Over a third of older adults in the U.S. experience significant vision loss, which decreases independence and is a biomarker of decreased health span. As the global aging population is expanding, it is imperative to uncover strategies to increase health span and reduce the economic burden of this age-related disease. While there are some treatments available for age-related vision loss, such as surgical removal of cataracts, many causes of vision loss, such as dry age-related macular degeneration (AMD), remain poorly understood and no treatments are currently available. Therefore, it is necessary to better understand the factors that contribute to disease progression for age-related vision loss and to uncover methods for disease prevention. One such factor is the effect of diet on ocular diseases. There are many reviews regarding micronutrients and their effect on eye health. Here, we discuss the impact of dietary patterns on the incidence and progression of age-related eye diseases, namely AMD, cataracts, diabetic retinopathy, and glaucoma. Then, we focus on the specific role of dietary carbohydrates, first by outlining the physiological effects of carbohydrates on the body and then how these changes translate into eye and age-related ocular diseases. Finally, we discuss future directions of nutrition research as it relates to aging and vision loss, with a discussion of caloric restriction, intermittent fasting, drug interventions, and emerging randomized clinical trials. This is a rich field with the capacity to improve life quality for millions of people so they may live with clear vision for longer and avoid the high cost of vision-saving surgeries.

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Whole bone strength and resistance to fracture are determined by a combination of bone quantity and bone quality – key factors in determining risk for osteoporosis and age-related fractures. Recent preclinical studies have shown that alterations to the gut microbiome can influence bone quantity as well as bone tissue quality. Prior work on the gut microbiome and bone has been limited to young animals, and it is unknown if the gut microbiome can alter bone tissue strength in aged animals. Here we ask if alterations to the constituents of the gut microbiome influence bone strength in older mice (12–24 months of age). Male C57BL/6J mice raised on a standard chow diet until 12 months of age were assigned to one of three diets: high glycemic, low glycemic, or low glycemic diet containing antibiotics (ampicillin and neomycin) to modify the constituents of the gut microbiome. The group fed the low glycemic diet containing antibiotics showed reductions in whole bone strength that could not be explained by geometry, indicating reduced bone tissue strength ( p < 0.007). The high glycemic diet group had larger bone cross-sectional area and moment of inertia and a corresponding greater bone strength as compared to the low glycemic groups, however tissue strength did not noticeably differ from that of the low glycemic group. These findings demonstrate that modifying the gut microbiome in aged mice can alter bone tissue quality.

Objectives High glycemic index diet has been demonstrated to induce obesity and insulin resistance. The role of gut microbiota, as a key mediator of several metabolic syndromes, has not been elucidated. The objective of this project is to understand the effect of gut microbiota in a high-glycemic diet-induced obesity and associated metabolic complications. Methods Male C57Bl6/J mice aged 8–9 weeks were fed with a high-glycemic diet (HG, amylopectin-based) or low-glycemic diet (LG, amylose-based) ad libitum for 8 weeks. Body composition was determined by MRIs. Intraperitoneal glucose tolerance tests were performed after 6 weeks on diet. Mice were euthanized after 8 weeks on diet. Results After two weeks on diet, the HG group (n = 12) mice had a significantly higher body fat mass by MRI analysis, as compared to the LG group (n = 12) despite having similar body weight and equal food consumption. After 6 weeks, mice in the HG group had a significantly higher fasting glucose level compared to the LG group. There was no difference in fasting triglyceride level. Gonadal, subcutaneous and brown fat adipose tissue weight were significantly higher in the HG group after 8 weeks on diet. 16S rDNA sequencing on feces showed that the HG mice have a significantly higher Shannon diversity and different overall microbiome structure compared to the LG mice. The microbial community in the LG group was predominated by Bacteroidetes, particularly by Bacteroides thetaiotaomicron (Relative abundance 48.65 ± 12.88% versus HG 14.69 ± 0.07%), while the HG group was predominated by Firmicutes. Ongoing analysis will investigate the relative role of key microbial taxa on obesity and glucose homeostasis. Conclusions Consuming two weeks of a high-glycemic index diet induced adiposity and hyperglycemia along with a shift of the overall gut microbiota composition compared to a low-glycemic index diet. Funding Sources NIH, USDA, Robert C and Veronica Atkins Foundation

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