Alzheimer’s: another reason to be sceptical about statins - Burne

Alzheimer’s: another reason to be sceptical about statins

November 5, 2012 By Jerome Burne

 

The front page of the Daily Express on Friday led with a new warning about statins – combining them with certain blood pressure pills could raise your risk of muscle pains, lung disorders and kidney damage. Hmm yes well.

Even as a cholesterol/statin sceptic I thought that was remarkably over-hyped – statin side effects are massively underplayed and finding they go up a bit when mixed with another drug is more of a clinical technicality than front page news.

However there is a statin risk which should be a serious cause for concern – lowering cholesterol may well raise your chances of developing Alzheimer’s. I’ll come to that in a moment.
First there is one aspect of the Express story that raises a wider issue – the way the buck is subtly passed when any new risk factor is identified. The standard official response is is to say: “If you are worried discuss it with your doctor.” It seems sensible but the implications aren’t reassuring. It’s a line that’s been trotted out rather a lot recently.

Need for serious sanctions

Earlier this week it was used in response to the report that found that more women are harmed by unnecessary treatment following a mammograms than benefit from detecting a cancer. The week before, when a brilliant BMJ investigation exposed the appalling corruption involved in official EU licensing of hip implants, you were also invited to discuss how it might affect you. In both cases serious sanctions would seem appropriate.

In the case of mammograms because convincing research showing that the dangers of over-diagnosis from breast screening dates back over a decade. A clear statement of risks and benefits has taken so long because of the readiness of the mammogram establishment to ignore or denigrate evidence of harm, as I described recently in the Mail. The fact that the European Medicines Agency allows licensing bodies to behave in a way that openly favours business interests rather than the patient, should also trigger an investigation.

Shifting responsibility

There’s nothing wrong with discussing safety with your doctor, but when that’s all that happens it is a brilliant way of shifting the responsibility for producing safe products from the authorities onto you. If in the future you suffer as a result of mammograms or hip implants or indeed statins then the fact you were told about the risk, discussed it and went ahead becomes just one of those things. For a book that discusses this see here.

To appreciate how odd the response to medical dangers is, look at what happens with when something dangerous about a car is picked up. In 2010 it was found that the throttle on some Toyotas could stick in the open position. But rather than saying: “If you are worried about the “dangerous acceleration” issue, discuss it with your dealer and decide if Toyota is right for you”, the company recalled nine million cars.

The truth is that medicine is far more dangerous than the motoring. An estimated 15 people died from driving 10 million cars at risk from the acceleration issue in the USA. If all drugs and other conventional treatments had to be withdrawn at that level of mortality, medicine would become impossible.

Drugs carry serious risks because of the way they work. A single molecule, such as cholesterol that is part of a complex interlocking system, is blocked or boosted with a drug – statins. Inevitably they do things you don’t want as well as the ones you do. And the more important the system you are blocking the more likely the harm. That’s why statins could cause the sort of brain damage that shows up in Alzheimer’s.

Last week I wrote about the growing evidence for links between the raised insulin and insulin resistance that diabetics suffer from and an increased risk of Alzheimer’s. What I didn’t appreciate then was that lowering cholesterol might be equally damaging.

You may be familiar with the idea that cholesterol is involved in brain function but maybe not just how important its role is. A review article in the European Journal of Internal Medicine last year makes it clear.

Cholesterol’s vital role

“The brain represents only 2% of the body’s total mass, but contains 25% of the total cholesterol,” reads an introductory paragraph. “Cholesterol is required everywhere in the brain as an antioxidant, an electrical insulator (in order to prevent ion leakage), as a structural scaffold for the neural network, and a functional component of all membranes. Cholesterol is also utilized in the wrapping and synaptic delivery of the neurotransmitters. It also plays an important role in the formation and functioning of synapses in the brain.”

Personally I’d want to know my odds of benefiting from blocking something that vital were better than the 100 -200:1 that is on offer from stains for primary prevention. The article goes on to describe a number of specific ways cholesterol is used in the brain.

It’s directly involved in the action of a gene known as ApoE. A harmful variation – ApoE4 – is well known to raised your risk of both heart disease and Alzheimer’s . So what does ApoE do? “It has an essential role in the delivery of fat, cholesterol, and antioxidants from the liver to all the cells of the body,” writes the author Stephanie Seneff, a Senior Research Scientist in the Computer Science and Artficial Intelligence Laboratory at MIT who has recently been turning her attention to biochemistry and medicine.

The ApoE4 variation causes brain problems because it doesn’t work so well and lowers the amount of cholesterol available to the hippocampus – the brain region crucial for memory.

More evidence for the harm from having too little cholesterol comes from research showing that Alzheimer’s patients have low levels of cholesterol in their spinal fluid, along with not enough lipoproteins, triglycerides, and free fatty acids. Parkinson’s patients, who also suffer brain damage, have low levels of cholesterol in their blood.

There’s still a lot more to be done to prove definitively that too too little cholesterol damages the brain along with too much insulin and glucose.But avoiding these two highly plausible risk factors is remarkably simple and doesn’t involve adding new risks the way drugs do. It’s what we advocate in our book. Make sure you have enough good fats and eat foods that don’t push up blood sugar.

It’s what Dr Seneff’s recommends too. “Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer’s disease.”
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Read the complete article here.

Alzheimer's: statin cure claims unfounded

Wed, 04 Apr 2012 15:33:00 EST

Cholesterol-lowering statin drugs “could stave off the symptoms of Alzheimer’s”, according to The Daily Telegraph. The front page of the Daily Express even boldly reported: “Statins halt Alzheimer’s.”

These attention-grabbing claims could easily lead readers to assume there has been a major breakthrough in the fight to cure Alzheimer’s disease. However, they are based on a small laboratory study which used mice that were bred to display signs of Alzheimer’s.

The early-stage research showed that the cholesterol-lowering drug simvastatin could improve learning and memory in mice genetically engineered to produce excess levels of amyloid protein in the brain, a characteristic feature of Alzheimer’s disease in humans. However, these improvements were only seen in younger mice, not older ones. The researchers took this to mean that statins would only be effective for blocking early-stage disease. The research also demonstrated that simvastatin caused some improvement in blood vessel function, which some researchers believe to be involved in developing the condition.

Even though these seem like positive results in mice, research has already looked directly at whether statins can stop Alzheimer’s and other forms of dementia in humans. For example, two recent high-quality reviews of research into statins and dementia suggest that there is no evidence that statins provide any specific benefit to humans with Alzheimer’s. While the new research suggests that the timing of statin use may allow it to have an effect, the evidence is far from conclusive and this would need to be explored further in a laboratory. Given the limitations of this research and the uncertainty over its results, the headline “Statins halt Alzheimer’s” is wildly misleading.

Dr Simon Ridley, head of research at Alzheimer’s Research UK, has put the study into context in a statement for Behind the Headlines. He said: “People should view the results with caution until further research has teased out how simvastatin might be working in these mice, and more importantly, until there is any significant new clinical trial data in humans.”

Where did the story come from?

The study was carried out by researchers from McGill University, Canada, and was funded by the Canadian Institutes of Health Research and the Heart and Stroke Foundation of Canada. The study was published in the peer-reviewed Journal of Neuroscience.

Newspaper headlines about this research were generally misleading and suggested that it directly applies to humans. Most media reports took a few paragraphs, and in some cases half the article, to inform readers of the key fact that this research was carried out in mice and not humans. While the Daily Express’ headline suggests that statins have been proven to “halt Alzheimer’s”, this is not justified by the newly published research. In fact, the current body of high-quality research on this topic suggests the opposite is true.

What kind of research was this?

This laboratory study assessed the effect of simvastatin on different signs and symptoms of a mouse model of Alzheimer’s disease. Simvastatin is a widely used statin drug, which can control levels of cholesterol in the body. Around the world, many millions of middle-aged and elderly people take statins. To date, analysis of these populations has not detected any protective effect of the drug against dementia, including Alzheimer’s.

Laboratory studies in mice represent the early stages of medical research. During these mice-based studies, researchers are able to manipulate mice into displaying key characteristics of human disease, which they can then study in detail to better understand the condition in humans. For example, mice may be genetically modify to have biological characteristics similar to a human disease. However, there are key differences between mice and men, and early, experimental results from studies in mice may not always translate into similar findings in humans.

Alzheimer’s disease is characterised by the presence of deposits of the protein beta-amyloid in brain cells. These deposits are also known as amyloid plaques. These can interfere with the normal functioning of brain cells, causing the symptoms of memory loss and other deterioration in cognitive function commonly associated with Alzheimer’s disease. The authors of this study also said that Alzheimer’s is associated with problems in the blood vessels and blood circulation in the brain, and that previous research suggests this compromised blood flow could be related to the progression of Alzheimer’s.

Because statins can help keep blood vessels free of fatty build-up, some people have speculated that they could have a role in preventing Alzheimer’s disease. Previous reviews have not found an apparent link between statins and Alzheimer’s. However, the authors of this new research say recent evidence suggests that the cholesterol-lowering drugs may have beneficial effects on the development and progression of Alzheimer’s disease.

What did the research involve?

This study involved mice that were bred to produce excessive amounts of beta-amyloid protein in their brains, thereby mimicking the key biological characteristic of Alzheimer’s in humans. The research looked at the effect of the statin drug simvastatin on the levels of amyloid in the brain, as well as its effects on blood flow and blood vessel function in the brain.

The study used three main types of mice:

• mice bred to have Alzheimer’s-like disease who received simvastatin (treatment group)
• mice bred to have Alzheimer’s-like disease who didn’t receive simvastatin (control group)
• mice that were not bred to have Alzheimer’s-like disease or receive simvastatin (natural group)

Simvastatin was given to the treatment group mice in their drinking water, while controls were given the same amount of water without the statin. Simvastatin was administered at 20mg per kilo of body weight per day for 3 days. This was increased to 30mg/kg/day for 4 days, and then to 40mg/kg/day for the rest of the treatment.

The treatment group was further divided into two age groups: adult and aged. Adult mice were six months old and had been treated with statins from three months of age for a period of three months. Aged mice were twelve months old and had been treated from six months of age for six months. Total cholesterol levels were measured to assess the effect of the statin.

Spatial memory and learning were assessed with a commonly used water maze test. This involves placing a mouse into a small pool of water containing an escape platform hidden beneath the water’s surface. Visual cues indicate its location, and researchers record how quickly the mouse learns the location of the platform on repeated attempts. The visual cues and platform location can be changed to further assess learning and memory.

Three days after they had completed the maze task, mice were anaesthetised and the blood flow in their brains was measured using a standard technique. This involved using lasers to gauge the amount of fluid moving through their blood vessels. In a subset of mice, a small sample of artery blood vessel tissue was taken from their brain and subjected to laboratory experiments. These were designed to assess its ability to contract and relax as a normal functioning blood vessel should.

The researchers then used appropriate statistical analysis techniques to examine their results.

What were the basic results?

The key finding of this study was that simvastatin fully restored short- and long-term memory in adult mice, but not in aged mice. The researchers found that these beneficial effects occurred without a decrease in the amount of amyloid plaque found in the brains of the mice.

In addition, simvastatin restored key aspects of the functionality of the arteries in the brains of mice with Alzheimer’s disease. This functionality was impaired in mice that did not receive the statin.

How did the researchers interpret the results?

The researchers concluded that simvastatin, and possibly other brain-penetrating statins, show “high therapeutic promise” in early Alzheimer’s disease and in patients with vascular disease who are at risk of developing Alzheimer’s disease.

Conclusion

News reports of this research have ranged from optimistic to misleading. The study’s early mouse-based results need to be viewed in context, particularly as no benefit of statin use on Alzheimer’s has been found when directly examined in humans.

This study shows that the cholesterol-lowering drug simvastatin could improve blood vessel function and learning and memory in mice with features of Alzheimer’s-like disease, but only when given “early in the disease process” (when the mice were at a younger age). However, improved performance in a water maze may not necessarily demonstrate reversal of Alzheimer’s, particularly as the researchers found no decrease in the amount of amyloid plaque found in the brains of the mice. This means that even in mice, the statin had no effect on amyloid, a key characteristic in the human form of the disease.

Furthermore, a recent systematic review of the literature on statins and dementia (including Alzheimer’s disease, which is one type of dementia with strict diagnostic criteria) concluded that the use of statins to prevent vascular disease did not appear to prevent Alzheimer’s. It concluded that “there is good evidence [from randomised controlled trials] that statins given in late life to individuals at risk of vascular disease have no effect in preventing Alzheimer’s or dementia.” This review sought to identify all high-quality literature published on the topic, and it is unlikely that these conclusions would change on the basis of the new, small animal study.

Similarly, a systematic review also looked at whether statins were effective at treating dementia, using high-quality studies published before March 2009. It included a study that assessed the effect of simvastatin on Alzheimer’s disease. It too concluded that there was insufficient evidence to recommend statins for the treatment of dementia, including Alzheimer’s.

This research is bound to be of great interest to people with Alzheimer’s disease and their loved ones, particularly given the impression they may have gained from reading newspaper accounts of it. Dr Simon Ridley, head of research at Alzheimer’s Research UK, the UK’s leading dementia research charity, has helped put the research into context in a statement issued to Behind the Headlines. He said:

“These kinds of studies, in which some characteristics of Alzheimer’s in mice are prevented or reversed, are often interesting and can help to guide both understanding of the disease as well as future studies in people. While some studies in humans have suggested that statin users may have a lower risk of Alzheimer’s, this has not been consistent.

“However, as with many trials for chronic diseases, there is always the issue of whether there is a critical time to give treatments that offers the best chance of success.

“Although simvastatin is a cholesterol-lowering drug, this study in mice did not explain exactly how simvastatin was having its beneficial effect. Interestingly, there did not seem to be a reduction in cholesterol in the mice treated with simvastatin, suggesting that the drug may be acting through a mechanism independent of its ability to lower cholesterol. Therefore people should view the results with caution until further research has teased out how simvastatin might be working in these mice, and more importantly, until there is any significant new clinical trial data in humans.”

Consequently, while the research may offer scientists some new clues on the development of Alzheimer’s disease, front-page headlines that “Statins halt Alzheimer’s” are not supported by this small animal study or by the weight of existing research on the topic.

Analysis by Bazian

Links To The Headlines

Statins could stave off symptoms of Alzheimer's, study finds. The Daily Telegraph, April 4 2012

Widely-prescribed statins may help to fight Alzheimer's if they're given in early stages. Daily Mail, April 4 2012

Statins halt Alzheimer's. The Daily Express, April 4 2012
 

Links To Science

Tong XK, Lecrux C and Hamel E. Age-Dependent Rescue by Simvastatin of Alzheimer's Disease Cerebrovascular and Memory Deficits. The Journal of Neuroscience, 4 April 2012, 32(14): 4705-4715
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Read the complete article here.

Fructose, Sunscreen, Statins and Flu Shots: a Recipe for Alzheimer's Disease.

Read the full article at SpaceDoc.com

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A Recipe for Alzheimer's Disease

by Stephanie Seneff
Senior Research Scientist at MIT (Massachusetts Institute of Technology)

Fructose, Sunscreen, Statins and Flu Shots: a Recipe for Alzheimer's Disease.

Alzheimer's is a dreaded diagnosis that immediately causes a patient to confront the frightening fact that the rest of their life will be defined by steadily eroding memory and cognitive function. Alzheimer's is alarmingly on the rise, and has been so for the past several decades. The cost to society, both financially and emotionally, is staggering.

Much research effort has been devoted to the search for a "cure" for Alzheimer's, most of it predicated on the notion that the characteristic amyloid-beta plaque and tau tangles are causative. Indeed, some drugs that attack the plaque have made it to phase III clinical trials, and, although they do indeed shrink the plaque, they unfortunately also accelerate the rate of decline [1].

I think a better tactic is to look for a cause rather than a cure. Together with colleagues, I published a paper this year on a theory for the cause of Alzheimer's [2], which was based on the idea that a key contributor is insufficient cholesterol in the brain.

Indeed, a recent article has shown that serum levels of cholesterol as well as the ability to synthesize cholesterol are inversely associated with mental decline in the elderly [3]. Furthermore, another study directly comparing Alzheimer's patients with age-matched controls showed a reduced serum level of LDL in the Alzheimer's patients, with the more severe cases showing further reduction in LDL [6].

When you look back to the earliest stages of Alzheimer's, the principle defect that is observed is an impairment in glucose metabolism in the brain [4]. Neurons ordinarily depend heavily on sugar as a fuel source, but sugar is toxic to cells if it's not carefully managed.

The cells have developed a mechanism for controlling the entry of glucose to be restricted to certain "gates" - regions of the cell membrane called lipid rafts that are heavily enriched in cholesterol and sphingomyelin. When cells don't have sufficient cholesterol in their membranes, they have fewer lipid rafts, and this leads to defective glucose uptake, and therefore increased risk to glycation damage from the glucose.

The proteins in the cell get gummed up with sugar and can no longer perform their functions. Fructose is far more damaging than glucose, and fructose consumption has steadily increased in the last decades. In our paper, we described ways in which amyloid beta can actually pitch in to try to divert neurons to alternative fuel sources, in order to minimize the damage caused by wayward sugars.

Since writing that article, I have discovered some compounding factors that I think make the situation much worse. Essentially all cells in the body are surrounded by an exterior coat made up of complex molecules called "GAGs" - glycosaminoglycans.

These contain sugars, proteins, and a large population of attached ions, particularly sulfate anions. These serve, I believe, an important role in helping to safely break down sugar. Simply stated, the sulfur atom deflects the reducing actions of sugars away from the vulnerable proteins.

The sulfate anions also provide a negative field around the cell, which is very useful for keeping bacteria out, because bacteria are also negatively charged, and hence repelled by the cell's negative electric field. So cells with lots of surrounding sulfate are afforded protection from invasive bacteria.

If a bacterium does get in, the cell will have to release oxidizing agents to kill it, and the cell itself will suffer damage from exposure to its own defense system. The fats in the cell membrane are more vulnerable to oxidative damage when there is insufficient cholesterol to protect them.

I now think that depletion of sulfate supply to the brain is another important contributor to Alzheimer's, and I further think that sulfate is supplied to the brain principally by sterol sulfates like cholesterol sulfate as well as their derivatives like vitamin D3 sulfate.

Both cholesterol sulfate and vitamin D3 sulfate are synthesized in the skin upon exposure to sunlight, and it is theorized that the skin is the major supplier of these nutrients to the body [5]. This is why I believe that excess sunscreen use and excess sun avoidance are another principal causative factor in Alzheimer's disease.

Statin drugs interfere with cholesterol synthesis in the liver, but the lipophilic statin drugs (like lovastatin and simvastatin) also interfere with the synthesis of cholesterol in the brain. This would then directly impact the neurons' ability to maintain adequate cholesterol in their membranes.

Indeed, a population-based study [7] showed that people who had ever taken statins had an increased risk to Alzheimer's disease, a hazard ratio of 1.21. More alarmingly, people who used to take statins had a hazard ratio of 2.54 (over two and a half times the risk to Alzheimer's) compared to people who never took statins.

What I think is happening is that the doctor is taking the patient off the statin drug once memory problems are noted, suspecting that the statin may be causing the problem. But it may well be too late at that point to recover. In my own studies on patient-provided drug side effect reports [8], I found a statistically significant increase in the mention of words and phrases associated with memory problems (p=0.011) in the statin drug reports compared to age-matched reports on a variety of other drugs.

Finally, I want to talk about flu shots. The elderly are greatly encouraged to renew their flu shots every single year, and I think this is another major factor that is steadily increasing their risk to Alzheimer's disease. This is mainly due to the aluminum contained in the flu shot.

It has been demonstrated without a doubt that aluminum in the water used in dialysis fluid eventually leads to dementia in dialysis patients, if care is not taken to extract all but trace amounts of aluminum from the water [9].

A very compelling article recently appeared on all the myriad dangers associated with aluminum in vaccines, and aluminum penetration into the brain as well as cognitive damage have both been well demonstrated in animal studies. The aluminum in the Hepatitis B vaccine is a likely source of the association found between this vaccine and autism [10], and I believe that the effects on the infant's brain and those on the elderly person's brain are similar and equally damaging.

The good news is that all of these factors are easy to correct, so the individual can become empowered to lead a lifestyle that will minimize the likelihood of having to face Alzheimer's as they age. The only challenge is to convince yourself that the misguided advice widely espoused by the medical establishment is dead wrong.

Stephanie Seneff is a Senior Research Scientist at MIT's Computer Science and Artificial Intelligence Laboratory.
Website at MIT: people.csail.mit.edu/seneff
Blog: stephanie-on-health.blogspot.com

References

[1] Eli Lilly and Company, 2010 PR Newswire, Lilly Halts Development of Semagacestat for Alzheimer's Disease Based on Preliminary Results of Phase III Clinical Trials, August 17, 2010, http://newsroom.lilly.com/releasedetail.cfm?releaseid=499794 (accessed on September 24, 2011).

[2] S. Seneff, G. Wainwright, and L. Mascitelli, "Nutrition and Alzheimer's Disease: the Detrimental Role of a High Carbohydrate Diet," European Journal of Internal Medicine 22(2):134-40, Apr 2011.

[3] R.S. Tilvis, J.N. Valvanne, T.E. Strandberg and T.A. Miettinen, "Prognostic significance of serum cholesterol, lathosterol, and sitosterol in old age; a 17-year population study," Annals of Medicine, 2011; Early Online, 110

[4] E. Steen, B.M. Terry, E.J. Rivera et al. "Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease-is this type 3 diabetes?" J Alzheimer's Dis 2005;7:63-80.

[5] C.A. Strott, "Cholesterol Sulfate In Human Physiology: What's It All About?" J Lipid Res 44, 1268-1278, 2003.

[6] P. Presecki, D. Mückseler, N. Mimica, et al., "Serum Lipid Levels in Patients with Alzheimer's Disease," Coll. Antropol. 35 Suppl. 1: 115120, 2011.

[7] T.D. Rea, J.C. Breitner, B.M. Psaty et al., "Statin Use and the Risk of Incident Dementia: The Cardiovascular Health Study," Arch Neurol. 62, 2005

[8] J. Liu, A. Li and S. Seneff, "Automatic Drug Side Effect Discovery from Online Patient- Submitted Reviews: Focus on Statin Drugs," Proc. IMMM, Barcelona, Spain, Oct. 2011.

[9] M.R. Wills and J. Savory, "Water Content of Aluminum, Dialysis Dementia, and Os- teomalacia" Environmental Health Perspectives 63:141-147, 1985.

[10] Gallagher OM and Goodman MS, "Hepatitis B vaccination of male neonates and autism diagnosis, NHIS 1997-2002." J Toxicol Environ Health A. 2010; 73(24):1665-77.

October 2011
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See also Stephanie's health blog here.

Why Statins Do More Harm Than Good - Stephanie Seneff

Why Statins Do More Harm Than Good

by Stephanie Seneff
Senior Research Scientist at MIT (Massachusetts Institute of Technology)

Americans have been well trained over the past few decades to avoid dietary fat and cholesterol and to stay out of the sun. Their conscientious implementation of this misguided advice has led to an epidemic in obesity and heart disease, along with a host of other debilitating conditions like arthritis and Alzheimer's disease.

Cholesterol is to animals as chlorophyll is to plants. Cholesterol, absent from plants, is what gives animals mobility and a nervous system. It is therefore not surprising that statin drug side effects mainly impact muscles and the nervous system.

The heart, as a muscle, is not exempt from statin toxicity. This is why the incidence of heart failure has steadily risen in step with the widespread adoption of statin therapy, now displacing cardiovascular disease as the number one killer. In this article I am going to take you on a whirlwind tour of the 60,000 foot view of my understanding of the principle causes of the current health crisis in America.
My extensive research has caused me to hypothesize a remarkable feat that the human body can perform in the presence of sunlight, which is to extract sulfur from hydrogen sulfide in the air and convert it to sulfate, taking advantage of the sun's energy to catalyze the reaction.

This process takes place in the skin upon sun exposure, and also in the endothelial cells lining blood vessels, and in the red blood cells, platelets, and mast cells in the blood. This feat is performed by a very interesting molecule called "endothelial nitric oxide synthase,'' a misnomer, since its main responsibility is to synthesize sulfate rather than nitric oxide.

The sulfate so produced plays a huge role in cardiovascular health, both by preventing blood clots and by keeping pathogenic microbes (bacteria and viruses) at bay. But it also plays another role that is just as important, which is to give cholesterol (as well as vitamin D and other sterols) a free ride through the blood stream.

Vitamin D3 (a highly touted nutrient) is synthesized in the skin from cholesterol (a highly demonized nutrient) and its chemical structure is almost identical to that of cholesterol. By attaching to cholesterol or vitamin D3, sulfate makes the molecule water soluble, and this means that it no longer has to travel packaged up inside an LDL particle. LDL, as you probably know, is the so-called "bad'' cholesterol, which will cause doctors to prescribe statins if the level is too high.

A great way to lower LDL levels is to get adequate sun exposure. It's not going to work to take a vitamin D supplement: you have to go outside and soak up the sun, because supplements are never sulfated and vitamin D is not cholesterol. Raw cow's milk is the only dietary source I know of that actually supplies sulfated vitamin D3, but even that is still not cholesterol sulfate.

Because most Americans have inadequate cholesterol in their skin and grossly inadequate amounts of sun exposure, they suffer from a huge deficiency in cholesterol and sulfate supply to the tissues. Not surprisingly, most impacted are the muscles and nervous system.

Because the heart muscle is indispensible, the body has developed a back-up strategy to give it special treatment, which is to synthesize cholesterol sulfate from LDL and homocysteine in the fatty deposits (plaque) that build up in arteries supplying the heart. The macrophages in the plaque extract cholesterol from damaged small dense LDL particles, and export it to HDL-A1. The platelets in the plaque will only accept cholesterol from HDL-A1, which they then convert to cholesterol sulfate.

They obtain the sulfate through yet another process which requires energy and oxidizing agents, extracting the sulfur from homocysteine. With insufficient homocysteine, the sulfur will most likely be extracted from cartilage, which gets its strength from extensive disulfide bonds. This, in my view, is the main cause of arthritis -- depletion of sulfur from the cartilage in the joints. So now you have both cardiovascular disease and arthritis as a consequence of a low-fat diet and aggressive sun avoidance.

Statin drugs dramatically lower LDL levels by interfering with cholesterol synthesis, and this wreaks havoc on the liver, the main back-up supplier of cholesterol to the tissues when cholesterol intake and cholesterol sulfate production are down. With the American diet, the liver has another huge task, which is to convert fructose to fat.

The fat cannot be stored or shipped (via LDL) if there is insufficient cholesterol. As a consequence, the liver abandons this task, and the fructose builds up in the blood, causing extensive glycation damage to blood proteins. One of the impacted proteins is the apoB in LDL, which interferes with LDL's ability to deliver its goods to the tissues, including cholesterol, fats, vitamins A, D, E, and K, and antioxidants. So LDL levels fall sharply with statins, and so does the bioavailability of all these nutrients.

Muscle cells come to the rescue, heroically, by extracting excess fructose from the blood and converting it to lactate, using anaerobic metabolism. They have to switch over to anaerobic metabolism anyway, because coenzyme Q10, another casualty of statin therapy, is in low supply. Coenzyme Q10 is crucial for aerobic metabolism.

Lactate is a great fuel for the heart and liver, but the problem is that the muscle cells get wrecked in the process, due to massive overdoses of fructose, in the context of inadequate cholesterol, which would have offered some protection. This is a principle contributor to the excessive muscle pain and weakness associated with statins. Eventually, the muscles can't do it any more, and you're now on the verge towards heart failure.

People on long-term statin therapy start to notice that their hair is receding faster, they're developing cataracts, they can't hear as well as they used to, they keep forgetting things, they can't open the pickle jar any more, and perhaps they'll need rotator cuff surgery soon, as their shoulders are so sore. They think it's just because they're growing old, but these are all side effects that my research, together with my students at MIT, has uncovered, by comparing statin drug side effects with side effects associated with other drugs in age-matched reviews.

Even more alarming are the rare but debilitating and even life-threatening side effects we've detected, such as ALS and Parkinson's disease, heart and liver failure, neuropathy and severe muscle damage. A 17-year study on the elderly confirmed what I already suspected: low serum cholesterol is associated with increased frailty, accelerated mental decline, and early death. (Ref 1.)

Statins are not the answer for anyone seeking to avoid cardiovascular disease. The answer, instead, is to modify the diet to include foods that are rich in cholesterol and saturated fat, to avoid empty carbohydrates, especially high fructose corn syrup, to eat foods that are good sources of sulfur, and, most especially, to spend plenty of time outdoors in the sun.

Stephanie Seneff is a Senior Research Scientist at MIT's Computer Science and Artificial Intelligence Laboratory.
She has a Batchelor's degree from MIT in biology with a minor in food and nutrition, and a PhD in Electrical Engineering and Computer Science, also from MIT. Her website at MIT: people.csail.mit.edu/seneff
Her blog: stephanie-on-health.blogspot.com

Ref 1. http://www.ncbi.nlm.nih.gov/pubmed/21254906

September 2011
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