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).

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!

Let’s start with the positive:

1) It’s much easier to understand that the current American Food Pyramid (2005):

This was so complicated (and seemingly needed to be individually tailored), that many people just carried on using the old American Food Pyramid (below – introduced 1992), which directed Americans to have: 6-11 grain portions a day; 2-4 fruit portions; 3-5 vegetable portions; 2-3 dairy servings and 2-3 meat/egg/fish/bean/nuts/egg servings per day. Hence Americans could have 26 portions of food a day – all having an impact on blood glucose levels. And we wonder why America led the world in getting fat and sick.

MyPlate is served with some advice, as a side dish

Here is the accompanying dietary advice in black; my comments in red alongside:

Balancing Calories
●     Enjoy your food, but eat less. (Less than what? An anorexic? Less than you are eating now? Less than you need for health?)
●     Avoid oversized portions. (Requires too much judgement to be useful advice – what is oversized to you may not be to me or vice versa. Plus – it is very difficult to ‘overeat’ real food – organic meat/fish/eggs/veg – it is very easy to ‘overeat’ processed food. Hence nature sorts out portion sizes for us)

Foods to Increase
●     Make half your plate fruits and vegetables. (i.e. Fructose & glucose & glucose).
●     Make at least half your grains whole grains. (there is debate on this in the informed nutritional world – whole grains have more nutrients than white grains (still far fewer than quality meat/fish/eggs), but white grains are less abrasive than whole grains and therefore less likely to cause irritable bowel syndrome or bowel cancer. It’s all glucose to the body either way).
●     Switch to fat-free or low-fat (1%) milk. (The UK is deficient in vitamins A, D, E and our government doesn’t bother recording vitamin K in the National Food Survey, but no doubt we are deficient in all four fat soluble vitamins. I doubt that the USA is any better, so we would be well advised to consume real fats in real food – like milk from ruminants freely living on grass. Nature sensibly puts real fat with real fat soluble vitamins in real food. Man stupidly takes them out).

Foods to Reduce
●     Compare sodium in foods like soup, bread, and frozen meals ― and choose the foods with lower numbers. (Don’t eat anything processed).
●     Drink water instead of sugary drinks.  (Good advice. Better still “Don’t drink anything processed”).

So the new MyPlate is simpler, but does this make it any better… Here are my key concerns for America’s national (public) health and for the nutritional advice in this new model…

Three national health concerns about MyPlate

1) This will do nothing to solve the obesity epidemic.

I have written 135,000 words on The Obesity Epidemic: What caused it? How can we stop it? In a nutshell we changed our diet advice (America in 1977-1980 and the UK followed suit in 1980-1983) and obesity has increased 10 fold since in the UK; America started from a slightly higher base, so has ‘only’ increased by a few multiples and not 10! We changed our advice away from “Farinaceous and vegetable foods are fattening, and saccharine matters are especially so” (Tanner, The Practice of Medicine, 1869) to “Base your meals on starchy foods.” This has had catastrophic consequences for human weight and health and cataclysmic benefit for the food, drink and drug industries, which profit from us being fat and sick.

MyPlate will do nothing to change this. It is still telling humans to “Base your meals on starchy foods” instead of realising, as we did for the 3.5 million years before the last 30 years of ‘conventional wisdom’, that carbs are uniquely fattening (and unnecessary for human health). Grains are just glucose, fruit is fructose and glucose (a particularly uniquely fattening combination – the same as sucrose – table sugar), vegetable are glucose (potatoes and starchy vegetables especially so) and dairy (processed yoghurts) and protein foods (beans etc) chosen can also have a carbohydrate content.

2) This will do nothing to solve the nutritional crisis.

We seem to have forgotten why we eat. We eat because there are 13 vitamins and c.16 minerals vital for human existence, let alone health and well being. All the plates and pyramids are obsessed with macro nutrients (fat, protein, carbohydrate); they seem to have forgotten mico nutrients (vitamins & minerals) entirely. Remember that slogan “Take care of the pennies/cents and the pounds/dollars look after themselves”? This applies nicely to nutrition. “Take care of the vitamins and minerals and the fats, protein and carbs will look after themselves.”

Our dietary advice should start from – how do we get our vitamins and minerals (notwithstanding that the concepts of “Recommended Dietary Allowance” (RDA), let alone “Adequate Intake” (AI) are a joke – as Sally Fallon Morell says “Why am I only allowed a certain  level of nutrition?”!) I did just this in my book The Obesity Epidemic. I’ve put three examples (for omnivores, vegetarians and vegans) as an Appendix to this post.

MyPlate will do little to nothing to improve the health of the American nation. We should be telling people to base their meals on meat and eggs from animals freely grazing on grass; fish and vegetables/salads. Quality dairy (again – only products from grass living animals are worth consuming), nuts & seeds (in moderation if overweight) and local, seasonal fruits (in moderation if overweight) are useful additions to the meat/fish/egg/veg base. Almost half the plate is taken up by fruits and grains – high glucose/low nutrition relative to meat/fish & eggs. No attention is given to the quality of food (other than the emphasis on whole grains, which is debatable (see red notes above)). The importance of eating animals that have predigested cellulose for us (arguably their role in the circle of life, along with fertilising the soil without needing oil) is not addressed. The epidemic of (type 2) diabetes will continue unabated with this level of carbohydrate intake.

3) The food industry will still love this.

The food industry, in fact, wasted no time in saying how much they loved it. Kellogg’s and General Mills (sponsors of the American Dietetic Association) (ADA) will love that grain segment – that’s cereals for breakfast then. Unilever and CoroWise (more  ADA sponsors) should be happy – dietitians will be telling people to put hydrogentated spreads on their copious amounts of bread – certainly not that natural butter product. The dairy industry (another ADA sponsor) will be very happy – they’ve got their own little segment all to themselves. When chips and potatoes count as veg, the fast food companies will be happy (Aramark – the ‘dining away from home’ ADA sponsor – should be happy anyway). Plus, no one is really going to opt for water instead of phenomenally promoted Coca-cola & Pepsi (not least when these are also ADA sponsors and therefore able to convince dietitians of the marvel of calorie-free, aspartame-laden, fizzy concoctions).

Here’s how it works for the fast food industry: Burger (protein), bun (grains), fries (vegetables), tomato slice (fruit), lettuce leaf & gherkin (more vegetables), strawberry milk shake (more fruit & dairy) – the perfect meal!

Anything that the food industry likes is a fail. The food industry would hate my advice – see below!

Three nutritional/technical concerns about MyPlate

1) The USDA appears not to know the difference between a food group and a macro nutrient!

There are 3 macro nutrients: fat, protein and carbs. There are essential fats (i.e. fats we must eat); there are essential proteins (i.e. amino acids we must eat); there are no essential carbs (i.e. there are no carbs that we must eat). Yes the brain does need glucose, but that doesn’t mean that we need to eat it. Indeed, anyone wanting to lose weight should relish in the fact that the brain needs glucose. Don’t eat it and then the body send out a signal to break down body fat to get glycerol/glucose. Result!

MyPlate has 4 food groups: vegetables, fruits, grains and dairy and one macro nutrient – protein! Protein is actually in everything. Literally everything from lettuce to apples to oats to beef. Hence MyPlate has protein in every segment. This is not necessarily a bad thing, but they still don’t know food groups from macro nutrients!

My food groups would be: meat; fish; eggs; dairy; vegetables & salads; nuts & seeds; fruits; beans & pulses and grains. That would make 9 in total. 5 of my food groups – meat; fish; eggs; nuts & seeds and beans & pulses – would end up in the one macro nutrient group on MyPlate – the protein segment. This should be the major part of the plate, not the minor part and the USDA should know a food group from a macro nutrient.

2) The USDA is as fat phobic as ever.

We changed our dietary advice c. 1980 (and started the obesity epidemic in so doing) because we developed this mad idea that fat is going to kill us. The Dietary Guidelines for Americans 2005 list: ice cream; sherbet; frozen yogurt; cakes; cookies; quick breads; doughnuts; margarine; sausages; potato chips; corn chips; popcorn and yeast bread as saturated fats. These are not saturated fats – not primarily, not even secondarily. They are first processed foods, secondly major sources of carbohydrates and thirdly, almost all then have more unsaturated fat than saturated fat (not that any real fat is better or worse than any other, but these are not real fats, and they are not saturated fats). Don’t eat any of these heaps of junk because they are processed heaps of junk. However, real fats in real food are absolutely vital for human health and we are suffering epidemic levels of deficiencies, in vitamins A and D particularly, in the UK and the USA.

Where is the fat on MyPlate? Where is the quality offal and red meat? the mackerel? the sardines? the quality dairy foods? the real butter? the free range eggs? Where are the vital fats that we need? Emphasizing protein and carbs and not fat is seriously harmful to health. Fats are vital, carbs are not. Protein is vital, but consuming protein in an unnatural balance (without the fat that nature provides naturally alongside) is a rapid route to vitamin A depletion and  liver and other health damage. Ask bodybuilders!

3) MyPlate is a visual guide, which is easy to understand but then falls victim to “The law of unintended consequences”.

MyPlate is clearly intended to be volume guide “Make half your plate fruit and vegetables” is one of the instructions. The UK eatbadly plate may appear to be a visual “this is how your plate should look”, but, when I asked the UK Food Standards Agency where the proportions in their food groups came from (listed below), the answer was based on weight.

33% Starchy foods (bread, potatoes, pasta, cereals etc)
33% Fruit and vegetables
15% Non dairy protein (meat, fish, eggs, beans etc)
12% Milk and Dairy products  
8% Foods high in fat and sugar  (101% due to rounding)

I did another interesting experiment in The Obesity Epidemic: What caused it? How can we stop it? I started with 100 grams of starchy foods and then calculated the weight of the other categories, to maintain the proposed proportions. The weight of fruit and vegetables would also be 100 grams; non dairy protein would be 45 grams; there would be 36 grams of milk and dairy and 24 grams of foods high in fat and sugar.

Using a sample of foods from the USDA food database, I estimated the calorie averages for 100 grams of each of these food groups as 333, 42, 188, 183 and 595 respectively.  This would give the estimated calorie values (for each of these weights) of 333, 42, 85, 67 and 144 respectively. If these are then scaled up in proportion for a 2,000 calorie a day diet, the five groups end up with 992, 125, 255, 198 and 430 calories respectively. The numbers will vary for each person’s interpretation of the plate, but you can see how one third of intake in the form of starchy foods can represent half of calorie intake and another third from fruit and vegetables just 6% of energy. The supposedly smallest segment, being so energy dense, can form a perhaps unanticipated 21% of calorie intake.

The same will happen with MyPlate – potatoes and chips as ‘vegetables’ not withstanding, the energy intake (which is what the body registers) for vegetables will be small relative to, say, nutritionally inferior grains.

MyAdvice

This would be my advice by the way:

1) Eat food – we shouldn’t need to call it real food.

2) Eat that real food three times a day – unless you are a cow, or want to be the size of one, stop grazing!

3) If you need to manage your weight, manage your carb intake. Gaining weight is literally defined by the formation of triglyceride (body fat) and this is beautifully facilitated by eating carbs, which provide glucose for the glycerol part of the triglyceride structure and insulin to enable fat storage. Losing weight is literally defined as breaking down triglyceride (body fat) which can happen when the brain wants the glycerol part for glucose or the body wants the fat part for energy/repair. So, weight gain happens in the presence of carbohydrate/glucose/insulin and weight loss happens in the absence of carbohydrate/glucose/insulin.

MyPlate

MyPlate will encourage you to eat 70% of your food intake in a form that contains carbohydrate and allows you to eat 100% in this way. Nothing like what we have been eating for 3.5 million years and nothing like what we need to eat to end the epidemics of being fat and sick.

This is another tragic missed opportunity to do something about the weight and health of Americans. Follow MyAdvice and not MyPlate and you’ll buck the trend.

Appendix

In The Obesity Epidemic, for Appendix 3, I did an experiment where I tried to get the Recommended Daily Allowance (RDA) for 12 vitamins (information for B7, Biotin, was not available) and 8 minerals (calcium, magnesium, phosphorus, copper, iron, manganese, selenium and zinc). These were the nutrients for which the United States Department of Agriculture database had information and for which there was an RDA. Having said this, there were no RDA’s for vitamins B5, D and K or for the minerals calcium and manganese – an ‘Adequate Intake’ was recommended.

- Omnivores can get the RDA’s/AI’s from the following 5 foods: 100 grams of liver, 200 grams of sardines, 200 grams of whole milk, 100 grams of sunflower seeds and 200 grams of broccoli (1,300 calories). There will be infinite combinations of real foods that can provide the RDA’s/AI’s, but I started from the ones known to be highly nutritious.

- For vegetarians, the RDA’s/AI’s’s could be met with these five foods: 500 grams of whole milk, 450 grams of eggs (10 medium eggs), 300 grams of spinach, 250 grams of raw mushrooms grown in sunshine and 50 grams of sunflower seeds (1,360 calories). Dietary advisors applaud people for choosing a vegetarian diet, but then tell them to avoid eggs and to consume low-fat milk. It then becomes practically impossible for a vegetarian to meet even minimal nutritional requirements.

- Vegans can’t get B12 naturally and they would need to eat 2.25 kilograms of (raw sunshine grown) mushrooms in a fat delivery mechanism (e.g. vegetable oil – unhealthy per se) to get the ‘adequate intake’ for vitamin D and an unusual food like oriental dried radishes to get their calcium – and to repeat this daily. For completeness, the five vegan foods would be 2.25 kilograms of mushrooms, 175 grams of porridge oats, 25 grams of sunflower seeds, 100 grams of oriental dried radishes and 300 grams of spinach (in more vegetable oil) and a vitamin B12 supplement. Without the calories in the vegetable oil, the vegan basket adds up to 1,644 calories – the highest of all three sample ways of getting our nutritional requirement.

The sub heading is “Wake up call for 5m Britons as diabetes toll also soars.”

When will public health advisors realise that we started this obesity epidemic? When will public health advisors realise that we started this diabetes epidemic?

Since Australopithecus Lucy first walked upright, an estimated 3.5 million years ago, we have eaten food provided by mother nature. For much of that time our main energy intake has necessarily come from animals and their by products (during the ice age this is all that our ancestors would have had; during much of the rest of our evolution animals – especially their fat – would have provided our much needed calories. Nuts, when available, would have been very useful also).

Look at the evidence – in the UK obesity didn’t rise above 2% since time began until the 1970′s. Obesity rates for men and women in the UK were 2.7% in 1972. They had reached 25% by the end of the millennium. So what happened to cause such a catastrophic change in obesity rates? We changed our diet advice. The USA changed in 1977-1980 and the UK followed suit in 1983-84. Obesity has increased up to 10 fold since. You may think that is just a coincidence – I don’t.

We used to know that floury foods were fattening and sugary foods even more so. We now tell people to base their meals on starchy foods. The average Briton eats 400 calories a day of sugar – with no vitamins and minerals of any value whatsoever. The average Briton eats 730 calories a day of flour – with so little nutrition that it is invariably fortified. We are just doing what we have been told to do – basing our meals on starchy food; following the Eatbadly plate advice (I refuse to call it Eatwell because it’s not).

That sub heading – this is a wake up call for 5m Britons. Boy I hope that it isn’t! The only hope Britons have is if they have ignored the dietary advice of the past 25-30 years and they have carried on eating real food, as mum and granny told them to: liver, sardines, eggs, milk, vegetables with butter on etc. Those who are avoiding real food and eating processed food; those who are avoiding fat and eating fattening carbohydrate instead – these people will continue to get fatter and fatter until someone sues the government for making them fat and we realise the horrors of the ‘experiment’ we have done with the ‘developed world’ since the turn of the 1980′s.

Who stands to gain if you think eggs (one of the most nutritious foods on the planet) are bad for you? (Kellogg’s and other cereal manufacturers).

Who stands to gain if you think butter (another wonderfully nutritious food) is bad for you? (Unilever and other margarine and spread manufacturers).

Who stands to gain if you follow the mad advice to snack/eat little and often (the best way to store fat and stay fat) all day long? (Kellogg’s, United Biscuits, makers of snack foods).

Who sponsors the British Nutrition Foundation? Kellogg’s, Unilever, United Biscuits, makers of snack foods and many, many more.

Who stands to gain if you eat what nature has provided for you? No processed food or drink company that’s for sure. No drug company – because you will be healthy. You stand to gain and you need to take charge of your own health and not trust dietary advisors who are conflicted.

If you want to know the full story behind The Obesity Epidemic: What caused it? How can we stop it? – click here.

As for diabetes – diabetes is a condition characterised by the malfunction of the pancreas and blood sugar handling system. In simple terms, type 1 diabetes is characterised by the pancreas no longer producing insulin, so the person needs to administer insulin in some way (usually injection). Type 2 diabetes is often called “insulin resistance”. Some insulin is still produced by the pancreas, but rarely the right amount, as the body has become resistant to insulin and the cells don’t respond to insulin as they should. Both types of diabetes are all about carbohydrates – the macro nutrient we didn’t used to eat much of and are now told to base our meals on, to snack on, to (basically) eat all the time. Our bodies are literally saying “enough is enough”. I can’t cope with this high quantity or low quality of carbohydrate any more – “I, your pancreas, am packing up”. Hence we now have 171 million diabetics world wide – a figure set to rise to 366 million by 2030. 95% of diabetics are type 2 – all pretty much avoidable if we went back to eating food – real food – and not the processed junk that food processing companies make so much money from.

Then you have Simon O’Neill, from Diabetes UK, saying “we must keep up the mantra of five fruit and veg a day”! More conflict of interest. Five a day was invented by a bunch (ha ha) of fruit and veg companies in California in 1991. Dieticians, nutritionists and now a spokesperson from Diabetes UK are sales reps for the fruit and veg industry. Diabetics should be eating low carb veg (green leafy vegetables, peppers, salads etc) but being very cautious about baked potatoes and fruit – especially tropical fruits. It’s more carbohydrate – it turns into glucose and fructose in the body as if we had eaten sucrose (table sugar – which is one molecule of glucose and one of fructose).

If we are serious about sorting obesity AND diabetes at the same time, we must stop our current diet advice madness and stop telling people to eat carbs virtually every waking minute. Meat, fish, eggs, vegetables (not potatoes), salads and dairy products should be our staples and whole grains, baked potatoes and fruit only if we are slim and not diabetic.

The study was an international collaboration, led by the University of London and involving teams from 14 institutions from London to Ontario. The results were published in the Journal of Applied Physiology and they were that that aerobic exercise does not benefit everyone in equal measures, and its usefulness is determined by a person’s genes. According to the results, 20% of people do not receive any health benefits from aerobic exercise (my emphasis).

The work was based on the belief among researchers that one of the best predictors of health is a body’s ability to take in and use oxygen during aerobic exercise. Participants in the study were asked to undergo rigorous aerobic training, while researchers took muscle tissue samples before and after. The team then identified a set of about 30 genes that predicted the increase of oxygen their body consumed.

- By the end of the study 20% of participants saw their maximum oxygen increase by less than 5%. (Zoe comment – This led to the conclusion that 20% of people receive no benefit from aerobic exercise).

- About 30 per cent showed no increase in insulin sensitivity, meaning that the exercise did not reduce their risk of diabetes. (Zoe comment – This was a secondary finding and other findings were connected to the role of exercise in specific conditions.)

What can we take out of this study?

1) This is about aerobic exercise (aerobic means ‘with oxygen’), but I expect the same will apply for anaerobic  (without oxygen) and ‘body sculpting’ exercise also.  Not everyone can be a long distance runner and some people simply do build more muscle more easily than others. Some people try everything from tablets to protein shakes to change their shape and some get an active job and it happens without them even trying.

2) The link between body, exercise and genetics can be no surprise. We have known for some time (and it is extremely obvious looking at parents and children) that height and build have a genetic element. It is highly UNlikely that two very tall, ‘column-like’, parents will produce short, stocky off-spring. Sometimes the genetics can be found from the wider family. As a home grown example, Andy’s boys are very different in build – both tall, but one has a large (rugby) build like Andy himself and the other has a more wiry (runner) build – like Andy’s own brother.

3) We can try to change fitness and/or build, but this study is saying that for c. 20% of people it will have no effect. (That’s just a headline grabber, remember, and should be taken as an indicator, not a fact). However, the mere suggestion that exercise may not be delivering benefit for some people does mean that doctors should try to find other ways to replicate the benefits of exercise for this group of people. Maybe breathing exercises/yoga/pilates etc may help oxygen utilisation. Maybe lifestyle changes and more ‘me-time’ can give some of the de-stressing benefits of exercise that this group may be missing. One of the most important findings of this study is the understanding that exercise will not have equal benefit for all people and will have no benefit for some.

4) We can sometimes get too hung up on the intensity of exercise. I spent some time with a professor of Biochemistry this week, looking at how the body uses food for fuel in different circumstances. He (like me) was a big fan of low intensity regular exercise – not running marathons and cycling for long times up hill, but just walking or gardening or doing ‘normal’ activity. This can also nicely raise the heart rate and generate the positive benefits that can be gained from more vigorous exercise. It would have been interesting for the study to have compared not just high intensity aerobic exercise in 14 different institutions, but to have low intensity exercise groups as comparators throughout.

5) There are two final points to make about exercise i) you don’t need to do exercise to lose weight – exercise is recommended by the calorie theorists to create a calorie deficit. The body will just try to get you to eat to overcome the calorie deficit and people are invariably likely to eat more than they use up (Time Magazine: Why Exercise won’t make you thin. 17.8.2009) and ii) any exercise that you enjoy is always a great thing to do (dancing, walking the dog, yoga etc – if you enjoy it, do it. If the thought of going to the gym at 6am makes your heart sink, don’t do it!). Here are some good reasons to exercise:  for your lean tissue maintenance; for your sense of well-being; for relaxation; for your joints; for your heart; for whole body health… Don’t ever think exercise is not a good thing to do – the only bad reason to exercise is because you are trying to force your body into calorie deficit. It will respond!