Nutrigenomics: Control Your Risk for Disease

As a registered dietitian and clinical exercise specialist, working in an integrative compounding pharmacy, I often face a daunting challenge to convince patients that what they eat, drink, and take through supplements and drugs influences their entire body, future health, and genes.Last year, I attended a presentation by Dr. Jeffrey Bland. Dr. Bland has a PhD from the University of Oregon and specializes in nutrigenomics, nutritional biochemistry, and applied clinical nutrition functional medicine; he is also a registered clinical laboratory director. I will give you a few of the highlights of Dr. Bland's presentation, along with my own tips for assessment and supplementation. Hopefully, you will be convinced to take serious consideration of what goes into your body, and to share this information with your patients.

Nutrigenomics

"Nutrigenomics" is the study of how foods interact with the genes in your body, and how diet can alter and affect the expression of disease. The Jan. 17, 2005 issue of Newsweek discussed this topic, as does the book Genome, which states, "Genes in and of themselves do not create disease. Only when they are plunged into a harmful environment unique to the individual do they create the outcome of disease." Let's look at biochemical markers, integrative therapeutic intervention, and disease risk and treatments.

Inflammation

Inflammation initiates insulin resistance, osteoporosis, arthritis, lupus, and cardiovascular disease. Omega-3 fatty acids (fish oil) make eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA and DHA modulate gene expression, are the cornerstone of all health therapies, and block inflammatory markers (series 2 prostaglandins).I recommend fish oil capsules, not flax, because alpha-linolenic acid requires adequate enzymes in order to convert to EPA and DHA. These enzymes can be reduced by stress, insulin resistance, and prescription medications. Purchase a high-quality fish oil to minimize mercury, PCBs, contaminants and burping. Appropriate dosing and distribution of EPA to DHA should be tailored to patients' individual needs.

Pre-Diabetes

Pre-diabetes is quickly becoming an epidemic. What can you do to prevent its onset? Measure fasting insulin level by serum; aim for 10 or less. Also test fasting glucose - look for a level between 70-99, and a triglyceride to high-density lipoprotein (HDL) ratio of 2:4. Control the type of carbohydrates you eat (refined and high glycemic foods), but do not omit carbohydrates altogether. Eliminating them can cause increased depression, fatigue and inadequate glycogen stores for exercisers.

Cardiovascular Disease

Cardiovascular disease (CVD) prevention includes decreasing inflammation, measuring C-reactive protein (hsCRP), maintaining good lipid control and a normal body weight (BMI of 19-24), getting adequate folic acid, B₆ and B₁₂, and exercising. Low hsCRP levels are correlated with less lumen thickening and CVD. Aim for hsCRP levels of less than 1. Lipids: Cholesterol, LDL, HDL and triglycerides should be measured after fasting for 10-12 hours. Food, supplements, and any necessary prescription medication should be chosen to fit those specific markers, and ratios should be determined.

Osteoporosis

Osteoporosis is a quiet, but serious threat to health. Approximately 10 million Americans over age 50 have osteoporosis and 34 million have osteopenia. Osteopenia is the beginning of osteoporosis. When I first started doing osteoporosis screenings, I was stunned at the number of young women (20-35 years) with osteopenia. U.S. Surgeon General Richard Carmona gave a moving speech at The American Dietetic Association meeting in October 2003 in Texas. He stated, "Osteoporosis is the second leading cause of death; you won't see it on the top ten list of diseases and is largely preventable!" By 2020, it is predicted that half of all Americans over age 50 will be at risk for fractures from weak bones.

During Dr. Bland's presentation, I heard many whispers when he related osteoporosis to other diseases. How can osteoporosis be related to other diseases? He proved his point with numerous clinical articles showing that bone loss is an inflammatory condition. So, what can you do? To prevent inflammation, get adequate calcium, vitamin D (measure serum D3 levels), green vegetables (vitamin K and alkali) and potassium (fruits and vegetables), and perform weight-bearing exercises; avoid too much vitamin, alcohol, caffeine, soda and sodium.

Patients with rheumatoid arthritis have a high rate of arterial wall thickening and calcium mobilization. High serum calcium increases the risk for CVD. What do these diseases have in common? Inflammation.

Immune conditions such as lupus and multiple sclerosis (MS) also are correlated to inflammation, adequate vitamin D status, and insulin resistance - the list goes on and on. However, I have tried to touch on the bigger and more common diseases in our society right now, in addition to giving you a taste of some things you can start to do to help prevent them.

To a large degree, it is possible to control gene expression. I am living proof. I have a strong family history of diabetes, depression, osteoporosis and obesity; but from the age of 10, I decided that I could be different. That decision has led me down a very clinical and integrative path, with a passion for helping people find their health by helping them find the tools and zest for better nutrition and exercise.

Resources

1. Creactive protein levels and outcomes after statin therapy. The New England Journal of Medicine 2005:352;29-38.
2. Selective inhibition of NF-KB blocks osteoclastogenesis and prevents inflammatory bone destruction in vivo. Nature Medicine 2004;10:617-24.
3. Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases. JAMA, July 28, 2004;292:490-495.
4. Vitamin A intake and hip fractures among postmenopausal women. JAMA 2002;287:47-54.
5. Inflammation and bone resorption as independent factors of accelerated arterial wall thickening in patients with rheumatoid arthritis. Arthritis Rheum November 2003;48(11):3061-7.