IMPROVE-IT study: Desperation of the Statin Industry

IMPROVE-IT touts ezetimibe and simvastatin therapy results as guidance to load up patients with ever higher doses of statins, satisfying the mythical NNTI of 100 patients dosed per 2 magical, precise, exact reductions of CVD incidence over 6 years.  Common sense would indicate that if you did nothing, normal variation would generate the same results given that there will never be 100% incidence of anything.  The impact of various statins piled one on top of each other in cardiovascular medicine is already being exaggerated based on a literal 1% decrease in incidence which could also easily be had by statistical manipulation. 

Stopping short of cutting cholesterol synthesis altogether, the ever lower recommendations for LDL to definitive hypocholesterolemia levels, which generates its own set of diseases such as increased infection and hemorrhagic type cerebral stroke, the ludicrous idea offered seriously to lower LDL levels in the populace to 60mg/dL and below will cause a whole swath of new death by low cholesterol.  What it says to the astute observer is that the normal range of LDL has never been culprit to atherosclerosis leading to ischemic events and that other unrecognized factors are causal, such as oxidation of cholesterol and proteins.

We're not seeing a remarkable 50% reduction here, just a flutter.  Moreover, the rate of death is exactly the same, barring a 0.1% difference.  For other drugs in oncology, this would be considered an unmet endpoint, and the drug would be canned, but not for the statin industry, whose sales must always increase year over year in order to inflate their stock price like other unrelated products.

IMPROVE-IT results

The real world data is that serum cholesterol levels are not related to CVD disease....at all.  Other factors associated with its transport do, but not cholesterol levels.  It is misdirected effort to reduce LDL-cholesterol across the board to hypocholesterolemia levels, especially as it pertains to the importance of cholesterol synthesis to cognition.  The thing with statins is that they are not targeted to particles, proteins, glycoproteins, etc.  They are designed to poison the mevalonate pathway, indiscriminately lowering cholesterol synthesis everywhere, having nothing to do with ApoB, ApoA, ApoE, ApoC, ApoJ, apo(a), triglycerides, phospholipids, plasmalogens, particle number, particle size, etc.  They have been proven dozens of times to have zero effect on the particle that is extremely more atherogenic than LDL, Lp(a), which nobody seems to check for.  One day in the future, it will be considered medical negligence not to check for Lp(a).  Statins do sometimes offer an anti-inflammatory mechanism, which may actually be their mode of action rather than poisoning the cholesterol synthesis enzyme chain.  The fact that lowering cholesterol lower and lower and lower had no benefit against heart disease says something to the tune of "obvious."

cholesterol-heart-disease-there-is-a-relationship-but-its-not-what-you-think

Real world data: Zero correlation (0.0) between cholesterol and heart disease.

1957: The Scurvy-Atherosclerosis Connection is Observed in Guinea Pigs

Dr. G.C. Willis made some of the first observations of this phenomenon in 1957. 

The Reversibility of Atherosclerosis (In Guinea Pigs)

Below is a picture of intimal hemorrhage induced by scurvy.

Below on the left is lipid accumulation (red) in a scurvy guinea pig liver,
and a normally supplemented liver on the right for comparison.

Dr. G.C. Willis' catalog of Vitamin C-Atherosclerosis work spanning back to 1957 is free for review here:

The Free Site for Dr. G.C. Willis' Work

Vitamin A Deficiency Causes an Irreversible Immunodeficiency??

Now, let's read this carefully again.  "A significant unresolved question is how vitamin A deprivation causes, and why retinoic acid fails to reverse, immunodeficiency. When depleted of vitamin A, T cells undergo programmed cell death (PCD), which is enhanced by the natural competitor of retinol, anhydroretinol."

But the TV pop-docs told us that vitamins have absolutely nothing to do with immune system function and that this vitamin-immune system connection is some kind of charlatan's ploy..

Wait a minute, now.  Vitamin A deficiency causes immunodeficiency?


Vitamin A depletion causes oxidative stress, mitochondrial dysfunction, and PARP-1-dependent energy deprivation.



While the title says one thing, the abstract clearly states another.  The disease is clearly multifactorial, but one cannot actually claim that vitamin deficiency has nothing to contribute to immunodeficiency because that would be simply false.  In fact, there is a 1-to-1 causality between various single nutrient deficiencies including macronutrients and immunodeficiency.  Nearly all nutrients are important to immune system function in one aspect or another.  It doesn't mean a well-nourished person will never get sick, just the same as living in the USA doesn't mean everyone will win the lottery.  It does mean that nutrient deficiency is an important causal factor to immunodeficiency, especially in impoverished countries and that there is no denying this fact.

Single Nutrient Deficiencies Known to Cause Cancer

Despite the "Reader's Digest" style expert "news" and other pop-sci mass media outlets that would lead one to believe this is some kind of quackery, it is well established in conventional global science that various single nutrient deficiencies are carcinogenic to the same degree as environmental carcinogens.  On the contrary, various single nutrient deficiencies may lead to severe cancer and the causal link has been established and known for a long time among conventional scientists.  Obviously, a compound nutrient deficiency could only worsen and aggravate carcinogenic processes.

Rather than go into a massive enumerated list-o-mania, or amazingly irrelevant political tirade, here are a few solid examples of independent conventional studies having proven the fact for a long time.

Selenium deficiency causes disseminated pyogranulomas.

Methionine and choline deficiency cause liver cancer.

Methyl donor nutrient deficiency causes liver cancer.

Vitamin B-12 deficiency causes genetic damage to B-cells.

Folate deficiency causes mitochondrial DNA deletions and chromosome breaks.

Zinc deficiency causes aberrant DNA damage repair.

Causing liver cancer by fighting glioma by depleting methionine??

Iodine deficiency causes dysplasia and neoplasia.

Riboflavin deficiency predisposes to cancer.

Riboflavin deficiency causes increased susceptibility to carcinogens.

Low Vitamin A causes Wilms tumor.

Experimental Vitamin A deficiency causes increased nephroblastoma.

Of course we don't ever forget about Vitamin C (ascorbate).

Maximal Ascorbate Cmax in Humans with Oral Dosing and Its Efficacy Threshold:

Taking 3 grams/4 hours can achieve 220uM Vitamin C in blood.

What type of cancer might respond to this oral dosing?  Lymphoma.

Proc Natl Acad Sci U S A. 2008 August 12; 105(32): 11105–11109.

What needs to be clarified is what direct cytotoxic effect additional ascorbate has and what immune cell augmenting effects that ascorbate has as an immune system side therapy.  The direct cytotoxic effect is one important mechanism, but it could not be the only one in the immunosurveillance against aberrant cells that happens routinely before solid tumor carcinogenesis.  It must be remembered that cells accumulate ascorbate against a gradient, often to 100 times higher concentration than what is in the serum environment.  1mM-4mM concentrations in lymphocytes is an unremarkable baseline concentration.  Given the stoichiometric depletion of ascorbate in an active immune response, it is not surprising that bowel tolerence in humans increases greatly in times of immune system challenge by any of the assorted antigens that it would face in fungal, bacterial, or viral infection as ascorbate is literally burned up like fuel.

Dynamic immune system cells operate in very extreme environments and burn through a lot of ascorbate.

Ascorbate burn rate by macrophages

Well known ascorbate burn by IL- therapy activating immune "killer cells" resulting in severe vitamin C depletion.

Neutrophils, our first line defense microbe eaters, use oxidative burst and may soak up an additional 8,000 umoles/L in times of attack.

So then, flux of reduced ascorbate through the physiology much like the running of water through a washing vessel of fixed volume may be more important than Cmax.  If the same dose of oxidized ascorbate remained stagnant through the vessel of the same size as a vessel through which reduced ascorbate were constantly running through, there would be less redox activity and more redox activity, respectively.  So the focus upon Cmax without examining immune cell function may be misguided especially in terms of daily immunosurveillance and prevention of cancer or immune system remission and/or mitochondrial reversion of early cancer.

The field of Vitamin C science has been partially demystified in the last 3 decades, but there is still much to be elucidated.

Vitamin C Reduces Field Rodent Lifespan Paper

A desperate absurdist attempt to "pull the wool over the sheep's eyes" was just made by picking up a field rodent that makes its own vitamin C and giving it two doses - a little bit more, and a lot more.  Typical for the people who want to make money off sick people, they touted this as new evidence that you shouldn't take extra vitamin C.  They measured the lifespan of these two groups and found that the group given a lot more died sooner than the group given a little more.

Here is the Achilles' Heel of the study.  There was no Zero Vitamin C group.  Why?  Because unlike humans and primates that do not make their own vitamin C, the field rodent would happily live its full life with zero dietary vitamin C.  So in effect, the little bit of vitamin C group is not zero + a little more, but what the rodent made in its own liver + a little more.  This is more than slightly misleading.  By not divulging the endogenous status of the field rodent's vitamin C synthesis, they are implying that the field rodent does not make vitamin C and that additional vitamin C kills the rodent.  Disingenuous yet with the cool dissimulation of people with an agenda to accept bribes from large corporations, it seems like a logical argument.  Except it isn't.

A person, any person anywhere on Planet Earth will die within a year without vitamin C in their diet.  The group omitted the zero vitamin C group, because the field rodent does not need it thanks to its own vitamin C generation in its own liver.  People do not possess this ability.  To properly match the studies, we would have demanded a zero vitamin C group for the field rodents and observed the life shortening qualities of vitamin C.  Then we would try this on humans and compare.

The results, which would be illegal and inhumane, would be the following:

Field rodents (n=100) + no vitamin C = full life span.
Humans (n =100) + no vitamin C = 100% mortality

The conclusion would then not be that supplemental vitamin C shortens human life, but extends it by 1,000,000%.  This absurd numerical conclusion of +1,000,000% is just as absurd as comparing the performance of a submarine on land versus in the ocean, or the effects of vitamin C on life extension in an animal that already makes its own to one that doesn't.

The last several decades of independent academic research have definitively and conclusively shown that Vitamin C and other antioxidants help to extend life span, not shorten it in humans.  A singular mass hypnosis piece in the pop media pimped by corporate funding contradicts thousands of scientists' findings across the globe.

What happens when a person doesn't take enough vitamin C, but just a tiny fraction of what you need?  This is still what will happen to you in 2013:

If some corporate shills had their way, we'd all just reverse centuries of scientific progress and go back to being scurvy pirates.  They should probably refresh themselves on medical documentation of scurvy.
 

OTC Saw Palmetto's Benefits against 5-alpha reductase II

Several unpatentable, human food plants can provide the same 5-alpha-reductase inhibitory effects as finasteride.  One is Saw Palmetto.

Potency of a novel saw palmetto ethanol extract, SPET-085, for inhibition of 5alpha-reductase II.