You’ve probably heard of the plethora of DNA or genetic testing products out there – 23andMe, GenoPalate, Helix, and many more.
You’ve also probably heard of epigenetics: how to modify your gene expression with nutrition.
While the science behind these genetic nutrition tests are a little shaky at the time of this writing, the science behind epigenetics and nutrigenomics is pretty solid.
Turns out, we have more control over our genes than we thought.
To go deeper, check out the work of Dr. Rhonda Patrick or Dr. Mitchell Gaynor. I’ve also included several reference links throughout this article to other great epigenetic resources.
How Epigenetics Works
Epigenetics means “on top of the genes”. When you ingest certain nutrients, those nutrients modify how your genes are expressed. Your genes don’t change, but your gene expression does.
The primary driver of epigenetic function is methylation and acetylation.
In terms of physics, it’s helpful to view methylation as an insulator and acetylation as a conductor. Methylation deactivates a gene (blocks the current) and acetylation activates a gene (allows the current).
Methylation is important because “global hypomethylation (undermethylation) is associated with nearly all human cancers” (R).
It’s also helpful to view epigenetics and methylation as dimmers, not on/off switches. Genes can be methylated or acetylated too far in one direction or another, harming our health.
Methylators are nutrients that either increase or decrease methylation, not both. The problem with this is that substances such as folate and alcohol can cause hypermethylation. Hypermethylation of genes can cause a whole slew of health problems.
Methylation adaptogens solve this problem and make sure that our methylation dimmers don’t go too far in either direction. We need both methylators and adaptogens.
Methylators & Adaptogens
Below is a list of methylators and adaptogens (R, R, R, R, R).
The nutrients and foods I mention here are commonly recommended in many conventional and alternative health resources for many years. Turns out that their health benefits are due in large part to their epigenetic power.
For each nutrient, I’ll list the specific genes and pathways it targets. Many times, one biochemical pathway can affect 100’s of genes, which could make targeting certain pathways more effective than targeting individual genes.
A glossary of genes and pathways is listed later in the article.
When a nutrient affects gene methylation universally, I will note that as well.
Here’s to hacking your health!
Curcumin
Type:
Adaptogen
Where to get it:
Turmeric – hard to absorb, black pepper increases absorption
Genes and pathways it affects:
More than 100 (R), including: NF-kB (R), Nrf2 (R), PI3K/AKT, and mTOR
Benefits:
Anti-cancer, anti-inflammatory (R)
Organosulfur Compounds
Type:
Adaptogen
Where to get it:
Garlic
Genes and pathways it affects:
Benefits:
Anti-cancer (R, R), anti-inflammatory, proimmunity
Quercetin
“[O]ne of the most widely used bioflavonoids for the treatment of metabolic and inflammatory disorders.” (R)
Type:
Adaptogen
Where to get it:
Berries, onions, broccoli, apples
Genes and pathways it affects:
p53 and others
Benefits:
Anti-cancer, anti-inflammatory (R), cardioprotective, anti-allergy, pro-immunity, anti-diabetic (R)
Resveratrol
Type:
Adaptogen
Where to get it:
Grapes – particularly grape skin, berries
Genes and pathways it affects:
BRCA, p53 (R) and others
Benefits:
Anti-cancer, anti inflammatory, antioxidant (R, R, R)
Genistein
Type:
Adaptogen
Where to get it:
Soy beans, fava beans
Genes and pathways it affects:
p16, hTERT and others
Benefits:
Anti-angiogenic, Anti-cancer (R)
EGCG
Type:
Adaptogen
Where to get it:
Tea – green, black, white, oolong
Genes and pathways it affects:
p16, hTERT and others
Benefits:
Anti-cancer, antioxidant (R)
Sulforaphane
Type:
Adaptogen
Where to get it:
The most sulforaphane potential is contained in broccoli seeds, broccoli sprouts, broccoli, and other cruciferous vegetables, in that order.
Genes and pathways it affects:
p16, p21, hTERT, Nrf2 (R), AMPK, NF-kB (R, R)
Benefits:
Anti-cancer, proapoptotic, antiproliferative (R, R), antioxidant, anti-inflammatory
Folate
Type:
Methylator
Where to get it:
Dark leafy greens, cruciferous vegetables, beans, legumes and seeds.
Genes and pathways it affects:
Universal
Choline
Type:
Methylator
Where to get it:
Beets, liver, mushrooms (also an adaptogen), seeds, turmeric
Genes and pathways it affects:
Universal
A Glossary of Important Genes and Pathways
hTERT
“hTERT is overexpressed in approximately 90% of cancers (R).”
mTOR
Affects autophagy, metabolism, cell growth, adipo- and angiogenesis and others (R).
Dysregulation can lead to diabetes, obesity, depression, and certain cancers (R, R). Some studies show that mTOR is overexpressed in almost 100 percent of advanced human prostate cancers.
Amino acids (too much protein), hormones, and growth factors are the primary drivers of overexpressed mTOR (R, R, R)
NF-kB
Inhibition reduces inflammation, controls immune and inflammatory responses, developmental processes, cellular growth, and apoptosis. Involved in cancer, arthritis, chronic inflammation, asthma, neurodegenerative diseases, and heart disease (R).
Activation is healthy in short bursts – exercise, stress, learning and overeating – but prolonged activation is harmful.
Blueberries have multiple compounds like anthocyanins, quercetin, and others that inhibit NF-kB (R). There are several other compounds listed above that do the same.
AMPK
Inhibits mTOR, master regulator of energy (R), initiates autophagy, regulates glucose, fatty acid, and protein synthesis.
Nrf2
Master regulator of cell defense (R, R), and regulates 100’s of genes. Is anti-inflammatory, involved in DNA repair, prevents cardiovascular disease, diabetes, Alzheimer’s, cancer, and skin aging.
Nrf2 is beneficial in the majority of cases, but there are some instances where it is harmful (R, R). E.g., potent and prolonged Nrf2 activation (R).
TP53 / p53
Most studied gene of all time, tumor suppressor, “guardian of the genome”, prevents mutations, pauses the life of a cell when there is risk of damage, repairing damage to the cell when possible, and initiating a cell’s death when the damage is too much to repair, mutated in more than 50% of all cancers (R).
Mentioned in over 8,500 articles, typically included in about two PubMed papers per day (R).
BRCA
A tumor suppressor gene mutation that is an indicator of breast and ovarian cancer risk.
MTHFR
A gene that can cause cardiovascular disease, stroke, hypertension, pre-eclampsia, glaucoma, psychiatric disorders and various cancers if mutated.
