Extracts of my contribution to the book by Dr Duane Gravelins MD
Tag Archives: CVD
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Why Statins are Toxic
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Statins are technically defined as HMG Co-enzyme A reductase inhibitors.
Inhibiting HMG Co-enzyme A reductase (mevalonate enzyme) has extremely
toxic implications because our cells rely on the products of this
mevalonate synthesis. Mevalonate, which is the basic building block for
cholesterol, CoQ10, dolichols and all the regulatory steroid hormones
etc…. (see diagram for more) This assembly line is so important
biochemists named it “The Mevalonate Metabolic Pathway” and teach it in
most basic courses.
The statin gamble – to reduce a symptom (not the
cause) i.e. sugar-damaged lipids. It works in that cholesterol
disappears, the lipids disappear, muscles and neurons start to
disappear. The myth pharma seek to exploit is lower LDL without causing
too much obvious toxic damage.
Sugar control will improve lipid
circulation, function and lipid health – without toxic consequences. It
won’t lower vital cholesterol! and raised LDL without sugar-damage
ensures longevity.
The cholesterol paradox essay link: http://bit.ly/1fkGYgb
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Why cholesterol drugs might affect memory
Dr Duane Graveline has agreed to share his comments on the article in Scientific American with you:
“When I saw Melinda Moyers’ first mistake I was amused for my morning walk
took place in Island Pond, Vermont not Merritt Island Island, Florida where
I currently reside. It was then I spotted the title “Why cholesterol
drugs might affect memory’ and began to get angry. I had spent 15 years
documenting the cognitive side effects of statin drugs and our FDA’s
Medwatch had recently reported over 7500 statin associated transient
global amnesia and memory loss reports received during the time period
2004-2014. A reasonably accurate title would not read cholesterol
lowering drugs might affect memory. The proper title would read
cholesterol lowering drugs affect memory. If Ms Moyer has done her job
she would know these facts just as I know them so why not use them.
Then
when my name came up again in the article I was surprised to read I
had been “following a healthy diet to keep my cholesterol low.” Never
since my research on the subject have I been even remotely concerned
about my cholesterol. It is irrelevant to heart attack and stroke.
Inflammation is the underlying cause. Many times in my writing I have
told my readers how ashamed I was to have raised my family on no eggs,
skim milk and margarine for 17 years so conned I had been as a much
younger doctor. Had Ms. Moyer but asked me I would have told her this.
And then she topped it off by saying “he says he has never felt better.”
Now I am really angry for she has never in the past decade asked me
and since the year 2000 I have almost completely lost the ability to
walk. I barely make it with cane and walker and am but a moment away
from wheelchair existence. Peripheral neuropathy says my neurologist
with my muscle biopsy showing denervation atrophy (no nerve, no
muscle). Ms Moyer conjured up this entire thing. If she had only called
me.
Duane Graveline MD MPH”
It’s Not Dementia, It’s Your Heart Medication: Cholesterol Drugs and Memory
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Cholesterol and insulin
Xia et al. inhibited a late step in the biosynthesis of de-novo cholesterol in murine and human pancreatic β cells [8] and published their findings in 2008. They had previously shown that insulin secretion was sensitive to the acute removal of membrane cholesterol. They now demonstrate that the depletion of membrane cholesterol impairs calcium voltage channels, insulin secretory granule creation, and mobilisation and membrane fusion.
This paper [8] clearly demonstrates that a direct causal link exists between membrane cholesterol depletion and the failure of insulin secretion. Their work is in close accord with data from some statin trials, which also connect cholesterol reduction with increased risk of type 2 diabetes; indeed, statin use has been shown to be associated with a rise of fasting plasma glucose in patients with and without diabetes [9]. The underlying mechanisms of the potential adverse effects of statins on carbohydrate homeostasis are complex [10] and might be related to the lipophilicity of the statin [11]. Indeed, retrospective analysis of the West of Scotland Coronary Prevention Study (WOSCOPS) revealed that 5 years of treatment with pravastatin reduced diabetes incidence by 30% [12]. The authors suggested that although lowering of trigliceride levels could have influenced diabetes incidence, other mechanisms such as anti-inflammatory action might have been involved; however, in the multivariate Cox model, baseline total cholesterol did not predict the development of diabetes [12]. Furthermore, pravastatin did not decrease diabetes incidence in the LIPID trial which included glucose-intolerant patients [13]. On the other hand, in the JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin), which studied apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels [14], the risk of diabetes was increased by a factor of 1.25 [95% confidence interval (CI), 1.05 to 1.51] among individuals receiving rosuvastatin 20 mg daily with respect to placebo. Strikingly, among persons assigned to rosuvastatin, the median low density lipoprotein (LDL) cholesterol level at 12 months was 55 mg per deciliter [interquartile range, 44 to 72 (1.1 to 1.9)].
It is intriguing that salutary lifestyle measures, which might exert their beneficial action through an anti-inflammatory mechanism without a strong cholesterol-lowering effect, beyond reducing cardiovascular events and total mortality, reduce also the risk of diabetes and other chronic degenerative diseases. This fact may represent a ‘justification’ not to use a drug in low-risk primary prevention populations: lowering cholesterol at the expense of increasing diabetes might be counter-productive over the long-term.
8. Xia F, Xie L, Mihic A, et al. Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells. Endocrinology 2008; 149: 5136-45.
9. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients. J Investig Med 2009; 57: 495-9.
10. Szendroedi J, Anderwald C, Krssak M, et al. Effects of high-dose simvastatin therapy on glucose metabolism and ectopic lipid deposition in nonobese type 2 diabetic patients. Diabetes Care 2009; 32: 209-14.
11. Ishikawa M, Okajima F, Inoue N, et al. Distinct effects of pravastatin, atorvastatin, and simvastatin on insulin secretion from a beta-cell line, MIN6 cells. J Atheroscler Thromb 2006; 13: 329-35.
12. Freeman DJ, Norrie J, Sattar N, et
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...the risk of mortality or acute coronary syndrome was positively associated with age; male gender; hypertension; uncontrolled diabetes; being a former smoker; HAVING LOW LDL; having low BMI....
Vitamin D Levels for Preventing Acute Coronary
Syndrome and Mortality: Evidence of a Non-Linear
Association
doi: 10.1210/jc.2013-1185
J Clin Endocrinol Metab
Low LDL and low BMI associated with increased mortality risk
Statin treatment accelerates atherosclerosis – Uffe Ravnskov
Recently two separate studies showed that people on statin treatment develop atherosclerosis more often than untreated people. One of them was published in Diabetes Care, the other one in Atherosclerosis. You can get more details about this shocking finding in Dr. Mercola´s interview with senior scientist researcher Stephanie Seneff from MIT, who also is a member of THINCS. Read also Dr. Mercola´s comments about statin treatment.
Uffe Ravnskov, MD, PhD,
Independent Investigator
Spokesman of THINCS
The International Network of Cholesterol Skeptics
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Liz & Glyn Wainwright 