Epigenetics: Nurturing Our Skin DNA for Beauty and Health

Factors outside your body can influence the genetics of skin disorders in the body and skin

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Credits: "Amber McCauley at Pixabay.com"
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The nature versus nurture debate is an ongoing point of contention in various fields. The argument revolves around whether we as humans are solely pre-programmed through our genetics—nature—or if we develop predominately with the influence of environment—nurture. Many skeptics of the nurture concept are looking for the underlying mechanism behind the influence of the environment. This is precisely where epigenetics comes in; it is the scientific mechanism behind the nurture argument.

 

What Is Epigenetics?

To understand the concept of genetics and epigenetics, one can use a simple analogy. Envision the human body as a city. There are buildings and streets at every turn, just as there are organs and tissues throughout the body. The development of this city relies upon blueprints. Genetics in the form of DNA can be likened to a large set of blueprints for the body. The concept of epigenetics is that these blueprints can be used in many different ways that can change how the buildings and streets are built. The blueprints essentially remain the same, but the selective use of the blueprints changes the ultimate design. There are three predominate mechanisms of epigenetics: DNA methylation, chromatin modification, and noncoding RNA interference.[1]

DNA methylation: silencing the DNA

DNA methylation is the act of adding methyl groups to certain sections of the DNA, making it invisible to the cellular reader, thereby turning it off. The enzyme in the body that adds these methyl groups can be thought of as a pencil modifying the blueprint with scribbles covering the page. These scribbles are not permanent and can be changed in the future.

Chromatin modifications: folding and tucking DNA away

Chromatin modification is another mechanism used to turn portions of the DNA off and on. Chromatin is the larger complex in each of our body’s cells that contains the DNA. It also possesses proteins called histones. There are so many DNA blueprints within a single cell that a folding system is required to fit all of the DNA. DNA wraps around histones, then histones come together to create chromatin. Modifying the histones through processes called methylation or acetylation adds bulky structures to make the histones difficult to fold together. This causes the DNA to unfold, making it accessible. If these bulky structures are removed, then the histones can fit together easily with the DNA wrapped tightly around them, making the DNA inaccessible. This process is similar to folding many blueprints numerous times; you will be unable to read any part of one blueprint without unfolding all of them.

Noncoding RNA: changing how the DNA is interpreted

The DNA in the body and skin are read and processed as molecules called RNA. Some parts of this RNA lead to the proteins of the body and skin; other parts of this RNA, known as noncoding RNA, controls whether the RNA can be read, needs to be modified, or whether it can actually be interpreted at all (even if the DNA is successfully read). Imagine that you have found the right blueprint that you needed for a building. You still need to get the right permits to be able to build the building, even if you have the blueprint. In some cases, the permit may change the way that the building is built. The noncoding RNA acts similarly to the permit. Noncoding RNA can allow the blueprint to be read more easily, alter the way the buildings are created after the blueprint is read, or prevent the building from being built at all.

 

Epigenetics in Action: How Does it Work?

The genetic code is permanent, so the only way to create diversity is by using the code in different ways. Epigenetics allows different parts of the DNA to be read at different times.[2] Alterations in epigenetics is crucial to the development of skin disease. Skin cancer development is an excellent example. Small sections of DNA, known as tumor suppressor genes, are important in the prevention of cancer development. If these genes are turned off, cancer is more likely to form. Ultraviolet radiation, the toxic component of the sun’s rays, can directly damage DNA. It is this damage that induces the DNA methylation of tumor suppressor genes, shutting them off and allowing skin cells to multiply, leading to cancer
development.[3] Psoriasis, a chronic skin disease due to an abnormally working immune system, is another example of epigenetic alterations at work. Specific noncoding RNAs known to increase inflammation in the body are increased in patients with psoriasis.[4] Knowing the epigenetic mechanisms that lead to disease can help with the diagnosis, treatment, and even prevention of many skin diseases.

 

Epigenetics in Skin Cancer 

Epigenetic changes can be both bad and good. As specific epigenetic changes are identified in skin diseases, so too are treatments to take advantage of these changes. In some cases, epigenetic changes can cause skin cells to go into overdrive and become cancerous.

Skin cancer - melanoma

Malignant melanoma, a deadly form of skin cancer, has a number of known negative epigenetic changes which scientists are using to detect, diagnose, and determine the progression of melanoma.[5] Chromatin modification in melanoma specifically is one of the changes that scientists hope to stop as a mode of treatment.[6]

Skin cancer - nonmelanoma

Nonmelanoma skin cancers are the most common type of cancer in the United States. These skin cancers represent another area of promise as epigenetic changes have been shown to be different between skin cancers that have a higher risk for spreading to the rest of the body.[7] These differences allow for doctors and scientists to determine how risky a skin cancer may be when a patient is diagnosed with one of these cancers.

 

Epigenetic Influence of Nutrition, Exercise, and Stress

The epigenetics of specific skin conditions can also assist in understanding the effects of nutrition, exercise, and stress on epigenetics and subsequent disease development.

Nutrition

Nutrition has been extensively studied, and the effects of a variety of foods and vitamins has been shown to modify epigenetics. For example, broccoli sprouts, garlic, and polyphenols have been found to increase histone acetylation, a form of chromatin modification.[8-10]

Exercise

Exercise also has direct epigenetic effects. In one study, biopsies of human muscle after exercise showed an increase in histone acetylation, which is typically seen when genes are being opened up to be read.[11] In another study, after brief exercise there was a significant increase in noncoding RNAs, which caused an immediate increase in neutrophils, a white blood cell important in immune function. This study shows that exercise does in fact impact the immune system, and it does it through epigenetics.[12]

Stress

Stress is a lifestyle factor commonly blamed for a multitude of disease processes. Various studies support this ideology. For instance, stress in early life via parental separation or abuse has been shown to affect DNA methylation both in a mouse-model and post-mortem human brains.[13,14] Knowing the mechanism of epigenetic alteration with nutrition, exercise, and stress may explain how these lifestyle components impact skin and overall health. 

Epigenetics explains how our DNA is expressed in so many different ways. As the epigenetic mechanisms become more apparent, our approach to disease and lifestyle will be refined and will expand molecular based research to include lifestyle factors. Since the completion of the Human Genome project in 2003, nature has been defined. Yet nurture in the form of epigenetics continues to unfold.

 

* This Website is for general skin beauty, wellness, and health information only. This Website is not to be used as a substitute for medical advice, diagnosis or treatment of any health condition or problem. The information provided on this Website should never be used to disregard, delay, or refuse treatment or advice from a physician or a qualified health provider.

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References

  1.  Lu Q. The critical importance of epigenetics in autoimmunity. J Autoimmun.2013;41:1-5; PMID: 23375849 Link to research.
  2. Mulder KW, Wang X, Escriu C, et al. Diverse epigenetic strategies interact to control epidermal differentiation. Nat Cell Biol.2012;14(7):753-763; PMID: 22729083 Link to research.
  3. Millington GW. Epigenetics and dermatological disease. Pharmacogenomics.2008;9(12):1835-1850; PMID: 19072642 Link to research.
  4. Sonkoly E, Stahle M, Pivarcsi A. MicroRNAs: novel regulators in skin inflammation. Clin Exp Dermatol.2008;33(3):312-315; PMID: 18419608 Link to research.
  5. Greenberg ES, Chong KK, Huynh KT, et al. Epigenetic biomarkers in skin cancer. Cancer Lett.2014;342(2):170-177; PMID: 22289720 Link to research.
  6. Yamamoto S, Yamano T, Tanaka M, et al. A novel combination of suicide gene therapy and histone deacetylase inhibitor for treatment of malignant melanoma. Cancer Gene Ther.2003;10(3):179-186; PMID: 12637938 Link to research.
  7. Darr OA, Colacino JA, Tang AL, et al. Epigenetic alterations in metastatic cutaneous carcinoma. Head Neck.2015;37(7):994-1001; PMID: 24700717 Link to research.
  8. Dashwood RH, Ho E. Dietary histone deacetylase inhibitors: from cells to mice to man. Semin Cancer Biol.2007;17(5):363-369; PMID: 17555985 Link to research.
  9. Druesne N, Pagniez A, Mayeur C, et al. Diallyl disulfide (DADS) increases histone acetylation and p21(waf1/cip1) expression in human colon tumor cell lines. Carcinogenesis.2004;25(7):1227-1236; PMID: 14976134 Link to research.
  10. Link A, Balaguer F, Goel A. Cancer chemoprevention by dietary polyphenols: promising role for epigenetics. Biochem Pharmacol.2010;80(12):1771-1792; PMID: 20599773 Link to research.
  11. McGee SL, Fairlie E, Garnham AP, et al. Exercise-induced histone modifications in human skeletal muscle. J Physiol.2009;587(Pt 24):5951-5958; PMID: 19884317 Link to research.
  12. Radom-Aizik S, Zaldivar F, Jr., Oliver S, et al. Evidence for microRNA involvement in exercise-associated neutrophil gene expression changes. J Appl Physiol (1985).2010;109(1):252-261; PMID: 20110541 Link to research.
  13. Murgatroyd C, Patchev AV, Wu Y, et al. Dynamic DNA methylation programs persistent adverse effects of early-life stress. Nat Neurosci.2009;12(12):1559-1566; PMID: 19898468 Link to research.
  14. McGowan PO, Sasaki A, D'Alessio AC, et al. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nat Neurosci.2009;12(3):342-348; PMID: 19234457 Link to research.