitochondrial function provides valuable insight into their potential roles in addressing obesity-related diseases. Accordingly, the goal of this review is to discuss key published work on the interplay between dietary bioactives, gut microbiota and their metabolites, and mitochondria function in the context of improving obesity-associated inflammation and metabolic dysfunction.

The US Department of Agriculture's Gus Schumacher Nutrition Incentive Program (GusNIP) funds produce prescription (PPR) programs that allow healthcare to support patients in accessing fruits and vegetables. This hybrid systematic narrative review identified 16 studies of PPR programs associated with GusNIP funding in some way that examined health outcomes, including clinical measures and healthcare utilization. Program designs were heterogeneous, sample sizes were generally small, and methodological rigor was often low, with most studies using a prepost design and none using a randomized control group. Fewer than half of the studies examining clinical values showed an association between PPR participation and improved health outcomes (for example, three of eight studies measuring weight or body mass index showed a statistically significant reduction, as well as two of the six studies measuring glycosylated hemoglobin). Only three studies examined healthcare utilization, two of which showed improvements in hospitalization and/or emergency department utilization. Overall, evidence for the health impact of PPRs is nascent but growing. PPRs with capacity should engage in rigorous study designs and examine a variety of downstream health and utilization outcomes.

There is widespread interest in fasting as a therapeutic or preventive regimen for improving health. This review provides an overview of the impact of fasting on adipose tissue metabolism, with special attention to sexually dimorphic regulation. During fasting, the storage of triacylglycerols in adipose tissue is inhibited via suppression of the extracellular lipolytic enzyme lipoprotein lipase. By contrast, the breakdown of stored triacylglycerols and subsequent release of fatty acids and glycerol in the blood are enhanced via stimulation of the intracellular lipolytic enzymes adipose triglyceride lipase and hormone-sensitive lipase. These metabolic alterations are driven by changes in humoral factors such as insulin, glucagon, corticosteroids, growth hormone, and catecholamines, as well as by neuronal pathways, and are mediated by transcriptional and posttranscriptional regulation of critical enzymes. Overall, fasting profoundly influences adipose tissue metabolism and leads to mobilization of stored triacylglycerols and the repartitioning of circulating triacylglycerols to nonadipose tissues.

The United States is experiencing rapid growth of racial and ethnic minority aging populations, with implications for health disparities research, as many of these groups experience excess prevalence of chronic diseases. The reasons for health disparities are multifactorial, including social determinants of health, with nutrition playing a critical role. The current inadequacy of dietary assessment methods limits this research. Evidence from food frequency questionnaires with multiethnic studies consistently shows lower validity among minority adults, even with some adaptation, relative to non-Hispanic White adults. This is likely to introduce not only error but also bias in estimates. In addition to adding foods, culturally specific recipes and portion sizes must be considered. Among those with low education, careful data collection with trained interviewers is essential. Important barriers to change include limited access to healthy foods, cultural preferences that influence dietary choices, and limited nutrition knowledge. Rediscovering traditional foodways may be an effective tool.

Hexoses, including glucose, fructose, and galactose, are six-carbon monosaccharides that play fundamental roles in mammalian metabolism, with glucose serving as the primary energy source and fructose and galactose metabolized through pathways converging with glucose metabolism. While glucose metabolism has been extensively studied over the past hundred years, the mechanisms of fructose metabolism and uptake, the transporters involved, and its roles in physiology and disease are far less explored. Recent data also suggest that excessive fructose intake can have detrimental effects on metabolic organs, including the liver. Emerging studies have uncovered novel regulatory mechanisms in glucose and fructose metabolism, including the role of posttranslational modifications of transporters and enzymes, and the discovery of regulators of transporters. Here, we highlight new findings on the regulation of glucose and fructose transporters and integrate recent molecular and clinical insights into how glucose and fructose contribute to metabolic diseases.

My scientific journey is not traditional; it begins with the career opportunities available for and expectations of young women during the outset of the women's liberation era and how life changed along the way. I've started my story when I was a child in the 1950s, daughter of a milkman and an immigrant fleeing the communists in her home country. My story reaches an apex when I became an internationally recognized vitamin E expert. Overall, I made transformative contributions to our understanding of α-tocopherol function in humans, and, using model systems, I have reported how its absence has a major impact on cellular metabolism. This is the story of my transformation. I have had some excellent mentors. I have a passion about learning why the body needs α-tocopherol. Certainly, when I started out, I had no expectations that I would become a world-renowned scientist, a term I now use to describe myself.