Further to
LIPITOR,® THIEF OF MEMORY Dr.Graveline has unraveled the impact of statins
on the immune system . The implications of this are huge. This is a must read
even though it is a bit technical for some (gets easier to understand as you
read). His comments could just as easily be applied to many other drugs.
"Tossing the statin sledgehammer into this system is perhaps quite comparable in
effect to the rampages of "a bull in a China shop" and it is far too soon to
tell about most malignant changes...
...statin's effect is based upon interference with our most basic immuno defense
system. The potential consequences are frightening."
Unlike foods/nutrients most drugs muck around with some very intricate
biochemical pathways and frequently mask, not cure as many pretend, the effects
of a disease at the expense of creating another.
Some examples are: Tomoxifin and Roloxifin, which are second generation anti-estrogen
medications which supposedly prevent breast cancer at the expense of upping the
chances of endometrial cancer and pulmonary embolus (twofold increase in embolic
event).
"The thiazolidinediones used to control Type II Diabetes are famous for causing
liver cancer. One of them, Rezulin, was approved in the USA through devious
political infighting, but failed to get approval in the UK because it was known
to cause liver cancer.... As of April 2000, lawsuits commenced to clarify this
situation (Law Offices of Charles H. Johnson & Associates (telephone 1 800 535
5727, toll free in North America)"...
Extracted from:
Our
Deadly Diabetes Deception
The drug companies, in many instances,
knowing release drugs that are harmful. Like professional criminals their
motto is "not guilty unless caught" As the probability of being caught is very
low and the cultivated public trust not to mention the profits so high they
continue to gamble with our health!
Chris Gupta
http://www.newmediaexplorer.org/chris/2004/08/11/statins_and_our_immune_system.htm
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Statins And Our Immune System
The pharmaceutical industry has long been attempting to develop a means
by which interference with cholesterol production might be achieved farther
along the biosynthetic pathway, beyond the point where vital intermediary
products such as
ubiquinones and
dolichols
originate. Thus far, their quest has failed. There is reason to believe that
such biochemical maneuvering, even if successful for restoring such products may
be completely inadequate to address the full spectrum of physiological
consequences from statin drug use. Certainly any hormonal consequence from
inadequate cholesterol availability, such as testosterone and progesterone
deficiency, would remain an issue. And, as Pfreiger has so brilliantly
demonstrated, impairment of synapse formation and function in our brain cells
from deficient cholesterol manufacture would continue unabated, resulting in the
incredible spectrum of cognitive dysfunction. Even if the clever and dedicated
researchers of the pharmaceutical industry finally discover a way around these
two, very substantial side effects, even greater hurdles exist from our recent
evidence that statins work not by cholesterol manipulation but by some basic
anti-inflammatory role.
Key to this is a substance known as nuclear factor
kappa B. All statins inhibit this vital step in our immune system's
ability to defend us from alien forces. Whether by being the recipient of a
donor kidney or under attack by bacteria or viruses, our immune system has
evolved a defensive strategy in which suppression of inflammation, triggered by
nuclear factor kappa B, plays a vital role. Such stimulants to inflammation
include the foreign by-products of arterial inflammation and damage. Statin
drugs are known to suppress this nuclear factor kappa B (NF-kB) response and
thereby open a veritable Pandora's box of unpredictable consequences.
At best, our HMG Co-A reductase inhibitors are blunt instruments and our
immuno-defense system is both delicate and complex. During eons of coexistence
of our complex multicellular life forms in the midst of competing, simpler
unicellular organisms, there have developed many different forms of defensive
and offensive strategy - all dealing with the needs of one or the other of these
duelling organisms to gain a survival advantage. We have had 3.5 billion years
to work out our defense systems against widely diverse challenges and NF-kB is
key to all of them. If we thought the complexity of cholesterol manufacture by
our body is complex, it's child's play compared to what is involved in
anti-infection and immuno-modulation. Now, throw in a statin and try to predict
the consequences.
NF-kB in its several forms is known to molecular biologists as a transcription
factor and my bringing more than a smattering of this complex subject to your
attention would risk losing you from terminal boredom, so skim the following
very lightly. I warmed you this is challenging - how could a history of a 3.5
billion year war be otherwise? NF-kB resides in the cytoplasm of each cell in
five different forms known to our molecular biologists as family. The offspring
of these family members, known as dimers, remain held in check in the cytoplasm
by certain inhibitory proteins until a release signal is received, allowing our
now activated NF-kB to enter the nucleus of the cell. It is there, in the
nucleus, that it completes its mission in life to stimulate genes and
manufacture proteins necessary for such diverse tasks as monocyte adhesion,
macrophage recruitment, smooth muscle migration and platelet activation, key
elements of our defensive inflammatory response.
With so many steps involved, a good strategist could predict many different
forms of assault by dedicated viruses, bacteria and other forms of single celled
life, for this war is basically that of the monocellular rulers originally
dominating life on our planet against we multicellular usurpers. Therefore it
should come as no surprise that some of these defenders have managed to gain an
advantage over us, their adversary, by inhibiting NF-kB while others succeed by
enhancing NF-kB. Others manage both sides of the coin. E. coli, one of our most
common infectious agents, prevents NF-kB from entering the nucleus, thereby
enabling this ubiquitous organism freer access to our bladder walls and
urethras. Through a similar process of checkmate, another common bacteria,
Salmonella, inhibits our anti-inflammatory response sufficiently long to allow
bacterial colonization of the lining of the gut, giving a decided advantage to
"their" side. On the other hand, some Chlamydia organisms, warring against the
urogenital systems of both men and women, have evolved a distinct advantage by
enhancing our NF-kB, thereby assuring increased survival of infected cells in
our urinary and reproductive systems. On a far more serious note, the very
common Epstein-Barr virus causing infectious mononucleosis uses NF-kB inhibition
to help destroy our protective "T "cells as part of our common teenage "mono"
presentation but when it decides to go on a malignant rampage, triggering
nasopharyngeal carcinoma and Burkitt's lymphoma, it does so through sustained
NF-kB activation. The list goes on and on with other microorganisms and foreign
antigens of all kinds, numbering thousands of variations of these basic themes.
So now let us return to statin drugs and their now well-established effect of
inhibition of NF-kB. What does this really mean in our ancient struggle with
disease organisms and our immune system's competence? It means while taking
statins we are likely to be far more susceptible to certain common infectious
agents but at the same time may be somewhat more resistive to others. In the
case of the Epstein Barr virus, perhaps we will see more " mono" but,
fortunately, less nasopharyngeal carcinoma and Burkitt's lymphoma. But the
reality is that we do not as yet know because this new statin role of NF-kB
inhibition has only just been recognized. The potential for increased risk of
both infectious disease and malignancy is there, for both depend upon our immune
system's competence. Tossing the statin sledgehammer into this system is
perhaps quite comparable in effect to the rampages of "a bull in a China shop"
and it is far too soon to tell about most malignant changes. The implications of
the very recent drug company promotion of statin drugs for organ transplant
recipients and as adjunctive therapy in the treatment of auto-immune diseases
are sobering, indeed, for these drugs can only work in this capacity at the risk
of causing mischief elsewhere. One must admire the drug companies' ability
for "positive spin" on a very alarming proposition, or is it arrogance? One
cannot have the one without the other. The sense of cynicism here is
overwhelming to me.
Increased cancer deaths among recipients of statin drugs already are being
observed. Ravnskov has reported of the recent PROSPER trial that statin
therapy increased the incidence of cancer deaths, completely offsetting the
slight decrease in deaths from cardiovascular disease. As Dr. Paul Roach
predicted in his Weston Price Foundation presentation of May 2003, the Japan
Lipid Intervention trial observed excess deaths from malignancy in their
so-called statin "hyper-responder" group. Of the 12 cancer deaths reported in
this group, whose cholesterols plummeted deeply with statin use, four were from
gastric cancer and two were from lung cancer. Although other factors may have
played a role, this heightened cancer risk may well be based on loss of immuno-resistance
secondary to NF-kB inhibition.
How strange it is that a class of drugs developed solely for the purpose to
interfering with the biosynthesis of cholesterol has now been shown to reduce
cardiovascular risk by an anti-inflammatory role completely unrelated to
cholesterol manipulation. Generally speaking this should be a welcome
observation, for atherosclerosis with all of its consequences is based primarily
upon inflammation within the arterial walls. Now, however, any optimism we might
have had is thoroughly tempered by our growing realization that statin's
effect is based upon interference with our most basic immuno defense system. The
potential consequences are frightening.
Duane Graveline MD MPH
References to NF-kappaB paper follow:
1. Pfrieger F.Brain researcher discovers bright side of ill-famed molecule.
Science, 9 November, 2001
2. Huang KC and others. HMG-CoA reductase inhibitors inhibit inducible nitric
oxide synthase gene expression in macrophages. J Biomed Sci.10(4):396-405, 2003
3. Zelvyte I and others. Modulation of inflammatory mediators and PPARgamma and
NF appaB expression by pravastatin in response to lipoproteins in human
monocytes in vitro.45(2):147-54, 2002
4. Zheng Y and others. Combined deficiency of P50 and cRel in CD4+ T cells
reveals an essential requirement for nuclear factor - kappa B in regulating
mature T cell survival and in vivo function. J Exp Med. 197(7):861-74. 2003
5. Knight JA. Reiew: Free radicals, anti-oxidants and the immune system. Ann
Clin Lab Sci. 30(2):145-58, 2000
6. Barnes PJ and Karin M. Nuclear Factor kappa B - a pivotal transcription
factor in chronic inflammatory diseases. NEJM. 15:1066-71, 1997
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