The thought that we are NOT destined to have the same diagnoses and medical conditions that our mothers, fathers, grandmothers and grandfathers had is very empowering. But is it possible to change our genes? This brings up the concept of epigentics. How our genes interact with our environment is basically epigentics at its core. Epigenetics does not necessarily change your DNA but how your body reads it. Epigenetics and epigenomics can turn genes "on" and "off" resulting in changes to expression of our genes. Epigenomics and epigenetics both emphasize how nutritional and environmental factors alter human gene expression from fetus to adult and across generations of families.
How does Epigenetics work?
Essentially all DNA in an organism are the same, but the cell types and functions are different due to gene expression and therefore control of gene expression is the epicenter of development. Epigenetic changes affect transcription, translation and subsequent protein modification of our genetic DNA to messenger RNA and finally the production of a protein. Epigenetic mechanisms include histone modification, DNA methylation, and varying RNA processes (Dolinoy DC).
DNA methylation: adding a methyl group to the DNA sequence. This group is added to specific places on the DNA, where it blocks the proteins that attach to DNA to “read” the gene essentially allowing the gene to be turned "on" or "off." Typically methylation turns genes "on" and demethylation turns genes "off."
Non-coding RNA: attaches to coding RNA preventing it from making proteins turning genes "off" or recruits proteins to modify histones to turn genes "on" or "off."
Histone modification: DNA wraps itself around proteins called histones. When histones are tightly packed the DNA cannot be read and the gene is turned "off," while conversely loosely packed histones allow for the DNA to be read and the gene to be turned "on."
Examples of epigenetics:
Fuso et al (2009) analyzed the methylation pattern of the PSEN1 promoter gene in the expression of neuroblastoma cells in mice. What they showed was a b vitamin deficiency promoted hypomethylation and the PSEN1 gene to turn "on" promoting neuroblastoma cell growth. B vitamins are found in foods like meat, seafood, poultry, eggs, dairy products, legumes, leafy greens, and seeds. Our vitamins are digested, absorbed and created by our gut bacteria. I.e. GET YOUR GUT RIGHT!
In a study by Fang, et al (2003), they looked at green tea polyphenols (epigallocatechin-3-gallate (EGCG)) and their affect on cancer cells. They found the major polyphenol from green tea, can inhibit variable DNMT (DNA methyltransferase) activity and reactivate methylation-silenced genes in cancer cells. DNMT essentially is methylating where it shouldn't which blocks tumor suppressor gene function leading to cancer evolution by stopping programmed cell death (apoptosis), DNA repair, cell interaction and angiogenesis. The ECGC in green tea has been shown to inhibit that process while reactivating tumor suppressor genes that were essentially silenced by the variable DNMT genes (Zang, et al). They demonstrated this in human colon cancer HT-29 cells, esophageal cancer KYSE 150 cells, and prostate cancer PC3 cells. The results show for the first time the inhibition of DNA methylation by a commonly consumed dietary constituent and suggest the potential use of EGCG for the prevention or reversal of related gene-silencing in the prevention of cancer. (Fang, et al).
The agoutic mice experiment which has been used to investigate the impacts of nutritional and environmental influences on the fetal epigenome. The agoutic gene produces either a black or yellow coated mouse. Yellow mice are hypomethylated while brown mice exhibit adequate methylation. Interestingly enough, the yellow, hypomethylated mice were more prone to obesity, diabetes, and tumor growth. Maternal supplementation with soy isoflavones increased methylation capacity in the mice to produce brown colored mice who were protected from obesity and the development of diabetes. They also looked at the effect of maternal BPA (bisphenol A) exposure on the mice development. BPA did not effect litter size, litter survival, wean weight, genotypic ratio, or sex ratio. Maternal dietary BPA exposure did shift the coat color toward yellow which means decreased methylation and increased obesity and diabetes development. The BPA-induced hypomethylation of the fetal epigenome was treated and eliminated by maternal dietary nutritional supplementation with methyl donors like methylated B12 and folic acid, betaine and choline or soy (Dolinoy, D.C.). This suggest that simple dietary changes can have a positive impact and protect against the harmful effects of environmental toxins on fetal development.
How do you change your gene expression for better health?
What we feed our bodies is central to the proper functioning of our cells. We need adequate nutrients for our cells to work and detoxify which means we need adequate gut function for optimal digestion, absorption and creation of our nutrients. Read more about gut health here, here, and here. We need a robust cell membrane to keep good materials in the cell and let toxins out. We need adequate detox. Cellular detoxification from toxins requires many nutrients and properly functioning cell membrane. Stress management and having a good immune system are also key and play a vital role in cellular detoxification.
Nutrition: This is at the heart of epigenetics. Adequate macro and micro nutrients plus vitamins and minerals are what makes our bodies rest, repair and regenerate. Get your gut right!
Exercise: promotes the release of happy hormones which decreases our stress, causes sweating for toxin removal, builds muscle and promotes insulin sensitivity.
Fasting: promotes autophagy (cell eating) for removal of old/damaged cells, increases mitochondrial functioning and efficiency, increases insulin senstivity and weight loss. *** discuss fasting with your healthcare practitioner prior to implementing. There are some instances where fasting can be harmful.
Sleep: restful, REM sleep promotes the release of growth hormone for r