Abstract
Considerable efforts have been dedicated to uncovering environmental and other risk factors that contribute to or alter the risk of acquiring a disease. But complex non-Mendelian traits and diseases were impervious to investigation by the use of traditional epidemiological and standard genetic approaches. The epigenetic approach, presented here, may contribute to a fruitful etiology that focuses, in this case, on the transgenerational inheritance following ancestors’ exposure during the slow stature growth period in mid-childhood. It is seen as part of the responses over generations following nutrition-related circumstances. When the requirements of nutrition were at its lowest, the child might have been overfed by the abundance after a very good crop, resulting in epigenetic marks transferred to descendants. The agents are supposed be nutritional or nutrition-related. The studies in humans of this specific kind of inheritance are scarce. Three settings have been Överkalix, Sweden, Bristol, the UK, and Taiwan. Recently a German and a Swedish study have explicitly tried to reproduce transgenerational findings of the slow stature growth period sensitivity to starving and loss of parent, respectively, influencing descendant’s mental health and birthweight, respectively. In a small strategic sample in Överkalix has been observed methylations in grandchildren’s pathways related to ancestor’s famine or excess food in mid-childhood, marks such as insulin processing and binding. The research in human transgenerational epigenetic inheritance is small but promises specific preventive and therapeutic measures, in public health and molecular biology, to diminish the plagues of diseases of complex etiology, such as cardiovascular disease.
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Bygren, L.O., Kaati, G. (2018). Slow Growth Period and Epigenetics. In: Patel, V., Preedy, V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham. https://doi.org/10.1007/978-3-319-31143-2_119-1
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DOI: https://doi.org/10.1007/978-3-319-31143-2_119-1
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