A recent (the first ever) audit on patient deaths from diabetes notes that approximately 70-75,000 diabetic patients die each year and it is estimated that approximately one third of these deaths could be avoided with better care of their condition.

This post is about the different types of diabetes, insulin non-production, insulin sensitivity, fat storage, insulin and obesity. It covers the issues related to diabetes, insulin and obesity and is intended to provide an understanding for why people are not keen to take medication for diabetes and why we could far better manage diabetes and avoid much of the incidence of diabetes if only we would return people to eating the real food that we ate before we had epidemics of obesity and diabetes – animals, vegetables and fruits in season, nuts & seeds where available. No cereals, no ready meals, no fortified margarines – none of the heinous products making us fat and sick.

Diabetes Type 1 & 2

Rosalyn Yalow and Solomon Berson are credited with having taken Sir Harold Himsworth’s distinction between what we now know as type 1 and type 2 diabetes (Ref 1), and demonstrating that type 1 diabetes was an insulin-deficient state, whereas patients with type 2 diabetes had substantial amounts of insulin in the blood and could be classified as insulin resistant (Ref 2). Type 1 diabetes can therefore be simplistically described as the type where the pancreas does not release insulin at all. In type 2 diabetes the pancreas is effectively releasing too much insulin and yet this still fails to regulate blood glucose levels normally, as cells have become resistant to insulin. This is a critical distinction and helps to explain why this Yalow and Berson study remains one of the most cited articles from the Journal of Clinical Investigation.

It follows that type 1 diabetes requires the administration of insulin and type 2 diabetes can be managed through medication to help optimise the insulin available and to help overcome insulin resistance. Both types of diabetes, I would argue, could be far better managed through diet, and I actually fail to see how type 2 diabetes can manifest itself in the absence of carbohydrate. Obesity in diabetics would be far less common if we adopted the low-carbohydrate principles from the nineteenth century, before the discovery of insulin in 1921, openly shared by William Banting in 1869 (Ref 3).

Insulin, obesity & diabetes

In their 1965 article (Ref 4), Yalow and Berson teamed up with Seymour Glick and Jesse Roth to review the relationship between insulin, obesity and diabetes. They opened with “Here we summarize several well established observations: A relatively high percentage of adult-onset diabetics (Ref 5) are obese and were so long before the onset of clinical diabetes. Diabetes occurs far more frequently in obese than in nonobese subjects. Obese patients without diabetes exhibit impaired glucose tolerance with abnormally high frequency.” With no claims of causation in any direction, the authors are merely observing associations between diabetes, obesity and insulin resistance. At the end of a rigorous study of blood glucose levels and insulin responsiveness in all permutations of lean and obese, diabetic and non diabetic people, their conclusion was as follows: “Thus, there is some degree of insulin insensitivity in obesity without diabetes and a greater degree of insensitivity in diabetes without obesity. When the two conditions coexist, insensitivity is greatest and results in the highest insulin concentrations if pancreatic reserve is adequate.”

This confirms that obese people are more likely to have type 2 diabetes and, even if not diabetic, they are more likely to display insulin sensitivity. Those who are both diabetic and obese are likely to be the most insulin resistant of all. The causation is likely circular, as obesity increases the person’s chance of developing type 2 diabetes and the accompanying insulin resistance makes obesity more likely. The subject of fat storage is very interesting to compare in type 1 and type 2 diabetes.

Type 1 diabetes

The first life event to trigger my interest in the subject of weight, insulin and carbohydrates was my brother developing type 1 diabetes when he was aged 15 and I was 13. As is classic in the onset of the condition, he lost approximately 20 pounds in a similar number of days (the condition took an inexplicably long time to diagnose, given the classic nature of the symptoms). His ‘energy in’ had undoubtedly increased – as he was sending me to the corner shop to buy litre after litre of sugary fizzy drinks. His ‘energy out’ undoubtedly decreased, as he seemed unable to move from his armchair. Having shared this story a number of times – the most common response is curiosity about any possible violation of the laws of thermodynamics – how could energy in go up and energy out go down and a human lose so much weight?

When type 1 diabetes occurs, sugar is lost in the urine. Indeed, diabetes means ‘sweet urine’ in Greek and diabetes is diagnosed by testing for sugar in the urine. At the 2010 Wales obesity conference Dr. Jeffrey Stephens a diabetologist, estimated that glycosuria (literally weeing out sugar in the urine) may account for 500 calories a day. That still doesn’t allow the first law of thermodynamics alone to explain the notorious weight loss in the sudden onset of type 1 diabetes. We seem more interested in calorie reconciliation than thinking about possible implications for obesity. I was always more interested in what this told us about the role of insulin in weight and weight loss.

What we observe, at the onset of type 1 diabetes, is, essentially, a human body incapable of storing fat in the absence of insulin. As soon as the condition is diagnosed we (unforgivably in my view) advise the person to eat carbohydrate at every meal and administer insulin regularly and the ability to store fat resumes. Invariably the person then struggles to avoid obesity for the rest of their life.

Type 2 diabetes

Conversely, just as onset type 1 diabetics, before diagnosis, are unable to store fat, type 2 diabetics are masters at this. Pre-diabetic individuals are often efficient ‘fat storing machines’ while insulin resistance is developing and before they are officially diagnosed with type 2 diabetes. Whereas the onset of type 1 is sudden and dramatic, type 2 diabetes can emerge over time and remain undiagnosed for months, even years. Any insulin resistant type 2, diagnosed or otherwise, would be well advised to avoid carbohydrates, as this is the one macronutrient that they cannot handle. Instead, we advise all citizens, diabetic or non-diabetic, to base their meals on starchy foods and to eat little and often and we maintain an excellent fat storage environment in so doing.

Insulin, fat storage & getting fat

Edgar Gordon wrote in the Journal of the American Medical Association (JAMA) 1963 “It may be stated categorically that the storage of fat and therefore the production and maintenance of obesity cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin. Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.” (Ref 6)

There are enough journal articles and medical references connecting insulin and weight to keep an obesity researcher engaged for years on this subject alone. The conclusion of all references, however, is that insulin leads to weight gain (and, therefore, by inference, that carbohydrate leads to weight gain). Nothing illustrates this better than medical journal forums seeking ways to encourage diabetics (especially young females) to take their insulin, because the doctors know that the diabetics know that insulin makes them fat.

The audit recently undertaken confirmed that the most at risk group was women aged 15 to 34 with diabetes. They were nine times more likely to die than non-diabetics of the same age. That’s because they know that insulin makes them fat and young women, particularly, don’t want to be fat. The solution is to lessen the intake of the macro nutrient that requires insulin to be administered – carbohydrates – but we do not advise this. Instead – we tell diabetics that this is a role model for healthy eating. It is, in fact, a recipe for making more diabetics and making current diabetics fat and sick.

The weight gain resulting from insulin is so well known that, as far back as 1925, Wilhelm Falta began using insulin to treat underweight adults and anorexia (Ref 7). The weight loss at the onset of type 1 diabetes is equally long known and remarkable. The non diabetic person can produce the same fattening effect of administering insulin by eating carbohydrates frequently and causing the pancreas to release insulin. The impact of insulin on weight is irrefutable and substantial, as we will also see in the next section on medication.

Diabetes & medication

The large-scale studies, such as the diabetes control and complications trial (DCCT) in patients with type 1 diabetes and the United Kingdom prospective diabetes study (UKPDS) in patients with type 2 diabetes, have quantified the weight gain resulting from the administration of insulin. The DCCT was a prospective trial involving 1,441 patients with type 1 diabetes randomised to either an intensive (three to four insulin injections/day or insulin pump) or conventional (one to two insulin injections/day) treatment protocol (Ref 8). At the nine year follow up, approximately 30% of men and 35% of women, receiving the intensive insulin dosage, were five points higher on their BMI scale. Men and women on the more conventional dose still gained weight, but far less. The study quantified the average (mean) weight gain as 4.75 kilograms greater for the three to four injections a day group.

The UKPDS study had 3,867 participants, newly diagnosed with type 2 diabetes (Ref 9). They were randomly assigned to either an ‘intervention’ group, with insulin or alternate drug treatment, or to a ‘managed through diet’ group. Weight gain over the 10 year study was a mean of 6.5 kilograms. Weight gain was significantly higher in the insulin/drug group (mean 2.9 kilograms) than in the diet group. Furthermore, of the drug treatment options, patients assigned insulin had a greater gain in weight (4.0 kilograms) than those given chlorpropamide (2.6 kilograms) or glibenclamide (1.7 kilograms). (The latter two named drugs are from the family of medication called sulphonylurea. They act to stimulate the release of insulin from the beta cells in the pancreas, thus trying to optimise any insulin that can be ‘squeezed out’ from the body more naturally than insulin administration).

The Glasgow report (Ref 10) presented numerous other studies confirming the same observed weight gain with the administration of either insulin or sulphonylureas. The latter produced lower weight gain than insulin, but gain none the less.

The weight gain with insulin is immediate and sustained, as the Yki-Jarvinen 1992 study showed, with a mean gain of 1.8 kilograms to 2.9 kilograms in 12 weeks with two injections and multiple injections respectively. Similarly the Yki-Jarvinen 1997 study, carried out over a one year period, showed a mean weight gain of 5.1 kilograms with 2-4 injections per day. All of these studies were done for management of type 2 diabetes, not type 1.

The people taking sulphonylureas fared better than those taking insulin, but still recorded notable weight gain. The largest weight gain, over a one year period, for a sulphonylurea, was a mean of 3.6 kilograms recorded by Marbury (1999) for glipizide (Ref 11).

Conclusion

The BBC article linked to in the opening line says of diabetes: “It means their bodies cannot use glucose properly. If they do not manage it, they can develop potentially fatal complications like heart or kidney failure.” This is a useful, if simplistic, description of both types of diabetic – “their bodies cannot use glucose properly.”

Q) So, how does the body get exposed to glucose? A) From our public health dietary advice:

- “Base your meals on starchy foods” (glucose);

- “Eat five-a-day” (glucose and fructose);

- Eat less fat” (which means that carbohydrate as a proportion, if not absolute amount, in the diet must increase – more glucose).

Insulin makes us fat. Glucose demands that insulin be released, so glucose makes us fat. Carbohydrates break down into glucose (and fructose) – fructose goes straight to the liver to be turned into fat and glucose stimulates and insulin response to make us fat. Medication for dealing with the complications of not being able to “use glucose properly” makes us fat. What doesn’t make us fat is the real food that the government tells us to eat less of – meat, fish, eggs and dairy products.

I hope that the government realises the consequences of their dietary advice before we make any more diabetics, let alone record the deaths of those we have already made.

References

Ref 1 : Sir Harold Himsworth, “Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types”, The Lancet, (1936).

Ref 2: Rosalyn Yalow, Solomon Berson, “Immunoassay of endogenous plasma insulin in man”, Journal of Clinical Investigation, (1960).

Ref 3: William Banting, “Letter on Corpulence addressed to the public”, (1869).

Ref 4: Yalow R.S., Glick S.M., Roth J., Berson S.A.,“Plasma insulin and growth hormone levels in obesity and diabetes”, Annals of the New York Academy of Sciences, (1965).

Ref 5: “Adult onset” was the common terminology used for type 2 diabetes at the time of the 1965 article. Type 1 diabetes similarly used to be called juvenile diabetes, as it manifested itself in children, adolescents or young adults. Type 1 and 2 are the favoured terms nowadays, not least because we are observing new cases of type 1 diabetes in middle aged people and, extremely worryingly, type 2 diabetes in children. The vast majority, 90-95%, of diabetics have type 2 diabetes.

Ref 6:  Edgar Gordon, “A new concept in the treatment of obesity”, The Journal of the American Medical Association, (1963).

Ref 7: Wilhem Falta, Endocrine diseases including their diagnosis and treatment, (1923).

Ref 8: DCCT Research Group, “Influence of intensive diabetes treatment on bodyweight and composition of adults with type 1 diabetes in the Diabetes Control and Complications Trial”, Diabetes Care, (2001).

Ref 9: UKPDS Group, “Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes”, The Lancet, (1998).

Ref 10: W.S. Leslie, C.R. Hankey and M.E.J. Lean, “Weight gain as an adverse effect of some commonly prescribed drugs: a systematic review” QJM, (June 2007).

Ref 11: Marbury T., Huang W.C., Strange P., Lebovitz H., “Repaglinide versus glyburide: a one-year comparison trial”, Diabetes Research and Clinical Practice, (1999).

I have the following points to make:

1) Association vs causation:

This study makes the usual and unforgiveable mistake of assuming that association means causation. To give an example, we can observe that people in the bath may be singing. This means that we could say singing may be associated with being in the bath. However, we can no more say that bathing causes singing than we can say that singing causes bathing!

If the study had measured sock colour, these men may also have worn blue socks – would the headline then be “wearing blue socks increases the chance of men getting prostate cancer?” Yes, it really is as daft as that. To jump from observed association to causation and risk is the most outrageous bad science and yet studies do it every day and the media amplifies it every time.

2) How risk is calculated:

Notwithstanding that association can say nothing about risk or causation, here is how ‘risk’ is calculated between two studies…  If in one study people ate no eggs and 1 in 100,000 people died and in another study people ate eggs and 2 in 100,000 people died – they will say “Eating eggs doubles your risk of dying”. They always ignore the denominator (the bottom number in the equation – in these cases the study size). The second group still only had a 1 in 50,000 chance of dying full stop and yet the headline tells you you’ve got twice the risk – this is indefensible scare tactics.

The summary of the original research article is here. The study followed 27,607 men over a 14 year period from 1994 – 2008.

The study looked at the 3,127 men initially diagnosed with what is called “non-metastatic prostate cancer” (“non-spreading” or localised prostate cancer) and then reviewed those who went on to develop, as they called it “lethal prostate cancer”. (I assume “terminal” would be a word we would more typically use). The findings were “we observed 199 events during 306,715 person-years”. That’s an incidence rate of 0.0649%. That’s a 1 in 1,541 incidence. To put this in perspective, our chance of dying in a car crash was put at 1 in 200 .

The summary stated: “Men who consumed 2.5 or more eggs per week had an 81% increased risk of lethal prostate cancer compared to men who consumed less than 0.5 eggs per week (HR: 1.81; 95% confidence interval (CI): 1.13, 2.89).”

There are three things wrong with this:

i) The completely unjustifiable leap from association to risk must be reiterated. For researchers to claim “increased risk” from an observed association is simply not valid. This is the kind of food survey that Harvard Public Health use in studies like this (if not the same one). This shows how many foods are being studied, in how many different quantities, relying on subject recall of what they have eaten – and that’s just the food, let alone other lifestyle factors – smoking, exercise, stress, location, marital status, financial circumstances etc.

ii) The study is claiming that in amongst the overall incidence of 0.0649%, those people eating 2.5 or more eggs per week had almost ‘double the chance’. As an example, those eating more than 2.5 eggs a week could have had a 0.09% incidence rate and the 0.5 egg group could have a 0.05% incidence rate (there’s a difference of 81% between those two percentages and the overall incidence can still be 0.0649%). Can you see the absolutely tiny number behind the 81% risk massive headline?

PLUS – this is critical and irresponsible not to have highlighted – after the number 1.81% the 95% confidence interval is given as 1.13 to 2.89. What this means is – the researchers are 95% confident that the observed differences between the higher and the lower egg consumption were somewhere in a range between 13% and 189% – that’s one heck of a range. This means that they cannot even establish an association within a fourteen fold range, let alone make a claim of 81% with any degree of accuracy.

iii) There is a very good NHS review here. This suggests that the NHS have obtained a full copy of the report (not just the summary) and they have been able to see that “Men who consumed more red meat or eggs tended to exercise less and have a higher BMI, and were more likely to smoke and have a family history of prostate cancer.”

Do you wonder if smoking, exercising less, having a higher BMI and having a family history of prostate cancer was more relevant that any egg consumption?!

Why would so called researchers mislead the public in this way? Academics have egos and they want their ‘research’ widely published and talked about. The headline “Smoking causes cancer” is not new; “Obesity causes cancer” has been said before (whether correct or not is immaterial – it’s not new news). How about “Family history of prostate cancer increases your risk of getting cancer” – hardly surprising. So, pick the one headline that would be new. “Wearing blue socks increases the chance of getting prostate cancer?” That would be new – but absurd, so let’s pick the one vague association that will get the Daily Mail headline – it must be the eggs!

Even if the eggs have any relevance at all – what else could be happening at the same time? Were the egg eating men Paleo dudes, or were they egg and soldier addicts (blame the bread), or egg and brown sauce addicts (blame the sugary gunge), or even egg and bacon addicts who hadn’t selected their bacon carefully enough (blame the processed meat).

3) Cholesterol is vital not evil:

The suggestion from the ‘experts’ that cholesterol could be the cause of harm is laughable. Cholesterol is protective – one of its most important functions is to repair cells – not attack them. The longevity facts associated with high cholesterol are related in major part to the protective benefits that cholesterol has for cancer (cell repair – it should be obvious). My book, The Obesity Epidemic: What caused it? How can we stop it?, has many studies showing the benefits for cancer and cholesterol. The body makes all the cholesterol it needs (cholesterol in food makes no difference), but you never know what survival signals the body could send out. Should the headline have been “men with prostate cancer crave eggs!”?

4) Common sense:

Would nature really put both the essential fats (omega-3 and omega-6), amino acids, complete protein and the most phenomenal range of vitamins and minerals in the tiny, humble egg if it were trying to kill us at the same time? By the way – the reason why eggs contain so much cholesterol is because it takes a lot of cholesterol to make a healthy chicken. It takes a lot of cholesterol to make a healthy human as well!

5) Conflict of interest:

Finally – always follow the money – remember who stands to gain if we demonise eggs – the sugary cereal companies. The Kellogg’s and General Mills who sponsor the American Dietetic Association , to make sure that dieticians are ‘on message’.

Eggs have only recently been exonerated for being harmful for cholesterol even though Ancel Keys, the man who started the war on fat and cholesterol  declared years ago “Cholesterol in food has no impact on cholesterol in the blood and we have known that all along”. No sooner have eggs been let out of jail for containing cholesterol – they need to be put back in jail or (heaven forbid) people will start eating eggs again for breakfast and not coco-pops.

Andy and I have just had a three egg omelette each for breakfast. Enjoy whatever real food you guys have!

Nutrition is a fascinating topic. There is little more important to human health than what and how we eat.  Modern epidemics of obesity and ill health are capturing media headlines and the attention of curious minds alike. This is a subject about which many people want to know more. However…

When I am asked to recommend a course on nutrition I can’t. I am not aware of a single programme being offered anywhere in the world, which is evidence based and which presents facts, rather than the current myths presented as facts. That doesn’t mean that there isn’t one, but I don’t know of one and I would be surprised if there were one given the extent of the misinformation being perpetuated by the vast majority of people working in this field.

What do you want to learn?

My starting advice to someone interested in studying nutrition would be to be specific about what you want to know. The British Dietetic Association curriculum for training as a dietician is detailed here. If this is your first higher qualification, the background in basic sciences and biology may be useful to you. For those who already have a degree and/or studied science to a reasonable level at school, reading a cell biology, physiology and biochemistry textbook will deliver the required background.

My passion is obesity. There is more than enough to study on this topic to do nothing else for the rest of one’s life. Hence I am not interested in (using the attached curriculum by way of example) immunology, microbiology, (food hygiene), clinical medicine, pharmacology, sociology and social policy, communication and educational methods and definitely not interested in ‘food’ science. Nature provides food – that’s the only food I want to understand. I’m not particularly interested in dietetics for the prevention of general disease (besides the fact that eating real food will achieve this naturally) and I’m only interested in public health to the extent of how we managed to get ourselves in the midst of an obesity epidemic.

Becoming a dietician

When I set out to study nutrition more formally, I investigated training as a dietitian. I rejected the prospect very quickly on two grounds:

i) With 1.5 billion overweight people in the world, this is more than a big enough arena in which to specialise. As detailed above, I have no interest in the vast majority of the dietician curriculum and have no time to ‘waste’ on such topics when I could be spending that time reading obesity journals.

ii) Upon investigation of the weight management part of the course, I discovered that the first lesson is the calorie formula. I would be told that energy in equalled energy out and that to lose one pound of fat a deficit of 3,500 calories must be created.

Thus the one part of the course that I would be interested in, would be of no use to me. Presumably I would need to reproduce answers that I know not to be true to pass, or fail as a result of giving my honest answer. A quick analysis of the 58 page curriculum document confirms that I made the right decision: the word weight does not appear once; the word obesity does not appear once; the word calorie does not appear once and the word diet only appears six times and in a very general context of the word diet e.g. UK diet or diet and lifestyle.

A third reason became apparent when I was researching for my book The Obesity Epidemic: What caused it? How can we stop it? Conflict of interest…

Here are the sponsors of The American Dietetic Association. Here are the program partners of the Dieticians Association of Australia. Here are the major partners of the Dieticians Association of Australia. Here are the associate partners. I detail in my book, The Obesity Epidemic, how unwilling the British Dietetic Association is to disclose its conflicts of interest. After a number of email exchanges, a BDA spokeswoman confirmed “we have been delighted to work with the Sugar Bureau…” The chief executive’s foreword (Andy Burman) in the 2008-09 annual report of the BDA notes “We now have our first national partners with Danone and Abbott and we hope to announce new partners over the coming year or so.” There is reference to a “Bird’s Eye” education award, but no mention of other partners or sponsors. The accounts for 2009 showed a turnover of £2,359,013 with no details of the source for this revenue. The notes to the accounts, which could add detail to this number, are for the eyes of BDA members only. A press release, dated 1 March 2007 entitled Kellogg’s: commitment to health and wellbeing, informed me that Kellogg’s had been the lead sponsor for the British Dietetic Association’s annual obesity intervention campaign since 2002 (and may still be).

Here are the members of the British Nutrition Foundation. Here are the sustaining members of the British Nutrition Foundation.

It is a complete disgrace that our nutritional ‘education’ has been infiltrated in this way. The partner that most disturbs me is Abbott Nutrition. This company makes an infant formula called Similac. The feeding guidelines on the Similac web site range from 1-2 weeks to 9-12 months, so this is clearly a product designed for babies. The can of baby formula, of the part that is not water, contained 43% corn syrup solids and 10.3% sucrose. “It’s a baby milkshake,” said a horrified Robert Lustig in the video “Sugar: The Bitter Truth“. I wanted to analyse a product for myself, so I chose Similac Isomil Advance, Soy Formula and the composition of this was 50% corn syrup, 14.2% soy protein isolate, 10.4% high oleic safflower oil, 9.7% sucrose, 8.2% soy oil and 7.5% coconut oil. If a baby is unfortunate enough not to be breastfed, the infant can be started on a diet of 60% sugar from the first moment something is put in its mouth.

It is clearly in the interests of ‘food’ companies to partner with those giving us dietary advice – and to start as close to birth as possible. Does the public know that our advice is so conflicted? How can we “Trust a dietician to know about nutrition” (their slogan) when this conflict of interest exists?

Nutritional ‘education’

That’s the conflict inherent in our nutritional training, what about the content of programmes?

I only know one way to learn and that is to “get the facts”. I am a thinker, not a feeler. If I am told something I need it to be evidence based. I want to know the source of everything – where did that come from? when did this become known and so on. This stood me in good stead studying economics (maths, statistics options) at Cambridge. Applying the same rigour to the subject of nutrition was the most shocking thing I have ever done.

During the three years of full time research for The Obesity Epidemic, the following nutritional beliefs did not hold up to scrutiny. Please note – these points are only in the part of nutrition related to dietary advice and weight loss. There may be many more errors in the teaching of nutrition outside my areas of interest.

Starting at the very beginning – dieticians state that “energy in = energy out.” “You can’t change the laws of the universe”, they say. But there is no law of the universe that says  “energy in = energy out.” I detail in The Obesity Epidemic exactly what the laws of thermodynamics say and which law we have misunderstood and which law we have ignored.

We are then told that 1lb = 3,500 calories. It doesn’t.

We are told that we will lose 1lb if we create a deficit of 3,500 calories. We won’t.

We are told that 98% of diets fail (true for calorie deficit diets) but are continually told to “eat less/do more” despite this.

Five-a-day is a marketing myth. Eight-a-day (drinking) is similarly fabricated. Alcohol guidelines are numbers “picked from the air.”Fruit is essentially sugar (fructose/glucose – aka sucrose) with vitamin C and not much else by way of nutrition. Offal, red meat and butter, the foods most often condemned by diet advisors, are nutritionally exemplary.

Saturated fat is life vital. Mother Nature is not trying to kill us.Cholesterol is life vital. Our own body (which makes our cholesterol) is not trying to kill us. The formula for cholesterol is C₂₇H₄₆O. There is no good or bad version.Grazing (don’t); fibre (pointless); sedentary behaviour (how humans were designed to be) – there’s so much that we have got terribly wrong.

As Kaayla Daniel said at the 2011 Weston Price Conference – “If you’re told it’s bad, it’s good and if you’re told it’s good, it’s bad – work on that basis and you can’t go far wrong!”

Check out this free ebook or any of these presentations: Calories, Energy Balance, Thermodynamics and Weight Loss; Ten diet myths; The Obesity Epidemic to find out more.

Conclusion

I cannot recommend any dietetic or nutrition course because I know of none that will teach the truth about everything from thermodynamics to the role of insulin in fat storage. My genuine recommendation is that you need to study via amazon (Sean Croxton, Underground Wellness, concluded the same) and medical journal web sites.

Read Mary Enig and Sally Fallon Morell on fats; Uffe Ravnskov, Duane Graveline and Dr Malcolm Kendrick on cholesterol and the lipid hypothesis; The Diet Delusion (Gary Taubes); critical reviews of all of these and weigh the evidence for yourself. There will be many more non- conventional wisdom works for different areas of interest. The seminal journals to be read include Benedict (1917); Newburgh & Johnson (1930); Hugo Rony (1940); The Minnesota Starvation Experiment/The Biology of Human Starvation (1950); Stunkard & McLaren-Hume (1959). The Seven Countries Study (1970); The COMA report (1984). There are 400 references here for convenience – the books and journal articles are recommended.

When I started to question the origin of the calorie theory (1lb = 3,500 calories, so to lose 1lb you need to create a deficit of 3,500 calories), I asked the Department of Health, the National Health Service, the National Obesity Forum, The National Institute for Clinical Excellence, the Association for the Study of Obesity, Dieticians in Obesity Management and the British Dietetic Association. None could source the calorie theory. None could prove it.

The British Dietetic Association reply was: “Unfortunately we do not hold information on the topic that you have requested.” It was suggested that I contact a dietitian. I happened to be with several dietitians at an obesity conference later that month (June 2009), so I asked fellow delegates and no one knew where the 3,500 formula came from. No one knew where the ‘eatwell’ plate proportions came from. One dietitian said to me “You’ve made us think how much we were just ‘told’ during our training, with no explanation. A group of us over there don’t even know where the five-a-day comes from.”

I rest my case!

Also available as a podcast

You can download the presentation slides HERE.

The study

The team looked at three studies for which there was food questionnaire information available:

- 37,083 men in the Health Professionals Follow Up Study (1986-2006);

- 79,570 women in the Nurses Health Study I (1980-2008);

- 87,504 women in the Nurses Health Study II (1991-2005).

In total 13,759 incidents of type 2 diabetes were recorded from 4,033,322 person-years of follow-up. That’s a 0.34% incident rate to start with. Hardly justifying the headline “Diabetes threat from two slices of bacon a day.”

The conclusion

You can see the conclusion in the abstract: “The pooled HRs (95% CIs) for a one serving/d increase of unprocessed, processed, and total red meat consumption were 1.12 (1.08, 1.16), 1.32 (1.25, 1.40), and 1.14 (1.10, 1.18), respectively. The results were confirmed by a meta-analysis (442,101 participants and 28,228 diabetes cases): the RRs (95% CIs) were 1.19 (1.04, 1.37) and 1.51 (1.25, 1.83) for 100 g of unprocessed red meat and for 50 g of unprocessed red meat, respectively. We estimated that substitutions of one serving of nuts, low-fat dairy, and whole grains per day for one serving of red meat per day were associated with a 16–35% lower risk of T2D. “

There must be an error with the two words that I have highlighted in red.  Is the article really saying that eating 100g of unprocessed red meat has 1.19 risk (presumably relative to not eating any unprocessed red meat) but that eating 50g of unprocessed red meat has a 1.51 risk? i.e. claiming that people who eat 100g of unprocessed red meat have ‘a 20% greater risk of diabetes’ but people who eat half this amount have ‘a 50% greater risk’?! Do they mean unprocessed at the first mention and processed at the second? (I’ve emailed Frank Hu – watch this space. Update – email back by return, fair play! Confirmation that this IS an error and AJCN will be asked to correct).

The overall conclusion is: “Our results suggest that red meat consumption, particularly processed red meat, is associated with an increased risk of T2D.”

Issues

1) On P2 of the full study we have the significant error at the outset. Under the heading “Assessment of meat consumption”, we have this telling passage: “Questionnaire items in unprocessed red meat consumption included ‘beef or lamb as main dish’, ‘pork as main dish’, ‘hamburger’ and ‘beef, pork or lamb as a sandwich or mixed dish’, and items on processed red meat included ‘bacon’, ‘hot dogs’, and ‘sausage, salami, bologna, and other processed red meats.’”

We reach the fundamental issue, which renders the study futile, in this one passage. Real food supporters define unprocessed meat as that which has been naturally reared and processed meat as any and every other meat. Take the Weston Price Foundation definition of real meat for any study. Real unprocessed meat comes from animals that have been living their entire life freely outdoors grazing on (ideally fast growing) grass in rain and sunshine. These animals must have been eating grass, which they are designed to eat and not grain which they cannot digest. Unless they have been chewing the cud, which, as ruminants they are designed to do and pre-digesting vitamin D blessed grass for those who cannot digest cellulose – humans – there is no point in consuming them.

Hamburgers are not real meat. Presumably a lamb curry takeaway qualifies as “beef or lamb as main dish” – this is not real meat, as real food supporters would define it. The fundamental point of the study is about red meat – processed and unprocessed. To make any relevant claims, the study should have looked at those who eat no meat (every single other factor unchanged), those who eat real meat (every single other factor unchanged) and those who eat processed meat (every single other factor unchanged). The fact that other factors cannot be held constant is one of the major reasons why the UK Food Standards Agency had to admit (in the context of fat and heart disease studies):

“However, the ideal controlled dietary trial for prevention of heart disease (a long-term intervention trial with differing levels of saturated fatty acids and measuring coronary disease endpoints) has not yet been done and it is unlikely ever to be done”.

Plus – the second critical point related to the so-called unprocessed meat – what is “beef or lamb as main dish” eaten with? rice? potatoes? carbs? What are hamburgers eaten with? burger buns? chips? ketchup? carbs? What are “beef, pork or lamb as a sandwich” eaten with – bit of a clue there – bread, likely hydrogenated fat margarine, emulsified mayonnaise, and, no doubt, more ingredients in the bread alone than in the varieties of real meat available to humans.

It doesn’t matter what the survey did or concluded next – they did not measure real meat vs processed meat or isolate this consumption from any other macro nutrient.

2) Diabetes is a condition related to blood glucose levels and insulin – either the body’s failure to release insulin to respond to a rise in blood glucose levels (type 1) or because cells are unresponsive (resistant) to insulin released (type 2). The macro nutrient most relevant to diabetes therefore is carbohydrate. Fat has no relevance and the relevance of protein is debatable, but negligible compared to that of carbohydrate. So, what is most likely to have any impact on diabetes – the processed (don’t call it unprocessed) hamburger, or the bun, fries and ketchup? To claim an association between one part of food intake and not the whole is meaningless.

The report even notes that they conducted a sensitivity analysis  with “adjustment for other major dietary variables (whole grain, fish, nuts, sugar-sweetened beverages, coffee, egg, potatoes, fruit and vegetables, all in quintiles).” Why not take the dietary questionnaires (however unreliable these notoriously are) and run an association with all dietary carbohydrate and incidence of diabetes over time. Biscuits, cakes, confectionery, bread, sugary cereals, pizza – the 400 calories of sugar and 700+ calories of flour that the average American eats daily. Are those eating more than their share getting more than their ‘share’ of diabetes?

This study was called “Red meat consumption and risk of type 2 diabetes…” Notwithstanding that it is about processed meat and even more processed meat and association with type 2 diabetes, when will we see the study “Carbohydrate consumption and risk of type 2 diabetes…”?

3) To be fair – the study did not claim causation. Research papers rarely do. They propose association and let the media run the “just two rashers of bacon can increase the risk…” headlines. Association does not mean causation – either way round. We should not be able to jump from association to ‘meat consumption causes diabetes’ any more than we should be able to jump from association to ‘diabetes causes meat consumption’. Not only is causation usually assumed, a direction of causation is assumed. The people who developed diabetes may have all worn blue socks – does that mean that wearing blue socks increases the risk of anything?

4) Table 2 of the report negates the idea that there is any trend. Data is presented for the three studies, for five different levels of meat intake. The serving sizes are determined relatively, by quintile, so, as an example, for the Health Professionals Follow-up Study for what the study assumes to be unprocessed red meat, the five different serving categories are 0.17 servings per day, 0.43, 0.65, 0.94 and 1.44 servings per day). Finally, three models are presented for each of these different meat intake levels, by study:

- an age adjusted model;

- a model adjusted for age, alcohol consumption, physical activity, smoking, ethnicity, menopausal stage for women, family history of diabetes/hypertension/hypercholesterolemia, quintiles of total calories and a dietary score for diabetes that the team made up (more on that below);

- a model adjusted for everything above and BMI.

All of this is then done for their opinion of unprocessed red meat, processed red meat and total red meat (that should be total processed meat). You can see that this is indeed a multi variate model!

There is not a steady trend between meat intake and the incidence of diabetes in every model variant of every study. For the Health Professionals Follow-up Study (HPFS), increased (what they call) unprocessed red meat intake from 0.65 servings per day to 0.94 servings per day was shown to have a reduced incidence of diabetes in all three models.

It is not clear how the dietary score for diabetes impacted the assumptions and therefore results, but the team “created a low diabetes risk score as a diet low in trans fat and glycaemic load and high in cereal fiber and the ratio of polyunsaturated to saturated fat.” What the ratio of two fats, which nature can put naturally in foods in different proportions and man can put very unnaturally in foods in different proportions has to do with the risk of diabetes I do not know.

5) The final point to make, as is the case with all presentation of numbers from studies to achieve maximum impact (and likelihood of media reporting) is that there are lies, damned lies and statistics. If you buy two lottery tickets each week, I can halve your chance of winning by allowing you only to buy one. Your odds of winning are now (for example) one in fourteen million instead of one in seven million – still absolutely naff all. However I have halved your chance of winning. Imagine I halved your ‘chance’ of developing diabetes in a similar, playing with numbers, kind of way…

Let’s take some actual numbers from Table 2 as an example:

Processed red meat, age adjusted model, from the HPFS…

- 0.02 servings of processed red meat per day (one serving is 28g so that’s half a gram of processed meat!) is associated with 340 incidences of diabetes in 138,550 person years. That’s an incidence rate of 0.25% or 1 in c. 400 people.

- 0.12 servings of processed red meat per day (that’s 3 grams – can any of you actually measure your intake to that level?) is associated with 409 incidences of diabetes in 121,238 person years. That’s an incidence rate of 0.34% or 1 in c 300 people.

(This is raw data – adjusted for age only – not adjusted for smoking, exercise, calorie intake, family history of diabetes, weight etc i.e. impossible to isolate two different minute meat intakes and assume that this is the only difference.) This aside, this is presented as – if at 0.02 servings per day you have a 1.00 ‘risk’ of developing diabetes, at 0.12 servings per day you have a score of 1.38 i.e. a 38% higher risk. There’s the headline “3 grams of bacon a day and you have a 40% greater risk of diabetes.” There’s how numbers are played with to frighten the life out of you and to make sure that you have sugary cereal for breakfast instead of eggs from grass living chickens.

The bottom line

This is a study about processed meat and even more processed meat and observed associations between intake of each and incidence of diabetes. No biochemical pathway is proposed for how fat/protein is supposed to impact a condition of glucose/carbohydrate handling deficiency. The obvious connection between the buns, chips and ketchup being consumed with the hamburger has not been made.

To let the media have the last word – the Mail article tells us how it is: “There is now widespread evidence that red meat drastically (my emphasis – couldn’t resist it) increases the likelihood of major health problems including heart disease, strokes, and some types of cancer.”

Accuse modern, processed meat of all this and more – all modern food in fact. Hang processed ‘food’ generally for crimes against human health – heart disease, strokes, cancer, diabetes, Alzheimers – all modern illness. Throw the book at the man-made horrors. But, if we really think that nature put all the essential fats, essential amino acids, full range of B vitamins, fat soluble vitamins, iron, calcium, magnesium and zinc in red meat and was trying to kill you at the same time, we wouldn’t be here today!

This is a review of  The Vegetarian Myth and the Amazon reviews confirm that it is the marmite of the book world – people love it or hate it. (Hopefully not about to be banned in Denmark however!) I have to confess that I loved it because it raised some huge issues – you don’t get much bigger than how can we feed the human species and neither ‘side’ has an answer to this one – we have way too many people already on this planet for any sustainable option and things are continuing to get worse.

This review is intended to provide a useful and convenient summary – reading the book for your self is still highly recommended. I will quote Keith verbatim where possible – her writing style is quite beautiful and should be read first hand.

Gary Taubes has his critics on the internet, but they pale into insignificance compared to those queuing up to attack Lierre Keith. In Chapter 1 she says: “I got hate mail before I’d barely started this book. And no, thank you, I don’t need any more.” There are many similar ‘cute’ comments and humour throughout the book, which I really enjoyed.

I also enjoyed the feminist passages in the writing, for which Keith has also been attacked. It took me back to my days at Cambridge when I saw an article written by the Student Union president referring to ‘she’ and ‘her’ all the way through. Why does this only apply to women, I wondered? And then, of course – silly me – this article does apply to both genders, but then so does every article talking about ‘he’ and ‘him’ and yet nothing ‘jars’ when we read that. Keith uses the female third personal singular a couple of times – just to keep you on your toes. She also gets (appropriately in my view) angry with those who think it has been OK to trash the planet during their infinitesimally small time as guests here – for their own greed and personal gain. They tend to be male (CEO’s, world leaders, lawyers etc) and they are certainly ‘macho’. Go girl!

Attacking the vegetarian

In Chapter 1, Keith notes exactly why her book has attracted the anger and outrage that it has. “’Vegetarian’ isn’t just what you eat or even what you believe, it’s who you are… I’m not just questioning a philosophy or a set of dietary habits. I’m threatening a vegetarian’s sense of self.”

Keith herself was vegan for 20 years and describes the health complaints that she has been left with, as a result of her dietary choice: from degenerative spine disease (irreversible) to depression and anxiety (much improved since ceasing to be vegan). She still suffers nausea and serious digestive problems and pain, which make it difficult for her to eat in the evening (if she plans on sleeping that night). Keith explains the chosen route was an obvious one made by her and friends when young: “All the friends of my youth were radical, righteous, intense. Vegetarianism was the obvious path, with veganism the high road alongside it.”

She pleads in the opening chapter: “You don’t have to try this for yourself. You’re allowed to learn from my mistakes… I’m asking you to stay the course, read this book, please. Especially if you have children or want to. I’m not too proud to beg.”

Keith ends this introduction with the humble statement: “Ultimately I would rather be helpful than right.” I was very little way into the book before I realised she is both.

The three arguments for (and against) vegetarianism

(Please note – the terms vegan/vegetarian can be used virtually interchangeably throughout the book – Keith applies the same arguments to both views. One just draws the line in the sand in a different place).

The book is perfectly structured. There are three arguments that vegetarians make as to why we should all be vegetarian and Keith structures the book in three parts to reflect this:

1) The moral argument – we should not kill;

2) The political argument – we can only feed the world if everyone is vegetarian;

3) The nutritional argument – it is healthier to be vegetarian.

The only thing that I won’t be able to answer, while writing this review, is how I would have responded reading it, had I still been vegetarian at the time. It would be wonderful if any vegetarians could try this and share their views. I know that there would have been a time when I would have been as angry as many vegetarian and vegan readers of the book have been. I don’t know, however, how I could have countered Keith’s arguments.

I do know that I never believed that there was a nutritional argument for being vegetarian. I have known enough about nutrition, for long enough, to know that liver, meat and fish are incomparably nutritious. This is why I never considered becoming vegan. I could not think how I could get vitamin A, B12, D, iron, zinc etc in anywhere close to sufficient amounts without supplements and it never felt right to be taking nutrients in a tablet when food could provide them.

I became vegetarian for the moral argument. I subsequently strengthened my belief by adopting the political argument. The essence of my belief was that I could be healthy enough without eating animals and animals would be better for this decision. I knew that I could not be optimally healthy, but felt that I was making a moral sacrifice in an age when humans were in a position to ‘do the right thing’.

Keith knocks down all three beliefs as follows:

The moral argument

I am covering the arguments in the order that Keith does and I could not believe how quickly Keith changed my views in this first part of the book. Even though the Barry Groves and Sally Fallon Morell presentations at the Weston A Price Foundation conference in March 2010 had ended my 15 year period of being vegetarian, I still believed that there was a clear line in the sand on ‘killing for food’ and that vegetarians were on the right side of the line. Oh boy!

In a nutshell the moral vegetarian argument is “we should not kill”. Keith’s response is:

a) There is absolutely nothing, nothing at all, that even a vegan can eat that something has not died for (several living things in fact);

b) Man is not at the top of a food chain – that is an arrogant view that only ‘man’ could hold. All humans are part of the circle of life. Our bodies end up as food for the soil, just as every other animal that dies (ideally on the prairie) leaves their nutrients and minerals to go back into the soil for new life.

a) When Keith expanded upon the first point, I was kicking myself within seconds. How could I have been so naive? Keith shared her original vegan view: “I wanted to believe that my life – my physical existence – was possible without killing, without death. It’s not.”

Before long, the examples came thick and fast and became irrefutable. How many slugs are killed for a lettuce? How many millions of species in a tablespoon of top soil are trashed every second by Cargill? How many rabbits and mice are killed in cultivated fields by industrial size farming equipment? How many fish die, so that rivers can be diverted to irrigate the vegan’s grains? How many wolves and bison have been killed because we turned their homeland into farmland – for grains and plant food? Keith answers the last one: “There were somewhere between 60 and 100 million bison in the United States in 1491. Now there are 350,000 bison and only 12 to 15,000 of those are pure bison that were not cross bred with domestic cattle. The land held between 425,000 and a million wolves; only 10,000 now remain.” “The North American prairie has been reduced to 2% of its original size and the topsoil, once twelve feet deep, can now only be measured in inches.”

b) Point (b) is so integrally linked to (a) – one of the reasons that no life is possible without death is that the soil upon which life depends relies upon death to return nutrients to the land. Keith explains her first hand experience of trying (and failing) to grow her own food without anything needing to die… (Any vegan that argues that they can grow their own lettuce, with nothing having to die, has to read the whole of this moral section of the book. Keith tried it and then some! The full story is funny and powerful at the same time).

Organic Gardening magazine soon explained to Keith that the first commandment of organic growing was “feed the soil, not the plant.” She learned that Nitrogen, Phosphorus and Potassium was the “triple Goddess of gardeners.” All three are minerals given back to the land when animals (including humans) die. (Calcium is also a limiting factor for soil – also found in the bones and remains of animals that die and so generously give back their nutrients to the land). We can get nitrogen from fossil fuels, or nitrogen can be given back to the land by the circle of life and death. We are not far from the time (peak oil and all that) when we have the stark choice – use fossil fuels for fertiliser for food or for running the power upon which modern life has come to depend. What do we do when the oil runs out? Manure and carcasses or fossil fuel for fertiliser? – that’s our choice.

As this part of the book unfolds, Keith hits you with one stark fact after another:

- “70% of all water from rivers and underground reserves is being spread onto irrigated land that grows one third of the world’s food,” writes Fred Pearce in When the rivers run dry.”

- “Of China’s 23,000 miles of large rivers, 80 percent don’t support fish anymore.” “Set aside the fossil fuel for the fertilizer and transportation. If you live in Vermont or California and eat vegan brown rice – this is what you’re eating: dead fish and dead birds from a dying river.”

- “We’re out of topsoil, out of water, out of species, and out of space in the atmosphere for the carbon we can’t seem to stop burning.”

You come to realise that the ultimate role that we (humans) can play in this universe is to continue to be a part of the universe when we die. Whatever happens to our soul, our body is food for worms, which are food for birds, which are food for cats, which are food for their predators and so on. Humans often look for significance – for a sense of purpose in life. Our purpose is as part of the whole circle of life. All of us have this part to play.

Keith continues, “The native prairie is now 99.8% gone. There is no place left for the buffalo to roam. There’s only corn, wheat and soy.” With all that land cultivated for vegetarian food, which was once home to free roaming animals, there is also no natural process by which the top soil can be rejuvenated. There is only so much that fossil fuel fertiliser can do to repair the damage being done by overworking our scarce land in the name of profit. No wonder (GM) Genetically Modified crops became a necessity – we have to modify crops when we have destroyed the earth to the point that it cannot yield ‘normal’ crops.

“’You can look a cow in the eye,’ reads an ad for soy burgers. What about a buffalo?” asks Keith. “Five percent of a species is needed to ensure enough diversity for long-term survival, and less than 1 percent of the buffalo are left.”

Keith concludes: “It is my conviction that growing annual grains is an activity that cannot be redeemed. It requires wholesale extermination of ecosystems – the land has to be cleared of all life.” We use 5.6 billion pounds (weight) of pesticides per year (a statistic I found elsewhere) – pesticides being designed to kill any living thing that also wants to feed on (our) growing food.

I realised in this part of the book that it comes down to black and white and shades of grey. To the vegan, the world is black and white – “meat is murder.” Keith describes this as “a simple ethical code… but it is the black-and-white thinking of a child.” This is a critical part of the book and one with which I resonated very strongly. I was far more black and white in my 20’s. Things were right and wrong. (Good days and bad days!) This is very child-like thinking. The simple world of a child is right and wrong. The more mature world of the adult has many shades of grey.

The shades of grey in this killing debate are inescapable – you may draw the line at eating cows, but not dogs; you may draw the line at eating chicken, but not red meat; you may draw the line at eating fish, but not meat; you may draw the line at eating eggs, but not the flesh of animals; you may draw the line by wearing leather shoes, but eating nothing from an animal; you may have a vegan diet and wardrobe – but bison, birds, fish, rabbits, mice and thousands of living creatures in top soil have died for your soya burger and lettuce.

It’s not that vegans are right and vegetarians are wrong, or vegetarians are right and omnivores are wrong, or omnivores are right and carnivores are wrong – it’s about where we each choose to draw our line. Better still, to return to the arrogant view that ‘man’ thinks he is at the top of a food chain, Keith concluded “I’m not going to draw a line. I’m going to draw a circle.” We are part of the circle of life, just as any other animal is. They and we need to live and die to give back to the land, so that birth and death can continue.

I remember non-veggies saying to me when I was veggie “If we didn’t eat the animals they wouldn’t be here” and I just couldn’t comprehend the point that they were making. Would that be such a bad thing? Surely the animals would be better off not living if they were just going to be killed for food? (‘Better to have loved/lived and lost, than never to have loved/lived at all’ kind of thing. That’s a massive philosophical argument in itself – we’re all going to die – is it worth being here at all?!) Couldn’t we keep animals and not kill them? I just didn’t think of the practicalities that no farmer keeps ruminants (that’s the collective term for grass grazing animals – cows, sheep, goats etc) as pets. Animals are kept for food and they always have been within communities throughout history. Each settlement would safeguard the delicate balance between the ‘goose and the golden egg’ – to protect any givers of eggs/milk and the time when it comes to eat the giver of these vital foods. I don’t want a world without sheep & lambs, or cows & calves, in the fields. I want natural manure from these grazing animals nourishing the land naturally. I don’t want oil used to mow the grass, which ruminants could have eaten and then more oil used in fertiliser instead of manure. Animals are a vital part of the circle of life, not a line that modern, arrogant, man thinks he can draw on the land. This brings us nicely on to…

The political argument

The political vegetarian argument is that we can only feed the world if everyone is vegetarian. Keith quotes Jim Motavalli, who, in turn quotes the British group Vegfam: “a 10-acre farm can support 60 people growing soybeans, 24 people growing wheat, 10 people growing corn or only 2 producing cattle.” The maths behind this is not provided and Keith can’t work out where it could come from, but she notes that any such statistics will always find against cattle because they start from the premise that the cattle is fed grain. Hence, of course land would produce more grain to be eaten as grain than if that grain were fed to cattle and the cattle output were subsequently calculated. What Keith (and every real food person) argues is – we should not be feeding grain to cattle. Not ever. Not in any circumstances. The maths then falls over.

Keith opens the political argument section with a detailed description of the digestive system of a ruminant. The term ruminant means a cud-chewing animal, characterised by having four stomach compartments – the first being called a rumen. Keith describes how a cow, for example, is entirely reliant upon a magical internal ecosystem comprising bacteria, fungi and multiples of microbial cultures. The cow is feeding on the bacteria and the microbes are living within (feeding upon) the cow – it is the way of life for/in a ruminant. Grains turn the normally neutral rumen (first stomach) acidic, which makes the cow sick and bloated (not dissimilar to the effect that grains have on many humans!) Hence we should not be feeding ruminants grains. Ruminants, by definition, need to chew on cud – grass.

Joel Salatin (one of the role models of the local sustainable model) then does the maths for his 10-acre farm in Virginia. He produces 3,000 eggs, 1,000 chickens, 80 hens, 2,000lbs of beef, 2,500lbs of pork, 100 turkeys, 50 rabbits and a few inches of topsoil. No fossil fuels needed whatsoever. The chickens get a bit of supplemental grain (they can ‘stomach it’, literally) and everything else eats grass. Keith compares the calories and nutrition from this organic farm vs. the malnutrition, pellagra and fatal disease that the soy, wheat, corn community would end up with. It is incomparable in favour of eating the sustainable (animal) way.

The arguments against the political vegetarian are numerous:

a) Agriculture (turning the little arable land that the world has into grain and soy fields) is destroying the planet. It ‘murders’ the top soil and is completely unsustainable, in that nothing is being done to reverse the damage. Instead – food manufacturers are looking to create GM ‘frankenfoods’, which can still grow when all life and health has been removed from the land. As Keith says: “Who cares if more food can be produced by farming when farming is destroying the world?”

b) Manure and animals living and dying on land is the natural way to fertilise – to replenish the top soil so vital to life. To replace animals in the food chain with soy and grain is to destroy the entire circle of life. This is also completely unsustainable. There is a finite amount of fossil fuel in the world to use for fertilisers. There can be a sufficient amount of manure from the right number of animals occupying the right land space.

As Keith challenges: “Political vegetarians need to answer this question – what is going to feed your food? Fossil fuel or manure?”

c) It is nonsense to say that we are feeding grain to cattle, which could be used to feed humans. We are feeding grain to cattle, which they cannot digest, because grain is so cheap and so subsidised, that grain manufacturers have to dump it somewhere. Grain to America is the butter mountain of Europe. If grain production were not so lucrative and well subsidised, there is no way that cattle would be fed grain – they might be left to eat the grass that they are supposed to eat. I say ‘might’ because grain also causes cattle to fatten quickly (as it does humans) and this makes the cattle heavier, quicker and thus makes the animals more lucrative in the process. Win win for Cargill. Lose lose for the ruminants and the earth, which they have not been allowed to renourish.

d) When we factor in all the water and oil and fossil fuels used to ‘feed’ the land in the way that animals would do naturally, the price of grain is the planet itself. Richard Manning is quoted as saying “A typical farm in 1940 produced two calories of food energy for every calorie of fossil energy used. By 1974 that ratio was 1.1. As of now, it takes more than a calorie of fossil fuel to produce a calorie of fuel for a human – somewhere between four and ten calories of fossil fuel for a calorie of food.” When fertilisers, pesticides, machinery, harvesting, transportation and so on are taken into account, an acre of corn requires about 50 gallons of oil.

e) What limited land there is in the world suitable for agriculture, America has more than its share. Encouraging the world to eat grains and soy (the USA food pyramid, the USDA dietary guidelines) makes the world dependent on America for its food – the ultimate dependence. Western countries support the giant food producers with subsidies totalling $360 billion. This substantially reduces world prices. As Oxfam has observed: “Exporters can offer US surpluses for sale at prices around half the cost of production – destroying local agriculture”. US aid is anything but – it is destroying local farmers and communities – making the world dependent on America to eat.

As Keith says “This is why there are no international aid agencies that suggest vegetarianism as a solution to world hunger: it isn’t one.”

Gary Taubes once joked “My wife says I blame everything on carbohydrates.”

In my view, the most serious thing that we need to blame on carbohydrates is that we have exploded the world population to completely unsustainable levels as a direct result of carbohydrates. When communities were based around sustainable, local, lands and foods, the population of the world could only ever be a number that could be sustained.

Agriculture and grains have enabled an unsustainable explosion in the number of people that we could feed, but this has never been done in a sustainable way. I thought I was a lone voice in thinking this until I read the following in The Vegetarian Myth:

“Breaking our dependence on the sun and nature’s fertility meant an explosion in grain production and a concomitant expansion in the human population. There are now over 6 billion humans. Understand: billions of us are only here because of fossil fuel, because we figured out how to transform stored energy into edible energy. As the natural gas and oil get more expensive, and then prohibitively expensive, there will be no way to keep that grain coming. And then? It doesn’t sound like a party I want to attend.”

The world population is due to reach 9 billion by 2050, about the time that the oceans are forecast to be empty of fish and long past peak oil. Keith estimates that we already have multiples too many people in the world – at least 10 times too many, maybe 100!

The stark reality is that this is an argument that neither the omnivores nor the vegetarians can win. There is no sustainable way to feed the current population – let alone the level that is forecast within the next 40 years. Grain, soy and agriculture are completely unsustainable, for any population level, as they destroy the planet without replenishing it in any way. Meat, fish and eggs are equally unsustainable, for the current population level, as there is not enough grazing land in the world for enough animals to feed us all and we have polluted and raped the oceans of their bounty. Had we not destroyed pastures for grain, the world population would have grown naturally and sustainably to sustainable levels.

Toward the end of this part of the book is a blunt message – forget peak oil. “Peak soil was ten thousand years ago, on the day before agriculture began.”

We then move to…

The nutritional argument

Even though I never bought this argument, I’ll cover it for completeness and because it is a very interesting part of the book and because many people do use this as a reason for being vegetarian. Unfortunately, dieticians and many charities (World Cancer Research Fund, British Heart Foundation, Diabetes UK) seem to be on hand to encourage this position. The nutritional arguments are as follows:

a) Humans evolved to eat plants and not animals;

b) Animal foods contain cholesterol and this will kill us;

c) Animal foods contain fat and this will kill us;

d) Vegetarian and vegan foods are healthy;

e) Animal foods contain fat and this will make us fat.

Keith devotes over 100 pages to this, Part 3, of the book and the attention that she devotes to each argument is impressive. As an example, I address the ‘what did we evolve to eat’ debate in Chapter 12 of The Obesity Epidemic, but Keith goes into it in far more detail. She goes through three roles of teeth, four actions of the jaw, four digestive processes, nine activities of the stomach, two of the gall bladder and every detail on gut flora, the colon and even the length of the small intestine to compare humans, dogs and sheep. She quotes Dr.s Michael and Mary Eades to provide the conclusion: “In anthropological scientific circles, there’s absolutely no debate about it – every respected authority will confirm that we were hunters. Our meat eating heritage is an inescapable fact.” I concluded the same from anthropological research.

I also looked, as Keith did, at the possibly of getting sufficient vegetarian food for the 3.5 million years since ‘man’ first walked upright. Notwithstanding the 30,000 years of ice age endured 40,000-10,000 years ago, when no vegetation would have been available, there is simply no evidence that our planet could have yielded sufficient vegetables and fruit for man to have consumed sufficient calories to survive. Grains were not available until the emergence of agriculture. Half the vegetables possibly available to our ancestors would not have been edible without cooking and fire was not discovered until somewhere between 1.5 and 0.5 million years ago. Let alone the seasonality of vegetation and the likelihood that nothing would have been available in certain parts of the world and for many months anywhere else.

That’s as far as I went. Keith also goes into the enzymes in plants and the toxins that they emit – in an effort not to be consumed and to survive – as any living thing tries to survive. She then picks up the argument – OK – should we have become vegetarian when grains did appear – notwithstanding the fact that we never had them before? She presents a compelling argument that we have simply not evolved to eat grains (this is the mainstream Paleo view) and that they are seriously harmful to human health. Lines such as these are punched out on successive pages:

- “Grains are essentially sugar with enough opioids to make them addictive.”

- “The diseases that insulin affects directly are the cause of the vast majority of death and disability in the US today. Heart disease, high blood pressure and diabetes are all caused by the insulin surges that grain and sugar demand.”

- “You can call it complex carbohydrates if you want, but it’s sugar.”

- “According to the USDA, we should be eating a diet that is 60% carbohydrate. Your body will turn that carbohydrate into almost two cups of glucose and each and every molecule has to be reckoned with.”

- Quoting the Eades again: “The actual amount of carbohydrates required by humans for health is zero.”

- And my favourite: “you’ve (vegetarians) damaged your digestion, from too many blood sugar highs and lows, and too much adrenaline. It can be fixed, but you’re going to have to eat real protein and fat and not sugars. You need to leave adrenaline for emergencies only; can we agree that breakfast shouldn’t be one?”!

b) The cholesterol argument has been covered more extensively by Kendrick and Ravnskov (and me in The Obesity Epidemic). Keith mentions a couple of the key points, and nails it beautifully with the following one liner: “One of the main functions of the liver is to make cholesterol, not because your liver wants you dead, but because life isn’t possible without cholesterol.”

c) The book provides another really nice summary on the position on fat. I go into this in more detail than I’ve seen it elsewhere with my original analysis of the Seven Countries Study and an assassination of the Truswell article, which is a summary of all the evidence relied upon by government authorities telling us that fat is a killer. (I also point out that when our governments talk about fat, they are in fact talking about refined carbohydrates, but that’s another story).

Keith’s summary is very clever. She explains that fat consumption declined almost 25% in the past 15 years (the book was published in 2009) and, at the same time, type 2 diabetes has increased by a factor of more than ten; cardiovascular disease recorded at time of hospital discharge has increased 25%, the incidence of stroke is rising and cancer “continues its relentless and increasing toll.”

Keith also covers the fat soluble vitamins, essential fats and other nutrients in real fat vs. the unnatural levels of omega-6 to 3 ratio, as a result of our obsession with cheap vegetable oils. “You tell me what to blame: the saturated fats we’ve always eaten – for four million years – or the industrially manufactured oils that until recently were used in paint.” Quite so!

d) Sugary cereals, soy (as it is called in the USA – it’s called soya in the UK) and vegetable oil spreads/margarines are promoted as healthy by the food industry. Of course they are – they are phenomenally lucrative. Kellogg’s alone is a $13billion company. They are new products, only introduced to the food chain in little more than the past 100 years in the case of cereals and in nearer 20 years in the case of modern soy and vegetable oil products. Keith states: “The food industry has developed over 100,000 new processed foods since 1990.” That is staggering and surely ‘foods’ should be in inverted commas!

These ‘foods’ rely as much on knocking real food, as they do on promoting themselves as healthy. Vilify eggs and promote sugary cereal as the alternative. Attack butter and hydrogenated margarine can come to the rescue. Lie about hormones in cow’s milk and everyone will turn to soya in their Starbucks. It is horrific to think that big business can get away with it. As Keith says “Try to comprehend the scale of this: food companies spend $33billion a year in advertising.”

Keith dedicates a few pages to a horrifying review of the health concerns surrounding soy(a). Quoting Dr Kaayla Daniel (one of the speakers at the March 2011 Weston Price Conference), author of The whole soy story: the dark side of America’s favourite health food the allegations unfold. Soy(a) is delivering hormone doses not dissimilar to the contraceptive pill (in snack size portions of soy – let alone the levels eaten by vegans). Soy(a) is implicated in serious thyroid disturbance (think thyroid, think weight). “Those who ate tofu at least twice a week had accelerated brain aging, diminished cognitive ability, and were more than twice as likely to be clinically diagnosed with Alzheimer’s disease.” “In fact, the more tofu eaten, the more cognitive impairment and/or brain atrophy.”

We had a vegan in our online club who said something about ‘you only ever get animal illnesses’ – bird flu and mad cow disease? Keith’s humour appears again when she closes the section on soy(a) with: “According to a vegetarian bumper sticker ‘There’s no such thing as mad tofu disease.’ You might want to rethink that”!

Food manufacturers must love vegans – virtually all vegan calories must come from food manufacturers. There’s very little that the vegan can get from the local farmer. That alone is reason enough for me to not want to be vegan!

e) The final argument was very interesting – especially people interested in weight loss. One of the arguments for avoiding animal foods is that fat contains (approximately) 9 calories per gram and carbs approximately 4. Hence many dieters become vegetarian as a convenient way of avoiding higher calorie foods. (The fact that these foods are zero carb doesn’t matter to calorie counters). Keith notes that “Somewhere between 30 and 50 percent of the girls and women seeking treatment for anorexia and bulimia are vegetarian.” Keith says “The overlap in my life is a perfect 100. Everyone I’ve known with an eating disorder has been a vegetarian and that includes two anorexic men who were both vegans.”

There is an interesting ‘chicken & egg’ argument – the dieter likely chooses to avoid animal foods to avoid calories but, also, vegetarian diets are typically low in tryptophan, which is the precursor of serotonin. Hence vegetarian diets can also cause depression, anxiety and eating disorders. “Veganism, I quip, is one part cult, one part eating disorder. I hear those words and I wish they weren’t true because of what they mean about me.” That’s what Keith said. I could have said the same.

Note on all 3 arguments

We need to make it clear that real foodies abhor factory farming every bit as much as vegans and vegetarians. We want it abolished. It is heinous – unhealthy for the animal and the human. It fails all three arguments. There is no moral argument for keeping animals in factory farms – their role is to graze freely on grass and to feed the soil with their manure and digestion. There is no political argument for factory farms – feeding grain to ruminants, who cannot digest it, is a terrible use of the world’s resources and is inevitably less efficient than feeding grain to humans (notwithstanding the harm that this could also do). There is no nutritional benefit in eating an animal that has never seen grass, let alone grazed freely on it. Much of the arguments made by vegans and vegetarians use the extreme examples of factory farming to make their case. We hate that too. Where we differ is on the value – morally, politically and nutritionally – of animals living freely and providing food for others in the circle of life, as they always have done.

The summary

The summary chapter in the book is a tour de force. Exquisitely written, it builds on a theme “what do I have for breakfast?” and all the things that we should think about to answer this question. We may not want to face the facts, but Keith sees this as no excuse to stay in denial. If delivered as a speech, you could see that no one in the audience would be sat down at the end. I have never seen such rousing prose.

The questions to be asked of vegetarians become these:

1) Moral – what do you think that you eat for which nothing has died? (I can understand that you may draw your line at not eating animals, but animals died for your food nonetheless. Please stop telling children “meat is murder” when bison, wolves, buffalo and rabbits died for your grains, as did the soil alongside).

2) Political – how can the agriculture that has destroyed, and continues to destroy, the planet be a sustainable way to feed the world? Without ruminants performing biological functions of soil, plants soon die as the soil structure is destroyed. Are you OK that your food is made from oil, not soil? What will feed your food when the fossil fuel runs out? (Let us work together to abolish the factory farming that we both abhor, and let us work together on the only sustainable way to feed the world – dramatically curtailing the world’s population).

3) Nutritional – (particularly for vegans) pick any non-animal food and let me pick any animal food and let’s compare vitamins and minerals. Where do you get retinol? B12? D? K2? Iron? and zinc? – to name just the most obvious nutrients provided by animal foods (some of those, exclusively so). What do you think we have eaten since time began? What did we eat during the 30,000 years of ice age? If there is any nutritional argument for being vegan, why would supplements be life critical? (not least, B12).

I sincerely hope that no one is vegetarian for nutritional reasons alone i.e. that the animal arguments are of no matter to them – they simply think that it is best to avoid real meat and fish and maybe eggs and dairy. If anyone is, they should be the easiest to return to healthy eating. If people choose not to eat animals, because of animals, then the question becomes – are you prepared for your health to suffer, as a result. Because it is less healthy to eat soya and grains than it is to eat meat and fish. Remember – in all of this – factory farmed meat and eggs don’t count. We are not talking about processed meat. That’s as bad as any processed food. We are talking about “Ermentrude”, grazing in the fields.

Keith pulls no punches in this final section: “You can’t have it both ways, vegetarians. If you want to save this world, including its animals, you can’t keep destroying it. And your food destroys it.”

Keith presents three questions to help answer the question – what should we have for breakfast?:

i) Does this food build or destroy topsoil?

ii) Does it use only ambient sun and rainfall, or does it require fossil soil, fossil fuel, fossil water, and drained wetlands, damaged rivers?

iii) Could you walk to where it grows, or does it come to you on a path slick with petroleum?

She gets stronger: “Despite the deepest longest of your hearts, vegetarians you are wrong. To save this world, we must know it, and then take our place inside it. As long as I believed the annual grains of a plant-based diet would save the world, I couldn’t see that they were destroying it. This exact moment – reading those words – will take courage. I know you’ve got it. Are you willing to use it?”

“What separates me from vegetarians isn’t ethics, or commitment. It’s information.” Lierre Keith.

And with that line, and with this book, we can no longer be in denial.

Why do we say “eat less/do more”? Does it work? What do the laws of thermodynamics actually say? (because it isn’t “eat less/do more”)

Why do we say “to lose 1lb of fat, we need to create a deficit of 3,500 calories”? Is any part of this equation correct? Do the 7 leading public health authorities in the UK know why they say this? Does anyone?

What is human fat tissue? How do we lose it? i.e. how do we lose weight? (because it isn’t “eat less/do more”)

And much more.

Hope you enjoy it!
Very best wishes – Zoe

Or you can listen to the talk and download it for listening later…

Or you can listen to the talk and download it for listening later…

And you can download the presentation slides here

Here’s the link to the presentation at last.

The book is based on comments made by overweight kids and teenagers on two identical sites run by Dr Pretlow: www.weigh2rock.com and www.blubberbuster.com. The sites look fun and interactive and the comments in the book reflect the value that young people get from them. The book content is almost entirely provided by verbatim comments made by the people using these sites. Dr Pretlow provides a narrative and asks questions for which the comments provide answers e.g. What do overweight kids say about their parents? We then get many examples of responses, as a factual illustration of what kids say in answer to this question. The title of the book is a well chosen one.

I must admit that the unedited verbatim comments don’t make comfortable reading for anyone used to writing for a living. You can read pages before finding one comment that is even close to being spelled properly, let alone grammatically correct. I know young people use text speak, slang  and abbreviations, but saying “board” when they mean “bored” or “choose” when they mean “choice” makes one wonder if there will be any authors in the future!

If you can tolerate reading 300 pages of essentially ‘text messages’, the content will in turn make you laugh and then make you cry. More will make you cry and they should all make us, as adults, feel guilty. We have failed these children. We have put profits of the food industry ahead of the health of our next generation and we have created, as just one example, a 500lb “Fat boy 15″ who has to be home schooled as a result of his weight. We have cut him off from the world before he is even an adult himself. What is he then most likely to do to overcome loneliness and boredom? Eat.

The minimum that these kids feel is embarrassed – embarrassed to go out, to be themselves, to have slimmer friends, to do activities required of them at school – to even be alive. Some have considered suicide. Weight, fat, size and diets are totally dominating and ruining the lives of these young people. The exhaustion of trying yet another diet and the despair of failure is palpable. It really is heartbreaking. It also made me angry. We didn’t have an obesity epidemic until we changed our diet advice away from what we evolved to eat – meat, fish, eggs, dairy, nuts, seeds, vegetables, salads and local fruits – foods provided by nature – to grains, grains, more grains, breads, cereals, man-made spreads, low fat this, low fat that. The food industry profits have got as fat as our children. The joy of shareholders is equal and opposite to the despair of the consumers.

We have been watching Jamie’s Food Revolution on TV in the UK these past few months – it aired first in the USA. My heart sank when I saw the USDA custodian for the region, ‘Rhonda’, saying that kids must have two breads with every meal and I nearly threw something at the screen when she confirmed that fries counted as a portion of veg. Carbs are uniquely addictive and uniquely fattening – processed carbs especially. Why is the USDA not insisting that children eat the most nutritious foods at school lunch? Where is the campaign to get liver, sardines, eggs and real milk (not low fat rubbish) into the school meal plan? How long will it be before Dr Pretlow is reporting overweight kids as saying “my government made me fat”?

The most commonly asked question on www.weigh2rock.com and www.blubberbuster.com is, unsurprisingly, how do I lose weight? There are the usual platitudes about ‘eat less/do more’, which the site would do well to counter and provide evidence for the futility of this route. Since Benedict, 1917, through Keys, 1945, and Stunkard and McLaren-Hume, 1959, to the most recent definitive study that I have seen – Franz et al 2007, all evidence confirms that ‘eat less/do more’ does not achieve sustained weight loss. Stunkard & McLaren-Hume quantified the failure rate as 98% – a statistic we often hear today and may not know from whence it came. What can work is eating better, eating what we ate before we had an obesity epidemic, eating the food provided by nature that we have evolved to eat.

I was encouraged by the number of children who had worked out the right advice for themselves – cut out the junk and stop snacking were tips that will have a significant positive impact. There were also some excellent tips for dealing with cravings and the support that kids get from each other in the site will undoubtedly help.

Dr Pretlow addresses the very real issue of food addiction – a topic that has also been a key area of interest for me. I was very pleased to see Pretlow exploring ways in which kids could eliminate the foods to which they are addicted from their diet. 68% of the respondents to one survey reported feeling addicted to food and 66% feeling out of control with food. My only surprise was that these figures were not in the 90% range. People cannot be addicts in moderation. We should no more advise food addicts to eat sugary processed food in moderation than we should tell alcoholics to drink in moderation. We need to start treating food addiction for what it is – a serious addiction with serious consequences. The work that the sites do in this area is invaluable.

This is a unique and important book. I have not before seen so many comments from so many young people about so many different aspects of one issue – their weight. We adults need to take responsibility for the part we have played in making our children overweight – starting with dieticians, who are little more than sales reps for the food and drink industry and whose professional body is sponsored by a who’s who of the food industry.

Even in this area, the children have clear views as to who should help them. 74% want an advisor who was overweight, but isn’t now. Only 5% want an advisor who has never been overweight.  Whether we have been overweight or not, whether young people can relate to us or not, we can all play our part. We can read this book, hear what young people are saying and do anything and everything we can to stop this horrific (childhood) obesity epidemic. For my part that means campaigning for a return to real food and a condemnation of the processed food that made us fat and sick. What will your part be?

This is a copy of possibly one of the most serious Diet & Health Today articles that I may do. It is dedicated to Anne (Annem in the club) who asked me a great question about cholesterol. It made me do what I had been meaning to do ever since I read Dr Malcolm Kendrick’s The Great Cholesterol Con…

Dr MK ran some analysis on World Health Organisation (WHO) data. The WHO has extensive data from almost 200 countries on more health measures than you could imagine – definitely worth a look one rainy, wintry afternoon. This is where Dr MK presented the world with two different Seven Country Studies – (for those of you who aren’t familiar with the history, it was the Ancel Keys’ Seven Countries Study that started all the fat heart hypothesis stuff). Dr MK took the seven countries with the lowest saturated fat intake and then the seven countries with the highest saturated fat intake. You may need to read this twice – but he found: “Every single one of the seven countries with the lowest saturated fat consumption has significantly higher rates of heart disease than every single one of the countries with the highest saturated fat consumption.”

The next chapter in The Great Cholesterol Con goes on to look at cholesterol and heart disease (and overall death rates) and quotes many great studies where it is shown that lower cholesterol is associated with higher mortality. However, it did leave me thinking – having run the data on saturated fat and heart disease, let’s just run all the data on the cholesterol and heart disease and get to the bottom of this hypothesis from all parts of the allegations.

It actually didn’t take that long – less than a couple of hours one Saturday afternoon. You go to the WHO statistics area of their web site and then pick data for cholesterol from risk factors (how judgemental to start with!) and then look under: Global burden of disease (mortality); All causes; Non communicable diseases and then G Cardiovascular disease (shortened to CVD). CVD deaths include ischemic heart disease and cerebrovascular disease – that means fatal heart attacks and fatal strokes to us. You find the most recent year where you can get both sets of data to compare like with like. This turns out to be 2002. You download their very user friendly spreadsheet data (CSV) – cut and paste it into an excel file and then try to remember how the heck to do scatter diagrams in excel!

Before telling you the results, we need to go back for a quick reminder on what we know about cholesterol and then hopefully this can serve as a factsheet for all the cholesterol questions we continually get.

The role of cholesterol

It is virtually impossible to explain how vital cholesterol is to the human body. If you had no cholesterol in your body you would be dead. Every single cell of your body is covered by a membrane (think of a membrane as the ‘skin’ or protective barrier around each cell). This membrane is made largely of cholesterol, fat and protein. Membranes are porous structures, not solid walls, letting nutrients and hormones in while keeping waste and toxins out. If cholesterol were removed from cell membranes they would literally explode from their internal water pressure. Human beings quite simply die without cholesterol.

Cholesterol is vital for hormone production – the sex hormones and therefore the entire human reproductive system are totally dependent on cholesterol. Hence, not only would humans die without cholesterol, the human race would die out.

Cholesterol is vital for digestion. The human body uses cholesterol to synthesise bile acids. Without cholesterol-rich, bile salts, the human body could not absorb essential fatty acids or the fat soluble vitamins (A, D, E and K) and serious, even life threatening, deficiencies could develop. (It is interesting, therefore, that nature puts cholesterol in virtually every food that contains fat – providing a digestion mechanism in tandem).

Cholesterol is vital for the brain, central nervous system and memory functions (hence how the side effects of statins include memory loss, mental confusion and people generally just not feeling themselves). Even though the brain is only 2% of the body’s weight, it contains approximately 25% of the body’s cholesterol. The vital connections between nerve endings in the brain, which help to conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, are largely made up of cholesterol.

Cholesterol is critical for bones and for all the roles performed by vitamin D. Vitamin D is best known for its role in calcium and phosphorus metabolism, and thus bone health, but we are continually learning more about potential additional health benefits of vitamin D from mental health to immune health. Vitamin D can be ingested (and is, interestingly again, found in foods high in cholesterol) and it can be made from skin cholesterol. Modern ‘health’ advice to avoid the sun, take cholesterol-lowering drugs, eat a low cholesterol diet (whatever the heck that is supposed to be) – combined with there not even being a recommended dietary allowance for vitamin D – is undoubtedly contributing to avoidable modern illness.

One of the key reasons that we need to spend approximately one third of our lives sleeping is to give the body time to produce cholesterol, repair cells and perform other essential maintenance.

This gives you the headlines of the vital functions that cholesterol performs, but hang on to that bottom line – it is utterly vital and we die instantly without it.

You may be familiar with the term essential fatty acids or essential amino acids (proteins break down into amino acids). The term ‘essential’ used like this in nutrition means that it is essential that we consume it in our diet because the body can’t make it. The body makes cholesterol. That says to me that cholesterol is even more vital than essential fatty acids or essential amino acids – even though these too are life critical – and therefore the design of the human body is such that it was not left to chance that we needed to get cholesterol from food. Of the 500 or so roles that the liver has – one is to produce cholesterol. It is too vital to be left to chance.

What went wrong?

So, how did something so life vital become more vilified than a mass murderer? I think it comes down to three things (and I don’t take credit for this view – it is there to be worked out by anyone who traces back the history and Kendrick, Uffe Ravnskov and all the thincs.org guys have led the way):

1) Rabbits;
2) Ancel Keys;
3) Money!

1) In 1913, a Russian chap called Nikolai Anitschkow decided to feed rabbits purified cholesterol and he managed to get their blood cholesterol levels in excess of 1,000 mg/dl (nearly 26 mmol/L! Most UK people have levels of 5-7 mmol/L). He then noticed the formation of “vascular lesions closely resembling those of human atherosclerosis” forming in the arteries of the rabbits. The obvious flaw in the experiment should have been that rabbits are strict herbivores. They do not eat animal products, which is the only source of cholesterol. Hence rabbits are in no way designed to digest cholesterol or animal fat and no one should be surprised if cholesterol or animal fat ended up stuck in any part of the poor rabbit. The only surprise is that no one thought to ask Anitschkow why he was feeding cholesterol and animal fat to herbivores. Interestingly, far less well known is that a parallel test was done on rats and dogs (omnivores) and feeding cholesterol to these species failed to produce lesions.

2) Ancel Keys. Remember the Minnesota experiment that I so often refer to? A brilliant and unbiased piece of research, which has given the world one of the best insights into low calorie dieting ever done – it was pure genius. This study made Ancel Keys the man of the moment and I guess he wanted to follow it with something equally impactful. There is an anecdote in The Great Cholesterol Con and on p113 of The Obesity Epidemic where Henry Blackburn, one of Keys’ closest colleagues, tries to explain what may have fuelled Keys drive to find a connection between diet and heart disease.

What is little known is that Keys originally tried to establish a link between cholesterol in food and cholesterol in the blood (our cholesterol levels when we have a blood test) because he thought (probably because of poor Bugs Bunny) that cholesterol in the blood causes heart disease.

Keys did multiples of studies, changing the diets of his human ‘guinea pigs’, and he presented his conclusions in The Journal of Nutrition, November 1955: “It is concluded that in adult men the serum cholesterol level is essentially independent of the cholesterol intake over the whole range of natural human diets. It is probable that infants, children and women are similar.” i.e. I only tested adult men and there is no relationship between cholesterol eaten and cholesterol in the blood and it is probable that there will similarly be no relationship for women or children.

In 1997 Keys put this even more assertively: “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”

Did you know – even the UK Food Standards Agency (FSA) and UK National Health Service (NHS) admit this?

- “However, dietary cholesterol has little effect on blood cholesterol. More important is the amount of saturated fat in your diet”. (National Health Service). (Notice the second sentence? They just couldn’t let the theory go).

- “But the cholesterol we get from our food has much less effect on the level of cholesterol in our blood than the amount of saturated fat we eat”. (Food Standards Agency). (This link may disappear, as the FSA is bowing out of giving nutritional advice).

What the government advice should say is: The body makes cholesterol. The cholesterol you eat has no impact on the level of cholesterol in your blood – not “little”, but “no” – (and we’ve known that all along). And they should also explain how saturated fat can determine blood cholesterol levels and then provide irrefutable evidence that it does. But it must be hard for public health bodies to even go this far. As we saw in a recent thread – the FSA also now accept that there is no limit on the number of eggs we can eat:

If only Keys had stopped here, but he wanted to find an explanation for heart disease and he was not about to be deterred. For some reason, which I find inexplicable, he then turned to fat (the entire literature on this topic is very vague about “fat” vs. “saturated fat” so his early writings are also very vague on the topic). Here’s a bit of Mensa logic for those who like this kind of thing:

i) Only animal foods contain cholesterol (meat, fish, eggs, dairy). NO non animal foods contain cholesterol.

ii) All animal foods contain fat – saturated and unsaturated. Some may be very low in fat (e.g. white fish), but they all contain some fat.

iii) If there is no link whatsoever between increased consumption of foods containing cholesterol and blood cholesterol levels, there can be no link whatsoever between increased consumption of animal foods and blood cholesterol levels since only animal foods can be increased in consumption to increase consumption of cholesterol!

So, Keys first did the graph that was presented at the Mount Sinai hospital (which is the one shown in the Tom Naughton video and in Dr Robert Lustig’s “Sugar: The Bitter Truth” ) and then went on to do the Seven Countries study – which I have read all twenty volumes of and take apart piece by piece in Chapter Eight of The Obesity Epidemic: What caused it? How can we stop it (on this page).

As Kendrick’s two unbiased seven country studies showed – there is not even an association between saturated fat and heart disease – let alone a causation. However, Keys published his seven countries study and the rest, as they say, is history.

3) The Robert Redford film All the Presidents’ Men that had the memorable quote “follow the money”. This is absolutely at the heart of everything in the diet industry from national dietary organisations to the food, drink and drug industries and individuals in between.

The Ancel Keys work interestingly claimed that saturated fat consumption (A) caused heart disease (C) not directly, but by raising cholesterol (B). Hence A was supposed to cause C through B. For this to even get off the starting blocks, A and C have to be related (plot one against the other and there has to be a clear relationship); A and B have to be related and B and C have to be related. None of these in fact holds. The Kendrick study shows that A and C are not related. There is no logic that A and B could be related – because of the problem of fat and cholesterol being found in the same foods and Kendrick presented many studies that showed B and C were not related. I aim in this article to put the nail in the coffin for any idea that high cholesterol is even associated with high heart disease. We will, in fact, show that the evidence confirms the opposite.

By having cholesterol as this middle-man, this has allowed an entire pharmaceutical industry (and stupid cook books) to come up with ways of lowering cholesterol. The most lucrative of these has clearly been statins – drugs designed to stop the body producing the cholesterol that it is designed to produce. It never hurts to remind people that one statin alone, Lipitor, is worth $12 billion to Pfizer. Taubes has a deeply troubling passage in The Diet Delusion where he looked at the committee who approved a lowering of the target cholesterol levels for the USA population. From memory (it’s a big book to find a reference!), a number of people were on the committee and all but one were funded by pharma companies and one didn’t want the target cholesterol level lowered. I wonder which one! (Anyone reading this – if you can find the page number I’d be so grateful – my copy has so many scribbles on I can barely read it).

So, cholesterol will remain the mass murderer for as long as statins are as lucrative as they are or until the public are enlightened and courageous enough to say no to doctors who try to put them on this medication (like my mum was after reading Dr MK!)

A small technicality

On p35 of The Great Cholesterol Con, Kendrick says: “How can eating saturated fat raise LDL levels? It is not merely biologically implausible, it is biologically impossible. Boy does that statement make me a hostage to fortune!”

I arranged to meet a biochemist at a local university to try to get to the bottom of this statement. The biochemist (who has more qualifications than I’ve had dark chocolate) was sadly so brainwashed in the ‘fat is bad’ theory that he just kept saying eating fat raises cholesterol. When I asked him to talk me through the biochemical pathway from fat digestion through to how this impacts cholesterol he said he didn’t know the digestive process well enough – we would need to add a dietician into the conversation. This was alarming enough. I then said – we eat 39 grams of butter per person per week in the UK and about 1.4 kilos of flour – didn’t he think it was more likely that the flour was making us fat and sick. He said it only took a drop of arsenic to kill us. I left shortly afterwards.

Kendrick has to be right (isn’t he always?) LDL (remember this is not cholesterol – it is a low density lipoprotein) is the left over from IDL (intermediate density lipoprotein), which is the left over from VLDL (very low density lipoprotein). VLDL is one of the measures you get in your blood cholesterol test (actually they estimate it – they don’t measure it – they only measure total cholesterol and HDL leaving two other unknowns in an equation with four variables and you thought this was scientific). (They also call VLDL ‘triglyceride’, which is confusing and unhelpful). Cutting a complex story short (it is explained in my book in different passages), carbohydrates can impact VLDL levels (starter for 10: Acetyl-CoA being the start of the process by which the body makes cholesterol and part of the Kreb’s cycle whereby the body turns glucose into ATP), but I really have found no way in which the fat that we eat can do so. Because fat is not water soluble, it is packaged into a lipoprotein in the digestive system. The lipoprotein that fat goes into is the biggest one – the chylomicron – and then it travels off into the body to go and do the essential repair and maintenance jobs that fat does. Does the fat say – hang on Mr chylomicron – we need to go via the liver and see if we can mess up the body’s VLDL production in some way?! Do ask this ‘how’ question (in detail) of someone who thinks that this is possible. I am still open to someone answering this, but I’m not holding my breath.

Fructose, on the other hand, we do know goes straight to the liver to be metabolised. Could that, and other carbs, impact VLDL production? The evidence I have already seen is strong that they do.

The serious bit

The WHO data is split into men and women. I first did the scatter diagrams for average (mean) cholesterol levels and CVD deaths. Then I ran the Pearson correlation coefficient on these numbers. This gives us the term called “r”. “r” tells us if there is some kind of a relationship: an r score of 0 would indicate no relationship; an r score of 1 would indicate a perfect relationship. A negative r score is called an inverse relationship e.g. the price of concert tickets is likely to be inversely related to the number of concert tickets bought – fewer tickets being bought at higher prices.

The “r” score for men revealed that there was a small relationship of 0.13 – however this relationship was inverse. The diagram and correlation shows that higher cholesterol levels are associated with lower CVD deaths and lower cholesterol levels are associated with higher CVD deaths. In women, the relationship is stronger – to the point of being meaningful. The r score was 0.52 – but, again, inverse. For women, higher cholesterol levels are quite significantly associated with lower CVD deaths and lower cholesterol levels are quite significantly associated with higher CVD deaths. Please note that I have added r squared on the graphs below (excel can do this for us) and it can confirm that you’ve got your r numbers right and r squared tells us the strength of any relationship we have observed.

All you need to do is to look at the lines going down to the right and wonder how on earth we ever got away with telling people that cholesterol causes heart disease. High cholesterol is associated with lower heart disease and vice versa – for all the data available in the world. High cholesterol is not even associated with high heart disease, let alone does it cause it.

It gets worse. I then kept the cholesterol information and changed the death rates to total deaths – all deaths from any cause – cancer, heart disease, diabetes, strokes – all deaths. You can see the diagrams for men and women again below. This time there is a significant relationship for both men and women: 0.66 for men and 0.74 for women – again inverse. There is a significant association between higher cholesterol levels and lower deaths and lower cholesterol levels and higher deaths for men and an even more significant relationship for women.

This is serious. I’ve shown it to a couple of academics (Professor sort of things) with whom I’ve been having great debates, as I want to see what the view is from people who wholly believe the fat/cholesterol/heart/death hypothesis. (Kendrick talks in his book about what happened when he showed an intelligent colleague his two seven countries studies and the evidence was just dismissed instantly). It is most useful to know what the resistance arguments will be before starting to invite the resistance. The two arguments I got back were:

1) “Ah yes – but this is only an association.”

Ah yes – but a) we changed global dietary advice back in 1977-1983 on the back of an association in Seven (carefully hand picked) Countries that miraculously became a causation even when the association was far from established and b) it is an association that’s the opposite to the one that the world currently holds true and c) that’s what epidemiology is supposed to be about – establish an association and then investigate if there could be any causation or useful learnings. So – go out with a new paradox – that high cholesterol is associated with low deaths and then see what dietary advice emerges.

2) “But that’s total cholesterol – the key thing is the ratio of good to bad cholesterol.”

Oh boy! The chemical formula for cholesterol is C27H46O. There is no good version or bad version. HDL and LDL are not even cholesterol, let alone good cholesterol or bad cholesterol. They are lipoproteins – see above – and they carry cholesterol, triglyceride, phospholipids and protein. Do you think that taxis are people? Or do you think that they are carriers of people (and luggage, and pets and fresh air and other things).

Back to – this is serious. Unless you have familial hypercholesterolemia (a hereditary condition suffered by c. 1 in 500 people), my personal view is that you can do real harm by lowering your cholesterol level – as measured by CVD deaths and total deaths. (New note – Uffe Ravnskov has emailed me to say high cholesterol is not a risk factor for people with FH either – I am sure he will be right. I’ll look at the papers he referenced asap and the “unless you have…” may disappear).

The doctors’ Hippocratic oath is “First do no harm”.

This also says to me – even though saturated fat has nothing to do with cholesterol, it doesn’t actually matter. Even if it did – cholesterol is only associated with CVD deaths in an inverse way. If fat did raise cholesterol – as public health officials like to claim – it could save lives! Please note I am always really careful with language in this area and never jump from association or relationship to causation. Someone may be in the bath and they may be singing – if we observe this in many cases, we may claim that there is an association. We cannot say that bathing causes singing or that singing causes bathing.

Our global dietary advice was changed in 1977 in the US and 1983 in the UK as a result of a biased study of seven handpicked counties. Had the data been available for the 192 countries we can analyse now, or had Keys even considered all the data that was available to him at the time (for France etc), our conclusion may have been that we need to protect cholesterol levels in the body. We may have realised that the last thing we should be trying to do is lowering cholesterol – unless we’re trying to lower life expectancy for some reason.

Zoë Harcombe