As stated in the previous article, epigenetic alterations are the key hallmark of aging. Indeed, multiple studies point to the fact that dysregulation of epigenetic mechanisms induces changes of gene expression that underlie the aging process in different tissues. These epigenetic mechanisms are: DNA methylation, histone acetylation and non-coding RNAs.
Dr. David Sinclair, Professor of Genetics at Harvard Medical School, claims in his acclaimed book, “Lifespan: Why We Age and Why We Don´t Have To”, that “epigenetic drift/noise, which are alterations to the epigenome [1] that take place with age due to changes in methylation, often related to an individual´s exposure to environmental factors, may be a key driver of aging in all species” [2].
In this article, we will explore the factors that affect these epigenetic alterations and that hence contribute to epigenetic “drift/noise”. Various factors are being shown to impact the aforementioned epigenetic mechanisms, such as: nutrition, smoking, alcohol consumption and physical activity.
There is emerging evidence that physical activity can regulate epigenetic mechanisms, many of which are associated with an array of human diseases. Summatively, and without getting into complex molecular mechanisms, a study conducted by Graziolo et al. found that moderate physical activity has the capacity to preserve and/or recover “positive” epigenetic markers that are known to be modified in important chronic diseases, including cardiovascular and neurodegenerative diseases. [3]
With regards to alcohol consumption, Van Engeland et al postulate that alcohol intake was associated with changes in methylation of tumour suppressor and DNA repair genes in colorectal cancer tissues [4]. Overall, exposure to alcohol has been shown to alter gene expression through epigenetic mechanisms. The alcohol-mediated chromatin remodelling in the brain promotes the transition from use to abuse and addiction [5].
Moving on to nutrition, there are a number of natural compounds that have been shown to affect (positively and negatively) epigenetic alterations. On one hand, compounds such as polyphenols (found in foods such as berries, herbs and spices, tea, vegetables, nuts and soybeans) have been shown to reverse in-vitro models some of the epigenetic aberrations associated with malignant transformation.[6] On the other hand, a Western Diet (which tends to be high in saturated fats, red meats, simple carbohydrates and low in fruits and vegetables, whole grains, etc.) has a well-established negative impact on the human body, and epigenetics, such as DNA methylation, may play a role in this process.[7]
Lastly, cigarette smoking is considered one of the most powerful environmental modifiers of DNA methylation.[1] As you´ll recall, DNA methylation is one of the key epigenetic mechanisms. Cigarette smoke induces DNA double-strand breaks, which causes recruitment of DNA methyltransferases (the enzymes that catalyze DNA methylation) and thus contributes to epigenetic drift/noise. Furthermore, according to Zong et al. transcription regulation by NF–κB, a key pro-inflammatory molecule, appears to have a main function in cigarette smoking-induced epigenetic changes in the mediation of inflammation.
We can hence conclude that all forms of toxicity, including smoking, diet and heavy metals, alcohol consumption, etc. trigger epigenetic alterations that contribute to the so-called epigenetic noise, as coined by Dr. David Sinclair. This in turn, as we discussed previously, is the crucial hallmark of aging.
The combined epigenetic noise in our bodies generate chronic inflammation and cellular ageing. At Longevity, we provide various personalised, preventive, integrative and regenerative medical wellness solutions to combat these negative effects.
[1] Refers to changes to a cell´s gene expression that do not involve altering its DNA code. Sinclair, D. and LaPlante, M.D. (2021) Lifespan: Why we age and why we don’t have to. London: Harper Thorsons.
[2] Sinclair, D. and LaPlante, M.D. (2021) Lifespan: Why we age and why we don’t have to. London: Harper Thorsons.
[3] https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-017-4193-5
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752894/
[5] https://pubmed.ncbi.nlm.nih.gov/30412425/
[6] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752894/
[7] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6275017/
[8] https://www.frontiersin.org/articles/10.3389/fgene.2013.00132/full
