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.


Maier, L et al. Extensive impact of non-antibiotic drugs on human gut bacteria. Nature doi:10.1038/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.

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.

Antibiotic Resistence – World Health Organisation.

Daily Mail.

The Telegraph.

Image Source: Dr Graham Beards at en.wikipedia [CC BY-SA 4.0 ( or GFDL (], 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.


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)!


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.


  • This entry was prompted by a cosmetics feature in the Daily Mail.
  • Image attribution - Wbensmith [GFDL ( or CC 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.


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).


  • 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).


  • 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).



  • 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.



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.



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:


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

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.



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.



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.


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.


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

    Statins Confirmed to Cause Parkinson’s - Implications for Additional Adverse Effects

    A new large study presented at the American Neurological Association Annual Meeting has found a strong connection between cholesterol-lowering medications and Parkinson’s disease. Contradicting previous claims that statins are protective against PD.

    In recent years there has been a considerable effort to try to find new applications for statins. Reports have tried to link statins with positive results on a wide range of conditions, such as: Alzheimer’s, Parkinson’s, Cancer, Multiple Sclerosis and Depression.  These claims have been somewhat surprising considering that the brain and nervous system have the highest requirements for cholesterol and low cholesterol levels are associated with cognition problems, increased suicide, and an increased risk for some types of cancer. Many people have suspected that the data is being carefully cherry picked in an attempt to show a false benefit and expand the use of statins into other areas.

    In the new study, researchers analysed data from the MarketScan Commercial Claims and Encounters database - including information on 30,343,035 persons aged 40 to 65 years. The use of cholesterol-lowering drugs was associated with a significantly higher prevalence of Parkinson's disease.

    This is not the first time that we have seen an absence of the predicted benefits of statins in real life data. For example, a large study in 2011 collected data from 289 of 290 municipalities in Sweden and found that the predicted benefits of statins had not materialised, despite a dramatic increase in statin use.

    An important finding of this new study is that all of the cholesterol lowering drugs included were associated with an increased risk of PD. Suggesting that the harms of the drugs could be directly related to the cholesterol-lowering effect. This adds to the mountain of data that now exists to show that having a low level of cholesterol is worse than having a high level.


    Melville, NA. Statin Use Linked to Increased Parkinson's Risk. Medscape October 26, 2016

    Nilsson, S 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

    Statin Benefits Exaggerated Yet Again

    Media reports from the UK during the last 24 hours have suggested that the benefits of statins have been underestimated and the harms have been exaggerated. These reports are based on research done by the clinical trials service unit at Oxford University. The first thing to note is that although this research group is part of Oxford University, it is funded by the pharmaceutical industry. The group is basically a research facility for the drugs companies. 

    The clinical trials service unit (CTSU) is run by Prof. Rory Collins. People who have been following the statins issue will already know Prof. Collins - he is the guy who tried to use his influence to have scientific papers critical of his research removed from the British Medical Journal. Prof. Collins first agreed to be interviewed for Statin Nation II, but then changed his mind and declined (see video excerpt below).

    Now, Prof. Collins has published a new report in the Lancet, and both the Editor of the Lancet and Prof. Collins have come out making comments in support of statins - making a number of wild claims. In fact, the CTSU and Prof. Collins have for some time now been making claims about statins that no one else can substantiate because they refuse to let anyone have access to their data. The worrying thing is that the claims that the CTSU and Prof. Collins make do not in any way at all fit with everything else we know about statins. For example, the published article in the Lancet and the press release that accompanied it states that if 10,000 people took a statin for 5 years in primary prevention, 500 major vascular events would be prevented (5% absolute risk reduction). Well, that is quite different from what the actual clinical trial data tells us. For example:

    The AFCAPS trial included around 7,000 people and found that the statin reduced the risk of a heart attack by 2.3%. But more people actually died in the group who took the statin. 80 people died in the statin group compared with 77 in the placebo group.

    The ASCOTT-LLA trial included 10,000 people and found that the statin reduced the risk of heart attack by 1%. And if we look at the number of deaths from all causes, there was no benefit associated with the statin.

    Numerous additional studies have confirmed that statin effects are within this ballpark - a reduction in the risk of heart attack by about 1 or 2%, but no actual extension in life expectancy overall. Looking at all of the data, the NNT group estimate that 104 people have to be treated for 5 years to prevent one heart attack (less than 1% absolute benefit). And again, no increase in life expectancy overall.

    Prof. Collins gets much better results for statins than anyone else seems to be able to. No one else is allowed access to his data to confirm these ‘benefits’. The data is owned by the people who make statins. We can all make our own conclusions about what is really going on.


    Drinking Water Better than Statins

    Most people are aware that the human body is mostly made up of water. By volume, two thirds of our cells' content is water. But because the water molecule is so small, a lot of water molecules are needed to make up this two thirds volume. And in fact, calculated in terms of the number of molecules, 99% of our bodies molecules are water molecules. It is perhaps then, not a huge surprise that our hydration status can affect the heart. 

    In 2002, researchers published a study that investigated the amount of water consumed each day and the number of heart disease deaths [2]. 

     Drawn using data from reference [2]. Showing the relationship between the number of 8oz (250ml) glasses of water consumed per day compared with the risk of dying of heart disease. Graph shown includes the data for Men.

    Drawn using data from reference [2]. Showing the relationship between the number of 8oz (250ml) glasses of water consumed per day compared with the risk of dying of heart disease. Graph shown includes the data for Men.

    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.

    None of the people included in this study had any prior signs of heart disease, so for many people, their baseline risk was already low. However, these are still dramatic results in favour of probably the simplest intervention possible - drinking more water. In addition, the results indicate that optimum water intake could be more effective at reducing heart disease mortality than statin medications. 

    Water consumption is not included in any of the cardiovascular risk calculators that doctors use. Since, current clinical guidelines encourage doctors to look for markers that have corresponding medications to treat. Globally, hundreds of billions of dollars have been spent on statins during the last two decades, and that does not even include the financial and health costs associated with the adverse effects of statins. On the other hand, drinking water is almost free and the only side effects are improved health in other areas. 

    As with the interpretation of all studies, we have to be careful about making associations. It has been said many times by many researchers that association does not prove causation. So, in addition to the data we should always ask if there is a plausible biological mechanism.

    The cardiovascular benefits of drinking water are at least in part due to improvements in blood viscosity and blood clotting factors. Increased blood viscosity (an increased general thickness and stickiness of the blood) is well known to increase the risk of heart disease [2-12].  Blood viscosity is a direct measure of the ability of the blood to flow through the vessels - it determines how much friction the blood causes against the vessels and how hard the heart has to work to pump blood and oxygen to organs and tissues. Blood viscosity is therefore a key fundamental aspect of heart disease. Although water intake is not the only factor that can affect blood viscosity, it certainly is one of the factors [13-15]. 

    It is well known within the medical community that heart attacks often happen in the morning and blood viscosity is also often increased in the morning [2,16,17].  During the night, fluid levels are of course not topped up as they are during the day, which could be one factor accounting for increased blood viscosity, and increased hearts attacks in the morning [2].  

    It should also be mentioned that drinks that have a mild diuretic effect, such as caffeinated drinks, can also increase blood viscosity due to fluid loss [18].  


    This is a very short excerpt from the book 101 Causes of Heart Disease: hint cholesterol isn't one of them. To be released 20 October. Preorder is available at a 20% discount.

    “Statins Protect Against Cancer” - Media Gets it Totally Wrong Again!

    This one really is incredible. It shows just how stupid the media have become regarding the reporting of data. I do mean stupid, its not an exaggeration. 

    Yesterday, most of the national newspapers in the UK reported on a study allegedly showing that statin medications dramatically reduce cancer deaths.  

    For example the headline in The Telegraph was:

    Statins linked to dramatically improved mortality rates for cancer patients”

    Researchers from Birmingham’s Aston University in the UK presented data at a medical conference in Italy. This data showed a very strong correlation between high cholesterol levels and a much reduced risk of dying of cancer.

    Actually, there is nothing revolutionary about this study - we have known for a long time that high cholesterol protects against cancer.

    An important paper, published in 2012, authored by Dr Uffe Ravnskov, Dr Kilmer McCully, and Professor Paul J. Rosch, looked at the connection between cholesterol and cancer. Nine studies were described where high cholesterol levels correlated with fewer deaths from cancer. 



    In addition to these studies, data from Japan and Korea also shows a strong correlation between high cholesterol and a greatly reduced risk of cancer.  As can clearly be seen in the screenshots below from Statin Nation II.

     Data from Korea shows a clear relationship between higher cholesterol levels and less liver cancer.

    Data from Korea shows a clear relationship between higher cholesterol levels and less liver cancer.

     Data from Japan also shows less liver cancer at higher cholesterol levels

    Data from Japan also shows less liver cancer at higher cholesterol levels

    The new study that was reported yesterday claimed that statins were responsible for the reduced risk of cancer. This is completely against all logic and common sense. Considering the huge amount of data showing high cholesterol protects against cancer, it is illogical to suggest that cholesterol-lowering statins are providing protection. Of course, we would expect the reverse to be true. And the authors had no basis for their assumptions. The authors did not even look at the number of people who were taking statins - they just made a completely unsubstantiated wild claim. Unfortunately, the main media outlets have long ago lost the ability to stop and think before they regurgitate press releases from research institutions. This is very wrong and very dangerous. 

    The Independent, a national newspaper in the UK, wrote:

    “The scientists said that the tests indicate the blocking of the hormone oestrogen, which causes high cholesterol through statins, could slow cancer growth dramatically.”

    This is a completely nonsensical statement. It simply does not make any sense whatsoever. “Blocking oestrogen”?....”Which causes high cholesterol through statins”? Its just complete nonsense! 

    In fact, if we look at the actual clinical trials that have been done, the PROSPER trial found that cancer diagnosis was more frequent for people who took the statin compared with those who did not. In this trial, any benefits that were achieved by slightly reducing the risk of heart disease were counteracted by the increased risk of cancer associated with the statin. Alarmingly, this was seen even with just three years of follow-up. 

    Another study published in the Journal of the American College of Cardiology also found that any cardiovascular benefits were offset by an increased risk of cancer associated with the statin. 

    It is obvious that the researchers from Aston University are motivated by a desire to receive research funding from the pharmaceutical companies that make cholesterol-lowering drugs. These researchers and the great majority of the media, unfortunately, are not the least bit interested in providing people with accurate health information. 



    Ravnskov,U, McCully,K and Rosch,P. The statin - low cholesterol - cancer conundrum. QJM. 2012 Apr;105(4):383-8

    Shepherd,J et al. Pravastatin In Elderly Individuals At Risk of Vascular Disease (PROSPER): A Randomized Controlled Trial. The Lancet 2002; 360:1623- 1630

    Alsheikh-Ali, AA et al. Effect of the Magnitude of Lipid Lowering on Risk of Elevated Liver Enzymes, Rhabdomyolysis, and Cancer. Journal of the American College of Cardiology 2007; 50:409-418

    The Independent’s article

    The Telegraph’s article

    The Sun’s article

    The Daily Mail's article

    The press release that prompted the 'news' reports

    Creating the ‘High’ Cholesterol Myth - Why Your Cholesterol Level is Normal and NOT High.

    Pharmaceutical companies and those people in the pockets of pharmaceutical companies have altered the definition of high cholesterol in order to increase the number of people who are eligible to take cholesterol medications. This article explains how many people who have been told they have ‘high’ cholesterol, in fact have a normal cholesterol level.

    What is Normal Cholesterol? 

    The measurement and recording of physical, biological and social data reveals that most things exhibit a normal distribution or bell shaped curve. This phenomenon has been observed for centuries. It is the most fundamental and the most widely used concept of statistical analysis. The bell curve has certain characteristics. For example, if we measure the height of the population within a country we would find that most people have an average height, a small number of people are very tall and a small number of people are very short. This is a normal distribution and is represented by the typical bell shaped curve. 

    As would be expected, the range of values that are found for cholesterol levels within a population also follow a normal distribution. And cholesterol levels vary tremendously between different people. Supporters of cholesterol-lowering medications would have us believe that the ideal cholesterol level is below 200 mg/dl (or 5 mmol/l), but we have known for decades that cholesterol varies from 105 mg/dl to 343 mg/dl (or 2.8 to 8.8 mmol/l) in people who are perfectly healthy. The figure below shows the range of cholesterol levels found in healthy people. 

                    Normal Distribution of Healthy Cholesterol Levels

                   Normal Distribution of Healthy Cholesterol Levels

    This same range of cholesterol levels has been seen in people who do have heart disease and people who do not have heart disease, as documented by Professor Brisson using data from the Framingham Study - which is one of the largest studies ever done on cholesterol. 

    Since the Framingham Study, other studies have also confirmed that people with heart disease have the same cholesterol levels as people who do not have heart disease.

    For example, in the UK, the typical person who has a heart attack tends to have the same cholesterol level that is seen for middle-aged and older people in the general population.  Something that is not unique to the UK. 

    A study published in the Lancet, included 5,754 patients from Australia and New Zealand who had already had a heart attack. The average cholesterol level of this group of people was around 220 mg/dl (5.7 mmol/l). Data from the World Health Organization Global Infobase shows that around the same time, the average cholesterol level for the general population was also 220 mg/dl (5.7 mmol/l). People who suffered a heart attack had the same average cholesterol level as the general population. 

    A study published in the American Journal of Cardiology included 8,500 American men with existing heart disease. The average cholesterol level for this group of people was around 215 mg/dl (5.5 mmol/l), which again, according to the World Health Organization is around the same or even slightly lower than the average cholesterol level for the general population. 

    It wasn’t that long ago that we were told anything above 250 mg/dl (6.5 mmol/l) was too high. And over the last few years the threshold has progressively been lowered and lowered - each time without scientific evidence to support the lowering of the threshold, and each time the decision to lower the threshold being taken by experts with links to the companies that make statins. Of course, each time the threshold is lowered, millions more people become eligible for cholesterol-lowering medications - massively increasing the market size for the drugs. 

    And in fact, despite all the hype about cholesterol, many industrialised countries around the world have seen a significant reduction in the average cholesterol level and even greater reductions in the number of people with so called “high” cholesterol - before the widespread use of statins!

    For example, in the United States, the number of people with a cholesterol level above 240 mg/dl (6.2 mmol/l) in 2002 was around half the number in 1962.  A similar trend can be seen in England. 

    The general perception is that people in industrialised countries have high cholesterol as a result of poor lifestyle choices. First of all, the cholesterol level has not risen - it was already falling before the widespread use of statins. Secondly, cholesterol levels are not high, but normal for most people. Thirdly, people with heart disease have the same average cholesterol levels as healthy people. And the fourth point is that cholesterol lowering does not reduce the risk of heart disease.

    For example in the UK, between 1994 and 2006 the percentage of men aged 65 to 74 with ‘high’ cholesterol decreased from 87% to 54%. Despite this, the rate of coronary heart disease for this age group stayed about the same. Other age groups have experienced an increase in the rate of heart disease as the number of people with ‘high’ cholesterol has decreased. 

    Those with vested interests have done a really good job of confusing people about normal cholesterol levels and created a huge amount of unnecessary fear about cholesterol solely for the purpose of turning healthy people into patients. 


    Brisson, G.J., 1981. Lipids in Human Nutrition: An Appraisal of Some Dietary Concepts Jack Burgess, New Jersey 

    Crossman, D. Science, Medicine, and the Future: The Future of the Management of Ischaemic Heart Disease British Medical Journal 1997; 314:356 

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

    Smith, R.L., 1993. The Cholesterol Conspiracy. Warren Green, Missouri 

    Allender S, Peto V, Scarborough P, Kaur A & Rayner M (2008a) Coronary Heart Disease Statistics. Chapter 10 blood cholesterol. London: British Heart Foundation. 

    Allender S, Peto V, Scarborough P, Kaur A & Rayner M (2008b) Coronary Heart Disease Statistics. Chapter 2 morbidity. London: British Heart Foundation. 

    Allender S, Peto V, Scarborough P, Boxer A & Rayner M (2007) Coronary Heart Disease Statistics. Chapter 2 Morbidity. British Heart Foundation: London. 

    Carroll MD et al (2005) Trends in serum lipids and lipoproteins of adults, 1960–2002. Journal of the American Medical Association 294 pp1773–1781. 

    Durrington P (2003) Dyslipidaemia. Lancet 362 717–731. 

    Rubins HB et al (1995) Distribution of lipids in 8,500 men with coronary artery disease. The American Journal of Cardiology 75 1202–1205. 

    Sachdeva A et al (2009) Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in get with the guidelines. American Heart Journal 157 111–117. 

    World Health Organization (2009) Global Infobase [online]. 

    The Rationale for the Use of Statins is (Again) Destroyed

    The diet-heart hypothesis (the basis for the introduction of statin medications) has again been annihilated by two recent studies.

    For about the last 60 years we have been told that eating foods containing saturated fat raises cholesterol levels and this increased cholesterol level causes plaques to form in the arteries - referred to as the lipid hypothesis or the diet-heart hypothesis. 

    Meta-analysis after meta-analysis has failed to show any link between dietary saturated fat and heart disease. And people who have heart attacks have repeatedly been shown to have normal or average cholesterol levels - not high cholesterol. Now, two more studies have recently been published to yet again destroy the diet-heart hypothesis and the basis for the use of statins - which are estimated to be taken by 100 million people around the world.

    The first study, published in the British Medical Journal, examined the validity of the diet-heart hypothesis by recovering and analysing previously unpublished data from randomised control trials. The study found that replacing saturated fat for vegetable oils did lower cholesterol levels, but this did not reduce the amount of heart disease or heart attacks. In fact, for each 30 mg/dL (0.78 mmol/L) reduction in cholesterol there was a 22% greater risk of death.

    This fits with all of the other studies done around the world, going back more than 40 years now, showing that low cholesterol correlates with increased deaths from all causes - in particular, deaths from cancer and other diseases related to the immune system.

     (The picture above is a screenshot from Statin Nation II, showing average cholesterol levels and rate of heart disease deaths for various countries. We can see for example that Lithuania and Portugal have roughly the same average cholesterol levels, but Lithuania has more than four times the number of heart disease deaths.)

    (The picture above is a screenshot from Statin Nation II, showing average cholesterol levels and rate of heart disease deaths for various countries. We can see for example that Lithuania and Portugal have roughly the same average cholesterol levels, but Lithuania has more than four times the number of heart disease deaths.)

    The second study was actually notification that a clinical trial had been stopped. This notification was published by the American College of Cardiology. A trial had started on a cholesterol altering drug called evacetrapib, but the results were so poor that the trial was stopped early.

    On average, patients taking this drug lowered there LDL level (so called bad cholesterol) by 37% and increased their HDL level (so called good cholesterol) by 130%. If we are to believe what we are told about cholesterol, then this should result in dramatic benefits in terms of heart disease reduction, however, the study actually found that these changes in so called ‘bad’ and ‘good’ cholesterol did not result in any reductions in anything at all to do with heart disease - there was no benefit.

    Stephen Nicholls, M.B.B.S, Ph.D., a professor at Australia’s University of Adelaide, cardiologist at Royal Adelaide Hospital and the study’s lead author, said:

    “Here we’ve got an agent that more than doubles the levels of good cholesterol and lowers bad cholesterol and yet has no effect on clinical events,” said  “We were disappointed and surprised by the results.”

    Actually Professor Nicholls absolutely should not be surprised if he has been taking even the most casual look at the medical literature, because this is just history repeating itself. Back in 2007, another drug with a similar name (torcetrapib) was tested in another clinical trial that had to be stopped early.

    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!