CANCER – When Cells GO CRAZY

Cancer - When Cells Go Crazy
Friday, 05 October 2012 22:43 Written by Dr. Tony Vendryes 

Like solders in a well-run army, the body’s cells are programmed to behave in a structured, orderly manner, to perform specific tasks to ensure health and well being. Sometimes a cell starts acting abnormally, breaking the conventional code of conduct, disregarding the rules and serious diseases like cancer can develop.    

What is Cancer? 
The word cancer comes from the Greek word for crab. Physicians of old noticed how in this disease,abnormal cells spread through the body in all directions seeming to crawl like a crab invading and damaging the patients organs and tissues.

Cancer is a disease of our cells and can develop from the cells in any organ or system in the body. Over 100 different types of cancer are known to modern medicine. It starts with one cell becoming abnormal. It then multiplies to produce more abnormal cells that over time invades and damages normal tissues and organs. Only then do symptoms manifest and this may take many years to happen. For example by the time the lump from a breast cancer is large enough to be felt, it would have been quietly developing over ten or more years. Medical tests like mammograms would only have discovered the lump one to two years earlier and by that time the cancer is no longer confined to the breast. Instead of just looking out for the symptoms of cancer we are better served if we address the causes of cancer.The ultimate solution to any problem is to determine the underlying causes and correct them.  

What causes CANCER?
Cancer cells act crazy. For one thing unlike normal cells they multiply indefinitely acting as if they are immortal and cannot die. But their behavior is suicidal as they end up killing themselves by destroying the very body they inhabit.
Why? The behavior of a cell is governed by the genetic material(DNA) that resides in the nucleus of that cell. Damaged DNA sends out abnormal instructions to the cells causing them to act insane and cancer results. Here are some of the common causes of cancer that science has identified.  

Poor nutrition: What you eat has everything to do with your cancer risk. My article last week highlighted how vitamins, minerals and herbs called antioxidants protect the cells from damage. A diet high in fresh fruit, vegetables (antioxidant rich) and fibre lowers your cancer risk while eating foods high in animal fats and low in fibre will increase your chances of getting cancer. This applies to many common cancers including colon, breast, prostate and lung cancer. The American Cancer Society recommends that for cancer protection we eat over 7 servings of fruit and vegetables daily. In addition regular use of the antioxidant supplements I listed last week will enhance cancer protection.  

Immune incompetence: Although abnormal cancerous cells form in our body regularly, we also have our own anti-cancer security system called the immune system that detects and destroys these abnormal cells. When cancer cells are allowed to proliferate, this indicates that the immune system is malfunctioning. There are many natural ways to enhance immune function. This is critical for our health in general as well as cancer protection in particular.  

Infection and Inflammation: The experts have clearly identifies chronic inflammation and infections particularly viral infections as definite causes of cancer. Common examples are the associations between the Human papilloma virus and cervical cancer and the hepatitis virus a liver cancer. Inflammation in the stomach and colon can set the stage for cancers there while chronic gum and tooth infections may also heighted your cancer risk.  

Hormones: Hormones are powerful chemical messengers that influence the behavior of all cells especially the cells of our reproductive organs. Hormonal imbalance is a major factor in causing cancers of the breast, prostate, uterus and testicles. This is related not only to changes in lifecycles and lifestyles but also to thousands of chemicals in the modern environment that have hormonal activity. The hormone estrogen and chemicals called xenoestrogens are major culprits.  

Chemical pollution and Radiation: In addition to the hormonal disruptors mentioned above, there are many other sources of chemical and electromagnetic pollution in our homes and work places. These invisible, subtle, ever present agents of cancer play multiple roles in the creation of malignancy. Every day objects like cell phones, plastic bottles or TV and computer screens may all add to a toxic burden that compromise our capacity to avoid cancer.  

Heredity: Our scientists have unraveled the human genetic code, and they are now working hard to identify genes that we can blame for cancer. This will allow for the development of new and expensive gene therapies. However it is estimated that less than 20% of our illnesses can be blamed on genes and over 80% is related to environment and lifestyle.

The fact that you are born with a gene, say for breast cancer does not mean that you will get breast cancer. It indicates that your risk is increased and that you should be particularly vigilant with your lifestyle practices. Genes exist and can be switched on (activated) or remain silent (inactive) by the factors mentioned above. You are not a helpless victim of even your genes.  

Mental attitude and Stress: As human beings we are not just a body, but an integration of body, mind and spirit. Just using those three different words encourages a division in our thinking that interferes with a truly holistic approach. I have coined a term “menscorp” to try to avoid this split.

Dealing with the body-mind, the menscorp is critical in addressing the cancer issue.
The research shows that ones mental state has a profound effect on delicate matters like immune function and hormonal balance, all of which influence cancer risk. Chronic anxiety, depression, negative thinking, emotional trauma can all tip the scales and initiate cancer. On the other hand optimism, joy, faith, prayer and gratitude reap powerful benefits for health and wellness. Your mental and spiritual attitudes are important instruments in your anti-cancer toolbox.   

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Learn More about YOUR Genes

 

 

Primary Benefits of the Gene SNP™ DNA Analysis: 

• Learn about your genetic risk based on variations in your unique genetic code
• Understand how your current nutrition, exercise and lifestyle choices interact with your unique genetic code
• Make informed decisions regarding eating habits, lifestyle choices and exercise based on your genes
• Learn how market-leading Isotonix® nutraceutical supplementation recommended in your personalized Health Action Plan can help you maintain your optimum health
• Track changes and progress in your Health Action Plan and, after following recommendations, update your Online Customer Profile to determine whether you have new nutrition, exercise, lifestyle or supplementation recommendations.

What Makes the Gene SNP™ DNA Screening Analysis Unique?
When it comes to our bodies, we want to make choices that have a positive impact on our health. But some of those decisions – eating the wrong foods, making certain lifestyle choices, even the way we exercise – could impact our body's ability to maintain optimum health. Even if we think we’re making the right choices, there are other factors that help determine our overall picture of health.
Genetics play a huge role in how our bodies process nutrients, how they respond to activity and how we react to our environment and surroundings. When it comes to your health, the answers are in your genes. Your DNA tells a story: how you process foods, how you react to exercise, how your environment affects your body, how your family history plays a part in your health.
What if you could learn about your health with a simple test, one that could give you realistic and reasonable recommendations to promote your quality of life? It’s time to make informed decisions about your health – no more guesswork, just facts.
The Gene SNP DNA Analysis combines your individual diet, lifestyle and environment information and is scientifically merged with your genetic background to provide an exclusive Health Action Plan designed specifically for you. It will help provide practical suggestions intended to promote your health and wellness. Based on variations in your DNA and lifestyle factors, the Gene SNP DNA Analysis will make recommendations based on how your body metabolizes food, utilizes nutrients, removes toxins and responds to physical activity. By understanding how your genetic profile affects your well-being, the Gene SNP DNA Analysis will help you take charge of optimizing your wellness. The Gene SNP DNA Analysis examines a wide variety of genes and SNPs, providing a customized Health Action plan that focuses on diet, nutrition, exercise and supplementation based on your genetic profile.    
Now you can be sure your personalized Health Action Plan includes the best possible supplementation thanks to the integration of the most advanced nutraceutical products available, Isotonix. Each product has been carefully chosen to provide you with the best supplementation based on your individualized Health Action Plan. By integrating the Gene SNP DNA Analysis with the Isotonix product line, you’ll be receiving the very best supplementation support to maintain the healthiest of lifestyles.
No longer will you have to accept a “one-size-fits-all” vitamin and nutrition regimen. Using our exclusive patent rights to screen genetic variations, Gene SNP DNA Analysis uncovers the ability of your genes to respond to nutritional and environmental factors that affect various areas of your health.
The best part is that the results remain accurate throughout your life since your gene makeup does not change. Since your genes don’t change, you have the ability to optimize the function of your genes through diet, exercise and nutritional supplementation. And while you can’t change your genes, you can change your lifestyle. As you progress through your Health Action Plan, following the recommendations specifically suited for you and your body, you can make changes to your online customer profile and receive an updated Health Action Plan with recommendations based on your new, healthier lifestyle.
Remember the Gene SNP Program is as easy as 1, 2, 3!
1)    Complete the Gene SNP DNA Analysis, including the Online Customer Profile
2)    Receive your Customized Health Action Plan
3)    Order your customized supplements

Frequently Asked Questions About the Gene SNP™ DNA Analysis:
What is the Gene SNP DNA Analysis?The Gene SNP DNA Analysis is a comprehensive kit that provides a laboratory analysis of specific gene variants in your genetic material (DNA) that have been found to influence health and an Online Customer Profile survey that provides valuable information about various lifestyle habits that relate to the gene variants being tested. These two pieces of information are then analyzed together to provide you with a personalized Health Action Plan outlining diet, nutrition, exercise and supplementation recommendations.
Who should use this product?Everyone over the age 18 concerned about how their genetic makeup plays a role in diet, nutrition and exercise should use this product.
How can understanding your genes promote a long, healthy life?Your health is a result of interactions between your genes and lifestyle factors such as diet, exercise, stress, smoking and alcohol. It is your genetic makeup that determines which nutrients are utilized, how they are used, the way toxins are removed and how effective these key processes are within the body. The best part is that the results remain accurate throughout your life since your gene makeup does not change. Since your genes don’t change, you have the ability to optimize the functioning of your genes through diet, exercise and nutritional supplementation. And while you can’t change your genes, you can change your lifestyle. As you progress through your Health Action Plan, following the recommendations specifically suited for you and your body, you can make changes to your online customer profile and receive an updated Health Action Plan with recommendations based on your new, healthier lifestyle.
Can I alter my genes through diet or lifestyle, or by using a vaccine?No matter what we do, our genes remain the same throughout our lifetime. No amount of food or exercise can physically alter our genes. With proper nutritional supplementation and lifestyle changes, you can maintain the functioning of your gene variations to maintain optimal health.
Will you be able to tell me if I’m ill?No, we can only determine what types of genes people have and how they relate to certain metabolic factors involved in well-being. If you think you may be ill, you should consult your doctor.
What is included in the Gene SNP DNA Analysis?Your Gene SNP DNA Analysis kit includes:

• Access to a secure Online Customer Profile
• Bubble envelope
• Pre-addressed return FedEx stamp for the envelope
• Two swabs
• One small paper envelope
• Gene SNP booklet
• Consent form, Genetic Assessment Request Form, instructions and Gene SNP Code wallet-card

What do I do with the Consent and the Genetic Assessment Forms? Both forms have to be filled out and signed before the laboratory can accept your swabs for processing and DNA analysis. Send the completed forms with your swabs in the padded envelope using the prepaid shipping label to the laboratory. 
How does the Gene SNP DNA Analysis testing process work?In the privacy of your home, you simply use a mouth swab to collect cheek cells, which contain your DNA. The swabs are put into the white swab envelope provided after drying. Send the swabs with the Genetic Assessment Request Form and the Consent Form in the padded envelope with a prepaid shipping label provided in the kit to the processing laboratory. Once at our certified laboratory, DNA is extracted from your swabs and then prepared for analysis. The DNA is analyzed using the latest genotyping technology to give the most accurate results. Your DNA analysis is then matched with the answers you provided into the Online Customer Profile. Once all of this data is compiled, it is entered into a sophisticated, algorithm-based computer software program that generates your confidential, easy-to-follow Gene SNP Health Action Plan. 
How long does it take to get my Gene SNP DNA Analysis results?Typically, it takes three to four weeks for you to receive your Gene SNP Health Action Plan. 
How accurate are the results of my Gene SNP analysis? The analysis of your DNA is in compliance with the Quality Assurance and Accuracy Verification Standards of the CLIA certified laboratory. The accuracy of the genetic analysis is greater than 95 percent. 
How can my sample fail the Gene SNP DNA Analysis? Sometimes the sample provided does not contain enough DNA because you just brushed your teeth, or if you did not let the swabs dry long enough before putting the swabs in the envelope, or if it took too long (longer than 10 days) to reach the laboratory for analysis. It is important to follow the Swab instructions in your kit.
How is my privacy protected?Protecting your privacy is at the core of Gene SNP DNA Analysis. We recognize your need for strong privacy protection and the careful management of your personal information. Any information you share is kept strictly confidential and is secured electronically using sophisticated encryption technology. The laboratory personnel and others who are required in the processing of your genetic results have been trained and tested to meet the requirements of Health Insurance Portability and Accountability Act (HIPAA). Your results are handled as Protected Health Information (PHI), as defined in HIPAA and regulations promulgated by the U.S. Department of Health and Human Services in accordance to that defined in 45 CFR, §160 and Subparts A and E of §164.
Should I worry about privacy issues?Your genetic information will be encrypted and will not be directly associated with your personal information collected from your Online Customer Profile, but will be stored in a database maintained in accordance to CLIA and HIPAA standards. While this information may be used by the laboratory research affiliates to conduct further analyses for commercial purposes, under no conditions will this information be released to third parties in a way that discloses personal information, except with your written permission, unless required by law. The laboratory is vigilant against breaches of security and improves security and privacy safeguards on a regular basis.
Can I use my PCID to allow more than person to take the Online Customer Profile?No, the PCID number is used to authenticate a unique person who is logging on and is used to identify specifically the supplements recommended for that person. 
What is the difference between the Nutri-Physical® and the Gene SNP DNA Analysis?The Nutri-Physical is an analytical tool that recommends a customized nutritional supplementation program based on your answers to a series of lifestyle and behavioral questions. These questions center around your current health and various lifestyle factors, including diet, exercise, medical history, current supplementation and related contributing factors.
The Gene SNP DNA Analysis is a specialized program which analyzes your DNA and lifestyle and customizes a program to your individual genes. It will help you identify the changes needed to promote your health and wellness. According to variations in your DNA and your lifestyle choices, the Gene SNP DNA Analysis will make recommendations based on how your body metabolizes food, utilizes nutrients, removes toxins and responds to physical activity. The Gene SNP DNA Analysis helps you understand how your genetic profile affects your well-being by a simple swab of your cheek.
Does my Gene SNP DNA Analysis Kit have an expiration date?You must send in your cheek swabs, consent forms and complete your Online Customer Profile within 180 days of the date the kit was purchased. All sales of the Gene SNP DNA Analysis kit are final.

* These statements have not been evaluated by the Food and Drug Administration.
This product(s) is not intended to diagnose, treat, cure or prevent any disease.

Scientific Studies Which Support the Gene SNP™ DNA Screening Analysis: 
Genes associated with cholesterol metabolism, triglyceride balance, vascular flow and tissue development: APOC3, IL-6, eNOS, LPL, CETP, MTHFR:

• Brousseau, M.E., et al, Cholesteryl ester transfer protein TaqI b2b2 Genotype is associated with higher HDL cholesterol levels and lower risk of coronary heart disease end points in men with HDL deficiency: Veterans Affairs HDL Cholesterol Intervention Trial. Arterioscler Thromb Vasc Biol 22, 1148-1154 (2002)
• Brull, D.J., et al, Interleukin-6 gene -174g>c and -572g>c promoter polymorphisms are strong predictors of plasma interleukin-6 levels after coronary artery bypass surgery. Arterioscler Thromb Vasc Biol 21, 1458-1463 (2001)
• Brull, D.J., et al, The effect of the Interleukin-6-174G > C promoter gene polymorphism on endothelial function in healthy volunteers. Eur J Clin Invest 32, 153-157 (2002)
• Chen, W. et al, Combined effects of endothelial nitric oxide synthase gene polymorphism (G894T) and insulin resistance status on blood pressure and familial risk of hypertension in young adults: the Bogalusa Heart Study. Am J Hypertens 14, 1046-1052 (2001)
• Dullaart, R.P., et al, Cholesteryl ester transfer protein gene polymorphism is a determinant of HDL cholesterol and of the lipoprotein response to a lipid-lowering diet in type 1 diabetes. Diabetes 46, 2082-2087 (1997)
• Leeson, C.P., Glu298Asp endothelial nitric oxide synthase gene polymorphism interacts with environmental and dietary factors to influence endothelial function. Circ Res 90, 1153-1158 (2002)
• Miyamoto, Y., et al, Endothelial nitric oxide synthase gene is positively associated with essential hypertension. Hypertension 32, 3-8 (1998)
• Shoji, M., et al, Positive association of endothelial nitric oxide synthase gene polymorphism with hypertension in northern Japan. Life Sci 66, 2557-2562 (2000)
• Brown, C.A., et al, A common polymorphism in methionine synthase reductase increases risk of premature coronary artery disease. J Cardiovasc Risk 7, 197-200 (2000)
• Christensen, B., et al, Genetic polymorphisms in methylenetetrahydrofolate reductase and methionine synthase, folate levels in red blood cells, and risk of neural tube defects. Am J Med Genet 84, 151-157 (1999)
• Chen, J, et al, A methylenetetrahydrofolate reductase polymorphism and the risk of colorectal cancer. Cancer Res 56, 4862-4864 (1996)
• Jacques, P.F., et al, Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation 93, 7-9 (1996)
• Ma, J., et al, Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer. Cancer Res 57, 1098-1102 (1997)
• Martinez de Villarreal, L.E., et al, Folate levels and N(5),N(10)-methylenetetrahydrofolate reductase genotype (MTHFR) in mothers of offspring with neural tube defects: a case-control study. Arch Med Res 32, 277-282 (2001)
• Slattery, M.L., et al, Methylenetetrahydrofolate reductase, diet, and risk of colon cancer. Cancer Epidemiol Biomarkers Prev 8, 513-518 (1999)
• Brown, S., et al. Interaction between the APOC3 gene promoter polymorphisms, saturated fat intake and plasma lipoproteins. Atherosclerosis. 170: 307-313, 2003.
• Fisher, R., et al. Common variation in the lipoprotein lipase gene effects on plasma lipids and risk of atherosclerosis. Atherosclerosis. 135: 145-159, 1997.
• Guzik, T., et al. Relationship between the G894T (Glu298Asp variant) in endothelial nitric oxide synthase and nitric oxide-mediated endothelial function in human atherosclerosis. American Journal of Medical Genetics. 100: 130-137, 2001.
• Wallace, A., et al. Variants in the cholesterol ester transfer protein and lipoprotein lipase genes are predictors of plasma cholesterol response to dietary change. Atherosclerosis. 152: 327-336, 2000.               

Genes associated with antioxidant function and detoxification: MnSOD, SOD3, GSTM1, GSTT1, GSTP1: 

• Ambrosone, C.B., et al, Manganese superoxide dismutase 9MsSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. Cancer Res 59(3), 602-606 (1999)
• Hirvonen, A, et al, Association between manganese superoxide dismutase (MsSOD) gene polymorphism and breast cancer risk. Carcinogenesis 5(22), 827-829 (2001)
• Kimura, K.Y., et al, Genetic association of manganese superoxide dismutase with exudative age-related macular degeneration. Am J Ophthalmol 130(6), 769-73 (2000)
• Stoehlmacher, J., et al, A genetic polymorphism of manganese superoxide dismutase (9MnSOD) predicts for risk of colorectal cancer in young individuals. Annals of Oncology 11(Suppl 4), 59 (2000)
• Wang, X.L., et al, Plasma extracellular cuperoxide dismutase levels in an Australian population with coronary artery disease. Arterioscler Thromb Vasc Biol 18, 1915-1921 (1998)
• Purdie, D., et al, Dietary antioxidants, manganese superoxide dismutase (MnSOD), and risk of epithelial ovarian cancer. Proc. American Assoc. for Cancer Res. 43, 4227 (2002)
• Cotton, S.C., et al, Glutathione S-transferase polymorphisms and colorectal cancer: a HuGE review. Am J Epidemiol 151(1), 7-32 (2000)
• Lampe, J.W., et al, Modulation of human glutathione S-transferases by botanically defined vegetable diets. Cancer Epidemiol Biomarkers Prev 8, 787-93
• Lin, H.J., et al, Glutathione transferase GSTT1, broccoli, and prevalence of colorectal adenomas. Pharmacogenetics 12, 175-179
• Mitrunen, K.N., et al, Glutathione S-transferase M1, M3, P1, and T1 genetic polymorphisms and susceptibility to breast cancer. Cancer Epidemiol Biomarkers Prev 10(3), 229-36 (2001)
• Pool-Zobul, B, et al, Mechanisms by which vegetable consumption reduces genetic damage in humans. Cancer Epidemiol. Biomarkers Prev. 7, 891-99 (1998)
• Rock, C.L., et al, Nutrition genetics and risks of cancer. Annu Rev Public Health 21, 47-64 (2000)
• Steinkellner, H., et al, Effects of crusiferous vegetables and their constituents on drug metabolizing enzymes involved in the bioactivation of DNA-reactive dietary carcinogens. Mutation Research, 480-481,285-297 (2001)
• Ambrosone, C., et al. Manganese superoxide dismutase (MnSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. Cancer Research. 59(3): 602-606, 1999.
• Chistyakov, D. A., et al. Polymorphisms in the Mn-SOD and EC-SOD genes and their relationship to diabetic neuropathy in type 1 diabetes mellitus. BMC Medical Genetics. 2(1): 4, 2001.
• Parke, D.V. “Antioxidants and disease prevention: mechanisms of action”. Antioxidants in Human Health. CABI Publishing, 1999.
• Gaudet, M., et al. Diet, GSTM1, and GSTT1 and head and neck cancer. Carcinogenesis. 25(5): 735-740, 2003
• Lampe, J.W., et al. Modulation of human glutathione S-transferases by botanically defined vegetable diets. Cancer Epidemiology Biomarkers Preview. 9(8):787-793, 2000.
• Verhoeff, B., et al. The effect of a common methylenetetrahydrofolate reductase mutation on levels of homocysteine, folate, vitamin B12 and on the risk of premature atherosclerosis. Atherosclerosis. 141(1): 161-166, 1998
• Change, A., et al. The effect of 677 C T and 1298 A C mutations on plasma homocysteine and 5,10- methylenetetrahydrofolate reductase activity in healthy subjects. British Journal of Nutrition. 83(6): 593-596, 2000.
• Jacques, P., et al. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation. 93(1): 7-9, 1996.
• Miller M., and Mohrenweiser, H. Genetic variability in susceptibility and response to toxicants. Toxicology Letters. 120(1-3): 269-280, 2001.
• Cosma, G., et al. Relationship between genotype and function of the human CYP1A1 gene. Journal of Toxicology and Environmental Health. 40(2-3): 309-316, 1993.
• Bosron, W. and Ting-Kai, L. Genetic polymorphism of human liver alcohol and aldehyde dehydrogenases, and their relationship to alcohol metabolism and alcoholism. Hepatology. 6(3):502 - 510, 1986.
• Takeshita, T. and Morimoto, K. Accumulation of hemoglobin-associated acetaldehyde with habitual alcohol drinking in the atypical ALDH2 genotype. Alcohol Clinical and Experimental Research. 24(1): 1-7, 2000.

 Genes associated with bone structure: VDR, COL1A1, IL6, TNFα: 

• Chen, H.Y., et al, Relation of vitamin D receptor FokI start codon polymorphism to bone mineral density and occurrence of osteoporosis in postmenopausal woman in Taiwan. Acta Obstet Gynecol Scan 81, 93-98 (2002)
• Dennison, E.M., at al, Birthweight, vitamin D receptor genotype and the programming of osteoporosis. Paediatr Perinat Epidemiol 15, 211-219 (2001)
• Eastell, R. and Lambert, H., Diet and healthy bones., Calcif Tissue Int 70, 400-404 (2002)
• Ferrari, S., et al, Bone mineral mass and calcium and phosphate metabolism in young men: relationships with vitamin D receptor allelic polymorphisms. J Clin Endocrinol Metab 84, 2043-2048 (1999)
• Ferrari. S.L., Osteoporosis, vitamin D receptor gene polymorphisms and response to diet. World Rev Nutr Diet 89, 83-92 (2001)
• Garnero, P., et al, Association between a functional interleukin-6 gene polymorphism and peak bone mineral density and postmenopausal bone loss in women: the ofely study. Bone 31, 43-50 (2002)
• Gong, G., et al, The association of bone mineral density with vitamin D receptor gene polymorphisms. Osteoporos Int 9, 55-64 (1999)
• Lorentzon, M., et al, Vitamin D receptor gene polymorphism is related to bone density, circulating osteocalcin, and parathyroid hormone in healthy adolescent girls. J Bone Miner Metab 19, 302-307
• MacDonald, H.M., et al, COL1A1 Sp1 polymorphism predicts perimenopausal and early postmenopausal spinal bone loss. J Bone Miner Res 16, 1634-1641 (2001)
• Mann, V., et al, A COL1A1 Sp1 binding site polymorphism predisposes to osteoporotic fracture by affecting bone density and quality. J Clin Invest 107, 899-907 (2001)
• Prentice, A., The relative contribution of diet and genotype to bone development. Proc Nutr Soc 60, 45-52 (2001)
• Ralston, S.H., Genetic control of susceptibility to osteoporosis. J Clin Endocrinol Metab 87, 2460-2466 (2002)
• Grant, S., et al. Reduced bone density and osteoporosis associated with a polymorphic Sp1 binding site in the collagen type 1 alpha 1 gene. Nature Genetics. 14: 203-205, 1996.
• Ortlepp, J., et al. The vitamin D receptor gene variant and physical activity predicts fasting glucose levels in healthy young men. Diabetic Medicine. 20: 451-454, 2003.
• Uitterlinden, A., et al. Interaction between the vitamin D receptor gene and collagen type 1alpha1 gene susceptibility for fracture. Journal of Bone and Mineral Research. 16: 379-385, 2001. 

Genes associated with inflammatory response: TNF, IL-6: 

• Abraham, L.J., et al, Impact of the -308 TNF promoter polymorphism on the transcriptional regulation of the TNF gene: relevance to disease. J Leukoc Biol 66, 552-566 (1999)
• Chung, H.Y., et al, The inflammation hypothesis of aging: molecular modulation by calorie restriction. Ann NY Acad Sci 928, 327-335 (2001)
• Grimble, R.F., Nutritional modulation of immune function. Proc Nutr Soc 60, 389-397 (2001)
• Nakajima, T., et al, Allelic variants in the interleukin-6 gene and essential hypertension in Japanese women. Genes Immun 1, 115-119 (1999)
• Terry, C.F., et al, Cooperative influence of genetic polymorphisms on interleukin 6 transcriptional regulation. J Biol Chem 275, 18138-18144 (2000)
• Vickers, M.A., et al, Genotype at a promoter polymorphism of the interleukin-6 gene is associated with baseline levels of plasma C-reactive protein. Cardiovasc Res 53, 1029-1034 (2002)
• Ferrari, S., et al. Two promoter polymorphisms regulating interleukin-6 gene expression are associated with circulating levels of C-reactive protein and markers of bone resorption in postmenopausal women. Journal of Clinical Endocrinology & Metabolism. 88: 255-259, 2003.
• Grimble R., et al. The ability of fish oil to suppress tumor necrosis factor alpha production by peripheral blood mononuclear cells in healthy men is associated with polymorphisms in genes that influence tumor necrosis factor alpha production. American Journal of Clinical Nutrition. 76(2): 454-459, 2002.
• Terry, c., et al. Cooperative influence of genetic polymorphisms on interleukin 6 transcriptional regulation. Journal of Biological Chemistry. 275: 18138-18144, 2000.
• Vendrell, J., et al. A polymorphism in the promoter of the tumor necrosis factor-alpha gene (-308) is associated with coronary heart disease in type 2 diabetic patients. Atherosclerosis. 167: 257-264, 2003.
• Witte, J.S., et al, Relation between tumour necrosis factor polymorphism TNFalpha-308 and risk of asthma. Eur J Hum Genet 10, 82-85 (2002)

Genes associated with glucose balance: VDR, PPARg2, ACE, TNF: 

• Chiu, K.C., et al, The vitamin D receptor polymorphism in the translation initiation codon is a risk factor for insulin resistance in glucose tolerant Caucasians. BMC Med Genet 2,2 (2001)
• Dalziel, B., et al, Association of the TNF-alpha -308G/A promoter polymorphism with insulin resistance in obesity. Obes Res 10, 401-407 (2002)
• Deeb, S.S., et al, A Pro12Ala substitution in PPARgamma2 associated with decreased receptor activity, lower body mass index and improved insulin sensitivity. Nat Genet 20, 284-287 (1998)
• Dengel, D.R., et al, Exercise-induced changes in insulin action are associated with ACE gene polymorphisms in older adults. Physiol Genomics 11, 73-80 (2002)
• Kadowaki, T., et al, The role PPARgamma in high-fat diet-induced obesity and insulin resistance. J Diabetes Complications 16, 41-45 (2002)
• Nicaud, V., et al, The TNF alpha/G-308A polymorphism influences insulin sensitivity in offspring of patients with coronary heart disease: the European Atherosclerosis Research Study II. Atherosclerosis 161, 317-325 (2002)
• Paolisso, G., et al, ACE gene polymorphism and insulin action in older subjects and healthy centenarians. J Am Geriatr Soc 49, 610-614 (2001)
• Li, S., et al. The peroxisome proliferator-activated receptor-gamma2 gene polymorphism (Pro12Ala) beneficially influences insulin resistance and its tracking from childhood to adulthood: the Bogalusa Heart Study. Diabetes. 52: 1265-1269, 2003.
• Ostgren, C., et al. Peroxisome proliferator-activated receptor-gammaPro12Ala polymorphism and the association with blood pressure in type 2 diabetes: Skaraborg hypertension and diabetes project. Journal of Hypertension. 21: 1657-1662, 2003.
• Paolisso, G., et al. ACE gene polymorphism and insulin action in older subjects and healthy centenarians. Journal of American Geriatric Society. 49: 610-614, 2001.
• Perticone, F., et al. Relationship between angiotensin-converting enzyme gene polymorphism and insulin resistance in never-treated hypertensive patients. Journal of Clinical Endocrinology & Metabolism. 86: 172-178, 2001.