Can Healthy Diets Really Change Gene Expression?

Epigenetics is the study of genetic variations that are caused within an individual, by external or environmental factors that can switch genes on and off, as opposed to changes in DNA sequence which happen as genes are passed down to the next generation. One of the most potent ways epigenetics can change is through nutrition.  In fact, one of the main reasons good nutrition is so important is because healthy food choices will minimize the expression of disease-causing genes we may have inherited.

Unlike behavior or stress, diet is one of the more easily studied, and therefore better understood, environmental factors in epigenetic change.

The nutrients we extract from food enter metabolic pathways where they are broken down, modified, and assembled into molecules the body can use. One such pathway is responsible for making methyl groups (CH3), which interact with important epigenetic tags that silence genes.

Familiar nutrients like folic acid, B vitamins, and SAM-e (S-Adenosyl methionine, a popular over-the-counter supplement) are key components of this methyl-making pathway. Diets high in these methyl-donating nutrients can rapidly alter gene expression, especially during early development when the epigenome is first being established.  Diet during early development can have long-lasting effects.

Your mother’s diet during pregnancy and your diet as an infant can affect your epigenome in ways that stick with you into adulthood. Animal studies have shown that a diet with too little methyl-donating folate or choline before or just after birth causes certain regions of the genome to be under-methylated for life.  For adults too, a methyl-deficient diet leads to a decrease in DNA methylation, but the changes are reversible when methyl is added back to diet.

Experiments in mice show just how important a mother’s diet is in shaping the epigenome of her offspring. All mammals have a gene called agouti.  When a mouse’s agouti gene is completely unmethylated, its fur is yellow and it is obese and prone diabetes and cancer.  When the agouti gene is methylated (as it is in normal mice), the fur is brown and the mouse has low disease risk.  Fat yellow mice and skinny brown mice are genetically identical.  The fat yellow mice are different because they have an epigenetic mutation.

When researchers fed pregnant yellow mice a methyl-rich diet, most of her pups were brown and stayed healthy for life. These results show that the environment in the womb influences adult health.  In other words, our health is not only determined by what we eat, but also what our parents ate.

Toxins and Supplements

Chemicals that enter our bodies can also affect the epigenome. Bisphenol A (BPA) is a compound used to make polycarbonate (soft) plastic.  It is in many consumer products, including water bottles and tin cans.  Controversial reports questioning the safety of BPA came out in 2008, prompting some manufacturers to stop using the chemical.

In the laboratory, BPA appears to reduce methylation of the agouti gene. In the strain of mice that was studied, yellow mothers gave birth to pups with a range of coat colors from yellow to brown.  When mothers were fed BPA, their babies were more likely to be yellow and obese, and die young.  However, when mothers were fed BPA along with methyl-rich foods, the offspring were more likely to be brown and healthy.  The maternal nutrient supplementation had counteracted the negative effects of exposure.


At the beginning of this essay, reference was made to “epigenetic tags” that can “silence or express genes.” These tags are single nucleotide polymorphisms within the genome (your DNA signature), frequently called SNPs (pronounced “snips”), and are the most common type of genetic variation between people.  Each SNP represents a difference in a single DNA building block, called a nucleotide.

While most biological and medical researchers welcome greater understanding of the roles of SNPs in  human health, not all are in favor of testing:

Here is an excellent, accessible, published research article clearly in favor of testing because of the overwhelming sense of empowerment created for patients:


To date, the SNP about which we know most is “methylene tetrahydrofolate reductase” (or MTHFR).

In 2003, a genetic study called the Human Genome Project was completed. From that study, we discovered that this important MTHFR gene, with many implications for health and well-being, is defective in a lot of folks, especially in Hispanic populations.


When it’s working right, the MTHFR gene begins a multi-step chemical breakdown process, called methylation, which works like this:

  • The MTHFR gene produces the MTHFR enzyme.
  • The MTHFR enzyme works with the folate vitamins (B9, folic acid), breaking them down from 5,10-methylenetetrahydrofolate to a more useful form, 5-methyltetrahydrofolate. These better folic acid supplements are now widely available in health food stores as 5-MTHF (this is NOT 5-hydroxy tryptophan, or 5HTP, the precursor to serotonin).
  • 5-MTHF helps convert the amino acid homocysteine into another essential amino acid, methionine, which is used to make proteins, utilize antioxidants, and to assist the liver in processing fats. Methionine helps with depression and to reduce inflammation. It also helps convert the strong estrogen, estradiol (E2) into the safe and breast-health promoting estrogen, estriol (E3).
  • Methionine is converted in the liver into SAM-e (s-adenosylmethionine), which is anti-inflammatory, supports immune functions, helps produce and excrete the brain chemicals serotonin, dopamine and melatonin, and is involved in the growth, repair and maintenance of all cells.
  • proper methylation is essential for binding and eliminating toxins and heavy metals; better detoxification can reduce risk for cancer and other health issues, including stress reduction by strengthening the adrenals.


What happens when you have a defective (mutated) MTHFR gene?

  • The SNP produces a defective MTHFR enzyme which functions less than optimally, such as performing at only 40% of its capacity, or 70% of its capacity. This means you won’t break down toxins or heavy metals well and you could carry a burden of too high minerals, including iron, copper, lead, or mercury. •The defective enzyme doesn’t break down folate vitamins properly, which causes high homocysteine, which can increase your risk of coronary heart disease , and high blood pressure, as well as increasing your risk for dementia.
  • Homocysteine is poorly converted to glutathione, which is your body’s chief antioxidant and detoxifier. You are then more susceptible to stress and toxin buildup.
  • Homocysteine is poorly converted to methionine, and less methionine can raise your risk of arteriosclerosis, fatty liver disease, anemia, inflammation, free radical damage, and significantly less production of the major methyl donor, SAM-e.
  • Less SAM-e can increase depression
  • And more broadly, an MTHFR defect can increase your risk of a variety of cancers (including breast and prostate cancer), stroke, heart problems, congenital defects, depression, irritable bowel syndrome (IBS), miscarriages, migraines, chemical sensitivities and many other conditions.
  • With a mutated MTHFR SNP, you will have problems converting inactive forms of folate and B12 to the active forms. So the inactive folate or B12 will simply build up in your serum, also inhibiting the active forms.
  • The journal Molecular Psychiatry states that “Schizophrenia-like syndromes, bipolar disorder, Parkinson’s disease, Alzheimer’s disease and vascular dementia have all been associated with one or more mutations of the MTHFR gene.” (2006;11,352–360)


Genes are passed down by both parents. Most literature states there are a good 40-50 different mutations of the MTFFR gene which could be passed down by one, or both or your parents.  But only two are particularly problematic: mutations on the points at C677T and A1298C. The numbers refer to their location on the DNA sequence.  You will also sometimes just see them written as just 677 and 1298.


If you test your saliva for your entire genome through, you will then need to interpret this data, which is now quite easy with a variety of free web programs including:

  • Genetic Genie, which will look at your methylation genetics just by reading your 23andMe raw data.
  • Live Wello, which gives a great deal of information to you based on 23and me, plus links to learn more about each gene’s potential problem.
  • Nutrahacker will tell you what supplements you need to take, and which ones plus more you need to avoid, due to your mutations. A vast amount of genetic information can be obtained from


What can I do about this?

You can’t change a defective gene. But you can help it do its job better and minimize problems.

One solution is to avoid supplements and many processed foods with synthetic folic acid, especially if you are homozygous for the SNP (having a copy of the same defective gene from each parent). Healthy foods that contain folate, like dark leafy greens, should be fine, since they contain the  active form of folate.  If you want to take a supplement to work around your body not absorbing folic acid well, look for the methylated versions:  methylfolate, or 5-MTHF.

Your serum B12 levels might also read high in a lab test, which, if you have the MTHFR SNP means you are not utilizing B12, and it’s simply building up in your blood. In this case it’s important to avoid the synthetic supplemental version of B12 called cyanocobalamin and instead favor the more useable methylcobalamin form (methyl B12).   Methyl B12 is needed for many detox functions, so start at a low dose (250-500 mcg) to avoid side effects like fatigue and head/body aches.

The other main B vitamin implicated by the MTHFR SNP is B6 (pyridoxine). Look for the methylated form, called P-5-P, or pyridoxyl 5 phosphate.

Dr. Ben Lynch, a SNP expert, says “repairing the digestive system and optimizing the flora should be one of the first steps in correcting methylation deficiency”, and that especially includes treating candida because of the toxins it releases, which inhibit proper methylation.

Some experts recommend eating clean, such as Paleo or the GAPS diet. As always, avoiding exposure to toxins is important.  Green your household cleaning supplies and don’t buy plastic.

If adding methylated B vitamins cause you to over-methylate, taking time-released Niacin, 50 mg, can slow it down. Symptoms of over-methylation include muscle pain or headaches, fatigue, insomnia, irritability or anxiety.

Minerals play a key role in several enzymatic functions. Vitamin C helps reduce oxidants.  Molybdenum (500 mcg) helps break down excess sulfates and sulfites.  This website offers suggestions on how to treat your SNPs.