103. Should Everyone Avoid Dairy Because of Results with Breast Cancer?

In the previous blog I explained how Jane Plant successfully cured breast cancer by changing her diet. Essentially she stopped eating milk and dairy products as well as any foods which contained them. (1)

However it is absolutely crucial to appreciate that the experience of Jane does not provide evidence to recommend that everyone should refrain from consuming dairy products. While I accept that the case for not smoking it extremely convincing, we have a long way to go before the same can be said of cows’ milk and any products derived from it.

First of all, although I do not question the success of the strategy for Jane, this certainly does not prove that it will work for everyone else. It is possible that this is so but it is equally possible that it may work for 50%, or 5% or 0.5%,.we simply do not know. Secondly, Jane was receiving chemotherapy at the same time, so did this treatment have a role? Thirdly were there special features about Jane that had a bearing on the outcome. She tells us she used to consume plenty of dairy produce so it may be that eliminating dairy produce from the diet is only effective in such people.

Milk is a very complex food, which consists of a wide range of different constituents. As the elimination of all dairy products prevents breast cancer, we still do not know which particular constituents of milk actively contribute to the development of the cancer. It is important to recognise that there is good evidence that some nutrients present in cow’s milk are particularly valuable. These include the short chain fatty acids which meet the demand for energy quickly and efficiently. Milk fat, especially from cows which have been fed a grass-based diet is one of the few good sources of vitamin K2. Recent research has demonstrated the critical role of Vitamin K2 in the effective utilisation of Vitamins A and D, as well as the mineral calcium (2, 3).

In a meta-analysis based on 6 studies it was found that those with the highest dairy consumption had a reduction of 13% in all-cause mortality compared with those who had the lowest consumption (4). With heart disease an analysis based on 9 separate studies also found a small reduction in death rate for those with a high intake of milk and milk products. For both ischaemic and haemorrhagic strokes the death rates were reduced in those with the highest dairy consumption. There were 5 different studies on the relationship between dairy consumption and diabetes: all of them found that there was a reduction in the incidence with a relatively high intake of milk and milk products. In the light of the totality of these results the authors commented that:

The similarity of the estimates of risk is remarkable and, although conclusions have to be tentative, it seems not unreasonable to conclude that there is no evidence that dairy foods as a total group are associated with harm to health either in terms of death, heart disease, stroke or diabetes, but are probably beneficial in relation to these disease outcomes.”

What is undoubtedly true is that Jane’s result raises many questions which can only be answered by major projects. To the best of my knowledge these have not been started and I doubt if any are planned for the near future. The fundamental problem as Jane herself recognises is that the research emphasis is in finding a drug which is a “magic bullet”. To quote her:

“…modern medical research in general, and especially in the case of cancer research , is aimed at trying to find pure form of a chemical compound which….can be administered in quantitative doses and shown in statistically designed clinical studies to significantly affect the outcome of the disease.”

She goes on to question the validity of this approach and concludes that if this is so, no amount of research and no amount of expenditure will produce the answer. The record to date suggests that she is correct because despite the enormous expenditure on cancer research, the progress achieved has been disappointing to put it mildly.

As mentioned above, the health professionals which Jane encountered showed little interest or understanding of the causes of her breast cancer. This type of attitude seems to be very widespread within the NHS. In fact it is characteristic of most of the medical establishment, especially in the USA, which has a major impact on medicine generally in the West. Nevertheless it is self-evident that unless the actual causes are removed as far as possible then the risks that the cancer will return remain high. In fact these risks may be increased even further by radiotherapy and chemotherapy which damage the immune system and therefore impair the body’s ability to deal with any incipient cancers which occur.

The reality is that the present focus in both research and treatment of cancer is on curing the disease. However if real progress is to be made there must be much greater emphasis on identifying the causes so that preventative action can be taken. It is highly relevant that one of the few areas has been with lung cancer where smoking where smoking tobacco was shown to be a major cause. Consequently the incidence has fallen in men as a result of a decline in the numbers who actually smoke cigarettes. Rather ironically the opposite applies to women, as more and more of them take up the habit.

Finally I must re-iterate the success achieved by Jane Plant. So despite what I have said here, I certainly would not wish to dissuade anyone from eliminating dairy from their diet in an attempt to cure or to prevent breast cancer. In the final analysis it is imperative that individuals makes up their own mind about what will be most suitable for each person.

REFERENCES

  1. http://vernerwheelock.com/?p=522
  2. http://vernerwheelock.com/?p=169
  3. http://vernerwheelock.com/?p=173
  4. http://vernerwheelock.com/?p=243

 

 

102. The Jane Plant Approach to Breast Cancer

Jane Plant is Professor of Geochemistry at Imperial College in London. For 5 years she was the Chief Scientist for the British Geological Survey. In 1987 she was diagnosed with breast cancer, which recurred 5 times and by 1993 had spread to her lymph system. She was not prepared to accept the advice of the conventional medical profession about the treatment and prognosis of her condition without question. Instead she applied her scientific training and expertise to try to identify the actual causes of the disease. As a result she devised simple changes to her diet and lifestyle which produced a complete cure. Her book describes how the story unfolds and contains details which may be used to cure or prevent cancers of the breast and prostate (1).

In this blog I will highlight some of the key points.

As a result of her initial investigations, Jane was astonished to learn how much had been discovered about breast and prostate cancer which was not generally available to the public. In reality there is knowledge of many ‘controllable’ risk factors which could be used to provide advice on how to make simple lifestyle changes that would help to prevent or treat these cancers. In the UK, the risk of developing breast cancer has been increasing progressively for years and would affect about 1 in 12 women at the time the book was written. By contrast, the risks were 50% or more lower in the Far East.

After the breast cancer was diagnosed, Jane agreed to have a mastectomy. While she was visiting the hospital, she repeatedly asked the medical staff what actually caused the cancer so that she could take steps to prevent a recurrence. As she had been advised that excess oestrogen was one of the causes she requested a diet which would reduce her oestrogen levels. Since doctors and nurses had difficulty in answering these questions she was referred to a dietitian, who did not keep a promise to investigate further and failed to respond to telephone calls.

Subsequently Jane made changes to her diet based her work on diets which were considered to be anti-cancer. Despite this about 5 years later, she became aware of a large hard lump under her left arm. This was removed by surgery, followed by a similar procedure to remove another one 2 weeks later. Although there were no signs that the cancer had spread, she agreed to a course of radiotherapy but this did not prevent the development of a small hard lump in a lymph node. After surgical removal, Tamoxifen was recommended, which Jane declined because she was aware it increased the risk of other types of cancer and had known several women on the drug who had died. Unfortunately the cancer re-emerged and this time it was decided that chemotherapy would be the treatment. The procedure involves tests on blood and urine so that the dose can be determined. On one occasion the doctor writing the prescription made a mistake and doubled the previous dose. This was noticed by Jane and a correction was made. However if this had not been detected, she may well have died of liver or kidney failure. The chemotherapy continued and Jane measured the size of the lump regularly, which did not show any decrease.

At this point, Jane decided to approach the problem using all her scientific training and expertise. A study of the different rates of cancer demonstrated the huge differences in the incidence of breast and prostate cancer throughout the world. In particular, the rates for breast cancer in rural China were only about 1/7 the rate of the UK. The difference for prostate cancer is even greater. Even in the industrialised areas of China and Japan the rates are still very much lower. Jane and her husband looked in detail at the information from the China-Cornell-Oxford project based on surveys conducted by a team led by Colin Campbell of Cornell University in the USA. They considered that the differences in cancer rates could be due to the high consumption of soya in the typical Chinese diet but doubted if this was the critical factor. However they then had the bright idea that perhaps milk and milk products would provide the answer to the puzzle. Working on the basis that the part of the body which is diseased is the key to the cause, they concluded that consuming a powerful biochemical from the mammary gland of one species might be sending the wrong signals to the mammary gland of another species, namely the human breast.

Prior to the initial diagnosis of breast cancer, Jane had consumed lots of dairy produce, including skimmed milk as well as low-fat cheeses and yoghurt. Although Jane had made adjustments to her diet, this contained milk, yoghurt and ghee (clarified butter). At this point Jane decided to cease eating all dairy produce immediately, including all other products which use milk or milk products as an ingredient, such as soups, biscuits, cakes.

Although the chemotherapy had not been effective up to that point, within days of commencing the new dietary regime the lump started to shrink. One week after she had eliminated dairy produce from her diet the lump began to soften and reduce in size. Jane continued to monitor the lump and remarkably found a straight line graph between size and time, which indicated that it would disappear completely. Sure enough, after 6 weeks she could find no sign of it. A couple of days later this was confirmed by her cancer specialist. Although the chemotherapy continued at the same time as the altered diet, none of the specialists had ever observed this effect from this type of treatment over a period of 20 years, so the effect must have been caused by the change of diet.

Jane is totally convinced that the link between dairy produce and breast cancer (and probably prostate cancer) is similar to that between smoking and lung cancer. There are some epidemiological studies which are consistent with this conclusion but this type of evidence does not prove “cause and effect”. Nevertheless the experience of Jane certainly cannot be discounted. She is a reputable scientist and there is absolutely no reason to doubt the veracity of her story.

REFERENCE

  1. Jane A Plant (2000) “Your Life in Your Hands: Understanding, Preventing and Overcoming Breast Cancer”. Virgin: London

 

 

 

101 More News from Australia

As I explained in the previous blog (1) Robert Clark has now submitted his report, following the Inquiry he conducted into the actions of Jennie Brand-Miller and Anthony Barclay at the University of Sydney set up in response to allegations made by Rory Robertson. Robertson has now had an opportunity to analyse the report and his comments have just been posted on his website (2).here are some of the key points he makes:

  1.  Five of seven of Professor Clark’s “Preliminary Findings of Fact” are factually incorrect.
  2. Clarke concluded that Statements made by the Complainant alleging that the United Nations FAO has falsified data are serious, and do not appear to be based on detailed evidence or inquiry”.However it is clear from the email correspondence between Robertson and officials at the FAO that this conclusion cannot be substantiated. Quite simply the only relevant information available to the FAO was that produced by the Australian Bureau of Statistics (ABS). Data up to 1999 was produced by the ABS but was discontinued after that because the organisation was not satisfied that it could prepare reliable figures. No doubt this means that there were question marks about the figures which were released for some years prior to this. However as Robertson makes clear the data which FAO produced for the years after 1999 were based essentially on that 1999 value. All of these points were put the FAO in a long and detailed email to FAO officials in December 2012. Apparently there was no reply. As the FAO is obviously using ABS data that lacks credibility, Robertson’s case is compelling and Clark has not provided a valid justification for his conclusion.
  3. Although Clark interviewed Brand-Miller and Barclay he did not interview Robertson. This is rather surprising as it is essential that an even-handed approach is adopted in any investigation of this type. When this is related to the fact that some of the key documentation was apparently not consulted there must be serious questions about the objectivity of the inquiry.
  4. Robertson’s prime objection is that the quality of the data, which have been used to conclude that the consumption of sugar has declined, is poor. This “fact” is absolutely crucial to the formulation of the “Australian Paradox”. This in turn has major implications for the food industry and for the formulation of public health policy.
  5. Clark failed to investigate properly misrepresentation of the information on the changes in soft drink consumption. In the original paper there is a graph which clearly shows that the consumption of sugary soft drinks increased from 35 to 45 litres per person per year between 1994 and 2006. It is obvious to anyone that this is an increase of about 30%. Nevertheless, the authors somehow conclude that there is actually a decrease of 10%. Clearly this is a blatant misrepresentation of what is straight forward information. There was a decline in sugar consumption between 2002 and 2006 which Brand-Miller and Barclay calculated to be 600g per person per year. In fact the correct value is only 150g per person per year. Even if there was small reduction in sugar from soft drinks between 2002 and 2006 this certainly does not conflict with the fact there was an increase of 30% between 1994 and 2006. It is surprising that Clark did not refer to this issue.

Now that I have had a chance to go through the report of the investigator in some detail and also have the benefit of the initial response from the complainer, I am forced to the conclusion that it is not the hard-hitting independent investigation that was needed. It certainly comes across as a “get us out of a hole” report. When questions were first raised it was evident that the authorities in the University of Sydney were not impressed and tried to play things down and hope that Rory Robertson would go away. It is difficult to understand why the academics were given the opportunity to present their case in person but Robertson was not. Furthermore the failure on the part of the investigator to ignore some of the documentation submitted makes one suspect that he did not do a totally thorough job.

Whenever dubious behaviour is alleged or suspected, a very good maxim is to “follow the money”. In this case, there is absolutely no doubt that Charles Perkins Centre is a major part of the University of Sydney operation. It represents a huge investment and the work on glycaemic index is very good income source for the University. It is perfectly understandable that the senior management will be keen to protect it. It is highly likely that Robertson will have been regarded as a bit of a nuisance to be swatted away. As it happens he is made of stern stuff and was not going to go away without a fight.

In these days universities have to fight hard for finance but they also have a responsibility as centres of learning and a duty to uphold standards of integrity and scholarship. The longer this controversy goes on the harder it will be to reach a satisfactory solution. The reality is that this incident has done enormous damage to the reputation of the University of Sydney. The fact that this blog is based at the other side of the world demonstrates the impact is not just restricted to Australia. Robert Clark talks about lessons to be learned but makes no comment about how this has been managed by the University. In fact, the University has a really big problem. It has to clean up this mess. Because of the failure to address the allegations when they were made originally, “the powers that be” will have to consider not just the roles of Brand-Miller and Barclay but also the handling of the issue by the senior management. Above all, they would do well to act on the famous advice of Denis Healey “When you are in a hole, the first thing to do is stop digging!”.

REFERENCES

  1. http://vernerwheelock.com/?p=513
  2. http://www.australianparadox.com/pdf/RR-response-to-inquiry-report.pdf
  3. http://www.australianparadox.com/pdf/FAOfalsifiedsugar.pdf

 

100. Australia: Report on Inquiry into Allegations against University of Sydney Academics

In my previous blog (1) I explained the background to the allegation against Jennie Brand-Miller and Alan Barclay by Rory Robertson. Essentially he argued that the so-called Australian Paradox which claimed that the increased incidence of obesity was not related to an increased consumption of sugar. Robertson concluded that the information showing that the sugar intake had fallen, over the period when obesity had increased was fundamentally flawed.

The University of Sydney commissioned Professor Robert Clark, Chair of Energy Strategy and Policy at the University of New South Wales and a former Chief Defence Scientist of Australia to conduct an Inquiry. He had just delivered his report, which is available on the internet although parts of it have been redacted (2).

The key statement in the Australian Paradox paper is that:

This analysis of apparent consumption, national dietary surveys and food industry data indicates a consistent and substantial decline in total refined and added sugar consumption by Australians over the past 30 years”(3).

Robert Clark dismissed 6 of the 7 allegations which Rory Robertson had made. On the face of it, this might appear to be a satisfactory outcome as far as the academics were concerned. The only allegation which was substantiated referred to the decline in sugar intake from sugar sweetened soft drinks between 2002 and 2006. In the paper Brand-Miller and Barclay has used a value of 600g per person. This figure was wrong. It should have been only 150g.

Nevertheless a close reading of the report shows that all in the garden is not rosy and that there are many lessons to be learned. In particular Clark was not impressed by the quality of the original “Australian Paradox” paper. He concluded that the paper was not tightly written and contained a number of arithmetic errors. He expressed the view that important new findings would usually be published in a high-impact, rigorously peer-reviewed journal. Subsequently the results would be considered in special edition publications of conference journal format. Clearly this had not been done as the original was published in what was regarded as a ‘soft’ journal, where the quality controls are less stringent. As a consequence it was recommended that a new one be prepared which specifically addresses the key factual issues raised in the inquiry. Furthermore this paper should be written in a constructive manner which respects the issues relating to the quality and reliability of data, raised by Rory Robertson.

The crux of the dispute is the conclusion in the Australian Paradox Paper which claims that there has been a decline in the consumption of the sugar from 1980 to 2003 during which time there has been a substantial increase in the incidence of obesity. This is fundamental to the Paradox, which is that the obesity is not caused by sugar, a phenomenon which contrasts with that of many other countries, including the USA and the UK.

However as Robertson has pointed out repeatedly the sources used by Brand-Miller and Barclay are subject to many criticisms. This raises serious questions about the reliability of the data and therefore casts doubt on the conclusions drawn.

The body providing the relevant information is the Australian Bureau of Statistics (ABS). Clark was provided with data from the ABS which showed that there had been a decline in the per capita consumption of sugar between 1975/6 and 1998/9. So the critical issue is to determine the reliability of these data. In correspondence between the ABS and Clark it is accepted that some errors may not have been taken into consideration. More specifically, in order to compute a value for the amount of sugar in the food supply it is essential to have information on all the different sources of sugar. These include all the different foods, especially those which are manufactured, which contain sugar. So in order to work out the total supply, the sugar content of all these foods must be known. This is extremely complicated because there must be variability within products and from time to time. Product formulation is continually changing. A good example is the growth in products which are promoted as “low fat”. Very often these are devised by removing the fat and replacing it with sugar. After 1998/9 the ABS discontinued publication of the figures. One of the reasons was that the ABS believed these conversion values were no longer appropriate. The inevitable question, of course, is “Were they ever accurate and reliable?” On top of all this, all the evidence amassed by Robertson, an experienced economist well used to number-crunching, shows that the trend is UP not DOWN

In view of the absolutely critical importance of the conclusions inherent in the Australian Paradox, it would have been incumbent on the authors to provide a cast-iron case. Clearly they have not done so and it is regrettable that Clark did not reach that conclusion. Furthermore he made no attempt to place this issue in the context of the growing appreciation of the role of sugar in the development of a range of different diseases. Of much greater concern than obesity is Type 2 diabetes (T2D) which in Australia has increased more than 3-fold in the past 30 years or so (4).

It is also becoming clear that sugar intake is a key factor leading to the development of heart disease, many cancers and Alzheimer’s Disease. The evidence continues to accumulate (5). The presence of fructose may be especially damaging to health (6).Bodies such as the World Health Organisation and the American Heart Association now accept that current levels of sugar consumption are not compatible with good health. Hence official recommendations are being reduced significantly.

Despite the somewhat unequivocal findings of Robert Clark there is no doubt that Rory Robertson’s campaign has had a genuine impact and that the credibility of the Australian Paradox has been seriously undermined as shown by some of the local media coverage (7).

REFERENCES

  1. http://vernerwheelock.com/?p=510
  2. http://sydney.edu.au/research/documents/australian-paradox-report-redacted.pdf
  3. A W Barclay & J Brand-Miller(2011) “The Australian Paradox: A Substantial Decline in Sugar Intake over the Same Timeframe that Overweight and Obesity Have Increased” 3. pp491-504
  4. http://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Maternal_Diabetes
  5. http://vernerwheelock.com/?p=325
  6. http://vernerwheelock.com/?p=234
  7. http://www.abc.net.au/radionational/programs/backgroundbriefing/independent-review-finds-issues-with-controversial-sugar-paper/5618490

 

 

99. What on Earth is Going on in Australia?

In February 2013 the official advisory body on nutrition In Australia issued its latest version of the Australian Dietary Guidelines. The report produced by the National Health and Medical Research Council (NHMRC) includes new stringent advice on the consumption of sugar (1). The public is recommended to:

“Limit intake of foods and drinks containing added sugars such as confectionary [sic], sugar-sweetened soft drinks and cordials, fruit drinks, vitamin waters, energy and sports drinks”

Compare this with the advice 10 years earlier in 2003:

Consume only moderate amounts of sugars and foods containing added sugars”

The advice on alcohol is:

If you choose to drink alcohol, limit intake”

So in effect the Australians have decided that sugar should be regarded in the same way as alcoholic beverages.

In reaching this position the Council recognized that the case for limiting sugar intake had become much stronger in the last few years. Consequently there is now convincing evidence that the consumption of sugar sweetened soft drinks (SSBs) is a key factor leading to excessive weight gain in children.

In the period leading up to the preparation of this report there was a serious attempt to cast doubt on the evidence relating to the damaging effects to health of excessive sugar consumption.

A research group in the University of Sydney published a paper which claimed that as the incidence of obesity continued to increase there was actually a decrease of 23% in the total amount of sugar being consumed in Australia between 1980 and 2003. As a result it was concluded that sugar could not possibly be responsible for the growing incidence of obesity, a phenomenon referred to as the Australian Paradox (2).

In an article in “The Australian” Bill Shrapnel, a dietitian and deputy chairman of University of Sydney Nutrition Research Foundation claimed that there was no evidence to justify the recommendation to restrict the intake of sugar (3). In fact he challenged the Council to produce the relevant information. His colleague Professor Jennie Brand-Miller focusing on sugar, distracts attention from saturated fat, salt and alcohol. They both contend that policy is based on myth and that there is no science to support the advice on sugar.

Following these public statement an independent economist, Rory Robertson decided to take an interest. Prior to this he had successfully lost 10 kg simply by restricting his intake of sugar. His experience helped to convince him that sugar (and fructose in particular) is the key to solving the obesity issue. In his view the conclusions of the University of Sydney researchers just did not ring true and so he studied the Australian Paradox paper.

In his opinion the conclusion is demonstrably false for the following reasons:

  • Some of the data presented shows clearly that over the period under consideration the trend is up not down
  • The primary source of their preferred indicator was abandoned as unreliable by the Australia Bureau of Statistics 10 years previously because it was decided that it was impossible to measure how much sugar was imported as it was already present in many thousands of manufactured products
  • The authors failed to mention official information on “sugar availability” which gives a reasonably good estimate of sugar consumption and is relatively high in recent years
  • National dietary surveys, coupled with on data food imports and industry information on soft drink consumption all indicate a high level of sugar consumption.

Robertson concluded:

All in all, we are left with a clear sense that there is no “Australian Paradox”, just an idiosyncratic and unreasonable assessment – and avoidance – of the available sugar data by those who coined the phrase” (4).

Details of the Robertson objections were published in “Business Day” and as a result the journalist Michael Pascoe received a communication from Jennie Brand-Miller (5). In this she claimed that the recent high values of “sugar availability” were caused by the fact that sugar required as a feedstock for the manufacture of ethanol, which is used as a fuel. She wrote that:

“Sugar availability takes no account of food wastage, use in animal food, beer and alcohol fermentation, or in non-food industrial use, and we cannot assume that a steady portion is lost in this way. Globally, raw sugar is an important ingredient for ethanol production. In Australia, ABARE data show that ethanol production as a biofuel for transport rose from 42 million litres to 209 million litres (almost four-fold) from 2005 to 2009.”

It was stated that the increase in ethanol production would require about 14 kg per head if 100% of raw sugar was used to make it. The reply continued:

Although there are no firm figures for how much raw sugar is presently being used for ethanol production, supplies of C-molasses alone are not adequate, and the absolute amounts are likely to be increasing”

Michael Pascoe commented:

“There’s a good reason why there are “no firm figures” – sugar is not used for ethanol production in Australia, as the most cursory of Google searches on Australian biofuels would show.”

In Australia fuel ethanol is produced from red sorghum and waste products from sugar and starch production.

Pascoe then informed the Professor of his findings and she accepted that he was correct.

At this point he assumed that the authors would correct or retract the original paper but instead published the same misrepresentations of the key facts in “Australian Paradox Revisited.”

More recently a group of academics at the University of Western Australia has conducted a detailed examination of the available data on sugar supply and consumption over the last 20-30 years(6). In particular they set out determine if there is sufficiently robust data to support the existence of an Australian Paradox.

They considered that it was essential to find out how much sugar was contained in manufactured products, especially those which had been imported. It was found that if all forms of sugar in the diet are taken into account, which includes sugar contained in processed foods and drinks as well as refined sugar, there was a steady increase in imports between 1988 and 2010. Although there were also exports these were small when compared with the imports. In 2010 there was an estimated

6 g of sugar per capita per day in highly processed food products exported from Australia compared with 30 g of sugar per capita per day imported into the country via similar products.

The FAO data used in the Australian Paradox paper did not include information on sugar present in imported products. The paper concluded when the data on imported food is included that the consumption of sugar was increasing in parallel with the increasing incidence of obesity. This clearly undermines any claim for the existence of an Australian Paradox.

The University of Sydney has conducted an investigation into allegations by Rory Robertson. The report has just been published and I will go through it and report on it shortly.

REFERENCES

  1. http://www.eatforhealth.gov.au/sites/default/files/files/the_guidelines/n55_australian_dietary_guidelines.pdf
  2. http://www.australianparadox.com/pdf/OriginalAustralianParadoxPaper.pdf
  3. http://www.theaustralian.com.au/news/health-science/a-spoonful-of-sugar-is-not-so-bad/story-e6frg8y6-1226090126776
  4. http://www.australianparadox.com/pdf/DitchingSugar27032012.pdf
  5. http://www.smh.com.au/business/pesky-economist-wont-let-big-sugar-lie-20120725-22pru.html
  6. W Rikkers et al (2013) http://www.biomedcentral.com/content/pdf/1471-2458-13-668.pdf

 

98.The High-Cholesterol Paradox

This is a repost by Glyn Wainwright which originally appeared on

bit.ly/1fkGYgb

I am very grateful  to Glyn for permission to post here. He can be contacted at
@Cholesterol_OK

Based upon a presentation to the European Conference WAPF London 2014

Glyn Wainwright MSc MBCS CITP CEng

Independent Researcher, Leeds UK

The Paradox

Being told you have ‘high cholesterol’ is commonly taken as a sign of an unhealthy destiny. Research suggests that for many elderly people the news that they have ‘high cholesterol’ is more often associated with good health and longevity (1).

 

For over 50 years this has been a paradox, the ‘High-Cholesterol Paradox’. What is really going on?

Hypothesis becomes Dogma

In the 1950s the prestigious American MD, Dr Ancel Keys (2), supported a popular theory that heart disease was caused by dietary Fats and Cholesterol (Lipids) circulating in the blood. In 1972 a British Professor, Dr John Yudkin (3), published a book called ‘Pure, White and Deadly’ which proposed over-consumption of refined sugar as the leading cause of diabetes and heart disease. The science was contested by ‘interested parties’, and the matter was resolved by ‘government decree’ in a US Senate report. On Friday January 14th 1977, Senator George McGovern’s Senate Select Committee on Nutrition and Human Needs published ‘Dietary Goals for the United States’.

This document sided heavily with Dr Keys’ lipid theory. Thus ‘hypothesis became dogma’, without the benefit of scientific proof. The McGovern report recommended that we consume more carbohydrates (sugar generating foods) with more limited amounts of fats, meat and dairy. Since the 1970s there has been a rise in the use of High-Fructose Corn Syrups in processed food, and the introduction of low-fat foods which tend to have added sugar to make them attractive to eat.

Until the 1970s there had been a small but consistent percentage of overweight and obese people in the population. By the 1980s obesity rates had begun to climb significantly. This sudden acceleration of obesity is very closely associated with the adoption of new high-sugar, low-fat formulations in processed foods – the consequences of the McGovern report recommendations being adopted around the world.

Advice to reduce our intake of saturated fats, obtained from meat and dairy, caused a rise in the use of plant based oils and so-called ‘vegetable fats’. This was misleadingly promoted as healthy. The biochemical destiny of dietary ‘Saturated Fat’ is not the same as that of excess ‘Carbohydrates and Sugars’.

Fats do not cause obesity or disease. It is the excess sugars (glucose and fructose – High Fructose Corn Syrup HFCS) which create abdominal obesity (4).

The erroneous idea, and fear, of artery blocking fats was exploited to market fat substitutes. Invite anyone talking about ‘artery blocking fats’ to hold a pat of butter in a closed fist. As the butter melts and runs out between their fingers, ask ‘How do fats, which are evolved to be fluids at body temperature, block the vascular ‘pipes’ in our bodies?’

Plant oils are not the natural lipids for maintaining healthy human or animal cell membranes. Animal sourced fats, and essential fatty acids (EFA), are identical to those we require for the maintenance of the healthy human body.

Let us explore some more big anomalies in the last 40 years of dietary health guidance.

Good Cholesterol? Bad Cholesterol? Spot the Difference?

All biochemists can confirm that all cholesterol molecules throughout the known universe are identical in every respect. So how can there be ‘good’ or ‘bad’ cholesterol. It is now possible to frighten people with unscientific descriptions like ‘Good’ and ‘Bad’ when talking about cholesterol.

This single misleading description may have prevented a whole generation from knowing the true causes of the very real disturbance in the levels of fatty nutrients (Lipids) circulating in our blood (4).

Healthy Lipids

If the total blood serum cholesterol (TBSC) is high and the organs are getting enough lipids, the blood lipid circulation is healthy. The large parcels of fatty nutrients (LDL lipids) sent by the liver are consumed by our organs (receptor-mediated endocytosis) and the smaller fatty wrappers and left-over lipids (HDL Lipids) return to the liver. The Fatty Nutrients (LDL) and the recycled lipids (HDL) are in balance. Such a healthy-lipid ‘High-Cholesterol’ person is well nourished and likely to have a long and healthy life.

Damaged Lipids

If the total blood serum cholesterol is high but the fatty nutrient droplets (LDLs) have sugar-damaged labels, the organs are unable to recognise and feed on them. The supply of fatty nutrients to organs is broken.

The liver continues to supply fatty nutrients (albeit with damaged LDL labels), but the organs’ receptors are unable to recognise them. The organs thus become starved of their fatty nutrients. Like badly labelled parcels in a postal service, the sugar-damaged lipids build up in the blood (raised LDL) and fewer empty wrappers are returned to the liver (low HDL).

LDL (erroneously called ‘bad’ cholesterol) is raised in the blood, awaiting clearance by the liver. There is less HDL (erroneously called ‘good’ cholesterol) being returned by the organs.

High Cholesterol (high levels of total blood serum cholesterol TBSC) when caused by damage to the LDL lipid parcels is a sign that lipid circulation is broken. These fats (LDL) will be scavenged to become visceral fats, deposited around the abdomen. This type of damage is associated with poor health

So it really doesn’t matter how high your total blood serum cholesterol (TBSC) is. What really counts is the damaged condition of the blood’s fatty nutrient parcels (LDL lipids). In our research review of metabolic syndromes (4) (e.g. diabetes, heart disease, obesity, arthritis and dementia) we explained that the major cause of lipid damage was sugar-related.

Sugar Damage (AGEs)

The abbreviation AGE (Advanced Glycation End-product) is used to describe any sugar-damaged protein. As we age, excessive amounts of free sugars in the blood (5)may eventually cause damage quicker than the body can repair it. The sugars attach by a chemical reaction and the sugar called fructose is known to be 10 times more reactive, and therefore more dangerous than our normal blood sugar (glucose). Since the 1970s we have been using increasing quantities of refined fructose (from high-fructose corn syrup). Its appealing sweetness, and ability to suppress the ‘no longer hungry’ receptor (6)(ghrelin receptor) is driving excessive food intake. Its ability to damage our fatty nutrients and lipid circulation is also driving waist-line obesity and its associated health problems (4,7).

Checking for Damage in our Lipids

There is a ‘simple to administer’ commonly available blood test used to check for sugar-damage. It is used to check the proteins in the blood of people who are diabetic or at risk of becoming diabetic. It tests for Glycated Haemoglobin (HbA1c) by counting the proportion of damaged molecules (per 1000) of Haemoglobin protein in the blood (mmol/mol). Researchers looking at ways of testing for damage to lipids, have found that sugar-damaged blood protein test (HbA1c), presents a very reasonable approximation of the state of sugar-damage in the blood lipids. Until there is a good general test for sugar-damage in blood lipids, this test (HbA1c) could be a sensible surrogate. This is a better way of assessing health than a simple cholesterol test (TBSC).

Improved sugar-damaged blood protein (HbA1c) scores in diabetic patients is accompanied by improvements in their lipid profiles. This could be very useful to anyone wanting to improve health outcomes by managing lifestyle and nutrition.

Clinical Consequences of Lowering Cholesterol

In 2008 Dr Luca Mascitelli asked me to examine a paper by Xia et al (8). It was very interesting to note that lowering cholesterol by as little as 10% (molecular in cell walls) in the pancreas (pancreatic beta-cells) prevented the release of insulin (cholesterol-mediated exocytosis). This paper described a mechanism by which ‘cholesterol lowering drugs’ directly cause diabetes. It was known that in statin drug trials which looked at glucose (blood sugar) control there was poor blood-sugar control in the statin user groups. Since 2011 the USA government (FDA) required statins to carry a warning about the risk of causing diabetes (9).

Memories are made of this – Cholesterol

The healthy human brain may only be 5% of body weight but it requires over 25% of the body’s cholesterol. The nervous system uses huge quantities of cholesterol for insulation, protection and structure (myelin). F W Pfrieger et al. (10) have shown that the formation of the memory (synapses) is dependent on good supplies of cholesterol.

Post-mortem studies show that depleted cholesterol levels in the cerebrospinal fluids are a key feature of dementias. It was also reported that behavioural changes and personality changes are associated with low levels of cerebrospinal cholesterol.

In another review paper on Dementia we commented extensively on the damage done by fructose and the depletion of cholesterol availability. Low cholesterol levels in the nervous system are not conducive to good mental health.

Consequences of Lowering Cholesterol

Drug treatments which lower cholesterol are acknowledged to cause adverse side-effects (ADRs) in at least 10% of Statin users (11). This figure may be as high as 30%. Conservative estimates indicate that in at least 1% of patients the side-effects are serious enough to be life threatening (e.g. Rhabdomyelitis, Dementia, Behavioural Disorders and Violence).

Our review (12) found that cholesterol lowering therapies were implicated in:

? Damage to muscles (including the heart) and exercise intolerance (13)

? Increased risk of Dementias (Impaired Synaptogenesis and Neuro-transmission) (14)

? Failure of Myelin Maintenance (Multiple Sclerosis Risks) (15)

? Neuro-muscular problems, aches and pains (Amyotrophic Lateral Sclerosis) (16)

? Diabetes (Insulin release inhibited) (8)

? Poor Maintenance of Bones and Joints

? Suppression of protective skin secretions (Apo-B) and increased MRSA infection (17)

Why would anyone want to lower cholesterol

What is needed is a lowering of damage to lipids – caused by sugar.

REFERENCES

1. Weiss, A., Beloosesky, Y., Schmilovitz-Weiss, H., Grossman, E. & Boaz, M. Serum total cholesterol: A mortality predictor in elderly hospitalized patients.

Clin. Nutr. Edinb. Scotl. 32, 533–537 (2013).

2. Mancini, M. & Stamler, J. Diet for preventing cardiovascular diseases: light from Ancel Keys, distinguished centenarian scientist.

Nutr Metab Cardiovasc Dis 14, 52–7 (2004).

3. Yudkin, J.

Pure, white and deadly: how sugar is killing us and what we can do to stop it. (2012).

4. Seneff, S., Wainwright, G. & Mascitelli, L. Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?

Arch. Med. Sci. AMS 7, (2011).

5. Bierhaus, A., Hofmann, M. A., Ziegler, R. & Nawroth, P. P. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept.

Cardiovasc Res 37, 586–600 (1998).

6. Lindqvist, A., Baelemans, A. & Erlanson-Albertsson, C. Effects of sucrose, glucose and fructose on peripheral and central appetite signals.

Regul. Pept. 150, (2008).

7. Seneff, S., Wainwright, G. & Mascitelli, L. Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet.

Eur. J. Intern. Med. 22, 134–140 (2011).

8. Xia, F.et al. Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells.

Endocrinology 149, 5136–45 (2008).

9. FDA publication. FDA Expands Advice on STATIN RISKS. (2014). at http://www.fda.gov/downloads/ForConsumers/ConsumerUpdates/UCM293705.pdf

10. Pfrieger, F. W. Role of cholesterol in synapse formation and function.

Biochim Biophys Acta 1610, 271–80 (2003).

11. Roger Vadon (Producer). BBC File on 4 Statins. (2008).

12. G Wainwright, L Mascitelli & M Goldstein. Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unstable membranes?

Arch. Med. Sci. 5, 289–295 (2009).

13. Hall, J. B.Principles of Critical Care – Rhabdomyolysis and Myoglobinuria. (McGraw Hill 1992, 1992).

14. Mauch, D. H.et al. CNS synaptogenesis promoted by glia-derived cholesterol.

Science 294, 1354–7 (2001).

15. Klopfleisch, S.et al. Negative impact of statins on oligodendrocytes and myelin formation in vitro and in vivo.

J Neurosci 28, 13609–14 (2008).

16. Goldstein, M. R., Mascitelli, L. & Pezzetta, F. Dyslipidemia is a protective factor in amyotrophic lateral sclerosis.

Neurology 71, 956; author reply 956–7 (2008).

17. Goldstein, M. R., Mascitelli, L. & Pezzetta, F. Methicillin-resistant Staphylococcus aureus: a link to statin therapy?

Cleve Clin J Med 75, 328–9; author reply 329 (2008).

 

Continuing Professional Development (CPD) WAPF talk accredited by:

The Naturopathic Nutrition Association

Federation of Nutritional Practitioners (FNTP)

British Association of Applied Nutrition (BAAN)

British Association of Nutritional Therapy (BANT

 

 

 

 

97. NICE but Naughty

So NICE has decided to go ahead with its proposal to recommend that those with a 10% risk of developing heart disease should be considered for treatment with statins. In an article in the BMJ, Professor Mark Baker, the director of the Centre for Clinical Practice at the NICE, stated that 77 people would need to take statins for 3 years for one to benefit (1). He justified this on the grounds that with blood pressure lowering drugs, 104 patients would have to be treated for one to benefit.

My initial reaction is to suggest that it is about time Mark Baker started living in the real world. In my experience, the vast majority of patients agree to take drugs on the strict understanding that it almost certainly will have an impact, which applies to them personally. If patients were actually told that there was only a one in 50 or even a one in a 100 chance that the drug would work in their case, how many would be prepared to undergo the treatment? Furthermore when the possibility of side-effects is factored into the equation, a person would have to absolutely desperate to have the treatment when the possibility of benefit is so small.

Baker’s response reminds me of the good old days in Belfast when somehow or other certain individuals had more than one vote in elections. One person was most indignant when he was accused of having 13 votes, because in reality he only had 9!!!

Surely it is time for legislation to be introduced, which will make it a mandatory requirement for the chances of success as well as the risks of side-effects to be presented to patients before agreeing to any form of drug therapy. After all it is standard practice to spell out the risks and chances of success before a person agrees to an operation so why should treatment with drugs be any different?

So to get back to the statins, let us consider what Baker does not tell us. The figures quoted only apply to those who have heart disease in the past. However when statins are used for primary prevention, which effectively is what is being proposed, there is no benefit in terms of improvement in life expectancy. Although there may be a very small benefit with respect to heart disease and strokes, this is more than outweighed by increased risks of developing diabetes and muscle damage (2). Baker also fails to mention that there is not a shred of reliable evidence to demonstrate that statins have any benefit whatsoever in women. In fact a comprehensive study conducted in Norway has found that for women from about age 60, when most deaths occur, the higher the cholesterol level the greater the life expectancy(3). The justification for using stains is primarily that they will lower cholesterol, which certainly does not make sense in the light of this information.

On side-effects Baker was incredibly complacent. He dismissed claims that GPs had reported seeing far more side effects from statins than were reported in the published trials. In his view:

The best evidence comes from placebo controlled trials, which show similar levels of side effects in statins and in placebos”.

He went on to say:

“Muscle pain has little or nothing to do with statins, and serious complications are extremely rare.” Furthermore the claims of a multitude of side effects:

“simply aren’t true”(1).

These statements beggar belief. As Dr David Newman points out, it often takes years of post-marketing surveillance (i.e., observational) studies and case reports for dangerous side effects to emerge. It is evident that these will not be picked up during trials, which usually focus on benefits and in any case are not specifically designed to get an accurate assessment of the adverse side-effects. A particular example is the Heart Protection Study, which was conducted in 2002 with Professor Rory Collins, director of the CTT project at Oxford University, as one of the leading investigators. This study commenced with 32,000 potential participants, who appeared to meet the criteria for treatment with statins. However about 12,000 of them were removed from the study because they had difficulty tolerating or taking a statin. In the publication of the results, information was limited to 20,000 who actually took part in the trial. What this means is that those with significant side-effects were eliminated before the trial commenced (4).

In the Women’s Health Initiative, data were collected from 153,840 postmenopausal women who were clear of diabetes at the start of the investigation. During the study, 10,242 participants developed diabetes. It was found that those who were on statins were 48% more likely to contract the disease. The results applied to all types of statin medication (5). This is undoubtedly a real effect. During the past 15 years here in the UK the incidence of diabetes has approximately doubled. There must be a strong possibility that the increased usage of statins has contributed to this increase. It is a particularly serious form of ill-health, which is not usually cured by medication.

Other adverse side-effects that have been reported include depression, memory loss, confusion and erectile dysfunction (6).

The reality is that the NICE position on statins is fundamentally flawed in the sense that it totally ignores relevant information which would have a critical influence on the final recommendation. In the past I have acted as external examiner for many Ph.Ds and I have no hesitation in concluding that this report is not up to standard.

It really is time that that Jeremy Hunt and his ministerial colleagues got a grip on things. This latest NICE recommendation will cost about £50 million to implement. Any marginal benefits will undoubtedly be more than counter-balanced by the adverse side-effects. In fact the net effect may well be a further deterioration in public health. There is simply no way that this expenditure can be justified. If this is true of statins, how many other drugs are currently being prescribed regularly for which the benefits are minimal or maybe even damaging to health?

Politicians seem to be cowed into submission by the specialists in the medical world. Yet the reality is that many of the issues are relatively straight forward. People like Mark Baker must not be allowed to get away with sweeping generalizations but should be required to present a proper logical case for the decisions they reach. If the Minister is unable or unwilling to demand answers to the crucial issues then he would be well advised to initiate an independent inquiry, which should be led by a person outside the medical profession and the pharmaceutical industries. A barrister or judge might be the most suitable person for such a task.

Alternatively this could be an ideal opportunity for the Parliamentary Committee on Health to pick up the baton.

The fact is that the current situation is an absolute disgrace and until it is addressed the NHS will continue to spend money on drugs with very little benefit to patients.

REFERENCES

  1. http://www.bmj.com/content/349/bmj.g4694
  2. http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/
  3. http://vernerwheelock.com/?p=105
  4. http://www.huffingtonpost.com/david-h-newman-md/assault-on-science_b_5423957.html
  5. http://archinte.jamanetwork.com/article.aspx?articleid=1108676
  6. http://drmalcolmkendrick.org/2014/06/27/another-backlash-begins/

 

 

96.Has Evidence Based Medicine lost its mind?

NICE has just announced that the proposal for all those with a 10% risk of developing heart disease should be offered statins has been confirmed. Effectively this means virtually everyone because even with the healthiest, fittest person there must be at least a 10% chance heart disease will cause their death. Perhaps “the great and the good” in NICE might care to reflect on what this means in practice. This is neatly illustrated in the story below by Pam Olver. I am very grateful to her for permission to publish it.

She can be contacted via her website at http://thismissionispossible.wordpress.com/enter-here/

And on Twitter @kiwikaidoc

This is Pam

Image

 

 

Posted on Thursday 17 July 2014 by thegintree

Have I lost my Mind? Or has Evidence based medicine failed itself?

Last night was a pretty ordinary night at the accident and urgent medical centre where I was doing an evening rostered shift. There was nothing extraordinary about Ted* (not his real name). In fact there was nothing extraordinary about his presentation either. Just another octogenarian. He could have been your dad or grandad, your brother or uncle. A person, an individual. Someone who is dear to you. Evidence based medicine has turned him into ‘just another octogenarian’. But he is Ted. He is a person, not a number. He is not actually quite the same as any other octogenarian even if they have the same clinical diagnoses. But evidence based medicine has turned everyone like Ted into generic Ted.

Let me tell you more. You can decide what to make of the story. You can decide what you would do.

Ted arrived at the after hours medical centre with his daughter. That’s what they had been told to do. “Arrive after 5 and someone will see you”. He was from out of town and staying with his daughter to recuperate from his foot infection. He had been staying with another daughter who lived a 45 minute drive from his usual place of residence. You see, Ted at the age of 81 was till living independently at his own house, near to his own GP. But he had an infected foot and was staying with his daughter. He then travelled here to stay with another daughter. She wasn’t sure how long it would be for. But he was going to run out of his medication. But the locum GP at his regular practice would not do a repeat prescription for him as he/she hadn’t seen him before. So now he was in my waiting room. He needed more pills and his foot was still painful. Oh, and he was constipated and just wanted a ‘good shit’. He didn’t need to be in an urgent care facility where there are 2 doctors and a full waiting room. He did need care. But this story is not about that kind of care (important nonetheless).

He had the requisite medipac of drugs. I right cocktail. At least he brought them along because he didn’t have a clue what the pills were or what they were for other than he’d had a ‘heart attack’ in January. Prior to this he had been on no medication at all. Nada. Nothing. And he had got to 81. Pretty good in my eyes.

The medicine list:

Aspirin 100mg daily

Metoprolol 23.5 mg daily

Enalipril 2.5 mg bd

Atorvastain 80mg daily (I kid you not!)

Ticagrelor

That’s exactly what happens when Evidence Based Guidelines are used for generic Teds. Except that Ted is Ted, not generic Ted.

But Ted came in also for review and dressings on his sore foot. It looked rather like a diabetic foot to me. He had a lovely macerated digital space between is 4th and 5th toes. But he is not diabetic. His finger prick glucose was 11. Pretty high considering he ate last at lunchtime.

The elephant in the room: are these drugs of any benefit at all for Ted? He has no idea of any benefits. He takes them because the doctor at the hospital discharged him on these because he ‘had a heart attack’. Because that’s everyone who has a heart attack gets. Ted is not everyone. Ted is Ted. What actual benefits will Ted get from this cornucopia of drugs.In all likelihood none at all. And about the side effects and drug interactions?

We know that there is a correlation between statin use and diabetes. And 80mg? Better than poison. We know that beta blockers aren’t that good if you have diabetes. And aspirin in the elderly – quite a high risk of bleeding. And ticagralor? Is there any safety data for use in the elderly? So here is Ted with his muscles very likely affected by his high dose statin, and a sore foot. That increases his risk of falling. So does blood pressure medication. Falls in the elderly have a high morbidity and mortality – broken hips, brain bleeds – and he is on two drugs that can make bleeding worse.

So is it possible then that drug side effects have contributed to his sore foot and increased his morbidity (and mortality) risk? If so, it means that the medicines he has been prescribed ‘because he had a heart attack’ may not be doing anything useful for Ted at all, but may indeed reduce his quality of life. Did anybody bother to ask Ted what he might want for himself. It’s called informed consent.

Ah, well at least Ted might not die from a heart attack. But will he live longer or better?

 

95. Mainstream Nutrition Myths (Debunked by Science)

This is a repost with permission which has been written by Kris Gunnars. I am very grateful to him for his agreement to publish here. This is an up-to-date commentary, which accurately summarises the deficiencies and problems of the current official advice promoted in many different countries.

He can be contacted via his web site which is at http://authoritynutrition.com/about/

Mainstream nutrition is full of nonsense.

Despite clear advancements in nutrition science, the old myths don’t seem to be going anywhere.

Here are 20 mainstream nutrition myths that have been debunked by scientific research.

Myth 1: The Healthiest Diet is a Low-Fat, High-Carb Diet With Lots of Grains

Several decades ago, the entire population was advised to eat a low-fat, high-carb diet (1).

At the time, not a single study had demonstrated that this diet could actually prevent disease.

Since then, many high quality studies have been done, including the Women’s Health Initiative, which is the largest nutrition study in history.

The results were clear… this diet does not cause weight loss, prevent cancer OR reduce the risk of heart disease (2345).

Bottom Line: Numerous studies have been done on the low-fat, high-carb diet. It has virtually no effect on body weight or disease risk over the long term.

Myth 2: Salt Should be Restricted in Order to Lower Blood Pressure and Reduce Heart Attacks and Strokes

 

The salt myth is still alive and kicking, even though there has never been any good scientific support for it.

Although lowering salt can reduce blood pressure by 1-5 mm/Hg on average, it doesn’t have any effect on heart attacks, strokes or death (67).

Of course, if you have a medical condition like salt-sensitive hypertension then you may be an exception (8).

But the public health advice that everyone should lower their salt intake (and have to eat boring, tasteless food) is not based on evidence.

Bottom Line: Despite modestly lowering blood pressure, reducing salt/sodium does not reduce the risk of heart attacks, strokes or death.

Myth 3: It is Best to Eat Many, Small Meals Throughout The Day to “Stoke The Metabolic Flame”

 

It is often claimed that people should eat many, small meals throughout the day to keep the metabolism high.

But the studies clearly disagree with this. Eating 2-3 meals per day has the exact same effect on total calories burned as eating 5-6 (or more) smaller meals (910).

Eating frequently may have benefits for some people (like preventing excessive hunger), but it is incorrect that this affects the amount of calories we burn.

There are even studies showing that eating too often can be harmful… a new study came out recently showing that more frequent meals dramatically increased liver and abdominal fat on a high calorie diet (11).

Bottom Line: It is not true that eating many, smaller meals leads to an increase in the amount of calories burned throughout the day. Frequent meals may even increase the accumulation of unhealthy belly and liver fat.

Myth 4: Egg Yolks Should be Avoided Because They Are High in Cholesterol, Which Drives Heart Disease

 

We’ve been advised to cut back on whole eggs because the yolks are high in cholesterol.

However, cholesterol in the diet has remarkably little effect on cholesterol in the blood, at least for the majority of people (1213).

Studies have shown that eggs raise the “good” choleserol and don’t raise risk of heart disease (14).

One review of 17 studies with a total of 263,938 participants showed that eating eggs had no effect on the risk of heart disease or stroke in non-diabetic individuals (15).

However… keep in mind that some studies have found an increased heart attack risk in diabetics who eat eggs (16).

Whole eggs really are among the most nutritious foods on the planet and almost allthe nutrients are found in the yolks.

Telling people to throw the yolks away may just be the most ridiculous advice in the history of nutrition.

Bottom Line: Despite eggs being high in cholesterol, they do not raise blood cholesterol or increase heart disease risk for the majority of people.

Myth 5: Whole Wheat is a Health Food and an Essential Part of a “Balanced” Diet

 

Wheat has been a part of the diet for a very long time, but itchanged due to genetic tampering in the 1960s.

The “new” wheat is significantly less nutritious than the older varieties (17).

Preliminary studies have shown that, compared to older wheat, modern wheat may increase cholesterol levels and inflammatory markers (1819).

It also causes symptoms like pain, bloating, tiredness and reduced quality of life in patients with irritable bowel syndrome (20).

Whereas some of the older varieties like Einkorn and Kamut may be relatively healthy, modern wheat is not.

Also, let’s not forget that the “whole grain” label is a joke… these grains have usually been pulverized into very fine flour, so they have similar metabolic effects as refined grains.

Bottom Line: The wheat most people are eating today is unhealthy. It is less nutritious and may increase cholesterol levels and inflammatory markers.

Myth 6: Saturated Fat Raises LDL Cholesterol in The Blood, Increasing Risk of Heart Attacks

 

For decades, we’ve been told that saturated fatraises cholesterol and causes heart disease.

In fact, this belief is the cornerstone of modern dietary guidelines.

However… several massive review studies have recently shown that saturated fat is NOT linked to an increased risk of death from heart disease or stroke (212223).

The truth is that saturated fats raise HDL (the “good”) cholesterol and change theLDL particles from small to Large LDL, which is linked to reduced risk (242526).

For most people, eating reasonable amounts of saturated fat is perfectly safe and downright healthy.

Bottom Line: Several recent studies have shown that saturated fat consumption does not increase the risk of death from heart disease or stroke.

Myth 7: Coffee is Unhealthy and Should be Avoided

Coffee has long been considered unhealthy, mainly because of the caffeine. However, most of the studies actually show that coffee has powerful health benefits.

 

This may be due to the fact that coffee is the biggest source of antioxidants in the Western diet, outranking both fruits and vegetables… combined (272829).

Coffee drinkers have a much lower risk of depression, type 2 diabetes, Alzheimer’s, Parkinson’s… and some studies even show that they live longer than people who don’t drink coffee (3031323334).

Bottom Line: Despite being perceived as unhealthy, coffee is actually loaded with antioxidants. Numerous studies show that coffee drinkers live longer and have a lower risk of many serious diseases.

Myth 8: Eating Fat Makes You Fat… so if You Want to Lose Weight, You Need to Eat Less Fat

 

Fat is the stuff that is under our skin, making us look soft and puffy.

Therefore it seems logical that eating fat would give us even more of it.

However, this depends entirely on the context. Diets that are high in fat AND carbs can make you fat, but it’s not because of the fat.

In fact, diets that are high in fat (but low in carbs) consistently lead to more weight loss than low-fat diets… even when the low-fat groups restrict calories (353637).

Bottom Line: The fattening effects of dietary fat depend entirely on the context. A diet that is high in fat but low in carbs leads to more weight loss than a low-fat diet.

Myth 9: A High-Protein Diet Increases Strain on The Kidneys and Raises Your Risk of Kidney Disease

 

It is often said that dietary protein increases strain on the kidneys and raises the risk of kidney failure.

Although it is true that people with established kidney disease should cut back on protein, this is absolutely not true of otherwise healthy people.

Numerous studies, even in athletes that eat large amounts of protein, show that a high protein intake is perfectly safe (383940).

In fact, a higher protein intake lowers blood pressure and helps fight type 2 diabetes… which are two of the main risk factors for kidney failure (4142).

Also let’s not forget that protein reduces appetite and supports weight loss, but obesity is another strong risk factor for kidney failure (4344).

Bottom Line: Eating a lot of protein has no adverse effects on kidney function in otherwise healthy people and improves numerous risk factors.

Myth 10: Full-Fat Dairy Products Are High in Saturated Fat and Calories… Raising The Risk of Heart Disease and Obesity

 

High-fat dairy products are among the richest sources of saturated fat in the diet and very high in calories.

For this reason, we’ve been told to eat low-fat dairyproducts instead.

However, the studies do not support this. Eating full-fat dairy product is not linked to increased heart disease and is even associated with a lower risk of obesity (45).

In countries where cows are grass-fed, eating full-fat dairy is actually associated with up to a 69% lower risk of heart disease (4647).

If anything, the main benefits of dairy are due to the fatty components. Therefore, choosing low-fat dairy products is a terrible idea.

Of course… this does not mean that you should go overboard and pour massive amounts of butter in your coffee, but it does imply that reasonable amounts of full-fat dairy from grass-fed cows are both safe and healthy.

Bottom Line: Despite being high in saturated fat and calories, studies show that full-fat dairy is linked to a reduced risk of obesity. In countries where cows are grass-fed, full-fat dairy is linked to reduced heart disease.

Myth 11: All Calories Are Created Equal, It Doesn’t Matter Which Types of Foods They Are Coming From

 

It is simply false that “all calories are created equal.”

Different foods go through different metabolic pathways and have direct effects on fat burning and the hormones and brain centers that regulate appetite (484950).

A high protein diet, for example, can increase the metabolic rate by 80 to 100 caloriesper day and significantly reduce appetite (515253).

In one study, such a diet made people automatically eat 441 fewer calories per day. They also lost 11 pounds in 12 weeks, just by adding protein to their diet (54).

There are many more examples of different foods having vastly different effects on hunger, hormones and health. Because a calorie is not a calorie.

Bottom Line: Not all calories are created equal, because different foods and macronutrients go through different metabolic pathways. They have varying effects on hunger, hormones and health.

Myth 12: Low-Fat Foods Are Healthy Because They Are Lower in Calories and Saturated Fat

 

When the low-fat guidelines first came out, the food manufacturers responded with all sorts of low-fat “health foods.”

The problem is… these foods taste horrible when the fat is removed, so the food manufacturers added a whole bunch of sugar instead.

The truth is, excess sugar is incredibly harmful, while the fat naturally present in food is not (5556).

Bottom Line: Processed low-fat foods tend to be very high in sugar, which is very unhealthy compared to the fat that is naturally present in foods.

Myth 13: Red Meat Consumption Raises The Risk of All Sorts of Diseases… Including Heart Disease, Type 2 Diabetes and Cancer

 

We are constantly warned about the “dangers” of eating red meat.

It is true that some studies have shown negative effects, but they were usually lumping processed and unprocessed meat together.

The largest studies (one with over 1 million people, the other with over 400 thousand) show that unprocessed red meat is not linked to increased heart disease or type 2 diabetes (5758).

Two review studies have also shown that the link to cancer is not as strong as some people would have you believe. The association is weak in men and nonexistent in women (5960).

So… don’t be afraid of eating meat. Just make sure to eat unprocessed meat and don’t overcook it, because eating too much burnt meat may be harmful.

Bottom Line: It is a myth that eating unprocessed red meat raises the risk of heart disease and diabetes. The cancer link is also exaggerated, the largest studies find only a weak effect in men and no effect in women.

Myth 14: The Only People Who Should go Gluten-Free Are Patients With Celiac Disease, About 1% of The Population

 

It is often claimed that no one benefits from a gluten-free diet except patients with celiac disease. This is the most severe form of gluten intolerance, affecting under 1% of people (6162).

But another condition called gluten sensitivity is much more common and may affect about 6-8% of people, although there are no good statistics available yet (6364).

Studies have also shown that gluten-free diets can reduce symptoms of irritable bowel syndrome, schizophrenia, autism and epilepsy (65666768).

However… people should eat foods that are naturally gluten free (like plants and animals), not gluten-free “products.” Gluten-free junk food is still junk food.

But keep in mind that the gluten situation is actually quite complicated and there are no clear answers yet. Some new studies suggest that it may be other compounds in wheat that cause some of the digestive problems, not the gluten itself.

Bottom Line: Studies have shown that many people can benefit from a gluten-free diet, not just patients with celiac disease.

Myth 15: Losing Weight is All About Willpower and Eating Less, Exercising More

 

Weight loss (and gain) is often assumed to be all about willpower and “calories in vs calories out.”

But this is completely inaccurate.

The human body is a highly complex biological system with many hormones and brain centers that regulate when, what and how much we eat.

It is well known that genetics, hormones and various external factors have a huge impact on body weight (69).

Junk food can also be downright addictive, making people quite literally lose control over their consumption (7071).

Although it is still the individual’s responsiblity to do something about their weight problem, blaming obesity on some sort of moral failure is unhelpful and inaccurate.

Bottom Line: It is a myth that weight gain is caused by some sort of moral failure. Genetics, hormones and all sorts of external factors have a huge effect.

Myth 16: Saturated Fats and Trans Fats are Similar… They’re The “Bad” Fats That we Need to Avoid

 

The mainstream health organizations often lump saturated and artificial trans fats in the same category… calling them the “bad” fats.

It is true that trans fats are harmful. They are linked to insulin resistance and metabolic problems, drastically raising the risk of heart disease (727374).

However, saturated fat is harmless, so it makes absolutely no sense to group the two together.

Interestingly, these same organizations also advise us to eat vegetable oils like soybean and canola oils.

But these oils are actually loaded with unhealthy fats… one study found that 0.56-4.2% of the fatty acids in them are toxic trans fats (75)!

Bottom Line: Many mainstream health organizations lump trans fats and saturated fats together, which makes no sense. Trans fats are harmful, saturated fats are not.

Myth 17: Protein Leaches Calcium From The Bones and Raises The Risk of Osteoporosis

 

It is commonly believed that eating protein raises the acidity of the blood and leachescalcium from the bones, leading to osteoporosis.

Although it is true that a high protein intake increases calcium excretion in the short-term, this effect does not persist in the long-term.

The truth is that a high protein intake is linked to a massively reduced risk of osteoporosis and fractures in old age (767778).

This is one example of where blindly following the conventional nutritional wisdom will have the exact opposite effect of what was intended!

Bottom Line: Numerous studies have shown that eating more (not less) protein is linked to a reduced risk of osteoporosis and fractures.

Myth 18: Low-Carb Diets Are Dangerous and Increase Your Risk of Heart Disease

Low-carb diets have been popular for many decades now.

 

Mainstream nutrition professionals have constantly warned us that these diets will end up clogging our arteries.

However, since the year 2002, over 20 studies have been conducted on the low-carb diet.

Low-carb diets actually cause more weight loss and improve most risk factors for heart disease more than the low-fat diet (7980).

Although the tide is slowly turning, many “experts” still claim that such diets are dangerous, then continue to promote the failed low-fat dogma that science has shown to be utterly useless.

Of course, low-carb diets are not for everyone, but it is very clear that they can havemajor benefits for people with obesity, type 2 diabetes and metabolic syndrome… some of the biggest health problems in the world (81828384).

Bottom Line: Despite having been demonized in the past, many new studies have shown that low-carb diets are much healthier than the low-fat diet still recommended by the mainstream.

Myth 19: Sugar is Mainly Harmful Because it Supplies “Empty” Calories

 

Pretty much everyone agrees that sugar is unhealthy when consumed in excess.

But many people still believe that it is only bad because it supplies empty calories.

Well… nothing could be farther from the truth.

When consumed in excess, sugar can cause severe metabolic problems (8586).

Many experts now believe that sugar may be driving of some of the world’s biggest killers… including obesity, heart disease, diabetes and even cancer (87888990).

Although sugar is fine in small amounts (especially for those who are physically active and metabolically healthy), it can be a complete disaster when consumed in excess.

Myth 20: Refined Seed- and Vegetable Oils Like Soybean and Corn Oils Lower Cholesterol and Are Super Healthy

Vegetable oils like soybean and corn oils are high in Omega-6 polyunsaturated fats, which have been shown to lower cholesterol levels.

But it’s important to remember that cholesterol is a risk factor for heart disease, not a disease in itself.

Just because something improves a risk factor, it doesn’t mean that it will affect hard end points like heart attacks or death… which is what really counts.

The truth is that several studies have shown that these oils increase the risk of death, from both heart disease and cancer (919293).

Even though these oils have been shown to cause heart disease and kill people, the mainstream health organizations are still telling us to eat them.

They just don’t get it… when we replace real foods with processed fake foods, we become fat and sick.

How many decades of “research” does it take to figure that out?

94. Growing doubt on statin drugs — the problem of drug-lifestyle interaction

This is a repost with permission which has been written by Dr John Mandrola. I am very grateful to him for his agreement to publish here.

He can be contacted via his web site which is at http://www.drjohnm.org/

Introduction

My mind is changing about statins. I’m growing increasingly worried about the irrational exuberance over these drugs, especially when used for prevention of heart disease that is yet to happen.

An elderly patient called my office last week to tell me thank you…not for a successful procedure or surgery, but rather, for helping with a problem that had dogged her for a decade. How did an electrophysiologist help a patient without doing a procedure?

I stopped her statin.

A few weeks later, the patient said, her muscle and joint pain were gone. “I thought it was arthritis. I’m walking now. I haven’t felt this good in years. I’ve even lost 5 pounds.”

So why was this elderly patient on a statin?

It was being used to lower cholesterol in the hopes that it would lower the risk of a future heart attack or stroke. This is called primary prevention. The patient had no vascular disease but had a high cholesterol level.

The problem of course is that statins have not been well-studied in elderly women. Her doctor, and the medical establishment writ large, have extrapolated findings of clinical trials on younger mostly male patients to all patients with high cholesterol levels. This is a striking jump to make given that low cholesterol levels in the elderly associate with higher death rates.

Anecdotes are not evidence but this one moved me to review some of the statin evidence. And to think (again) about treating people versus disease.

As always, let’s start with the truth–absolute not relative values. Then I will move on to some new revelations about statins, and then an interesting theory of why potent cholesterol-lowering drugs have such painfully small effects on overall cardiovascular outcomes.

The Truths:

When statins are used in low-risk patients without heart disease (primary prevention) there is no mortality benefit. That’s right. Your chance of dying are the same on or off the drug, regardless of how much the statin lowers the cholesterol level.

When statins are used for primary prevention there is a small lowering of future vascular events (stroke/heart attack) over 5-10 years. The absolute risk reduction is in the range of 7 per 1000. That means you have to treat 140 patients with a statin (for five years) to prevent one event. Or this: for 99.3% of statin-treated patients, there is no benefit. I like to call this the PSR or percent same result.

There is also general agreement that statins increase the risk of developing diabetes, especially in women, and that risk is about the same as preventing a stroke or heart attack, approximately 1%.

Another fact is that patient-level (raw) data from the industry-sponsored cholesterol trials have not been independently analyzed. Systematic reviews from the Cochrane group have analyzed only published data rather than the raw data. There is likely a difference.

There is great debate about the incidence of statin side effects, such as muscle pain, cognitive issues, decreased energy, sexual problems, kidney and liver injury, among others. In the industry-sponsored randomized controlled clinical trials, discontinuation of statins was not significantly different from placebo. Observational data, and the observations of any clinician, provide a different picture.

No statin drug has ever been compared to lifestyle interventions for the prevention of cardiovascular disease.

New Revelations:

A study presented in April 2014 at the Society of General Internal Medicine Meeting in San Diego showed that individuals prescribed statin therapy for high cholesterol consumed more calories and more fat than non-statin users. And, not surprisingly, this increase in calories paralleled an increase in BMI (Body Mass Index) in statin users.

An analysis of a prospective cohort study of men (published in JAMA-IM) revealed that physical-activity levels were “modestly” lower among statin users compared with nonusers independent of other cardiac medications and of medical history.

Possible Connecting Theory: Drug-Lifestyle Interaction

These two recent studies are troublesome. As pointed out in the excellent coverage from heartwire journalist Michael O’Riordan, there may be an interaction between medication and lifestyle. Namely, if statin users consume more calories, gain weight and exercise less it becomes easy to see why cardiovascular benefits are so small.

It’s been really hard to explain why the striking reductions in bad cholesterol (LDL)–up to 30-50%–from statins hasn’t translated into significant future benefit.

One possibility is that cholesterol levels are a lousy surrogate for outcomes. That surely seems true in the elderly, but what about in younger patients and those with familial high cholesterol? These patients are definitely at increased cardio-vascular (CV) risk. So cholesterol levels are surely not unimportant. There is convincing data, for instance, that higher HDL (good cholesterol) levels associate with lower CV risk.

Another possibility for lack of statin benefit is analogous to AF rhythm-control and high blood pressure issues. As in, yes, it’s better to be in regular sinus rhythm and have normal blood pressure, but getting to those goals with pills isn’t the same as being there naturally. With rhythm-control and blood pressure drugs the achievement of the desired outcome is muted by side effects from the drugs. Perhaps it’s the same with statin drugs?

You don’t have to posit malfeasance on the part of big pharma here. All you have to do is think past the disease-specific mindset of modern-day medicine. We are much more than our cholesterol level. A statin drug, like so many drugs which block enzyme pathways far upstream in major cellular pathways, is going to have much more biologic action than just moving an easily measured cholesterol level.

When you step back and look at medications as chemical modifiers of cellular processes in complex biologic systems like our body it’s easy to understand that health comes not from pills. Not even statins.

JMM

REFERENCES

  1. Should people at low risk of cardiovascular disease take a statin? BMJ 2013;347:f6123
  2. The above authors reply to criticism: http://www.bmj.com/content/347/bmj.f6123/rr/678736
  3. The Cholesterol Myth | YouTube video of Australian TV investigative journalism piece: http://youtu.be/F0kIC-dbW2gMore commentary on statin drugs…
  4. CW: Really good news about the safety of statin drugs
  5. Statins are so misunderstood…
  6. Statin drugs are much more than cholesterol lowering agents…