Endocrine Abstracts

Current knowledge supports the notion that the onset and progression of endocrine and age-related diseases depend on an individual’s metabolic flexibility. With respect to cardiometabolic diseases, especially in older persons, several factors act in concert and converge to challenge metabolic flexibility. These include an inadequate diet, insufficient physical activity, chronodisruption, decreased metabolic reserve, altered gut microbiome, and reduced immune system capacity. At the personal level, all these factors interact together and with an individual’s genetic make-up to either promote or disrupt a program of metabolic flexibility in the context of endocrine disorders, aging, and obesity as well as the end point of many of these ailments, which are cardiovascular diseases.

Specifically, within the context of personalized nutrition or nutrigenomics, we seek to identify new metabolite-based markers, substantiate intake of certain foods, nutrients or dietary patterns, define the degree and mechanisms by which circadian control affects cardiometabolic diseases, and to describe the roles of microRNAs in these diseases.

Excellent examples of progress in this area are the results obtained for i) the APOA2 locus, dietary fat and obesity; ii) the LPL locus, polyunsaturated fatty acids, and triglyceride levels; and iii) the TCF7L2, Mediterranean diet and stroke. The results of the studies undertaken to date, indicate that huge progress has been made in identifying polymorphisms in genes related with endocrine and cardiometabolomic diseases. Therefore, while the current scientific evidence level of applying genotype data to personalized treatment is at its early stages, future prospects are encouraging. Outcomes of this research will generate new and better strategies for the prevention of age-related disorders and for slowing the aging process using nutritional and behavioral approaches.