Dr. Roberts & Nutrigenomics
Last weekend, I attended a one day lecture in Columbus given by Dr. James Roberts, an integrative cardiologist who practices in Toledo. Dr. Roberts has been using Dr. Yasko's genetic testing and protocols with adult patients for several years. This was a great follow up to what I learned from Dr. Yasko a few months ago.
Beware, this information is DENSE and technical...if you've had genetic testing done and know some of your specific SNPs, you may find a few helpful tidbits here, but don't expect to absorb and understand the whole thing. Some of the information won’t even apply, so see what resonates and drill down on the information that is pertinent to you.
First, a few key takeaways:
There are three main ways our genes determine our health:
Genes/genetic errors we inherit from both parents
Epigenetic programming--the way our genes are "methylated" (marked) helps determine expression
Interaction between our genes and our lifestyle, exposures and even emotions
In a study done with rats, pups of mothers who were fed a low protein diet demonstrated a methylation pattern of their genes that predisposed them to high blood pressure in adulthood.
The prevalence of MTHFR 677 defects is increasing and is considered to be an adaptive mutation that protects against certain types of cancers.
Folate can stand in for BH4 (tetrahydrobiopterin) when there is a deficiency in BH4. BH4 is critical for the formation of neurotransmitters, and is negatively affected by several genetic mutations.
Insufficient SAMe (resulting in a low SAM/SAH ratio) inhibits COMT, an enzyme that helps break down estrogens and catecholamines (stress neurotransmitters).
When homocysteine is elevated, SAM:SAH ratios, glutathione, DNA methylation and BH4 levels are all compromised.
SAMe is involved in:
Carnitine production
Inactivation of catecholamines
Clearing estrogens safely
Metabolizing bioflavenoids
Generating phosphatidylchole
Creatine production
Clearing niacin (if you've had a bad reaction when using niacin, you are likely to be deficient in SAMe)
Alcohol consumption inhibits the MTR enzyme, which directly impacts/lowers SAMe.
Studies done on healthy Finnish men aged 45-64 revealed:
High homocysteine and COMT defects (V158 and H62) was a significant cardiovascular risk factor because of persistent elevations in catecholamines.
Similarly, increased cardiovascular risk was seen in those with COMT defects who drink coffee.
With CBS upregulations due to genetic errors:
Homocysteine remethylation to SAMe is compromised
Excess sulfite (neurotoxic) is produced
Excess sulfate (increases fight-flight neurochemicals) is produced
Increased hydrogen sulfide (causes brain fog and platelet activation)
Glutamate (excitotoxic) increases, especially if heavy metals, particularly lead, are present
Ammonia levels go up, using up BH4
Cysteine and glutathione levels compromised, impairing detoxification
There is a predisposition to GERD, allergies and asthma
Things that act as methylation thieves:
Fibrates by decreasing GFR (glomular filtration rate)
Cholestyramine by blunting folate and B12 absorption
Niacin by blocking B6 synthesis and using methyl groups
Estradiol by unknown mechanism
Testosterone by increasing creatine need
Methotrexate by blocking DHFR enzyme
Dilantin by slowing MTHFR and MTR enzymes
Carbamazepine by depleting folate
Cyclosporin by decreasing GFR and slowing MTHFR function
Levodopa by increasing SAH generation
NAC (N-acetyl-cysteine) by thiol-disulfide exchange
PPIs (proton pump inhibitors) and H2 blockers (both of these are acid-blocking drugs) by decreasing B12 absorption
Oral contraceptives by decreasing B12, B6, folate, B2, C and Zinc
Alcohol by decreasing MTR activity and causing folate deficiency
Mercury by decreasing MTR activity
Lead, aluminum, cadmium and organic pollutants by multiple enzyme dysfunctions
Even though cardiovascular mortality rates rise when cholesterol increases above 200, all-cause mortality, or death from ALL causes also RISES when cholesterol is UNDER 150.