“Let us imagine that, say, 10% of those prescribed statins quietly flushed their drugs down the toilet. That’d make the drug look up to 10% less likely to cause side-effects!”

Not to mention, it could also put those 10% of prescribed statins into the water table, inadvertently exposing people to the effects of statins. Seems like that could also skew the side effect profile. After all, if people (supposedly) not exposed to the drug experienced some of the same muscle aches, it could bolster the arguments of those who claim these aches and pains are just a placebo effect.

I’m not sayin’ … I’m just sayin’ …

Thee I got religion and started eating 4 to 6 eggs in a day. Salmon and chicken rerplacerd wheat and ri e. My hdl is 55 and trigs are 50 to 60. I am off stations and my total cholesterol is 180.

Can somebody comment what they make of it? I know hdl is said to be a proxy for sat fat intake. Is increased fat intake correlated with higher cholestrol ?

Hilarious, Mark, thank you!

http://people.csail.mit.edu/seneff/why_statins_dont_really_work.html

‘Every individual gets at most only one chance to grow old. When you experience your body falling apart, it is easy to imagine that this is just due to the fact that you are advancing in age. I think the best way to characterize statin therapy is that it makes you grow older faster. Mobility is a great miracle that cholesterol has enabled in all animals. By suppressing cholesterol synthesis, statin drugs can destroy that mobility. No study has shown that statins improve all-cause mortality statistics. But there can be no doubt that statins will make your remaining days on earth a lot less pleasant than they would otherwise be.

To optimize the quality of your life, increase your life expectancy, and avoid heart disease, my advice is simple: spend significant time outdoors; eat healthy, cholesterol-enriched, animal-based foods like eggs, liver, and oysters; eat fermented foods like yogurt and sour cream; eat foods rich in sulfur like onions and garlic. And finally, say “no, thank-you” to your doctor when he recommends statin therapy. ‘

Blimey, a correction is needed urgently before Collins or Sever or Baigent exerts undue eminence upon the host (let them try!) I meant 75% – 74% was an unintentional typo.

‘Oxidative stress’ is a bit more demanding of the intellect than is the fat/cholesterol hypothesis but if I could figure the outline and then understand what others have written then almost anybody should be able – cos I am bit ordinary and thick.

Oxidative stress is brought on by compromised capacity for detoxification by the detoxicant process of methylation (and perhaps compounded by compromise to detoxification by transulfuration, too). Methyl groups (CH3) are passed from donor to recipient and they zap the recipient which is likely a reactive oxygen species or ‘free-radical’. The process is essential to every cell and takes place billions of times per second.

Oxidative stress invokes ‘inflammation’, which is actually incidental and not causal to the process. So don’t let anyone convince you inflammation ’causes’ CVD, it does not. ‘Inflammation’ is much like a two-bar heater in that inflammation; ‘heat’ arises when current meets with resistance. One difference is that we might have to envisage ions as conveyors of current, but that is exactly what ions do, so let’s accept this and move on swiftly.

Adequate methylation and transulfuration (and other processes too) are essential to maintain wellness. Conversely inadequate methylation capacity hastens ageing and onset of chronic illness. Methylation is the front-line of detoxification. Thing is elevated levels of the excito-hormones that form the basis of the fright, flight, or fight responses driven by the hypothalamic – pituitary – adrenal axis (HPA-axis) elevate the level of competition for would-be methyl donors — which is often indicated by rising levels of homocysteine (Hcy), btw.

That Hcy might oxidise cholesterol and thence cholesterol converts to oxycholesterol and oxycholesterol drives necrosis of certain cells (not cholesterol) leading to arterial disease (atherosclerosis) is now where my curiosities are focussed.

Of course stress has long been a well-received risk-factor for cardiovascular disease of the kind that involves and follows from atherosclerosis (plaques forming and consequential narrowing). But stress is an epi-physiological risk-factor that must commute through some stepwise physiological events to feed into whatever physiological developments actually cause atheromas to form. Increasingly I feel competition for methyl donating antioxidants, which increases for several reasons, not least a rise in the levels of the fright, flight, or fight hormones raises that level of competition.

I kinda figured this, very sketchily, for myself and then landed on an essay by Stan Field and written in 2006. As a consequence of figuring and then landing on some measure of confirmation, I can tell you, I half scared myself to death.

It isn’t just that the fat/cholesterol hypothesis is under attack, it is crumbling, and with some hope the house of statin secrets whose head is Lord Statin of Oxford, the head of CTT collaboration, Professor Sir Rory Collins, is to crumble too, Because it should be inadmissible to claim benefits arising in data you hold secret and deny open access to. Waht the fat-headed cholesterol faithful do not realise is that the much needed (and likely) successor to the fat/cholesterol hypothesis is already out there, its being developed, and more attentive and interested parties are contemplating its merits.

The biggest merit this methylation, homocysteine, oxidation, oxidised cholesterol theory has going for it is that risk factors like stress, and smoking, and obesity, can be linked either to the endocrinological aspects or to the oxidation sides of this delicate balance. In other words, for the first time risk factors can be discussed intelligently, epi-physiological risk factors (smoking, stress, etc.) can be logical split from those that are more physiological, and the nature of convergence to some physiological process in common can be explained. Smoking introduces a whole cocktail of toxins that add greatly to the workload of methylation.

So, when faced by a GP who si about to prescribe a statin inquire what thought he/she has given to ‘convergence’, ‘methylation’, and how on earth an HMG-CoA reductase inhibitor can prevent oxidation of cholesterol. If they were connected to the bp monitor, we could see their bp and bpm rising, for sure, for a patient with level of understanding would scare them half to death; I give you my word.

Link to Stan Fields essay ; http://www.svhi.com/lateschmart/methylmagic.pdf

Clowns to the left, joker to the right, lets drive that wedge between em, baby!

I discovered this very rarely cited report.

Dement Geriatr Cogn Disord 2009;28:75–80
DOI: 10.1159/000231980 Can be downloaded in full.
Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later
Alina Solomon et al.
I came across this paper first on the WebMD site in 2009. Not properly referenced therein and I enquired from
both WebMD and WebMD-BOOTS (UK version) about this use of statins and my comments Both declined to
answer.
From the full paper, the following extracts are very pertinent:
Extract from Introduction:
“Thus, the best approach implies not only early diagnosis and treatment, but also emphasizes prevention.
However, chronic diseases with a long preclinical phase (such as AD) pose inherent difficulties in the
identification of their risk factors. Since disease onset cannot be pinpointed, the chances are that true risk
relationships (factors increasing the probability of getting the disease) and reverse causality (the effects of
the disease itself on various factors) get confused.”

Comment: Indeed and three decades use of drugs, with an acknowledged adverse reaction of polyneuropathy
and other neurological adverse reactions is ignored as a factor in the development of Alzheimer’s. Now that takes some bias.

Extract from Strengths and Limitations of the Study
Information on lipid lowering treatments, which have been suggested to decrease dementia risk , was not available for this study.

Comment: The patient records were available for many possible factors such as age, sex, race, education and other medical conditions (Table 1) but not the therapeutic records. This is unbelievable; patient records without treatment details im plies either gross incompetence or negligence or that the records were withheld DELIBERATELY for the purpose of obfuscation and protection of Big Pharma profits.

I therefore did a quick 2×2 Chi-square test using Table 2 of the paper using both the combined and separately the AD and VaD numbers using guidelines on therapy, i.e. cholesterol blood levels over 200 and over 239 mg/dl should be treated with statins while cholesterol levels less than 200 mg/dl would not usually be treated. The results are shown below in the table. As the results were significant it is quite clear why the data on therapy was NOT available; Big Pharma would certainly not approve of results that implicated statins as a possible cause of Alzheimer’s and VaD
PMID: 168669 14 [PubM ed – indexed for MEDLINE]
Table Showing 2 x 2 analysis (CSS) for combined AD and VaD and assuming TC values above 239 mg/dl as treated with statins. Given guidelines this is almost certain.

The table below will have to be copied to a word processor and columns aligned manually. Columns delineated by “|” Tabs do not copy.

Cholesterol categories| No dementia (%age)| AD & VaD (%age)| TOTAL (%age)

NO TREAT (239 mg/dl) | 2932 (50.31)| 215 (3.69)| 3147 54.00

Totals | 5477 (93.98)| 351 (6.02)| 5828 (100)

CHI2 = 7.92 p= 0.0049
V2 = 7.91 p= 0.0049
Phi2 = p = 0.0014

This is highly significant and the fact that the actual therapies used were “unavailable” suggests doubtful, if not corrupt, practice and bias.

The Relative Rate (RR – much loved by medical statisticians) is a
58% INCREASE associated with the recommended prescription for statins. (Based on US guidelines
http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf)

Total Cholesterol
240 mg/dl = ~6.2 mmol/L High )

Using the combined AD and VaD figures from Table 2 for cholesterol levels >200 mg/dl (5.2 nmol/L) is shown below. Again the results are highly significant but suggest that the treatment of lower levels of
cholesterol may have been less aggressive.

Cholesterol categories | No dementia (%age)| AD & VaD (%age)| TOTAL (%age)

NO TREAT (200 mg/dl) | 6703 (68.09) | 460 (4.67) | 7163 (72.77)

Totals | 9248 (93.95) | 596 (6.05) | 9844 (100)
Chi2 = 6.24 p= 0.0124
V2 = 6.24 p= 0.0124
Phi2 = p = 0.0006

CONCLUSION: No wonder that details of therapy were “not available”. This is emphasised by the acknowledged “unavailabilty” of treatment data on the medical records. We are asked to believe that the
medical records did not include treatment records. I find that this is incredible; it is clear that the treatment records were deliberately withheld to obfuscate the real result of this study.

— The Great Cholesterol Myth

Dr Briffa, how terrible that some Professionals find it easier to stand by and

deny a mistake even though it can cause Death.

Is it loss of Face or loss of Wealth I wonder.

Thank you for what you do.

You are right PL. Because of the reigning dogma of the TSH test (another stellar

example of Junk Science) thousands of people with Thyroid disease are every week

sent home with a prescription for antidepressants, and told to get some exercise,

” Is it really possible that one treatment can prevent so many diseases? ”

Yes, of course it’s possible.
If you die from the first illness you don’t get the others.

Just not the desired way to prevent illnesses.

‘On the money’, John D! Made me smile.
I wrote a letter to the Indy in 2008 (!) which of course they did NOT publish. Might as well publish it here 🙂 Quote:

Sir,

Statins ability to ‘halve’ the risk of dementia? (Independent, Tues. 29 July)

And a subsequent10-minute Internet search finds additional claims to:

moderate an influenza pandemic, prevent onset of Alzheimer’s, prevent Parkinsons, reduce the incidence of cardiovascular events, reduce the risk of stroke, reduce the risk of flu death, aid recovery after pneumonia, assist secondary prevention medication, reduce risk of sepsis, assist periodontitis patients, cure one of the most common forms of learning disability, cure acne and associated skin conditions, reduce the risk of lung cancer, prevent lung cancer, fight colon cancer, alleviate erectile dysfunction in men, lower cholesterol in children and infants, help treat Hep.C. and, as if all this healing power wasn’t enough, statins have now been ‘shown’ also to stop depression.

Now pull the other one!

M. Peralta