154. The Acidity of the Body

These days we are given all sorts of advice on healthy eating. There is much controversy about what actually constitutes a healthy diet. Readers of these blogs will know that there are many criticisms of the current official recommendations. There is a convincing case that complying with these will do more harm than good. Furthermore there is considerable variation in how individuals respond to a particular diet. Therefore it would be very helpful if there was a simple test which would enable people to assess their progress towards achieving good health.
In fact there is evidence which indicates that this can be done by monitoring the pH, which is a measure of the acidity/alkalinity of the body. The pH is a log scale with the range from 0 to 14. Low values are acid and high values are alkaline. A value of 7 is neutral (neither acid nor alkaline). The body pH can be measured using litmus strips on a sample of saliva or urine. The optimum value is about 7.5 which is slightly alkaline. The strips are readily available and inexpensive. It is quite easy for individuals to check their own pH themselves.
Metabolic syndrome (MetS) is defined as a condition characterised by a number of metabolic features including low HDL Cholesterol, raised triglycerides, hypertension, obesity and insulin resistance. These are invariably associated with common chronic diseases such as diabetes, heart disease, various cancers and all-cause mortality. In a recent study with 148 participants it was found that as the number of MetS features increased the pH of the urine decreased progressively. For those with no features the pH was 6.15 but for those with 4 features it had fallen to 5.7 (1).
In a recent European study a total of 66,484 women were followed for 14 years. During this period there were 1,372 cases of type 2 diabetes (T2D). It was found that those with a high acid-forming potential had a much higher incidence of T2D than those with a low value. Interestingly the difference was greater for those with a “normal” Body Mass Index (BMI) than for those who were “overweight“ with a BMI >25 (2). This was the first time that a large prospective study has demonstrated that the dietary acid load was positively associated with T2D risk, independently of other known risk factors,
Other studies have shown that the incidence of T2D is higher in people with a low pH in their urine when compared with those who have a higher urinary pH. The low pH was associated with the uric acid and the presence of stones in the urine. It was found that this condition was prevalent in patients with glucose intolerance and T2D (3).
The famous German Nobel Prize winner, Otto Warburg, discovered that there is only one cause for cancer which is the replacement of the respiration of oxygen in normal body cells by the fermentation of sugar. All normal body cells meet their energy needs by the respiration of oxygen but cancer cells depend on sugar as a source of energy for the fermentation process. Because of this crucial difference between cancer and normal cells, this knowledge can be utilised to devise methods of curing the disease. Protocols which deprive the body of sugar are proving to be effective in this context. Furthermore the fermentation causes the immediate environment of cancer cells to become acidic and therefore reduce the pH below the optimum value of 7.4.
In a highly significant investigation it was noted that the pH range of tumours in mice was between 6.5 and 6.9 (compared with 7.2-7.5 for normal tissue). When the pH was raised by treatment with sodium bicarbonate (baking soda) this resulted in significant reductions in the number and size of metastases to the lungs, intestine and diaphragm (5). The tumours used were models for breast and prostate cancer in humans. This is a practice which has been used successfully for the treatment of various forms of cancer.
Consequently there is considerable interest in understanding the relationship between various foods and their impact on the pH. Various attempts have been made to determine the impact of different foods on the pH of the body.
Chris Woollams has spent years developing his Canceractive website which contains an enormous amount of reliable information which relates to the prevention and curing of cancers. People diagnosed with cancer invariably have an acidic pH and there are strong indications that the consumption of a high proportion on of foods which are known to be alkaline can help to prevent and even cure cancer (6).
These include:
Vegetables
Beetroot, Cabbage, Carrots, Cauliflower, Celery, Cucumber, Fresh green beans, Lettuce
Mushrooms, Parsnips, Potatoes, Spinach, Swede, Watercress
Fresh fruits
Apple, Avocado, Blackberries, Blackcurrants, Cherries, Grapes, Lemons
Olives, Pears, Olives, Raspberries
Others
Fresh ginger, Fresh juices, Green tea, Olive oil, Seeds
By contrast, here are some of the foods which are acidic producers:
Vegetables
Brussel sprouts, Lentils, Peanuts, Rhubarb, Tomatoes
Fruits
Bananas, Grapefruit, Oranges, Plum, Prunes
Others
All alcohol, Coffee, Fizzy drinks, Sauce, Sugar, Sweets

The above list is certainly not meant to be comprehensive and the degree to which individual foods can exercise their effect on the pH does vary and of course will be influenced by the amount consumed.
For those whose pH levels are in the acidic range it should be possible to raise it into the alkaline range by making adjustments to the diet. The alkaline-producing foods should be reduced at the expense of the acid-producing ones. However it is critical to understand that it is the balance that is important. While there are some acid-producing foods which should be kept to a minimum such as fizzy drinks and sugar, there are others such as Brussel sprouts and tomatoes which should be include in a healthy diet. The above information is simply a guide which hopefully will enable a person to try out different possibilities and discover what actually works and what is feasible.
The significant advantage of the pH is that it provides a means by which anyone can monitor their progress in response to dietary adjustments. As things stand at present we do not have absolute proof that the rationale is sound but it is certainly worth trying. There is no suggestion that attempting to alter the pH by dietary means will cause any possible harm. On the face of it, pH should be a routine check as already applies to body temperature or blood pressure. It would be extremely valuable if the research could be instigated which would explore how this could be achieved.

REFERENCES
1. N M Malouf et al (2007) Clinical Journal of the American Society of Nephrology 2 (5) pp883-888
2. G Fagherazzi et al (2013) Diabetologia doi:10.1007/s00125-013-3100-0
3. K Sakhaee et al (2002) Kidney International 62 (3) pp 971-979
4. http://www.healingcancernaturally.com/warburgcancer-cause-prevention.html
5. I F Robey et al (2009) Cancer Research 69 (6) pp 2260-2268
6. http://www.canceractive.com/cancer-active-page-link.aspx?n=978

153. Public Accounts Committee Report on Tamiflu and Publication of Drug Evaluation Results

A report from the House of Commons Public Accounts Committee concludes that information is routinely withheld from doctors and researchers about the methods and results of clinical trials on treatments currently prescribed in the United Kingdom (1). Invariably the bodies responsible for the approval of new drugs only have access to the results of studies which present the drug under investigation in a positive light which those which do not as well as those which show no benefit or even undesirable effects may never be revealed. Essentially this means that the regulatory authorities do not have the total picture which is needed if sound decisions regarding approval for usage are to be made. Although this problem has been recognised for many years there has been a failure on the part of government, industry and the professional bodies to take the necessary action to deal with it. It was recommended that the full methods and results are available to doctors and researchers for all trials on all uses of all treatments currently being prescribed.

The report considered what happened with Tamiflu, which had been stockpiled between 2006-07 and 2012-13, on the basis that it would be needed in the event of a pandemic of influenza. During this time the Department of Health spent £560 on antiviral medicines, of which £424 was for Tamiflu and £136 for Relenza. Valuable insight into the background to this policy can be gained from some of the evidence presented to the Committee by Ben Goldacre author of “Bad Pharma” and Fiona Godlee, editor-in-chief of the British Medical Journal.

With respect to Tamiflu, Fiona referred to the work of a team at the Cochrane Commission led by Tom Jefferson who discovered that there had been about 123 trials conducted on Tamiflu and that the pharmaceutical company Roche was aware of 74 completed trials. Of those, it appears that the European Medicines Agency (EMA) had access to only 15 incomplete accounts. In the UK, the National Institute for Health and Care Excellence (NICE) had received 4incomplete accounts of trials.

She described those involved in Cochrane Commission reviews as

“slightly obsessive and very scientifically determined people”

While it might be expected that the regulatory bodies would require all the evidence to be provided for evaluation in practice according to Fiona they do not ask for it even though they are entitled to have it. Because they are under-resourced and stretched they tend to take the manufacturer’s word for it. By contrast, in Germany, manufacturers have a legal obligation to provide the Institute for Quality and Efficiency in Healthcare (IQWIG), which performs a similar role to NICE, with a full list of clinical trials and supporting clinical study reports.
In a letter to the Chair of NICE, Sir Michael Rawlins, Fiona described the response from IQWIG when it discovered that had not been provided with all the relevant data on reboxitine, a drug produced by Pfizer(2). The company was told it would only approve the drug for reimbursement if all the results were made available to the Institute. The full dataset showed that the drug was ineffective and possibly harmful. This illustrates very effectively how the regulatory bodies can actually be misled and in reality manipulated by the drug companies.
The report implied that those responsible for the expenditure involved in stockpiling the Tamiflu did not have the evidence which clearly demonstrated the efficacy of the drug, especially in the light of the Cochrane report cited above. Hence it is particularly relevant that when the Chief Medical Officer, Dame Sally Davies, was presenting evidence to the Committee she attempted to cast doubts on the credibility of the Cochrane conclusions. In particular she claimed that the Cochrane group

“extracted data from 25 studies but excluded 43 and took no data from published studies.”

The reply to this comment included the following points:
• Not all the trials on conducted on Tamiflu, produced by Roche had been published in the scientific literature
• Not all of those published have been totally accurate. The original results are contained in “Clinical Study Reports” which are extremely detailed and comprehensive. The experience of the Cochrane group has provided examples of discrepancies between the information in these Clinical reports and what appeared in the scientific paper. The group cited 2 examples which stated that:
“there were no drug related serious adverse events”
and
“No serious adverse events were noted in the major trials and no significant changes were noted in laboratory parameters”

However, the equivalent clinical study reports for these two trials describe 10 serious adverse events (in nine participants), some of which were classified as “possibly” related to Tamiflu. They also discovered many of the authors of the scientific papers had not actually seen the raw data. At least one paper had been ghost written.
As a consequence the team decided that there were serious doubts about the reliability of the scientific papers from Roche and that they should restrict their analyses to the original Clinical Study Reports, a strategy which seems entirely reasonable
• There was one study, which was the largest treatment trial of Tamiflu, where the only published information was a 300-word abstract of a conference presentation. The author, Professor Treanor did not participate in the original study and admitted on Channel 4 News that he could not even remember presenting it at a conference in 2000
• Hence it was not correct for Dame Sally to conclude that 42 studies had been excluded. The position was that for 42 studies it was possible to obtain sufficient information to determine their suitability for further assessment and analysis in the review… a very different context

The work of the Cochrane team was fraught with difficulties and in some cases the information was only released in response to Freedom of Information requests and even then there was great reluctance to provide it. The claims of the regulators that they had all the information needed to make sound decisions just do not stand up to rigorous examination.
There is absolutely no reason to doubt the Cochrane conclusion its review has had access to the most extensive data set ever used in these particular drug types and therefore provides a transparent assessment. Consequently it has not been possible to draw conclusions about its effect on complications or transmission. Accepting that it is incomplete at this stage, it is certainly the best that has been produced so far and must carry mush more weight than anything from the regulators who have not had access to such comprehensive evidence.
The Government and the officials in the Department of Health would do well to take note of the Public Accounts Committee Report.

REFERENCES
1. http://www.publications.parliament.uk/pa/cm201314/cmselect/cmpubacc/295/295.pdf
2. http://www.bmj.com/tamiflu/nice

152. You Must Be Nuts!

I have just been watching the video entitled “You must be nuts!” which has been made by Obhi Chatterjee and colleagues. It can be viewed on You Tube here:

The stimulus for this video was to try to understand why Obhi’s father had developed dementia and to identify ways in which the condition could be alleviated. It is absolutely staggering to learn that that the incidence of Alzheimer’s Disease (AD) has increased from about 2% in those over 85 years old about 40 years ago to over 50% to-day. So it cannot be shrugged off on the grounds that it is just because people are getting older. In any case much of the increased life expectancy is the result of reduced infant mortality. In addition, AD is now being detected in young people, which is a new phenomenon.
This is an excellent compilation of information which conveys a prime facie case that changes to our diet, food production methods and medical treatments have combined to produce what is in effect a toxic environment. A number of individuals who can speak with authority on the different aspects have been interviewed and some of the relevant research has been cited. For anyone who is unaware of how bad things have become, the conclusions will come as a great shock. The big advantage of this form of presentation is that the messages come across very clearly and therefore should have a big impact on those who actually take the time to sit down and watch it.
The so-called “Lipid hypothesis”, which is based on the level of cholesterol in the blood (TC) as a risk factor for heart disease, underpins the conventional advice on healthy eating and is the justification for the use of statins. This leads to the conclusion that if we can lower our TC, then we will reduce the risk of heart disease. It is argued that because saturated fat (SFA) in the diet increases TC, it should be reduced and by the same reasoning the polyunsaturates (PUFA) should be increased. As statins lower TC so the story goes, they should be prescribed for virtually all men and women when they reach their 60s. The original work by Ancel Keys which led directly to the Lipid hypothesis has now been totally discredited.
Unfortunately those who have been diligent in following the advice, like the Chatterjee family, are now probably suffering the consequences. There is very convincing evidence that many of the individual fatty acids are actually important nutrients in their own right and play a critical role in supplying energy to the vital organs like the heart and brain. On the other hand, the PUFAs are highly reactive and can be converted to trans fats by various processes including heat, which are damaging to health. As the PUFAs in in “cholesterol lowering” foods such as margarine/spreads are mainly omega-6s the effect has been to increase the omega-6:omega-3 ratio from about 1-4 to 15 or even as much as 50, which is bad news!
But it gets worse. As shoppers try to avoid the fat, they invariably opt for the “low fat” variants. This is absolutely disastrous because not only are they missing out on the fat but also increasing their intake of sugar and/or sweeteners. In fact anyone who chooses processed foods will inevitably increase their intake of sugar because it is added to many of them. There can be no doubt that the increased consumption of sugar and refined carbohydrates is the prime reason why Type 2 diabetes (T2D) has doubled in the last 15 years. Those with T2D have a much increased risk of developing AD, not to mention heart disease, obesity and cancer. AD is often referred to as Type 3 Diabetes.
On top of all this we have the drugs which are being prescribed more and more. The video explains how crucial cholesterol is for brain function and why restricting the supply may have disastrous consequences. This of course is exactly what the statins would do. Despite all the hype, any benefits resulting from the use of statins is very small and is restricted to men who have suffered from heart disease in the past. Then there are other drugs which are also widely prescribed such as aspirin and omeprazole, which is supposed to protect the stomach from the damaging effect of the aspirin. Last May the FDA in the USA, warned against the general use of aspirin for the primary prevention of a heart attack or stroke.
Another concern is the widespread and extensive use of pesticides which may reduce the availability of the minerals in the foods which are being produced. A specific example is Vitamin B12 which is depleted by glyphosate or “Round up”.
To sum up, the case is made that the following factors have combined to cause this serious deterioration in our health as shown by the increased incidence of AD and T2D:
• The unscientific advice, especially to reduce SFA
• Routine use of drugs for the elderly
• High carbohydrate diet/processed foods
• Use of chemical fertilisers and pesticides in horticulture and agriculture.
I strongly recommend that everyone watch this video. It presents a very powerful series of arguments that things have gone badly wrong in the past 40-50 years. The case presented may not be correct in every aspect, but that is not the point. It is vital that these issues are addressed and that the resources are made available to get to the fundamental causes. Despite the comments at the end from Paul Burstow MP, I believe that politicians are reluctant to face up to what is undoubtedly a systemic failure with respect to policy formulation and regulatory controls. This will only change with pressure from the grassroots. Viewing this video should help to generate this pressure.

151. Praluent: New Cholesterol Drugs Get Riskier By The Day

This is a re-post of the article by Francois Lubbe of The Cholesterol Truth. I am most grateful to him for permission to post here.
The original is available at

http://www.thecholesteroltruth.com/praluent-cholesterol-drugs-side-effects-hypercholesterolemia/

Big Pharma seems intent in sticking to its backward way of thinking when it comes to cholesterol. So far their efforts, to create a drug that can prevent heart disease failed miserably.

Fortunately, many people have cottoned onto the fact that lowering cholesterol to ridiculously low levels with drugs is a bad idea because it can seriously put your health at risk. In the last few years, even some mainstream experts are beginning to agree that the Big Pharma has got it all wrong and that cholesterol is not the villain it is made out to be.

As a result, fewer people are taking cholesterol-lowering statin drugs and there is no doubt Big Pharma will feel this in their pockets — these drugs are among the top-selling of all time raking in billions of pounds each year.

However, instead of trying a different approach, Big Pharma and its cronies have their minds set on developing new cholesterol-lowering drugs, which are proving to be even more dangerous.

Cholesterol drugs: Going one step too far

Recently, the pharmaceutical giant Sanofi submitted its application to the European Medicines Agency (EMA) for the approval of a new cholesterol-lowering drug, Praluent (alirocumab).

Praluent is in a class of drug known as PCSK9 inhibitors. It is intended for the treatment of patients with hypercholesterolemia — people with hereditary high cholesterol. PCSK9 promises to reduce LDL cholesterol levels to previously unheard of lows… dangerously low levels!

The bigwigs at Sanofi are probably rubbing their hands together as they wait for the EMA’s approval, because as far as they are concerned they have struck gold.

Statin drugs reduce your cholesterol by blocking an enzyme in your liver that is responsible for making cholesterol. When taking a statin drug, people are usually able to reduce their cholesterol to between 70 and 100 mg/dL. However, patients with hypercholesterolemia usually cannot reach the ridiculously low targets set by the mainstream and that’s where PCSK9 inhibitors come into the picture.

According to Dr. Elliott Antman, president-elect of the American Heart Association and a dean at Harvard Medical School, PCSK9 inhibitors can reduce cholesterol levels to below 50 mg/dL.

That’s just madness! Too low cholesterol levels — even for those with hypercholesterolemia — will make patients vulnerable to a host of health problems. For example, research published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, showed that low cholesterol levels are associated with poor memory and even memory loss in middle-aged adults. That’s because cholesterol helps your brain form memories and it is vital to your neurological function.

Here’s where the prospect of Praluent hitting the market gets a bit more disturbing: When the company submitted its approval for Praluent to the American Food and Drug Administration (FDA), the first thing the agency said was that it was concerned about the neurocognitive side effects these drugs have shown.

That’s right, PCSK9 inhibitors damage your brain.

In fact, the FDA is so concerned about the detrimental effect these drugs can have on your brain that it asked Sanofi to show neurocognitive testing in outcomes trials. In other words, the drug maker needs to show that Praluent won’t fry your brain.

Furthermore, studies have also shown that if your cholesterol levels are too low, and if these low levels begin to affect your brain, you increase your risk of dementia, violent and aggressive behaviour, depression, suicide, cancer, Parkinson’s disease — and likely heart disease, as a result of cholesterol sulphate deficiency.

Cholesterol drugs: It’s time to dig deeper

Yes, that’s right, too low cholesterol levels may cause heart disease. A well-respected researcher at the Massachusetts Institute of Technology, Dr. Stephanie Seneff, recently said in an interview: “Heart disease, is a cholesterol deficiency problem, and in particular a cholesterol sulphate deficiency problem…”

Dr. Seneff points out that all of the information is available in research literature, to support her statement. By carefully dissecting all the research available on heart disease, she has come to the conclusion that the mechanism we call “cardiovascular disease,” of which arterial plaque is a hallmark, is actually your body’s way to compensate for not having enough cholesterol sulphate.

Now there’s a surprise, especially since conventional medicine has been telling us for years that heart disease is due to elevated cholesterol levels and it has been recommending that we lower our cholesterol to extremely low levels… levels that clearly harm our overall health…

Perhaps it’s time for Big Pharma to throw in the towel. Their drugs seem to be becoming more vicious and more damaging and they still have not figured out what really lies at the root of the problem.

And if you pay attention to what Dr. Seneff says, then these snake oil salesmen definitely have been pulling the wool over our eyes for much longer than we know.

As a sufferer of with hypercholesterolemia, one thing is certain, you won’t see me taking a statin drug and you certainly won’t ever see me anywhere near PCSK9 inhibitors.

Heart to a healthy and happy heart,

Francois Lubbe
Editor
The Cholesterol Truth

Sources:

Arteriosclerosis, Thrombosis, and Vascular Biology June 30, 2008

New Cholesterol Drug PCSK9 Is Likely to Prematurely Kill You, published online 03.06.13, articles.mercola.com

Could THIS Be the Hidden Factor Behind Obesity, Heart Disease, and Chronic Fatigue?, published online 17.09.11

Praluent (anti-PCSK9), published online, consensus.druganalyst.com

150. “Pure, White and Deadly”: What Sugar Does to You

Following on from the previous blog (1) based on the epidemiological evidence in John Yudkins’ book “Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do to Stop It” this will focus on results from the experiments conducted with sugar. Here is a selection:
• One way of assessing the capability of the liver to produce fat is to measure the activity of some of the enzymes which are involved in the synthesis of fat. Using young rats it was found that those given sugar had 5 times the activity of one of these enzymes when compared with those not given any sugar. In another study, when sugar replaced starch in the diet of the rats. The activity another enzyme was doubled. With starch it is only glucose that is produced but sucrose is broken down to release both glucose and fructose. This particular result is consistent with other studies which confirm that the role of fructose is different from that of glucose and may possibly be even more damaging. It was also found that the sugar-fed rats show an increase in blood pressure, a deterioration in the ability to cope with high levels of blood glucose, an alteration in the properties of blood platelets and a change in the level of insulin in the blood. These are all observed in people with heart disease. When sugar was included in the diet of pigs, there was an increase in the level of triglycerides, which gives a much better indication of risk of heart disease than total blood cholesterol or LDL cholesterol. There was also an increase in the level of insulin in the blood.
• Studies with young men by Professor Ian MacDonald at Guy’s Hospital in London that consuming sugar for a few days caused a rise in blood triglycerides. With women it was observed in those after the menopause but not before. In Yudkins’ research team, it was found that in a group of 19 young men, they all had raised triglyceride levels after 2 weeks on a high sugar diet. In addition, 6 of them also gained about 2 kgs in body weight, there was an increase in insulin in the blood and the stickiness of the blood platelets increased. All of these changes reverted to the original values when they resumed their usual diet. These results raised a number of interesting issues:
1. The possibility that some individuals are susceptible to a heart attack specifically because of sugar.
2. The increased level of insulin in these men was in agreement with other researchers who had suggested insulin could be a critical factor in the development of atherosclerosis.
3. The rapid gain in weight which provided a clue about the relationship between excess weight and the risks of developing heart disease.
• Further studies with those who showed an increase in insulin concentration, confirmed that after a period on a high sugar diet, the platelets behaved like those of people with atherosclerosis, which returned to normal after cessation of the experimental diet.
• When Dr Robert Ahrens from the USA spent a period with Yudkins in London he studied the effect of sugar in the diet on blood pressure in young men. He observed a rise blood pressure, which was proportional to the amount of sugar added to the diet. In a review on sugar and heart disease he wrote that coronary heart disease:
“continues to increase on a world-wide scale in rough proportion to the increase in sugar consumption but not in proportion with saturated-fat intake”
• In another experiment with those who produced high insulin levels it was found that a 40% rise in insulin after 2 weeks on the high-sugar diet was accompanied by a rise of 300 to 400% in the level of the adrenal hormone. A further study in which volunteers reduced their intake of sugar from150 gms to 55 gms per day showed that this was associated with a reduction of about 30% in the oestrogen level. These findings confirm that the sugar is causing a disturbance in the hormone balance.
• Discussing the significance of these results, Yudkin emphasises that because of the effects of sugar on the liver. kidney and the hormone balance, sugar is a food which does have a considerable impact on the body and the way in which it functions. In particular the disturbance of hormones would explain why sugar may be responsible for a number of different forms of ill-health as well as the differences between individuals. It is known that many people who have definite atherosclerosis have a high level of insulin in the blood. The risk of coronary disease is increased by other factors including cigarette smoking, being overweight , peripheral vascular disease and Type 2 Diabetes (T2D) and all of these are associated with increased insulin in the blood. Similarly, a reduction in excess weight and/or increased physical activity both reduce the risk of heart disease, result in a fall in insulin levels.
However the most compelling reason for believing that insulin, or possibly some other hormone, plays a central role in the development of heart disease is multiplicity of changes that accompany the disease. It is difficult to see how these could occur unless there has been some disturbance of the hormone levels. He considers that insulin is the most likely hormone to be involved. Yudkin suggests that a continuing high-sugar diet means that there is a persistent high demand for the pancreas to produce insulin. Because insulin has many different functions the excess may well be deleterious in other ways, such as upsetting the established hormone balance. It might be expected that the insulin would increase the deposition of fat resulting in obesity. It could also increase the accumulation of fatty material inside the arteries and alter the properties of the platelets thereby leading to atherosclerosis.
CONCLUSION
All of these comments are extremely perceptive. There is now little doubt about the role of insulin not only in heart disease but in a range of other diseases and conditions. There can no question that even if all his ideas do not prove to be absolutely accurate, he has been totally vindicated by the subsequent events. In fact, the incidence of obesity and T2D continued to increase enormously since the second edition of his book. This would have been entirely predictable on the basis of his work. Furthermore, it is self-evident that current policies are failing and failing badly.
It is a great pity that there was no-one in a position to influence policy who recognised the significance of the work of Yudkin and those who had taken a similar stance. The time has come when his ideas must be applied. Unfortunately there is still powerful opposition as politicians and their acolytes continue to defend the indefensible.

REFERENCE
1. http://vernerwheelock.com/?p=680

149. “Pure, White and Deadly”: The Epidemiological Evidence

“Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do To Stop It” is the title of a book written by Professor John Yudkin, who was in the Department of Nutrition at Queen Elizabeth College, London for many years (1). The first edition was published in 1972 and a revised edition appeared in 1986. Professor Yudkin died in 1995 and for many years the book was out of print. However in 2012 Penguin decided to publish it again with an introduction by Robert Lustig, Professor of Pediatrics at the University of California, San Francisco and an ardent campaigner for reducing sugar consumption.
We have now reached a point where there is overwhelming evidence that the official advice to reduce total fat/ saturated fat (SFA) formulated over 30 years was fundamentally flawed. In fact, it is virtually certain this recommendation has been one of the crucial factors contributing to the increased incidence of obesity, Type 2 Diabetes (T2D) and related conditions/diseases. It is arguably the most disastrous policy failures in the field of public health which has ever occurred. The inevitable consequence is that millions of people have suffered and died prematurely.
In order to understand how and why this happened we have to look at the developments in research in the period after the war, when there was a concerted effort, particularly in the USA, to tackle heart disease because it was one of the leading causes of death. It was accepted that the habitual diet was one of the factors involved but 2 different theories emerged. In the USA, Ancel Keys put forward the proposition that excess fat/SFA was a primary cause and therefore the amounts of these constituents in the diet should be reduced. By contrast, John Yudkin argued that the key issue was excessive sugar in the diet. It was of course Keys who prevailed and his views were effectively endorsed by publication of “Dietary Goals for the United States” for the McGovern Committee of Congress in February 1977 (2). An excellent account of the politics and other relevant issues is given by Nina Teicholz in “The Big Fat Surprise” (3).
Once the Americans decided that fat was the key problem, the same approach was adopted by the WHO and so many other countries devised nutrition/public health policies using similar “principles”. It is also meant that anyone who did not follow the party line, including John Yudkin, was effectively marginalised. He must have been extremely frustrated at the time of his death although he has been totally vindicated by the recent developments which I am convinced will inevitably force the politicians to re-shape policies on nutrition and public health.
In the meantime it is fascinating to re-visit “Pure, White and Deadly” to discover what exactly the views and conclusions of John Yudkin about 30 years ago. Here is a selection:
• The view that everything that increases cholesterol in the blood is likely to cause heart disease and vice versa is simplistic and naïve. It has hindered a proper understanding of the disease and its causes, which is why more progress has not been made on prevention. The reality is that there are more extensive disturbances than just a rise in in the blood cholesterol. These a rise in the blood triglycerides, a fall in the HDL cholesterol, changes in the blood glucose similar to those which occur with diabetes, including an increase in the insulin level in the blood. The activity of many enzymes is altered and the behaviour of the blood platelets is changed. As many as 20 different indicators are changed in people with severe atherosclerosis and so it does not make sense to focus specifically on cholesterol, which any case is not a specially reliable indicator of heart disease. All of this has been confirmed by subsequent research and events.
• With reference to the role of fat in heart disease, he notes that few people were not happy about the original work of Ancel Keys which was based on analyses of data which related the amount of fat consumed to the incidence heart disease in 6 different countries to produce a straight line. Although this showed an association it certainly did not confirm cause and effect. However Yudkin commented that the straight line disappeared when data from other countries, were incorporated into the study. More recently Zoe Harcombe has done a detailed critique of the Keys work, which completely destroyed any credibility which still existed (4).
• Epidemiological studies with sugar and heart disease for many countries showed that the there was a closer relationship than with fat. Accepting the limitations of this approach it at least makes the point that the case against sugar is at least as strong as that against fat. In addition the information for Great Britain demonstrated that the rise in sugar consumption preceded very closely the rise in deaths from heart disease. Data from South Africa showed that black population, which consumed little sugar, had a low incidence of heart disease. By contrast, the whites and the Indians who consumed much the same as the British, Americans or Australians, had comparable rates of heart disease. Furthermore, as sugar consumption by the blacks increased there was also an increase in heart disease. A similar picture was observed in Yemenis who moved to Israel. When they arrived, the incidence of heart disease was relatively low but it increase as they adapted to the typical diet in Israel, which has a high sugar content. Coronary disease is common on the island of St Helena where the residents consume less fat than in the USA or Great Britain, are very active because there is little mechanical transport and cigarette smoking is limited. However their consumption of sugar is about 40 kg per year which is high. It is clear that the totality of the epidemiological evidence is undoubtedly consistent with the case that sugar is a prime (but not the only) factor causing heart disease.
• In order to go beyond the study of populations, Yudkin and colleagues decided to investigate the sugar consumption of individuals to see if there was any differences between those with heart disease and those without. In one study, patients who had just suffered their first heart attack were compared with a control group. The sugar intake of the coronary patients was 113 gms per day but in the controls it was 58 gms per day. This study was criticised on the grounds that it had not been blinded (those obtaining the data knew which people had suffered a heart attack). In a second study, blinding was done but the results were essentially similar. The coronary patients were consuming 74 gms per day. This time there were 2 control groups: one had 67 gms and the other 74 gms per day. This type of study had NEVER been done for fat. Once again, the results were consistent! Although Yudkin goes to great pains to emphasise that this evidence does not constitute absolute proof and even if sugar is shown to be a cause of heart disease it will not be the only one.
THE NEXT BLOG CONTINUES WITH MORE FROM JOHN YUDKIN

REFERENCES
1. John Yudkin (2012) “Pure, White and Deadly” Penguin London ISBN: 978-0-241-96528-3
2. http://zerodisease.com/archive/Dietary_Goals_For_The_United_States.pdfin
3. Nina Teicholz. (2014)“The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” Simon & Shuster: New York
4. Zoe Harcombe (2010) “The Obesity Epidemic” Columbus

148. BMJ Joins the Debate on Saturated Fat

When the article entitled “Saturated fat is not the major issue” by cardiology specialist DR Aseem Malhotra appeared in the BMJ there were over 30 responses. These give us a valuable insight into the debate.
Dr Malhotra concludes that the advice to reduce saturated fat (SFA) has increased the risks of cardiovascular disease (CVD) rather than lowered them. In particular he refers to the evidence that SFA reduces the large buoyant LDL particles (Type A) which are protective when it is the small dense LDL particles (Type B) that are implicated in CVD. He also notes that a number of prospective cohort studies have indicated that SFA are actually protective for CVD.
The article has received substantial press coverage but it is especially useful to consider the points raised by those who made responses. At the time of writing there had been 33 responses of which 14 were generally supportive, 7 were opposed and effectively supported the status quo and the remaining 12 did not take a position.
Here is a selection of the points raised by the respondents:
• Mark Burkitt was critical of both supporters and critics of Dr Malhotra because many of them argued their case solely from the position of statistical ‘risk factors’ without any attempt to consider the underlying mechanisms. Nevertheless he agreed with the main thrust of the article. There is strong evidence that the key factor is the oxidation of the LDL Cholesterol and therefore the focus should be on understanding what causes this and how it can be prevented. Unfortunately diets which are high in polyunsaturates and low in SFA can logically be expected to promote the oxidation of the LDL Cholesterol (2). Essentially the same point was made by Richard Hoffman who advocated a diet rich in antioxidants in order to reduce/prevent the oxidation of the LDL Cholesterol
• Alison Tedstone and Vicki Pyne of Public Health England presented the current UK government position that SFA should be no more than 11% of total food energy. This was based on the advice of the Scientific Advisory Committee on Nutrition. They refer to a Cochrane Collaboration systematic review which concluded that reducing saturated fat by reducing and/or modifying dietary fat intakes lowered the risk of cardiovascular events by 14% (3). However they failed to mention that there were no clear effects of modified fat diets on total or cardiovascular mortality, despite the inclusion of over 13,000 participants in studies of over six months which presents a rather different picture. A few days earlier I had pointed out that the intake of SFA had fallen from 56.7 g/day in 1969 to 29.2 g/day in 2000. Furthermore the target set in 1984 to reduce SFA from 20% to 15% of food energy had been reached in 2003. Over this period the incidence of obesity had continued to increase. In men it had doubled since 1993. Furthermore since 1994 the incidence of diabetes has more than doubled for both men and women. Regrettably these contributors made no attempt to answer my question that if reducing SFA in the past had obviously not produced the predicted results, how can we justify that it will succeed in the future.
• Peter Clifton claimed that the article had done a disservice to the public debate on nutrition. He cited one paper in which hundreds of experiments had showed that SFA elevates LDL cholesterol (4). It is difficult to understand the significance of this statement as the main focus of this paper was the ratio of Total Cholesterol: HDL Cholesterol. In fact the authors emphasised the dubiousness of relying on cholesterol alone as a marker of the risk of coronary artery disease. Although many studies predict the effects of the various fats on the fats in the blood, this cannot determine whether a fat will cause the disease. It is all too true that many people simply ignore this important proviso and assume that changes in the blood fats automatically reflect the impact on the incidence of heart disease.
• Malcolm Kendrick, a GP in Cheshire and author of “The Great Cholesterol Con” was particularly enthusiastic about the article. He commented that for those who look at the evidence rather than accept the dogma, the facts are clear. SFA is healthy, trans fats are not. The recent epidemic of obesity has been driven by the lunacy of replacing fat with sugars.

The above contribution just about sums up the current position. Those critical of Dr Malhotra are either nit-picking or have to rely on sources which have been discredited time and time again. How often do people have to be told that an association does not demonstrate “cause and effect”? On the other it is very encouraging that so many of the respondents have come to the same conclusion as Dr Malhotra. When the recommendations on fat and SFA were initially devised it was accepted that final proof did not exist but it was confidently predicted that it would emerge from major investigations which were planned or were already in progress. As it happens, these studies failed to deliver the expected results. There has been enormous success in reducing the intake of SFA in the UK and in many other countries with a similar type of food supply. Despite this, obesity is now prevalent and diabetes continues to increase. There is now convincing evidence that it is the increase in sugars and refined carbohydrates which is responsible for the deterioration of public health. The emphasis on SFA has been a great mistake. Unfortunately there are still many people, especially those in a position to implement a totally re-vamped healthy eating policy, who fail to recognise reality. The tragedy is that until this is put into place large numbers will continue to suffer poor health and premature death. Hopefully the positive response to the Malhotra paper will increase the pressure needed to bring about change.

REFERENCES
1. http://www.bmj.com/content/347/bmj.f6340
2. http://www.bmj.com/content/347/bmj.f6340?tab=responses
3. L Hooper et al (2012) Cochrane Database of Systematic Reviews 5 Art. No.: CD002137. DOI: 10.1002/14651858.CD002137.pub3
4. R P Mensink et al (2003) American Journal of Clinical Nutrition 77 (5) pp111

147. Avandia: More Bad News About the Drug Industry

In a previous blog (1) I explained how concerns about the increased incidence of heart attacks associated with treatment for diabetes by the drug Rosiglitazone (marketed by GSK under the brand name Avandia) had resulted in an investigation by the US Senate Finance Committee. The committee staff had access to about 250,000 documents and produced a comprehensive report which revealed details of the way in which one major drug company conducted its’ business (2).
A paper by Nissen and Wolski in 2007 was the first public warning that there might be serious side-effects with Avandia (3). However the Senate report was able to investigate what was known within the company before this.
In response to the Nissen/Wolski alert GSK published an interim report of its’ own trial referred to as “RECORD” (4). According to one of their senior executives in a sworn statement in 2007 this was:
“very reassuring”.
In a letter to The Lancet, GSK maintained that RECORD trial was “compelling evidence” for the safety of Avandia
Despite these claims it was apparent that some executives in GSK were aware of the limitations of the RECORD trial. A briefing document in June 2005 noted that the results of RECORD will not be available until 2009 and that the current observed endpoint is very much lower (about 3.5% per annum) than anticipated in the original protocol (11% per annum).
A slide presentation devised in 2004 acknowledged that RECORD did not have sufficient “power”, which means that the study would not provide enough data to test for cardiovascular safety. One reason could be that the number of participants was too small to detect a genuine difference between the treatments used. The slide presentation also revealed that RECORD was primarily a marketing exercise and was designed to counter the results of PROactive, a trial with a similar type of drug, namely Actos. This product was produced by the Japanese company Takeda and was regarded as the main competitor to Avandia.
This was demonstrated by an email in June 2005, which discussed the need to respond to PROactive which included the following:
“Clearly no patients will be recruited until [we] have made a decision based on the go-no go criteria from the PROactive data. However, there is a great deal of EU commercial push to initiate this study in 2005.’’
A briefing document for a meeting in July 2005 stated that:

“Publication of the PROactive data may result in important commercial disadvantage in Europe. We therefore have the opportunity to start a CV (CardioVascular) outcomes study with the aim of getting superiority data in 2007”

In fact the possibility that Avandia might be responsible for an increase in problems linked to heart disease had emerged as early as 2004. Notes of a meeting held in June state that:
“There was disappointment verbalized about the morbidity and mortality table that showed that there were ten ischemia-related adverse events in the rosiglitazone group versus five events in the placebo group.”

Later in 2004, GSK initiated a clinical trial to compare Avandia with a placebo which involved 11,586 participants. Analysis of the data in 2005 found that the Hazard Ratio (HR) for myocardial ischaemia was 1.29. This means that those patients treated with Avandia were 29% more likely to have a heart attack than those on the placebo. This is not too far away from the value of 43% in the Nissen /Wolski report. In a further clinical trial with 14,237 patients, analysis of the results in 2006 produced a HR of 1.31, which essentially confirmed the finding of the previous trial.
The experience of Dr John Buse of the University of North Carolina is especially relevant because it not only demonstrates another nasty aspect of the GSK culture but also shows that questions had been raised about the cardiovascular safety of Avandia as early as 1999. This issue was considered by the Senate Finance Committee in 2007. Here is an extract from its report:
“In particular, GSK’s attempt at intimidation appears to have been triggered by speeches that Dr. Buse gave at scientific meetings in 1999. During those meetings, Dr. Buse suggested that, aside from its benefit of controlling glucose levels in diabetics, Avandia may carry cardiovascular risks. The effect of silencing this criticism is, in our opinion, extremely serious. At a July 30, 2007, safety panel on Avandia, FDA scientists presented an analysis estimating that Avandia caused approximately 83,000 excess heart attacks since coming on the market. Had GSK considered Avandia’s increased cardiovascular risk more seriously when the issue was first raised in 1999 by Dr. Buse, instead of to smother an independent medical opinion, some of these heart attacks may have been avoided.
According to documents provided to the Committee by, among others, GSK, and the University of North Carolina, it is apparent that the original allegations, regarding Dr.Buse and GSK’s attempts at silencing him are true; according to relevant emails, GSK executives labelled Dr. Buse a “renegade” and silenced his concerns about Avandia by complaining to his superiors and threatening a lawsuit.
Even more troubling, documents reveal that plans to silence Dr. Buse involved discussions by executives at the highest levels of GSK, including then and current CEO Jean-Pierre Garnier. Also, GSK prepared and required Dr. Buse to sign a letter claiming that he was no longer worried about cardiovascular risks associated with Avandia. After Dr. Buse signed the letter, GSK officials began referring to it as Dr. Buse’s “retraction letter.” Documents show that GSK intended to use this “retraction letter” to gain favour with a financial consulting company that was, among other things, evaluating GSK’s products for investors. After cutting short Dr. Buse’s criticism, GSK executives
then sought to bring Dr. Buse back into GSK’s favour. While publicly silent subsequent to signing the “retraction letter,” Dr. Buse still remained troubled about Avandia and its possible risks. Years later, he wrote a private email to a colleague detailing the incident with GSK:
“[T]he company’s leadership contact[ed] my chairman and a short and ugly set of interchanges occurred over a period of about a week ending in my having to sign some legal document in which I agreed not to discuss this issue further in public.”

Dr. Buse ended the email, “I was certainly intimidated by them…. It makes me embarrassed to have caved in several years ago.”

“GSK’s behaviour since the Committee first brought these allegations to light has been less
than stellar. Instead of acknowledging the misdeed to investors, apologizing to patients, and pledging to change corporate behavior, GSK launched a public relations campaign of denial. Specifically, GSK sent out a press release entitled
“GSK Response to US Senate Committee on Finance” which stated that the allegations raised by the Committee were “absolutely false.” Further, CEO Jean-Pierre Garnier denied having any knowledge of the alleged intimidation of Dr. Buse in an interview that ran in July in The Philadelphia Enquirer” (4).

CONCLUSION
There is little doubt that on the basis of this evidence GSK has been totally irresponsible and that the recent bribing in China cannot be dismissed as an isolated event. The reality is that this is a company which is totally unscrupulous and has been responsible for an estimated 83,000 excess cases of heart disease, many of whom died as a consequence. GSK is one of the leading global players and its’ approach to business may well be typical of the industry as a whole. Despite the reports of the Senate Finance Committee, there is no convincing evidence that there has been any significant change in company culture. How many more people will die prematurely before governments decide to address this issue?
REFERENCES
1. http://vernerwheelock.com/?p=463
2. Available at http://www.finance.senate.gov/newsroom/chairman/release/?id=bc56b552-efc5-4706-968d-f7032d5cd2e4
3. S E Nissen and K Wolski (2007) New England Journal of Medicine 356 (24) pp 2457-2471
4. P D Home et al (2007) New England Journal of Medicine 357 (1) pp 28-38
5. http://www.finance.senate.gov/newsroom/ranking/release/?id=3a1d9e3e-6ea8-4200-a86f-8aadc9338f5e

146. Hanging on for Dear Life

In his third Reith Lecture Dr Atul Gawande, focuses on the approach by doctors to patients with diseases which may be terminal (1). One of the big changes that has occurred in the last 50 years or so has been the increase in the number of people who now die in hospital or other institutions, currently about 8 out of 10 deaths. Dr Gawande is especially concerned that the medical profession could do a lot better in the way it deals with these people. He describes how his daughter’s music teacher contracted cancer that was almost certainly terminal but that he felt incompetent to decide what was best for her. As a cancer surgeon, he could operate but while that might give her extra time it would also make her feel worse. On the other hand he was not comfortable about doing nothing.
So he talked to various people about the circumstances and asked them what was they thought best way forward. Here is what he discovered.
• There has been a failure to recognise that people have priorities other than the desire to live as long as possible and they would like to have support in meeting those priorities. These can include help to maintain their cognitive function, spending more time at home rather than in hospital or even just having the company of their dog.
• The most reliable way to learn what these priorities are is to ask the people themselves. As a general rule this just does not happen. In a study with cancer patients who were in a very advance stage – less than a third of them had had a conversation with their physician about their priorities and goals for their end of life. It was significant that this group did far better and had less suffering. They were more likely to get the care that they wanted, less likely to die in the hospital or ICU, and more likely to die at home or with family. Interestingly, 6 months after their death their family members were less likely to be depressed or to have post-traumatic stress disorder symptoms. In a study conducted at Massachusetts General Hospital patients with Stage IV lung cancer were divided into 2 equal groups. One got the usual oncology care but the other also had the usual care plus access to a palliative care physician who would discuss with them what their priorities and goals might be for the end of life. The group who had that discussion ended up choosing to stop chemotherapy sooner. They were much less likely to go onto the fourth round of chemotherapy, which meant that there was a saving of about one third in the chemotherapy costs. Their time in hospital was also reduced by a third. They were much less likely to die in the hospital and they moved to a hospice earlier. Essentially they had a better quality of life than those who were not given the opportunity to discuss their circumstances and effectively have a say in how they treated as the end of their lives approached. To cap it all, they actually survived for about 25% longer than those in the other group.
• Doctors have a tendency to blind patients with information but Dr Gawande discovered that this is not very helpful. On the other hand, if people are given the opportunity to express themselves, they are much more likely to come to terms with their worries and anxieties. He realised that he had been doing far too much talking, up to 90 % of the time. People told him that he should not be talking for more than 50% of the time in order to allow the patients to ask questions and explain their preferences and concerns.
Instead of bombarding patients with facts and figures, the physician should concentrate on encouraging them to be forthcoming and one way to do this is by asking a number of questions.
CONCLUSION
The scenario painted here is probably familiar to many. A person who has just been diagnosed with a terminal illness is probably shell-shocked and therefore not in a fit state to have any kind of rational discussion. Even after some time, the tendency will be to rely on the physician to spell out the options and the prognoses. The work of Dr Gawande described here and in the previous blog (2) confirms that there is excessive use of many treatments and procedures. The study at Massachusetts General Hospital has produced some fascinating results with less treatment resulting in improved quality of life and a greater life expectancy not to mention the cost saving due to the reduction in treatments. With respect to cancer, we are left without the answer as yet to the intriguing question “Would the patients have done even better without any conventional radiotherapy and chemotherapy?”
Dr Gawande has made no attempt to deal with the fundamental causes of cancer although it is relatively uncommon for this issue to be raised in conventional medicine. However the reality is that even if a tumour is removed the chances of a recurrence must be very high if the lifestyle remains unchanged. It has been established that diet (or rather a poor diet) is one of the major factors which contributes to the development of various cancers. The work of the Otto Warburg showed that in cancer cells energy is utilised by means of fermentation so that glucose is the prime source. On the other hand, unlike healthy cells, the cancer cells cannot utilise fat. Hence with a diet which is low in sugar and carbohydrates generally, the growth of the cancer cells is retarded and may even cease completely. Furthermore there are many foods which can boost the immune system and therefore improve the ability of the body to repair itself. Dr Gawande would be doing us all a great service if he was to turn his attention to the potential of dietary changes to overcome some of our common chronic diseases. Obviously he has the ability to reach out beyond conventional thinking. Even more important he has established a unique international reputation so there is every possibility that when he speaks people in high places will listen.
REFERENCES
1. http://downloads.bbc.co.uk/radio4/open-book/2014_reith_lecture3_edinburgh.pdf
2. http://vernerwheelock.com/?p=672

145. What is Wrong with Modern Medicine?

It seems to be the accepted wisdom that the prime problem with our health services is a lack of resources and therefore all will be well if we can find enough money to meet all the demands. However we have only to look at the USA to appreciate that this view is nonsense. The Americans spend more than twice the amount on health care per capita as other developed nations, but ranks 49th in life expectancy worldwide. I have just been listening to the Reith Lectures by Dr Atul Gawande who is a surgeon and commentator on health policy issues (1). In 2010 he was named as by Time magazine as one of the world’s influential thinkers.
In an article in the New Yorker in 2009 he compared the medical facilities between 2 communities in Texas. One was McAllen and the other was El Paso County. Both of these counties have a population of roughly seven hundred thousand, similar public-health statistics, and similar percentages of non-English speakers, illegal immigrants, and the unemployed. Yet in 2006, Medicare expenditures which is the best approximation of the costs of health care in El Paso was $7,504 per enrollee—half as much as in McAllen (2). There was no evidence to indicate that the treatments and technologies available at McAllen were any better than those found elsewhere in the country. The annual reports that hospitals file with Medicare show that those in McAllen and El Paso offer comparable technologies—neonatal intensive-care units, advanced cardiac services, PET scans, and so on. Public statistics show no difference in the supply of doctors. In fact Mc Allen actually has fewer specialists than the national average.
Dr Gawande eventually gained access to commercial insurance data which revealed that compared with patients in El Paso and the country as a whole, patients in McAllen were given more diagnostic testing, more hospital treatment, more surgery and more home care. More detailed information was obtained from Medicare payment data. This showed that between 2001 and 2005, critically ill patients received almost fifty per cent more specialist visits in McAllen than in El Paso, and were two-thirds more likely to see ten or more specialists in a six-month period. In 2005 and 2006, patients in McAllen received 20% more abdominal ultrasounds, 30% more bone-density studies, 60% more stress tests with echocardiography, 200% cent more nerve-conduction studies to diagnose carpal-tunnel syndrome, and 530% more urine-flow studies to diagnose prostate troubles. They received one-fifth to two-thirds more gallbladder operations, knee replacements, breast biopsies, and bladder scopes. They also received two to three times as many pacemakers, implantable defibrillators, cardiac-bypass operations, carotid endarterectomies, and coronary-artery stents. And Medicare paid for five times as many home-nurse visits. So Dr Gawande had absolutely no doubt that the primary cause of McAllen’s extreme costs was, very simply, the across-the-board overuse of medicine.
A study conducted at Dartmouth’s Institute for Health Policy and Clinical Practice, analysed the treatment received by a million elderly Americans diagnosed with colon or rectal cancer, a hip fracture, or a heart attack. It was found that patients in higher-spending regions received 60% more care than elsewhere. They got more frequent tests and procedures, more visits with specialists, and more frequent admission to hospitals. Despite all this they did no better than other patients, as determined by survival, ability to function, or satisfaction with the care they received. If anything, they seemed to do worse.
In 2006 there were at least 60 million surgical procedures performed on people living in the USA, which is one for every 5 citizens. About 100,000 people die as a result of complications which arise during surgery, which is greater than the number who die in car crashes.
It is evident that where costs of medical treatment are excessively high, many of the treatments are unnecessary and may well do more harm than good. Dr Gawande considered the workings of the Mayo Clinic which has a fundamental philosophy that “The needs of the patient come first”—not the convenience of the doctors, not their revenues. In contrast to some other medical organisations the object is not to get more money out of the patients. Some years ago, it decided that all the income would be pooled and that doctors would be paid a salary, thereby breaking any link between the choice of treatment and remuneration. This was an integral part of a strategy which aimed to raise quality and to help doctors and other staff members work as a team. So it was no great surprise to discover that unnecessary costs are avoided so that The Mayo Clinic is not only very cost-effective but the quality of care extremely good.
Further probing in Texas revealed that in McAllen the growth of profit became accepted as legitimate in the practice of medicine and consequently many doctors
“came to treat patients the way subprime-mortgage lenders treated home buyers: as profit centers”.
This goes a long way to explain why there has been so much use of treatments and procedures which are not absolutely essential. So the crux of the issue is the focus of the doctor. Is the over-riding objective to meet the needs of the patient above all else or is it to maximize revenue?
Although Dr Gawande is based in the USA he does have insight into the way medicine operates in Europe. Even so his studies and analyses are particularly valuable because understanding what actually motivates people is critical in the formulation of policy irrespective of where it is applied.
It should certainly serve as a warning to those involved in any re-organisation of the NHS here in the UK. It does not mean that privatisation per se will be detrimental to patients. It will all depend on how the how the contracts are set up. For privatization to be effective it is essential that:
1. Contractors are paid a fixed price, which is agreed at the outset. They must not be given an open cheque book so that they are re-imbursed for costs of all treatments and procedures, which is apparently what happens in the USA.
2. It is essential to incentivize for high quality care and any failure to maintain high standards should be penalized.
My prime concern is that I am not convinced that the authorities have either the will or the competence to devise contracts which will provide the incentives to achieve what is best for the patient and will ensure that procedures are in place to guarantee that the terms and conditions are fulfilled. Those responsible for the commissioning could learn a lot from how the food supermarkets deal with the suppliers of own label products.
Dr Gawande also highlights the widespread usage of unnecessary procedures and treatments that may well be doing more harm than good which is not confined to the USA… a subject I will return to in a later blog.
REFERENCES
1. http://downloads.bbc.co.uk/radio4/open-book/2014_reith_lecture3_edinburgh.pdf
2. http://www.newyorker.com/magazine/2009/06/01/the-cost-conundrum?currentPage=all