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Death of the Great Cholesterol Diet Fairy Tale, Familial Hypercholesterolaemia, BRCA1/2 Myths, Insulin 101, Cancer and 50 Shades

Posted May 23 2013 9:25pm



Sorry for the delay.... Old scathing editorial in QJM (hat tip: Peter D'Adamo), by D.D. Adams ' The great cholesterol myth; unfortunate consequences of Brown and Goldstein’s mistake .'



The Mistaken Implication of FHC and Elevated Blood Cholesterol

Abstract  Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D.

Unfortunate consequences of Brown and Goldstein’s mistake
Brown and Goldstein’s burst of fascinating information dazzled the medical profession, most of whom consequently accepted the false cholesterol hypothesis. This has led to unfortunate consequences that include



The author concludes 'The fact that of the thousands of people involved in achieving this spurious result did not include a single elementary mathematician with intellectual independence is in accord with the whole sorry story of the great cholesterol myth, starting with the false statistics used in analysing the Framingham data.10 The meta-analysis of Ray et al.,13 showing no prolongation of life by use of statins in randomized controlled trials involving 65 229 participants, is the final nail in the coffin of the great cholesterol myth.'



Insulin 101, Diabesity and Cancer Malignancies....

The lifetime risk of developing any invasive cancer is over 1:3 (males nearly 1:2) currently and by 2020, the WHO estimates, the stats will be 1:2 for both males and females.  The XX chromosomes no longer will protect us gals.

Why?

Does it have anything to do with 'Great Cholesterol Diet Myth' that the above authors have dispelled on unfounded, false scientific interpretations?  The refined whole-wheat-unhealthy-heart debacle may be nearing its end after this editorial, perhaps.

Is our diabesity and cancer epidemics related to the growth over the last few decades of 'low fat,' government-sanctioned, high refined carbs, grain-based propaganda and GMO ( Bt-gut busting zonulin-opening lectins ), pesticide laced grains and grain-fed commercial meat, poultry, dairy and eggs?  And the environmental havoc that plays out...  Our original gut flora are nearly extinct much like most of the rainforest species.  Compound this with other endocrine- and gut-disrupting toxins like mercury and arsenic that  rain out from coal burners which still supply greater than 50% of USA energy.  BTW China is now #1 globally for coal utilization, eeking out over the USA in recent years. Go China for exceeding USA's giant industrial pollution footprints.

http://www.avonbreastcare.org/files/SusanLuckWebinar.pdf



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).
  • Compared with noncarriers, women carrying at least one CYP19 8r allele had 20% higher estrone (P = 0.003), 18% higher estradiol (P = 0.02), and 21% higher free estradiol concentrations (P = 0.01). Women with the COMT Met/Met genotype had 28% higher 2-hydroxyestrone (P = 0.08) and 31% higher 16α-hydroxyestrone concentrations (P = 0.02), compared with Val/Val women.  Cancer Epidemiol Biomarkers Prev 13; 94.

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 )



Other Citations:

http://www.ultrawellnesscenter.com/files/2010/05/Functional-Diagnostics-Redefining-Disease.pdf
http://www.ultrawellnesscenter.com/files/2010/05/Cholesterol-AT.pdf
http://www.cancer.org/cancer/cancerbasics/lifetime-probability-of-developing-or-dying-from-cancer
http://whattofeedyourkids.blogspot.jp/2009/10/xenoestrogens-and-breast-cancer-why-we.html
http://www.scientificamerican.com/article.cfm?id=earth-talk-the-coal-truth
http://www.lef.org/magazine/mag2012/nov2012_Epigenetics_Breast_Cancer_01.htm
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.
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