131. The Banting Diet

William Banting was a London undertaker during the 19th century who in his later years suffered from obesity. Having tried various strategies he was advised to consume a diet which was low in sugar and other saccharine foods, which proved so successful that he decided to write a pamphlet describing his experience. This blog is based entirely on the fourth edition, published in 1869,  for which he charged one shilling (5p in today’s money) in order to cover his costs of production (1).

Here are a few extracts from the preface which have the advantage of recording some of the responses to the earlier editions:

  • “It is with no slight degree of pride and satisfaction that I presume to publish a fourth edition of my Letter on Cor­pulence, in the hope and belief that it may still further interest and benefit the Public
  • It has happily attained a world-wide circulation, and afforded me a vast amount of pleasure and gratification, derived from the conviction that I have been the means of bringing under public consideration and discussion one of the little known and much neglected laws of nature. The popularity of my unpretending brochure is manifest, not only in the surprising sale of no less than 63,000 copies, in this country alone, but by its translation into foreign languages and its large and rapid circulation in France, Germany, and the United States. In addition to this I have received nearly 2,000 very complimentary and grateful letters from all quarters of the world
  • The great principle which Mr. William Harvey (my medical adviser), of Soho Square, inculcated, having been confirmed by my own personal experience, I was enabled to speak with perfect confidence, and I became invulnerable to the ridicule, contempt, or abuse which were not spared in the earlier stages of the discussion. I believe I have subdued my discourteous assailants by silence and patience; and I can now look with pity, not unmixed with sorrow, upon men of eminence who had the rashness and folly to designate the dietary system as “humbug,” and to hold up to scorn the man who put it forth, although he never derived nor sought pecuniary or personal recompense, but simply desired, out of gratitude, to make known to other sufferers the remedy which he had found so efficacious to himself. I heartily thank the public press for the general fairness of its criticisms, and feel deeply indebted to the Morning Advertiser for its able article on 3rd October, 1865, when I was so sadly and unjustly attacked by certain pro­minent members of the British Association, whose feelings, now that the subject has been more widely and intelligently examined and discussed, I do not envy
  • It has been reported to me that many medical men have argued that I could not have consulted any eminent mem­bers of their fraternity on the subject of obesity. I beg leave emphatically to assure the public that, for the 20 years, previous to consulting Mr. Harvey, I had no occasion to consult a medical man, for any other ailments except those which are the inevitable consequences of corpulence; and that, although my medical advisers were neither few, nor of second-rate reputation, not one of them pointed out the real cause of my sufferings, nor proposed any effectual remedy, until I appealed to my friend, Mr. Harvey, the celebrated aurist, on account only of deafness
  • It is possible, and I think probable, that even Mr. Harvey was somewhat surprised at the extraordinary and speedy result of my rigid adherence to his advice, because he had long before prescribed the proper dietary system to reduce or cure corpulence, but his patients having hitherto impru­dently slighted his prescriptions, it was only my very strict compliance that completely proved the accuracy of his judgment. My only merit consists in entire obedience to Mr. Harvey’s advice. To him alone belongs all the credit of the remedy. He was the first to lead me on to the true road of health, and I was probably the first of his many patients who kept to it
  • Another eminent medical man, whose letter will appear among the rest, was actually giving my pamphlets in the course of his practice. I was greatly surprised to hear of it, and wrote to ascertain the fact. He invited me to call on him, and showed me that my information was correct by pointing to a pile of them lying upon his table. He complimented me upon the publication, as it contained sound advice in cases like my own; and added, that the discovery was not Mr. Harvey’s, but was derived from “Mons. Bernard, of Paris.” I replied that Mr. Harvey had told me he had first derived his information from lectures which he had heard in Paris, by Mons. Bernard, in regard to diabetes, and some other complaints, but that he had himself applied it to cases of corpulency. He admitted that the simple record of my own experience of the value of the system had brought it to the clear light of day, and that if it had been written by a medical man, it would scarcely have been noticed by the general public at all
  • Probably no one was ever subjected to more ridicule and abuse than I have been, in English as well as in foreign journals. My only object, however, has been the good of my fellow creatures. To have accomplished this object, in any degree, is a sufficient reward for my expenditure of time and means, and an ample compensation for the insolent contempt of some, and the feeble ribaldry of others
  • I have ascertained, by repeated experiments, that five ounces of sugar distributed equally over seven days, which is not an ounce per (lay, will augment my weight nearly one pound by the end of that short period. The other forbidden elements have not produced so extraordinary a result. In these, therefore, I am not so rigid. Some people (as will be seen by their letters) find other things detrimental. I never eat bread unless it is stale, cut thin, and well. toasted. I very seldom take any butter, certainly not a pound in a year. I seldom take milk (though that called so, in London, is probably misnamed), and I am quite sure that I do not drink a gallon of it in the whole year. I occasionally eat a potato with my dinner, possibly to the extent of 1 lb. per week. I spoke of sherry as very admissible, and I am glad of this opportunity to say, that I have since discovered it promoted acidity. Perhaps the best sherry I could procure was not the very best, but I found weak light claret, or brandy, gin, and whisky, with water, suited me better; and I have been led to believe that fruit, however ripe, does not suit me so well taken raw as when cooked, without sugar. I find that vegetables of all kinds, grown above ground, ripened to maturity and well boiled, are admirable; but I avoid all roots, as carrot, turnip, parsnip, and beet. I have not taken any kind of medicine for eighteen months, and find that my dietary contains all the needful regimen which my system requires. In the firm belief and conviction that the quality in food is the chief desideratum, and that the question of quantity is mere moonshine, I take the most agreeable and savoury viands, meat and game pies, that my cook can concoct, with the best possible gravies, jellies, &c., the fat being skimmed off; but I never, or very rarely, take a morsel of pie or pudding crusts
  • The subjoined correspondence is only a portion of upwards of 1,800 letters which I have received. There is scarcely one out of the whole which does not breathe a spirit of pure thankfulness and gratitude for the benefits derived from the dietary system, and contain the most flattering encomiums on my character and motives.”

COMMENT

The publication of the pamphlet obviously had an enormous impact. It is quite revealing that Banting tried so many different approaches which turned out to be complete failures. The success achieved by so many others who followed his example was absolutely phenomenal and provided convincing evidence of its validity. Despite this Banting, was subject to criticisms from many quarters. In particular, the ignorance and arrogance of the mainstream medical profession is clearly demonstrated.

Here are some extracts from the main body of the pamphlet:

  • Few men have led a more active life—bodily or mentally—from a constitutional anxiety for regularity, precision, and order, during fifty years’ business career, from which I had retired, so that my corpulence and subsequent obesity were not through neglect of neces­sary bodily activity, nor from excessive eating, drink­ing, or self indulgence of any kind, except that I par­took of the simple aliments of bread, milk, butter, beer, sugar, and potatoes more freely than my age required, and hence, as I believe, the generation of the parasite, detrimental to comfort if not really to health and comfort
  • Although no very great. size or weight, still I could not stoop to tic my shoe, so to speak, nor attend to the little offices humanity requires without considerable pain and difficulty, which only the corpulent can understand; I have been compelled to go down stairs slowly backwards, to save the jar of increased weight upon the ancle and knee joints, and been obliged to puff and blow with every slight exertion, particularly that of going up stairs. I have spared no pains to remedy this by low living (moderation and light food was generally prescribed, but I had no direct bill of fare to know what was really intended), and that, con­sequently, brought the system into a low impoverished state, without decreasing corpulence, caused many obnoxious boils to appear, and two rather formidable carbuncles, for which I was ably operated upon and fed into increased obesity
  • Bread, butter, milk, sugar, beer, and potatoes, which had been the main (and, I thought, innocent) elements of my subsistence, or at all events they had for many years been adopted freely
  • These, said my excellent adviser, contain starch and saccharine matter, tending to create fat, and should be avoided altogether
  • For breakfast, at 9.0 A.M., I take five to six ounces of either beef mutton, kidneys, broiled fish, bacon, or cold meat of any kind except pork or veal; a large cup of tea or coffee (without milk or sugar), a little biscuit, or one ounce of dry toast; making together six ounces solid, nine liquid.
  • For dinner, at 2.0 P.M., Five or six ounces of any fish except salmon, herrings, or eels, any meat except pork or veal, any vegetable except potato, parsnip, beetroot, turnip, or carrot, one ounce of dry toast, fruit out of a pudding not sweetened, any kind of poultry or game, and two or three glasses of good claret, sherry, or Madeira— Champagne, port, and beer forbidden; making together ten to twelve ounces solid, and ten liquid.
  • For tea, at 6.0 P.M., Two or three ounces of cooked fruit, a rusk or two, and a cup of tea without milk or sugar; making two to four ounces solid, nine liquid.
  • For supper, at 9.0 P.M. Three or four ounces of meat or fish, similar to dinner, with a glass or two of claret or sherry and water; making four ounces solid and seven liquid.
  • For nightcap, if required, A tumbler of grog—(gin, whisky, or brandy, without sugar)—or a glass or two of claret or sherry
  • This plan leads to an excellent night’s rest, with from six to eight hours’ sound sleep
  • My former dietary table was bread and milk for breakfast, or a pint of tea with plenty of milk, sugar, and buttered toast; meat, beer, much bread (of which I was always very fond) and pastry for dinner, the meal of tea similar to that of breakfast, and generally a fruit tart or bread and milk for supper. I had little comfort and far less sound sleep
    • I have not felt better in health than now for the last twenty-six years.
    • Have suffered no inconvenience whatever in the probational remedy or since.
    • Am reduced nearly 13 inches in bulk, and 50 lbs. in weight.
    • Can perform every necessary office for myself.
    • The umbilical rupture is cured.
    • My sight and hearing are suprising at my age.
    • My other bodily ailments have become mere matters of history.
    • Total loss of weight in 12 months 46 lbs
    • All symptoms of acidity, indigestion, and heartburn (with which I was frequently tormented) have vanished. I have left off using boot-hooks, and other such aids, which were indis­pensable, but being now able to stoop with ease and freedom, are unnecessary. I have lost the feeling of occasional faintness, and what I think a remarkable blessing and comfort is, that I have been able safely to leave off knee-bandages, which I had worn necessarily for many years, and given up the umbilical truss
    • The great charm and comfort of the system is, that its affects are palpable within a week of trial, which creates a natural stimulus to persevere for few weeks more, when the fact becomes established beyond question
    • I only entreat all persons suffering from corpulence to make a fair trial for just one clear month, as I am well convinced, they will afterwards pursue a course which yields such extraordinary benefit, till entirely and effectually relieved, and be it remembered, by the sacrifice merely of simple, for the advantage of more generous and comforting food. The simple dietary evidently adds fuel to corpulent fire, whereas the superior and liberal seems to extinguish it.”

CONCLUSION

Banting certainly enjoyed a wide range of tasty foods. He limited the intake of carbohydrates but had plenty of others which contained fat. Essentially he followed the same basic principles which so many in recent years have found works very well as means of controlling Type 2 Diabetes (T2D) but is also effective as a means of losing weight. However there may well be serious doubts about recommending his intake of alcoholic beverages to all and sundry. Despite the success of the Banting approach and the widespread dissemination of how it was achieved, the valuable lessons have been forgotten as shown by the obesity crisis. It is rather ironic that so many people find themselves in the same position of Banting in the days before he encountered the progressive Mr Harvey. Banting died in March 1876 aged 81 years.

Although all this happened 150 years ago, the insight gained is just as applicable today as it was then. What is more there is now sound science, which provides detailed confirmation of the experience of Banting. Despite all the opposition which still exists, most people who reduce their intake of sugar and other carbohydrate-containing foods, will not only lose weight but also lower the risks of developing heart disease, T2D, cancer and Alzheimer’s Disease.

 

REFERENCE

  1. http://www.lowcarb.ca/corpulence/corpulence_full.html

 

130. A Little Bit of History about LDL Cholesterol

The cholesterol lowering campaign really took off in 1985 with the recommendations of a Consensus Conference sponsored by the National Institutes of Health in the USA (1). I have just come across a commentary written at the time by Gerald Reaven which is absolutely fascinating (2). It is certainly highly relevant to recall the key points which were made almost 30 years ago!

The main conclusion was that raised levels of LDL Cholesterol in the blood plasma are causally related to the development of Cardiovascular Disease (CVD). Therefore steps should be taken to lower the LDL Cholesterol by the use of diet and/or drugs, in order to reduce the incidence CVD.  In particular, everyone except children under the age of 2 years should be advised to adopt a diet that reduces the intake of fat from 40% calories as it was then to 30%. Saturated fat (SFA) should be reduced to less than 10% calories while polyunsaturated fat (PUFA) should be increased. In addition, massive education programmes should be launched to ensure that health professionals were aware of the importance of treating hypercholesterolaemia and the food industry was to be encouraged to develop and market products in line with the dietary advice.

First of all, Gerald Reaven pointed out that Implementation of the recommendations would mean there would inevitably be an increase in the carbohydrate content of the national diet in the USA but that there had been no attempt by the Conference to assess the impact of this. In his view, there was enough credible evidence to postulate that a “low fat high carbohydrate (LFHC) diet” would result in metabolic changes in many people, which would be deleterious to health. In particular changes in blood glucose, insulin and HDL Cholesterol would actually increase the risks of developing CVD. This is rather ironic since the justification for the changes was to reduce risks of CVD.

He suggests that the older the individual and /or the more glucose intolerant the greater the chance that LFHC diets would result in significant increases in postprandial blood glucose, which is a risk factor for CVD. Furthermore for those consumers who have impaired glucose tolerance or full blown Type 2 Diabetes (T2D) the recommendation is even more questionable.

He then goes on to consider the role of insulin and states quite bluntly that raising the level of insulin in the blood increases the risk of CVD even in those who do not have T2D. Furthermore there is abundant evidence that increasing the carbohydrate content of the diet will augment the plasma insulin response of normal individuals. Therefore it is predictable that the insulin levels will be raised. While this might not be a major problem in those who are young, slim and physically active, it is almost certainly damaging for those who are getting on in years, well-nourished and sedentary.

A LFHC diet is known to raise the level of triglycerides in the blood, which is associated with an increased risk of CVD. While the importance of this has been questioned, Reaven argues that there is enough evidence to take this seriously. In particular he notes that this may be related to a fall in the level of the HDL Cholesterol, which could be another reason why an LFHC diet would increase the risks of CVD.

Even accepting the “Consensus” position that the LDL Cholesterol should be reduced and that the HDL Cholesterol is beneficial then it follows that the objective should be to increase the HDL:LDL in order to reduce the risks of CVD. Obviously this is what would happen if the LDL Cholesterol is lowered and the HDL Cholesterol is unchanged. Unfortunately because an LFHC diet also reduces the HDL even more than occurs with the LDL Cholesterol, the net effect is to lower the ratio! This is not exactly what the Consensus Conference was trying to achieve.

Finally here is a comment on the organisation of the conference which speaks for itself:

The most efficient way to reach a consensus concerning a complex issue within a short period is to make sure that controversial views are not represented on the panel. It is clear that the panel assembled by the NIH met this criterion; ie, no one who had published scientific evidence that might have led to the presentation of formidable arguments contrary to conventional wisdom was a member of the panel. I believe it is the responsibility of the organizers of such conferences to make sure that dissenting voices are present, and their absence raises substantial questions concerning the utility of the recommendations that are issued.”

 

CONCLUSION

Although the information presented here is entirely from the USA, the circumstances in many other countries are virtually the same. Here in the UK, over the past 30 years or so there has been an enormous increase in the use of the lipid lowering drugs (by a factor of about 20) (3). At the same time some of the fat in the diet has been replaced by carbohydrates (4). Although there has been quite an improvement in longevity the impact of this on the quality of life has been tempered by the increase in dementia. The incidence of obesity is evident, while the fact that T2D has doubled in the past 15 years and is expected to continue increasing is clearly a major public health issue. There is absolutely no question that Gerald Reaven has been totally vindicated by events. The fears which he outlined in 1985 have materialised.

It was evident that the doubts which he and others expressed were simply swept aside by those who were determined to implement their own agenda. The current position is now even worse because it is clear that the policy has been a disaster. Yet there is still a complete failure on the part of governments and health professionals to face up to reality. In the meantime huge numbers of people who faithfully comply with the official advice are suffering unnecessarily and many die prematurely. It is difficult to imagine a greater public health policy disaster. It is right up there with those wars which have been started on a false prospectus.

REFERENCES

  1. http://jama.jamanetwork.com/article.aspx?articleid=397825
  2. http://jn.nutrition.org/content/116/7/1143.full.pdf
  3. http://www.bhf.org.uk/plugins/PublicationsSearchResults/DownloadFile.aspx?docid=508b8b91-1301-4ad7-bc7e-7f413877548b&version=-1&title=Coronary+Heart+Disease+Statistics+2012+&resource=G608%2f1012%2fCHA
  4. http://vernerwheelock.com/?p=606

 

 

129. “A CALORIE IS A CALORIE”

The conventional view of energy in food is that it is measured by the bomb calorimeter, which many of us used in our physics classes in school. A known amount of material is placed in the calorimeter and incinerated. The rise in temperature is then used to calculate the energy/calorie content. Using the same principle humans can be placed inside a much more sophisticated and bigger calorimeter so that the calories expended can be measured. If these are greater than those consumed this means some of the body’s reserves have been used and therefore the individual exhibits weight loss. Similarly if more calories are consumed than are the total lost then there will be weight gain. As a consequence it has led to the assumption that weight loss can be achieved by reducing the total number of calories consumed. This has been the accepted mantra by health professionals, those who wish to lose weight and especially the weight loss industry.

The reality is that it does not work! (1). In a recent article in the Journal of the American Medical Association (2, 3) David Ludwig and Mark Friedman pose the questions:

“But what if we’ve confused cause and effect? What if it’s not overeating that causes us to get fat, but the process of getting fatter that causes us to overeat?”

They put forward the view that that there are certain factors, which stimulate the fat cells in the body to take up and store excessive amounts of constituents which are rich in calories and consequently are not available to meet the normal requirements for maintenance. In order to survive the brain makes the person feel hungry and so more food is consumed. So while the immediate problem is solved in the short term, the long term result is weight gain and ultimately obesity. Essentially the reason the usual approach to slimming fails is that it is accompanied by persistent hunger and the only ones who succeed are those who effectively starve themselves.

The article emphasises that there is no doubt that the hormone insulin is the dominant factor which influences the storage of calories in fat cells. When excess insulin is used to treat T2D it causes weight gain whereas insulin deficiency causes weight loss. From a dietary perspective it is the consumption of sugar and refined carbohydrates which cause the production of insulin by the pancreas in order to control the build-up of glucose in the blood. So the more of these foods that are consumed the more insulin will be available. Therefore it is quite consistent that the increase in the consumption of sugar and refined carbohydrates in the USA, the UK and many other countries has been accompanied by an increase in the incidence of obesity.

In an earlier study David Ludwig and colleagues compared diets which contained the same amount of calories but very different proportions of carbohydrates and fats (4). The subjects were middle-aged men and women who were overweight or obese. They found that those on the diet containing 60% fat and 10% carbohydrates had a total energy expenditure of 3137 Kcalories /day whereas those on the low fat diet with 20% fat and 20% carbohydrates had only 2812 Kcalories/day….a reduction of over 300/day. This is a huge difference but the most important conclusion to emerge is that this confirms the fact that not all calories are equal! This should come as no surprise to anyone who recognises that the ways in which fat, protein and carbohydrate are metabolised and utilised in the body are totally different. Nevertheless the significance of the impact on the energy expenditure is absolutely crucial because it demonstrates the futility of formulating diets on the basis of calorie content irrespective of the constituents. This insight also helps to understand why the odds are stacked against the conventional calorie control approach to lose weight since a low fat diet seems to be utilised very efficiently with energy loss kept to a minimum. The study also monitored some of the other indicators of health and in general that the more favourable results were obtained with the high fat diet. In particular, the levels of triglycerides, a heart disease risk factor was 107 mg/dl in those on the low fat diet but only 66 mg/dl in those on the high fat one. In fact work with rats has suggested that even on a low calorie diet which is high in refined carbohydrates, there is a tendency towards obesity as shown by fat deposition (5).

There really is nothing new about the findings. Over 50 years ago, Kekwick and Pawan conducted a series of experiments with iso-caloric diets (all with the same calorie content) and concluded that the:

“..rate of weight loss varied so markedly with the composition of the diet on a constant calorie intake, it is suggested that obese patients must alter their metabolism in response to the contents of the diet. The rate of insensible loss of water has been shown to rise with a high-fat and high-protein diets and to fall with high-carbohydrate diets” (6).

There have been a number of other investigations which all reach similar conclusions but have not been accepted by mainstream nutritionists on the grounds that the results do not comply with the First Law of Thermodynamics. This states that the  total energy of an isolated system is constant; energy can be transformed from one form to another, but cannot be created or destroyed. However this logic is totally fallacious because the First Law relates to an isolated system and therefore we need to have information on all the energy inputs and outputs. As the study by Ludwig and Friedman showed there is marked variation in the energy loss with the diets of different composition, the fact that weight loss varies is entirely consistent with the First Law. Those who claim that the variation in weight loss is in conflict with the First Law are obviously making the false assumption that the energy retained in the body will be precisely the same for every diet irrespective of the composition. Clearly this is impossible and therefore wrong because the biochemical steps involved in the breakdown and utilisation of fat, protein and carbohydrate are all different. There is ample evidence available to confirm this. For anyone interested in a more detailed consideration of this issue plus a discussion of the role of the Second Law of Thermodynamics, consult this reference (7).

CONCLUSION

The focus on calorie control as a means of weight loss is based on a fundamentally flawed concept. It does not work and there are millions of people who can confirm this from their own personal experience. The message is quite clear. It is not the amount of food which determines your weight or your ability to lose it but the quality in terms of the relative proportions of fat and carbohydrate. If you wish to lose weight and improve your health then it is abundantly obvious that the answer is to reduce the carbohydrates and increase the fat.

7. As the rate of weight-loss varied so markedly with

REFERENCES

  1. http://vernerwheelock.com/?p=218
  2. http://jama.jamanetwork.com/article.aspx?articleid=1871695
  3. http://www.nytimes.com/2014/05/18/opinion/sunday/always-hungry-heres-why.html?_r=0
  4. http://jama.jamanetwork.com/article.aspx?articleid=1199154
  5. http://www.ncbi.nlm.nih.gov/pubmed/15337404
  6. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(56)91691-9/fulltext
  7. http://www.nutritionj.com/content/3/1/9

 

127. Beware of Fructose!

The original work of Ancel Keys which eventually led to the dietary guidelines recommending a reduction in total fat and particularly saturated fat (SFA) was based on epidemiological studies which related the national fat data to the incidence of heart disease (1). However almost invariably countries which have a high intake of fat also have a high intake of sugar and it is very likely that if this had been the focus of attention, similar associations would have emerged for sugar and heart disease. The work of Keys has been subjected to devastating criticism and in the view of many who have analysed his results it has been totally discredited.

By contrast there is growing evidence that an excessive intake of carbohydrates is a critical factor which contributes to a variety of diseases/conditions which include obesity, hypertension, diabetes and heart disease. This is confirmed by the improvements in health which have been observed by those who make substantial reductions in the amount of carbohydrates in the regular pattern of food consumption.

Recently the spotlight has focussed specifically on sucrose (table sugar) and High Fructose Corn Syrup (HFCS). Sucrose breaks down to a 50:50 mixture of glucose and fructose. HFCS is essentially similar and is widely used in foodstuffs, especially in the USA where there has been a progressive increase in the amount consumed since it was first introduced in the 1970s. Over the next 30 years the fructose consumed in the USA had increased by 30% (2). HFCS-55, which consists of 55% fructose and 42% glucose, is used primarily in sweetened beverages and is also used to sweeten other products (e.g., baked foods and confectionaries).

There are a variety of reasons which taken together make a very compelling case that sugar and HFCS are largely responsible for the deterioration in standards of public health which have been observed in many different countries. The epidemiological evidence shows that there is a close association between the increase in the consumption of these sugars and the increase in the incidence of obesity. Further understanding emerges from a consideration of the different roles of glucose and fructose in the body. At the outset it is crucial to emphasise that although they are very similar in chemical structure they have distinctly different functions and are metabolised by totally different pathways. There is now growing evidence that it is the fructose which is responsible for many of the public health concerns that have arisen in recent years.

In 2002 it was suggested that fructose plays a critical role in the development of Metabolic Syndrome, which is a cluster of diseases/conditions namely obesity, diabetes, hypertension, raised blood triglycerides and low HDL Cholesterol. This was based on evidence from both animal and human studies. In particular when comparisons are made between fructose and sugar (which produces fructose and glucose) it was found that there was greater weight gain, raised blood pressure and raised blood triglycerides with the fructose treatment on its own (3).

Here are some specific examples:

  • The level of triglycerides in the blood was raised when young men were given a diet which was supplemented with 200 g sucrose/day but when the sucrose was replaced with starch, which breaks down to glucose only there was no change(4)
  • In a study conducted in Denmark with healthy men and women aged between 20 and 50 years a comparison was made between supplementation of the regular diet soft drinks containing sucrose and artificial sweeteners. It was found that after 10 weeks the blood pressure had increased in the sugar group but in the other group it had decreased. The body weight increased in the sucrose group but decreased in those using the sweeteners (5)
  • A comparison was done over 8 weeks in which healthy men and women consumed 25% of their energy either as fructose or glucose. Although both groups gained the same amount of weight, those consuming fructose synthesised more fat in the liver and had a greater amount of subcutaneous fat. This is consistent with the fact that virtually all the fructose has to be utilised by the liver which primarily converts it into fat that is stored. The fructose group also had more oxidised LDL Cholesterol and a higher concentration of small dense particles of LDL Cholesterol, both of which are risk factors for heart disease. Insulin sensitivity was reduced in the fructose group but not in those consuming glucose (6).

All of these results provide convincing evidence that fructose is much more damaging to health than glucose. The experimental data fits in very well with the epidemiological information which relates the changes in the incidence of various diseases with the patterns of consumption. There seems very little doubt that increasing consumption of sugar and of HFCS has been the critical factor responsible for the obesity epidemic. Therefore it would be sensible to emphasise the importance of reducing sugar consumption in the advice given to the public. Regrettably because of the obsession with fat and SFA in particular the message is not getting through. Sales of Sugar Sweetened Soft drinks remain at a very high level. Furthermore “low fat” foods continue to be promoted heavily and consumers purchase them in the belief that they are healthy even though the fat taken out has largely been replaced by sugar!!!

REFERENCES

  1. A Keys (1970) Circulation 41 (1) pp 188-195
  2. G  A Bray et al (2004) American Journal of Clinical Nutrition 79 (4) pp 537-543
  3. S S Elliott et al (2002) American Journal of Clinical Nutrition 76 (5) pp 911-922
  4. P A Akinynju et al (1968) Nature 218 (5145) pp 975-977
  5. A Raben et al (2002) American Journal of Clinical Nutrition 76 (4) pp 721-729
  6. K Stanhope et al (2009) Journal of Clinical Investigation 119 (5) pp 1322-1334

126. What Every Woman Should Know about Mammography

Mammography is a procedure in which the breast is examined using a special X-ray machine to detect signs of cancer. The rationale is that early detection enables treatment to be started before symptoms become evident thereby increasing the chances of curing or controlling the disease. This approach is utilised in many countries and in the UK is being actively promoted by the NHS.

As long ago as 1978 the Office of Technology Assessment (OTA) in the USA reported that questions were being raised about the safety of the procedure (1). In a report the OTA noted that many in the medical profession believed that it was efficacious and safe for all women, but there is no scientific information derived through controlled studies to support such a view. It was concluded that the technology had been introduced on an extensive scale before doubts about its safety raised questions about its effectiveness.

These fears were confirmed by the results of a study based on data collected in the Norwegian Breast Cancer Screening Program. The incidence of breast cancer in one group consisting of 119,472 women aged 50-69 at the outset who were screened using mammography on 3 separate occasions was assessed. This was then compared with the results for a similar control group of 109,784 women who were only screened on one occasion which was at the end of the 6-year period. It was found that the cancer incidence in those who had been screened 3 times was 22% higher than in those who were screened once. As expected the incidence of breast cancer was considerably higher in those who were screened at the beginning of the 6-year period because many cancers were only detected due to the screening. The authors were surprised to find that there was still a higher incidence in the group which had multiple screenings at the end of the period. If the screenings were performing as expected then this group should have had less cancer because the rationale is that the detection should enable the cancer to be treated. The explanation suggested was that many cases of breast cancer recover spontaneously. This means that the treatment for these particular cases is totally unnecessary and may actually be counter-productive (2).

A more recent evaluation was conducted by the Nordic Cochrane Collaboration which concluded that if 2000 women are regularly screened for 10 years one will benefit from the screening, as she will avoid dying from breast cancer. At the same time, 10 healthy women will, as a consequence, become cancer patients and will be treated unnecessarily. These women will have either a part of their breast or the whole breast removed, and they will often receive radiotherapy, and sometimes chemotherapy. These numbers were derived from the randomised trials of mammography screening. However, since the trials were performed, treatment of breast cancer has improved considerably. More recent studies suggest that mammography screening may no longer be effective in reducing the risk of dying from breast cancer. Screening produces patients with breast cancer from among healthy women who would never have developed symptoms of breast cancer. Treatment of these healthy women increases their risk of dying, e.g. from heart disease and cancer. It therefore no longer seems beneficial to attend for breast cancer screening. In fact, by avoiding going to screening, a woman will lower her risk of getting a breast cancer diagnosis (3).

Nevertheless here in the UK the NHS continues to claim that mammography screening will save 1400 lives per year. However a paper by Peter C Gøtzsche and Karsten Juhl Jørgensen of the Nordic Cochrane Centre published in the Journal of the Royal Society of Medicine entitled “The Breast Screening Programme and Misinforming the Public” challenges this position (4). They argue that the harm has been “downplayed” and that the information provided for the public has remained largely unaffected by “repeated criticism and pivotal research” which has questioned the benefits of screening and documented substantial over-diagnosis.

The paper states that information regarding lives saved through the screening programme is much exaggerated. “The claim that death rates have fallen ‘in part from earlier diagnosis associated with screening’ is astonishingly misleading,” says Peter Gøtzsche, who is the Director of the Nordic Cochrane Centre. “Deaths from breast cancer are falling because treatment is improving. There’s been a similar fall in the age-groups not invited to screening. In this respect, and many others, the Programme persists in misinforming the public. It was forced to revise its leaflet inviting women for mammography but the new leaflet and their latest Annual Review continue to repeat incorrect mortality estimates.”

According to the NHS Programme, screening will prevent one death from breast cancer for every 400 women screened regularly over ten years. Gøtzsche and Jørgensen were unable to find any evidence for this estimate in reports from the Programme or elsewhere. Based on studies in Sweden a more realistic estimate would be one death prevented for every 2000 women screened, which means the NHS figure is 5 times too high.

The authors also point out that the NHS publicity is ambiguous with respect to the over-diagnosis, which means that those considering screening do not appreciate the risks involved. Information from Denmark shows that the incidence of mastectomies is increased substantially as a direct result of over-diagnosis. However the impression presented by the NHS is that screening will reduce the chances of a woman requiring a mastectomy and is therefore seriously misleading.

This is another example of how the hierarchy in the medical profession persists in pushing a strategy which quite simply flies in the face of the latest evidence. The fact that more and more people can do their own investigations using the internet will ultimately undermine the official policy. In the meantime many people will suffer unnecessarily and public money will be wasted on a procedure that is clearly “not fit for purpose”.

Further insight into this topic can be found on the Canceractive website (5).

REFERENCES

  1. http://www.princeton.edu/~ota/disk3/1978/7805/780501.PDF
  2. P-H Zahl et al (2008) JAMA Internal Medicine 168 (21) pp 2311-2316
  3. http://www.cochrane.dk/screening/index-en.htm
  4. http://www.rsm.ac.uk/media/pr295.php
  5. http://www.canceractive.com/cancer-active-page-link.aspx?n=1420

 

BLOG 2014 125. Rubbish on NHS Choices Website

I have just been looking at a section of the NHS Choices website entitled “The Truth about Carbs” (1). I just cannot believe the utter rubbish that is presented here about carbohydrates.

Here are some extracts:

  • “Carbs” has become a dirty word in recent times, especially in the weight loss world, due in no small part to the popularity of low-carb diets such as the Atkins, Dukan and South Beach. The “carbs are bad” mantra from Dr Atkins and co has left many people confused about carbohydrates and their importance for your health, including maintaining a healthy weight.
  • Carbohydrates are a source of energy. When eaten, the body converts most carbohydrates into glucose (sugar), which is used to fuel cells such as those of the brain and muscles.
  • Carbs are important to your health for a number of reasons. In a healthy balanced diet they are the body’s main source of energy. High fibre, starchy carbs release sugar into the blood more slowly than sugary foods and drinks.
  • Carbs should be the body’s main source of energy in a healthy balanced diet, providing about 4kcal (17kJ) per gram. Carbs are broken down into glucose (sugar) before being absorbed into the bloodstream. From there, the glucose enters the body’s cells with the help of insulin. Glucose is used by your body for energy, fuelling all of your activities, whether going for a run or breathing. Unused glucose can be converted to glycogen found in the liver and muscles. If unused, glucose can be converted to fat, for long-term storage of energy.
  • Vegetables, pulses, wholegrain varieties of starchy foods, and potatoes eaten with their skins on are good sources of fibre. Fibre is an important part of a healthy balanced diet. It can promote good bowel health, reduce the risk of constipation, and some forms of fibre have been shown to reduce cholesterol levels. Many people don’t get enough fibre. On average, most people in the UK get about 14g of fibre a day. We are advised to eat an average of 18g a day.
  • Carbohydrate contains fewer calories gram for gram than fat, and starchy foods can be a good source of fibre, which means they can be a useful part of a weight loss plan. By replacing fatty, sugary foods and drinks with high-fibre starchy foods, it is more likely you will reduce the number of calories in your diet. Also high fibre foods add bulk to your meal helping you feel full. “You still need to watch your portion sizes to avoid overeating,” says Sian. “Also watch out for the added fats used when you cook and serve them: this is what increases the calorie content.”
  • While we can most certainly survive without sugar, it would be quite difficult to eliminate carbs entirely from your diet. Carbohydrates are the body’s main source of energy. In the absence of carbohydrate, your body will use protein and fat for energy.
  • However, cutting out starchy foods from your diet could put you at increased risk of a deficiency in certain nutrients, leading to health problems …, unless you’re able to make up for the nutritional shortfall with healthy substitutes.
  • It may also be hard to get enough fibre, which is important for a healthy digestive system and to prevent constipation. Healthy sources of carbs such as starchy foods, vegetables, fruits, legumes and dairy products are an important source of nutrients such as calcium, iron and B vitamins.
  • Cutting out carbohydrates and replacing those calories with fats and higher fat sources of protein could increase your intake of saturated fat, which can raise the amount of cholesterol in your blood – a risk factor for heart disease.
  • When you are low on glucose, the body breaks down stored fat to convert it into energy. This process causes a buildup of ketones in the blood, resulting in ketosis. Ketosis as a result of a low carbohydrate diet can be accompanied by headaches, weakness, nausea, dehydration, dizziness and irritability particularly in the short term.
  • Try to limit the amount of sugary foods you eat and instead include healthier sources of carbohydrate in your diet such as wholegrains, potatoes, vegetables, fruits, legumes and lower fat dairy products.

 

Many of the statements above cannot be substantiated. There simply is not the evidence to support them. I could spend a long time explaining why this is so but what I find particularly fascinating is the comments posted by people who have also been appalled by what is presented as official policy. Let them speak for themselves with some of their views:

  • since switching to a low carb (not no carb) diet my endurance training has improved dramatically. I never feel tired or lethargic, so carbs don’t have to be your main source of energy. By the way, I have also lost nearly 2 stones in weight and my blood pressure has fallen into the “ideal” zone. I eat loads of butter and cream, lots of green veg and eggs, and about the same amount of meat as before (but with the fat left on, which I used to trim off after years of ‘brain washing’!).
  •  The article still contains rubbish like :-”Can we survive without carbs?

    While we can most certainly survive without sugar, it would be quite difficult to eliminate carbs entirely from your diet. Carbs are the body’s main source of energy. In the absence of carbs, your body will use protein and fat for energy.”

    An unbiased article would point out that calories can be obtained from any of the three macronutrients and that your body has the largest energy store in the form of fats, not carbs.

    Bacon and egg is a carb free breakfast, steak with two green veg has a few grams. Nobody advocates zero carb diets but restricting to <100 grams per day gives many people benefits to health.

    If you want to lose weight reduce calories and make sure the ones you reduce are all carbohydrate – the optional macro nutrient.

  • There are essential Amino and Fatty acids but I have never heard of essential carbs. Carbs especially refined sort are the cause for obesity and excessive insulin which both combined are disastrous to the biological function and yet the NHS prescribe this diet (high insulin diet) which I find a real irony. NHS how much did you get paid by our sugar industry for this article
  • I hold the NHS very highly, therefore I am acutely embarrassed by the bad science in this article.
    Due to my recent diagnosis of diabetes I’ve been reading a lot of peer reviewed modern studies, and I’m becoming more and more mystified and frustrated by the nutritional advice by the NHS.
    Frankly, your recommended low-fat high-carbs regime is almost the last thing diabetic people should eat, which is bad news as correct nutrition is the first line of defence against diabetes.I’m going with Sweden and their sensible LCHF approach, instead. They’re at the forefront of research on obesity and diabetes, whereas you’re still using 40 years old fallacious and financially biased science from the United States.

VW note:

Apparently the article which I have cited was updated in the light of comments about the previous version. Here are extracts made in December 2013 and January 2014 in response to that:

  • Have the NHS been infiltrated by certain members of the food lobby or are they really this ignorant?
    No wonder this country has an obesity crisis!
  • Dreadful article. Old 70′s health myths dressed up as common sense advice.
    I do not understand how this is allowed to be put out as public information from the NHS.
  • Hello Sian, I am concerned that you are pushing the low fat dogma despite the relentless science and research that shows that the dogma is nonsense. The NHS has a public duty to admit low fat calorie obsession is a dead end. You do not deal with hormones, metabolism and gut health. Food quality and healthy metabolism are key to health, not carbs. Please stop defending the mistakes of the past. (Sian is the author of the article).
  • This is a very unbalanced article. It’s fine as a “pro carbohydrate” item but needs to be balanced by an article stating the opposing case based on the insulin hypothesis of obesity and the problems of carbohydrates in diabetes etc.There is a problem with the “science” above in that the article http://www.nejm.org/doi/full/10.1056/NEJMoa022207 does in fact demonstrate a statistically significant improvement in weight loss at both months 3 and 6 of around 4% of weight loss. Most of us would take an extra weight loss of 3 to 4 kg in 6 months and say “thank you very much, Dr Atkins”. That could be an extra half stone to some of us.

    At 12 months with a high dropout rate and the use of “baseline data carried forward” for the dropouts the weight loss difference is reduced to a mere 2% of body weight with P=0.26 so there is still an 80% probability of getting a better weight loss on the low carb arm of this one study.

    This article should be withdrawn and re-written.

  •  Perfectly sufficient fibre and associated food factors such as vitamins can be gained from a diet based on leafy greens and raw coloured vegetables.
  • This commentary is full of inaccuracy, fallacy, opinion, and error. Point wise:1. Fibre is a carb. strictly, but it is not digested or metabolised, so should not be described nutritionally as a carb.
    2. We do not need carbs at all – none.
    3. Starchy foods when cooked do not release energy slowly, they dump glucose into the blood quickly. This is contraindicated – utterly.
    4. There is no requirement, and no reason why grains need to be in the human diet at all.
    5. Carbs are the main source of energy when they make up the largest portion of intakes, sure – but there is no reason why this needs to be so. Fats and protein also contain energy.
    6. So what if fats contain 2.25 x the energy per g than carbs? If carbs cause you to eat 3 to 4 times as much total energy per day (which they do, due to insulin response).
    7. Glycogen shortage is not a problem during exercise in properly fat adapted individuals.
    8. This author has provided no supporting literature at all, it is an opinion piece, its full of ridiculous errors and fallacies, and its plain ignorant. NHS choices, really; come on.
  • I have been low carb for over a year. Result ; lower triglycerides, ldl static, hdl increased, fasting blood sugar lowered, energy levels increased. Oh and not to mention two and a half stone lighter. I eat lots of saturated fat and enjoy it. Am i constipated? No.You need to examine the huge and growing scientific evidence on low carb high fat diets.

CONCLUSIONS

I think there is no need for me to add anything further. The comments from the different contributors have addressed most of the issues which would be of concern to me. Although the article has been revised it looks to me that most of the earlier comments are still applicable, which means that there has been little improvement. It seems that the NHS has got into such a pickle that it is having to defend the indefensible. The tragedy is that while some individuals have been able to work things out for themselves, the vast majority are still at the mercy of people like the author of this article. The inevitable consequence is that many are suffering unnecessarily and dying prematurely. It is obvious that the current policies are not working and a complete re-think is required. The knowledge and information is readily available. It is an absolute scandal that it has not been incorporated into the NHS strategy.

If one wants inspiration then take a look at what is happening in South Africa, starting with a link to The Real Meal Revolution website (2).

REFERENCES

  1. http://www.nhs.uk/livewell/loseweight/pages/the-truth-about-carbs.aspx
  2. http://realmealrevolution.com/

 

 

124. Cancer: Evidence Points to Carbohydrates not Fat

INTRODUCTION

When the dietary recommendations were being devised initially a high intake of fat was considered to be a risk factor for certain types of cancer and in particular breast cancer in women. This conclusion was based largely on international comparisons and the results of animal studies.

RESULTS OF VARIOUS STUDIES

However the results of the Nurses’ Health Study which were published in 1999 completely undermined the conventional wisdom at the time. This major project commenced in 1976 when 88,795 female registered nurses aged 30 to 55 years free of cancer were recruited. The participants were followed up for 14 years. In 1980 they completed a food frequency questionnaire and this exercise was replicated in 1984, 1986 and 1990. A total of 2,956 women were diagnosed with breast cancer.  When the cancer incidence was related to diet there was absolutely no evidence of increased risk of breast cancer with increased intake of animal fat, polyunsaturated fat, saturated fat or even trans unsaturated fat. In fact it was found that the risk of breast cancer tended to be highest among those with the lowest fat intake. Certainly there was no suggestion that lower intake of total fat or of any particular types of fat over the 14 years of the study was associated with a decreased risk of breast cancer. So it was concluded that a reduction of total fat in mid-life was unlikely to prevent breast cancer.

This study included more cases, longer follow-ups and more person-years than any previously published prospective study on diet and breast cancer. The quality and the reliability of this work are enhanced by the fact that the diet of the participants was assessed on 4 different occasions (1).

In Korea 829,770 men and 468,615 women aged between 30 and 95 were given a medical check in the years 1992-1995. They had a follow-up examination after 10 years during which time there had been 20,566 cancer deaths in the men and 5,907 in the women. The results (Tables 1 and 2) show that the deaths from all causes and from several cancers increased progressively with the concentration of blood glucose. When the results for the first 5 years were excluded the same trends were evident which eliminates the possibility that the increase in blood glucose is actually caused by the cancer (2).

TABLE 1. RELATIVE MORTALITY RATES FOR SELECTED CANCERS AND BLOOD GLUCOSE LEVELS IN KOREAN MEN

Cause of deaths                                        Fasting Blood Glucose levels, mg/100ml
<90 90-109 110-125 126-139 >140 Diabetes
All causes 1.00 1.04 1.28 1.50 2.09 1.83
All cancers 1.00 1.04 1.17 1.28 1.29 1.27
Colorectum cancer 1.00 1.07 1.27 1.23 1.31 1.28
Pancreatic cancer 1.00 1.08 1.28 1.45 1.91 1.71

 

TABLE 2. RELATIVE MORTALITY RATES FOR SELECTED CANCERS AND BLOOD GLUCOSE LEVELS IN KOREAN WOMEN 

Cause of deaths                                   Fasting Blood Glucose levels, mg/100ml
<90 90-109 110-125 126-139 >140 Diabetes
All causes 1.00 1.01 1.24 1.42 2.35 1.99
All cancers 1.00 1.00 1.01 1.12 1.23 1.31
Colorectum cancer 1.00 0.96 1.05                  0.85 1.11
Pancreatic cancer 1.00 1.45 1.70                  2.05 1.71
Breast 1.00 1.15 0.89                  1.24 2.23

 

In an Austrian study, 63,585 men and 77,228 women whose mean age at baseline was 43 years were followed up for an average of 8.4 years. Over 5,000 cases of cancer were diagnosed. The average age of diagnosis was 64 years. Those who developed cancer in the first year were excluded.

Table 3 shows that with cancers of the liver, gallbladder and bile duct, thyroid and multiple myeloma the tendency is for the mortality rate to increase as the level of fasting blood glucose increases based on results for men and women. It should also be noted that with some of these cancers there is an increased rate at relatively low levels of blood glucose. For leukaemia, there is no consistent trend. For breast cancer in women (Table 4) a relatively high death rate is only apparent in those over 65 at the highest blood glucose level (3).

TABLE 3 FASTING BLOOD GLUCOSE CONCENTRATIONS AND THE INCIDENCE OF VARIOUS CANCERS IN MEN AND WOMEN

                                 Fasting blood glucose at enrolment, mmol/L
  2.2-4.1 4.2-5.2 5.3-6.0 6.1-6.9 >7.0
Liver cancer 1.37 1.00 1.89 2.45 3.56
Gallbladder and bile duct 0.92 1.00 1.90 3.74 3.36
Thyroid cancer 1.24 1.00 2.22 2.34 -
Multiple myeloma 1.54 1.00 2.26 2.42 -
Leukaemia 0.78 1.00 1.47 1.00 -

TABLE 4. FASTING BLOOD GLUCOSE AND THE INCIDENCE OF BREAST CANCER IN WOMEN AT DIFFERENT AGES

                                 Fasting blood glucose at enrolment, mmol/L
Breast cancer 2.2-4.1 4.2-5.2 5.3-6.0 6.1-6.9 >7.0
All 0.96 1.00 0.99 0.91 1.38
<50 years 0.99 1.00 0.61 0.67 -
50-65 years 1.05 1.00 1.08 0.80 1.12
>65 years 0.80 1.00 1.09 1.03 1.63

 

Breast cancer patients with diabetes are more likely to die prematurely from breast cancer than patients without diabetes (RR 1.76) which suggests that besides affecting the incidence rate diabetes also promotes breast cancer mortality (4).

A recent systematic review confirmed that patients with breast cancer and pre-existing diabetes suffer all-cause mortality that is increased by about 50%. This finding was consistent across different populations and was generally independent of possible confounding variables. The main implication of this study is that diabetes is associated with adverse outcomes in breast cancer throughout its full course, from initial presentation, during treatment (which influences the choice of therapy), and, ultimately, to mortality (5).

In a Canadian investigation 512 women treated for breast cancer were followed for an average period of just over 4 years. Women with diabetes were excluded. The breast cancer recurred in 76 of the women and there were 43 deaths. The relationship with the blood insulin (Table 5) show that those with the highest levels were more likely to experience a recurrence (by a factor of 2) and to die (by a factor of 3.1) when compared with those with the lowest levels (6).

TABLE 5. BLOOD INSULIN LEVELS AND RISK OF BREAST CANCER AND DEATH

Insulin level, Pmol/L 8.1-27.0 27.0-35.3 35.3-51.9 51.9-339.8
RR, breast cancer 1.0 1.3 1.5 2.0
RR, death 1.0 1.5 2.0 3.1

 

Insulin has been shown to stimulate cell proliferation in normal breast tissue and in human breast cancer cell lines. It has also been established that the administration of insulin promotes breast tumour growth in animal models. In the Women’s Health Initiative (WHI) 93,676 post-menopausal women aged between 50 and 79 years were followed for over 6 years commencing between 1993 and 1998. Fasting insulin levels were measured and the results (Table 5) showed that the incidence of breast cancer was more than doubled at the higher levels when compared with the lowest level. It should be noted that any women with diabetes were excluded from the study and all those involved were not on hormone therapy (7).

TABLE 6 FASTING INSULIN LEVELS AND BREAST CANCER INCIDENCE

Insulin level, µIU/ml <3.9 3.9-5.6 5.6-8.8 >8.8
Hazard Ratio 1.00 1.00 1.59 2.65

 

Because of the potential role of insulin in the development of cancer there is considerable interest in studying the effect of various therapies for diabetes. An investigation in Saskatchewan with 10,309 participants (55% men) who had used anti-diabetic drugs for less than a year resulted in 245 deaths. However there were marked differences in death rates depending on the drug used. It was found (Table 7) that people exposed to sulfonylurea or exogenous insulin (agents that increase circulating insulin levels) were significantly more likely to have a cancer-related death than people exposed to

metformin (which does not increase insulin levels). When adjustment were made to the death rates to allow for other factors such as the age of the patients it was found that the risk of cancer-related mortality was even greater for insulin exposure (90% relative increase) than for sulfonylurea exposure (30% relative increase) (8).

TABLE 7. CANCER THERAPY AND MORTALITY

Therapy Cancer mortality   rate, per 1,000 person-years
Metformin 6.3
Sulphonyl urea 9.7
No insulin 6.8
Insulin 9.9

 

STUDIES WITH MICE

In an investigation with mice the development of tumours was compared for different diets. The control contained 55% carbohydrate which is roughly the same as the national diets in the UK or the USA. The experimental diets contained 8, 10 and 15% CHO. With mice that were particularly susceptible to tumour growth it was found that at 1 year old almost half of those on the 55% carbohydrate diet had developed tumours but none were detected in those on the 15% carbohydrate diet. In total 70% of the mice on the high CHO diet developed tumours and only one reached the normal life span. Less than 30% of those on the low CHO diet developed tumours while more than half reached or exceeded the normal life span. The low CHO diet reduced the plasma insulin levels which in results in a reduced glucose uptake by the tumour cells. There was a positive correlation between plasma insulin levels and tumour size which confirms that the glucose supply is related to tumour growth (9).

CONCLUSION

There is little doubt that excessive amounts of sugar and refined carbohydrates in the diet is the primary cause of Type 2 Diabetes (T2D). Confirmation is shown by the fact that T2D can be effectively cured by a diet which is low in carbohydrates and high in fat (10). It is now becoming clear that the rationale to reduce fat and especially the saturated fats (SFAs) was fundamentally flawed (11). The evidence presented here flags up the dangers of consuming excessive carbohydrate with respect to many different cancers. The fact that the risks increase as the concentration of glucose in the blood increases is particularly relevant. The case for limiting the intake of sugar and refined carbohydrates has now reached the point where it is extremely convincing. Unfortunately this is in direct conflict with the official dietary recommendations in many countries. Although there is growing awareness of the risks associated with sugar consumption, many people have difficulty in adapting their diets because they are still convinced the SFAs are dangerous. In reality, there was never any justification recommending a reduction in these fats. On the contrary they should be considered as valuable nutrients (12).

REFERENCES

  1. Michelle Holmes et al (1999) JAMA 281 (10) pp.914-920
  2. S H Jee et al (2005) Journal of the American Medical Association 293 (2) pp194-202
  3. K Rapp et al (2006) Diabetologica  49 (5) pp 945-952
  4. F Xue & K B Michels (2007) American Journal of Clinical Nutrition 86 (3) pp S823-S835
  5. K S Peairs et al (2011) Journal of Clinical Oncology 29 (1) pp 40-46
  6. P J Goodwin et al (2002) Journal of Clinical Oncology 20 (1) pp 42-51
  7. M J Gunter et al (2009) Journal of the National Cancer Institute 101 (1) pp 48-60
  8. S L Bowker et al (2006) Diabetes Care 29 (2) pp254-258
  9. V W Ho et al (2011) Cancer Research 71 (13) pp 4484-4493
  10. http://vernerwheelock.com/?p=558
  11. Nina Teicholz. (2014)“The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” Simon & Shuster New York
  12. http://vernerwheelock.com/?p=155

 

123. Changing Patterns of Food Consumption

Epidemiological studies into changing patterns of food consumption and disease statistics can provide valuable insights into the relationships between diet and health. In Great Britain data from national statistics show that amount of fat consumed has fallen from 120gm/day in 1969 to 74gm/day in 2000. When expressed as a proportion of energy consumed the fat intake has decreased from 42.6% in 1980 to 37.7% Calories in 2010.At the same time there has been an increase in the energy as carbohydrate from 44.4 t0 47.4%. Consideration of the different types of fats shows that between 1969 and 2000 that the intake of saturated fat (SFA) has fallen from 56.7 to 29.2 g/day. In other words it has been reduced by almost half!

Healthy Eating has now been actively promoted in the UK for at least a quarter of a century. There is no question that one of the driving forces for these changes was the official UK Committee on Medical Aspects of Food Policy (COMA) in 1984 which recommended:

  • Total fat as a percentage of total daily energy should be reduced from 42 to 31-35% calories
  • Saturated fat should be reduced from 20 to 15% calories
  • Polyunsaturated fat could be increased.

It is evident that the national diet has changed in accordance with these recommendations. The response from the food industry and from consumers has been very positive as demonstrated by the development of extensive ranges of low fat products. A good example of the success of these strategies is the growth in sales of semi-skimmed milk which is now the predominant liquid milk product. However it should also be noted that the reduction in total fat has been largely replaced by an increase in carbohydrates much of which consists of sugar.

Table 1 Changes in the intakes of fat in Great Britain

Year Total fat, g/day Saturated fat , g/day Monounsaturated fat, g/day Polyunsaturated fat, g/day
1969 120 56.7 46.5 11.0
1972 112 52.0 42.9 11.5
1975 107 51.7 39.8 10.1
1980 106 46.8 39.6 11.3
1985  96 40.6 34.7 13.1
1990  86 34.6 34.8 13.9
1995  78 30.8 28.7 13.4
2000  74 29.2 26.3 13.4

 

Source: National Food Survey.

Note: The National Food Survey was replaced by Family Food in 2000 so that data collected since then is not comparable.

. The justification for recommending a reduction in total fat was that as a concentrated source of calories it was a major contributor to obesity. As SFA were considered to raise the level of blood cholesterol (TC) it was concluded that reducing SFA would lower the TC with a consequential reduction in the risk of heart disease. Therefore it is highly relevant to see what has actually happened to some of the key indicators of public health.

The Health Survey for England is a valuable source of information on the state of public health and this has been used to prepare the following tables (1).

Table 2 shows that there have been large increases in the prevalence of obesity. The value for men has almost doubled since 1993.

TABLE 2 PREVALENCE OF OBESITY (BASED ON BMI>30)

YEAR ALL MEN ,% ALL WOMEN,%
1993 13.2 16.4
1998 17.3 21.2
2003 22.2 23.0
2008 24.1 24.9
2010 26.2 26.1

 

In Great Britain the life-time risk of developing bowel cancer in men has increased from 3.5% in 1975 to 6.9% in 2008. In women there has been an increase from 3.9% to 5.4% over the same period. For females aged between 40 and 59 years the breast cancer rates have increased from 134/100,000 in 1979 to 215/100,000 in 2008 (2).

Table 3 shows that between 1994 and 2010 the incidence of diabetes has more than doubled for both men and women (1). The importance of these results cannot be underestimated.  According to Diabetes UK there are 145,000 new cases of diabetes every year which means that the total number in the UK is about 2.6 million. In addition it is estimated that there are about 1 million people who have diabetes which has not been diagnosed and that 7 million people have pre-diabetes which means that they are up to 16 times more likely to develop diabetes than those who do not have the condition.

TABLE 3 PREVALENCE OF DIABETES

YEAR ALL MEN, % ALL WOMEN,%
1994 2.9 1.9
1998 3.3 2.5
2003 4.3 3.4
2006 5.6 4.2
2009 6.5 4.5
2010 6.3 5.3

 

However diabetes is in many ways just the tip of the iceberg because those who suffer from it are likely to experience further complications. These can include damage to small blood vessels which in turn leads to blindness, kidney failure and nerve damage.  Deterioration of the larger arteries can contribute stroke and heart disease as well as difficulties in pregnancy and infection. The American Heart Association has concluded that adults with diabetes are two to four times more likely to have heart disease or a stroke than adults without diabetes.

EXPERIENCE OF OTHER COUNTRIES

The changes in food consumption patterns which have occurred in the UK over the past 25-30 years are in direct contrast with what happened in Spain between 1964 and 1991(3). Over this period the consumption of the main sources of carbohydrate in the diet: bread, pulses, pasta and rice declined from 43.8 to 20.4% of the total food intake. At the same time one of the main sources of fat, dairy products increased from 13.3 to 22.8% of food intake. Other important sources of fat including meat, fish and eggs increased from 10 to 19.7% (Table 4).

TABLE 4 CHANGES IN FOOD CONSUMPTION PATTERNS IN SPAIN BETWEEN 1964-65 AND 1990-1991

                1964-1965              1990-1991
FOOD                                           Gm/person/day
Bread 361.7 164.1
Pasta 12.7 11.7
Rice 27.6 17.9
Potatoes 292.2 137.5
Vegetables 155.8 165.3
Pulses 41.4 22.5
Total fruits 164.8 326.7
Total meat 73.3 229.3
Fish 62.2 87.6
Eggs 43.8 27.9
Milk 219.5 380.0
Cheese 4.4 15.5
Sugar 38.7 25.2
Wine 131.4 68.8
Total fats/oils 76.0 58.8

 

Between 1976 and 1990 the mortality rates from CHD declined from 126/100,000 to 110/100,000 in men and from 59/100,000 to 49/100,000 in women. The decline in deaths due to strokes was even more impressive. It fell from 171/100,000 to 104/100,000 in men and from 147/100,000 to 86/100,000 in women (Table 5).

The reduction in carbohydrates and the increase in fats would be expected to be accompanied by an increase in the death rate from heart disease if the rationale which underpins the dietary recommendations for the UK. In fact the reverse has actually happened with a decline in these death rates.

TABLE 5 CHANGES IN MORTALITY

                                           Mortality/100,000
  1976 1990
Coronary heart disease    
                    Men 126 110
                    Women 60 49
Stroke    
                    Men 171 105
                    Women 147 86

 

Essentially similar results have been reported for Japan.  Between  1958 and 1995 the fat intake in the national diet increased by a factor of 4 due to the increased consumption of meat, eggs and dairy products(4).  Inevitably much of the increased fat was saturated. Despite this change in the pattern of consumption there was no change in the incidence of heart disease. By contrast, the incidence of stroke fell by 85%.

REFERENCES

  1. Health Survey of England 2010 Adult Trend Tables
  2. Cancer Research UK
  3. L. Serra-Majem et al (1995) American Journal of Clinical Nutrition 61 (supplement) pp. 1351S-1359S
  4. A. Okayama (1993) Journal of International Epidemiology 22 (6) pp 1038-104

 

 

122. Disclosure of the Results of Clinical Trials: Case Study of Tamiflu and Implications for Statins

One of the key issues to emerge from the recent spat between Sir Rory Collins and the BMJ about statins (1) has been the refusal of the Cholesterol Treatments Trialists’ Collaboration (CTT) at Oxford University to allow open access to the original clinical trial data. The independent panel set up by the editor of the BMJ concluded that it:

“strongly believes that the current debates on the appropriate use of statins would be

elevated and usefully informed by making available the individual patient-level data

that underpin the relevant studies” (2).

There have been suggestions that the information which is released for publication and to the regulatory bodies is not a true representation of the primary data obtained in the clinical trials (3).

Recently the original data on ‘flu vaccines have been released and it is especially pertinent to discover the insight this example provides.

Tamiflu is one of the medicines used to treat or prevent many different types of flu including bird flu and swine flu. It is recommended by the World health Organisation (WHO) and has been approved by the Food and Drugs Administration (FDA) in the US and by the European Medicines Agency (EMA). In the UK the government has spent £424m in recent years but much of this has had to be discarded because it was never used according to a critical report by the National Audit Office (4).

It is claimed that it will reduce the duration and severity of the flu but questions have been raised about the evidence on which this is based.

The House of Commons Select Committee on Science and Technology has been conducting an Inquiry into “Clinical Trials and Disclosure of Data”. In particular the inquiry focused on the need for transparency of the results of clinical trials, which are primarily concerned with the evaluation of drugs prior to approval (5).

Specific information relating to Tamiflu was presented in a submission from the Cochrane Collaboration which is an international network of volunteer scientists who carry out reviews of evidence on interventions in health care using highly structured and reproducible methods. Cochrane reviews are considered as the gold standard in evidence-based decision making for interventions and are used by many governments in the formulation of public health policies. It is independent of the pharmaceutical companies and any other potential conflicting interests. A group of their researchers had been reviewing 2 vaccines used for ‘flu, namely zanamivir (Relenza, GW now GSK) and oseltamir (Tamiflu, Roche). In their submission they explained the problems encountered in their attempts to obtain the information which was required for their evaluations. In 2009 the team was doing an update of an earlier review which had been published in 2005, when it received a query from a Japanese paediatrician. Dr Keiji Hayashi wanted to know how it was possible that in our 2005 update we had included 8 unpublished Tamiflu trials contained in extreme summary form within another review funded by Roche and carried out by Roche staff and consultants. How could we possibly have done that as we had not seen the original studies? As a consequence Roche was approached but only agreed to release the original raw data if the reviewers would sign a confidentiality clause. Obviously this was not possible because it would compromise the independence, transparency and reproducibility of the report. However as result of coverage on Channel 4 News and in the British Medical Journal Roche publicly promised full study reports. Despite only 4-5 parts of the 10 trials were handed over as Roche claimed that would all that was needed. Subsequently the documents were released and much to their surprise the researchers discovered that there is a clinical study report for each drug trial conducted. This is a complex document containing hundreds or thousands of pages of information with minute details about trials, their planning and execution. Up to that point the Cochrane reviewers were totally dependent on a journal article of a few pages.

At the outset they were aware of 26 trials but it subsequently emerged that there were 123 trials on Tamiflu. The fact that so many were kept under wraps may have had damaging effects on public and clinician confidence in the rigour of how medications are assessed in the UK for safety and effectiveness. There is also a risk that NHS funds have not been used for interventions which offer the best value for money.

  • Nevertheless the Cochrane team did succeed in gaining access to the material which Roche had submitted to the EMA as well as comments made by the FDA on Tamiflu. As a result the team was able to compare the more detailed information with relatively few publications which had been available previously. They found that there were discrepancies in reporting harms and some important aspects of study design between publications and regulatory reports. There were also suggestions that the drug interferes with the natural antibody production. If this is the case it would mean that the use of Tamiflu weakens natural host defences and may weaken response to any antigen stimulating interventions such as vaccines. The regulatory evidence released from EMA and FDA indicates that the positive effects of the drug are not as marked as those claimed by the manufacturer and its consultants in industry-sponsored publications. In agreement with the FDA there was no reliable evidence to conclude that Tamiflu is effective against influenza complications (e.g. pneumonia) and person-to-person transmission.

CONCLUSIONS

In the light of the evidence which has come to light the authors question whether the government would have agreed to stockpile Tamiflu if the complete picture was available when the decision was made. They also note that the WHO and the Centers for Disease Control (CDC) in the US apparently disregard this information and continue to recommend Tamiflu.

This particular case study is confirmation that information has been manipulated by one company in order to improve the chances of approval being granted by the regulatory authorities. There is also no doubt that this type of action is used to advantage in the market place.

Clearly this revelation has major implications for statins. It would not be in the least surprising that a similar approach is being used by the manufacturers of statins. It would certainly explain why Rory Collins and his colleagues at the CTT are so reluctant to allow any outsiders to have access to the clinical trial data which they have. There are already serious doubts about the value of statins, especially when used as a preventive measure in people who have not had problems with heart disease (6). The Department of Health and other bodies such as NICE must insist that the statin data at the CTT and elsewhere is open to scrutiny as a matter of urgency.

NOTE: It is extremely unfortunate that the Cochrane team which recently review statins did not show anything like the same determination as the one investigating Tamiflu. Had it done so it might well have reached a conclusion which was much less favourably disposed towards the use of statins (7). It is rather ironic that relied so heavily on the information provided by the CTT and apparently did not have access to the original trial data. As a consequence, the reputation of the Cochrane Collaboration has become somewhat tarnished, which is a great pity!

REFERENCES

  1. http://vernerwheelock.com/?p=528
  2. http://journals.bmj.com/site/bmj/statins/Final%20report%20of%20the%20independent%20panel%20310714.pdf
  3. http://vernerwheelock.com/?p=575
  4. http://www.nao.org.uk/report/access-to-clinical-trial-information-and-the-stockpiling-of-tamiflu-2/
  5. http://www.publications.parliament.uk/pa/cm201314/cmselect/cmsctech/104/104vw05.htm
  6. http://vernerwheelock.com/?p=432
  7. http://vernerwheelock.com/?p=545

 

 

121. Time for a Reality Check on the NHS

According to a report in The Guardian:

The NHS is generally acknowledged to be facing a growing funding crisis after four years of tight settlements, deepening demographic pressure and an inefficient system that splits health and social care. The Nuffield Trust has suggested there will be a financial shortfall of £2bn in 2015-16” (1).

The politicians are desperately trying to overcome the problems by finding more money.

The critical feature is that there is an almost total failure to conduct any kind of hard-nosed analysis to identify the fundamental issues and devise suitable objectives for the NHS. We have to face the reality that health is deteriorating as shown, for example, by the doubling of diabetes, primarily Type 2(T2D) in the past 15 years. The number of people who require care and nursing is growing steadily. It is therefore no surprise that the costs continue to increase. Clearly this is not sustainable in the long term. If we carry on in this way we will finish up like the USA which spends more than twice the amount on health care per capita as other developed nations, but ranks 49th in life expectancy worldwide.

Instead of accepting that there is a need for additional funds the politicians should be trying to determine what should be done to prevent standards of public health getting worse and working out how to reverse current trends so that a steady improvement can be achieved. Conceptually this is not difficult. The current approach is primarily “curative”. Unfortunately a cure is impossible in the vast majority of cases and the best that can be done is to “manage” the condition or disease. The obvious answer therefore is to place much more emphasis on preventing the disease in the first place.

So why have we come so far down the wrong road? To understand this we have to consider the role of the drug companies. Most of us have been conditioned or “brain washed” into believing that there should be a “cure” for every possible form of ill-health we experience. Even if one is not available at present all we have to do is pour money into research and eventually the scientists will come up with a remedy. While this may work for a number of diseases (eg antibiotics and certain infections) it is definitely not the answer for all diseases. With many of them the damage is permanent. For others, a “cure” may be possible in the short term but if the primary cause (eg exposure to toxins or poor diet) is not removed then the likelihood is that disease will re-cur.

Any analysis of the current difficulties of the NHS must examine the role of the
drug companies. The expenditure on drugs by the NHS is about £14B, which is almost 10% of the total budget (2). It is vital to appreciate that for many of the drugs being prescribed, there is no reliable evidence to demonstrate that they are effective. Quite the contrary, many of them are ineffective. One way of assessing this is to determine the NNT (Number Needed to Treat), which is the number of people who have to be treated in order that one will benefit. This may come as a surprise to many who quite naturally assume that if they have treatment with a drug it will almost certainly help them to recover. However if the NNT is 10 it mean there is a 10% chance of benefit and with an NNT of 100, then there is only a1% chance. Some examples from the NNT website, which only uses high quality studies in its analyses, are shown in Table 1(3). I believe most people would be absolutely astounded to see these results. The normal expectation is that any treatment will have a positive effect for the individual involved. This is certainly true of antibiotics so it somewhat disconcerting to learn that there is only a 1 in 4 chance that the treatment will prevent a respiratory tract infection. However for other treatments the odds of success are even smaller. With thrombolytics for a major heart attack, only 1 in 43 benefits and even then that is dependent on the treatment being applied within 6 hours. The results are even worse if treatment is delayed. Furthermore there were some risks that serious harm could also occur. Despite all the hype it turns out that the NNT team only find benefits for statin treatment in those with known heart disease even then it only applies to 1 patient out of 83. However the risks of developing diabetes are 1 in 50 while 1 in 10 may expect muscle damage. It seems highly likely that perceptions of the benefits of drug treatments are very much greater than the reality. It would be fascinating to discover how many people would agree to these treatments if they were informed of the chances of personal benefit beforehand. Even more astounding is the revelation that although some drugs have limited benefits for some conditions, when used for others there is no benefit whatsoever and in many cases those treated suffer adverse side-effects. This is appalling. It is quite obvious that the benefits of drug use have been grossly exaggerated. Hence it follows that most of the money spent by the NHS and any other body/individual on drugs is wasted. Effectively the pharmaceutical industry is sucking resources out of the system which could be spent in other ways that would facilitate patients. From a policy perspective, reducing expenditure on drugs by the NHS should be a top priority. Unfortunately there is no indication that any politician is aware of this information let alone prepared to tackle this issue head on.

TABLE 1. The Benefits and Harm Associated with Various Medical Treatments

Treatment Benefits Harm
Beta Blockers for Acute Heart Attack (Myocardial Infarction). None were helped 1 in 91 were harmed by cardiogenic shock
Early Invasive Management for Acute Coronary Syndromes None were helped (preventing death)1 in 9 were helped by feeling less pain in chest1 in 59 were helped by avoiding a heart attack in the next year 1 in 33 were harmed by suffering a heart attack.1 in 33 were harmed by suffered major bleeding
Anti-Hypertensive Treatment for the Primary Prevention of Cardiovascular   Events In Mild Hypertension None   were helped (preventing death, stroke, heart disease, or   cardiovascular events 1 in 12   were harmed (medication side effects and stopped the   drug)
Statins Given for 5 Years   for Heart Disease Prevention (With Known Heart Disease) 1 in 83 were helped (life saved)1 in 39 were helped (preventing non-fatal   heart attack)1 in 125 were helped (preventing stroke) 1 in 50 were harmed (develop diabetes)1 in 10 were harmed (muscle damage)
Statins for Acute Coronary Syndrome None   were helped (life saved; heart attack, stroke, or heart   failure prevented) An unknown number were harmed (medication side   effects/adverse reactions)
Statin Drugs Given for 5 Years for Heart Disease   Prevention (Without Known Heart Disease) None were helped (life saved)1 in 60 were helped (preventing heart attack)1 in 268 were helped (preventing stroke) 1 in 50 were harmed (develop diabetes)1 in 10 were harmed (muscle damage)
Blood Pressure Medicines for Five Years to Prevent   Death, Heart Attacks, and Strokes 1 in 125 were helped (prevented death)1 in 67 were helped (prevented stroke)1 in 100 were helped (prevented heart attack)  1 in 10   were harmed (medication side effects, stopping the drug)
Thrombolytics Given for Major Heart Attack 1 in 43 were helped (life saved, given within   6 hours)1 in 63 were helped (life saved, given between   6-12 hours)1 in 200 were helped (life saved, given   between 12-24 hours) 1 in 143 were harmed (major bleeding episode)1 in 250 were harmed (hemorrhagic stroke)
Thrombolytics   for Acute Ischemic Stroke None   were helped (stroke symptoms improved) 1 in 20   were harmed (symptomatic intracranial hemorrhage)
Prophylactic   Antibiotics for Reducing ICU Respiratory Tract Infections and Mortality in   Adults 1 in 18 were helped (life saved)1 in 4 were helped (prevented one respiratory   tract infection) An unknown number were harmed (medication side effects/adverse   reactions)

 

Once the limitations of drugs are appreciated it follows that we have to accept that many diseases cannot be cured. Whilst some alleviation may be possible, the reality is that if these diseases are to be overcome, the only effective strategy is prevention. Essentially this means lifestyle. In this blog I will focus primarily on diet because there is now overwhelming evidence that it does play a critical role in determining an individual’s personal health. This brings us up against another fundamental difficulty which is that much of the official advice is fundamentally wrong and has therefore been a crucial factor contributing to many of our common health problems.

There are convincing reasons why T2D, not obesity, should be regarded as the indicator of public health status. During 2013-2014 there were 45.1 million items prescribed for diabetes, with a net ingredient cost of £803.1million (4). This represents an increase of 66.5% in the number of items and 56.3% in the net ingredient cost since 2005-2006. In England it is estimated that 6% of the population has diabetes and the total cost is currently about £10billion (5). It is estimated that by 2025 there will be 5 million people with diabetes in England (6). Those with diabetes have a reduced life expectancy and an increased risk of retinopathy, stroke, kidney failure, heart disease and amputation of limbs.

A man diagnosed with T2D at age 40 will lose almost 12 years of life and 19 Quality Adjusted Life Years (QALYs) compared with a person without diabetes. A woman of the same age will lose about 14 years of life and 22 QALYs (7). Despite the huge expenditure on drugs, there are serious questions about the effectiveness of treatments of T2D to lower the blood glucose. In a meta-analysis of data from 13 randomized controlled trials there was no benefit, in adults with T2D, from intensive glucose lowering in terms of all-cause mortality or deaths from cardiovascular disease (8). Furthermore, an increase in all-cause mortality of 19% cannot be ruled out. Only one study showed a protective effect on myocardial infarction but this was counterbalanced by an increase in total mortality. The authors pointed out that drugs for the treatment of diabetes are being approved on the basis of their effectiveness in lowering blood glucose, despite the fact that there is no evidence based on clinically relevant criteria. It all adds up to more evidence about the misplaced confidence in the use of drugs to cure many diseases.

There is ample evidence that T2D can be controlled, possibly even cured completely by making changes to the diet (9). The condition is directly due to the increased level of glucose in the blood. As a result the pancreas has to produce insulin to prevent excess glucose in the body. Excessive insulin damages many of the organs, which can eventually lead to a range of diseases. If there is too much glucose over a prolonged period the pancreas is unable to cope and the glucose becomes rampant, causing all sorts of damage. The solution is obvious. Reduce the amount of glucose which enters the body by altering the diet. Sugar is one of the main culprits, so it should be avoided like the plague. In addition starch is broken down to produce glucose. This means that foods such as refined flour, rice or pasta should be limited because the starch is released quickly giving rise to big increases in the blood glucose.

Essentially this means a diet which is low in carbohydrates (LC). The big problem is that the official advice is to increase carbohydrates. There is a strong possibility that those diagnosed with T2D will be advised to replace fat with carbohydrates. This is fundamentally wrong! The recommendation to reduce fat and especially saturated fat (SFA) does not stand up to rigorous examination. In fact, many of the individual SFAs are important nutrients (10). So what we should be doing is limiting the carbohydrates and consuming plenty of fats

In order to make progress it is essential to alter the dietary advice. However this will not be easy. Although there is growing appreciation to limit sugar intake, the official advice from government and the NHS is to reduce fat. This means that those people who are genuinely attempting to consume a healthy diet will opt for low fat versions of dairy, meat and other types of food. Unfortunately this are usually formulated by removing the fat and replacing it with sugar and/or sweeteners. So the consumers are missing out on valuable nutrients and pushing up their intake of sugar. The official advice is to replace the fat with complex carbohydrates, such as wholemeal bread, potatoes, rice and pasta. All of these contain starch which is broken down to glucose, which inevitably raises the level of glucose in the blood. This approach is fully supported and promulgated by the vast majority of professional dietitians and nutritionists, who in any event feel compelled to comply with the official doctrine.

While recognizing the difficulties, it is the responsibility of the politicians to set the agenda and formulate policy objectives accordingly. Clearly it will mean that they have to take on very powerful vested interests, who will fight tooth and nail to maintain the status quo because they are doing very nicely. Politicians must be prepared to tackle bodies such as NICE which is “not fit for purpose” (11).

The current strategy is not working. Vast sums of public money are being wasted. Many people are suffering unnecessarily and dying prematurely. This is a huge challenge for the politicians. Are there any out there with the intellectual ability, determination and astuteness to address this issue?

REFERENCES

  1. http://www.theguardian.com/politics/2014/sep/22/ed-miliband-speech-tax-tobacco-nhs-labour-conference
  2. http://www.theguardian.com/society/2013/nov/06/drug-industry-nhs-cap
  3. http://www.thennt.com/
  4. http://www.hscic.gov.uk/catalogue/PUB14681/pres-diab-eng-200506-201314-rep.pdf
  5. http://www.diabetes.org.uk/Documents/About%20Us/Statistics/Diabetes-key-stats-guidelines-April2014.pdf
  6. http://www.diabetes.org.uk/Documents/Reports/State-of-the-Nation-2012.pdf      
  7. http://jama.jamanetwork.com/article.aspx?articleid=197439
  8. Remy Boussageon et al (2011) http://www.bmj.com/content/343/bmj.d4169.pdf%2Bhtml
  9. http://vernerwheelock.com/?p=422
  10. http://vernerwheelock.com/?p=153
  11. http://vernerwheelock.com/?p=569