Purpose of review Purines have several important physiological functions as part of nucleic acids and as intracellular and extracellular signaling molecules. Purine metabolites, particularly uric acid, have been implicated in congenital and complex diseases. However, their role in complex diseases is not clear and they have both beneficial and detrimental effects on disease pathogenesis. In addition, the relationship between purines and complex diseases is affected by genetic and nutritional factors. This review presents latest findings about the relationship between purines and complex diseases and the effect of genes and nutrients on this relationship. Recent findings Evidence from recent studies show strong role of purines in complex diseases. Although they are causal in only few diseases, our knowledge about their role in other diseases is still evolving. Of all the purines, uric acid is the most studied. Uric acid acts as an antioxidant as well as a prooxidant under different conditions, thus, its role in disease also varies. Other purines, adenosine and inosine have been less studied, but they have neuroprotective properties which are valuable in neurodegenerative diseases. Summary Purines are molecules with great potential in disease pathogenesis as either metabolic markers or therapeutic targets. More studies need to be conducted to understand their relevance for complex diseases.
Background: Several innate and environmental factors affect the rate and degree of cognitive decline with each factor representing a potentially valuable intervention point to slow progression of this decline. Serum urate, a product of purine metabolism and potent antioxidant, and weight loss have been associated with cognitive decline.
Objectives The objective of this study was to determine whether and how a parent's own weight and their lifestyle choices impact the weight of their children. Methods Data were collected for 383 participants, 244 children (48.77% male, mean age 11.87 years) and one or both parents (24.82% male, mean age 41.38 years) via anthropometric measures and a questionnaire. Participants described factors related to their lifestyle and household environment including smoking status, sedentary behavior, and sleep duration. BMI-for-Age percentile (BfaP) was calculated for all children. These data were used to explore how parental and environmental factors relate to a child's weight status via correlation and regression analyses. Results Parents who were overweight or obese were more likely to have children with higher weight status; the relationship between a mother and child's weight status remains similar throughout adolescence (r = 0.26, P < 0.001), but a father's weight status is more reflective of the weight status of older children (r = 0.46, P = 0.015) rather than younger (r = 0.25, P = 0.10). Children were more likely to be overweight or obese if they lived in smoking households (non-smoking mean BfAP 57.29 (SE 2.6) vs. smoking BfAP 67.1 (SE4.9)). Fathers (r = 0.09, P = 0.5) and mothers (r = 0.06, P = 0.4) who spent more time on sedentary activities had children with higher BfAP. Children with parents who ate fast food more often were more likely to carry excess weight (r = 0.15, P = 0.03 for mothers, r = 0.10, P = 0.4 for fathers). Children with fathers who slept fewer than eight hours per day were more likely to be overweight or obese (r = −0.21, P = 0.05); a mother who engaged in very little or in large amounts of sleep was more likely to have offspring who were overweight or obese (P = 0.01). Conclusions Within this cohort, parental weight status predicts a child's weight status. Parents making healthier lifestyle choices for themselves will likely impact their child's weight in a desirable manner, providing guidance for future child obesity prevention and intervention programs. Funding Sources Funding for this research was provided by NIDDK.
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