BRCA1/2 and Chopping Off B**bies
Breast cancer is complex, yet it is quite simple. Is it necessary to contemplate IMHO surgical removal and reconstruction of any beautiful body part that may fall to cancer? Where does one logically start? Where does one end because everything that undergoes DNA replication and editing may fall to cancer and mutations... Ms. Angelina Jolie, I lurrv u, please stop. Your message is IMHO short-sighted and not sustainable.
Pardon, Let's Look at A Couple of BRCA1/2 Facts:
BRCA1/2 is a defect in DNA repair and fails to fix 8OHdG (oxidative DNA damage product, 8-hydroxy-2'deoxyguanosine)
BRCA1/2 raises risk in men of breast, prostate, pancreatic, gastric and hematologic cancers
BRCA1/2 raises risk in women of breast (73%), ovarian (41%), colon (2-fold), pancreas (3-fold), stomach (4-fold) and fallopian tube (120-fold) cancers
BRCA1/2 like all mutation genes is under epigenetically controlled regulation -- for example, silencing of the gene occurs with polyaromatic hydrocarbons (pollution), insulin, and hypomethylation (lack of methyl donors -- either depletion or dietary deficiency -- or COMT, MTHFR , etc variants). Best food sourced methyl donors are methylB12, choline and methylfolates (free range egg yolks, liver, meat, seafood -- sorry no plant sources you crazy vegans). Insulin 101 : Insulin is a growth hormone and one function is to induce stimulation of female ovaries to increase testosterone secretion. Unfortunately, in both men and women, normal levels and excess testosterone may be converted into estrogens under insulin induction by P450-aromatase (aka, CYP19), in many tissues including fat tissues, breast cells, endothelial cells and prostate cells.... Certain gene variants accumulate significantly more estrogens than non-carriers (COMT, CYP19).
BRCA1/2 silencing may be epigenetically avoided by diet, resveratrol and other antioxidants
BRCA1/2 needs a genetic 'cofactor' like MTHFR , COMT, CYP19 (aromatase which converts testosterone to estrogens), CYP1B1 (pathway increases 16OHE1, estrogen carcinogen adduct) and CYP1A1 to be carcinogenic according to emerging evidence. These genetic polymorphisms are all related to raised toxic estrogen metabolites and creation of estrogen dominant states.
Functional Medicine and Tracking/Lowering 8OHdG
GDX/Metametrix Labs and other functional medicine lab testing centers offer a wonderful test that measures and helps practitioners to track oxidative DNA damage, the 8OHdG biomarker. This goes up and down with oxidative damage. Many things have been shown to lower and raise 8OHdG. Diet and supplements (melatonin, vitamin C, berry extracts, resveratrol, etc) have been shown to lower 8OHdG. Please check out more HERE and HERE (p. 361 of 'Lab evals for integrative and functional medicine' 2nd ed, 2008).
In a hepatitis C trial in participants at risk for hepatic carcinoma and iron overload, a low-iron diet and phlebotomy lowered 8OHdG to near normal 8OHdG rates after 6 yrs. Additional observed benefits were improvements in liver function: lower ALT and liver function tests, improved scarring and hepatitis, no progression to carcinoma. Viral Hep C titers remained the same but cancer was avoided despite originally sky-high 8OHdG six years prior at trial onset.
Prior animal pharm:
Pesticides May Be Behind USA Diabesity, Disrupting Insulin and Tissue Insulin Resistance
50 Shades of F_cked Up (Cancer medical management in the USA )
Aromatase up-regulation, insulin and raised intracellular oestrogens in men, induce adiposity, metabolic syndrome and prostate disease, via aberrant ER-α and GPER signalling.
MTHFR Polymorphisms, Dietary Folate Intake, and Breast Cancer Risk Results from the Shanghai Breast Cancer Study [hat tip: Todd Lepine MD]
Breast. 2008 Oct;17(5):441-50. Counseling for male BRCA mutation carriers: a review.
Methionine-Dependence Phenotype in the de novo Pathway in BRCA1 and BRCA2 Mutation Carriers with and without Breast Cancer. [need for methyl donors]
Epigenetic diet: impact on the epigenome and cancer.
Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.
Epigenetic impact of dietary polyphenols in cancer chemoprevention: Lifelong remodeling of our epigenomes.