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Majid Ali, M.D. |
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Editor,
The Journal of Integrative Medicine
Formerly, Associate Professor of Pathology (adj.), College
of Physicians
and Surgeons of Columbia University, NY
Formerly, President of Staff and Chief Pathologist,
Holy Name Hospital, Teaneck, NJ
Fellow, Royal
College of Surgeons of England -
Diplomate,
American Board of Anatomic and Clinical Pathology
Diplomate, American Boards of Environmental Medicine
Past President Capital University of Integrative
Medicine |
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WHY DON'T STATIN DRUGS WORK FOR WOMEN?
There are no controversies in clinical medicine; only levels of learning,
understanding and enlightenment
The term primary prevention with drugs means drugging people for diseases they
do not have. The title of this chapter asks a crucially important question for
women who are taking statin drugs for the primary prevention of heart attacks
and stroke. Simply stated, such women are spending thousands of dollars on
statin drugs only to buy a real risk of poisoning their livers, muscles, and
other body organs for preventing diseases that they do not have. This question
is equally important for men who also are spending thousands of dollars on
statin drugs only to buy a real risk of chemical poisoning for sake of the seven
to ten in a thousand chances that the drugs will save them from a future heart
attacks and/or stroke.
Why don't statin drugs work for women? In 1997, My colleague Omar Ali and I
addressed this question at length in an article published in The Journal of
Integrative Medicine.1 We marshalled 13 lines of evidence to support our view
that the use of statin drugs is ill-advised for the vast majority of people
taking such drugs. I reproduce text concerning those lines of evidence later in
this chapter. Specifically we asserted that there is no evidence that statin
drugs used for primary prevention confer any survival benefits on women. In
2007, the British journal The Lancet published an article which fully validated
our statement made ten years earlier.2 In this article professors, John Abramson
of Harvard University and James Wright of University of British Columbia,
analyzed published data for over 40,000 women who were given statin drugs for
primary prevention. Consider the opening paragraph of their paper:
The last major revision of the US guidelines, in 2001, increased the number of
Americans for whom statins are recommended from 13 million to 36 million, most
of whom do not yet have but are estimated to be at moderately elevated risk of
developing coronary heart disease. In support of statin therapy for the primary
prevention of this disease in women and people aged over 65 years, the
guidelines cite seven and nine randomized trials, respectively. Yet not one of
the studies provides such evidence.
Yet not one of the studies provides such evidence! This comment should surprise
only those who have never critically examined the data on the subject published
during the last few decades.
The Great Deception: Drug Docs Masquerade Their Sales Slogans As "US Guidelines"
In the face of clear evidence to the contrary, why do doctors continue to
prescribe statin drugs for women who do not have any evidence of heart disease?
For the answer to that question, I return to the first sentence of the above
Lancet quote: The last major revision of the US guidelines, in 2001, increased
the number of Americans for whom statins are recommended from 13 million to 36
million.... What does the phrase the US Guidelines mean to the U.S. doctors,
pharmacists, and general public? They uncritically accept those guidelines as a
mandate from the US government. They are convinced that those recommendations
are based on careful and diligent analysis of all the available scientific
evidence concerning the subject. The reality could not be further from the
truth.
The 2001 US guidelines mentioned in the Lancet article are actually shameless
sales slogans foisted on gullible doctors by a panel of doctors paid by drug
companies. Those doctors—bagmen for drug monsters, as a young cardiologist put
it—engaged in pernicious distortion of the data to serve their masters. Note
again the closing sentence of the Lancet quote cited above: Yet not one of the
studies provides such evidence.
When Was the Last Time You Saw a Chick Emerge From An Egg And Drop Dead of a
Heart Attack?
One memory of 1966 is still very sharp in my mind. In July of that year, I
started my internship in Louisville, Kentucky. For my medical rotation I was
assigned to a Harvard-trained internist. During the first round with him, he
told me that he had not touched an egg since he joined Harvard Medical School
several years earlier, and that he planned not to touch an egg ever. I asked him
why he had decided not eat eggs. With a condescending look, he told me the
yellow of an egg is nearly all cholesterol and unhealthy fats. My thoughts
drifted to my father back in Pakistan. He ate two to four eggs almost every day,
sometimes even more. My father, I might tell the reader, worked as an attorney
until the day before his last final illness in his nineties. He never suffered
from heart disease. Some years after my education by that internist I heard that
he suffered a heart attack.
There is something profoundly ironic about the state of the knowledge of that
Harvard- trained internist. He prescribed statin drugs to block an enzyme
involved in the production of cholesterol called HMG-Co-reductase ("HMG"). I
wonder if he knew that egg is a physiological and healthful inhibitor of that
enzyme. Yes, egg is a physiological and healthful HMG inhibitor. I might explain
here that the production of cholesterol is a highly orchestrated metabolic feat
of the cells, which in health produce only as much cholesterol as is needed.
When we eat eggs, the cholesterol and other healthful fats in them down-regulate
the production of excess cholesterol by a physiological inhibition of HMG
enzyme.
When my patients express confusion about the difference between my advice
concerning the use of statin drugs and their other doctors who push it, I
briefly explain the above-described relationship between the cholesterol taken
in with food and that produced in the body, and later ask them a question: When
was the last time you saw a chick emerge from an egg and drop dead of a heart
attack?
Objectives of This Essay on Cholesterol
In addition to addressing the question raised in the title, in this chapter I
also wish to provide information for everyone to which should help them in
making well-informed and intelligent decisions about the use of statin drugs for
healthy living and healthful aging. Specifically, I hope this information
should:
Support the decision of those who have refused statin prescriptions given to
them by their doctors;
Assist others in decision-making while they consider the use of statins; and
Provide information for those who now take statin drugs and will one day—I am
confident— want to discontinue them
To provide a framework of reference for providing information concerning the
above matters, first I address the following questions:
1. What is cholesterol?
2. What does cholesterol do to preserve human health?
3. What are "good" and "bad" cholesterols?
4. When does cholesterol become a health hazard?
5. How important is the issue of inflammation in consideration of blood
cholesterol levels?
6. What are statin drugs?
7. How do statin drugs work?
8. What are the deceptions in the reported health and life-span benefits of
statins among men?
9 What are the adverse consequences—not merely side-effects—of statin drugs?
10. When may statins be recommended?
1. What is cholesterol?
Cholesterol is a precious commodity. It is the premium intelligence molecule of
the body. It is also an essential ingredient of cells of the human body. Nearly
all cell populations of the human body can produce cholesterol in times of
chronically increased demands for this guardian angel of cell membranes.
Cholesterol is highly soluble in fats, a feature allows it to freely move in and
out of all cell populations in the body. In quantitative terms, the liver is the
body organ most involved in cholesterol production. The adrenals glands, gonads
(ovaries and testes), and the gut are other body organs with a higher capability
for cholesterol production than most other body organs.
Cholesterol is a steroid and the source of all other steroids in the body,
including testosterone, estrogens, progestins, 31 hormones produced in the
adrenal glands, and other hormones. In addition, cholesterol serves as the raw
substance for the production of some other essential substances in the body,
such as vitamin D. Bile acids are essential for digestion of fats and also
derived from cholesterol. Each molecule of cholesterol contains 27 carbon atoms
and has a molecular weight of 386 daltons. The molecular structure of
cholesterol contains three hexagons (6- cornered configurations) and a single
pentagon (5-cornered configurations).
2. What does cholesterol do to preserve human health?
Cholesterol is a guardian angel of the human body, and not a villain as doctors
paid by drug companies want us to believe. It is essential for all
health-preserving functions as well as for healthful aging. Specifically, it:
Is an antioxidant;
Participates in the oxidant/antioxidant equilibrium;
Protects cell membrane structure;
Preserves cell membrane functions by:
Exerting gating (in-and-out traffic); and
Separate internal order of a cell from external disorder;
Serves as the raw material for the production of many hormones;
Mediates cellular cross-talk; and
Regulates intelligence between the cell and the matrix (cement substance that
glues cells together).
Through all of its molecular attributes, cholesterol:
Protects neurons and reduces the risk of depression, suicide, and several
neurodegenerative disorders;
Protects coronary (heart) arteries and prevents heart attacks;
Protects cerebral (brain) arteries and prevents strokes;
Protects renal (kidney) arteries and prevents renal failure; and
Protects peripheral (limb) arteries and prevents leg cramps and gangrene.
Protects muscle cells and prevents chronic fatigue states;
Protects liver cells and prevents liver injury.
3. What are "good" and "bad" cholesterols?
There are two answer to this question: A short one and a long one. First, the
short answer: The "good" is HDL cholesterol and it is good because it prevents
heart attacks. The "bad" cholesterol is LDL cholesterol and it is bad because it
causes heart attacks. Doctors use this short answers when they prescribe statin
drugs. This is a short but stupid answer.
Now the long answer. Cholesterol is produced in the body through highly complex
enzyme reactions. This process is exquisitely orchestrated to provide an ample
supply of several types of health-promoting, all of which serve essential roles
in the ever-changing "cholesterol kaleidoscope."This kaleidoscope continuously
adjusts itself to fill the ever-changing metabolic, hormonal, and intelligence
needs of the body. In this model of cholesterol metabolism, it is silly to
designate HDL cholesterol "good" and LDL cholesterol. Furthermore, it is equally
silly to claim that HDL-2 component of HDL cholesterol is "most protective" and
the HDL-3 fraction is less protective. I include here some brief comments
concerning the salient aspects of cholesterol metabolism to shed some more light
on the subject.
Cholesterol is a precious commodity. I repeat this for emphasis here. How
precious? Consider this: The body allocates 36 parts of ATP (the basic units of
the body's energy economy), 18 parts of a high-energy substance in the body
called acetyl CoA, and 16 parts of another valuable substance in the body called
NADPH. With such resource consumption, Nature would not been expected to be
frivolous in its intelligent design of the cholesterol kaleidoscope. And it
certainly is not. For optimal conservation and utilization of its precious
commodity cholesterol, evolution has created a vast and exquisitely regulated
network of enzyme pathways, binding proteins on cell surfaces (receptors), and
transporters within cells, as well as in the blood. Under physiological
conditions, the body closely balances cholesterol supply in the food (exogenous
cholesterol) with production in the body (endogenous). So vigorously is this
balance protected that dietary restriction of cholesterol has limited effect
(less than 15% drop) on the blood cholesterol level. Fasting rapidly stimulates
cholesterol production in the body; by contrast, ready availability of
cholesterol in the food—with, let's say, an egg breakfast—decreases cholesterol
synthesis in the body.
Now, humankind faces three sets of unrelenting threats to cholesterol
homeostasis (balance): toxic environment, toxic foods, and toxic thoughts. Most
notably, incremental chemicalization of cells disrupts the body's energetic and
enzymatic pathways. Facing progressive oxidizing, acidifying, and
de-oxygenizing, the body tries to cope by producing more antioxidants, including
cholesterol and uric acids. Additionally, blockade and/or inactivation of the
protein receptors and blood transporters involved with efficient distribution of
cholesterol fractions creates abnormal proportions of various cholesterol
fractions. To cite one such relationship, normally cholesterol free in cells
suppresses several enzymes involved with its production there, including HMG
enzyme (the target of statin drugs). This involves oxygen—there is evidence that
intracellular oxygenation of cholesterol turns it into a more potent inhibitor
of HMG enzyme. One would expect that a functional oxygen deficit would decrease
the potency of cholesterol in its inhibition of HMG enzyme.
Cholesterol is not cholesterol is not cholesterol. LDL cholesterol is not just
one substance in the sense that glucose is. Nor is HDL cholesterol is just one
substance in the sense that insulin is. It is sad how few doctors understand
this crucial point. The so-called LDL (low-density lipoprotein) cholesterol is
not a different type of cholesterol from that in the so-called HDL (high-
density lipoprotein. The difference between LDL and HDL cholesterols is the
amount of proteins attached to cholesterol molecules; HDL has more of proteins
and LDL has less. Cholesterol in both is identical. So, in reality whether
cholesterol is bound to more proteins or less of them depends on the metabolism
of proteins which, in turn, depends on the metabolism of oxygen, free radicals,
and acidity in the body.
There are yet other factors that disrupt cholesterol homeostasis. For example,
the excess insulin state is now pandemic, and this state increases production
and storage of fats of all types, including cholesterol. (See my Darwin's
Drones, Dysox and Diabetes (2007) for a full discussion of the subject). Clearly
what is needed to normalize cholesterol homeostasis is not statins to further
block crucial liver enzymes. Rather, what is required is to effectively address
the issues of toxic environment, toxic foods, and toxic thoughts.
4. When does cholesterol become a health hazard?
In its natural, native, and unoxidized (un-rancid) form, cholesterol is an
antioxidant and serves all of the above-listed redox-active and metabolic roles.
Every antioxidant turns into an oxidant when it scavenges free radicals.
Cholesterol is not an exception. In its oxidized state, cholesterol is an
oxidant. In that state, indeed it injures cell membranes, matrix, and
endothelial cells (cells lining the inside of blood vessels).
5. How important is the issue of inflammation in consideration of blood
cholesterol levels?
This is a crucially important issue. Any and all types of chronic, subacute, or
occult inflammatory processes incremental oxidize cholesterol, and so increase
cholesterol toxicity. Notable among such infections are: (1) periodontal
abscesses and other oral infections; (2) altered states of gut ecology; (3)
chronic systemic collagen disorders; (4) chronic skin disorders; (5) chronic
urinary tract infections; (6) chronic infections of the genital tract; and (7)
others. The common denominator in all of the above pathologic entities is
increased acidity (acidosis), incremental free radical activity (oxidosis), and
dysoxygenosis (dysox).
6 What Are Statin Drugs?
Statin drugs are a class of drugs which are used to blood cholesterol levels.
These drugs include Pravachol, Zocor, Lipitor, Crescor, and Vytorin.
7 How do statin drugs work?
Drug companies teach doctors that statin drugs block an enzyme in the liver
called (HMG Co-reductase inhibitors). That is a partial truth. If it were true,
we would not see evidence of liver and muscle injury in many individuals taking
statin drugs. Nor would such individuals develop chronic fatigue and muscle pain
from other toxic effects of drugs, such as diffuse dissolution of the muscle
cells called rhabdomyolysis.
8 What Are the Deceptions in the Reported Health and Life-Span Benefits of
Statins Among Men?
In most reported clinical trials of statin drugs, the reported reduction in
deaths after five or more years of drug therapy are less than one percent.
However, those dismal numbers are grossly bloated and reported as "risk
reduction" numbers. Consider the following quote from The new England Journal of
Medicine (1996;335:1239):
West of Scotland study found an absolute reduction in cardiac mortality of 0.7
percent after five years of pravastatin therapy (40 mg per day, costing $100 per
month). Therefore, 143 men with hypercholesterolemia must spend a total of
$858,000 (drug cost only) to delay 1 such death...The problem is that outcome
events in primary prevention are always rare, even in coronary disease, leading
to the paradox that pravastatin is both highly effective and of very little
benefit.
I return to this crucial subject with more illustrative examples to support my
case. For additional information on this subject, I refer the reader to my book
RDA: Rats, Drugs and assumptions (2004).
9. What Are the Adverse Consequences—Not Merely Side-Effects—of Statin Drugs?
Liver injury
Muscle injury
Chronic fatigue
Chronic, severe, muscle cells death (potentially fatal rhabdomyolysis)
Increased incidence of depression, suicide, eating disorders, and some forms of
neurodegenerative disorders caused by abnormally low blood cholesterol levels.
10. When May Statins Be Recommended?
Individuals with advanced coronary artery and/or stroke who stubbornly refuse to
consider effective oxystatic and detox therapies to reverse coronary and
cerebral (brain) arteries;
Smokers and others with advanced coronary artery or stroke and significantly
raised blood cholesterol levels;
Individuals with advanced coronary artery and recurrent episodes of congestive
heart failure;
Individuals with advanced coronary artery and recurrent episodes of stroke; and
Thirteen Lines of Evidence Against the Cholesterol Theory
Below, I reproduce some text from our 1997 paper published in The Journal of
Integrative Medicine1 (available without charge at www.jintmed.com) in which we
marshalled 13 reasons of evidence against the so-called cholesterol theory of
coronary artery disease which is used to promote the use of statin drugs:
1 Cholesterol is an antioxidant, albeit a weak one, and cannot be expected to
cause oxidative injury that clearly initiates atherogenesis;
2. A majority of patients who develop severe IHD (ischemic heart disease)
including episodes of myocardial infarction, do not have elevated blood
cholesterol levels.64,469,470
3. When death occurs within six to eight hours of myocardial infarction, no
acute coronary thrombotic occlusions are found at autopsy in more than 75
percent of cases; however, when death occurs after 48 hours, acute thrombotic
occlusion is almost always found (personal unpublished data).
4. The range of frequency of acute thrombotic coronary occlusion in survivors of
out-of-the- hospital cardiac arrests extends from 36 percent as determined by
angiography237 to 95 percent in autopsy studies.238
5. There is a well recognized paradox of IHD coexisting with normal
angiograms.68-70
6. Reduction of atherosclerotic lesions does not follow when the death rate from
myocardial infarction falls.59-61,471
7. Lowered blood cholesterol levels in women are not associated with the
reduction in the rate of acute ischemic myocardial events to the same degree as
is seen among men.67
8. Lifestyle stressors,239-247 tobacco smoking,269-273 and physical
inactivity261-266 are recognized independent risk factors of IHD and exert
potent prooxidant effects. We are not aware of any valid reason to believe that
the oxidative stress of all those factors is confined to oxidative modification
of LDL.
9. The cholesterol theory does not explain the recognized risk factors of IHD,
such as hypertension and diabetes.
10. The cholesterol theory does not explain the cardioprotective role of
coenzyme Q1087,88,316-322 nor does it explain how
hyperhomocysteinemia95,96,290-304 increases risk of IHD.
11. The cholesterol theory does not explain the recognized risk factors of
increased body stores of iron71,72, copper73 and mercury75,—transition metals
with potent oxidizing potential.
12. The cholesterol theory does not explain the protective effects of
selenium77,78,346,347 and chromium,79,80,472-475 minerals with recognized
antioxidant effects.
13. The cholesterol theory does not explain the epidemiologic data showing
reduced mortality from IHD in patients taking ascorbic acid81,82 and vitamin
E.83,84 (see the full text on www.jintmed.com for all citations)
To the above lines of evidence, I add the following three additional mechanism
by which inflammation and cellular toxicity promote atherogenesis to further
expand the frame of reference for the reader:
1. Patients who have low CRP levels after statin therapy have better clinical
outcomes than those with higher CRP levels, regardless of the resultant level of
LDL cholesterol. Strategies to lower cardiovascular risk with statins should
include monitoring CRP as well as cholesterol. (N Eng J Med. 2005;352:20-28.)
2. Tumor necrosis factor alpha (TNF-alpha) is a potent pro-inflammatory
substances and promotes atherogenesis.
3. TNF-alpha causes increased production of another potent proinflammatory
substance called PAI-1 (plasminogen activator inhibitor). Specifically, TNF-alpha
increases the production of PAI-1by 32%, via protein kinase C- and nuclear
factor-kappaB-dependent pathways. PAI-1 is an important mediator of
atherosclerosis and liver fibrosis in insulin resistance.
At this point, the reader should not need any explanation for the fact that
statin drugs do not work for women. Still, I will furnish a simple answer:
statin drugs do not work for women in the primary prevention of heart disease
because natural, unoxidized, un-rancid cholesterol does not cause coronary
artery disease. Rather, it prevents that.
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