Epigenetic Modifications Induced by Nutrients in Early Life Phases: Gender Differences in Metabolic Alteration in Adulthood

Abstract

Metabolic chronic diseases, also named noncommunicable diseases (NCDs), are considered multifactorial pathologies, which are dramatically increased during the last decades. Noncommunicable diseases such as cardiovascular diseases, obesity, diabetes mellitus, cancers, and chronic respiratory diseases markedly increase morbidity, mortality, and socioeconomic costs. Moreover, NCDs induce several and complex clinical manifestations that lead to a gradual deterioration of health status and quality of life of affected individuals. Multiple factors are involved in the development and progression of these diseases such as sedentary behavior, smoking, pollution, and unhealthy diet. Indeed, nutrition has a pivotal role in maintaining health, and dietary imbalances represent major determinants favoring chronic diseases through metabolic homeostasis alterations. In particular, it appears that specific nutrients and adequate nutrition are important in all periods of life, but they are essential during specific times in early life such as prenatal and postnatal phases. Indeed, epidemiologic and experimental studies report the deleterious effects of an incorrect nutrition on health status several decades later in life. During the last decade, a growing interest on the possible role of epigenetic mechanisms as link between nutritional imbalances and NCDs development has been observed. Finally, because of the pivotal role of the hormones in fat, carbohydrate, and protein metabolism regulation throughout life, it is expected that any hormonal modification of these processes can imbalance metabolism and fat storage. Therefore, a particular interest to several chemicals able to act as endocrine disruptors has been recently developed. In this review, we will provide an overview and discuss the epigenetic role of some specific nutrients and chemicals in the modulation of physiological and pathological mechanisms.

The “Elderly” Lesson in a “Stressful” Life: Italian Holistic Approach to Increase COVID-19 Prevention and Awareness

“…The anti-inflammatory effects of the Mediterranean Dietary Model could be mediated by epigenetic mechanisms already operating from in-utero life and early years of postnatal life, although a further analysis is needed to corroborate this hypothesis (34). Epigenetic factors are heritable from cell to daughter cell within the same organism, and there is growing evidence that this heritability can be transgenerational among organisms (47). Moreover, a recent study concluded that a 1-year Mediterranean-like-nutritional intervention can promote epigenetic rejuvenation in the elderly (48).…”

Applying epigenetic science to the understanding of eating disorders: a promising paradigm for research and practice

“…For example, research in animals, living humans, and postmortem human brains has shown associations between early environment (e.g. trauma) and DNA methylation [ 18 ▪ , 19 – 24 ]. Likewise, exposure to gestational distress (e.g.…”

“…Likewise, exposure to gestational distress (e.g. maternal depression, malnutrition) has been associated with peripheral DNA methylation outcome later in life [ 18 ▪ , 20 , 22 – 24 ]. Although the studies in question are heterogenous with respect to methodology and results [ 18 ▪ , 23 ], available findings point to the potentials of epigenetic processes to constitute molecular mechanisms that could link environmental impacts, experienced at various moments throughout the life cycle (perinatal, childhood and adult) to mental-health outcomes, including eating disorders [ 8 , 18 ▪ , 23 ].…”

The Impact of Unbalanced Maternal Nutritional Intakes on Oocyte Mitochondrial Activity: Implications for Reproductive Function

“…It is exactly in this peri-conceptional period that nutrition might cause short-, medium-, and long-term effects on reproduction and on the health of the offspring. All these adverse outcomes have been imputed especially to epigenetic modifications and mitochondrial impairments [ 2 , 3 , 4 ].…”