Glycation is favored by genetic and behavioral factors. Its consequences, cellular aging and age-related diseases, seem to be transmitted to future generations by epigenetic means.
Epigenetics is an extension of genetics and a branch of biology that focuses on the involvement of genetics and the environment to understand the transmission of acquired traits.
Thus, studies have highlighted the role of epigenetics in the phenomenon of metabolic memory in diabetes (1).
Similarly, fetal exposure to maternal glycation, following an excessively sweet diet before pregnancy, could be associated with a higher risk of glycation in the child (2); a risk greater than that attributable to genetic factors.
These results are particularly worrying: we are witnessing a maternal transmission of risks of accelerated aging (3).
And this is how a diet too rich in sugar would have, in a few generations, irreversible consequences on the aging of future generations.
© AGE Breaker updated 05 2023[Glycation is one of the major causes of aging. Resulting from the fixation of sugars on the proteins constituting the organism, glycation generates toxic compounds that cause cellular aging. Glycation is particularly involved in metabolic disorders, skin aging and cognitive decline.] [AGE BREAKER, patented nutritional supplements, based on rosmarinic acid, recognized by aging specialists around the world for their properties to reverse the effects of glycation.]
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1: A. El-Osta et Al. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. The Journal of Experimental Medicine. 2008; doi: 10.1084 / jem.20081188092608c
2: N. Foussard et Al. Skin Autofluorescence of Pregnant Women With Diabetes Predicts the Macrosomia of their Children. Diabetes, 2019 Aug;68(8). doi: 10.2337/db18-0906
3: A. Perrone et Al. Advanced Glycation End Products (AGEs): Biochemistry, Signaling, Analytical Methods, and Epigenetic Effects. Oxidative medicine and cellular longevity. Published online 2020 Mar 18. doi: 10.1155/2020/3818196