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 to 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 [28] 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 over two decades ago, and 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 [3]. Several distinct observations are strongly suggestive of a role played by these viruses [22]. 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 [12] 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 [16].
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 [21], 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) [24]. 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 [27], 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.
Wednesday, July 29, 2009
Tuesday, July 21, 2009
Statins, Pregnancy, Sepsis, Cancer, Heart Failure: A Critical Analysis
Introduction
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.
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.
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:
- find a substance whose concentration can be measured cheaply
- find a prevalent disease whose presence correlates with a high concentration of that substance
- find a drug that reduces the concentration of that substance
- advertise aggressively to the general public and medical professionals, claiming a miracle cure.
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.
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.
2. Statins and Pregnancy
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
"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.
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
"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.
3. Very Low LDL: Good or Bad?
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 [10] (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.
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 [10] (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.
4. Do Statins Protect against Sepsis?
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 [27]. (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," [7] 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.
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 [27]. (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," [7] 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.
5. Do Statins Cause Sepsis?
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. This other effect would protect against infection and inflammation. Yet protecting against infection and inflammation 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. [25] 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." [25]
"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.[6] (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)." [27] (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.
An article by Wilson et al. [25] 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." [25]
"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.[6] (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)." [27] (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.
6. Very Low LDL and Vitamin D
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 [8],[13],[17] (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.
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 [8],[13],[17] (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.
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