188. Report by Credit Suisse Research on Nutrition

An extremely valuable contribution to our understanding of contemporary nutrition has just been released. This is a review of research which has been conducted by a team from the Credit Suisse Bank. The primary purpose is to understand the basic concepts which should be used to devise a diet consistent with good health. In my opinion, the work is objective and extremely competent. Hence the conclusions should be regarded as reliable.

There can be no disagreement that there are fundamental problems with the quality of the diet in many countries as demonstrated by the high incidence of obesity and type 2 diabetes (T2D). However there is debate about the relative importance of the different fats and carbohydrates. This blog will highlight the key points in the report:

  • Natural fat consumption is lower than “ideal” and if anything could increase safely well beyond current levels.
  • Although saturated fat (SFA) was blamed for being the main cause behind an epidemic of heart attacks this cannot be substantiated because consumption declined between 1930 and 1960. Smoking and alcohol were far more likely factors behind the heart attack epidemic.
  • SFA has not been a driver of obesity: fat does not make you fat. The most likely causes are carbohydrates and the solvent-extracted vegetable oils (canola, corn oil, soybean oil, sunflower oil, cottonseed oil). Globally consumption per capita of these oils increased by 214% between 1961 and 2011 and 169% in the U.S. Carbohydrates and vegetable oils accounted for over 90% of the increase in calorie intake in this period.
  • Total blood cholesterol (TC) and LDL cholesterol (the “bad” one)—are poor indicators of CVD risk. In women in particular, TC has zero predictive value if we look at all causes of death. Low blood cholesterol in men could be as bad as very high cholesterol. The best indicators are the size of LDL particles and the ratio of TG (triglycerides) to HDL (the “good” one). A VAP test to check your pattern A/B costs less than $100 in the USA, yet few know of its existence.
  • The intake of foods rich in SFA (butter, palm and coconut oil and lard) poses no risk to health and particularly to the heart. SFA should be regarded as a healthy source of energy and it has a positive effect on the pattern A/B.
  • Transfats have negative health effects.
  • Most research on consistently shows benefits from additional intake of omega-3 fatty acids. Additional intake of 1 gram per day of omega-3 reduces the risk of CVD death by 5-30%. It has also been shown to be beneficial in lowering the risk of mental illnesses such as Alzheimer’s Disease or dementia.
  • An analysis based on a group of 22 European countries shows that there is a positive correlation between the increase in omega-6 intake and the level of CVD deaths.
  • Two surveys of doctors, nutritionist and consumers revealed that all three groups had only superficial knowledge of the potential benefits or risks of increased fat consumption. Their views are influenced significantly more by public health bodies or by WHO and AHA rather than by the results of research. With respect to cholesterol, 40% of nutritionists and 70% of the general practitioners surveyed still believe that eating cholesterol-rich foods is bad for your heart.
  • Consumers have a positive perception of fish, nuts, chicken, eggs, yogurt and milk as sources of fat and a negative view of beef, pork, cheese, margarine and butter. They are neutral to positive on vegetable oils in general, but olive oil commands a very positive “healthy” image.
  • Health care officials and government bodies have been consistently behind developments on the research front. Research showed that transfats were quite unhealthy as early as 1993, yet a full ban of transfats in the U.S. will only happen in 2018. In Europe only Switzerland and Denmark have so far banned them. The stance of most officials and influential organizations such as WHO or AHA is now well behind research in two main areas: SFA and polyunsaturated omega-6 fats.
  • Carbohydrates are one if not the major cause behind the fast growth of metabolic syndrome cases in the U.S.—4% a year—which includes T2D and obesity.

The research team analysed the changes which changes in consumption which occurred in the USA between 1971-75 and 2009-10 during which time the percentage of obese males rose from 12.1% to 35.5%. Over this period, total fat consumption increased just 2%, SFA declined by 7% and protein increased just 7%. By contrast, carbohydrate consumption increased by 30%. The corresponding changes in specific foods is also relevant. Red meat consumption declined by 24%, butter and lard by 39% and eggs by 21%, and dairy rose by just 5%. Conversely, the consumption of vegetable oils (rich in omega-6) soared by 89%, chicken by 139% (which contains saturated fat and omega-6 in almost equal quantities), maize by 100% (rich in omega-6) and sugar by 25%.This led to the conclusion that:

“It seems clear that saturated and monounsaturated fats have very little to do with the soaring levels of obesity among the U.S. population but that carbohydrates and/or polyunsaturated fats (mostly omega-6) have a lot to account for and are also the two main factors behind the overall increase in calorie intake. Excessive consumption of carbohydrates and omega-6 have been shown to trigger insulin resistance through an inflammatory response. Note that obesity is not just an isolated “illness.” Most obese people have a higher probability of experiencing cardiovascular problems, diabetes, and other metabolic illnesses. In retrospect, it would be easy to conclude that in the U.S. the stance of many health officials and medical researchers against saturated fat—and the concomitant switch into carbohydrates and potentially omega-6—created a health disaster of major proportions.”

By focussing on the fundamental changes in the food consumption patterns, the research team has been able to obtain insight into those factors which may have been contributing to the changes. Even more significant, it is shows conclusively that the SFA could not possibly have any involvement in the development of obesity and related health problems. This approach contrasts favourably with that of many academic researchers who restrict themselves to investigations of doubtful validity while ignoring what is happening in the real world.

This is illustrated very neatly in this report with an evaluation of an epidemiological work on omega-6s. A meta-analysis reached the conclusion that replacing 5% of SFA with polyunsaturated fats lowered coronary events by 13%. But there was no breakdown of the relative proportions of omega-3s and omega-6s. Because omega-6s cause inflammation and omega-3s are anti-inflammatory, this information is essential if any sound conclusion is to be drawn. Furthermore there was no information on the content of transfats present in the SFA. In the absence of this information it was totally impossible to reach a definitive conclusion. The fact that the research team identified these weaknesses certainly inspires confidence in the quality of the investigation.

Based on the results, forecasts are made about how demands for various foods and ingredients are likely to change in the future which include:

  • Fat consumption per capita is expected to grow from the 26% of total energy intake registered globally in 2011 to close to 31% by 2030.
  • Carbohydrates will decline from 60% of global energy intake in 2011 to 55% by 2030. This substantial decline is likely to happen because of that the rising awareness of the link between excess carbohydrate consumption (and particularly sugar) and T2D, cardiovascular issues and mental illnesses.
  • SFA is likely to experience the fastest growth, rising from 9.4% in 2011 to 12.7% of daily energy intake by 2030, monounsaturated will increase from 10.2% to 12.2%. On the other hand omega-6s are expected to decline slightly from 6% to 5.4% and omega-3s to grow from 0.50% to 0.55%.
  • Meat consumption is expected to grow 23% over the next fifteen years. The perception of red meat is likely to improve with the acceptance of SFA as healthy rather than harmful.
  • The two leading processed oils: rapeseed and soybean oil should decline somewhat. Palm oil should gradually improve its image and see the benefits of a trend towards “natural” oils and should grow by 10%. There is also a good future for olive oil and coconut oil.
  • The growth in the demand for fish and nuts should be maintained.
  • Eggs should do particularly well as the more people understand that the cholesterol theory has been discredited. By 2030, it is predicted that everyone will be consuming about 5 eggs per week.
  • Demand for butter and cheese should continue to grow at a fast pace, in line with growth rates in the last 3-5 years. Milk and milk-related products should grow by 50% or 2.5% a year. Butter should continue to replace margarine and benefit from the full ban on transfats.


Publication of this report represents a significant step forward in progress towards a total re-evaluation of the current official dietary recommendations in most countries. As it clearly recognises, the guidelines developed in the USA during the 1970s have proved to be an unmitigated disaster. Awareness that changes are required is growing but there is inertia within governments to take the necessary policy initiatives. The fact that these issues are now being considered seriously by the business/financial interests will certainly help to drive things forward. While the implications in the marketplace for some products are poor there are others which will provide opportunities that can be exploited by progressive entrepreneurs. There are indications that this is already happening in Sweden where there has been a shortage of butter reported (2).

I am delighted that the conclusions here are in total agreement with several of my earlier blogs on topics including:

  • Cholesterol (3)
  • Saturated fat(4)
  • Omega-s/omega-6s(5)

A very welcome report which is further ammunition for those of us who to are keen to get these concepts widely accepted.


  1. Credit Suisse Research (2015) “Eat: The New Health Paradigm” https://doc.research-and-analytics.csfb.com/docView?language=ENG&source=ulg&format=PDF&document_id=1053247551&serialid=MFT6JQWS%2b4FvvuMDBUQ7v9g4cGa84%2fgpv8mURvaRWdQ%3d
  2. http://www.dietdoctor.com/butter-shortage-in-sweden
  3. http://vernerwheelock.com/?p=838
  4. http://vernerwheelock.com/?p=854
  5. http://vernerwheelock.com/?p=710




187. Letter to Health Minister in New South Wales about Official Advice on Low Carb

SUBMISSION TO: Hon. Jillian Skinner, MP, Government of New South Wales

FROM: Dr Verner Wheelock

I am extremely concerned about the expulsion of Jennifer Elliott from the Dietitians Association of Australia (DAA) because of her recommendation to lower carbohydrate diets to people with insulin resistance and type 2 diabetes (T2D). Furthermore I find it incomprehensible that the Southern New South Wales Local Health District (SNSW Health) has issued the following instruction that:

“Nutritional advice to clients must not include a low carbohydrate diet. Jennifer will be advised on the information that she may provide to clients…. ”

The impact of this is that people who have effectively cured their T2D by lowering their blood glucose, losing weight and stopped all medication will be told to increase their carbohydrate intake, which caused the T2D in the first place.

There is absolutely no doubt that reducing carbohydrate consumption (coupled with an increased intake of healthy fats….low carb/high fat (LCHF)) is extremely successful in the treatment of T2D in very many people.

There is convincing research which has been collated in an excellent paper prepared by many of the leading practitioners in the field (1). This explains in detail how and why restriction of carbohydrates is an extremely effective treatment for T2D. Patients find it easy to do, weight loss is not essential and there are no adverse side effects.

Even more impressive is the enormous number of individuals who have successfully cured T2D by adopting this strategy. I am well aware that some who claim to be “scientists” discount these on the grounds that they are “anecdotal”. If it was limited to a few then this might be a reasonable point of view but when there are so many, this type of criticism simply lacks credibility. When so many find the official advice does not work while the LCHF approach is successful, then this has to be of major significance. Is it is reasonable and logical to condemn all these people as liars and charlatans?

As a person who has been in business for 25 years it is essential to be able to make judgments based on the totality of evidence which is available. It is completely unrealistic to wait until the academics in business management have come to a conclusion. Is this specific issue any different?

Recently the BMJ published a report from 2 GPs describing how one of their patients with T2D had improved his health significantly by changing his diet and lifestyle (2). He has come off sugar altogether and cut out bread (he previously consumed a lot of this), potatoes, pasta, cereals, and rice. This has led to greater consumption of green vegetables, but also eggs, full fat Greek yoghurt, and cheese. This is in direct contradiction of the instructions issued by SNSW Health. The result was that he lost 16kg in body weight. HbA1c fell from 52 to 43 mmol/mol (6.9% to 6.2%) and blood pressure from 130/80 mm Hg to 117/70 mm Hg. As a consequence he stopped all medication. What was even more remarkable was the response to the article from almost 40 people (3). Many of these were from diabetics, including those with T1D. Here are some extracts from these responses:

    • “I see patients who have type-1 or -2 diabetes among others at my private practice. Some of them have come to the same conclusion as the patient of the article by reading themselves about low carb, or their doctor had recommended it. Those patients usually have lost weight and many do fine with none or less medication. As high blood sugar is a cause of retinopathy, the better HbA1c reflects to their eye health too.” (Ophthalmologist in Finland)
    • “I am an elite outrigger canoe paddler and Type 1 of 19 years. I have been quite successful over the years with multiple World Titles and WR’s. During my years training and racing there was always the worry of hypos and not only effecting performance but also endangering life. I had tiredness and hunger constantly…….Starting in October 2014 in between major comps I started my LCHF lifestyle and have had the best months of my diabetic life. No hunger, great energy, good recovery, level BGL, and performance is fantastic.” (Athlete from Brisbane)
    • “I’m a 49 year old type 1…I cannot understand the current recommendations in my country by the ADA on giving 30-60 carbs per meal. It’s a proven, scientific fact that carbs raise glucose….and high glucose causes an entire slew of complications such as blindness, loss of limbs to neuropathy and kidney failure…so why recommend eating so many carbs?? I eat 30 grams or less of carbohydrate per day and all those are from non-starchy veggies. I am well nourished, never hungry and my last 5 A1C’s have been in the 4’s. ..with the last one 4.8..”( Hair replacement specialist USA)
    • “As an obesity medicine physician who uses low carb high fats diets in all of my patients I cheer the publication of this article. Nowhere in medical school or after is the concept of taking someone OFF medications discussed. Why should we? Patients are supposed to just get sicker, right? This attitude is not only pervasive but more important WRONG. They get sicker only when they are taught to eat a diet that makes them sicker. Unfortunately, this is the low fat diet pushed by all so called “patient advocacy groups” such as the American Diabetes Association. When taught to eat a whole foods low carb high fat diet patients do get better and “deprescribing” is a daily occurrence in our clinic.” (Physician, USA)
  • “I was diagnosed T2 in 2000 with an HbA1c of about 11. The presenting symptoms were peripheral neuropathy & extreme tiredness. I was advised that T2 was progressive & however well I complied with the NHS/Diabetes UK diet – complex carbs, low fat, sugar & salt – my condition would worsen, progressing to increased medication, insulin, amputation, blindness … & the Dr helpfully computed my probability of a heart attack at 25%. WOW! I went out in a state of shock. For 7 1/2 years I carefully followed the recommendations until in 2008 my neuropathy condition was crippling. It was painful to get out of bed. Driving was becoming dangerous. HbA1c was about 7 so the Dr considered hospital referral, rather than a diabetes control problem. I had other diabetes related symptoms…..  


  • In May 2008 I cut out all the obvious carbs, increasing veg & fatty foods. My diabetes control & health rapidly improved. In 3 months I was out of pain & able to play tennis again. I have been taking 3×500 mg metformin, & continue to do so. Seven years on, at age 76, I am fit & well, playing tennis at club standard & with no diabetes symptoms or health complications. My HbA1c range is between 6 & 6.6. “(Retired scientific consultant, England).


On 16th September 2015 when the American Diabetes Association (ADA) asked on Facebook

“What was your most recent blood glucose reading?”

it was overwhelmed with over 800 responses, almost all of which were highly critical (4). Here is a selection:

  • I was dx’d two years ago, was force feeding myself to reach the daily carb requirements, I was taking boatloads of insulin, going low then high and very down emotionally because of it. Then I found the better way. I used to walk around with tears in my eyes and a lump in my throat, now I have a skip in my step…low carb and typeonegrit have been a game changer for me!
  • Been using whole food diets void of sugars, grains, processing and industrial veggie oils for fifteen years with my patients. Reversing diabetes while reducing CV risk. Lots of good evidence to support this approach. http://denversdietdoctor.com/medical-weight-loss/
  • Time to see the handwriting on the wall, ADA. Love all the comments below showing that the best way to get optimum blood glucose control isn’t with the ADA recommendations but with a low carb high fat moderate protein diet. That’s what diabetics should be eating, American Diabetes Association!
  • Been off insulin for 2 1/2 years now do to low carb diet. No more highs or lows! My blood sugar is PERFECT! Lost 130 pound (but stopped insulin only 2 weeks in cause I normalized that fast!) No more fatty liver, cholesterol is perfect! And the weight continues to come off! Why is American Diabetes Association still recommend such high carb levels! Following those recommendations almost killed me! It’s already acknowledged low carb is best…but still changes nothing. A little angry over this…
  • Wow. Just reading through these threads and finding hundreds of people who have reversed Type 2 diabetes by NOT listening to the ADA. I just clicked on Diabetic Living magazine, and shortcake is on one cover and shells are on another cover! What? This is poison.
  • The ADA diet is responsible for the deaths and maiming of many diabetics. If you want to live with diabetes and be healthy, low carb is the only way.
  • I went from “Prediabetic” to Type 2 thanks to following ADA diet recommendations. I gained more weight on your diet than at any other time in my life. And I felt worse than ever. If I hadn’t decided to be “noncompliant” and reduce my carb load to 60gm/day I know I’d be even worse off. I now eat LCHF and my sugars run between 70-90s and no huge spikes anymore since I know WHAT to eat. I test 8-12 times a day in order to “keep an eye” on my sugars. And because of LCHF I’ve lost 26 lbs of the weight your stupid plan added! Why on earth would you tell DIABETICS to eat CARBS especially in the asinine levels you recommend? The ADA should be ashamed and either revamp or go away. I’m all for a class action suit. My fbs this morning? A healthy 74!
  • The ADA is probably so sorry they asked the question and have no idea how to reply to all these wonderful people fighting against ADA and their shameful advice that is killing people
  • I was following the ADA diet while being a “diabetic” for 30 yrs, now on wheat belly life style I have been insulin free with normal AlC’s for 10 months . My doc. Says GREAT!! Keep up doing what you are doing. All my labs are also normal range , I’m down to only 2 ordered drugs and I’m almost 80 yrs old . I feel really good. I follow dr. William Davis’s wheat belly life style and am now in love with him for showing me a new way to good health.
  • They won’t listen. They will use their studies that are funded by pharma companies and the grain association to tell all of you normal people that have seen changes by eating low carb or grain free that you are wrong and it is all in your head.
  • Interestingly, FACEBOOK is now blocking all my attempts to comment or “like” postings which show: Dr. Richard K. Bernstein’s, Diabetes Solution, saying that “this message contains content that has been blocked by our security systems.”


    • Really? Now even FB wants to interfere with the exchange of knowledge taking place here??
  • My experience as a nurse for 41 years reinforces that many of the approaches that traditional healthcare has used for many years have NOT been effective for many persons. That spurred my own quest to find additional information and learn more about research — even am back n school (doctoral program ). And these days, Dr. Bernstein’s book, Diabetes Solutions, stays on the shelf in my desk hutch – within easy reach and reference!!


    • And yes, I changed how our our family eats as I learned more from the research publications, and looked for these forums as well.
  • 95. After years of taking statins, thiazides and beta-blockers, which some peer-reviewed research tells me might have been the cause, a year and a half ago my fasting glucose was no longer high-normal but suddenly 131. I went on a lowcarb/moderateprotein/highfat diet, and now my formerly awful lipid profile looks fine without statins, my fasting glucose is good, and I’ve dropped 40 pounds. One of my doctors is sure this will kill me no matter how good my bloodwork looks the same doctor who refuses to believe that excessive protein raises my blood glucose, but I have piles of data to prove it, and piles of friends with similar piles of data. Dr. Bernstein’s book is my bible. You can’t argue with facts, try as you may. And you will.
  • The latest information from CSIRO are recommending 50grams of carb per day for DIABETICS. This information will be released to the public within the next few months. A 2 year study that has PROVEN results with 50grams or less of carb per day plus 3 strength sessions per week WILL LOWER your HBA1C. Switch over to low carb and enjoy a long life without complications.


I could go on and on. The evidence is overwhelming. It is absolutely appalling that literally millions of people all over the world are being given advice which is WRONG and making their health even worse. As a consequence they have to endure considerable suffering and their life span is reduced. As these case studies demonstrate most of this is unnecessary. We have all been let down by the professionals fuelled by a toxic combination of incompetence, corruption and hubris. There is no doubt that things are changing slowly because people are being empowered by the information which can be accessed via the internet. But the process could be accelerated if the politicians grasped the nettle and took effective action. You have an opportunity to make a real difference by taking initiatives to stop the nonsense currently being promulgated by official bodies which are responsible to you. Even more important is to promote the dietary principles which are so obviously successful all over the world. By doing this you would be helping to improve the health of the citizens of New South Wales and the financial savings would be absolutely huge. No doubt some of these will be members of your own family and friends. I can assure you that this action would be widely welcomed in many different countries. You would be recognised as the trailblazer with the imagination and determination to make the breakthrough that so many politicians have shirked because of their timidity and ineptness.

The reality is that if T2D is not controlled the incidence will continue to grow to a point where it will become so expensive and damaging to public health that it will not be sustainable.

There is no question that the policy changes will have to be implemented eventually. So why not sooner rather than later.


  1. R D Feinman et al (2015) http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/pdf
  2. D Unwin & S Tobin (2015) http://www.bmj.com/content/351/bmj.h4023
  3. http://www.bmj.com/content/351/bmj.h4023/rapid-responses
  4. https://www.facebook.com/AmericanDiabetesAssociation/posts/10153140618374033?comment_id=10153144986604033&ref=notif&notif_t=like&hc_location=ufi

186. Diabetes Prevention Programme

In March 2015, NHS England announced the Diabetes Prevention Programme (DPP) which is a joint initiative with Public Health England (PHE) and Diabetes UK (1).The object is to achieve a significant reduction in the number of people with Type 2 Diabetes (T2D) which is expected to be about 4 million if no action is taken. It is claimed that there have been well-designed trials conducted in Finland, the USA, Japan, China and India which show that reductions of up to 60% can be obtained in adults at high risk by means of intervention programmes to encourage changes in lifestyle.

The justification has been developed by NICE. The initial proposals were subject to severe criticisms by specialists in the treatment of T2D (2). For example great emphasis was placed on the importance of weight loss and exercise in spite of limited evidence in support of this strategy. But this was in conflict with the drugs recommended which actually promote weight gain.

As a consequence substantial amendments were made and a revised consultation document was issued (3). The guidelines are set out in a document entitled “Type 2 diabetes in adults” (4). In addition there is whole raft of appendices.

In view of the importance of developing a policy which will successfully control this key public health issue, it is worth analyzing the DPP carefully.

The Rationale

T2D is defined as a:

“condition of insufficient insulin production often exacerbated by insulin resistance, the primary treatment for which is weight loss and exercise. Pharmacological measures to increase insulin sensitivity or to increase insulin release can be added to lifestyle interventions, but insulin therapy may eventually be needed by the majority of people as their insulin secretion declines.”

Subsequently it goes on to explain that:

“The underlying disorder of type 2 diabetes is usually that of a background of insulin insensitivity where the body is unable to respond to normal levels of insulin, and insulin deficiency where the pancreas is unable to secrete enough insulin to compensate for this resistance. Insulin insensitivity is usually evidenced by excess body weight or obesity, and is exacerbated by overeating and inactivity. It is commonly associated with raised blood pressure, a disturbance of blood lipid levels, and a tendency to develop thrombosis. This combination is often recognised as ‘metabolic syndrome’, and is associated with fatty liver and abdominal adiposity (increased waist circumference). Insulin deficiency is progressive over time, such that the high glucose levels usually worsen relentlessly over a period of 30 years, requiring continued escalation of blood glucose lowering therapy.”

This really is quite remarkable because the insulin resistance is caused by the excessive production of insulin. It is obvious that those responsible for these proposed guidelines have a very limited perspective. While it is true that Type 1 Diabetes (T1D) is the result of insufficient insulin production because of damage to the pancreas, there seems to be a failure to appreciate that T2D is a totally different disease. The fundamental issue with T2D is excessive levels of glucose in the blood. This in turn stimulates the production of extra insulin which is needed to cope with the large amounts of glucose. While this may be perceived as a requirement for more insulin, it is inevitable that if more insulin is supplied it will exacerbate the insulin resistance, which contributes to the ill-health. It really does not take a genius to work out that if there is a reduction in the blood glucose then there should be a corresponding reduction in the requirement for insulin to be produced. The level of blood glucose is determined by the diet and therefore it follows that alteration to the diet is the obvious solution to the problem.

The Solution

Although the main emphasis in the DPP was on the use of drugs to treat T2D there is one chapter which is devoted to “Lifestyle and non-pharmacological management”. This concludes that:

there was little new evidence to warrant any change to previous views in this field. The major consensus-based recommendations from the UK and USA emphasise sensible practical implementation of nutritional advice for people with type 2 diabetes. Management otherwise will concentrate on principles of healthy eating (essentially those for optimal cardiovascular risk protection), and reduction of high levels of free carbohydrate in foods that may cause hyperglycaemia in the presence of defective insulin secretory reserve”.

Here again, note the term “defective insulin secretory reserve” where the underlying assumption seems to be that the body should be able to cope with whatever is thrown at it. Would it not be much more sensible to regard a diet which produced excessive glucose in the blood as toxic? Obviously this question never arose because it is certainly not addressed in the current official recommendations which are to:

“Emphasise advice on healthy balanced eating that is applicable to the general population when providing advice to adults with type 2 diabetes. Encourage high-fibre, low-glycaemic-index sources of carbohydrate in the diet, such as fruit, vegetables, wholegrains and pulses; include low-fat dairy products and oily fish; and control the intake of foods containing saturated and trans fatty acids”.

It goes on to state that:

“If people are currently gaining weight, weight maintenance is advantageous”.

Finally some suggestions for future research are presented on the grounds that:

“Type 2 diabetes is associated with obesity, and lifestyle interventions including diet and physical activity are thought to be useful in helping to control the condition and improve patient outcomes such as reducing the risk of long-term complications and increasing quality of life. Low carbohydrate diets have been a source of discussion over the past two decades and there is much debate regarding its effectiveness and safety in controlling blood glucose levels, particularly in the longer-term. Specifically, there is little consensus on the optimal intake of daily carbohydrates, where the risk of adverse effects such as hypoglycaemia is minimised. A randomised controlled trial addressing this clinical question would help to provide a better understanding of the effects of low carbohydrate diets on diabetes control and maintenance to inform appropriate management strategies”.

During the consultation period a number of pertinent comments were made (5). It was pointed out that there was no reliable evidence to support a recommendation to reduce SFA therefore the advice to consume low fat dairy produce could not be justified. The response was:

“Thank you for your feedback. It was not within the scope of the guideline to update the evidence review on dietary advice therefore it is not possible to make changes to this section”.

When it was suggested that longer-term trials need to be undertaken to test the long-term efficacy and safety of low carbohydrate diets, the reply was exactly the same.

Essentially what we have is a passing reference to “Diet and lifestyle” which simply goes along with the current approach. The response to the comments made during the consultation exercise reveals that there are no plans to change things as they are. Presumably this is accurately reflected in what appears on the NHS Choices website (6) which proffers the following advice on how to cope with T2D.

For diet, the strategy is to increase the amount of fibre and to reduce fat, especially SFA. Specific advice includes:

  • Increase consumption of foods such as wholegrain bread and cereals
  • Choose foods that are low in fat – replace butter, ghee and coconut oil with low fat spreads and vegetable oil
  • Choose skimmed and semi-skimmed milk, and low fat yoghurts

If you have a BMI of 30kg/m2 or over you should lose weight by gradually by reducing your calorie intake and becoming more physically active. Losing 5-10% of your total body weight over the course of a year is considered to be a realistic initial target.

With respect to exercise for adults who are aged between 19 and 64 years, it is recommended that there should be a minimum of:

  • 150 minutes (2 hours and 30 minutes) of “moderate-intensity” aerobic activity, such as cycling or fast walking, a week, which can be taken in sessions of 10 minutes or more, and
  • muscle-strengthening activities on two or more days a week that work all major muscle groups (legs, hips, back, abdomen, chest, shoulders and arms).


Although there is relatively little emphasis on diet and lifestyle, it is evident that there is heavy reliance on weight loss. This seems to be unduly optimistic, especially as there are no plans to review the existing dietary recommendations, which have not exactly been a howling success. On the face of it, the chances of success do not appear to be high so I will be doing a more detailed critique in subsequent blogs.



  1. http://www.england.nhs.uk/2015/03/12/diabetes-prevention/
  2. http://www.pulsetoday.co.uk/clinical/diabetes/nice-risks-making-itself-a-laughing-stock-over-guidance-on-metformin-alternatives-say-experts/20009139.article#.VdhZxnlRHIU
  3. http://www.nice.org.uk/guidance/GID-CGWAVE0612/documents/type-2-diabetes-guideline-consultation-2
  4. http://www.nice.org.uk/guidance/gid-cgwave0612/resources/type-2-diabetes-full-guideline2
  5. http://www.nice.org.uk/guidance/GID-CGWAVE0612/documents/type-2-diabetes-first-consultation-comments-table-with-responses-2
  6. http://www.nhs.uk/Conditions/Diabetes-type2/Pages/Treatment.aspx


185. Type 2 Diabetes Policy is an Absolute Shambles

Diabetes UK has just issued another warning about Type 2 Diabetes (T2D) in a press statement (1).

According to this, there are now almost 3.5 million people in England and Wales who have been diagnosed with T2D, which is an increase of over 60% in the past 10 years. The true value is probably about 4 million if those who were undiagnosed are taken into account. The organisation claims there is a need for urgent action to ensure that all those affected are provided with high quality care as recommended by NICE. It also advocates that there should be more emphasis on prevention. The Chief Executive said that there is huge potential to save money and reduce pressure on NHS hospitals and services by providing better care to prevent people with T2D from developing devastating and costly complications.

The current official approach to the prevention and treatment of T2D is based on a concept of the disease which is fundamentally flawed.

Diabetes UK lists the following factors which increase the risks of developing T2D:

  • Being overweight or having a high Body Mass Index (BMI).
  • Waist circumference greater than 80 cm in women and 94 cm in men
  • African-Caribbean, Black African, Chinese or South Asian background and over 25 years old
  • From another ethnic background and over 40
  • Have a parent, brother or sister with T2D
  • Have had high blood pressure, a heart attack or a stroke
  • Have a history of polycystic ovaries, gestational diabetes or have given birth to a baby 4.5kg
  • Suffer from schizophrenia, bipolar illness or depression, or you are taking anti-psychotic medication.

There is no suggestion that T2D can be cured. Anyone who is diagnosed with the disease is given information on how to manage it. As a general rule the advice given by Diabetes UK in agreement with the official position of the NHS.

In particular, weight loss is regarded as one of the prime objectives. This can be achieved by a combination of diet and exercise. According to this the fibre content of the diet should be increased by consuming foods such as whole grain bread and cereals, beans and legumes as well as fruit and vegetables. In addition the intake of fat, especially saturated fat (SFA) should be restricted so low fat spreads and vegetable oil are recommended instead of butter as well as low fat versions of other foods.

This approach is a good an example of a failure to see the wood for the trees. T2D is caused by excess glucose in the blood. This in turn stimulates the pancreas to produce insulin which has a variety of different functions. One of these is to direct the glucose to the liver where most of it is converted into fat for storage, thereby leading to body weight gain. Continuous excessive production of insulin results in insulin resistance to many different organs in the body. Effectively this is damage which may eventually cause chronic disease such as atherosclerosis and various cancers.

Ultimately the ability of the pancreas to produce insulin is impaired so that the glucose cannot be effectively controlled. The excess glucose also causes damage. For examples by becoming attached to proteins, which prevents them functioning properly. This is full blown T2D.

It does not take a genius to work out that there is just one single factor which is causing these problems, which is the amount of glucose which is entering the blood stream from the food supply. The obvious answer therefore is to reduce it. The first step must be to reduce the sugar intake. As sugar breaks down to glucose and fructose it is a particularly dangerous combination. This is because fructose can only be metabolised in the liver which means a big reduction in the capacity to deal with the glucose. By contrast the glucose can be metabolised throughout the body. It is important to understand that sugar is present as an ingredient in many different manufactured foods. Rather ironically many “low fat” foods are formulated by removing the fat and replacing it with sugar. Hence those who follow the official advice may well finish up with increasing their sugar intake. In addition the starch, which is present in foods such as bread, flour, potatoes, rice and pasta, is broken down during digestion to release glucose and therefore contributes to the amount present in the blood.

There is now a comprehensive body of evidence which confirms that this strategy of reducing the consumption of sugar and carbohydrate-containing foods is effective and should also be the first approach (2). Furthermore there are numerous personal case histories of individuals who have adopted similar protocols and achieved great success (3). It also follows that increasing incidence of T2D is the direct result of the increasing consumption of sugar and other foods which contain carbohydrates. One of the main reasons for this has been the emphasis on reducing fat that has obviously had an impact as shown by the success of the low fat foods in the market place. When this is combined with the growth in consumption of Sugar Sweetened Beverages (SSBs) there has inevitably been an increase in the consumption of carbohydrates. So it is not in the least surprising that T2D incidence has increased. The only sensible policy that will counter T2D is to introduce measures which will alter the national diet so that there will be a very substantial reduction in the intake of sugar and other carbohydrate-containing foods.

It is difficult to understand how weight loss would be effective. There is no evidence to indicate that overweight/obesity is the cause of T2D. A more rational explanation is that both conditions are caused by a common factor, namely excess blood glucose. In reality the relationship between obesity and T2D may be rather complex. It turns out that several countries with a high incidence of T2D have low rates of obesity and vice versa. In Sri Lanka, the prevalence of T2D increased from 3% in 2000 to 11% in 2011, while the obesity rate remained constant at 0.1%. (4).

It has also been found that up to 20% of people who have a BMI which is “normal” have been diagnosed with T2D. Even more worrying is that the death rate in this group is about double that of those who are overweight or obese when diagnosed with T2D (5).

Another major concern is that the initial damage caused by T2D, such as retinopathy, may not be detectable for several years prior to clinical diagnosis (6).


The present policies for tackling T2D are doomed to failure. First of all, they are far too late and quite considerable damage is likely to have occurred before the disease is actually recognised. Secondly, there is no reliable evidence to demonstrate that weight loss is an effective strategy for coping with T2D. The probability is that it will make things worse since the standard conventional advice is to reduce fat to help with the weight loss but also to reduce the risk of heart disease, which is another rather dubious approach. To compensate for the reduction in fat, an increase in complex carbohydrates is usually recommended. If there is to be a genuine attempt to control T2D, then the only logical strategy is to focus on prevention. Essentially this means there will have to a concerted effort to reduce the consumption of carbohydrates, with the emphasis on eliminating sugar from the diet. However for this to be totally successful, there will have to be some increase in the consumption of SFAs, which is in direct conflict with current government policy in the UK.


  1. https://www.diabetes.org.uk/About_us/News/diabetes-up-60-per-cent-in-last-decade-/
  2. http://www.sciencedirect.com/science/article/pii/S0899900714003323
  3. http://vernerwheelock.com/?p=842
  4. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0057873
  5. http://jama.jamanetwork.com/article.aspx?articleid=1309174
  6. http://care.diabetesjournals.org/content/15/7/815.abstract

184. Getting to Grips with the Saturated Fats

The main thrust of the healthy eating recommendations which have been promulgated as official policy for the past 40 years or so has been to reduce the intake of total fat, especially the saturated fats (SFAs). Numerous evaluations of the rationale to support this advice have concluded that it was fundamentally flawed. What is more, there are convincing reasons to believe that those who complied have damaged their health because of the changes they made to their habitual diet. In particular, the increase in the consumption in sugar and other carbohydrate-containing foods is probably why there has been such a disastrous increase in the incidence of obesity, Type 2 Diabetes (T2D) and related conditions.

The most recent study has just been published in the BMJ (1). It has been conducted by a team of researchers based in Canada. The object of the investigation was to do a systematic review of the associations between the intakes of SFAs and the trans fatty acids (TFAs) with respect to all-cause mortality (ACM) as well as cardiovascular disease (CVD), coronary heart disease (CHD), stroke and T2D.

This type of work has been bedevilled by misuse of associations because there are far too many examples of wrongly using this type of information to conclude that there is cause and effect. So if there is no association it is highly unlikely that there is a cause and effect.

The main focus of this blog will be on ACM because that is the prime concern of most people. In the past there has been too much emphasis on a single disease such as CHD to the exclusion of all others. It now evident that those who were pushing the “cholesterol theory” totally ignored the increase in the incidence of cancer which is invariably observed at low values of blood cholesterol and LDL cholesterol.

Here are some of the key results from the Canadian study:

  • For the studies on SFAs, the team started out with 20,413 potentially eligible articles. These were ultimately whittled down to 6 which met the stringent criteria that had been established.
  • There was no association between SFA intake and ACM.
  • There were a few studies which suggested that ACM increases at high intakes of TFAs. However there was reliable and strong positive associations between TFA intake and CHD and CHD mortality which was consistent with several previous systematic reviews and meta-analyses. TFAs may cause inflammation, which can be the starting point for many chronic diseases.
  • The damage to health was restricted to TFAs produce by industrial processes. There was no indication of increased risks associated with the TFAs present in cows’ milk.

Any attempt to establish the facts in this field is beset with difficulties, which are rarely appreciated by the researchers so the reality is that many of the studies are very poor and should never have been used as a basis for the development of policies. First of all, there are many different individual saturated fatty acids and it certainly cannot be assumed that they all have a similar function in the body. In fact it would be remarkable if they did. The number of carbon atoms can vary from 1 or 2 up to 20 or more. There is convincing evidence that the short and medium chain fatty acids (MCTs) are especially valuable nutrients. This is because they do not need to be emulsified by bile salts and so are rapidly absorbed into the blood stream from the small intestine. They are especially valuable because they boost the immune system and possess anti-microbial, anti-viral and anti-tumour properties. Lauric acid (C12) is particularly effective.

Much of the case used to condemn the SFA is based on some rather dubious studies which conclude that the SFAs “lower cholesterol” but again it depends on which individual fatty acid is being considered. It is recognized that certain ones such as stearic acid (C18) does not have any effect. But all this is only of academic interest since it is now known that the ACM is raised at low values of both Total Cholesterol and LDL Cholesterol in the blood (2, 3).

The source of SFAs used in the different studies can actually vary considerably. In some, fat from animal products has been wrongly labelled as saturated so results from this type of investigation are quite meaningless.

It is also crucial to allow for the effect of other nutrients which may be present. The Canadians note that there were differences between studies on T2D. In one of these adjustments had been made for the magnesium and fibre levels in the diets but in the other this had not been done. It was also found that replacing the SFAs with either carbohydrates or other fats produced differences in the results.

It is significant that there the case for lowering the intake of the SFAs has been found wanting when subjected to rigorous examination. In recent years, there have been several studies which have all come to the same conclusion. Earlier this year Zoe Harcombe and colleagues analysed the results of all the studies which had been done prior to the introduction of the recommendation to reduce SFAs in 1983 (4). They found that there were no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions. Although there were reductions in mean serum cholesterol levels which were significantly higher in the intervention groups, this did not result in significant differences in CHD or all-cause mortality.


An earlier meta-analysis conducted in 2010 concluded that there was:

no significant evidence to conclude that dietary saturated fat(SFA) is associated with an increased risk of CHD, stroke or CVD” (5).


Despite all this the UK Government carries on with its discredited policies. In a response to a letter from me forwarded by my MP to the Health Minister. The reply from the one of the junior ministers, Jane Ellison, contained the following statement:

“There is good evidence that saturated fat consumption influences serum cholesterol levels and thereby increases the risk of cardiovascular disease. On this basis, the PHE will continue to advise people to consume a diet that is low in saturated fat”

What a load of absolute rubbish!!


  1. http://www.bmj.com/content/351/bmj.h3978
  2. http://vernerwheelock.com/?p=838
  3. https://www.karger.com/Article/Pdf/381654
  4. http://openheart.bmj.com/content/2/1/e000196
  5. P. Siri-Tarino (2010) American Journal of Clinical Nutrition 91 (3)  pp. 535-546

183. The Significance of the Low Carb Summit in Cape Town, February 2015

There is no absolutely no doubt that the dietary recommendations which were formulated by the US Senate Committee chaired by George McGovern have proved to be disastrous. Effectively this resulted in public health policies all over the world advising that total fat, especially the saturated fats (SFAs) should be reduced and that there should be an increase in the intake of carbohydrates. Consequently there has been a shift in food consumption patterns as various measures have been implemented as a response. In particular, the food industry has altered the composition of many products so that they can be promoted as “low fat”. Very often the fat has been replaced by sugar. In addition the use of sugar as an ingredient in manufactured products has become widespread. The growth in the consumption of soft drinks has contributed to the increased sugar intake.

In parallel with these changes in food consumption, there have been progressive increases in the incidence of obesity, Type 2 Diabetes (T2D) and many other related conditions such as kidney disease. We have now reached a point where the science confirms that the change in diet is one of the primary causes of the deterioration in public health standards. It follows therefore that these changes which have occurred over the past 40 years or so will have to be reversed. Hence the carbohydrates will have to be reduced and replaced by healthy fats summarised by the Low Carb High Fat (LCHF). In an ideal world, the logic of the case would lead to initiatives designed to achieve this objective. Unfortunately there is resistance from very powerful interests including businesses that feel threatened and scientists who are not prepared to admit that they have been wrong.

Nevertheless things are starting to move. The most recent significant event was the Low Carb Summit which was held in Cape Town in February 2015 hosted by Tim Noakes and organised by Karen Thomson, who is a grand-daughter of Professor Christiaan Barnard. It was the first time that most of the leading figures in the world from a variety of disciplines and backgrounds came together to share their experience and knowledge. This meeting was highly successful. The presentations by speakers representing a range of disciplines and backgrounds were extremely impressive and provided a very powerful and compelling case in support of an LCHF diet. The rationale is extremely convincing, especially as the same message is coming through loud and clear from a wide variety of perspectives.

At the end of the conference the following statement was issued which was endorsed by all the speakers:

“The mainstream dietary advice that we are currently giving to the world has simply not worked. Instead it is the opinion of all 15 speakers at the Old Mutual Health Summit that this incorrect nutritional advice is the immediate cause of the global obesity and diabetes epidemics.

This advice has failed because it completely ignores the history of why and how human nutrition has developed over the past three million years. More importantly, it refuses to acknowledge the presence of insulin resistance (carbohydrate intolerance) as the single most prevalent biological state in modern humans eating according to those current dietary guidelines which promote low-fat and high-carbohydrate intakes.

Persons with insulin resistance are at an increased risk of developing a wide range of chronic medical conditions if they ingest high carbohydrate diets for any length of time (decades).”

It was extremely relevant that the Summit was held in South Africa because of the developments there. Last year Tim Noakes and colleagues produced a comprehensive book which described the background to the flawed recommendations and explained the rationale of the new approach based on LCHF which is also referred to as a Banting diet (1). However the book also contained a variety of recipes for very attractive meals which were admirably illustrated. The initial print run was 3,000 but it proved to be an immediate success topping the best seller lists in South Africa for at least 20 weeks. It has now sold over 200,000 copies and has been launched overseas. Clearly it struck a chord. It came as a pleasant surprise that meals prepared from ingredients which had been portrayed as “unhealthy” such as meat and full fat dairy products could now be regarded as “healthy”. Even more significant was there were many individuals who discovered that they started to lose weight and that within a matter of months had reached an acceptable level. To cap it all, their general health improved. Further evidence of the impact is that there is a growing number of restaurants which provide and promote menus based on the Banting principles.

The conference speakers have produced a wealth of knowledge which will be invaluable for anyone who is interested in understanding the background research which demonstrates the dangers of excess sugar and carbohydrates and why the case for reducing the SFAs was full of holes. The whole cholesterol story has turned out to rubbish which means that there is absolutely no justification for recommending the polyunsaturated (omega-6s) on the grounds that they “lower cholesterol”. In reality the excessive amounts consumed in most countries contribute to the development of inflammation, which can lead to a range of serious chronic diseases.

The conference proceedings are now available and will be invaluable to anyone who accepts the ideas presented here and has doubts about the current advice promulgated by the mainstream professionals. Individuals concerned about their personal health and/or wishing to lose weight will be very encouraged by the various presentations. In addition, professionals who genuinely wish to tune into the latest thinking will be amazed at the way everything fits together and just makes such good sense!

To find out more and to purchase log on to this link:



1. Having tried various ways to lose weight, he eventually succeeded with a diet based on meat, fruit and vegetables but avoiding sugar and starchy foods. He wrote a pamphlet, which proved to be very popular. By all accounts those who followed the advice managed to lose weight. It is worth noting that these principles were effectively accepted until the late 1960s.

182. The Reality of Science: Conflicts of Interest Must Be Addressed

There is an impression that science and scientists are dedicated to conducting independent studies which will provide objective results that can be regarded as definitive. Unfortunately the reality is anything but. Individuals who happen to be working as scientists are subject to all the pressures and prejudices which are common to everyone. Invariably people have preconceived ideas about what to expect from any investigation, which can influence the way in which the results are presented and interpreted. Hence the quality of any study is determined not only by the competence of the individuals involved but also their intellectually honesty and integrity.

Within the area of medicine, health and nutrition there are fundamental characteristics which mean that many of the issues to be addressed are difficult and complex. For a start, there are the variations between people because of genetics, gender and age. Secondly, there can be a long time span between cause and effect. Chronic diseases such as Type 2 Diabetes (T2D) and cancers can take years to develop. Thirdly, unlike infectious diseases where there is just a single cause, chronic diseases are usually the culmination of several different factors. All of this means that designing studies that will provide results which are genuinely sound is not easy. Inevitably finance is usually a key issue. Ideally the more participants the better because this is one way of overcoming the variation between individuals but this pushes up the expense. At the present time, much of the money for research is provided by companies. This then raises the possibility that the source of funding may have an influence on the results which are produced.

A study on research in the biomedical field Identified 37 eligible studies conducted between 1980 and 2002 which provided adequate information on the financial relationships between the industry, scientific investigators and the academic institutions involved (1). The relationship between industry sponsorship and outcome in original research was examined. It was found that there was a statistically significant association between industry sponsorship and pro-industry conclusions which favoured the industry by a factor of 3.6. Industry sponsorship was also associated with restrictions on publication and data sharing.

It was concluded that financial relationships among industry, scientific investigators, and academic institutions are widespread. Conflicts of interest arising from these ties can influence biomedical research in important ways.

In the field of food and nutrition, a recent investigation has examined reviews on the relationship between Sugar-Sweetened Beverages (SSBs) and weight gain to compare those financed by industry with those financed by independent sources (2).

In all 17 suitable reviews were found that were analysed in the study which reached 18 conclusions. Six of these declared potential conflicts of interest with industry, and 11 declared having no potential conflicts of interest with industry or did not report on potential conflicts of interest. The results showed that 61% of the conclusions from the 17 reviews (11/18 conclusions) supported an adverse association between SSB consumption and weight gain or obesity; none reported any significant benefit.

Among the reviews that reported having no conflict of interest (11 with 12 conclusions), 83.3% conclusions (10/12) were that SSBs were directly associated with increased weight gain or obesity. In contrast, 83.3% (5/6) of the conclusions from reviews that reported having some conflict of interest with the food industry were that there was insufficient scientific evidence to support a positive association. This means that those which had industry support were five times more likely to present a conclusion of no positive association than those without them.

Commenting on the results, the authors contend that the fundamental objective of scientific endeavour should be seek the truth irrespective of financial or other interests. They conclude that:

“If other concerns influence the results of research, nutrition science as a whole is likely to suffer, partly because of incorrect information and partly through a loss of confidence in the discipline from the general public. Eventually, nutrition research itself might be at risk because perceived biases would threaten to make it irrelevant. The influence of biased reviews on policy makers and medical practitioners might also be another potential threat for public health.”

The report on “Carbohydrates and Health” (3) which has just been published was prepared by a panel chaired by Professor Ian Macdonald of the University of Nottingham. A Channel 4 Despatches programme revealed that he was in receipt of money from Unilever, Coca Cola and Mars (4). This information was not shown on his university website although he had informed the government of his financial links with these companies. However the eminent pharmacologist David Colquhoun says that the Macdonald case is a “shocking conflict of interest”. He advocates that all these interests should be declared in every research paper and presentation.

However even this may not be sufficient as Mark Wilson, a researcher in Canada has pointed out (5). Within the field of medicine and the relevant science, specialised knowledge, training and practice is needed if the implication of bias are to be assessed properly. It is all very well having these financial links on the record but this information simply draws attention to a potential conflict. It flags up the possibility of bias. As Wilson notes:

“But it does nothing more. It does not inform the public whether the person with a commercial COI is the grip of bias or not. Nor does it provide the means to assess the implications of a bias. And to suggest that these tasks can be accomplished simply through disclosure is to endow this accountability tool with extra ordinary super governance powers. It is not surprising then that disclosure has had a poor record on combating bias on Wall Street and in psychiatric medicine. It has been mythologised as a cure-all”.

The BMJ has made a determined effort to get to grips with these financial conflicts of interest. It has now concluded that declaration of these interests does not go far enough. Although it accepts that transparency is essential, it is not sufficient to eliminate bias or the perception of bias. As a consequence much more stringent conditions will be introduced in an effort to get to grips with this issue. Hence it has decided that:

“From next year our clinical education articles will be authored by experts without financial ties to industry … By industry we mean companies producing drugs, devices, or tests; medical education companies; or other companies with an interest in the topic of the article. We are phasing in this policy to start with editorials, clinical reviews, and most practice series. We hope that by the end of 2016, this will have extended to the rest of our education section: our specialist state of the art reviews and diagnostics and therapeutics series. “(6)

The journals concern was triggered by specific examples where clinical decisions based on information biased by commercial interests had resulted in harm to patients. It is attempting to achieve a shift in culture by promoting authors without financial ties to industry and offering them appropriate prominence and visibility. In this way it is hoped that readers will be able to trust the information.


  1. http://jama.jamanetwork.com/article.aspx?articleid=195843
  2. http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1001578
  3. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/445503/SACN_Carbohydrates_and_Health.pdf
  4. http://www.dailymail.co.uk/debate/article-2543052/Obesity-tsars-sugar-firms-paying-fortune-VERY-unhealthy-relationship.html
  5. http://jrs.sagepub.com/content/107/6/216?ijkey=5e297b9c0fa73fcf7c0c0505d7d09d2c72b972f5&keytype2=tf_ipsecsha
  6. http://www.bmj.com/content/349/bmj.g7197

181. Another Success Story with Type 2 Diabetes

There is now overwhelming evidence that Type 2 Diabetes (T2D) can be reversed by simply altering the diet by reducing the intake of sugar and carbohydrates, which can be replaced by healthy fats (1). One of the latest developments is a case study from the general practice of Dr David Unwin and Dr Simon Tobin in the North of England. Details are given in a paper in the BMJ (British Medical Journal) (2).

The person involved was a 52-year old man with a history of T2D for 14 years and hypertension for 9 years. He was taking 4 drugs, namely aspirin (75 mg per day), metformin (500mg three times per day), perindopril (4mg per day) and simvastatin (40 mg at night). Because of the adverse side effects he was experiencing, he was keen to explore ways of reducing or eliminating his use of drugs.

It was clear to the doctors that the patient had Metabolic Syndrome (MS), which is a constellation of diseases/conditions which include T2D, hypertension, fatty liver, insulin resistance and obesity. They fully appreciated that there was research which demonstrated that the MS could be overcome by reducing the dietary intake of sugar and foods which contain starch that is broken down to glucose during digestion.

It was considered that none of the drugs were essential because they had all been prescribed to reduce the risk of cardiovascular events and the complications of diabetes rather than to treat an actual disease.

An evaluation of the various lifestyle strategies led to the conclusions that:

  • Physical activity is as effective as low to moderate intensity statins at reducing our patient’s risk of cardiovascular disease and outperforms aspirin.
  • The Mediterranean diet is nearly as effective as metformin.
  • Both of these (physical activity and Mediterranean diet) have a low risk of harm compared with the drugs listed and reduce the risk of comorbidities such as osteoarthritis, some cancers, and gallstones.

At this point it is interesting to note that weight loss was identified as one of the objectives. It is highly significant that the patient himself had decided that he should adopt a diet which was low in foods containing carbohydrates, namely sugar, rice, pasta, potatoes and bread. This is in direct contrast with the conventional approach which is to focus on lowering the intake of fatty foods (because they are a concentrated source of calories). Equally important is that it also conflicts with the usual advice from dietitians to those with T2D which is to reduce fat (in order to lower the risks of heart disease) and increase the intake of complex carbohydrates (not processed).

The results

The patient stopped consuming sugar as far as possible. He had been used to eating lots of bread but cut this out completely as well as potatoes, rice, pasta and cereals. Instead he increased his consumption of green vegetables, eggs, full fat Greek yoghurt, and cheese. Over a period of 7 months the patient reduced his weight from about 109 to 93kg and this enabled him to take more exercise, join a gym, and take up yoga. The goal of coming off all drugs was achieved in a stepwise manner as he lost weight—first metformin, then perindopril, followed by simvastatin and aspirin.

His HbA1c (a measure of his blood glucose) was reduced from 6.9% to 6.2%. His blood pressure and various indicators of his general health all improved.

All the nasty side effects have gone, he now needs an hour and a half less sleep a day and reports feeling “just much younger again.”

There is nothing particularly novel about this result. There are hundreds, if not thousands, of other individuals who have achieved similar success (3, 4). What is significant is that this has been published in one of the leading medical journals and that the strategy adopted contradicts the official policy of the NHS.

The NHS Choices website tells us that with respect to T2D:

There is no cure for diabetes. However, treatment aims to keep your blood glucose levels as normal as possible, which will control your symptoms and minimise the risk of health problems developing later on.” (5).

Furthermore it continues:

“….. as type 2 diabetes is a progressive condition, you may eventually need to take medication to keep your blood glucose at normal levels. You may need to take tablets initially, but move on to injected therapies, such as insulin, at a later stage.”

To put it bluntly if your GP/ dietitian goes along with this, you will have to accept there is no cure for the disease, it will get worse and you may expect to be on drugs for the rest of your life.

This is a policy of absolute despair which is utterly and completely wrong as the above case study proves!

The official position is an example of appalling ignorance. The fundamental reason T2D develops is because there is far too much glucose in the blood, which causes the pancreas to produce large amounts of insulin to remove the glucose. This excess insulin damages the internal organs, which can result in chronic conditions such as heart disease and cancers. Ultimately the pancreas cannot produce sufficient insulin and further damage is caused by the glucose. This is full blown T2D. One does not have to be a genius to understand that the answer is to remove the cause which is to cut down the amount of glucose which is coming into the blood. This is readily achieved by eating less foods which contain sugar and carbohydrates.

It follows therefore that the only logical and sensible way forward is to look for a solution based on changing the diet as the first approach. Provided the correct changes are made this should bring about an immediate improvement in the vast majority of people. Obviously there may be some who have severe permanent damages s that there is little scope for much improvement.

It is to be hoped that many GPs will take note of this case study and have a complete re-think about their approach to T2D. For the time being at least, they seem to have the freedom to do so.

From the perspective of national policy, it is evident that the current approach is a total failure. It is scandalous that most patients are not even being advised a change in diet could well be extremely beneficial. It is unbelievable that the official advice to reduce fat and increase carbohydrates will actually make things very much worse. So we have immense suffering which could be avoided, not to mention the enormous costs incurred for drugs, other treatments and care.

T2D has already doubled in the UK in the past 15 years and it is projected that the numbers afflicted will continue to increase. There is not the slightest doubt that if there is to be any progress, there will have to be a major shift in the patterns of national food consumption. The fact that the recent report from the Scientific Advisory Committee on Nutrition (SACN) recommended that 50% of the energy intake should be carbohydrates shows just how far away we are from any kind of rational policy (6).


  1. http://www.thehealthedgepodcast.com/wp-content/uploads/2015/03/Dieatary-carbohydrate-restriction-Diabetes-2015.pdf
  2. http://www.bmj.com/content/351/bmj.h4023.full?ijkey=AN2nBwW6h3wuQJK&keytype=ref
  3. http://vernerwheelock.com/?p=422
  4. http://vernerwheelock.com/?p=229
  5. http://www.nhs.uk/conditions/Diabetes-type2/Pages/Introduction.aspx
  6. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/445503/SACN_Carbohydrates_and_Health.pdf


According to a report prepared by Public Health England (PHE) children in local authorities with water fluoridation schemes have less tooth decay than those in local authorities without such schemes (1). It also claims that as many as 45% fewer children aged one to four in fluoridated areas are admitted to hospital for tooth decay – primarily to have decayed teeth extracted under a general anaesthetic – than in non-fluoridated areas. The report concludes that there is no evidence of harm to health in fluoridated areas. PHE has found no differences between fluoridated and non-fluoridated areas in their rates of hip fracture, osteosarcoma (a form of bone cancer), cancers overall, Down’s syndrome births or all-cause mortality (all recorded causes of death).

So everything in the garden is rosy then! We can carry on with the policy of fluoridation and fluoride can be introduced into the water supply in areas which currently are not doing so.

It is important to appreciate that the figures which are being bandied about in the media are relative rather than absolute. Digging into the report it emerges that the actual rate of decayed teeth was 30% in fluoridated areas and 33% in non-fluoridated areas. These differences are very small and could well be due to other factors which have not been taken into consideration or may simply be due to chance. In any case these figures certainly do not demonstrate “cause and effect”. The values for hospital admissions are per 100,000 per year which means they are relatively small and therefore the differences may not be real. In any event they do not constitute proof that the low values are the result of the presence of fluoride in the drinking water.

Of much greater significance is the complacent assumption that fluoridation is undoubtedly beneficial and that there can be no possible adverse effects. It is very clear that much highly relevant but inconvenient information has been totally ignored.

The fundamental weakness in the approach adopted by the report is that dental caries is a very good indicator of other health problems in any given individual. There is widespread agreement that dietary sugar is one of the major causes of dental caries. But excess sugar is obviously the prime cause of diabetes (which has doubled in the last 15 years), obesity, kidney disease, heart disease and cancer. So that rather than fiddling about with fluoridation the public health authorities should focus their attention on reducing sugar consumption because of the beneficial effects that will have on general health. So even if fluoridation is effective, it is really only scratching the surface.

In addition, here are some facts that should certainly be of interest to those who are currently consuming fluoridated water and those who may be required to do so in the future.

The PHE report refers to a review of fluoridation conducted by the National Research Council of the US National Academy of Science (NAS) which was published in 2006 and implies that it provides support for the PHE conclusions. However Dr John Doull, who chaired the review, says that the safety of fluoridation remains “unsettled” and that:

we have much less information than we should, considering how long it has been going on”.

Here are some of the issues which were identified in the NRC report (2):

  • Fluorides have the ability to interfere with the functions of the brain and the body by direct and indirect means. Fluorides increase the production of free radicals in the brain through several different biological pathways. These changes have a bearing on the possibility that fluorides act to increase the risk of developing Alzheimer’s disease. The possibility has been raised by studies conducted in China that fluoride can lower intellectual abilities
  • Evidence of several types indicates that fluoride affects normal endocrine function or response; the effects of the fluoride-induced changes vary in degree and kind in different individuals. Fluoride is therefore an endocrine disruptor in the broad sense of altering normal endocrine function or response
  • Several lines of information indicate an effect of fluoride exposure on thyroid function
  • Exposure to fluoride appears to bring about increases in blood glucose or impaired glucose tolerance in some individuals and to increase the severity of some types of diabetes. As diabetic individuals usually have higher than normal water intake, this means they will have higher than normal fluoride intake for a given concentration of fluoride in drinking water
  • There is no question that fluoride can affect the cells involved in providing immune responses
  • A few human studies suggested that high concentrations of fluoride exposure might be associated with alterations in reproductive hormones, effects on fertility, and developmental outcomes, but design limitations make those studies insufficient for risk evaluation
  • The possible association of cytogenetic effects with fluoride exposure suggests that Down’s syndrome is a biologically plausible outcome of exposure
  • Human kidneys concentrate fluoride as much as 50-fold from plasma to urine. Portions of the renal system may therefore be at higher risk of fluoride toxicity than most soft tissue
  • Fluoride appears to have the potential to initiate or promote cancers, particularly of the bone

In the light of these conclusions the PHE statement that there is no evidence of harm is complacent in the extreme. The NRC review has clearly identified a range of possible harms that may be associated with fluoridation of the public water supplies. It is simply not good enough for the PHE to discount these possible risks in this way. It is blindingly obvious that there are huge gaps in our knowledge of the role of fluoride in the body. Hence a much more precautionary approach is needed, especially as the benefits are so marginal.

It would certainly be helpful if the UK government could explain why 97% of the population in Western Europe have water which has not been subject to the fluoridation process (3). It does not happen in Austria, Belgium, Denmark, Finland, France, Germany, Greece, Iceland, Italy, Luxembourg, Netherlands, Northern Ireland, Norway, Portugal, Scotland, Sweden or Switzerland. Despite the lack of fluoridation the rates of teeth decay have fallen at least as fast, if not faster, than in those few countries where it is allowed. If the PHE report was to have any credibility it should have included these results from other European countries!


  1. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/296329/Water_fluoridation_health_monitoring_for_England.pdf
  2. http://www.nap.edu/catalog.php?record_id=11571
  3. http://fluoridealert.org/articles/fluoride-facts/


A comprehensive review on the role of cholesterol in health and a critique of the use of statins has recently been published by a team of Japanese researchers (1). This pulls together information from a range of different sources. The focus is on all-cause mortality because fundamentally that is the key parameter most people understand and wish to control. Determination of individual diseases are subject to bias and lack of objectivity, which does not apply to death. The relationship between all-cause mortality and the cholesterol in the blood has now been investigated repeatedly in many different countries and the results which are incredibly consistent may come as a surprise to many people. In this blog I will refer to a selection of what is available.


In the Ibaraki Prefecture Health Study, 91,219 men and women aged 40-79 years without any history of stroke or coronary heart disease (CHD) were followed for just over 10 years. It was found that the all-cause mortality was inversely correlated with the level of LDL cholesterol. In other words the higher the LDL cholesterol the greater the life expectancy, which of course is in direct conflict with the conventional wisdom.

In the Isehara Study, data was collected from those who had an annual check-up. The final database contained information on 8,340 men (aged 64±10 years) and 13,591 women (61±12 years). Again it was found that the level of LDL cholesterol was inversely related to the all-cause mortality rate. Interestingly it was reported that, the mortality rates due to cancer in men and to respiratory disease without cancer (mostly pneumonia) in men and women were lowest in those groups with the highest values.

The Jichi Medical School Cohort Study is one of the most recent, large epidemiological studies conducted in Japan in which 12,234 healthy adults from rural communities were followed for almost 12 years. Once again, the highest death rates from all causes was in those with the lowest TC values. In this investigation even the exclusion of deaths within the first 5 years did not alter the relationship between low TC levels and the high mortality. The exclusion of deaths caused by liver disease also made no difference to this conclusion. However in this study the relationship between the death rates and TC levels in men was U-shaped so there was some increase at the higher values. But in women it was clear that as the higher the TC, the lower the death rate.


The results of the Jichi Study are very similar to those obtained in the HUNT Study conducted in Norway, in which 52,087 men and women aged 20-74 years were followed over a 10-year period (2). TC levels were measured and details of any deaths which occurred were recorded. The results are shown in Table 1.

For both men and women, the highest all-cause mortality was in those with the TC levels below 5.0 mmol/L.

In men, there was no increase in the all-cause mortality with raised TC. Those with a TC level between 5.0 and 5.9 mmol/L had the lowest death rate, which was 23% lower than those with a TC below 5.0 mmol/L. At higher values, the rate increased again.

For women the pattern is different. The higher the TC, the lower the risk of dying from all causes. Compared with those with a TC below 5.0 mmol/L, those with the highest TC levels were 28% less likely to die from all causes.

Table 1. Variation in mortality due to all causes and to cardiovascular diseases (CVD) with TC in men and women

TC, Mmol/L (mg/100ml)                          MEN                    WOMEN
All-cause CVD All-cause CVD
<5.0          (<194) 1.00 1.00 1.00 1.00
5.0-5.9     (194-228) 0.77 0.80 0.92 0.90
6.0-6.9     (232-267) 0.84 0.87 0.84 0.81
>7.0          (>270) 0.98 1.05 0.72 0.74


In a subsequent paper the research team provided the information for the different age ranges (3). This detailed break-down shows that as expected most of the deaths occur after the age of 60 years (Table 2). Although the optimum TC level for men aged 60-69 is in TC range 5.0 to 5.9 mmol/L, for those over 70 the lowest death rate is in the higher TC level of 6.0 to 6.9 mmol/L. For women it is very clear that the death rate for the over 60s decreases as the TC increases. For this age range it is evident that the highest death rates are for those with a TC level which is below 5.9 mmol/L. The relatively high death rates for those aged 60+ years at low TC values should also be noted.

Table 2. All-cause mortality rates (per 1000 person years) and TC levels at different age ranges

Age ranges                               TC LEVELS, mmol/L(mg/100ml)
<5.0(<194) 5.0-5.9(194-228) 6.0-6.9(232-267) >7.0(>270)
20-29 1.10 0.38 0.30 0.00
30-39 0.80 0.57 0.72 0.47
40-49 2.22 1.38 2.27 3.37
50-59 4.54 4.93 6.22 5.74
60-69 20.31 16.20 17.37 18.47
70-74 49.18 40.37 37.93 41.25
20-29 0.35 0.30 0.24 0.60
30-39 0.31 0.43 0.82 0.69
40-49 0.89 1.85 1.69 1.12
50-59 2.95 3.59 3.53 3.79
60-69 22.31 10.32 10.47 9.51
69-74 31.46 22.50 21.58 19.23


The authors commented as follows:

‘’If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but beneficial.’’

They went on to conclude:

‘’Our results contradict the guidelines’ well-established demarcation line (5 mmol /L) between

‘good’ and ‘too high’ levels of cholesterol. They also contradict the popularized idea of a positive, linear relationship between cholesterol and fatal disease. Guideline-based advice regarding CVD prevention may thus be outdated and misleading, particularly regarding many women who have cholesterol levels in the range of 5–7 mmol/Litre and are currently encouraged to take better care of their health’’.

The Netherlands

In the Netherlands, a study with residents in Leiden with an average age of 89 years, it was found that those with the highest TC levels had the lowest mortality, while those with low TC values had the highest mortality (4). Those with the high life expectancy was due to particularly low incidences of cancer and infection.


In the Honolulu Heart Programme the TC was measured between 1965 and 1968 in 7961 men of Japanese origin who were born between 1900 and 1919. During the period of this study the men were monitored on 3 occasions and there were 2072 deaths. The results (Table 3) confirm that in this group of men the death rate attributed to coronary heart disease is directly associated with the TC level. However for deaths from stroke there are high death rates for both high and low cholesterol values. For cancer, it is evident that the death rate is inversely related to the TC levels. In this study there were twice as many deaths due to cancer at low TC levels when compared with whose TC was above 6.98 mmol/L.  For all-cause mortality the lowest death rates were found in the cholesterol range between 4.65 and 6.18 mmol/L (180 and 239 mg/100ml). The authors concluded that manipulation of TC levels below the range shown above would not be desirable if it was to result in an increased risk of death from cancer and other diseases (5).

Table 3. Relationship between death rate and total cholesterol for various causes of death 


<4.65      (<180) 1.68 1.80 7.32 17.46
4.65-5.40(180-209) 2.01 1.17 5.30 14.09
5.43-6.18(218-239) 2.38 1.40 5.33 14.07
6.20-6.96(249-268) 4.24 1.65 5.34 15.92
>6.98      (>269 ) 4.87 1.74 3.83 17.31



In Austria, 67,41men and 82,237 women aged 20–95 years were followed over a 15-year period (1985–1999) as part of the Vorarlberg Health Monitoring and Promotion Programme. It was found that in both men and women in the 50–64 and ?65 age groups, TC levels were a negative risk factor for all-cause mortality (6).


A study done in the Finnish city of Kuopio monitored 490 elderly persons aged over 75 (28% men) for 6 years. None of them were on cholesterol lowering medication. Those with TC lower than 5mmol/L had a death rate that was double that of those who whose TC was greater than 6 mmol/L (7).

In another study done in Finland 623 people aged over 75 years were monitored for 17 years (8). The TC was monitored as well as lathosterol, which indicates cholesterol synthesis and sitosterol indicates cholesterol absorption. The reults showed that TC declined in old age, and low cholesterol was associated with poor health and multi-morbidity. TC levels below 5.0 mmol/L were associated with accelerated all-cause mortality Lathosterol when they were all low it was reduced to 5.6 yearsand sitosterol both decreased with deteriorating health. Low lathosterol, sitosterol, and TC predicted mortality additively and independently of each other. When all three sterols were high the age expectancy was 9.9 years but when they were all low, it was reduced to 5.6 years. It was concluded that reduced synthesis and absorption of cholesterol, and low TC levels are associated with deteriorating health and indicate impaired survival in old age.


Without exception all-cause mortality is highest in those with the lowest levels of TC. In older people those with the highest cholesterol have the highest survival rates, irrespective of where they live in the world. The picture which emerges is totally consistent. The research which triggered the concern about heart disease was based almost entirely on middle-aged men and was restricted to heart disease. But what is so striking about all the studies cited here is that when the focus is on older people, which is when the vast majority deaths occur, and on all-cause mortality the perception of the risks associated with cholesterol are reversed. It is also highly significant that these results do NOT conflict with the research on middle-aged men and heart disease. The data from Honolulu confirm that in those involved in the study with low cholesterol there was a low death rate from heart disease but crucially the incidence of cancer was relatively high and demonstrates why it is vital to consider the big picture. The emphasis on TC and LDL cholesterol as risk factors was based on a complete failure to do so. There is absolutely no logical justification for advising people to lower their TC or their LDL cholesterol. On the contrary all the evidence which is now available indicates that that the higher the better. The results for women are quite exceptional and show consistently that those with the highest TC values invariably have the greatest life expectancy.

By contrast, we can be reasonably certain that the cholesterol lowering strategies which have been applied have not resulted in any benefit and probably have been damaging to health. In particular, the rationale for the use of drugs such as statins is totally destroyed by the evidence presented here. All the indications are that cholesterol is beneficial and the higher the better!

It really is astonishing and irresponsible for the authorities to continue the various programmes which still use TC as a risk factor for heart disease and push cholesterol-lowering strategies. It is time they were abandoned because they are not achieving anything positive and are almost certainly doing more harm than good, not to mention that there are a sheer waste of valuable resources.


  1. https://www.karger.com/Article/Pdf/381654
  2. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 159-168.
  3. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 170-171.
  4. A W Weverling-Rijnsburger et al (1997) Lancet 350 pp 1119-1123
  5. G.Stemmerman et al (1991) Archives of Internal Medicine 151 pp.969-972
  6. Ulmer et al (2004) Journal of Womens Health 13 pp 41–53
  7. P Tuikkala et al (2010) Scandinavian Journal of Primary health Care 28 (2) pp 121-127
  8. R S Tivlis et al (2011) Annals Medicine 43 pp 292-301