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Applying nutrigenomics to cardiovascular medicine: prevention and treatment.

Nutrigenomics provides us with an expanded perspective on the prevention and treatment of cardiovascular disease. In cardiovascular management, nutrigenomics encompasses genetic testing, metabolomics, the identification of single nucleotide polymorphisms (SNPs) and nutrient-genetic interactions, and the newest concept, gene expression testing. These tests provide indication of whether or not your patients' genetics are expressed and their risk of cardiovascular disease.

Most genetic expression is driven by inflammation, and the majority of the genes, once turned on, promote an inflammatory response. Most of the loci on genes associated with Ml, CHD, and CHF are expressed through inflammation, oxidative stress, and immune-vascular dysfunction. This dynamic starts in the vascular endothelium, vascular smooth muscle, and cardiomyocytes, leading to angina, coronary artery vasospasm, obstructive coronary heart disease, diastolic and systolic dysfunction, and cardiomyopathy. Regardless of the type of insult, blood vessels respond to insults via three fundamental mechanisms: inflammation, oxidative stress, and immune-vascular dysfunction.

Consequently, the inflammatory pathways have become the primary focus in the management of genetic expression and of genetic risk for CVD. That management goes beyond an emphasis on the top five traditional risk factors such as hypertension, dyslipidemia, diabetes, obesity, and smoking. It is probable that 80% or 90% of outcomes in cardiovascular disease are not genetic per se, but actually reflect environmental influences on genetic expression. Reduction and prevention of CHD is not likely to improve without using genetic markers and gene expression testing to identify these underlying risk factors.

Nutrients. Nutritional factors provide information that determines whether our genes are turned on or turned off, with a corresponding beneficial or detrimental outcome. One change in a single ubiquitous nutrient such as magnesium may cause 300 or 400 different changes in downstream metabolic pathways and cardiovascular function and health. This is just one example of environmental influences and the importance of genetic expression. When there is interference with a metabolic pathway, a single area of abnormality can result in a myriad of defects and a spoke-like effect, resulting in a ripple of downstream changes in many metabolic pathways.

Epigenetics. There are several issues we want to define when we initially examine patients. One is their genetic profile, the genes they were dealt. The genetic profile includes their proteome, transcriptome, metabolome, and to some extent the gut microbiome. The gut has a tremendous influence, obviously, on cardiovascular illness. There are also epigenetic influences that are not genetic such as DNA methylation, histone modification, and non-coded messenger RNA. These influences are not in the genetic code, but can be passed on from mother to fetus and from generation to generation. The final aspect is gene expression, as genes express themselves in response to nourishment or insults from different types of information coming in from the environment. Genetic polymorphisms and transcription factors must also be included in the general workup to determine if a patient is at risk for cardiovascular disease. Genetics have become important in determining not only dietary intake, but also medication intake in many patients, based on their genetic profile.

There are more than 400 known risk factors for cardiovascular disease. Aggregating all these risk factors, regardless of their mechanism of action, it becomes clear that they all ultimately result in the same three finite responses in the body: inflammation, oxidative distress, and/or immune dysfunction. These risk factors ultimately translate into vascular disease.


Mediterranean Diet. We know the Mediterranean diet (MedDiet) turns on numerous beneficial genetic pathways that can reduce risk for cardiovascular disease, as well as risk for type II diabetes, so this is currently one of our best strategies for disease prevention. If our patients consume a Western diet, that will result in totally different outcomes in terms of gene expression, since most of the foods included in a Western dietary pattern have been shown to express 30 to 40 different inflammatory and immune pathways.

The MedDiet has an advantageous effect on genes such as transcription factor 7. If you can turn off that one gene, you can reduce the risk of diabetes by as much as 40%. In a clinical trial of this diet, other prevalent beneficial effects were related to atherosclerosis and hypertension. The Mediterranean diet, in combination with CoQ10, has been shown to be the most beneficial intervention for healthy aging, and preventing processes and diseases related to chronic oxidative stress and CHD. Changes in genetic expression toward a protective mode were often associated with improvement in systemic markers for inflammation, immune function, oxidative stress, hypertension, and CHD:

* Modulating 43% of genetic pathways, including nine pathways in response to diets emphasizing olive oil, and four pathways with diets emphasizing nuts.

* Decreasing oxidative stress, high sensitivity C-reactive protein (hsCRP), and interleukin 6 (IL-6).

* Increasing oxidative defenses, enzymes, hippurate, and phenols, while improving mitochondrial function, fatty acid beta oxidation, and ATP energy production.

* Preventing cardiovascular diseases with a relative risk reduction of 30% and reduced diabetes mellitus by 40%.

Pritikin and DASH Diets. The Pritikin diet is one of the most effective ways to turn off the gene expression that increases risk for cardiovascular disease. As reported in recent Annals of Internal Medicine, the Pritikin diet can reduce risk of cardiovascular disease by as much as 30% to 35%. That benefit is directly correlated with the diet itself, but is also enhanced when supplementing with nutrients such as CoQ10. The DASH-1 and DASH-2 diets have also been found beneficial in relation to changes in inflammatory genes and improved response to the types of medications prescribed for hypertension.

Specific Nutrients

Electrolytes. These nutrients, particularly sodium, potassium, and magnesium, can change genetic expression, salt sensitivity, intravascular volume, blood pressure, risk for heart disease, risk for coronary heart disease, heart attack, cardiac arrhythmias, and congestive heart failure. In terms of salt sensitivity, for example, there are genetic variations between Caucasians and African Americans. One of the most important is cytochrome P4A11 (expressed as CYP4A11), which relates to sodium and water diuresis and the role of the epithelial sodium channel (ENaC) function. Patients who have resistant hypertension due to CYP4A11 who are treated with the drug Amiloride, have dramatic reductions in blood pressure and often can discontinue or reduce the dose of other anti-hypertensive drugs.

Omega Fatty Acids. Omega 3 fatty acids affect huge numbers of genes that reverse changes in our metabolic profile and in our transcriptome, genes that can improve beta oxidation, mitochondrial health, mitochondrial biogenesis, and transcription factors. As a result, ATP production goes up, cells are healthier, and patients live longer. We know that omega 3 fatty acids by themselves have dramatic effects on PPARs and many nuclear receptor proteins that function as transcription factors such as retinoid X receptors, liver X receptors, and farnesoid X receptors. These receptors can have dramatic influences, reversing inflammation, oxidative stress, blood pressure, and risk for heart disease. It is also very important to balance omega 3s and omega 6s in a way that achieves these beneficial effects and reduces inflammation. Assessing the omega 3 pathway and determining the omega 3 index in the red blood cell can lead to specific treatments to improve CVD:

* In specific studies, omega 3 fats changed expression of 610 genes in men and 250 genes in women.

* Omega 3s improved cardiovascular markers, decreasing saturated GPC (glycerol phosphocholine) and LPC (lysophosphatidylcholine), and increasing oxidative stress defense factors, nuclear transcription factors, acylcarnitines, hexose, and leucine.

* Polymorphisms contribute to the complexity of nutritional effects seen with omega 3s and their role in reducing cardiovascular disease, inflammation, glucose levels, and lipids.

Monounsaturated Fats. Lipids such as olive oil that contain oleic acid can also have a positive impact on different SNPs and PPAR receptors, improving coronary heart disease and diabetes mellitus, while reducing oxidized LDL. Even without the MedDiet, olive oil given as a supplement can have dramatic and highly beneficial influences on genetic expression related to the three finite vascular responses for reducing cardiovascular disease.

* Extra virgin olive oil (EVOO), taken for 6 weeks at 20 grams (<1 1/2 tablespoons) per day in healthy adults improved 133 of 238 proteomic biomarkers for CHD, CKD (chronic kidney disease), dyslipidemia, and DM.

* EVOO down-regulated CHD genes; reduced oxLDL, glucose levels, AGEs (advanced glycation end products), HbA1C, ROS (radical oxygen species), collagen peptides, and inflammation; and prevented some forms of atherosclerosis.

* EVOO upregulated cholesterol efflux capacity (CEC), improved reverse cholesterol transport (RCT), and increased HDL-C.

Gut Metabolites. We've also known that changes in the gut microbiota, particularly those various microbiomes that metabolize phosphatidylcholine, L-carnitine, and other vital nutrients, can produce changes that are relevant to cardiovascular disease. This is another example of why the gut is so important in determining what happens within the cardiovascular system.

* Gut microbiota signatures (GMS) act as important determinants in the pathogenesis of inflammatory-induced obesity, CHD, atherosclerosis, and T2 DM.

* High-fat intake and elevated glucose in the presence of altered GMS promote increases in lipopolysaccharides (LPS), endotoxins from the cell walls of gram negative bacteria that can lead to ED and atherosclerosis. LPS crosses the enterocyte barrier coupled with lipoproteins, stimulating the innate immune system, TLR4 in adipocytes, and vascular tissue, activating NFkb, and increasing inflammation, oxidative stress, and immune dysfunction.

* A diet of saturated fatty acids (SFA) and/or high refined carbohydrates (CHO) increased LPS concentration by 70%, as well as gram negative concentration in the gut.

* SFA and CHO decreased bifidobacteria levels. Similar reductions occurred in association with obesity, DM, MS, and NAFLD, promoting alterations in the intestinal barrier and enterocytes leading to increased intestinal permeability.

* Increases in the abundance of Pseudomaoadaceae were observed in CVD patients compared to healthy individuals.

* Firmicutes species are lower in CVD patients, and CHD plaque also has higher ratio of Pseudomaoadaceae to Firmicutes bacteria and DNA.

* Higher Prevotella species relative to Bacteroides are reported in patients with high TMAO and CHD. Healthy flora becomes very important in maintaining a healthy gut microbiome, and of course, one must nourish the flora with good prebiotics to assure health.

* Diets with fermentable fibers, prebiotics, probiotics, and plant polyphenols favorably regulated microbial activities and decreased gram negative bacteria within the gut.

* Saccharomyces boulardii increased HDL and improved serum lipid levels.

* Certain probiotics were found to reduce blood pressure.

Genes Relevant to Cardiovascular Risk

Gene 9p21. One of the primary genes we are now measuring is the 9p21 gene, which increases the risk of atherosclerosis and coronary heart disease. Patients who have a heterozygote SNP for 9p21 have a risk for Ml that is increased by 50%. When a patient has a homozygote SNP, risk goes up to approximately 100%, so this is one of the top genetic risks that we measure for CHD and MI. The 9p21 gene is associated with coronary heart disease and Ml, but also with cancer through the MTAP (methylthioadenosine phosphorylase) pathway. However, there are many other genes that should also be evaluated, not just for coronary heart disease, but also for hypertension and dyslipidemia. A gene called GLU 1q25, for example, increases the risk of heart disease in diabetics, related to glutamic acid, glutamine synthesis, and insulin levels.

Apo E4 Genotype. The Apo E genotype is not new information, but we must remind ourselves that this genotype increases risk for CVD and people with the genotype have varied responses, particularly to different types of fats in their diet. Consequently, it is important that their genotype be identified before starting these patients on specific types of nutrients such as omega 3 and 6 fats. Management of risk factors for patients with the APO E4 allele addresses issues such as:

* Increased cholesterol absorption and delayed clearance, resulting in higher serum LDL.

* Increased CVD risk with smoking and alcohol intake and overall increased incidence of CHD, CVD, MI, Alzheimer's, and dementia.

* Inability to repair vascular endothelium to produce nitric oxide.

* Less response to statins.

* Best reduction of LDL occurs through dietary restriction of carbohydrates, with low fat diets, and omega 3 fatty acids.

* Response to phytosterols and cholesterol absorption

COMT Polymorphisms. One of the newest genes that we're looking at is COMT (catechol-O-methyltransferase) which provides instructions for the breakdown of norepinephrine and epinephrine. If this genetic SNP is present, the patient will have higher levels of norepinephrine and epinephrine and increased risk of hypertension and coronary heart disease. There is a variation in response depending on which of the specific COMPT SNPs the patient carries; for example, aspirin or vitamin E may be beneficial for patients with one type of COMT SNP, but detrimental if one of the other SNPs is present.

Glutathione-Related SNPs. The risk of myocardial infarction can be increased by 71% if a SNP affecting glutathione metabolism (GSH-Px) is present. This selenium-dependent enzyme expresses different capacities to neutralize hydroxyl radicals and other oxidative molecules related to increases in oxidative stress and CVD. For these patients, glutathione peroxidase and selenium levels would be key measurements to track for the risk of CVD:

* Low GSH-Px is a major CHD risk factor.

* Higher levels of glutathione peroxidase support more rapid recycling of glutathione, resulting in higher availability of glutathione.

* Increased glutathione peroxidase (GSH-Px) decreases BP, MI, LVH, and CHF.

* GSH-Px confers more cell, tissue, and organ protection than SOD (superoxide dismutase) or catalase, or the combination of both.

Hypertension. There is a whole host of genetic influences on blood pressure, probably 30 different genes that we have recognized to date, all of which are helpful in determining both risk for hypertension and risk for cardiovascular target organ damage, as well as response to nutrients, caffeine, medications, and various types of diets. We know, for example, that someone who consumes large amounts of caffeine and has the SNP cytochrome P-450-1A2 will increase their risk of tachycardia, hypertension, aortic stiffness, and myocardial infarction. Of course, one could have the right type of SNP for caffeine detoxification and that will reduce their risk. Approximately 60% of the population has cytochrome P-450-1 A2FF, which is the wrong kind of gene to have, because they are slow metabolizers and their risk for CHD and Ml actually go up with caffeine consumption. Before you tell patients it's okay to be drinking caffeine, you need to check the gene for cytochrome P-450 function.

Lab Testing

You want to be able to measure whether your patients' genes are expressing inflammation, oxidative stress, or immune dysfunction, which will put them at increased risk for cardiovascular disease.

Measuring Genetic Expression. A test is now available that measures gene expression; this evaluation, with the acronym Corus CAD, is available from a company in Southern California, CardioDx. The evaluation uses a score of 0 to 40, expressing the patient's risk for obstructive coronary heart disease. This evaluation is very accurate, highly sensitive, has published studies, and good medical background information. We use not only genetic testing for SNPs, but also the Corus gene expression test to determine patients' risk at baseline. Once you have established the baseline, you can do an intervention, and then repeat the test in about six months to see if that intervention is reducing the gene expression testing score, which implies that you are reducing the risk for future cardiovascular events.

Metabolomic Testing. Changes in endothelial physiology and biochemistry, reflected in metabolites, often precede hypertension by decades. One strategy applied in a series of studies evaluated just 36 of the known 4,229 metabolites, primarily dicarboxylacylcarnitines, medium- and longchain acyl carnitines, and fatty acids. Successful prediction of various forms of CVD risk were made in study after study, in patients at risk of CHD, coronary artery disease, adverse events after coronary artery bypass grafting, and those at increased risk due to the effects of aging. Metabolic measurement predicted CVD beyond any degree possible using readily available clinical characteristics and other CHD risk factors.

Cardiovascular SNPs. Obviously, there are large numbers of cardiovascular SNPs that we could check. At this point I recommend testing for those that have the best validation, the highest correlation with risk prediction, and those that are easily attainable. Currently 23andMe provides far too much information. The genetic tests listed in the table here define risk for coronary heart disease, arrhythmias, heart failure, and hypertension; these are the genetic factors I recommend that you look at in all your high-risk cardiovascular patients. From these tests and the Corus gene expression test, you will be able to determine the nutritional programs, medications, and other interventions the patient requires. Most of these tests can be obtained through Boston Heart Lab, Cleveland Heart Lab, Vibrant America Lab, Quest Labs, Doctor's Data, Genomics, Genova, or Pathway Genomics; there are also a number of companies that offer various test panels. I use a checklist of the companies that provide the best genetic testing, and for each patient, I simply check off the relevant tests for that individual and submit the list.

Genetic Trends in Cardiovascular Disease

* Genetic predisposition to CHD accounts for less than 50% of the susceptibility to CHD depending on gender, age, ethnicity and other factors.

* Positive family history increases risk of CHD by less than 3%.

* If onset of heart disease occurs before age 46, genetics account for approximately 100% of risk.

* There are 30 to 60 loci associated with Ml and CHD, but only a minority of loci mediates effects on CHD through the known top five risk factors.

* More than 50% of these genetic variants occur in over 50% of the population. Ten of the risk variants occur in over 75% of the population.

* Homozygotes for 9p21 SNP have 100% increase in risk and heterozygotes have 50% increase in risk.

* In the Swedish Twin Registry, genetic factors accounted for 57% of risk for CHD in men and 38% in women.

Top 25 Environment and Functional Risk Factors for Cardiovascular Disease

* Hypertension (24 hour ABM)

* Dyslipidemia (advanced lipid testing)

* Hyperglycemia, metabolic syndrome, insulin resistance, and diabetes mellitus

* Obesity/body composition

* Smoking/tobacco

* Hyperuricemia

* Renal disease

* Elevated fibrinogen

* Elevated serum iron/ferritin

* Trans fatty acids and refined carbohydrates

* Low dietary intake of omega 3 fatty acids and omega 3 index

* Low dietary potassium and magnesium with high dietary sodium intake

* Micronutrient deficiencies

* Caffeine intake with CYP 1A2 SNP, IF/IF allele

* Inflammation: increased hsCRP

* Increased oxidative stress and decreased oxidative defenses

* Immune vascular dysfunction/imbalance

* Lack of sleep

* Lack of exercise/sedentary lifestyle

* Stress, anxiety, and depression

* Hyper-homocysteinemia

* Subclinical hypothyroidism

* Hormonal imbalances in both genders

* Chronic clinical or subclinical infections

* Heavy metals

* Environmental pollutants

Testing for Early Detection and Prevention of Cardiovascular Disease

1. Genetic Expression Scoring and Testing: Corus CAD.

2. Top five CHD Risk Factors treated to new goals:

a. Hypertension: 24 hour ambulatory BP monitor (ABM).

b. Dyslipidemia: Advanced lipid testing.

c. Dysglycemia: FBS, 2h GTT, HbA1c, insulin, proinsulin, C-peptide.

d. Obesity: BW, BMI, WC, WHR, body impedance analysis (BIA).

e. Tobacco: stop all forms.

Genetic Testing

1. 9p21 (GG/CC) (inflammation, plaque rupture, thrombosis, AAA, ASCVD, CHD, MI, DM, IR)

2. 6p24.1 (CHD and DVT)

3. 4q25 (atrial fibrillation)

4. ACE I/D (DD allele) (HBP, LVH, CRI, nephroangiogenesis microalbuminuria, carotid IMT, CHD, MI)

5. COMT: Val/Val or Met/Met allele (CHD, MI, HBP and use of ASA and vitamin E)

6. 1q25 (GLUL) (CHD in DM)

7. APO E (E4/E4) (CHD, lipids, dietary response, omega 3 FA)

8. MTHFR (A1298C and C677T) for methylation (endothelial dysfunction, hypertension, thrombosis, CVD, CHD, MI, CVA and hyper-homocysteinemia).

9. CYP 1A2 (IF/IF) and caffeine (HBP, Ml, CHD, tachycardia, stiff aorta, PWV, Al, SBP, PP, vascular inflammation, increased catecholamines)

10. Corin (hypertension, volume and sodium, CHF with ANP and BNP, CRF, CVD, eclampsia)

11. CYP 11 B2 (TT allele) (HBP and aldosterone)

12. GSH-Px (glutathione peroxidase) (ALA-6 alleles, selenium) (CHD and Ml)

13. NOS 3 (Nitric oxide, HBP and CHD)

14. ADR B2 (AA allele vs GG allele) (HBP, PRA and DASH diet and RAAS drugs)

15. APO A1 and A2 (lipids)

16. HETE CYP4AII and CYP4F2 (HBP, sodium and volume overload, ENac) (amiloride)

17. MMP-2, MMP-9, and TIMP-1 (cardiovascular remodeling, DD, LVH, CHF, and hypertension)

18. AGTR1, NR3C2, HSD11B1, and B2 (HBP, potassium) and AGTR1 (AA/AC) and ARB response

19. AT1R-AA(AT1R autoantibodies); hypertension (ARB vs ACEI)

20. Blood group type A, B, and AB (vWF and thrombosis)

Conclusions and Key Take Away Points

* Evaluate and treat the Top 5 CFID Risk Factors utilizing the new definitions and testing methods.

* Evaluate and treat the Top 25 Modifiable CHD Risk Factors.

* Evaluate micronutrient testing (MNT).

* Evaluate specific genetics, SNP's, genetic expression testing (Corus CAD, GET, and GES), epigenetics and metabolomics for CVD, CHD, hypertension, and dyslipidemia.

* Obtain noninvasive CV testing (Endopat, CAPWA, TMT, CAC, CTA, Carotid IMT, rest and exercise ECHO, MCG, ABI, AAA, 24 hr ABM).

* Traditional Mediterranean diet (TMD) with 5 tablespoons EVOO/day (50 grams) and CoQ10.

* Modified low glycemie DASH 2 for hypertension. B2-AR AA/ GG alleles.

* 10 servings of fruits and vegetables per day (6 veg/4 fruit).

* High mixed fiber (40 grams), prebiotics, and probiotics general and specific species (alternating species).

* Omega 3 fatty acids for all patients, dose dependent (1-5 grams per day of balanced DHA, EPA, GLA and gammadelta tocopherol).

* 2 grams sodium, 5-10 gram potassium and 1000 mg magnesium/day.

* Avoid caffeine in CYP 1A2 SNP (IF/IF and IF/IA alleles).

* Selective use of ASA, vitamin E depending on COMT phenotype (met/met).

* 5 methyl folate and B vitamins depending on MTHFR genotype.

* Selenium with GSH-Px (ALA 6 alleles).

* Specific anti-hypertensive drug selection based on genotypes such as ACE l/D, Corin, CYPII B2, HETE and CYP 4A11, AGTR1, and AGTAA.


Dr. Mark Houston is an author, teacher, clinician, and researcher, currently Associate Clinical Professor of Medicine at Vanderbilt University School of Medicine, Clinical Instructor in the Department of Physical Therapy and Health Care Sciences at George Washington University, Director of the Hypertension Institute and Vascular Biology and Medical Director of the Division of Human Nutrition at Saint Thomas Hospital in Nashville, TN. Dr. Houston was selected as one of the Top Physicians in Hypertension in the US in 2008-2014 by the Consumer Research Council, and by USA Today as one of the Most Influential Doctors in the US in both Hypertension and Hyperlipidemia twice in 2009-2010. He was selected for The Patient's Choice Award in 2010-2012 by Consumer Reports USA. He is triple boarded certified by the American Board of Internal Medicine (ABIM), the American Society of Hypertension (ASH) (FASH) and the American Board of Anti-Aging and Regenerative Medicine (ABAARM, FAARM). He holds two Master of Science degrees, one in Human Nutrition from the University of Bridgeport, Connecticut, and another in Metabolic and Nutritional Medicine (University of South Florida School of Medicine-Tampa). Dr. Houston has presented over 10,000 lectures nationally and internationally and published over 250 medical articles and scientific abstracts in peer reviewed medical journals, as well as book chapters and books.


Stephen T. Sinatra and Mark C. Houston (editors). Nutritional and Integrative Strategies in Cardiovascular Medicine. Boca Raton, FL: CRC Press; 2015.

Dr. Stephen Sinatra and Dr. Houston are coauthors of a book on integrative cardiovascular medicine published in spring 2015 by CRC Press, available on and in various book stores. This is one of the first and only books that takes an integrative approach to cardiovascular medicine from the perspective of functional medicine, metabolic medicine, nutrition, nutritional supplements, and pharmacology. The book discusses all the essential aspects of cardiovascular disease, written for health care providers.

Other best-selling books by Dr. Houston include What Your Doctor May Not Tell You About Heart Disease (Grand Central Publishing, 2012); What Your Doctor May Not Tell You About Hypertension (Time-Warner Books, 2003); The Handbook of Hypertension (Wiley-Blackwell, 2009); and Vascular Biology in Clinical Medicine (Hanley and Belfus, 2002).

Workshop--January 27, 2016 Scripps Natural Supplements: An Evidence-Based Update Preconference in San Diego Integrative Cardiovascular Symposium Mark Houston, MD, and Mimi Guarneri, MD

This new interactive seminar will emphasize practical applied clinical cardiovascular medicine for health care providers and will review each topic with an emphasis on proper diagnosis and clinical treatment primarily with nutrition and nutritional supplements.

* Applied Clinical Vascular Biology & Vascular Aging for the Clinician

* Cardiovascular Disease (CVD) & Stress / Depression / Spirit / Heart Math

* Integrative Management of Hypertension Part 1

* Integrative Management of Hypertension Part 2

* Integrative Management of Dyslipidemia

* Integrative Management of Coronary Heart Disease (CHD) & Congestive Heart Failure (CHF)

For More Information Contact:

Scripps Conference Services & CME

Phone: 858-652-5400



Gene Expression Testing

The Corus CAD gene expression test, provided in tandem with a clinical assessment, can quickly, accurately, and safely help clinicians rule out obstructive coronary artery disease (CAD) in symptomatic patients. This test can now be ordered through CardioDx and through Quest Diagnostics and is covered by Aetna and Medicare.


600 Saginaw Drive,

Redwood City, California 94063

Phone: 650-475-2788

Fax: 650-475-2799



Jerry Stine, NC. Thanks to Jerry Stine, NC, of Lifespan Institute for technical support on this article. Lifespan provides consulting on nutritional biochemistry and individualized antiaging programs. Phone: 707-431-2143.

Nancy Faass, MSW, MPH. Ms. Faass is a writer and editor in San Francisco who has worked on more than 45 books for publishers that include Elsevier, Harper, McGraw-Hill, New Harbinger, New World Library, North Atlantic, and others. Director of The Writers' Group, her work focuses on the development, writing, and editing of copy, web content, articles, manuals, and white papers in the fields of integrative medicine.

For more information see: Phone:415-922-6234.
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Date:Dec 1, 2015
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