'Good' Cholesterol (HDLs) Found to be Bad in New Study

We all know the official line - the higher your cholesterol level the greater your risk for heart disease. And a high level of LDLs or a low level of HDLs is bad.

 Image by TLECOATL ZYANYA

Image by TLECOATL ZYANYA

In fact, every aspect of this hypothesis has been repeatedly destroyed, but the vast majority of the medical community continue to ignore the facts, as astonishing as this is.

We have studies going back more than 40 years showing a strong link between higher cholesterol and a longer life. Other studies have shown a strong link between higher cholesterol levels and reduced incidence of cancer and infections (see this video clip).  

A dietary trial published in the British Medical Journal in 2016 found that for each 30 mg/dL (0.78 mmol/L) reduction in cholesterol there was a 22% greater risk of death (see previous post here).

We also know that people who have a heart attack do not have high cholesterol - they have the same average total cholesterol levels as other people of a similar age (see this previous post here).

And we know that cholesterol-lowering at the population level does not reduce the risk of heart disease (see Statin Nation).

The LDL level (so called bad cholesterol) is also actually lower in people with heart disease, not higher - according to a large study published in the American Heart Journal.

Higher levels of so called ‘bad’ cholesterol also predict better athletic performance (see here).

Drugs that increased HDLs (so called good cholesterol) have increased the number of deaths. The drug Torcetrapib reduced "bad" LDLs by 25% and increased "good" HDLs by 72%, and at the same time increased the number of deaths due to cardiovascular causes by 40% and doubled the number of deaths from all causes (see Statin Nation book and this blog post).

Now, a new study has again challenged the idea that HDLs are good. The new study has been published in the American Heart Association journal Arteriosclerosis, Thrombosis, and Vascular Biology. The researchers found an association between higher HDL levels and an increase in carotid plaque in women.

Medscape recently reported comments from Robert Rosenson, MD, Mount Sinai Icahn School of Medicine, New York City, who has chaired four international working groups on the biology HDLs.:

"HDL can be a good, bad, or neutral particle," he said.

And that’s not all. A few days ago Professor Sheriff Sultan (featured in Statin Nation II) informed me about a study recently completed in China at Sichuan University and funded by a Sichuan Province-Supporting Technology Project. The study compared blood cholesterol and blood glucose in patients with coronary artery atherosclerosis and healthy individuals.

The researchers found that the cholesterol levels did not correlate significantly with artery atherosclerosis but blood glucose levels did.

The researchers stated: “Hyperlipidemia is not an important cause of coronary atherosclerosis”.

And yet again there is a lack of reporting from the media about these studies - because most journalists are lazy and they only write about cholesterol and statins when a press release is issued from a drugs company that they can cut and paste into their newspaper or website.

New Study Finds Statin Use Associated With Another Type of Muscle Damage.

It is already well-known that statins damage muscles. This is the most common of all the statin adverse effects, and somewhat ironically includes damage to the heart muscle.

Now a new study has found another link between statins and muscle damage. This time Idiopathic inflammatory myositis (IIM) - a varied group of autoimmune related muscle disorders that are characterised by chronic inflammation that results in muscle weakness. These conditions can cause gastrointestinal, cardiac and pulmonary dysfunction. According to the British Society for Rheumatology these muscle conditions are a significant problem for morbidity and mortality.

Lead author Gillian E. Caught from Adelaide Medical School, University of Adelaide, South Australia, told theheart.org | Medscape Cardiology:

Neuropathology_case_XII_02.jpg

"They are severe, debilitating conditions that can result in permanent disability and death, and unfortunately, do not go away when the statin is discontinued because the statin has triggered an autoimmune response. That is why these patients need to be treated aggressively with steroids to help try to get the condition under control."

Dr Caught also said that the general musculoskeletal adverse effects associated with statin use are well known and are estimated to affect between 7% and 29% of all statin users.

The new study is published in the Journal of the American Medical Association (JAMA).

It is a population-based case-control study using the South Australian Myositis Database and the North West Adelaide Health Study, using data from confirmed cases of IIM diagnosed between 1990 and 2014 in patients 40 years or older.

Patients with Idiopathic inflammatory myositis were 79% more likely to be taking statins than the control group.

As more studies emerge confirming what patients have been saying for decades about statin adverse effects, the real risk / benefit ratio associated with statin use is becoming more clear. Increasing, data is showing that statins cause far more harm than we have been led to believe.

Media Silence and Misinformation

As far as I can see this important finding has not been reported anywhere in the mainstream media. Instead, articles like this one published in the Irish Independent continue to suggest that statins are saving lives.

A Huge Problem

Recently, the CDC found that 50% of men and 38% of women aged 60 years and older in America were taking a medication to lower cholesterol.

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Higher Cholesterol Builds Muscle

Back in 2011 during the making of Statin Nation, I communicated briefly with Dr. Steve Riechman at Texas A&M University. Dr Riechman had completed some studies that showed people with higher cholesterol levels tend to gain more muscle mass. At the time, I didn’t realise that Dr Riechman had actually given a presentation to explain these studies. I recently found this and I think its worth sharing.

Dr Riechman was initially looking at what genetic influences determine muscle gain but he discovered that the genetic effects would get lost in what people ate - food seemed to be more important than genetics. He fairly quickly discovered that cholesterol helps to build muscle. During his studies the more cholesterol the person ate the more muscle they gained with resistance training.

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The diagram above is taken from Dr Riechman's presentation. It shows the amount of cholesterol consumed against the amount of learn muscle mass gained. It is worth noting that the level of cholesterol consumption that was for decades recommended by the American Heart Association is associated with the least lean muscle gain.

Dr Riechman then compared this data on dietary cholesterol levels with total blood cholesterol levels. The yellow bars in the diagram below represent ‘healthy’ blood cholesterol levels as recommended. Low blood cholesterol levels are supposed to be ideal but low cholesterol levels resulted in an actual loss of lean muscle mass - even though the trial participants were resistance training.

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Furthermore, it was the so called ‘bad cholesterol’ (LDLs) that predicted the muscle gain. The so called ‘good cholesterol' (HDLs) did not make any difference to muscle gain. Those who had higher levels of ‘bad cholesterol’ had greater muscle gain than those with lower levels of ‘bad cholesterol’.

Dr Riechman battled for 2 years with medical journals to get this research published.

In his presentation, included below, Dr Riechman then goes on to explain more about the actual mechanisms involved and also discusses some of the other important uses of cholesterol within the body.

Another important point he makes is that there is an incredible need tor cholesterol during periods of recovery and the body can’t get enough of it at these times.

Six Things Better than Taking a Statin

Here is a list of six things to consider doing instead of taking a statin. Each of these individual interventions ha been shown to provide greater benefits than statin medications. Just image what can be achieved if all of these are combined.

Exercise

We all know that exercise strengthens the cardiovascular system and protects us from heart disease. In fact, general fitness is strongly associated with protection from dying of all causes. People with the lowest capacity for exercise have 4.5 times the risk of dying when compared with people who have the greatest capacity for exercise.


Exercise does not have to take place in a gym. Any kind of physical movement that increases the heart rate is likely to be beneficial. Health authorities recommend at least thirty minutes of movement or exercise on as many days during the week as possible.


Exercise is also very beneficial for people with diabetes and for the prevention of diabetes, because exercise increases insulin sensitivity (insulin resistance is the hallmark of diabetes). Exercise also helps to reduce visceral fat. This should be a source of encouragement for people who struggle to lose weight when exercising. The harmful visceral fat could still be reducing even if the number on the scale does not change very much. Waist circumference is a better indicator than a bathroom scale.

Drink more water

In 2002, researchers published a study that investigated the amount of water consumed each day and the number of heart disease deaths.

The study included around 20,000 men and women between the ages of 38 and 100, who were followed for 6 years. The researchers found a strong correlation between increased water consumption and a reduction in heart disease deaths. On average, the people drinking five or more glasses of water per day had about half the risk of dying of heart disease compared with people who drank two glasses or less per day.  The association remained the same even after eliminating a wide range of other factors such as age, smoking status, high blood pressure, body mass index, education level, and estrogen replacement therapy in menopausal women.

Coq10 supplement

Some of the most dramatic results were found in a Swedish study published in 2013 that included 440 people aged 70-88 who were split into two groups; one group received a placebo, while the other group received supplemental selenium and CoQ10.  After five years, those in the placebo group had a cardiovascular death rate of 12.6 percent, while those in the group who received selenium and CoQ10 had a cardiovascular death rate of 5.9 percent. This dramatic reduction in cardiovascular mortality is considerably greater than any reduction ever seen in any statin clinical trial.

Vitamin C supplement

Vitamin C is used to make collagen - which lines all of the blood vessels.
In 2004, The American Journal of Clinical Nutrition published an analysis of nine studies that included information on intakes of vitamin E, carotenoids, and vitamin C. The most significant finding was that people who took 700 mg or more of supplemental vitamin C had significantly fewer heart attacks.

Relaxation and meditation

A study published in the journal Circulation in 2012 investigated the use of transcendental meditation for people with heart disease. Participants were split into two groups; one group completed twenty minutes of meditation twice every day, while the other, dubbed the “health education group”, was instructed to spend the same amount of time doing other health-promoting activities such as preparing healthy meals, exercising, or nonspecific relaxation.
After five years of follow-up, 31 percent of the people in the health education group had either had a heart attack or stroke, or died, compared with 20 percent of those in the meditation group, representing an absolute risk reduction of 11 percent associated with meditation, above the benefits associated with more common health-promoting activities.

Not taking a statin

In the studies that have been most supportive of statins, the reduction in heart attack deaths has typically been between 1% and 3%. However, the side effects of the medication are experienced by around 20% of people. And these side effects include an increase in the amount of calcified plaque. Overall, almost everyone will be better off not taking a statin, than taking a statin.


From: STATIN NATION:The Ill-Founded War on Cholesterol, What Really Causes Heart Disease, and the Truth About the Most Overprescribed Drugs in the World


References:

Myers J, Prakash M, Froelicher V, Do D, Partington S, Atwood JE. Exercise capacity and mortality among men referred for exercise testing. N Engl J Med. 2002;346(11):793–801.
Chan J, Knutsen SF, Blix GG, Lee JW, Fraser GE. Water, other uids, and fatal coronary heart dis- ease: the Adventist Health Study. Am J Epidemiol. 2002;155(9):827–833
Knekt P, Ritz J, Pereira MA, et al. Antioxidant vitamins and coronary heart disease risk: a pooled analysis of 9 cohorts. Am J Clin Nutr. 2004;80(6):1508–1520.
Alehagen U, Johansson P, Bj rnstedt M, Rosén A, Dahlstr m U. Cardiovascular mortality and N-terminal proBNP reduced after combined selenium and CoQ10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. Int J Cardiol. 2013;167(5):1860–1866
Schneider RH, Grim CE, Rainforth MV, et al. Stress reduction in the secondary prevention of cardiovascular disease: randomized, controlled trial of transcendental meditation and health educa- tion in blacks. Circ Cardiovasc Qual Outcomes. 2012;5(6):750–758. doi:10.1161/CIRCOUTCOMES.112.967406.

How Much L-Arginine?

One of the biggest problems with statins is that they are prescribed to lower a perceived risk factor without full consideration to the other effects they have. But the prescription of natural nutritional supplements can also fall into this same trap.

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There are a number of nutritional supplements that have been shown to be much more effective than statins. But I think it is important to also warn people about the potential dangers of some of them.

L-arginine is a widely available nutritional supplement for lowering blood pressure and is often recommended for the prevention of cardiovascular disease. L-arginine is an amino acid that converts into nitric oxide. Nitric oxide is an extremely important substance for dilating the blood vessels and is therefore critical for adequate circulation. Through this mechanism l-arginine does lower blood pressure and may also help with erectile dysfunction.

However, when I interviewed Professor Sherif Sultan, one of the world’s leading vascular and endovascular surgeons, for Statin Nation II, he explained that L-arginine supplementation has been shown to cause a number of adverse effects. L-arginine can cause some types of cancer to spread. Some forms of irregular heartbeat can also be made worse by L-arginine, and L-arginine can actually cause blood pressure to become dangerously low for some people.

A study published in the Journal of the American Medical Association in 2006 looked at the effect of giving L-arginine to patients after they had suffered a heart attack. It found that L-arginine, surprisingly, did not improve vascular stiffness measurements. In fact, six patients in the L-arginine group died during the six-month trial compared with no deaths in the placebo group. The researchers understandably concluded that “L-Arginine should not be recommended following acute myocardial infarction".

The results of this study are in conflict with other studies done on l-arginine by others such as Nobel Prize winning researcher Louis Ignarro. Published in 2004. However, those studies were done on mice instead of humans and they also included other nutrients such as vitamin C that we would expect to have a beneficial effect - the benefit could be from the vitamin C rather than l-arginine.

To add more confusion, a study published in the journal circulation in 1996 found that l-arginine supplementation had beneficial effects for patients with severe heart failure.

In the 2006 study that found l-arginine to be harmful the study participants were given 3grams of l-arganine 3 times a day for 6 months. And in the 1996 study that found a benefit for heart failure patients, a larger amount of l-arginine was used (5.6-12.6grams per day), but just for 6 weeks. So, all of this makes it very difficult to determine an appropriate dose. Obviously it depends very much on the individual person and any existing health conditions. Caution suggests that the dose should be kept below 8grams per day.

Anyone who feels l-arginine is benefiting them personally should also try to investigate if this benefit cannot be attributed to other nutrients they are taking, We cannot yet be sure about the overall effects of l-arginine.

References:

-Long-term combined beneficial effects of physical training and metabolic treatment on atherosclerosis in hypercholesterolemic mice. Proc Natl Acad Sci U S A. 2004 Jun 8; 101(23): 8797–8802. Published online 2004 May 28. doi:  10.1073/pnas.0402734101
PMCID: PMC423275

-Rector TS1, Bank AJ, Mullen KA, Tschumperlin LK, Sih R, Pillai K, Kubo SH. Randomized, double-blind, placebo-controlled study of supplemental oral L-arginine in patients with heart failure. Circulation. 1996 Jun 15;93(12):2135-41.

-Schulman SP, Becker LC, Kass DA, et al. L-Arginine therapy in acute myocardial infarction. The Vascular Interaction With Age in Myocardial Infarction (VINTAGE MI) randomized clinical trial. JAMA. 2006;295(1):58–64. doi:10.1001/jama.295.1.58

The Real Causes of Heart Disease - [and Statins don't help]

My latest article about the real causes of heart disease has just been published in Positive Health.

Heart disease is the leading cause of death worldwide. For decades our health authorities and the majority of the medical profession have told us that dietary saturated fat and cholesterol are primary causes of heart disease. This has been the main justification for an estimated thirty-five to forty million people in the United States, seven to eight million people in England, and millions more people worldwide being prescribed cholesterol-lowering statins. However, in this article I will argue that the way we have been looking at the causes of heart disease is fundamentally flawed and taking statins offers very little to no protection.

http://www.positivehealth.com/article/heart/the-real-causes-of-heart-disease-and-statins-don-t-help

The Real Issues Concerning Salt and Cardiovascular Disease

Various health authorities tell us that consuming too much salt is bad for the heart. More specifically, experts are concerned about the intake of sodium compared with potassium. The World Health Organization advises adults to consume less than 5 grams of salt, less than 2 grams of sodium, and more than 3.5 grams of potassium each day.

The concern is largely based on observations that a high sodium intake, or a low potassium intake relative to sodium, can increase blood pressure. The American Heart Association has even stricter guidance and recommends an intake of no more than 1.5 grams of sodium per day. This guidance is based on studies that have suggested that sodium intake below this level is associated with lower blood pressure. The mechanisms by which sodium intake influences blood pressure are not yet fully understood, but they are thought to be related primarily to the intimate relationship between sodium and water.

When sodium is absorbed through the gastrointestinal tract, it brings water with it, keeping the body hydrated. The major liquids of the body are sustained because of sodium. Without sodium the liquid component of blood and the liquids that surround the body’s cells would lose their water, leading to dehydration and death.

 Image credit: By © 2011 by Tomasz Sienicki via wikki commons.

Image credit: By © 2011 by Tomasz Sienicki via wikki commons.

The body uses various systems to try to keep the correct balance of sodium and water. Information is sent from the blood vessels and the brain that tells the kidneys to retain sodium or excrete sodium in the urine. Sodium intake also causes changes in thirst as a means of regulating water relative to sodium.

If too much sodium is consumed, sodium’s affinity with water is believed to cause an increase in the liquid volume and an increase in the pressure within the blood vessels. Potassium does not have the same affinity with water. In fact, potassium and sodium are antagonistic to each other; potassium counters the effects of sodium, and vice versa.

The intracellular space (inside the body’s cells) contains a lot more potassium than the extracellular space (the liquid surrounding the body’s cells) and the reverse is true for sodium. Therefore, the body clearly requires an appropriate balance of sodium and potassium, but the current recommendations for sodium intake might not be serving us well.

Studies on salt intake are somewhat problematic. Comparing data between various studies is difficult because two different methods are used for measuring salt intake: measuring urinary sodium excretion and estimating dietary intake. Twenty-four-hour urinary sodium excretion might be the most accurate method, since 90–95 percent of sodium intake is excreted in the urine. However, it is not practical to collect twenty-four-hour’s worth of urine, particularly during an extended study period, so researchers have suggested that fasting morning urine is a reliable substitute. Urinary sodium excretion does not account for sodium loss due to sweat.

Dietary intake is measured with the aid of food diaries and questionnaires. However, there is considerable room for inaccuracies if the study participant does not recall all of the foods they consumed. Further inaccuracies can arise because of differences in the sodium content of common foods and if table salt is not included in the analysis. In addition, portion size needs to be accurately accounted for.

Dietary recommendations for salt intake are largely based on clinical studies that use urinary analysis. But population surveys have used dietary recall for the analysis, and there is no existing method for comparing these two different measurements.

The analysis is made more complicated by differences in how each person consumes sodium. One person might have a higher sodium intake because of consuming processed foods such as ready- made meals, whereas another person might be getting their sodium from a more balanced diet that also includes more fresh fruit and vegetables. Therefore, some diets might be high in sodium but also high in potassium. Some people’s diets could also be high in other cardio-protective nutrients that could be offsetting the otherwise negative impact of the sodium.

Notwithstanding these difficulties in interpreting the data, studies have generally, on balance, shown a connection between lower sodium intake and lower blood pressure, although the reduction in blood pressure associated with lower sodium intake is often quite small. For example, an analysis completed by the Cochrane Hypertension Group found that a modest reduction in sodium intake resulted in an average reduction of 5 mmHg in systolic blood pressure and a reduction of 2.7 mmHg in diastolic blood pressure for people with high blood pressure. People with normal blood pressure had smaller reductions (2.3 mmHg for systolic and 1 mmHg for diastolic). Mathematically, if a 2 mmHg reduction in diastolic blood pressure is applied across a very large population (such as nationwide), this would result in an overall 6 percent reduction in heart disease risk. But how relevant these small reductions in blood pressure are for individual people is debatable.

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Since blood pressure fluctuates as a result of a wide range of different conditions, it is important to look for a connection between lower sodium intake and an actual reduction in cardiovascular problems, rather than looking at changes in blood pressure alone. Such studies have had mixed results; some have confirmed an increased risk of cardiovascular disease in connection with a high sodium intake, while others have not. In fact, overall, researchers have suggested that the relationship between sodium intake and cardiovascular disease follows a J-shaped curve whereby both a low and high sodium intake could involve an increased risk.

Statistically, the lowest cardiovascular risks have been seen with a sodium intake of 3–5 grams per day, with an increased risk associated with both higher levels (above 5 grams per day) and lower levels (below 3 grams per day). This is important because although the data does confirm some kind of connection with sodium intake, the current recommendations are set too low and are associated with an increased risk. As mentioned above, health authorities currently recommend a sodium intake of 1.5–2 grams per day. Overall, this level of intake is associated with an increase in cardiovascular problems.

Health authorities could have become blinded by the blood pressure–lowering effect of a very low-sodium diet, and they could have failed to consider the other effects of such a diet. A very low-sodium diet has been shown to alter levels of some hormones and cytokines that are involved in cell-to-cell communication. A moderate, rather than low, sodium intake has even been shown to improve outcomes for some heart failure patients.

As mentioned, we should also consider potassium intake, not just sodium intake, as there is some evidence that potassium might exhibit a similar relationship. A study that analyzed the data from approximately 39,000 patients in the United States who had already suffered a heart attack found a U-shaped curve. Similar to sodium, both low and high levels of potassium were associated with an increased cardiovascular risk, with the lowest risk associated with moderate potassium levels.

The J-shaped and U-shaped curves for sodium and potassium respectively might be a further indication that the levels relative to each other are what is most important. Indeed, there is some data suggesting that a higher sodium-to-potassium excretion ratio is more strongly associated with increased cardiovascular risk than that of sodium or potassium alone.

Sodium/Potassium Balance after Heart Attack

The importance of the correct balance of sodium and potassium is further illustrated by the observation of heart muscle tissue after a heart attack. In an acute heart attack, tissue damage can be seen in three zones of heart muscle tissue. The core area consists of necrotic tissue and dead cells due to the absence of oxygen. Next to this there is an area of severe injury that is composed of cells that will die if the metabolic derangement cannot be corrected. Last, surrounding this area is a less ischemic zone, where cellular function is impaired but is reversible. In short, there is a gradient of extent of damage and metabolic derangement, with the extent of damage gradually reducing with increasing distance away from the necrotic core.

The damage gradient correlates with the amount of sodium inside the cell. As mentioned, there is a lot more sodium outside the cell (the extracellular space) than inside the cell. Under healthy conditions, there is a powerful mechanism for constantly pumping excess sodium out of the cell, the sodium-potassium pump; however, after a heart attack the membrane of the cell is damaged and additional sodium enters the cell. The excess sodium increases the liquid volume of the cell, causing it to swell, and cellular function and the ability to pump the excess sodium out of the cell is impaired.

The outer area of tissue damage typically corresponds with a 50 percent increase in the amount of sodium in the cell. The intermediate zone corresponds with a 200 percent increase in sodium, and the inner necrotic core has a 300 percent increase in sodium.

At the same time a similar, but reverse, situation is observed with potassium. Normally there is much more potassium inside the cell than outside, but after a heart attack there is a decrease in the potassium content inside the cell that again corresponds with the degree of tissue damage within the three affected zones.

These observations led Dr. Demetrio Sodi Pallares of Mexico City to develop a polarizing solution to help correct the sodium-potassium deregulation after an acute heart attack. The solution was based on earlier work done by Henry Laborit, a French researcher, and consisted of glucose, insulin, and potassium. The insulin helps the glucose and potassium into the cell.

Dr. Pallares had quite dramatic positive results using the polarizing solution in the 1960s, and a number of prominent cardiologists around the world also started administering it. At that time, and in a number of studies completed since, the polarizing solution reduced the number of deaths, the amount of tissue damage, and complications such as arrhythmias after a heart attack.

In fact, the potential benefits of the polarizing solution also extend into other areas of medicine that are beyond the scope of this topic and involve the electrical potential across the cell membrane and the additional use of electromagnetic fields. A more detailed discussion is available in the excellent book Bioelectromagnetic and Subtle Energy Medicine.

Statins Damage Gut Microbiome and Contribute to Antibiotic Resistance

Our digestive tract contains about 2 kg of microbes (the microbiome). These microbes, often referred to as friendly bacteria, help with digestion, the production of vitamin B and vitamin K, and play a major role in the immune system.

A recent study published in Nature has found that statins disturb the gut microbiome - they inhibit the growth of some potentially useful bacteria in the gut and allow other bacteria to flourish and become superbugs resistant to antibiotics.

The study found that a wide range of commonly prescribed medications interfere with the gut microbiome, including simvastatin.

The study confirms what has previously been seen in studies done on mice given statins. These previous studies have found that rosuvastatin, atorvastatin and pravastatin also cause profound alterations in the balance of gut microbes. And this imbalance is similar to what has been seen in diet-related obesity.

 Antibiotic Resistance -the white paper discs contain antibiotics. Most of the bacteria in the dish on the left are sensitive to the antibiotics. The bacteria in the dish on the right are resistant to antibiotics.

Antibiotic Resistance -the white paper discs contain antibiotics. Most of the bacteria in the dish on the left are sensitive to the antibiotics. The bacteria in the dish on the right are resistant to antibiotics.

The human body contains about one third more bacteria cells than human cells, and scientists are still investigating the many ways that these colonies of bacteria live in symbiosis with us. The implications of the changes in the bacteria caused by statins is difficult to predict, however the changes are likely to weaken the host's immune system and ability to produce some specific nutrients. Researchers for the article published in Nature say that statins are also contributing to the global problem of antibiotic resistance.

Antibiotic resistance, according to the World Health Organisation, is one of the most urgent public health problems and “Antibiotic resistance is rising to dangerously high levels in all parts of the world”.

This is an important example of how medicine has become unsustainable. This will likely become yet another serious adverse effect of the widespread use of statins that will simply be ignored in the push to keep hundreds of millions of healthy people as patients for profit.

References:

Maier, L et al. Extensive impact of non-antibiotic drugs on human gut bacteria. Nature doi:10.1038/nature25979. https://www.nature.com/articles/nature25979

Caparros-Martin, JA et al. Statin therapy causes gut dysbiosis in mice through a PXR-dependent mechanism. Microbione 2017; 5: 95. doi: 10.1186/s40168-017-0312-4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550934/

Nolan, JA et al. The influence of rosuvastatin on the gastrointestinal microbiota and host gene expression profiles. Am J Physiol Gastrointest Liver Physiol. 2017 May 1;312(5):G488-G497. doi: 10.1152/ajpgi.00149.2016. https://www.ncbi.nlm.nih.gov/pubmed/28209601

Antibiotic Resistence – World Health Organisation. http://www.who.int/mediacentre/factsheets/antibiotic-resistance/en/

Daily Mail. http://www.dailymail.co.uk/health/article-5521767/Statins-hayfever-pills-fueling-antibiotic-resistance.html

The Telegraph. https://www.telegraph.co.uk/science/2018/03/19/statins-hayfever-pills-could-driving-antibiotic-resistance-warn/

Image Source: Dr Graham Beards at en.wikipedia [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

Cholesterol and Looking Younger

We already know that cholesterol is the raw material used to make all of the sex hormones within the body, vitamin D, and bile acids. We also know that the brain and nervous system need a lot of cholesterol, and that cholesterol plays an important role in the immune system. Epidemiological studies have shown a strong association between higher cholesterol levels, reduced risk of cancer, reduced risk of infections and a longer life. Cholesterol is also an essential part of the cell membrane and it is this function that has now led to cholesterol being used in a range of anti-aging skin products.

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The outermost layer of the skin (medically called the stratum corneum) protects us from dehydration and external dangers. Three major lipids are important for this layer: ceramides, free fatty acids, and cholesterol.

When the level of cholesterol and the other fatty acids within the stratum corneum is reduced it is thought that tiny gaps can appear between the cells and the skin loses moisture quicker, becomes tight, dull and deflated. The skin ages faster and is less able to function as a protective barrier.  This has led to the development of anti-aging cosmetics that contain cholesterol and other fatty acids.

Cosmetics containing cholesterol like the one shown retail for around £100 (US$140)!

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Yet another reason not to worry about cholesterol-rich foods and to think twice before artificially lowering cholesterol with statins or anything else.

This mechanism could also be one of several reasons why a range of skin problems have been reported with statins.

Notes:

  • This entry was prompted by a cosmetics feature in the Daily Mail.
  • Image attribution - Wbensmith [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons
  • The product image is for illustrative purposes only and there is no intention to endorse the product shown. The best way to ensure adequate cholesterol levels is to consume a balanced diet which includes cholesterol containing foods.
  • Also see, Lipids and Skin Barrier Function. Contact Dermatitis. 2008 May;58(5):255-62. doi: 10.1111/j.1600-0536.2008.01320.x.

 

Statins and the Nocebo Effect?

There have been numerous and relentless attempts to play down the extent and severity of statin adverse effects. One of these relates to the nocebo effect.

The nocebo effect suggests that health problems from other causes are blamed on a prescribed medication. The idea is that after taking the tablet the patient reports adverse effects from the medication but these adverse effects have a different cause or may be induced through an expectation of adverse effects due to a widespread belief that the medication can be harmful. In some ways the opposite of the placebo effect.

The nocebo idea, in general, is an interesting concept worthy of debate, however, I believe the way this idea has been applied to statins does not represent what's really happening concerning statin adverse effects.

Claims that statin adverse effects are due to the nocebo effect arose from studies that have found the same number of adverse effects in the statin group as the placebo group. The most recent of these, and probably the most cited, is a study published in the Lancet in May 2017:

Gupta, A, Thompson, D and Whitehouse, A et al. Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid-Lowering Arm (ASCOT-LLA): a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension phase. Lancet 2017 Vol 389 No. 10088 p2473-2481.

This study looked at data from the ASCOT trial. Researchers compared data from the trial period itself with data from a follow-up period where patients were told if they were receiving the statin or a placebo and also given the option to start a statin. During the trial itself about the same number of patients in both the statin group and the placebo group reported muscle aches and pains. But during the follow up period (where patients knew if they were taking a statin or not) considerably more people started to report muscle aches and pains in the statin group than the non-statin group. The researchers and other commentators have suggested that once patients knew they were taking a statin the rate of muscle aches and pains increased in the statin group. A result of the nocebo effect.

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However, the following points have been overlooked or deliberately ignored:

The researchers suggested that the muscle-related adverse effects were the result of patients now knowing they were taking a statin and can blame the statin for any muscle-related problems (real or imaginary) experienced.

This idea of a nocebo effect relies on the idea that patients have an expectation that statins cause muscle problems. It has even been suggested that the nocebo effect is due to exaggerated reports about statin adverse effects in the media. However, the data that was used for the 2017 Lancet paper was actually collected between 1998 and 2005. Long before statins became a household name and patients could create preconceived ideas about statins.

It is also worth mentioning that:

During the initial trial period there was a statistically significant increase in renal and urinary adverse effects in those people who were given the statin. Something that has never been mentioned before when discussing this study.

During the unblinded phase there was also a statistically significant increase in musculoskeletal and connective tissue disorders and blood and lymphatic system disorders in the people who took a statin.

In the ASCOT trial no one lived any longer as a result of taking the statin.

The idea of the nocebo effect is one reason doctors reject their patients’ reports of adverse effects after starting a statin. Doctors are advised by opinion leaders to watch out for these “false” reports of statin adverse effects and have other explanations ready, such as telling the patient its just due to old age.

Statins Debate

Last November, Professor Sherif Sultan took part in a debate about the use of statins at the VEITH symposium in New York. Professor Sultan argued against the use of statins and he won the debate. Statins were of course a hot topic at the event and after the debate itself the discussions continued. The video below is a (after debate) discussion between Drs Ron Waksman, Ido Weinberg, David Spence and Sherif Sultan.

Other related Video clips and Notes

It is important to note the following, particularly in regard to the comments made by David Spence:

  • The seven countries study referred to by David Spence was the work of Ancel Keys and it is widely now known that Ancel Keys’ work was fraudulent. The seven countries study selectively chose data to fit a preconceived hypothesis. A hypothesis that has repeatedly been shown to be false. (See video clip one about the six nations study and the lipid hypothesis).

VIDEO ONE

  • While some of the comments about the Mediterranean diet are correct, David Spence seems unaware that the Mediterranean diet is different things for different people. For example, he mentions the island of Crete. The island of Crete was used as another example in Statin Nation II, specifically the village of Anogia, where the people eat large amounts of animal fat but have no heart disease, again challenging the lipid hypothesis. (See video clip two).

VIDEO TWO

  • Dr Spence describes how he thinks it is a good idea to scare his patients into complying with statins by showing them images of atherosclerotic plaque - he doesn’t mention that the statin he is prescribing will actually increase the amount of plaque in the arteries. (See video clip three and four).

VIDEO THREE

VIDEO FOUR

  • Dr Spence suggests that “we don’t need much LDL”. Dr Spence should he reminded that LDLs provide the transport mechanism for delivering all the vital nutrients to the cell including:

--coenzyme Q10 (CoQ10) - this is needed for energy production within the cells of the body. In particular, it is needed in the heart muscle cells. CoQ10 is also an antioxidant.

--beta-Carotene (vitamin A) - these are thought to protect against diseases, in particular, protect against cancer and eye disease.

--vitamin E- an antioxidant. It is also involved in the immune system and helps to dilate blood vessels - improving circulation. It also helps prevent coagulation, which is a key feature of heart disease.

Not to mention that people live considerably longer with higher LDL levels and are protected from serious diseases.

This fundamental oversight by Dr Spence displays just how academically corrupted much of the medical profession has become. Someone in his position should know better, especially considering that he claims to be in support of nutritional interventions.  

 

New York Times Article Is Wrong (Errors and Omissions in Statins Article)

The New York Times has just published an article supposedly examining the pros and cons of the elderly taking statins. On the face of it the article appears to be balanced however, there are a great number of errors and omissions in this article and as a result the article creates completely the wrong impression about statins.

The New Times Article can be found here, it might be worth comparing the article with the information below.

The first problem with the New York Times article is found in the second paragraph where the author incorrectly states “[statins] get much of the credit for the nation’s plummeting rates of heart attacks and strokes”.

In fact, heart disease death rates have been declining rapidly in the United States (and the UK) since the 1970s (see figure 1). Statins were introduced in the mid to late 1990s - around 20-25 years after the sharp decline was already well under way.

  FIGURE 1

FIGURE 1

The reduction in heart disease deaths in the United States (and the UK) is mostly due to the reduction in the number of people who smoke cigarettes (see figure 2). Improvements in hospital treatments has also contributed.

  FIGURE 2

FIGURE 2

In addition, retrospective studies have also failed to find any benefit associated with statins. Although statin clinical trials have predicted a slight reduction in heart attacks in some patient groups, studies that have looked retrospectively have found that these predicted benefits have not actually materialized.

Clinical trials are perceived as the gold standard of clinical research but in recent decades there has been a greater understanding of how the clinical trial process can be manipulated by commercial interests in order to get the result that is favorable to the company sponsoring the trial. Therefore, it is also important to look retrospectively at the risks and benefits as the drug is used widely in the general population.

For example, researchers collected data from all but one of the municipalities of Sweden and they found that statins had not provided any benefit despite a huge increase in usage.

In 2012 the British Heart Foundation published a report detailing a wide range of heart disease statistics. One of the highlights of this report was the decline in heart disease death rates that had been seen in the UK between the years 2002 and 2010. The report listed the improvements that had led to this decline in deaths - statins were not mentioned at all.

Doctors in the pockets of drugs companies and lazy reporters often repeat the myth that statins have contributed to the decline in heart disease deaths, but there is not any to data to support this.

There are many other problems with the New York Times article, such as quoting relative percentages instead of absolute percentages (relative percentages hugely misrepresent the data), and also a failure to mention the other common adverse effects of statins that the elderly are more vulnerable to. However, I want to take particular issue with the fact that the New York Times article also fails to inform people of the strong connection between low cholesterol levels and shorter life expectancy and increased cancer rates - a correlation particularly strong in the elderly. As explained in the excerpt below from Statin Nation II:

References:

Figure 1 taken from Factors Influencing the Decline in Stroke Mortality
A Statement From the American Heart Association/American Stroke Association

https://doi.org/10.1161/01.str.0000437068.30550.cf
Available here

Figure 2 is published by the CDC and is available here

Swedish Study: Nilsson et al. No connection between the level of exposition to statins in the population and the incidence/ mortality of acute myocardial infarction: An ecological study based on Sweden's municipalities. Journal of Negative Results in BioMedicine 2011, 10:6

British Heart Foundation report: Coronary Heart Disease Statistics 2012. Available from https://www.bhf.org.uk/publications/statistics/coronary-heart-disease-statistics-2012

Ditch the Carb, Not the Fat

Its that time of year again when many of us are planning to start a healthier lifestyle. The incorrect advice to follow a low-fat diet persists so its worth reminding ourselves of some of the key reasons why we should aim to reduce carbohydrates and sugars instead of fat.

Low-Fat Diets Paradoxically Increase Blood Fat levels.

Fats in the bloodstream are known as triglycerides. A higher level of triglycerides in the blood can increase the risk for heart disease. High levels of triglycerides are also a very common feature of diabetes and diabetics are up to five times more likely to have heart disease than non-diabetic people.

For decades, the idea has perpetuated that eating fat will cause the level of triglycerides in the blood to increase. However, when we look at the data from scientific studies it is clear that this is not the case. In fact, every dietary trial that has been done has found that a low-fat diet causes the level of triglycerides to increase - no studies have found that increased dietary fat increases triglycerides.

Initially, this may seem to be a paradox, however, what these and other studies reveal is that dietary fat is not the villain it was once thought to be. A low-fat diet will inherently involve the consumption of more carbohydrate and sugar. Guidelines from health authorities actively encourage people to substitute foods that contain fat with foods that are carbohydrate based. What is often overlooked is the effect that a low-fat / high-carbohydrate diet has on blood glucose levels.

The chart below compares the effects that a high-carbohydrate diet has on blood glucose levels with the effects of a high-protein / higher fat content diet, during a 24 hour period. It can be seen that the high carbohydrate diet causes wild fluctuations in blood glucose and much higher levels of blood glucose overall. It is worth pointing out that the carbohydrate content of the high-carbohydrate diet used for this analysis was 55 percent - which is considerably lower in carbohydrate content than the diet many people are consuming today.

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Why is this so important? Well, high blood glucose is a serious situation that the body has to rectify as a priority. High levels of blood glucose cause circulatory problems and damage to the inside wall of blood vessels. And a high level of blood glucose triggers the release of the hormone insulin, which is required to lower blood glucose levels.

Insulin enables the body’s cells to use some of the glucose, but if there is too much glucose insulin converts the excess glucose into fat (triglycerides). This explains why low-fat /high-carbohydrate diets increase blood triglyceride levels.

It is worth mentioning that the presence of a high level of insulin, in response to the high glucose level, by definition, blocks the ability to burn body fat. Insulin is a fat storing hormone. This is one reason my people who follow a low-carbohydrate diet tend to lose more body fat.
When the level of triglycerides is high we also find a low level of HDLs - the so called ‘good cholesterol’.  Again, every single dietary trial completed has found that a low-fat / high-carbohydrate diet reduces HDL levels.

We can really start to appreciate the topsy turvy world we live in where HDLs are called ‘good’ and at the same time low-fat diets are promoted as healthy - the very diet that is the best way to reduce HDL ‘good cholesterol’ levels.  Just one of the many fundamental inconsistencies associated with the lipid hypothesis.

 

References:

Liu, S et al. ”Dietary Glycemic Load assessed by Food-Frequency Questionnaire in Relation to Plasma High-Density- Lipoprotein Cholesterol and Fasting Plasma Triacylglycerols in Postmenopausal Women” American Journal of Clinical Nutrition 2001;73:560-566

Radhika, G et al. “Dietary Carbohydrates, Glycemic Load and Serum High-Density Lipoprotein Cholesterol Concentrations among South Indian Adults” European Journal of Clinical Nutrition. Advance Online Publication November 7, 2007

Garg, A, Grundy, SM and Koffler, M “Effect of High Carbohydrate Intake on Hyperglycemia, Islet Function, and Plasma Lipoproteins in NIDDM” Diabetes Care 1992; 15:1572-1580

Garg, A et al. “Effects of Varying Carbohydrate Content of Diet in Patients with Non-Insulin-Dependent Diabetes Mellitus” Journal of the American Medical Association 1994; 271:1421-1428

Samaha, FF et al. “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity” New England Journal of Medicine 2003; 348:2074-2081

Yancy, WS et al. “A Low-Carbohydrate, Ketogenic Diet Verses a Low-Fat Diet to Treat Obesity and Hyperlipidemia”. Annals of Internal Medicine 2004; 140:769-777

Gardner, CD et al. “Comparison of the Atkins, Zone, Ornish and LEARN Diets for Change in Weight and Related Risk Factors among Overweight Premenopausal Women”. Journal of the American Medical Association 2007; 297:969-977

Stern, L et al. “The Effects of Low-Carbohydrate Verses Conventional Weight Loss Diets in Severely Obese Adults: One-Year Follow-up of a Randomized Trial”. Annals of Internal Medicine 2004; 140:778-785

Foster, GD et al. “A Randomized Trial of a Low-Carbohydrate Diet for Obesity” New England Journal of Medicine 2003; 348:2082-2090

Appel. LJ et al. ”Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood Pressure and Serum Lipids” Journal of the American Medical Association 2005; 294: 2455-2464

Mozaffarian, D, Rimm, EB, and Herrington, DM “Dietary Fats, Carbohydrate, and Progression of Coronary Atherosclerosis in Postmenopausal Women” American Journal of Clinical Nutrition 2004; 80:1175-1184

Smith, J., 2009. “$29 Billion Reasons to Lie about Cholesterol: Making Profit by Turning Healthy people into Patients” Troubador, Leicester

Gannon, MC and Nuttall, FQ “Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes” Diabetes 2004; 53:2375-2382

Zhengling, Li et al. “Men and Women Differ in Lipoprotein Response to Dietary Saturated Fat and Cholesterol Restriction” Journal of Nutrition 2003; 133:3428-3433

Walden, CE et al. ”Lipoprotein Lipid Response to the National Cholesterol Education Program Step II Diet by Hypercholesterolemic and Combined Hyperlipidemic Women and Men” Arteriosclerosis, Thrombosis, and Vascular Biology 1997;17:375-382

Lichtenstein, AH et al. “Efficacy of a Therapeutic Lifestyle Change/Step 2 Diet in Moderately Hypercholesterolemic Middle- Aged and Elderly Female and Male Subjects” Journal of Lipid Research 2002; 43:264-273

Sniderman, AD, Scantlebury, T and Cianflone, K “Hypertriglyceridemic HyperapoB: The Unappreciated Atherogenic Dyslipoproteinemia in Type 2 Diabetes Mellitus” Annals of Internal Medicine 2001; 135:447-459

 

Don’t Let STATINS Break Your Heart!

Despite the fact that statins are currently prescribed to around 100 Million people worldwide for the prevention of heart disease these medications, somewhat ironically, actually damage the heart. This damage occurs through a number of different mechanisms.

Statins damage the heart in the following major ways:

  • Statins block Coenzyme Q10 (CoQ10), which is essential for all cellular energy production. The heart contains the most CoQ10 since the heart has the greatest requirements for energy production. Statins block CoQ10 because they act very high up in the mevalonate pathway. The mevalonate pathway is the biochemical step by step process used by the body to create a wide range of essential compounds. Statins inhibit this process - that’s how they lower cholesterol levels and also lower CoQ10 levels.

Statins have the effect of lowering LDL levels (so called ‘bad cholesterol’). However, LDLs provide the main transport mechanism for moving CoQ10 around the body. Therefore, this is another way that statins reduce the availability of CoQ10.

Low levels of CoQ10 weaken the heart and can cause or contribute to heart failure.

Incidentally, LDLs also provide the transport mechanism for a number of other vital nutrients such as vitamin E, and various carotenoids such as beta-carotene.

 

  • Statins increase the amount of calcified plaque in the arteries. Atherosclerosis is a hardening and narrowing of the arteries. The process involves calcification. The confirm registry found that statin use is associated with an increased number and extent of calcified coronary plaques.

Other studies have shown that statins do not reduce coronary artery calcium, and that the disease continues regardless of the statin use.

The Veteran Affairs Diabetes Trial found that statin use was linked with the progression of coronary artery calcification despite the fact that the statin users had significantly lower and nearly optimal LDL ‘cholesterol' levels.

  • Statins inhibit vitamin K2 and selenium, both of which normally have a protective effect on the heart and blood vessels.

 

  • Statins increase the risk of Type 2 Diabetes and Diabetes increases the risk of heart disease death by up to 400%.

 

  • Statins block the response to exercise. After exercise, the heart normally gets stronger as part of the normal adaptation process. Statins hinder this process. This means that the benefits of exercise cannot be obtained by people who take statins. The response to exercise is important for everyone however, it is particularly importance for anyone recovering from a cardiac event.  

 

The video above has been created to create more awareness of these issues and to encourage people to think carefully before starting statins. T-shirts and posters are also available as part of this campaign to help spread the message.

 

References

Nakazato R, Gransar H, Berman DS, et al. Statins use and coronary artery plaque composition: Results from the International Multicenter Confirm Registry. Atherosclerosis. 2012;225(1):148–153.

Raggi P, Davidson M, Callister TQ, et al.. Aggressive versus moderate lipid-lowering therapy in hypercholesterolemic postmenopausal women: beyond endorsed lipid lowering with EBT scanning (BELLES). Circulation. 2005;112(4):563–571. doi:10.1161 /CIRCULATIONAHA.104.512681

Schmermund A, Achenbach S, Budde T, et al. Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter randomized, double-blind trial. Circulation. 2006;113(3):427–437. doi:10.1161/CIRCULATIONAHA.105.568147

Saremi R, Bahn G, Reaven PD, et al. Progression of vascular calcication is increased with statin use in the Veterans Affairs Diabetes Trial (VADT). Diabetes Care. 2012;35(11):2390–2392. doi:10.2337 /dc12-0464

Crandall JP, Mather K, Rajpathak SN on behalf of the Diabetes Prevention Program(DPP) Research Group, et al Statin use and risk of developing diabetes: results from the Diabetes Prevention Program BMJ Open Diabetes Research and Care 2017;5:e000438. doi: 10.1136/bmjdrc-2017-000438

Sattar N  et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet 2010;375:735–42.doi:10.1016/S0140-6736(09)61965-6

Thakker D et al. Statin use and the risk of developing diabetes: a network meta-analysis. Pharmacoepidemiol Drug Saf 2016;25:1131–49.doi:10.1002/pds.4020

Thakker D et al. Statin use and risk of developing diabetes in cardiovascular disease: systematic literature review and meta-analysis. Value Health 2014;17:A478.doi:10.1016/j.jval.2014.08.1378

Ridker PM et al. Cardiovascular benefits and diabetes risks of statin therapy in primary prevention: an analysis from the JUPITER trial. Lancet 2012;380:565–71.doi:10.1016/S0140-6736(12)61190-8

Culver AL et al. Statin use and risk of diabetes mellitus in postmenopausal women in the Women’s Health Initiative. Arch Intern Med 2012;172:144–52.doi:10.1001/archinternmed.2011.625

Mills EJ et al. Efficacy and safety of statin treatment for cardiovascular disease: a network meta-analysis of 170,255 patients from 76 randomized trials. QJM 2011;104:109–24.doi:10.1093/qjmed/hcq165

Baker WL et al. Differing effect of statins on insulin sensitivity in non-diabetics: a systematic review and meta-analysis. Diabetes Res Clin Pract 2010;87:98–107.doi:10.1016/j.diabres.2009.10.008

Nakata M et al. Effects of statins on the adipocyte maturation and expression of glucose transporter 4 (SLC2A4): implications in glycaemic control. Diabetologia 2006;49:1881–92.doi:10.1007/s00125-006-0269-5

Chamberlain LH. Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes. FEBS Lett 2001;507:357–61.doi:10.1016/S0014-5793(01)03007-1

Mikus CR, Boyle LJ, Borengasser SJ, et al. Simvastatin impairs exercise training adaptations. J Am Coll Cardiol. 2013;62(8):709–714

 

 

Cholesterol-Lowering Industry Still Worth More Than $19 Billion and Increasing

The London-based research firm Visiongain has recently published a new report detailing market analysis for cholesterol-lowering drugs for the next ten years. The report itself costs more than $3000 to buy, however, Visiongain have issued a press release containing highlights from the report, which tells us everything we need to know.

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In 2017 the global cholesterol-lowering industry is worth $19.2 Billion and is forecast to grow 4.9% each year during the next five years. Which means that the industry will be worth $24.4 Billion in 2022.

This data flies in the face of the numerous media reports we have seen in recent years referring to statins as cheap, costing a few pennies. Those people supporting the mass use of statins have also tried to claim that the financial incentive to lie to people about statins and cholesterol no longer exists because statins are cheap and most statins are off-patent.  Clearly, the financial incentive to keep this terrible mess going is very much still there.

Back in 2009, I estimated the global cholesterol-lowering industry to be worth around $29 Billion, including both drugs and the revenue food manufacturers receive by marketing cholesterol-lowering or "low in cholesterol" products.

The new market analysis includes a range of drugs in addition to statins including cholesterol absorption inhibitors, ion exchange resins, vibrates, PCSK9 Inhibitors, and others.

In the statins category, Crestor was leading in 2016, being associated with a market share of 26.7%.

The largest clinical trial done on Crestor is the JUPITER trial, which is full of controversy (see the excerpt from Statin Nation below) and the results of this trial have been questioned by other researchers.

The 'New Study' Showing Everyone Needs Statins

Recently, most of the British media ran a story suggesting statins should be taken by millions of people in their 20s and 30s. The articles made statements such as:

Millions of people in their 20s and 30s should be offered statins” Telegraph

Statins DO work” Daily Mail

Statins Cut Heart Deaths by 28%” The Times

Several of the reports made reference to a "new trial", running for 20 years and being the longest of its kind. In fact, the study they are referring to is WOSCOPS and this study was completed in 1995!

The WOSCOPS study included 6,595 men in the West of Scotland, with high cholesterol levels. During this five year study, 1.7% of people who were given the placebo died of heart disease, compared with 1.2% of those who were given the statin. And overall, the use of the statin increased the chances of still being alive after 5 years, from a 96% chance to a 97% chance.

 Pharmaceutical companies are always looking for ways to get more people to consume their products.

Pharmaceutical companies are always looking for ways to get more people to consume their products.

An interesting feature of the WOSCOPS study is that around 80% of the people included were current smokers or ex-smokers. It is well known that smoking drastically increases the risk for heart disease. In fact, the heart disease death rate is 80% higher in heavy smokers than in non-smokers. We also know that smoking causes inflammation and this inflammation can take 5 years to return to normal levels after smoking has been stopped. Heart disease is an inflammatory condition and statins reduce inflammation. Therefore, the slight benefits that were achieved in the WOSCOPS trial back in 1995 could be due to the effect the statin had on inflammation, and it is possible that this had nothing to do with cholesterol at all.

Further evidence for any benefits found in the WOSCOPS study having nothing to do with cholesterol lowering can be seen in the fact that the people in the higher band of total cholesterol level benefited less than those in the lower band. This was also the case for LDL ‘cholesterol’.

The WOSCOPS Follow Up

In 2007, a follow-up study of WOSCOPS was published in the New England Journal of Medicine. For this, researchers undertook a 10 year follow up of the trial participants. There are a number of problems with this follow-up. After the original WOSCOPS trial had ended some of the people who were in the placebo group started taking a statin, and some of those who were in the statin group stopped taking the drug. The researchers did not take account of this in the WOSCOPS follow up study. This means that any results obtained 10 years on are meaningless. The original groups were now mixed with some taking a statin and others not taking one.

To make matters worse, the researchers did not know how many people were taking statins after 5 years – the follow up period was 10 years but they only had data on this aspect for the first 5 years.

Another point is related to the fact that more people got cancer in the group who were originally given the statin. The authors of the study dismissed this as a chance finding.

The data from the WOSCOPS follow up period actually shows that with increasing time, people who were in the original statin group had a higher incidence of cancer than those who were not given the drug.

An accompanying editorial to this study was also published in the New England Journal of Medicine at the time. The author stated that “there should no longer be any doubt that the reduction of LDL cholesterol levels has a role in the prevention and treatment of coronary heart disease”. The Times newspaper also featured this study in an article that took up the whole of the front page. The Times article suggested that “statins have benefits after dosage is stopped” and that statins should be used for even more people, “including younger people in whom heart disease has yet to get a start”.

The 'new study' more recently being reported is a follow-up of the follow-up and has further exaggerated all of the problems associated with the previous follow-up and original study. This kind of post hoc analysis is also unreliable because it is very easy to find data to support what you are looking for, retrospectively, long after the trial was done.

People should be aware that the motivation for this study was to deceive more people into becoming patients for profit and the media reports describing it are lazy and grossly inaccurate.

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Shepherd, J et al. “Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia” New England Journal of Medicine 1995; 333:1301-1308

Ford, I et al. “Long-Term Follow-Up of the West of Scotland Coronary Prevention Study” New England Journal of Medicine 2007; 357:1477-1486