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.

Screen Shot 2018-01-01 at 18.05.49.png

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!


    Statins DO Cause Muscle Damage - New Study

    For decades, many health authorities have played down or even ignored the muscle damage caused by statins. We are repeatedly told that the risk of muscle damage is low.

    However, a new study conducted by the Cleveland Clinic that will be published in the Journal of the American Medical Association, has again confirmed that large numbers of people do indeed suffer muscle damage due to statins.

    This study is unusual because it only included people who had previously reported that they are intolerant to statins - these people were given a statin or a placebo.

    The people who took the statin had a 61% increased risk of muscle damage compared with those who took the placebo. Which shows that people do not just imagine the muscle pain, as has previously been suggested by statin supporters.

    In response to the study Dr Steven Nissen, chairman of Cardiovascular Medicine at Cleveland Clinic, said:

    "The study has important implications for both guidelines and regulatory policy, because it provides strong evidence that muscle-related statin intolerance is a real and reproducible phenomenon.”

    72 million people are eligible for statins in the United States, 12-17 million people in the UK, and millions more in other countries. We already know that most of these people will not obtain any benefit from the statin - they are being exposed to significant adverse effects for no prospect of a health benefit.

    This latest study should prompt our health authorities to rethink the billions of dollars that are being spent on cholesterol-lowering. However, unfortunately, this study is already being used to suggest that patients should simply switch to another, more expensive, medication.

    The study was funded by Amgen Inc., the maker of a PCSK9 Inhibitor - an injection that lowers cholesterol. These PCSK9 Inhibitors have been approved based on the dramatic reductions in cholesterol associated with them - despite that fact that low cholesterol is strongly associated with increased deaths from all causes.

    As a reminder of this, please see the video excerpt below:

    When it suits them, pharmaceutical companies and those experts paid to support pharmaceutical companies, scoff at the suggestion of statin adverse effects. But when they want to get more people to take another product instead, then they will admit to statin damage.



    Strangely the publication itself has been hidden from the general public - only large media organisations can view it prior to the embargo.

    Press release issued by the Journal of the American Medical Association

    The Telegraph - Statins Do Cause Muscle Pain Scientists Conclude


    U.S. Government Lifts Restrictions on Dietary Cholesterol

    Recently, the secretaries of health and agriculture in the United States revised dietary guidelines and said that dietary cholesterol was “no longer a nutrient of concern”.

    The committees have finally acknowledged that there is no link between the amount of cholesterol that is eaten and the level of cholesterol in the blood. This change to the dietary guidelines was suggested last year, and was officially implemented during the first week of January this year.

    As I mentioned in my book, the dietary cholesterol guidelines came out of the cholesterol consensus conference in 1984 - a recommendation was published not to consume more than 250-300mg of cholesterol per day - that’s about the amount of cholesterol found in one egg.

    This recommendation was introduced despite the fact that there was absolutely no evidence at all that dietary cholesterol influences blood cholesterol levels. Something that was also covered extensively in Dr Uffe Ravnskov’s classic text The Cholesterol Myths.

    In fact, even the UK National Diet and Nutrition Survey, published in 2001, stated that “dietary cholesterol has a relatively small and variable effect on blood cholesterol levels”.

    Although this change in the guidelines is a step in the right direction, it really just illustrates the absurdness of the cholesterol idea (or lipid hypothesis) because the authorities are still clinging to the idea that cholesterol and saturated fat causes heart disease. 

    Of course, its not easy for the authorities to accept that they got it wrong for so long, and its not easy for those people who have built a career out of demonising cholesterol either. Like Dr John McDougall (author of several books promoting the avoidance of saturated fat and cholesterol) who has joined a small group of physicians who are suing the agriculture secretary over the change in the guidelines. 

    How Wikipedia, and other Popular Websites Manipulate Our Opinions.

    If you really want to appreciate how we are continuously and ubiquitously misled by a whole range of issues, you just have to pick one topic and investigate that for yourself, in detail, with an open mind. After doing so, the illusionary world immediately crumbles right in front of you, and you can never read any article or listen to any news report in the same way again.

    Investigative journalist Sharyl Attkisson, summarises this well in her TEDex Talk below. She describes how astroturf, or fake grassroots movements funded by political, corporate, or other special interests very effectively manipulate and distort media message. And how the information on Wikipedia is controlled.

    Sharyl, rather appropriately, discusses this with the aid of the example of a fictitious cholesterol medication.

    ‘Bad’ Cholesterol is Very Good for You

    As many will already know, statin medications target LDL ‘cholesterol’ (so called ‘bad’ cholesterol). Much of the medical community believes that lowering LDLs as low as possible is beneficial to health.

    The keenness for lowering LDLs is nothing short of bizarre considering the incredibly important functions that LDLs provide.

    People think that a higher level of LDLs increases the risk for heart disease. This is not correct. One of the very few large scale studies done on this (available here) found that people with heart disease have lower levels of LDLs - yes, lower, not higher.

    LDL ‘cholesterol’ Info Sheet / Poster PDF

    LDL ‘cholesterol’ Info Sheet / Poster JPEG

    Statins Increase Kidney Disease Risk by 30-36%

    A large study, published in the American Journal of Cardiology has found that statins increase the risk of kidney disease by 30 - 36%.

    The study included 43,000 people, with a median 6.4 year follow up. This follow up time is important because statin trials are typically only around 4 years in duration, and in some cases less than 3 years duration. So this new study gives us a rare insight into what happens in the real world with long-term statin use. 

    Acute kidney injury, chronic kidney disease, and nephritis/nephrosis/renal sclerosis were increased in those who took statins.

    Amazingly, one of the lead authors, Dr Ishak A Mansi, said: "patients who are taking statins should not stop taking them based on this study".  Probably, the study could not have been published if this comment was not included. Those people who follow this subject will know that this is a standard line printed in just about every statin study regardless of the actual data or outcomes. 

    The authors did also say that there is an urgent need for more longer-term studies like this one in order to know what statins are really doing to people in the long term.

    Also amazingly, at the same time, the United States Preventative Services Task Force has just come out officially stating their support for the widespread use of statins for people with low risk of heart disease. This task force did not mention the increased kidney disease, or the increase in arterial plaques, or the increased diabetes risks...etc., associated with statin use. 

    The task force article (being pro-statins) has been picked up by some of the large media organisations. Unfortunately, the study showing the increased risk of kidney disease has not - not yet anyway. 


    chronic nephritis 

    chronic nephritis 

    Different People: Different Diets

    Its the time of year when many people start thinking about improving their lifestyle and eating more healthily. Some people will be tempted to follow one of the many fad diets.

    This article is an excerpt from the Ebook 29 Billion Reasons to Lie About Cholesterol, and describes the need for an individual approach to nutrition.

    A multi-billion dollar diet industry has emerged that includes an exhaustive range of fad diets. One of the main differences between each of these diets concerns the proportions of carbohydrate, protein and fat that is recommended. Some experts recommend a low carbohydrate/high protein and fat approach, whereas others advocate a high carbohydrate/low protein and fat program. The recommendations between different diets can be poles apart yet each program has numerous success stories in support of it. How can completely opposite approaches achieve the same results?

    When the authorities establish nutritional recommendations for a whole country, they attempt to provide a simple ‘one size fits all’ set of guidelines. This certainly makes their job easier but unfortunately it bears no relation to the realities of nutritional science. If we look around the world we can see that different cultures have historically eaten very different kinds of foods. Genetically people adapted to the range of foods that were available to them in their immediate environment. Nutritional wisdom was passed down from one generation to the next and each successive generation remained healthy.

    During the 1920s and 1930s a dentist by the name of Dr Weston Price travelled around the world to study the foods eaten by traditional cultures. His work is summarised in a classic book titled Nutrition and Physical Degeneration (1). Dr. Price studied a great variety of different cultures from North American Indians to Australian Aborigines and New Zealand Maori.

    Within each of the cultures he studied, Dr Price found that people stayed healthy as long as they stick to their traditional diets – the foods that were eaten by their ancestors. However, whenever a group of people tried to follow a different diet, and in particular, consumed processed ‘modern’ foods, they became affected by the degenerative conditions that plague the industrialised world.

    Our metabolisms evolve over tens of thousands of years. Modern technology has allowed people to migrate across vast distances but during this time our metabolic makeup has not changed a great deal. Here in the UK, as with many other countries around the world, we have a real melting pot of cultures and genetic heritage. This has resulted in a wide range of different nutritional requirements. Some people may be suited to the general high carbohydrate/low fat diet that is recommended to everyone. However, many other people will not be suited to this and they may need much more protein and fat than carbohydrate in order to have lots of energy and good health.

    Over the last few decades experts have been trying to find the villain in our food. Some say it is carbohydrate, and others blame fat. As we have already seen, dietary saturated fat and cholesterol have bore the brunt of this approach. However, an assessment of nutrition from a global perspective reveals a number of case studies that may help us to learn more about the link between what we eat and our health. The purpose of this chapter is to discuss a few of these examples that demonstrate the need for an individualised approach to nutrition.

    Alaskan Eskimos

    In the early 1920s Dr Victor Levine from the Creighton School of Medicine planned a trip to Alaska to study the health of native Eskimos. In a New York Times article he was quoted as saying: “The Eskimos seem to be more capable of resisting disease and hardships than those of more southern climates. Yet they defy all the known laws of nutrition. They eat large amounts of protein and fats, but are short on other vital elements without which we in this part of the world could not live at all for any length of time” (2).

    Indeed, the native Eskimo at this time was highly admired for having excellent health. Dr Western Price also commented on the health of the native Eskimo, by stating that it was amongst the best that he had encountered on his travels, and that he was “deeply concerned to know the formula of his [the Eskimos’] nutrition in order that we may learn from it” (1).

    Another researcher: Dr Cleave, a surgeon captain in the Royal Navy, was interested in the low rate of heart disease in Eskimo communities. Dr Cleave observed that the Eskimo followed a highly carnivorous diet, being abundant in meat and fat, yet there was an absence of heart disease (3).

    Dr Cleave studied many traditional cultures around the world. He documented the importance of wholesome natural foods and an evolutionary approach to nutrition. In particular, he was concerned with the effect of consuming refined carbohydrates such as white flour. These investigations led to the discovery of what Cleave referred to as the incubation period for degenerative disease. This is related to the amount of time it takes for signs of disease to become apparent within a community after people start consuming refined carbohydrates. Cleave generally found that this incubation period was 20 years for diabetes and 30 years for heart disease.

    Back in 1974, when Dr Cleave published his book summarising his research (3), he had already begun to understand the mechanism by which high blood glucose (sugar) levels damage the arteries and cause heart disease. He also commented on the absurdity of the idea that saturated fat causes heart disease – stating that this idea has no logical foundation from an evolutionary point of view.

    The findings of Dr Levine, Dr Price, Dr Cleave and many others, have since been confirmed by the increasing rates of disease in all countries that increasingly adopt refined foods and abandon traditional foods. Of the many examples of this, the story of the Eskimo is among the most striking. Since when native Eskimos abandon their traditional eating patterns and follow a western diet their rate of diabetes and heart disease increases drastically.

    Native Eskimos in America now have a higher rate of disease than the general population. Having once been studied for their incredibly low rates of diabetes and heart disease, Eskimos who eat western foods suddenly be- come at high risk for these diseases. For example, native Eskimos are now 2.3 times more likely to have diabetes, 1.6 times more likely to be obese, and 1.2 times more likely to have heart disease than their white American counterparts (4).

    The decline in the health of native Eskimos has been more rapid than what has been seen in other cultures. But this was predicted by Dr Price decades ago and it is exactly what would be expected when we look at nutrition from an evolutionary point of view. As stated above, the traditional diet followed by Eskimos consisted mostly of protein and fat based foods. These foods included large quantities of dried salmon (as each piece of fish was broken off it was dipped in seal oil), fish eggs, whale skin and the organs of sea animals. Other foods included caribou, nuts, kelp, and cranberries (1).

    Native Eskimos from Alaska are given the same nutritional guidelines as the rest of the American public. They are advised to eat more fruits and vegetables (up to nine servings a day), eat whole grains, cut down on fatty foods and limit the amount of fat in their diet (5, 6).

    Dietitians and other ‘experts’ focus on reducing the fat content of the diet, but surely attention should be given to the dissimilarities between the traditional Eskimo diet and the one which is now being advised. Traditionally, the Eskimo would simply not have any grain based foods available to them. Neither would they have access to the majority of fruits and vegetables that are found in warmer climates. Their metabolisms have evolved to thrive on protein and fat based foods – the foods that were available to them. Otherwise these people would not have survived.

    It is curious that the most significant health problem among native Eskimos is diabetes. As we have seen in the previous chapter, one of the main contributing factors to the development of diabetes is having high blood glucose levels - being caused by a diet that has a high glycemic load. A high carbohydrate/low fat diet that contains grain based foods has a high glycemic load and causes blood glucose levels to rapidly increase after eating.

    It is logical to suggest that native Eskimos are more susceptible to the adverse effects of a diet that has a high glycemic load. Their metabolisms have historically only had to deal with relatively small amounts of glucose. An Eskimo’s body is not used to dealing with the rapid increase in blood glucose that is associated with a low fat / high carbohydrate diet. It would take tens of thousands of years for them to adapt to this but it has been introduced to them suddenly in just a few decades.

    North American Indians

    American Indians suffer similar rates of obesity, diabetes and heart disease as do native Eskimos (4). The traditional diet of the American Indian was in many cases almost entirely made up of the wild animals of the case (1). This included: deer, buffalo, bear, moose, and fish. A small amount of plant food from berries, wild celery and corn was also eaten (7). When Dr Price visited the American Indians who were following their traditional way of life he was shown how they managed to keep themselves free from diseases such as scurvy.

    When a moose was killed it was opened up at the back and two “balls of fat” just above the kidneys were taken out and cut up into small pieces. Each member of the family was then given a piece to eat. The Indians knew that eating a small amount of this part of the animal would prevent them from getting scurvy (1). The “balls of fat” were in fact the adrenal glands of the animal. We now know that the adrenal glands provide one of the richest sources of vitamin C available from any food. The vitamin C available from the adrenal glands of the moose protected the American Indians from scurvy. They had discovered this nutritional secret long before ‘modern civilisation’ had built laboratories to measure the nutrient content of foods.

    American Indians are advised to reduce their fat intake, eat plenty of fruits and vegetables, eat low-fat cheese, skimmed milk, egg substitutes and soft margarines, and to cook with vegetable oils (7). Again, these guidelines rep- resent a diet that is very different from their traditional diet – which included a large amount of protein and just a small amount of carbohydrate. The glycemic load of the traditional diet would be much lower than the diet that is now being recommended to American Indians. Increasing the glycemic load in this way, can only increase the risk for diabetes and heart disease for these people.

    In addition, low-fat foods that are more heavily processed such as low-fat cheese, skimmed milk and egg substitutes are not whole foods – they are denatured and low in vital nutrients. Whereas the meats that was traditionally eaten were packed with life supporting nutrients. A lower intake of vital nutrients further increases the risk for disease. For example, these nutrients are needed to protect the blood vessels and arteries from damage.

    Australian Aborigines

    Australian Aborigines are probably the oldest living race of people in the world (1). The traditional diet of the Aborigines depended on the district. Those who came from the coastal regions thrived on dugong, sea cow, shell fish and other types of sea food. This was supplemented with some sea plants. Whereas people living in the interior districts thrived on land animals (such as kangaroo and wallaby), eggs, insects, leaves, berries, peas and roots (1).

    Dr Price found that ‘modern’ nutrition was having a disastrous effect on Australian Aborigines. After consuming ‘modern’ foods for a relatively short period of time the fertility of these people had reduced to the point where the death rate far exceeded the birth rate. In summary, Dr Price wrote: “They demonstrate in a tragic way in inadequacy of the white man’s dietary program” (1).

    In the mid 1980s Professor Kerin O’Dea published an article in the journal Diabetes to document how a group of Australian Aborigines virtually recovered from diabetes in five weeks by returning to their traditional diet (8, 9).

    Swiss – Loetschental Valley

    At the time when Dr Price visited Switzerland, the most serious disease for the country as a whole was tuberculosis. However, the beautiful Loetschental Valley had not experienced a single case of this disease. The food here consisted mainly of rye bread and cheese. The cheese was eaten in slices as large (and thick) as the slice of bread and it was made from the milk of cows that grazed on the grass near the snow line of the mountains. This cheese contained natural butter fat, which was the pride of the people and revered for its life-giving properties. All of the dairy foods were unpasteurised and provided an excellent source of vitamins and minerals.

    African Tribes

    Although the Swiss of the Loetschental Valley thrived on a diet that contained a significant amount of grains (in the form of rye bread) certain African tribes have not fared so well. For in Africa, there appears to be a connection between the health of a particular group of people and the portion of the diet that is made up of grain based foods. Table 4A lists some of the African tribes that were studied by Dr Price. Generally, the tribes that consumed larger amounts of animal based foods were much more immune to dental cavities.

    Among tribes who traditionally ate more foods of animal origin (which contained large amounts of saturated fat and cholesterol) it was not uncommon to find a complete absence of dental cavities. However, those tribes that extensively used cereal grains as food had around 6-7% of their teeth affected by dental cavities. It is widely accepted that dental health is a reliable indicator of nutritional status and general health. In addition, the tribes who consumed more animal based foods were generally physically stronger than those following a cereal or grain based diet.

    Animal Vs Plant Based Food

    Researchers with an interest in the evolution of dietary habits and how this relates to health have investigated traditional diets around the world. They have found a huge variety in the composition of traditional diets. For example, the amount of meat that was eaten ranges from 270 grams to 1,400 grams per person per day (10). Figure 4A illustrates the composition of various traditional diets. It can be seen that the percentage of the diet that was made up of animal foods and plant based foods varied tremendously.

    Although there is tremendous variation in traditional diets, it has also been revealed that:
    • 73% of hunter-gatherer societies ate more animal foods than plant foods
    • 14% of hunter-gatherer societies ate more plant foods than animal foods (11)
    In fact, across all hunter-gatherer societies, the median consumption was around 66-75% animal foods and just 26-35% plant foods (11).

    It is well established that humans are omnivores (having the biological requirement to eat both animal and plant foods). However this data shows that animal foods would have been the preferred energy source for the majority of worldwide hunter-gatherers (11).

    In addition, 97% of the world’s hunter-gatherers would have exceeded the fat intake that is recommended to people in the UK and America (11).

    These facts can help to explain why the UK and America, along with other countries, are experiencing a rapid increase in the incidence of diabetes. Genetically, a large proportion of humans are not able to cope with a high carbohydrate/low fat diet. As mentioned above, the high glycemic load of this diet results in high blood glucose levels that can cause or contribute to diabetes.

    High blood glucose levels can also damage the walls of the arteries that supply blood and oxygen to the heart. Some of the mechanisms associated with this are discussed in chapter 12.
    However, it would be inappropriate to suggest that diabetes and heart disease would be eliminated overnight by the ubiquitous adoption of a high protein/high fat diet. Since there are those people who do function best on a low fat / high carbohydrate diet. The challenge is try to establish what proportion of carbohydrate, protein and fat suits you as an individual.

    Two Laws of Nutrition

    The work of Dr Price and numerous other researchers over the last century has been remarkably consistent and has revealed two fundamental laws of nutrition.
    These are:

    1. Food is most nutritious in its natural state (as described in the appendix)
    2. Each person has totally unique requirements for foods based on their genetic heritage and lifestyle. This applies to the macronutrients (carbohydrate, protein and fat) and to micronutrients (vitamins, minerals and trace elements).

    These two simple rules should form the basis of any nutritional guidelines. If these laws are not obeyed, we can be absolutely certain that disease and degeneration will occur. Unfortunately, nutritional advice in the 21st century is heavily influenced by politics and commercial interests. While this is the case, the general public will be subjected to a continuous deterioration in health.

    Finding Your Own Nutritional Requirements

    Dr Roger Williams, the great biochemist who discovered many of the B vitamins, said that at the metabolic level we are all as unique as we are in our fingerprints (12). Our metabolic individuality determines our individual nutritional requirements. This individuality permeates a number of different levels within the body.

    It is of course practically impossible to determine our own individual genetic heritage by working back through our family tree. In order to do this we would have to trace our heritage back for tens of thousands of years. We can however develop ways to measure how our individual metabolism is functioning today.

    Rather than trying to find a simple set of nutritional recommendations to suit everyone, it makes much more sense to develop tools that enable individual people to determine their own individual requirements for foods. A range of these tools already exist. Although, in order to understand each metabolic level it may be necessary to complete several, or a range of metabolic tests.

    This area of metabolic testing is also related to functional medicine - it is evolving all the time and beyond the scope of this book. Suffice to say that it is best to work with a qualified practitioner who is metabolic-individuality-inclined. Failing that, there is a great deal that can be done through trial and error and listening to the way your body responds to different amounts of protein, fat and carbohydrate.

    The main purpose of this chapter is to demonstrate that a ‘one size fits all’ approach to nutrition will never work, and that the idea that everyone should follow a low fat diet is flawed.

    This article is Chapter 4 from the Ebook 29 Billion Reasons to Lie About Cholesterol (2nd Edition). Please click here for more details..