email@example.com Last updated November 22, 2009
Over the last few decades, the American pharmaceutical industry (henceforth, "Big Pharma") has applied a very successful formula to market fear and convert it into a multi-billion dollar industry. The algorithm goes like this:
In a substitution of variables, the substance is cholesterol, the disease is heart disease, and the drug is Lipitor, and, voila! Through aggressive advertising campaigns, Big Pharma has managed to convince the American public and the American doctors that statin drugs are the best thing since sliced bread.
But are they right? I think the evidence shows that very few people currently taking statin drugs are actually benefiting from them. Furthermore, many of them are actually worse off than they would have been had they never been on statins. Below, I will argue that any benefits incurred in combating heart disease are more than offset by increased susceptibility to fetal damage, toxic infection, and cancer.
I am certainly not alone in my concern about the ever increasing usage of statin drugs to fight a "disease," "hypercholesterolemia" [high cholesterol], that I would argue is not a disease at all. The Weston A. Price Foundation is trying hard to spread the word about the many roles of cholesterol and the myriad side effects associated with statin usage. They share with me the growing alarm over the ever widening definition of who qualifies for statin drugs:
"Who suffers from hypercholesterolemia? Peruse the medical literature of 25 or 30 years ago and you'll get the following answer: any middle-aged man whose cholesterol is over 240 with other risk factors, such as smoking or overweight. After the Cholesterol Consensus Conference in 1984, the parameters changed; anyone (male or female) with cholesterol over 200 could receive the dreaded diagnosis and a prescription for pills. Recently that number has been moved down to 180. If you have had a heart attack, you get to take cholesterol-lowering medicines even if your cholesterol is already very low--after all, you have committed the sin of having a heart attack so your cholesterol must therefore be too high. The penance is a lifetime of cholesterol-lowering medications along with a boring lowfat diet. But why wait until you have a heart attack? Since we all labor under the stigma of original sin, we are all candidates for treatment. Current edicts stipulate cholesterol testing and treatment for young adults and even children." (Statin Drugs: the Problem) .
Let me first briefly introduce a bit of biology and terminology. Cholesterol is a biological substance that is a direct precursor to many very important substances, including the sex hormones estrogen and testosterone, the adrenal hormones hydrocortisone and aldosterone, bile acids which help you digest fats, and, most especially, vitamin D. It is well known that vitamin D plays a critical role in fighting infection and cancer, in addition to its essential role in calcium metabolism and bone health. Since cholesterol is so crucial to well-being, the body is able to manufacture as much as it needs in the liver, even in the absence of a supply from food sources. There is plenty of evidence that cholesterol is protective against infection, a topic that will be central to this essay. (Cholesterol Benefits) .
When you have your cholesterol measured, the numbers will come back factored into three components: LDL, HDL, and "other." In simple terminology, LDL delivers cholesterol (from the liver) to the peripheral tissues, and HDL delivers cholesterol (e.g., from food sources) to the liver, where it is converted to bile acids and released into the digestive system to break down consumed fats. LDL is the one that is usually labelled as "bad," but, as you will see later, this is a misnomer.
Big Pharma is intent on getting as many people as possible on as high a dose of statins as they can possibly justify. They are arguing now that people whose cholesterol levels are fine should take statins if their C-reactive protein, an indicator of inflammation, is high (C-Reactive Protein and Heart Disease) . They also claim that people with a known heart condition should aim to achieve an LDL level below 70 mg/dl ( 70 mg/dl LDL Goal ) . This can be accomplished (relatively easily in many cases) by taking 80 mg (four times the standard dosage) of a statin drug every day. They are now even prescribing statins for women in their 20's who are married and fertile, without regard to the damaging effect these drugs are known to have on a fetus.
What I find particularly frustrating, and what is perhaps my main reason for writing this essay, is that, in my view, many of the health benefits of high cholesterol are currently being mis-represented, paradoxically, as benefits of statin drugs. There is currently a barrage of news items on the Web claiming that statins are protective against cancer, sepsis, and Alzheimers' disease. The researchers behind the retrospective studies where an apparently beneficial effect is observed are careful to say that "randomized controlled studies have yet to be conducted," but the media miss those subtleties and turn the claims into "facts." At the same time, when it became clear that very low values of LDL are problematic for both infection and cancer, Big Pharma tried to distance itself from the tight association statin drugs have with cholesterol levels. Incredibly, they claim that, because low LDL is problematic regardless of whether it occurs naturally or artificially through statin use, statins are somehow exonerated. While I agree with their claim that statins are not "carcinogenic," in the sense that they don't directly cause cancer, statistics show that, over the long term, people who sustain a lower cholesterol level in the blood are at higher risk for cancer (and infection) than people with high cholesterol. Essentially, by taking a statin, you are shifting the odds on what you die of. Pay the money, suffer the side effects, and as a result you may end up dying of cancer or a runaway infection before you would have died of heart disease if you had never taken the drug in the first place.
Alzheimer's is such a big and complex topic that I have written an entire separate essay on that subject, which can be found here. The specific sections most relevant to statins are 4. The Relationship between Cholesterol and Alzheimer's. and 5. Do Statins Cause Alzheimer's?. Suffice it to say that, after having done extensive research on Alzheimer's, it seems evident to me that the incidence of Alzheimer's will rise sharply in the coming years as long-term statin users become elderly.
In the next section, I hope to make it clear that one demographic that should never be prescribed a statin drug is pre-menopausal women. In the following sections I will discuss sepsis (blood poisoning), and cancer, and will show how Big Pharma has successfully manipulated the truth to make it appear that statins are protective against both of these, when in fact the exact opposite is true. The last section before the summary presents the infectious theory of atherosclerosis, which has recently received considerable attention. I will describe, in as simple terms as possible, how cholesterol may play a central role in the artery wall in fighting the infective agent. The arguments presented there lead to the conclusion that statins work against even the long-term health of the heart itself.
You may not be old enough to remember the disaster incurred by the widespread practice in Europe in the 1950's of treating depression with the then newly discovered drug Thalidomide. When you take a Lipitor tablet you are taking a drug that, like Thalidomide, is labeled "Class X" with respect to its potential harm to the fetus, and is even worse than Thalidomide in terms of the kind of damage it can do to your unborn child. A woman who is in the childbearing age group should never be advised to take a statin drug. While there are warnings associated with the ads and on the labels claiming that you should "stop taking Lipitor" should you become pregnant, the drug companies seem intent on hushing up the fact that these drugs are toxic to the developing fetus.
Clearly it would be unethical to conduct a controlled experiment that intentionally exposes a pregnant woman to statins, and therefore such controlled studies have not been done. However, in one of the few available retrospective studies of statins and pregnancy, researchers from the U.S. National Institutes of Health found that statin use during the first trimester of pregnancy led to severe central nervous system defects as well as limb deformities. Twenty out of 52 women who had been exposed to statins during the first trimester had babies with severe deformities, which is nearly a 40% rate of severe birth defects.
"Of the 20 babies born with malformations, five had severe central nervous system defects, and five had malformed limbs. One baby had both, according to Muenke. There were also two cases of a very rare birth defect called holoprosencephaly, which occurs when the brain fails to divide properly." (Statins and Birth Defects) .
Doctors in Liverpool have even had the audacity to propose that statins be prescribed to pregnant women, an idea that these authors find wildly disturbing: (Statins during Pregnancy) . There seems to be a general lack of awareness, even among doctors, of the degree of harm these drugs can inflict on the developing fetus.
Great Britain now has the dubious distinction of being the only country where you can buy statin drugs over the counter (NonPrescription Statins) . This means that any naive young woman thinking she can self-treat high cholesterol may end up with a severely malformed baby, and chances are she won't even realize it's due to the drug.
In the following pages, I will first make a case for why very low values of LDL are dangerous. I will then tell two remarkable stories about how statin makers are trying to convince the media and the public that black is white: they argue that statins are actually protective against both cancer and sepsis (blood poisoning), whereas the evidence is the exact opposite, as I will now show.
I am going to start my story with a recent article that appeared in the Annals of Clinical and Laboratory Science in 2007 (Low LDL Bad) . This article involved a very simple study, inspired by the recent practice of cardiologists to recommend to their patients with known heart disease that they more aggressively lower their LDL cholesterol levels. The consequences of a very low LDL level, as evidenced by the outcome of the experiment described in the above article, can be dramatic and alarming. The authors examined 203 patients' charts in a hospital and divided them into two groups: those whose LDL was below 70 mg/dl, and those whose LDL was above 70 mg/dl. They found that the below 70 group had a fifteen fold increase in the incidence of cancer, and a five fold increase in the incidence of sepsis (more familiarly known as blood poisoning or septicemia), when compared with the above-70 group. Thus, nearly all of the patients who had cancer and most of the patients who had sepsis also had low LDL, strongly implying that people with low values of LDL are much more likely to suffer from cancer and dangerous infection than the general population.
Statin proponents are scrambling to come up with convoluted explanations that exonerate statin drugs, as evidenced in the way another article along similar lines is pitched  (Not Even Looking for Cancer) . Even though they weren't initially investigating cancer at all, but were rather concerned about liver and muscle damage, these authors found a highly significant (p=.009) inverse correlation between achieved LDL levels and cancer -- the lower the LDL level the higher the incidence of cancer. The review process for this article was very heated, and an argument was made that it should not be published because it might discourage people from taking their statin drugs. It starts to become humorous when you read the explanation developed here: (Statins aren't to Blame) . The argument goes like this: people who have natural low values of LDL (< 70 mg/dl) have increased cancer risk even if they aren't taking statin drugs. Statin drugs don't directly cause cancer, they just promote it indirectly by knocking down your LDL levels into the range where increased risk occurs. Guns don't kill you, they just release bullets that do.
Quite surprisingly, you can easily find web pages that hail the benefits of statins beyond their ability to lower cholesterol (already a dubious achievement). The claims they make directly contradict the actual effects of statins. For example, if you do a web search on "statins cancer", you will find several hits claiming that statins may be protective against cancer. Several recent articles on the Web have suggested that statins may protect against sepsis. I am almost certain that both of these claims are false.
We'll start with sepsis, and with an article that illustrates how sloppy science gets turned into truth when it migrates into the media. (Statins Reduce Sepsis Risk) . I quote here the lead sentence of the story:
"Cholesterol-lowering drugs can reduce the risk of severe infection in patients suffering from heart disease or stroke, scientists said on Wednesday."
This sounds like a fact, but instead it is the result of a flawed study, as I will argue below. The conclusion was drawn on the basis of a retrospective study of patients who had had a heart attack or stroke. "Retrospective" means to take a look back at something that has already taken place. Some of the patients had been prescribed statins and some had not, a decision surely based on their cholesterol profile. Thus, those who were not prescribed statins must have had naturally occurring low cholesterol, even though they suffered from a disease commonly treated with statins. Although high cholesterol is correlated with heart disease incidence, it is by no means the case that if you have heart disease you must have high cholesterol.
Another very strong risk factor for heart disease and stroke is diabetes, (in fact, it is sometimes referred to as a cardiovascular disease) (Diabetes and Heart Disease) . (Diabetes and Stroke) . Diabetes is also a risk factor for sepsis (Diabetes and Sepsis) , because untreated diabetes often leads to sores in the extremities that won't heal, which can lead to subsequent gangrene and amputations. It is quite plausible that those in the retrospective study who did not have high cholesterol were more likely to have diabetes (the causative agent of their heart attack or stroke), a condition which causes increased risk to sepsis.
The above claim that cholesterol-lowering drugs can reduce the risk of severe infection in patients suffering from heart disease or stroke is directly contradicted in the conclusion of an excellent article that carefully examined several studies on sepsis. These authors concluded that statin therapy should be temporarily halted during a sepsis event . (Statins Following Sepsis Event) .
"Statins are effective at lowering lipid levels, but lipids are the wrong target in sepsis. Higher lipid levels are desirable in these patients."
He goes on to say: "Research has shown that hypocholesterolemia [low cholesterol] in critical illness and multisystem organ failure correlates with decreased patient survival rates." This can be translated into "if your cholesterol is low, you have a worse chance of surviving."
A careful study of all the available evidence that statins may protect against sepsis, titled simply, "Statins and Sepsis,"  was published by Professor Fang Gao at the University of Warwick in the U.K. in the British Journal of Anesthesia in 2008. (Statins and Sepsis: Review Study) . At the end of the study, he wrote this caveat: "However, there have been no RCT [randomized controlled clinical trials] of statins in sepsis, and large randomized controlled clinical trials with clinically relevant primary endpoints are desperately needed." In the paper, he mentioned the ASEPSIS trial, that was underway at the time, and which he claimed would be completed by 2008. A "Declaration of interest" at the bottom of the paper said the following:
"Professor Gao is the Chief Investigator of RCT on Statin therapy in the ASEPSIS trial. The trial received a pump-prime research grant from Pfizer. Professor Gao and Dr Thickett have received travelling sponsorships from pharmaceutical and industrial companies to attend national and international conferences."
I.e., Professor Gao receives funding and perks from Big Pharma that surely influence his research bias.
Since it is now June, 2009, I was eager to find the results of the ASEPSIS trial on the Web. I did find a pointer to the trial itself, (ASEPSIS Trial) , and a very encouraging title: "Randomised double-blind placebo-controlled trial of 40 mg/day of Atorvastatin on reduction in severity of SEPSIS in ward patients." The trial web site indicated that indeed the trial had been completed in January, 2008, i.e., eighteen months ago. But there was nothing there to indicate what the outcome was. The web search turned up no other pointer to this trial -- no papers, no media coverage. You can be sure that if this trial had had an outcome favorable to statins, it would have been all over the media. Thus, it is highly likely that this randomized double-blind placebo-controlled trial showed the exact opposite of the effect that was so eagerly anticipated. Once you remove the cholesterol bias, the effect goes away.
Researchers who are trying to make sense of the idea that statins might protect against sepsis are led to the false conclusion that statins must have some other biological effect ( besides their dramatic ability to interfere with cholesterol production) that is making them protective against sepsis; i.e., infection. Yet protecting against infection is something that cholesterol itself does extremely well. Based on biology, I would expect that, if the difference in cholesterol levels between the control group and the treatment group are eliminated, the apparent beneficial effect of statins for sepsis would disappear. In fact, I would expect the effect to go in the wrong direction, i.e., statins cause an increased risk to sepsis.
An article by Wilson et al.  in the journal Critical Care studied changes in blood cholesterol levels following trauma, infection and multiple organ failure. I quote their abstract in full here:
"Hypocholesterolemia is an important observation following trauma. In a study of critically ill trauma patients, mean cholesterol levels were significantly lower (119 ± 44 mg/dl) than expected values (201 ± 17 mg/dl). In patients who died, final cholesterol levels fell by 33% versus a 28% increase in survivors. Cholesterol levels were also adversely affected by infection or organ system dysfunction. Other studies have illustrated the clinical significance of hypocholesterolemia. Because lipoproteins can bind and neutralize lipopolysaccharide, hypocholesterolemia can negatively impact outcome. New therapies directed at increasing low cholesterol levels may become important options for the treatment of sepsis." 
"Hypocholesterolemia" is low cholesterol. Patients who died had low cholesterol to begin with, and saw their cholesterol drop on average by 33%. Patients who survived experienced a 28% increase in cholesterol level over the course of the disease -- they were able to marshall all their defenses toward manufacturing cholesterol at full capacity to fight the disease. "Lipopolysaccharide" is another term for the endotoxins that bacteria release triggering a sepsis event. "Lipoproteins" is the second "L" in "LDL". So the statement, "lipoproteins can bind and neutralize lipopolysaccharide" means that cholesterol is mobilized to bind and neutralize the endotoxins released by bacteria during an acute phase of infection, the one thing that most critically needs to be done to get out of a sepsis crisis. The article advocates drugs to support increasing cholesterol levels, i.e., the exact opposite of a statin drug.
CAH (cholesterol-7alpha-hydroxylase) is an enzyme that plays an important role in the liver to break cholesterol down and dispose of it as bile acids. In experiments conducted on hamsters, Feingold et al. (Endotoxins and CAH) exposed the hamsters to bacterial endotoxins and observed an immediate biological response that inhibited the activity of CAH, which then promoted the availability of more cholesterol to devote to fighting the infection. In the summary, they conclude, "Thus the decrease in CAH may play a role in facilitating the formation and secretion of lipoprotein in the liver, thereby contributing to host defense." I.e., by preventing the breakdown of cholesterol in the liver, more cholesterol is made available to fight the disease.
If statins lowered the risk of sepsis in the individual, then they should have done so in the general population as well, yet the results of epidemiological studies yield dramatically different results.
"In the United States, there were an estimated 750,000 cases of severe sepsis in 1995, resulting in 215,000 deaths, and there was an annualized increase in the incidence of sepsis of 8.7% between 1979 and 2000. Sepsis now rivals acute myocardial infarction as a frequent cause of death. It is the leading cause of death in noncoronary intensive care units (ICUs)."  (Sepsis is on the Rise) .
Let me repeat: 8.7% increase in sepsis incidence every year. Statin drugs were first introduced as prescription drugs in the 1980's, and have enjoyed steadily increasing usage statistics since then. (Statin History) . If they protect against sepsis, why does the incidence of sepsis keep going up every year as more and more people take statins?
The answer to this question is the same as the answer to the question of why the effect goes away when you perform a randomized double-blind trial. It is cholesterol, not statins, that protects against sepsis. In the retrospective studies, the control group are the ones who did not meet the requirements for statin prescription, i.e., who must have had very low cholesterol indeed, if they were not being prescribed statins in spite of heart disease or stroke. It is their low LDL that makes them susceptible to sepsis. In the placebo-controlled ASEPSIS trial, there would not have been a distinction in the pre-treatment cholesterol levels between the treatment group and the controls, and this is what caused the apparent benefit of statins to disappear: it was actually a benefit of cholesterol that was measured instead.
While it is less well known than the number one and number two killers, heart disease and cancer, sepsis is nonetheless a very nasty condition that kills fast and viciously. To quote from Wikipedia,
"In the United States, sepsis is the second-leading cause of death in non-coronary ICU patients, and the tenth-most-common cause of death overall according to data from the Centers for Disease Control and Prevention (the first being multiple organ dysfunction syndrome). Sepsis is common and also more dangerous in elderly, immunocompromised, and critically-ill patients. It occurs in 1-2% of all hospitalizations and accounts for as much as 25% of intensive-care unit (ICU) bed utilization. It is a major cause of death in intensive-care units worldwide, with mortality rates that range from 20% for sepsis to 40% for severe sepsis to >60% for septic shock." (Wikipedia on Sepsis) .
The flawed studies suggesting a link between taking statins and preventing sepsis are actually instead showing a link between very low cholesterol and increased sepsis susceptibility. Cholesterol is doing the work, and statins are stealing the credit. All the while, statins are slowly crippling the work horse.
As a final blow to the theory that statins may protect against infection, a carefully designed study that just came out has shown that statin drugs increase the risk of pneumonia requiring hospitalization in the elderly by 61% (Statins Increase Risk for Pneumonia) . The study, published in the British Medical Journal, involved over 3,000 Group Health patients. The study was inspired by the recent hype that statins might protect against infection, an idea that is looking more and more like the result of the benefits of high cholesterol rather than any immune resistance role for statins. The result is consistent with the view that the effect of statins to reduce cholesterol levels in the blood is actually serving to decrease immunity and promote infection.
Very low values of LDL leave you at risk to sepsis and cancer not only because cholesterol itself is protective against these things, but also because cholesterol is the precursor to vitamin D, which is also a miracle drug with respect to fighting cancer and sepsis. A strong indicator that LDL is directly tied to vitamin D supply is that low levels of LDL are associated with an increased risk of bone fractures for menopausal women (LDL and Bone Fractures) . Vitamin D is perhaps best known in its role in promoting calcium absorption and therefore keeping bones strong and healthy.
There are many articles on the Web that support the notion that vitamin D protects from a broad range of different cancers. Epidemiologically, there has been found to be a strong inverse correlation between cancer incidence and sunny places. That is, despite the widely-promoted idea that the sun causes cancer, it actually protects from all cancers, due to the fact that sun exposure causes the skin to produce vitamin D. (Sun Protects from Cancer) .
If you have adequate cholesterol in the skin, a mere twenty minutes in the sun per day is enough to get all the vitamin D you need, i.e., on the order 10,000 IU. There is considerable circumstantial evidence that the sun has a healing effect for cancer (by comparing cancer statistics with climate conditions, contrasting sun with rain and north with south). However, it is very difficult to do controlled studies on this effect because it's hard to quantify how much sun exposure was obtained. Most of the controlled studies, therefore, have compared people who took vitamin D supplements with those who didn't. How much vitamin D they obtained naturally then becomes a complicating effect that is difficult to tease apart.
A controlled study published in the American Journal of Nutrition followed three groups of women, one of which was given large doses of Vitamin D along with calcium supplements, the second was given only calcium, and the third was given nothing. The study was not even designed to investigate the relationship between vitamin D and cancer, but rather was interested in the question of bone health. But they discovered by surprise that the group taking vitamin D supplements had a 60% decreased risk for all cancers. (Vitamin D Prevents Cancer) . Another large epidemiological study showed that people who took at least 400 IU/day of vitamin D had a 43% reduced risk for pancreatic cancer. (Vitamin D Protects from Pancreatic Cancer) .
Vitamin D also appears to help you recover from cancer once you're diagnosed with it. This has been shown to be true, for example, for both colon cancer (Vitamin D Fights Colon Cancer) and lung cancer (Vitamin D Fights Lung Cancer) .
Recall that LDL delivers cholesterol to the tissues . Vitamin D is manufactured from cholesterol in the skin upon exposure to sunlight (Vitamin D Synthesized from Cholesterol) . If your LDL is low, then you are not going to be able to supply adequate amounts of cholesterol to the skin, and the result will be severe vitamin D deficiency, and, ultimately, an increased susceptibility to cancer. Even if you spend gobs of time out in the sun, your vitamin D levels will still be low, because your supply chain of LDL is insufficient for production of vitamin D.
However, this process will take some time to be noticed due to the buffering effects for both cholesterol in the skin and vitamin D in the blood. Thus, short term studies will not necessarily reveal the problem, and long-term studies have yet to be done. Chris Masterjohn, in contrasting the situation for vitamin D deficiency with another worrisome consequence of statin usage, coenzyme Q10 depletion, wrote the following:
"We would expect statins to take even longer to cause a drop in vitamin D levels, because, whereas coenzyme Q10 is measured directly in the blood, the 7-dehydrocholesterol takes time to migrate to the surface of the skin and accumulate there. So what is the effect of statins on vitamin D levels one year down the road? Two years? Five? Ten? The truth is we have no idea, because no one has bothered to study it."
Vitamin D also protects against infection, by boosting the effectiveness of the immune system. (Vitamin D and Flu ) . Sepsis comes about as a direct result of an inability to fight off an infection, most often a bacterial infection. Vitamin D plays a critical role both in preventing sepsis and in enabling recovery if it occurs ,, (Vitamin D and Sepsis) .
If you start taking a statin, it will take considerable time before the debilitating effects on vitamin D are felt in the system, because vitamin D has an excellent buffering system. Considerable sun exposure in the summer can give you a stockpile of vitamin D that can often carry you through the winter months. And the cholesterol already in the skin has to be consumed before the deficiency in the supply chain (low LDL) will be apparent. This gives statin manufacturers an opportunity to exploit observed long-term benefits of life-time high vitamin D levels and claim them as short-term benefits of the statin drug that were taken only in the previous few months of a person's life. And what is particularly ironic and disturbing is that the statin drug is in the process of eroding the very benefits for which it is given undue credit.
As we have already seen, sustained low LDL will lead to low levels of vitamin D, because LDL supplies the cholesterol to the skin that manufactures the vitamin D.
Inadequate vitamin D, in turn, is a major risk factor for sepsis. An article published in the Journal of translational Medicine  provides strong evidence that vitamin D deficiency is associated with increased risk of sepsis. A direct quote from this article states, "Patients with severe infections as in sepsis have a high prevalence of vitamin D deficiency and high mortality rates."
This quote from the web shows all kinds of epidemiological evidence that vitamin D is protective against sepsis, and also explains the role it might play:
"Dr. Grant points out that septicemia incidence is highest in the winter and lowest in the autumn, that rates are also generally highest in the Northeast and lowest in the Southwest, and that African Americans (who have lower levels of vitamin D) have 1.7 to 4.3 times higher incidence rates than do whites. There is also a rapid increase in risk with age, and several other chronic and infectious diseases are closely associated with that increase. All of these factors indicate vitamin D deficiency; therefore, such a deficiency could play a strong causal role in septicemia, especially since deficiency inhibits the production of cathelicidins, which not only break down the cell walls of noxious germs, but also help to reduce the endotoxins resulting from the breakdown." (Vitamin D and Sepsis) .
To summarize, doctors have argued recently that people with known heart disease should target a level of LDL that is below 70 mg/dl. People prescribed statins due to C-reactive protein will also likely achieve a similar low level of LDL, as statins are very effective at reducing cholesterol. However, such a low value for LDL is dangerous, because of the increased vulnerability you now have to infection and sepsis, due to both insufficient cholesterol and insufficient vitamin D.
If you do a web search on "statins cancer," you will come up with a number of web sites claiming that statins may protect against cancer, such as this one: (Statins May Protect Against Cancer) . The study this article referred to was large : it involved 37,248 patients who were taking a statin, and compared them against 25,594 patients who were not. It was noted that, over the course of the study, only 9.4% of those who took the statin drugs developed cancer, as contrasted with 13.2% of those who did not take the drug. The authors provide a caveat, however, that the results are far from conclusive, and offer the following direct quote from Eric Jacobs, the strategic director of pharmacoepidemiology at the American Cancer Society:
"While statins remain important drugs for the prevention of heart disease, they should not be used in the hopes of preventing cancer. Randomized trials have definitively shown that using statins does not reduce cancer risk, at least in the short-term, and most previous observational studies have not found clear evidence that even long-term statin use can protect against cancer," said Jacobs.
Is it the statin drug that reduced the risk of cancer, or rather the highly correlated fact that, statistically, those not prescribed statin had low cholesterol, and were thus more vulnerable to cancer?
In the above study, an especially high benefit was observed for lung cancer and colorectal cancer. There was a well known "Seven Counties Study"  carried out by Ancel Keys in the mid 1980's, before statins were even available by prescription. One clear result revealed by this study was an increased risk for lung cancer as being especially associated with low serum cholesterol levels. A study by Winawer et al. , reported in 1990, also mostly preceded the widespread use of statin drugs. It showed that a decline in cholesterol levels was a predictor of subsequent colon cancer . Thus low or declining cholesterol are risk factors for both lung and colon cancer.
The following website provides a more complete picture by summing up several controlled studies in a single informative chart: (Statins and Cancer: Summary) . The effect of statins on cancer seems to be a complete wash, i.e., only statistically insignificant differences were observed between the statin users and the controls (some up, some down) for several studies included in the chart.
Among the cancers that statin drugs allegedly suppress, prostate cancer is perhaps the poster child. The evidence in epidemiological studies that statins reduce the incidence of prostate cancer seem convincing (Statins Guard against Prostate Cancer) . Furthermore, a seemingly solid reason for this protective effect is tied to the male sex hormone, testosterone. Testosterone is manufactured in the adrenal glands and the gonads from cholesterol via a biochemical process. These glands don't have to depend on delivery of cholesterol by LDL, as they can even manufacture cholesterol themselves, but this process is also controlled by the very same HMG-CoA reductase enzyme that statins interfere with (Cholesterol and Testosterone Manufacture) . As expected based on biochemistry, the ability of statins to reduce total testosterone has been shown definitively to be true, at least for diabetic men, where the observed reduction on average was from 13.4 nmol/L down to 11.9 nmol/L .
For the past several decades, medical students have been taught in medical school that testosterone "fuels the fire" of prostate cancer. Further positive evidence in favor of statins protecting from prostate cancer comes from the observation that statins appear to lower levels of PSA, a biomarker for prostate cancer that can be measured from blood samples (Statins Lower PSA) .
Of course, arguing this idea is a mixed blessing for Big Pharma, because it means they might have to concede that statin drugs could cause sexual dysfunction. Neither loss in libido nor erectile dysfunction are listed as possible side effects of statin drugs. However, there is plenty of anecdotal evidence on the Web suggesting that they are (Statins and Erectile Dysfunction) .
You may feel that a loss in libido is justified if it leads to a decreased risk of prostate cancer, the second most common cancer diagnosis for men (Prostate Cancer Common) . However, if you want the full story, please read the next section.
A person on statin drugs has enjoyed the protective benefit of high cholesterol all his life, up until the time he was treated with the drug. Cancer takes a long time to develop to a level where it can be detected, and the effect of depleted cholesterol on vitamin D supply also takes time to become a problem, due to the body's ability to store both vitamin D and cholesterol in the skin. Even controlled clinical trials are never conducted over a long enough time period to pick up on the slow erosion of cancer protection consequent to sustained statin usage.
Perhaps the first time alarm bells started to go off in the general public on the idea that statin drugs might cause cancer was when the results of the Vytorin study finally came out, and showed that there was a statistically significant 64% increase in all types of cancer among those who took Vytorin, as contrasted with the placebo group. A scathing review of the situation has been written by Bryan Richards of CNN:
"The only surprise about the cancer data is that it was reported at all. Normally Big Pharma would have swept such incriminating data under the rug. The reason they couldn't is because all their Vytorin data is now under such scrutiny they can't dispose or alter undesirable data like they normally do."
"This cancer information has very broad implications for the entire statin industry -- indicating that as cholesterol levels are forced abnormally low under the pretense of heart disease prevention, cancer rates are going to rise. Any fleeting benefits to high dose statin therapy or other means of aggressively and unnaturally lowering cholesterol are rapidly disappearing." (Vytorin Causes Cancer) .
Vytorin is actually a trade name for a pill that combines two cholesterol reducing drugs, Zetia (ezetimibe) and Zocor (simvastatin), into a single pill, to achieve a remarkably greater drop in cholesterol levels than those realized by people taking Zocor operating alone. In fact, after eight weeks of treatment, average LDL levels had been driven down to just 52 mg/LDL in the people taking Vytorin. (Very Low LDL with Vytorin) . The increased incidence in cancer was significant at the 95% level, meaning that there is only a 5% chance that the result was a chance occurrence.
For at least two types of cancer, an increased risk due to statin exposure has been demonstrated, non-melanoma skin cancer and liver cancer. Liver cancer is no surprise, since one of the severe side effects of statin exposure is liver damage. The liver is the "control center" for cholesterol, the place where cholesterol is manufactured and broken down. Skin cancer is a direct consequence of sun exposure. However, vitamin D, which is protective against all cancers, is manufactured in the skin, and immediately made available to the epithelial cells to protect them from cancer. A depleted supply of cholesterol due to statin exposure interferes with the ability to produce vitamin D and thus foils this protective response.
In a study conducted at the University of California at San Francisco, statins were shown to cause liver cancer in rodents. Again, this article has been kept under wraps by Big Pharma, but was picked up by statin skeptics and posted on the Web. By contrast, this cancer-causing effect was notably not found for drugs that lower blood pressure.
"All members of the two most popular classes of lipid-lowering drugs (the fibrates and the statins) cause cancer in rodents, in some cases at levels of animal exposure close to those prescribed to humans." (Statins and Liver Cancer) .The observation of increased risk of non-melanoma skin cancer, of course, has been kept in the back room by Big Pharma, but was picked up by one of the most vocal and convincing skeptics of the benefits of statin therapy, Dr.Ravnskov, the Director of THINCS, the "International Network of Cholesterol Skeptics." (Statins and Non-Melanoma Skin Cancer) .
In the Heart Protection Study, there was an increase in non-melanoma skin cancer observed in people treated with simvastatin, but, with a significance value of p = 0.06, it barely missed the significance level cutoff of 0.05. However, by combining these results with those of another study of simvastatin, the p value becomes 0.028, well within the range of significance. Such a technique of combining the results of multiple trials to gain significance is a perfectly legitimate scientific method.
But what about prostate cancer? It took a lot of digging on the Web to finally obtain a full and rational explanation for the various pieces of the puzzle, but the final full story that emerges leads to the likely conclusion that statins increase risk to prostate cancer, at least for those whose LDL levels are driven below 70 mg/dl. The document that is central to the argument that follows is a book chapter written by the Harvard urologist, Dr. Abraham Morgentaler, and reprinted in full here : (Testosterone and Cancer) . A shorter version of the story can be found here: (Short Version) . His chapter is fascinating and extremely well written, and it describes how he ultimately came to believe that a "fact" that he had been taught long ago in medical school was actually a myth. He wrote in the introduction:
"How the original fear about T [testosterone] and prostate cancer came to be is a fantastic story involving Nobel Prize winners, medical breakthroughs, and a critical paradox that took two-thirds of a century to solve. In the end, it is also a cautionary tale of how it may take years -- even decades -- to correct a medical 'truth' once it has been established."
It was through the practice of treating patients with naturally low testosterone who complained of sexual dysfunction that Dr. Morgentaler eventually discovered that what he had long ago been taught in medical school was in fact the exact opposite of the truth. Not only does a high testosterone level not cause or fuel prostate cancer, but, in fact, a low testosterone level increases susceptibility to prostate cancer. He discovered this because he thought testosterone supplements would help his patients' symptoms, but was afraid to give testosterone to anyone who might have prostate cancer. Because of this concern, he decided to test his patients for prostate cancer, to ensure that any who already had cancer would not be given the treatment. Much to his surprise, he found that a much larger than typical percentage of his patients had prostate cancer . Despite the fact that their PSA level was below 4.0 ng/mL, their cancer incidence was an astounding 15%.
"The way I look at these numbers is that men with low testosterone have a cancer rate as high as men with normal T who are a decade older."
And he continues with this comment that makes it quite conclusive that it is the low testosterone that causes the increased risk:
"More importantly, in our study of 345 men, we found that the degree of testosterone deficiency correlated with the degree of cancer risk. Men whose testosterone levels were in the bottom third of the group were twice as likely to have cancer diagnosed on biopsy as men in the upper third. This finding adds to the concern that low testosterone is a risk factor for prostate cancer."
Now we can look back on the studies that suggest that statins protect from prostate cancer in a new light. Since low cholesterol and low testosterone go together, it is logical that high cholesterol and high testosterone do too. People who are prescribed statins have enjoyed a natural protection against prostate cancer all their lives, due to their elevated cholesterol levels. This inate advantage is what causes the statistics to show that statin users have a lower incidence of prostate cancer. Statin drugs are fast eroding this advantage, however. And when statin drugs drive cholesterol to the below 70 mg/dl mark, they are likely leaving the patient extremely vulnerable to prostate cancer.
A recent study published in 2008 in the American Journal of Epidemiology  (Statins Increase Risk for Prostate Cancer) bears out my prediction that men taking statins would have an increased risk to prostate cancer when compared against other men who are the same age. The authors conducted a population-based study of 1001 prostate cancer cases diagnosed between 2002 and 2005, and 942 age-matched controls. They were expecting to find that statins protect against cancer, but no evidence of such protection emerged from the study. Instead, they found that, for obese men, statins lead to a statistically significant increase in risk. They observed a 50% increase in risk overall, and a significantly larger 80% risk for those who had taken statins for at least five years.
Another indicator that statins may increase risk is based on the inicidence of prostate cancer worldwide. In fact, the rate of prostate cancer is much higher in the West than in the East. For example, blacks in the U.S. have 60 times the incidence of prostate cancer compared to men in Shanghai, China (Prostate Cancer Statistics) . The U.S. has the dubious distinction of having the highest prostate cancer incidence worldwide, with European rates being somewhat lower, and prostate cancer rates among Asians sharply lower.
In summary, while the statin manufacturers would like you to believe that statins are protective against cancer, it has been shown conclusively that this is not true. To the contrary, there is considerable evidence that statins contribute to an increased risk of cancer, in at least three categories: liver cancer, nonmelanoma skin cancer, and prostate cancer.
You might think that it is not a big deal if you don't manufacture vitamin D in the skin -- you can just pop vitamin D supplements to compensate. But biology is never that simple. Vitamin D taken orally is a very different thing from vitamin D manufactured under the influence of sunlight. An important consideration is that the vitamin D manufactured in the skin is immediately put to use in situ to ward off skin cancer. In a sense, people who regularly apply sunscreen are simulating the same condition brought on by low LDL. An SPF level of 8 or more completely disables the reaction that converts cholesterol to vitamin D, while at the same time not protecting you from the most harmful high frequency rays. This, I suspect, is why the incidence of melanoma cancer in children has been increasing by 3% per year since the 1970's , as more and more people buy into the sunscreen scare.
Secondly, disabling the natural production mechanism and replacing it with oral supplements is a lot like destroying the pancreas' ability to make insulin and taking insulin shots to compensate. Your body's natural mechanisms have exquisite control over production levels, turning the spigot on and off based on carefully monitored biological needs:
"The body has two mechanisms to prevent an excess of vitamin D from developing: first, further irradiation converts excess vitamin D in the skin to a variety of inactive metabolites; second, the pigment melanin begins to accumulate in skin tissues after the first exposure of the season, which decreases the production of vitamin D." (Vitamin D Regulation) .
Thus, you can never suffer from a vitamin D overdose if you get your vitamin D exclusively from sun exposure. Even if you get it in part from foods that are natural sources, such as fatty fish and eggs, it is never present in the potentially toxic concentrations that can be found in pills, and it is always accompanied by fats that are an important factor in aiding absorption.
A series of thoughtful and provocative articles by Marshall et al. ,, have urgently argued that the current trend towards recommending vitamin D supplements to just about everybody is misguided and potentially very dangerous (Oral Vitamin D Dangerous) . Like much of what is wrong with modern medical practice, the arguments in favor of vitamin D supplements are deceptively simple and appealing. It is becoming increasingly evident that vitamin D plays a critical role in protecting from cancer and infection, in addition to its critical role in calcium metabolism and bone development. There has been a growing awareness that our nation faces a vitamin D deficiency epidemic. Instead of simply recommending that people spend more time out in the sun, the solution that is recommended is to give everybody a life-time "prescription" of oral vitamin D supplements.
However, Marshall argues that this growing practice may be problematic because it is exposing gut bacteria to concentrated doses of vitamin D, which is acting essentially like an antibiotic. Many of the original bacteria in the gut succumb, and a new mix of biota emerges, with adverse consequences, possibly even contributing to the obesity epidemic:
"Is it possible that the chronic addition of immunomodulatory "Vitamin D" to the diet of Homo sapiens has disturbed the historic composition of gut microbiota, and thus is as at least partly responsible for the current epidemic of obesity? Physicians know that chronic administration of corticosteroids encourages obesity. More research is needed to better define the immunomodulatory activities of this secosteroid, before encouraging even more of it to be added to the food chain." 
But perhaps even more alarmingly, he hypothesizes that the bacteria may be evolving to produce factors that inhibit a critical step that converts the ingested vitamin D into the active form (from 25-D to 1,25-D). The bacteria would be inspired to do this in self defense: the process of natural selection would select for the ones who had acquired this defense mechanism. This is directly analogous to the mechanism that is causing bacteria to become resistant to just about every antibiotic we throw at them. It is unclear what would be the long-term consequence, but it seems really alarming to imagine a situation where the step that activates the vitamin is foiled. One outcome he suggests is an increased incidence of autoimmune disease, something that is definitely happening at this time. But surely there would also be an increased susceptibility to infection and cancer, since the oral vitamin D is being neutralized by the bacteria and therefore wasted.
It is of course widely believed that statins are beneficial in the treatment of heart disease. However, the only aspect of heart disease they have been shown to benefit with statistical significance is the incidence of minor heart attacks in men in their 50's with cardiovascular issues. Another way that problems with the heart can kill you besides heart attacks is heart failure, and it is not a disease you want to die of. It is a slow and painful death.
Doctor Peter Langsjoehn believes that statins are inducing an epidemic rise in the incidence of heart failure. He wrote: "In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, "statin cardiomyopathy". Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with 'normal' cholesterol levels. We are in the midst of a CHF epidemic in the US with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes. " (Statins and Heart Failure) .
This idea seems entirely plausible to me, if only for the simple reason that the heart is a muscle, and statin drugs are known to cause muscle damage. Muscle pain, muscle weakness, and the potentially fatal disease rhabdomyalysis (where destroyed muscle fibers are released into the blood stream and ultimately induce kidney failure) are all known side effects of statin drugs. (Statins and Muscle Damage) . A heart that is already weakened due to heart disease, viewed as a muscle, seems very vulnerable to abuse from statin drugs.
Sally Fallon and Dr. Mary G. Enig of the Weston Price Foundation seem to agree with this assessment, and they explain it as likely due to the depletion of Coenzyme-Q10 directly due to statin interference: "We are currently in the midst of a congestive heart failure epidemic in the United States--while the incidence of heart attack has declined slightly, an increase in the number heart failure cases has outpaced these gains. Deaths attributed to heart failure more than doubled from 1989 to 1997. (Statins were first given pre-market approval in 1987.) Interference with production of Co-Q10 by statin drugs is the most likely explanation. The heart is a muscle and it cannot work when deprived of Co-Q10." (Heart Failure Epidemic) .
You may believe that if you just get your LDL low enough, a "heart attack" diagnosis will be averted. This is not true. In fact, if you have a heart attack, or, at least, the type of heart attack referred to as "NSTEMI", which characterizes over half of the heart attack patients, your chances of surviving three years are significantly greater if your LDL levels are high. this disturbing result was shown in a recent study  that involved 517 patients who were admitted into the hospital with a diagnosis of NSTEMI, between 1997 and 2000, and were tested for fasting lipid profiles within 24 hours of admission. They were divided into two groups based on whether their LDL was below or above the median LDL value of the group (105 mg/dL). As would be expected, more of the patients (36%) in the low-LDL group had already been taking statins than in the case of the high-LDL group (24%). All-cause mortality was significantly higher after three years in the low-LDL group (p=0.005). There was no difference in age, gender, or severity of coronary artery disease between the two groups.
If you have recently been tested for C-Reactive Protein (CRP) and your doctor says you now should take a statin drug despite the fact that your cholesterol levels are fine, you are not alone. Within the last year, the media picked up on the story that high C-Reactive Protein is an even better predictor of heart disease than high cholesterol. The logic goes like this: if you have heart disease, you're almost certain to be prescribed a statin. If you don't have heart disease, but you have elevated CRP, an indicator for future heart disease, then that's almost like having heart disease, and you should take a statin drug. Never mind that your cholesterol levels will be driven down into the danger zone.
Drug companies are already hard at work trying to come up with a drug that will lower the concentration of CRP in your blood. Their reasoning is the same as their reasoning for cholesterol: if a high concentration of CRP is associated with heart disease, then reducing the concentration will surely defend against heart disease.
However, fortunately for CRP, we now have a very high-tech new cutting edge method to test the hypothesis that a substance causes a particular disease. It's a powerful and elegant new tool, and it depends upon genetic sequencing. What is especially good about this method is that you don't have to give to thousands of people a drug (i.e, that reduces CRP) that might be doing them harm, which is what's necessary if you're going to do a placebo-controlled study of a new drug.
The method, termed "Mendelian randomization," relies on knowledge of the gene sequence associated with a particular substance, such as CRP. All you need to do is to sequence that gene for hundreds of thousands of people, something that is now relatively straightforward, and it does nothing to interfere with their well-being. You can then use statistics to determine which alternative patterns of that gene are associated with higher or lower concentrations of CRP in the blood. Now you just have to look at how the two groups (low and high CRP tendencies) distribute over heart disease incidence.
This method was applied very successfully in a study involving over 100,000 people. These people were monitored over the course of nearly twenty years, and their genetic signatures for CRP were compared with their heart disease risk. Results are reported in a 2009 article in the Journal of the American Medical Assocation . The New York Times picked up on the story, and you can read about it here: (C-Reactive Protein Exonerated) .
The results of the study revealed that CRP does not cause heart disease! Apparently, its concentration goes up in response to the changes in the blood vessels that lead to heart disease. It might even be protective against heart disease. I.e., if heart disease were a fire, then CRP could be the water hose rather than the match. Its concentration would go up in order to defend against whatever else is causing the damage to the vessels.
Now here's where it gets interesting. Suppose cholesterol is the same as CRP? I think it can not be ruled out that high cholesterol is a response rather than a cause. If the kind of test that was applied to CRP can be applied to cholesterol (e.g., if there aren't technical issues that make it infeasible for cholesterol) then I think someone ought to perform this test. I'm certain that Big Pharma will never fund such a study, however, since they have thoroughly convinced the medical community and the public at large that cholesterol causes heart disease. They have nothing to prove, and everything to lose, if they turn out to be wrong about cholesterol and heart disease.
The next section will examine the theory that heart disease results from a response to an infectious agent. We will show that, if this is true, then cholesterol plays a crucial role in fighting the infection. Statin drugs, by reducing the bio-availability of cholesterol, interfere with this protective response.
Atherosclerosis is the technical term for "hardening of the arteries," a process that can eventually culminate in a heart attack. The process starts with an infusion of LDL into the artery wall and ends with a rapid cascade of events leading to plaque rupture and the subsequent release of clotting agents that cause the artery to be completely blocked. As a consequence, the section of the heart supplied by the artery becomes nutrient starved, and it quickly becomes non-functioning and is converted into inert scar tissue. The remainder of the heart then has to work harder to pump blood throughout the body. However, plenty of people survive a minor heart attack and go on living for many years with no obvious disability.
The most clear and unambiguous benefit of statin drugs is that they reduce the incidence of nonfatal heart attacks in men in their 50's. The mechanism by which they achieve this outcome is surely directly tied to their ability to reduce the concentration of LDL in the blood. In careful studies of atherosclerosis, it has been determined that cholesterol in LDL plays a critical role in all stages of the atherosclerotic process. When the supply of LDL is reduced, the entire process is slowed down and the heart attack is delayed or possibly even arrested.
This is surely a good thing? Well, it seems to me that the atherosclerotic process is so intricate and so purposeful that it is hard to believe it plays no role in sustaining health. An excellent and widely referenced article written in 1995 on atherosclerosis  provides a fascinating account of all that happens in between the time that the LDL first penetrates the vessel wall and the time of the acute event triggering the heart attack.
Under normal circumstances, the cholesterol enters and leaves the artery wall at the same pace, and no fatty streak accumulates. However, sometimes the LDL "decides" to linger in the wall and also transforms to a weakly oxidized state. This oxidation is a signaling device that encourages white blood cells to join the party. They in turn release chemicals which further oxidize the LDL and trigger an inflammatory response. The newly arrived white blood cells are converted into macrophages, and the LDL, which had been hanging in the extracellular matrix, now take up semi-permanent residence inside the macrophages that are being steadily recruited from the blood supply. Once the LDL becomes highly oxidized it can even become toxic to the macrophages. They release their lipid (fat) droplets which are then consumed by nearby smooth muscle cells lining the artery wall. Over time, the resulting lesion grows outward until it eventually reaches the adventitia, the outermost layer of the artery wall. This situation is deemed a crisis condition, presumably because any further expansion in that direction would penetrate into the heart muscle.
Highly oxidized LDL penetrating all the way to the adventitia triggers a remarkable series of events intent on closing off the artery. High concentrations of "tissue factor" are released from the macrophages, and this tissue factor induces blood clotting by the platelets. The oxidized LDL also inhibits vasodilation, causing the vessel to constrict and furthering the goal of complete closure. Plaque rupture ensues, and more platelets are recruited to the wound site to further encourage a blood clot. In short, systematic biological mechanisms have been preprogrammed to shut down and isolate this segment of the heart.
What could possibly be a good reason to want to kill off a segment of the heart? The article that so beautifully laid out the sequence of events leading to a heart attack never mentioned the idea of an infective agent. However, the entire process would suddenly make sense if you imagine that, when LDL first entered the artery wall, it encountered an infective agent such as a bacterium or a virus, and it was this that triggered it to linger in the artery wall and enter the mildly oxidized state. The macrophages were then recruited to release toxic chemicals with the intent of disabling or even killing the viruses, and then to consume their debris. Meanwhile, the LDL could work on the parallel task of neutralizing toxins released by the infective agents. Further penetration towards the outer wall of the artery was necessitated because the viruses or bacteria were advancing in that direction. Once the enemy reached the outer wall, a crisis ensued because the next step would be penetration of the virus or bacterium into the heart muscle. Such an infection of the heart itself, myocarditis, was something to be avoided at all cost. A minor heart attack, which would essentially turn this segment of the heart into necrotic tissue, would also isolate the infective agent, a preferred outcome to the alternative of letting the infective agent grow unchecked within the heart muscle, leading directly to heart failure.
The notion of heart disease being due to an infective agent was proposed at the beginning of the 1900's. It was mostly ignored over most of that century, but is gaining increased traction in recent times. One clear possibility is the extremely common herpes virus, also known as HCMV (Human Cytomegalovirus), which is estimated to infect from 60 to 99 percent of the world's population . Several distinct observations are strongly suggestive of a role played by these viruses . One such observation is that they are capable of triggering many of the steps involved in the above process of atherosclerosis. Another line of evidence comes from a clinical study that showed that patients with high titres of CMV antibodies were at greater risk to atherosclerosis. Direct evidence of their existence in atherosclerotic lesions has been found in the form of HCMV nucleic acids, detected in 90% of the severe atherosclerotic lesions that were examined. A final line of evidence comes from transplant patients --those who tested positive for HCMV infection were at much higher risk to arterial blockage.
A compelling argument for a relationship between an infective agent and atherosclerosis is in the case of children who were infected with typhoid fever. As early as 1911, Klotz and Manning  observed that atherosclerosis was particularly pronounced in children who had died from typhoid fever. They concluded that the production of fatty tissue in the arterial wall was the result of a direct irritation of that tissue by the presence of infection or toxins. Many studies have implicated a variety of other common infective agents as being cofactors in causing arterial disease. These include Chlamydia pneumoniae (a common source of pneumonia), Helicobacter pylori (the bacterium that causes stomach ulcers), and HSV and CMV (the one discussed above), both of which cause Herpes .
Another indirect argument for the relationship between infection and heart disease is that people who experience an acute heart attack or stroke have disproprortionately just recovered from an infectious disease. These diseases include tuberculosis, sepsis, HIV, chickenpox, tooth infections, and infections of the urinary tract. People with heart disease are encouraged to take steps to prevent gum disease, due to the observed correlation between infections in the gum and atherosclerosis.
A strong proponent of the theory that heart disease is the result of an infective agent is Uffe Ravnskov, a Swedish doctor who has been a tireless advocate of cholesterol as a much-abused and vital biological substance. In his recent book on cholesterol , the next-to-last chapter, titled simply "The Real Cause," argues persuasively for the point of view that atherosclerosis is the direct result of infective agents, and also makes a case for LDL's critical role in plaque build-up to protect against the infective agents. Oxidation is the usual way that macrophages destroy bacteria and viruses. Thus the presence of intense oxidation in the plaque is very suggestive of an attempt to neutralize a pathogen. LDL is able to bind and neutralize the alfa-toxin produced by staphylococcus baceteria, and, as we have seen before, it also neutralizes lipopolysccharide, another common bacterial endotoxin. By subsequently changing their structure to induce the macrophages to consume them, the LDL particles effectively render inert the bacteria and their harmful products.
The endotoxins that are released by bacteria are thus clearly implicated in heart disease. Since LDL can bind with and neutralize bacterial endotoxins, one reason why it might settle in the arterial wall, then, is to be available to neutralize the endotoxins of resident bacteria. It has also been shown that bacterial endotoxin stimulates the expression of tissue factor by macrophages (cells that were derived from the white blood cells) . As we have seen from the above discussion on atherosclerosis, tissue factor is probably the single most contributory component for initiating the final cascade in a heart attack. This would presumably occur because the presence of unneutralized endotoxin indicates that the body's defenses have lost the battle against the bacteria at this site. Statins have been shown to inhibit the migration of white blood cells to inflammatory sites , which would reduce the bioavailability of tissue factor and therefore possibly prevent the heart attack, but would allow the bacteria and their endotoxin to remain in place and continue to do harm to the surrounding tissues, eventually invading the heart muscle itself.
Thus, the observed rapid rise in the incidence of heart failure subsequent to widespread statin usage may not be just due to the fact that statins may directly harm heart muscle cells, but also to the possibility that they indirectly put them in harm's way to the bacteria and viruses that have broken through the protective arterial wall.
Clearly, high-dosage programs for statins have the same goal as Vytorin, to aggressively reduce LDL to levels below 70 mg/dl. My prediction is that they will also yield the same unwanted result -- alarming increases in the incidence of cancer, sepsis, heart failure, and birth defects. Under the influence of Big Pharma, medical doctors appear to be embracing these aggressive treatment plans with abandon. It will be in the end a very positive outcome if high-dose statins become the smoking gun that finally causes us to realize the absurdity of trying to play God to this degree. We need to step back and realize that we should stop demonizing cholesterol -- that it is an amazing biological substance with widespread roles in diverse mechanisms throughout the body, that we have only barely begun to understand.
In 1990, a group of researchers from 19 studies around the world met at a workshop in Bethesda, Md., and pooled their collective results into tables of the relationship between total cholesterol levels and all-cause mortality . The tables were computed separately for men and women, and subjects were binned into four categories with dividing points at 160, 200, and 240 mg/dl.
Men in the two middle categories had equivalent optimal values, with mortality increasing sharply for the >240 range. However, mortality was even higher for the group whose cholesterol was abnormally low (below 160). For women, the results were even more dramatic in that the upper two bins (cholesterol > 200) had equally good and optimal mortality rates. All-cause mortality was higher for those whose cholesterol was between 160 and 200, and even higher for those whose cholesterol was below 160. So, for both men and women, below 160 mg/dL was the highest mortality group.
With those numbers in mind, it is interesting to take a look at the current situation with respect to heart patients. A comprehensive study involving 136,905 heart attack patients from 541 hospitals around the country was done recently to assess lipid levels in these patients (Heart Attacks and Cholesterol Levels) . It can be inferred from the numbers they quote that a substantial percentage of these patients are in the <160 bin with respect to total cholesterol. Half of the patients with a prior history of heart disease had LDL levels below 100 mg/dL, and 54% of all the patients had an HDL level below 40 mg/dL. 100 plus 40 is just 140, which, if augmented by 20 mg/dL in the "other" category would just hit the 160 mg/DL boundary needed to get out of the lowest and highest mortality bin. The article claimed that nearly 75% of the patients had met the current guidelines -- i.e., had cholesterol levels low enough to be considered good with respect to heart disease. The authors, funded by GlaxoSmithKline and Pfizer, two statin drug producers, argued that we need to further reduce the guidelines in order to encourage more people to take statin drugs.
Is there no end to this madness? Can it possibly be considered that cholesterol is not the cause of heart disease for these patients who still have heart disease despite having artificially achieved cholesterol levels not normally seen in nature? Big Pharma may succeed in reducing the incidence of heart disease in the population just by virtue of the fact that they kill off these people with sepsis and cancer and heart failure before they would have died of a heart attack if left untreated.
The following quote portends what is to come as high-dosage statins become a routine program for more and more people:
"In articles posted at MedicationSense.com in recent months, I discussed the findings of two major studies of maximum-dose 80-mg Lipitor (atorvastatin). Despite the authors' claims that these studies proved the benefit of maximum-dose Lipitor for preventing heart attacks and strokes, the MedicationSense.com articles revealed that maximum-dose Lipitor caused far more liver injuries than placebo or low-dose Lipitor. Even worse, despite a reduction in heart attacks and a slight reduction in strokes, there was no improvement in overall mortality because more subjects on maximum-dose Lipitor died of other causes including cancer." (High Dose Statins and Liver Damage/Cancer) .
When you become obsessed with getting your LDL numbers low, you're just trading off death by heart attack with death by cancer or infection or heart failure. At the same time, you're incurring additional expense, along with often annoying and in some cases devastating side effects associated with statin drugs. Doesn't this seem counterproductive?
While Americans seem to want to rely on a magic bullet to solve their medical problems, they would be much better off to focus on the things that take effort: stop smoking, start exercising, lose weight, eat healthy foods, get plenty of sleep, spend some time outside in the sun without sunscreen, and reduce the effect of stress through relaxation exercises. Achieving these goals is much more rewarding and beneficial than popping a pill. These are the true secrets to a long and healthy life.
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I would like to express extreme gratitude towards Professor Tim Berners-Lee, the inventor of the World Wide Web. While the presentation of information on the Web may be biased, it is still possible to uncover the full story if you dig deeply enough. And it would have been impossible to find the truth without the easy access to a broad spectrum of information, both authoritative and anecdotal, that can be found there.
Estonian translation courtesy of Martin Aus.
Finnish translation courtesy of Elsa Jansson.
Georgian translation courtesy of Ana Mirilashvili.
German translation courtesy of Maximilian Neumann.
Serbian translation courtesy of Branca Fiagic.
Turkish translation courtesy of Zoltan Solak.