Written by Dr. Kristine Blanche
I spent the first half of my medical career in a conventional mindset. Throughout my work in surgery, emergency medicine, & critical care, I realized that there was a very limited focus on prevention in the medical world. Prompted by a series of family illnesses, I became “obsessed” with the prevention of illness and disease.
I have always told my patients:
“Genes load the gun, but the environment pulls the trigger.”
Everyday people are born with genetic mutations, which can increase the risk of illness and disease; however, mutations are rarely the ultimate cause of the disease. Many factors influence whether the mutation is expressed, and you have control over many of these factors.
Lets take a look a very common genetically linked disease in the US: type-two diabetes. During my first pregnancy, I developed gestational diabetes. Upon further tests, I discovered that I was born with a gene that significantly increases my risk of developing type-two diabetes. I have been pre-diabetic all my life, and did not even realize it. However, now that I am fully aware of the risk, I can prevent myself from becoming diabetic by maintaining a stable blood sugar level, staying active, and rarely indulging in sweets. By taking simple preventative actions, I can remain diabetes-free for the rest of my life, despite my genetic predisposition. The United States government spends approximately $245 billion a year on the co-morbidities of diabetes (National Diabetes Statistics Report, 2014) while approximately 1.7 million people are diagnosed a year (CDC, 2012). Type-two diabetes is one of the most preventable diseases on the planet. Yet, it is predicted that 1 in 3 people in the United States will have diabetes by 2050. These staggering numbers are a result of the non-existent focus on prevention.
Even though type-two diabetes can be prevented with a few lifestyle changes, many medical practitioners chose prescribing insulin instead of prescribing a healthy lifestyle. Type-two diabetes can be prevented despite genetic predisposition – Can cancer prevention work in the same way?
Further research is necessary to learn the relationship between certain genes and cancer. Recently, the BRCA gene, which has been proven to increases the risk to breast and ovarian cancer, has become the frontier for studying genetic links to cancer. However, the mechanisms behind the function and expression of the gene are not yet fully understood. The recommended conventional treatment is to undergo prophylactic mastectomies and oophorectomies – surgery to cut out the potential problem. But what if you could prevent the expression of the BRCA gene, and bypass all the pain and money spent on procedures? If type-two diabetes can be prevented, despite genetic predisposition, what effect will prevention have on cancer genes?
Similarly to the BRCA gene, research suggests that the MTHFR gene mutation also increases breast cancer risk. (Dong 2014) However, the mechanisms of action are more clearly understood and continue to be further studied. The MethyleneTetraHydroFolateReductase,orknown as the MTHFR gene mutation, can be detected with a simple blood test. Simply put, the MTHFR gene mutation slows down methylation and the ability to create anti-oxidants and detoxify the body. Because toxins are a common environmental trigger to cancer, and the genetic mutation impairs this detoxification process, it is speculated that this particular gene mutation is the link to cancer risk – yet thousands of people are unaware they have the MTHFR gene.
After learning of the MTHFR gene at a conference with Dr. Ben Lynch, I began testing for MTHFR A1298C and MTHFR C6777T in all my patients nine months ago. Alarmingly, 85% of people I have tested in my New York practice are either homozygous or heterozygous for one or both of the MTHFR genes mutations. These numbers are staggering. Empowered with this information, my patients are now able to identify a potential increased risk for cancer and heart disease, and institute simple changes to their lifestyle to help prevent the onset of disease.
The right lifestyle and nutrient recommendations can assist a patient in ultimately “feeding their genes” in order to increase methylation and minimizing the negative effects of the MTHFR mutation.
As Dr. Ben Lynch has written for many years, any people with a MTHFR gene mutation should take these simple steps:
- Maintain a gluten and dairy free lifestyle
- Eat organic foods
- Avoid toxins – cleaners, perfumes, and skincare chemicals
- Detoxify regularly – saunas
- Ensure adequate amounts of methylcobalamine and methylfolate
- Take precautions to ensure gut health – probiotics
- Avoid folic acid
(Matheos, Laura, Holy MTHFR, LLM,December 31, 2012)
The above diagram is a great visual of the complex biochemical pathways that are affected by the MTHFR gene. The diagram effectively illustrates the significance of methyl B12 and folate, and identifies how the MTHFR gene is central to many biochemical processes.
It is clear toxins increase the risk of cancer. A study by Darbre (2004) discovered Parabens, chemicals found in most skin care products and deodorants, in 99% of breast tumors removed in women being treated for primary breast cancer. Parabens are just one of the many chemicals that have an established link with breast cancer incidence (Darbre, 2008). BPA is another toxin linked to breast cancer (Li, 2014).
My passion is cancer prevention. I strive to learn more about the genetic mutations linked to the development of cancer. Personally, I have not treated a single patient with breast cancer who tested negative for the MTHFR mutation. If the gene is discovered pre-cancer development, simple measures can be taken to prevent the progression towards disease, including detoxification protocols and the supplementation of methylfolate and methylcobalamine (Wei, 2014).
In preventative medicine, the goal is to identify risk factors and implement a plan to reverse these risk factors and prevent disease. The connection between toxins and breast cancer is firmly established (Barr, 2012, Darbre 2008, Li, 2014). Screening for impaired detoxification pathways and implementing nutritional changes to optimize methylation and detoxification can stop cancer before it even starts.
Health is our greatest asset. We simply MUST demand PREVENTION.
For more information please visit https://www.indiegogo.com/projects/fund-cutting-edge-research-natural-approach-to-preventing-breast-cancer
Kristine Blanche, RPA-C
“Together we can change the face of medicine!”
Integrative Healing Center
403 Main Street #1~ Inspiration Wharf
Port Washington, NY 11050
Barr, L., Metaxas, G., (2012) Measurement of paraben concentrations in human breast tissue at serial locations across the breast from axilla to sternum
Darbre, P., Aljarrah, A., & Miller, W. (2004). Concentrations of parabens in human breast tumours. J Appl Toxicol, 24, 5–13.
Darbre, P., & Harvey, P. (2008). Paraben esters review of recent studies of endocrine toxicity, absorption, esterase, and discussion of possible health risks. J Appl Toxicol, 28, 561–578.
Stankova J, Lawrance AK, Rozen R (2008). “Methylenetetrahydrofolate reductase (MTHFR): a novel target for cancer therapy”. Curr Pharm Des 14 (11): 1143–50. doi:10.2174/138161208784246171. PMID 18473861.
Li K, Li W, Dong X (2014) Association of 677 C.T (rs1801133) and 1298 A.C (rs1801131) Polymorphisms in the MTHFR Gene and Breast Cancer Susceptibility: A Meta-Analysis Based on 57 Individual Studies. PLoS ONE 9(6): e71290. doi:10.1371/journal.pone.0071290
Lynch, Benjamin. MTHFR C677T Mutation: Basic Protocol. MTHFR.net. Feb. 24, 2012.
Weiwei Z, Liping C, Dequan L. (2014) Association between dietary intake of folate, Vitamin B6, B12 & MTHFR, MTR Genotype and breast cancer risk. Pak J Med Sci 2014;30(1):106-110. doi: http://dx.doi.org/10.12669/pjms.301.4189