A UK TV programme (Monday 6th August 2012) generated much interest about Calorie Restriction and Intermittent Fasting. The programme was a Horizon documentary, by Michael Mosley, called “Eat, Fast and Live Longer” (The comma is very important!)
I did a review of the programme, so you’ll be able to see what it was about by reading this - it will be long gone from iplayer. This free download will also explain the difference between Calorie Restriction (CR) and Intermittent Fasting (IF) and the three things that can vary within IF options.
The document also asks and answers – what has been proven by research into Intermittent Fasting? Has it been proven to make humans live longer? (No) Has it been proven to reduce the human risk of Alzheimer’s? (No) And so on.
Michael Mosley tried a number of options for the programme – a four day fast (if a cup-a-soup doesn’t count!); alternate day fasting and fasting two days a week. He simply found the latter option – two days a week – more bearable than the other options and thus “The Fast Diet” was born and 5:2 became a familiar term in UK dieting speak.
One of the people interviewed in the programme was Dr Krista Varady. She had been researching alternate day fasting for some time, which Mosley tried and rejected in favour of starving for fewer days each week.
In PR interviews for the book this week, two very interesting comments were made by Varady:
1) On BBC Breakfast, on January 14th 2014, at approximately 1 min 40 secs in, Suzanna Reid mentions “the 5:2 diet” and asks Varady “You were involved in the research for that diet?” To which Varady replies: “There’s actually not any research on 5:2 itself, so all of the research quoted in that book is actually on every other day dieting. So when they talk about all the cholesterol lowering effects and weight loss effects, they’re actually reporting fasting every other day and not two days a week.”
2) On Woman’s Hour, on January 15th 2014, just after 23 mins in, Jane Garvey asks some brilliant questions. Here’s how the conversation goes:
Garvey: “You were part of that Horizon programme, all about fasting. So, outline what you believe, are the benefits of fasting.”
Varady: “It involves something called a feast day, where people can basically eat whatever they like, alternated with something we call a diet day, where people would eat about 500 calories, as either a lunch or a dinner. I’ve run about 10 years of studies involving 5-600 people, so we’ve looked at a lot of aspects … the heart protective and diabetes protective effects…”
Garvey: “Hang on – heart protective? diabetes protective? How and why?”
Varady: “After about four weeks or so this diet helps to lower cholesterol levels, triglyceride levels, blood pressure, blood sugar levels, insulin…”
Garvey: “How does it do that?”
Varady: “How does it do it? It’s basically the weight loss.”
Garvey: “OK, so that’s linked to weight loss, but not necessarily weight loss through fasting.”
Varady: “I really think all the benefits are through the weight loss. We have yet to tease apart the effect of fasting from the weight loss.”
LISTEN TO SNIPPET
And that’s all you need to know.
The front cover of the book claims “The only fasting diet proven by science.” But the person who has been researching this for 10 years still can’t “tease apart” the effect of fasting. Weight loss, by whatever method, is the factor that may deliver health benefits.
There are a number of new diet books out this New Year, as would be expected. The Honey Diet has already been the subject of a feature in the Daily Mail.
I was particularly curious about this one, as I’m often asked “Can I have honey?” and my reply is “No – it’s just sugar!”
The best starting point to get the nutritional facts about honey is the global ‘bible’ of food information – the United States Department of Agriculture database, available on nutritiondata.com. Honey can be found here – in the “sweets” section! Bit of a clue for starters.
Per 100g, honey has 304 calories. It is 82% carbohydrate and 18% water. All the carbohydrate is sugar. It differs from table sugar (sucrose) in the following ways:
i) Table sugar is 100% carbohydrate/sugar; honey is 82% carbohydrate/sugar.
Table sugar (sucrose) has no water content. If it did it would be sticky – like honey. Honey is slightly lower in carbohydrate than sucrose, simply because it has a water content – and that’s also why it’s sticky.
ii) Table sugar is 100% empty calories; honey is virtually all empty calories.
If you look at the nutrition data information for honey for yourself, you can see that 100 grams of honey has no essential fats, no protein, traces of a couple of vitamins and traces of a few minerals. The highest contribution honey makes to any one nutrient requirement is that 100 grams of honey provides 0.1mg of manganese. You would need to consume 2.3 kilograms of honey daily, at a calorie intake of almost 7,000, to get this one nutrient from honey. Or, you could have 60 grams of cocoa powder, at 137 calories, in the delicious form of very high cocoa content chocolate and get your daily requirement of manganese in one hit.
iii) Table sugar is 100% sucrose = 50% glucose/50% fructose; honey is virtually the same = 46% glucose/50.5% fructose/3.5% galactose .
Sucrose is a disaccharide (two sugars). It is made up of glucose and fructose in equal measures. Hence table sugar is 50% fructose and 50% glucose. The USDA database tells us that honey is 1% sucrose, 43.5% glucose, 50% fructose, 1.75% maltose and 3.75% galactose. Maltose is also a disaccharide – providing two molecules of glucose and we know that sucrose is a disaccharide providing one molecule of glucose and one of fructose. Hence, if we break honey down into the monosaccharides (single sugars), the maltose gets added to the glucose line, as does half the sucrose and we end up with the simple sugar composition of honey being 45.75% glucose (say 46%), 50.5% fructose and 3.75% galactose.
Honey is thus a cross between table sugar and High Fructose Corn Syrup (HFCS) in terms of its sugar composition.
You can see that the differences between sucrose and honey are small and not necessarily good ones. There is nothing good about honey from a nutritional point of view.
The claims about honey in the article
1) “Honey’s unique combination of natural sugars make it a near-perfect weight loss food.”
As John McEnroe famously said “You cannot be serious!” You have seen in the sugar composition of honey that it is somewhere between the 50/50 glucose/fructose ratio of table sugar and the 45/55 glucose/fructose ratio of HFCS. It is sugar and nothing but sugar. There is nothing beneficial to weight loss about sugar. Sugar is the single substance best avoided by anyone wanting to lose weight.
2) “By substituting sugar for honey throughout the day and taking a large spoonful of honey in a hot drink before going to bed, the mechanisms in the brain that spark ruinous sugar cravings can be shut down altogether.”
I don’t see how. If you substitute one nutritionally pointless sugar for another nutritionally pointless sugar throughout the day, you are still consuming unnecessary nutritionally pointless sugar throughout the day. If you crave sugar, consuming sugar feeds those sugar cravings – it does not make them go away. Would you try to kid an alcoholic that consuming one alcohol instead of another would make alcohol cravings go away? Or a smoker that one brand of cigarettes instead of another would stop them craving cigarettes? This really is disingenuous.
The average human body, with an average five litres of blood, needs 0.8-1.1 grams of glucose per litre of blood = 4-5.5 grams of glucose per person at any one time. One tablespoon (let alone a large one) of honey has 17 grams of sugar. We know that 46% of this is, or breaks down into, glucose – that’s almost 8 grams. That’s twice what the blood stream needs in total at any one time.
If you were in a state of stable blood glucose before going to bed – a tablespoon of honey will whack you out of stability and force the body to release insulin to get you back into the normal blood glucose range. Do this too often and don’t be surprised when you develop type 2 diabetes. If you had high blood glucose anyway before bed – a spoon of honey will make it even worse. Even if you had slightly low blood glucose, you do not want anything to shoot your glucose levels over the top and out of the normal range. You should just go to bed and your body will break down triglyceride (body fat) while you sleep to keep your blood glucose stable throughout the night.
You lose weight while you sleep by going to bed without having chucked sugar into your mouth last thing at night – not by having done so.
The fructose part of honey, by the way, doesn’t go into the blood stream – it goes straight to the liver where the liver turns it to fat.
3) “The hundreds of micro-nutrients in every teaspoon of honey change the way the substance reacts in our digestive system.”
This statement fails in the first few words. First of all there are not even hundreds of micro-nutrients. Micro-nutrients are otherwise known as vitamins and minerals. There are precisely 13 vitamins and there is some debate as to the number of minerals that are relevant to include, but a number of 16 would be accepted by most people. That’s not even 30 micro-nutrients to assess.
Then – you’ve seen the nutritional content of honey in the opening section – and that was for 100 grams. Look back at the nutrition database for yourself and use the drop down menu at the top to change the quantity to either 1 tablespoon (21 grams) or 1 packet (14 grams). One teaspoon is not even 7 grams, so either divide the tablespoon values by 3 or the packet values by 2 and the nutritional value of a teaspoon of honey is even less than either of these. You will see that even the traces of vitamins and minerals have now disappeared to register zero contributions of virtually every micro-nutrient.
4) “In fact, tests conducted by medical research laboratories in Dubai show a spoonful of honey appears to lower blood-sugar levels rather than raise them as a spoonful of white sugar would.” (The article’s emphasis, not mine).
This is not true – not as the first response anyway. This article appears to be the one in question – a Dubai study assessing the impact of honey on blood glucose levels. It was interesting to search for articles about honey. The author, Al-Waili, comes up again and again. He is Mr Honey. Pubmed alone has 30 articles under his name extolling the virtues of honey. He declares no conflicts of interest, but he will certainly be popular with the honey producers, even if they aren’t funding him.
Al-Waili’s areas of research involving honey are very varied – from the topical application of honey vs. acyclovir for the treatment of herpes to the prophylactic effects of crude honey on chronic seborrheic dermatitis and dandruff! Most of Al-Waili’s studies review the value of applying honey as an ‘ointment’ to different parts of the body and there may be value in honey for such purposes. I don’t know and it’s not my area of interest. I’m interested in food, health and weight and I can’t see a value for honey in this arena.
Back to the Dubai study allegedly showing that honey lowers blood-sugar levels: You only need to read the abstract to see that a number of experiments were undertaken in this study, but the one we need to look at is the first – Dextrose solution was compared with honey solution to assess the impact on plasma (blood) glucose levels (PGL) in eight people.
The dextrose solution contained 75 grams of dextrose in 250mL water and the honey solution contained 75 grams honey in 250mL of water. The result was that “In healthy subjects, dextrose elevated PGL at 1 (53%) and 2 (3%) hours, and decreased PGL after 3 hours (20%). Honey elevated PGL after 1 hour (14%) and decreased it after 3 hours (10%).”
So, honey did not lower blood glucose levels. Honey raised blood glucose levels at the one hour marker and then lowered them after three hours. This is a normal response to putting too much glucose into the blood stream. Blood glucose levels rise and then insulin is released; the excess glucose is converted to glycogen and blood glucose levels fall.
We don’t know from the abstract if blood glucose levels stayed within the normal range, or fell below the normal range. I interpret the expression “decreased PGL after three hours” as the blood glucose level ended up lower than it was before the consumption of the dextrose/honey solution. This would generate a classic hypoglycaemic response and a lower than normal blood glucose level would lead to the person seeking glucose and thus having cravings for more sugary food. This is the reason why I advise people never to start on the sugar ingestion roller coaster – or you will be on it, incessantly craving sweet things, for the rest of the day.
The other important factor to highlight in this study is that honey was not being compared with white sugar (what people would assume to be table sugar). Honey was being compared with dextrose. Dextrose is pure glucose (some athletes consume dextrose tablets to get a quick shot of glucose into their blood stream). Hence this experiment compared 75 grams of glucose in water with 28 grams of glucose in water (that’s the amount of glucose in 75 grams of honey). Is it any surprise that putting more than twice the glucose into the blood stream has more impact on blood glucose levels? Had this experiment compared dextrose with table sugar, table sugar would have produced less of a response than dextrose, since table sugar has half the glucose of dextrose. This is also disingenuous.
The diet rules
These are only nine rules in the article, and the wording and order differs to the book, so here are the rules taken from the book:
1) Rule Number 1: Switch sugar for honey;
2) Rule Number 2: Have a honey drink every night before bed (1-2 tablespoons only – we are reminded that there are 64 calories in a tablespoon, which can mount up!) ;
3) Rule Number 3: No more junk food;
4) Rule Number 4: Enjoy a good breakfast;
5) Rule Number 5: Enjoy unlimited salads and vegetables;
6) Rule Number 6: Full-fat dairy products are OK;
7) Rule Number 7: Drink lots of water;
8) Rule Number 8: One no-carb day each week (the menus for the no-carb day list tomatoes, apple, mushrooms, unlimited salad & vegetables, beans, avocado, yoghurt and cheese, so this should be a no grains day?);
9) Rule Number 9: Switch to brown carbohydrates (and not too many);
10) Rule Number 10: Include protein in every meal or snack;
11) Rule Number 11: No more than two pieces of fruit (not juice) per day.
Only two of these rules are needed – (Rule 3) Don’t eat junk food and (Rule 9) limit even your unrefined carb intake and that’s it. Rules 8 and 11 are also intended to curtail carb intake – because this is a low carb diet at the end of the day. Rule 10 is pointless – protein is in everything (except oils and sucrose). So, unless you plan to sit down to a meal of olive oil, or honey!, you will consume protein.
It is interesting to note that the first chapter in the book – “The key to weight loss” – has a number of references listed at the back, but none of them are about honey. They are about errors we have made in dietary advice – fat is not the enemy, carbohydrates are etc – the kind of stuff I write and talk about on an hourly basis. All good stuff, but naff all to do with honey. Chapter 2, all about the benefits of honey for sleep, similarly has an impressive number of references – about sleep and obesity generally. I couldn’t see honey in a single title listed. Chapter 3 gets into more general benefits claimed for honey – and there may be some – but this is billed as a weight loss diet and honey is not featuring in the rationale for weight loss – the efficacy of low carbohydrate intake is, however.
There is a 7-day plan presented in the article and you will be able to see immediately why this plan would help weight loss – and it has nothing whatsoever to do with honey. It’s a plan largely based on real food and low carbohydrate intake – rules (3) and (9).
Monday has bacon, one tomato, a handful of olives, a three-egg omelette, celery sticks with cream cheese, salmon and steamed broccoli and plain yoghurt with honey. Monday is described as the “no carb” day. Honey is pure carb; salads and vegetables are carbs and dairy foods have a carb content, so we’ll assume that the author, Mike McInnes, means “no grains” day and has ignored the honey.
You can see the rest of the meal options in the article – they are based on real food and low carbohydrate. In fact the only rubbish in there is honey! Every day has to feature honey (or it wouldn’t be the honey diet). Monday, Tuesday and Thursday have honey in yoghurt – far better to leave the honey out and just have natural live (bio) yoghurt. Wednesday has honey cake. On Friday you are supposed to make 12-15 apple and walnut cookies (with honey of course) and eat only one (see the recipes). On Saturday you are supposed to make 12 honey banana muffins and, again, eat only one. On Sunday, it’s rhubarb and banana crumble – with 2 tablespoons of honey slipped in.
The rest of the foods listed are healthy – eggs, chicken (but ignore the advice to remove the skin – that’s where the nutrients are), tuna salad, pork casserole, frittata, steak, salads and vegetables etc. Eggs feature heavily in the diet and the meals are real food/low carb. It really is only the honey and the cakes/muffins etc, which have been concocted to include honey, providing empty calories in this diet.
This diet should ditch the honey completely and therefore dump its first rule. However, if you ditched the honey, this wouldn’t be The Honey Diet. It would be just another low carb diet!
Why are diabetics being told to eat what made them diabetic?
Thursday November 14th (2013) was World Diabetes Day.
The International Diabetes Federation (IDF) defines diabetes as follows :
“Diabetes mellitus, or simply diabetes, is a chronic disease that occurs when the pancreas is no longer able to make insulin, or when the body cannot make good use of the insulin it produces. Insulin is a hormone made by the pancreas, that acts like a key to let glucose from the food we eat pass from the blood stream into the cells in the body to produce energy. All carbohydrate foods are broken down into glucose in the blood. Insulin helps glucose get into the cells.
Not being able to produce insulin or use it effectively leads to raised glucose levels in the blood (known as hyperglycaemia). Over the long-term high glucose levels are associated with damage to the body and failure of various organs and tissues.”
Note the mention of the word “glucose” five times and the acknowledgment that all carbohydrate foods are broken down into glucose.
The different types
The IDF definition describes the two types of diabetes – type 1 diabetes is the type where the body is no longer able to make insulin and type 2 diabetes is the type where the body cannot make good use of the insulin it produces.
We used to call type 1 diabetes “juvenile diabetes”, as it only used to occur in young people. The typical age of onset was during teenage years – some children developed type 1 younger and a few in their early 20s, but it was largely a teenage condition. If you hadn’t developed type 1 diabetes by the time of your 21st birthday, you were highly unlikely to do so.
Type 2 diabetes used to be called “maturity onset diabetes”, as it only used to occur in older people. It was typically associated with ‘granny’ who had a sweet tooth, always had humbugs in her handbag and it developed after years of drip feeding glucose.
Neither type 1 nor type 2 diabetes are called juvenile or maturity onset anymore and that’s because these labels no longer apply. We are seeing type 1 diabetes in middle aged people and older. We are seeing type 2 diabetes in children. The latter is particularly horrific. I attended an obesity conference a few years ago where a doctor specialising in childhood diabetes and obesity said that he was seeing an increasing number of type 2 diabetic children come through his door. He had no means of assessing what this would do to their life expectancy, but his prediction was that few children with type 2 diabetes would reach their 40th birthday – such was what he knew about the impact of type 2 diabetes on the body.
The IDF also informs us that more than 371million people have diabetes. Type 1 is seen as an autoimmune condition, with a strong hereditary connection (this is why we are asked for family members with diabetes in medical questionnaires). Type 1 is the rarer of the two types by far – 92-95% of the incidence of diabetes is type 2.
What causes type 2 diabetes?
If the vast majority of diabetes is type 2 – the type that we used to develop with age – what causes it?
The UK NHS lists four risk factors. Please note – this is not saying what causes type 2 diabetes, but listing risk factors. You can have one of these risk factors and not develop type 2 diabetes and you can develop type 2 diabetes and not have one of these risk factors. Despite this page being called “Causes of type 2 diabetes”, it is not telling us what causes diabetes.
The NHS’s four risk factors are presented as: “You are more likely to develop type 2 diabetes if you:
- are over 40 years old
- have a relative with the condition
- are of South Asian, African-Caribbean or Middle Eastern origin
- are overweight or obese.”
I accept the age factor – this is the maturity onset aspect of the condition. However, I do not accept that it is age alone that is associated with type 2 diabetes. I think that type 2 diabetes depends on what people eat as they age.
The risk factor related to relatives with the condition is positioned as: “A child who has a parent with type 2 diabetes has about a one-in-three chance of also developing it.” I also think that this is related to diet. A child is eating what their parents eat. If the parents are eating such that they developed type 2 diabetes, the child will be doing the same.
The third ‘risk factor’ may apply in the UK, but it is not accurate globally. The IDF has a chart for the top 10 countries in the world for incidence of diabetes. Six of the ten countries are in the Pacific Ocean and the other four are in the Arabic/Middle East. It would be useful to study the diets of these nations.
The final risk factor seems an obvious one – we know that people who are overweight or obese more often have diabetes – yes?
The evidence is compelling: The JAMA (1999) article “The Disease Burden Associated with Obesity and Overweight” estimated that a male under 55 and with a BMI of over 40 has 90 times the chance of developing type 2 diabetes than a normal weight male of the same age. (Ref 1) Although this study found the risk for women slightly lower, other studies have corroborated this multiple for women. Colditz et al (1995) found that women with a BMI of more than 35 had 93 times the risk of developing type 2 diabetes than women whose BMI was less than 22. (Ref 2) A BMI of 35 is also not breathtakingly high – 1.2 million people in the UK currently have a BMI of over 40. An average height woman (5’4”) who is 14 stone seven pounds has a BMI of 35 and an average man (5’9”) who weighs 17 stone has a BMI of 35.
I question causation, however. Does obesity cause diabetes? Or does diabetes, with all the accompanying insulin problems, cause obesity? Or do the same foods that cause obesity also cause diabetes?
My view on type 2 diabetes
I think that type 2 diabetes is the body saying “enough’s enough”. Every time we consume carbohydrate – any carbohydrate, as the International Diabetes Federation tells us – glucose enters the blood stream. The body can only tolerate approximately one teaspoon (approximately 16 calories) of glucose in the blood stream at any one time. Any amount beyond this requires the body to call upon the pancreas to release insulin to turn the excess glucose into glycogen (the stored form of glucose) to return blood glucose levels to safe levels.
Only in the past 10,000 years have we even had ‘our daily bread’ and this bread has historically been dense, unrefined, unsweetened and limited in quantity. We used to have vegetables and fruits in season and that was the extent of our carbohydrate intake. No sugary cereal and fruit juice for breakfast; no muffin/cereal bar mid-morning; no sandwich/crisps and drink meal deal at lunch time; no confectionery late afternoon; no pasta/pizza for dinner and no TV munchies in the evening.
Can you imagine how many times we make demands on our pancreas during a typical “base your meals on starchy foods” day? How many times can we do this before the body says “enough’s enough! I simply cannot keep responding to your unprecedented consumption of glucose in this way.”
Age is not the issue – a Paleo pensioner is not going to develop type 2 diabetes; a carb addict child might.
Genetics are an issue for type 1 diabetes, but need not be for type 2. If the type 2 diabetes parents realises what they have done wrong and changes the family diet as a consequence – the child may well be saved from developing type 2 diabetes.
The ethnicity need not be the issue – if Brits, of Asian and African Caribbean origin, recognise that they are particularly unused to the appalling British diet and particularly susceptible to its effects – they too can change their diet to avoid type 2 diabetes.
As for the fourth NHS risk factor, the people who manage carbohydrate intake can avoid both obesity and type 2 diabetes.
Dietary advice for diabetics
The IDF definition of diabetes mentions the word glucose five times and tells us that all carbohydrate foods are broken down into glucose. It warns us how damaging high glucose levels are and how diabetes is the condition whereby glucose cannot be cleared from the blood effectively.
So answer one question – why on earth would diabetics be advised to consume glucose?
This is the dietary advice from Diabetes UK entitled “Healthy Eating”:
Diabetics are advised to consume the following EACH DAY:
* 5-14 portions of Starchy Foods per day “One-third of your diet should be made up of these foods, so try to include them in every meal.” A slice of bread is given as an example portion – a diabetic should therefore eat the starch equivalent of up to 14 slices of bread every single day.
*”Aim for at least 5 portions” of Fruit & Vegetables (5-a-day of course!) That’s a combination of glucose and fructose.
* 3 portions of Dairy Products, and diabetics are told to “choose low-fat alternatives.”
* 2-3 portions of Meat, Fish, Eggs & Pulses. One portion is listed as 2-3oz meat, so the daily guidelines are between 4-9oz meat or bean/pulse/nut equivalents. If the bean/pulse/nut options are chosen instead of meat or fish, this means that every single food that the diabetic consumes during the day will include sugar.
Starchy foods break down into glucose. Vegetables break down into glucose. Fruit breaks down into fructose and glucose. Dairy products (lactose) break down into glucose and galactose. Pulses, beans and nuts also provide glucose.
Can you imagine the strain that this dietary advice places on an already malfunctioning pancreas/insulin/glucose handling system? If my vacuum cleaner isn’t working, I’m not going to spend the day hoovering! If my glucose handling system isn’t working, why would I spend the day consuming things that break down into glucose? That’s where the analogy ends. If my vacuum cleaner isn’t working, I buy another one. Once we have exhausted our glucose handling system, to the point of it being broken, we cannot buy another one. We cannot repair it. We can, however, dramatically curtail consumption of the substance that made it break in the first place – glucose.
Which bit of that do Diabetes organisations not understand?
Ref 1: Must A., Spadano J., Coakley E.H., Field A.E. et al, “The disease burden associated with overweight and obesity”, Journal of the American Medical Association (JAMA), (1999).
Ref 2: Colditz G.A., Willet W.C., Rotnitzky A. et al, “Weight gain as a risk factor for clinical diabetes mellitus in women”, Annals of Internal Medicine, (1995).
This is a review of a book written by James & Hannah Yoseph entitled How statin drugs really lower cholesterol: and kill you one cell at a time (and many thanks to Eric who posted a comment to say that there is a ‘made easier’ version of this here.)
I won’t reiterate the importance of cholesterol – you can read this on this post. Suffice to say your body makes cholesterol because it is so utterly vital, the body cannot leave it to chance that you would consume it. You would die instantly without cholesterol – it is a fundamental part of every cell in your body.
This book should be read by every person BEFORE they either prescribe or take statins. I would be interested to know if any person could prescribe or take statins AFTER reading it…
There is an interview with the Yosephs here.
The three key contributions of the Yoseph book
There are three key contributions of this book:
1) The explanation of precisely how statins work in the human body (and in animals where they have been used for drug testing).
2) The documentation of medical journal articles proving that the precise mechanism as to how statins work has been known by their proponents throughout.
3) The detailing of the conflict of interest endemic in the pharmaceutical industry and approval processes, which have monumentally failed the human race. The book takes one drug company, Merck, and the American Food & Drug Administration (FDA) and a number of other related bodies (e.g. the National Cholesterol Education Programme NCEP) and a handful of individuals and traces in incredible detail the role that each played in this scandal. And it is a scandal.
Let us look at the three main findings that the Yosephs have given us:
1) How statin drugs really lower cholesterol
Every cell needs sustenance. The cell says “I’m hungry” and makes a protein called “reductase.” Reductase activates something called the mevalonate pathway. Mevalonate is cell food just as glucose is brain food. Mevalonate is utterly vital for the life of every cell in the human body.
The Yoseph’s put it this way: “Mevalonate is the essence of cell renewal. In all cells, mevalonate travels down the mevalonate pathway to make cholesterol and isoprenoids (five-carbon molecules). Both stimulate the cell to grow, replicate its DNA and divide into two cells. This is the ‘cell cycle’. This is life.”
Cell renewal is continuous throughout the body – cells lining the gut are turned over every 10 hours to 5 days; skin cells are recycled every two weeks; liver cells are replaced every 300-500 days and bone cells last a decade.
Without the cholesterol and isoprenoids made by the mevalonate pathway, none of this cell rejuvenation happens. Isoprenoids make our cells replicate and renew. Without mevalonate and without isoprenoids, cells age and die. They cannot be replaced.
CoQ10 is an isoprenoid. CoQ10 is vital for cell energy. Heme-A is an isoprenoid. Heme-A is vital for cell energy and drug metabolism. Isopentenyl adenine is an isoprenoid. Don’t worry about the names in all of this – just remember that Isopentenyl adenine is vital for DNA replication. DNA is the blueprint of every cell. Before a cell divides, it replicates its DNA and the new cell can be formed from the same blueprint. There are other vital isoprenoids – all are stopped from functioning by the disruption of the mevalonate pathway.
In the simplified flow chart above, showing the cholesterol production pathway in the body, we can see why statins are called HMG-CoA Reductase inhibitors – this is the part of the pathway that they disrupt. Statins disable reductase. Without reductase, the mevalonate pathway cannot function properly. Without the mevalonate pathway, cells cannot rejuvenate properly. It follows that the life of every cell in the human body is catastrophically impaired by statins.
How long does it take cells to be affected? That depends on the life cycle of the cell – 300-500 days for liver cells and up to 5 days for the cells lining the gut.
In chapter four of the Yoseph’s book there is one of the most incredible explanations about what statins actually do, which I have not seen elsewhere. The Yosephs describe the fact that statins are not just HMG-CoA reductase inhibitors, they are also reductase stimulators…
Life preserving responses are hard wired at the cell level – our body will do whatever it takes to keep us alive; every cell will do its bit to keep us alive. Because reductase is the ‘food’ for cell reproduction, taking something that impairs this process (statins) triggers the body to try to overcome the damage that is being done. Reductase production increases to try to reopen the mevalonate pathway. It’s a terrific attempt by the body to fight back. However, the Yosephs sadly note: “So far, they have not figured out how to save statin-fed dying cells except by adding back mevalonate.”
The book describes that there are two ways in which every cell of the body can get the cholesterol it so vitally needs: 1) it can make cholesterol and 2) it can take cholesterol from the blood stream.
When someone takes statins, the cells are impaired from making cholesterol so they try to take the cholesterol from the blood stream. The LDL receptors on each cell go into overdrive and try to ‘receive’ more LDL from the blood stream to compensate for the fact that the cell can’t currently make as much itself. This lowers the cholesterol in the blood stream. (Please remember that LDL stands for Low Density Lipoprotein – it is not cholesterol, let alone bad cholesterol. Similarly HDL stands for High Density Lipoprotein – it is not cholesterol, let alone good cholesterol).
That’s how statins lower cholesterol and that’s how statins kill us one cell at a time.
Familial Hypercholesterolemia (FH)
It is time to mention Familial Hypercholesterolemia (FH) here. FH is a genetic condition caused by a gene defect on chromosome 19. The defect makes the body unable to remove LDL from the bloodstream, resulting in consistently high levels of LDL. Bearing in mind that FH is rare to start with – one in 500 people – in some cases of FH the LDL receptors work to an extent (just not very well); in other cases the LDL receptors work barely at all.
My logical consideration of FH suggests to me that the problem is that the LDL receptors don’t work properly and therefore the LDL (lipoproteins) cannot get into the body’s cells in the way that they are supposed to. This means that cells don’t get the vital LDL, carrying the vital protein, lipids and cholesterol needed for the cell’s health. LDL in the blood stream is high because the LDL has stayed in the bloodstream and has not been able to get into the cells – where it is supposed to go. Hence high LDL blood levels are the sign that someone has FH. The high LDL levels are, however, a symptom and not a cause or a problem per se. The problem is that the health of every cell is compromised by LDL not getting to the cell. This includes heart, brain and muscle cells – all cells. An FH sufferer can therefore have heart problems – because of too little LDL reaching the heart cells – not because of too much LDL! How differently things can be seen when one is not blinded by thinking that cholesterol or lipoproteins are bad.
This also explains why high HDL would be seen as good. HDL is the lipoprotein that carries used lipids and cholesterol back to the liver for recycling. If the LDL were not able to get to the cells to do its job then there is little for HDL to carry back to recycle. Hence HDL would be low and this would be seen as bad with impaired understanding as to why.
Ironically, the most serious form of Familial Hypercholesterolemia would receive no benefit from statins anyway. As the extreme form of FH is characterised by LDL receptors working barely at all, even the body going into crisis mode, and trying to take LDL from the blood stream with increased LDL receptor activity, will not work if the LDL receptors are not working well enough in the first place. Hence the LDL will stay in the blood stream with an extreme sufferer of FH and yet the statin has reduced what little chance the FH sufferer’s body had of making cholesterol within the cell. The FH sufferer should ideally be given medication (if anything existed) to stimulate cholesterol production within the cell, so that the cell would at least get the vital cholesterol it needs, even when it couldn’t get it from the blood stream.
2) What was known by whom and when as statins were pushed through to approval?
We need to introduce some key players here:
- Brown & Goldstein were awarded a Nobel Prize for their work with lipoproteins. We will see what they knew along the way and their involvement with statin approval.
- Akira Endo was a Japanese biochemist who graduated from Tohoku University in 1957 and joined Sankyo Pharmaceuticals in Tokyo. Endo is the guy who discovered the poison that statins are made of. In 1971 he began his search for a fungal mycotoxin that would lower cholesterol. (Definition: “Mycotoxins are secondary metabolites produced by microfungi that are capable of causing disease and death in humans and other animals”). (A metabolite is a small molecule produced during metabolism.)
In 1976 Endo managed to extract something called citrinin, a disease-causing mycotoxin from Penicillium Citrinum. He discovered that citrinin lowered blood cholesterol and published a report on this. In the same year he abandoned his work with citrinin because it was too toxic. He extracted another mycotoxin from Penicillium Citrinum called “ML-236B”, which was less toxic but still lowered cholesterol. ML-236B became Endo’s first experimental statin. (There’s a great story in the book about how Sankyo, with Japanese cultural traits of trust and honour, approached the American drug company Merck to develop the statin together. Merck shafted Sankyo and Endo was wrongly seen as the betrayer and was ostracised by Sankyo). Endo was then ‘out on his own’ and he approached Brown & Goldstein, seeing the work that they were doing with lipoproteins, and this is how these guys got together.
(Also – if you are thinking that Penicillium Citrinum sounds like an antibiotic, you’d be right. The book states “Statins – secondary fungal metabolites – are anti-life or anti-bios. Statins are antibiotics. Because antibiotics are anti-bios and kill ‘good’ vitamin-producing bacteria in the gut, most are prescribed for as short a term as possible. Statins, on the other hand, are often prescribed for life. Most antibiotics also have specific action on specific microbes. Not so with statins. Statins indiscriminately kill any cell including human cells.” (Their emphasis). This could explain the warnings about gut health on statin patient leaflets.)
In 1953 Watson and Crick discovered the structure of DNA. In 1979 Marvin Siperstein discovered that DNA replication (cell rejuvenation) required isoprenoids from mevalonate (specifically the isoprenoid called isopentenyl adenine). (p10 in the book) (I won’t dwell on Marvin Siperstein, but he’s one of the good guys in the Yoseph book – writing his important discoveries and highlighting serious issues in medical journals. These articles were sadly ignored.)
In 1976, Beecham Labs in the UK (what became SmtihKline Beecham and then Glaxo SmithKline) had discovered a statin named “compactin”. Sankyo Pharmaceuticals had discovered the same compound in parallel in Japan. They called it Mevastatin. “Stat” in statin means to stop and mevastatin means “to stop mevalonate”. So they knew exactly what they were stopping when they named this drug. Within an hour of adding compactin to cholesterol-rich cells, the cell reproduction cycle was completely stopped. Within minutes of adding back a small amount of mevalonate, DNA replication and cell cycles were completely restored.
This bit is key – because the cells were given ample cholesterol before the experiment (they were “cholesterol-rich cells”), it was clear that the problem was not cholesterol deprivation but isopentenyl adenine deprivation (that isoprenoid that enables DNA replication). The absence of this isoprenoid prevented DNA replication and the entire cell cycle.
As the Yosephs state “Cells are poisoned by statins because statins block the making of isoprenoids from mevalonate. If cells cannot replicate, they inevitably die.”
In 1977 (p37 of the Yoseph book), Endo, Brown and Goldstein published a paper documenting that statins caused an increase in reductase. It was therefore known back this far that statins should not necessarily be called reductase inhibitors, but reductase stimulators. They didn’t detect the increase in LDL receptor activity at this time.
In 1978 Merck developed their own statin.
In 1979 Endo patented another statin and sold it to Sankyo to try to restore his honour.
On p143 of the book, The Yosephs present an image of a paper written by Brown and Goldstein in The Journal of Biological Chemistry (1979). This incredible quotation from their paper is extracted: “Mevalonate, the product of HMG-CoA reductase, also supported growth, confirming that compactin was exerting its killing effect by a specific inhibition of HMG-CoA reductase.” So Brown and Goldstein admitted that the first statin, compactin, had a killing effect and this was a result of inhibiting reductase. They went on to develop further statins, which also inhibited reductase and also had a killing effect.
In 1980, Brown and Goldstein wrote the following in The Journal of Lipid Research (we’ll see who’s behind this journal shortly): “When the regulator of reductase is identified, it may be possible to administer this compound to animals and perhaps to patients, preventing the compensatory rise in reductase…” Hence Brown and Goldstein knew by 1980 that statins both inhibited and stimulated reductase. They also knew that the “compensatory rise in reductase” was something to be prevented.
In 1980, Brown and Goldstein co-authored a paper in The Journal of Biological Chemistry stating: “CoA reductase is inhibited by compactin, mevalonate formation is blocked and cultured cells die.” (p14)
In 1980, Brown and Goldstein co-authored a paper in The Journal of Lipid Research stating: “Incubation of cultured cells with compactin blocks mevalonate production and converts the cells into mevalonate auxotrophs.” (p172) An auxotroph is something that has lost the ability to synthesise certain substances needed for its growth and metabolism.
In 1980, Endo co-authored a paper in The Journal of Biological Chemistry entitled “Isolation and characterisation of cells resistant to ML236B (compactin) with increased levels of HMG-CoA reductase”. The extract (p146 of the Yoseph book) states: “…cholesterol alone is ineffective in preventing cell death…Addition of other mevalonate-derived metabolites to the culture medium along with cholesterol including ubiquinone [That’s CoQ10 remember], dolichol and isopentanyl adenine [that’s the isoprenoid vital for DNA replication] did not prevent the toxic effect of ML236B.” i.e. nothing we could add back to the cell, to compensate for the damage we had done, could prevent the toxic effect.
Also in 1980, Sankyo cancelled clinical trials of their statin on humans after half their laboratory dogs died of cancer. Merck called Sankyo to try to learn from this and Sankyo told them to sod off – quite right! Merck stopped statin development (sadly, only temporarily).
In 1982 Brown and Goldstein wrote in The Proceedings of the National Academy of Sciences: “If reducatase cannot increase sufficiently to overcome the inhibition by compactin, the cells die.” (p144)
Incredibly, given all of this going on, in 1982 Merck was allowed to give Lovastatin to humans in the first human trial. At this time:
- It was known that statins were toxins.
- It was known that statins blocked the mevalonate pathway.
- It was known that blocking the mevalonate pathway caused cell death.
- It was known that nothing could be added back to the body (not cholesterol, not isoprenoids, nothing) to prevent cell death and the toxic effect of statins.
- It was known that statins not only inhibited reductase, but they stimulated it too. It was known that inhibition of reductase “had a killing effect”. The consequences of stimulating reductase were not precisely known, but caused enough concern for the 1980 Brown and Goldstein article in The Journal of Lipid Research to discuss what might be administered to “prevent(ing) the compensatory rise in reductase…”
In 1984 lovastatin was approved by the FDA in record time.
In 1985 Brown and Goldstein were awarded the Nobel Prize!
3) The conflicts of interest:
We need to introduce some more players at this stage:
Daniel Steinberg is the overall ringmaster. If you do an internet search you will find remarkably little about him personally and this seems to be deliberate. The Yosephs should be commended for what they have managed to piece together about this orchestrator. (You will find his “Cholesterol Wars”, where he writes that “after much controversy, cholesterol and lipoproteins were implicated, indicted and ultimately found guilty.”)
Steinberg was the founder and first editor in chief of The Journal of Lipid Research (a vehicle for Endo, Brown and Goldstein and lipid theory supporters to use).
Steinberg was Chairman of the Council on Arteriosclerosis of the American Heart Association and used his position to recommend treating high cholesterol as early as 1969. (Introducing the theory that this life vital substance, made by the body, should be treated rather than revered).
Steinberg was co-chair of the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT). This trial was led by the National Institutes of Health (NIH), costing the taxpayer $150 million over 13 years. In January 1984 the results were published and claimed that the long sought evidence was now available – absolute differentials were less than 2% in different groups observed.
Steinberg was Merck’s scientific advisor when lovastatin was approved in record time in 1984.
Steinberg was the first speaker at the FDA advisory committee meeting on statins, held at the NIH, in February 1987.
In 2006, writing in his own Journal of Lipid Research, Steinberg reported that “the Goldstein/Brown laboratory showed that this huge over production of reductase, representing an attempt by the cell to overcome statin inhibition, is accompanied by a huge buildup of endoplasmic reticulum, the organelle [place] in which the reductase resides. As a result the cells look “abnormal” but of course they are not cancer cells.” Steinberg admits that the cell tries to overcome what the statin is doing, he uses the unscientific word “huge” twice – neither time in his favour – and he is apparently able to single-handedly declare that abnormal cells are “of course not cancer cells”.
The same article “The discovery of statins and the end of the controversy” (how arrogant is that?!) declared: “…there was no hard evidence that compactin would be toxic in humans, only rumors about toxicity in dogs…” Rumors? Merck contacted Sankyo to understand why half their dogs had developed cancer.
Steinberg chaired the NIH consensus panel, which in December 1984 declared that LDL cholesterol was the cause of Coronary Vascular Disease (CVD) and recommended that a National Cholesterol Education Programme (NCEP) be adopted. Since this time the NCEP has set continually lower cholesterol targets. Their recommended age for statin use is now nine!
The members of the NCEP
The 2004 NCEP financial disclosure report reveals that all members of the 2004 guideline participants had received payments and/or grant funds from the following organisations:
Dr Scott Grundy: Abbott, Astra Zeneca, Bayer, Bristol-Myers Squibb, Glaxo SmithKline, Kos, Merck, Pfizer, Sankyo.
Dr Bairey: Astra Zeneca, Bayer, Bristol-Myers Squibb, Kos, Merck, Novartis, Pfizer, Procter & Gamble, Wyeth.
Dr Brewer: Astra Zeneca, Esperion, Fournier, Lipid Sciences, Merck, Novartis, Pfizer, Sankyo, Tularik.
Dr Clark: Abbot, Astra Zeneca, Bristol-Myers Squibb, Merck, Pfizer.
Dr Hunninghake: Astra Zeneca, Bristol-Myers Squibb, Kos, Merck, Novartis, Pfizer.
Dr Pasternak: Astra Zeneca, BMS-Sanofi, Pfizer, Johnson & Johnson, Kos, Merck, Novartis, Takeda.
Dr Smith: Merck.
Dr Stone: Abbot, Astra Zeneca, Bristol-Myers Squibb, Kos, Merck, Novartis, Pfizer, Reliant, Sankyo.
The members of the 1987 FDA Panel
On February 19th 1987 the FDA held an advisory committee meeting to review the NIH clinical guidelines for altering cholesterol with Merck’s new statin, lovastatin. The NIH hosted the event. This would be like the NHS hosting the approval meeting for a drug in the UK; implicit support. Incredibly a Merck consultant, Fred Singer, was in the Chair.
Steinberg and the Nobel prize winners Brown and Goldstein were present in support of Merck. The FDA advisory committee comprised 4 FDA employees, 8 FDA advisors (2 were Merck consultants) and 11 Merck speakers and guests. That put the vote 13-10 in Merck’s favour from the outset.
The Yoseph book fully documents the actual comments made in the meeting and by whom – the record was sequestered through a Freedom of Information request. A Merck toxicologist (MacDonald) admitted that rabbits on lovastatin died rapidly. He attributed this to “elevated blood levels” and got away with no one asking him elevated blood levels of what? MacDonald glossed over the fact that statins failed to lower cholesterol in rats, mice and hamsters. This was because rodents are able to reopen the mevalonate pathway – this is why they live. The rabbits couldn’t do this. This is why they died. Dogs were somewhere in between. MacDonald had to admit to liver cell damage in dogs but, again, got away with “We clearly do not understand the mechanism”. It was denied that cataracts had been observed in rats (a few cases in dogs were skimmed over).
A pharmaceutical consultant called Dr Richard Cenedella said: “I have consulted for many drug companies over the years. All of the hyper-lipidemic drugs induce cataracts in mice; it’s an early observation that holds up.” Cenedella wrote to the Journal of the American Medical Association in 1987 “…to caution against the possible complication of cataract development that might result from long-term use of this agent” [statins]
Jonathan Tobert was Merck’s Clinical Director for all trials. In March 1988 he stated that to date there had been no cataracts seen in humans taking lovastatin. The year before he co-authored a paper documenting an increase in lens opacities (i.e. cataracts) in 101 lovastatin consumers. The Yosephs pull no punches in the book. This is just one of a catalogue of examples where they are able to prove contradictory statements made by Tobert. On p121 they say “You can tell when Tobert is lying. He is either writing or his lips are moving.” And I thought I was bold!
Interestingly cataracts are back in the news as I publish this, but I have not seen any reduction in statin prescription or usage since the headlines that emanated from this JAMA research.
In April 2009 an extraordinary letter was written to President Obama by FDA scientists to say that “The FDA is fundamentally broken” and detailing examples of suppression of truth, distortion and the “FDA failing to fulfil its mission.” Nothing has happened as a result of this letter.
The remarkable Yoseph book has brought us the most precise understanding of how statins lower cholesterol. It has shown that the dangers were known all along – by those pushing through the launch and approval of statins. It has shown how a few key players – Steinberg, Endo, Brown and Goldstein could work with Merck and how Merck and other drug companies could infiltrate the FDA, influence the NIH and even see the establishment of a National Cholesterol Education Programme comprised of drug company funded representatives.
The scandal has been brilliant, meticulously planned and success guaranteed. Billions and billions of dollars have been generated from first demonising cholesterol and secondly discovering a poison (Definition: “Mycotoxins are secondary metabolites produced by microfungi that are capable of causing disease and death in humans and other animals”) that could stop the body making cholesterol. Or, as we now know more accurately – a poison that could drive cells to remove cholesterol from the blood stream, as those cells fight to avoid death.
The mevalonate pathway should never be blocked in a living creature. A rat may get away with it, a human won’t. If only humans died as quickly as rabbits, maybe statins would have never have been approved. The fact that they are killing us one cell at a time, but just more slowly, is little consolation.
The Executive Summary:
Cholesterol is utterly life vital. We die instantly without it. We need it for every single cell of the body, the muscles, the brain, hormones, bile production, fat digestion, reproduction – it simply cannot be emphasised enough how vital cholesterol is.
It is so vital that the body makes it – the body cannot afford to leave it to chance that we would need to get cholesterol from our diet. This makes cholesterol even more vital to the body than essential fats and protein – as we need to eat these.
Statins stop the body from making the cholesterol that it was designed to make (not entirely, or they would have an immediate 100% death rate).
Statins block something called “the mevalonate pathway”. This is catastrophic. Blocking the mevalonate pathway means that cells cannot replicate or repair themselves properly. Blocking the mevalonate pathway means that every cell in the body dies. The only thing that varies is how long each cell takes to die – some take more time than others.
Nothing can compensate for blocking the mevalonate pathway. Nothing except adding mevalonate back in to the body and we don’t do this. (We don’t even know if we can do this in humans. We shouldn’t block this pathway in the first place.) Adding cholesterol makes no difference, adding CoQ10 makes no difference. Blocking the mevalonate pathway is so flipping serious that anyone who does it should be shot. (I really think using the ‘F’ word here is quite appropriate).
The body tries to respond to the crisis that it detects. As cells realise that their ability to make cholesterol has been impaired, they try to take the cholesterol they need from the blood stream. This lowers blood cholesterol levels and ignorant doctors are happy. They know not what they have done.
There is a second way in which the body tries to save itself – it tries to increase the production of reductase, hoping that this may unblock the mevalonate pathway. It can’t. Hence reductase is both stimulated and inhibited at the same time. Who knows how the body responds to this mechanism being totally confused.
LDL receptor activity and reductase activity increase in parallel. The LDL receptors (the ‘doors’ on each cell responsible for letting LDL in to the cell, with the cholesterol and other good stuff that it is carrying) work harder to try to get LDL from the blood stream into the cells. The reductase production increases to try to reboot the mevalonate pathway, so that cells can make cholesterol as they are designed to do.
The inventors of statins knew what statins were really doing throughout the development of this drug (mevastatin literally means to stop mevalonate – they knew exactly what mevastatin would do). They knew that statins blocked the mevalonate pathway. They knew that this caused cell death. They knew that nothing could compensate for this other than putting the vital mevalonate back. They knew that CoQ10 was affected and this was serious. They patented adding CoQ10 to their statins but then never bothered to add it.
Statins were only originally intended for the 1 in 500 people with Familial Hypercholesterolemia. This would not have enabled drug companies to reach the profit potential of their dreams. Hence cholesterol has been demonised and targets have continually been reset by conflicted bodies so that the norm is no longer the norm and everyone can be told that they need statins.
Ironically, the most serious form of Familial Hypercholesterolemia would receive no benefit from statins anyway. As the extreme form is characterised by LDL receptors working barely at all, even the body going into crisis mode, and trying to take LDL from the blood stream with increased LDL receptor activity, will not work if the LDL receptors are not working sufficiently. Hence the LDL will stay in the blood stream with an extreme sufferer of FH and yet the statin has reduced what little chance the FH sufferer’s body had of making cholesterol within the cell.
There’s a great message on p304 of the book where the Yosephs suggest a notice that should be put up in washrooms:
Employees must wash hands before returning to work.
And do not touch the mevalonate pathway!
On Saturday 12th October 2013 I thought that the Daily Express front page had been mixed up with the Daily Mail. The Express is notorious for its statin scare tactic headlines. The Daily Mail is usually more balanced when it comes to these heinous drugs. Indeed the comments on most statin articles on The Mail on line show readers to be very knowledgeable about the lucrative and harmful cholesterol scam.
“Wonder drugs cut toll of strokes by 40%” was the Mail headline on Saturday. The Telegraph proclaimed “Strokes fall by 40% due to increased statin use” and The Mirror went with “Statins reduce number of stroke sufferers by 40% in 16 years”. (Those words recorded the original headlines. You may notice that all of these headlines have changed – see the Press Complaints Commission review at the end of this blog).
This is the original article from which these headlines totally inexplicably came. I have a copy of the full article and it doesn’t mention the word “statins” once. You can see that neither does the abstract.
The Daily Mail, The Telegraph & The Mirror
I have written to Jenny Hope, Rhiannon Williams and Damien Fletcher at The Mail, Telegraph and Mirror respectively asking them the following:
Please can you help me understand how this headline (their own particular headline inserted) came from this original article?
I have a copy of the full article, as well as the abstract, and neither mention the word statins even once. Neither claim that statins and strokes are even associated, let alone the causation you claimed.
Best wishes – Zoe
I will update this article with any replies received.
The Mail article appeared on line on Friday 11th October at 23.06pm and it formed the front page of the actual newspaper on Saturday 12th. The Telegraph online article is dated 12th October 12.35am. The Mirror article is dated 12th October 08.50am. It may be the case that the Telegraph and Mirror simply copied The Mail – we will see.
The lead researcher
I also emailed the lead researcher on the article – Dr Yanzhong Wang to ask:
Dear Dr Wang
Please are you aware of any press release that accompanied your recent article in the Stroke Journal?
I am struggling to see how your interesting original article was reported as follows when your article makes no mention of the word statins.
Thank you for your time
Kind regards – Zoe Harcombe
Dr Wang replied by return to say:
Thanks, Zoe. Yes, it’s our paper and you’d better ask DM journalists why and how they linked statins to our paper. A good summary of our paper in the media can be found here.
The study is an interesting one and the Guardian article is indeed a pretty fair summary.
I’ve gone through the full journal article and would give the headlines as follows:
The SLSR is the South London Stroke Register and it covers a defined region of Lambeth and Southwark. The study has managed to cover 357,308 people in this area and the region is multicultural – enabling the researchers to make comparisons between black and white people as well as men and women and people of different ages and people exhibiting different lifestyle factors (smokers or not, diabetic or not for example).
During a 16 year study (1995-2010) 4,245 first ever strokes were recorded among the population. That means that each person in the study (and there was no upper age limit for excluding people) had a 1 in 84 likelihood of having a first stroke during the entire 16 year study. That’s a 1 in 1,346 chance in any one study year. I don’t know about you, but I wouldn’t lose any sleep over those odds.
The study abstract noted that “Total stroke incidence reduced by 39.5% during the 16-year period from 247 to 149.5 per 100 000 population.” This is a relative, not absolute reduction: 247 in 100,000 is 0.247%; 149.5 in 100,000 is 0.1495%. Moving from 247 out of a big number to 149.5 out of the same big number is a 40% reduction but the absolute numbers are too small to get your head around. It’s the big 40% number that makes the headlines and makes things look much more impressive than they are. Would this, more accurate, headline be quite as attention grabbing?
“First time stroke incidence in South London falls from 0.247% to 0.1495% in 16 years”?
The most interesting findings of the study are:
1) That stroke incidence has fallen in this study, but…
2) …that this has not happened in all groups in the study. There has been no significant decline for the entire 15-44 age group. That alone is quite a finding. There has also been no decline in stroke incidence in black people.
3) The average (mean) age of first stroke has decreased from 71.7 to 69.6. This is another significant finding. We do not want people to be having their first stroke at a younger age.
4) The incidence of stroke is so massively correlated with age – you almost don’t need to worry about anything else. Table 4 has the incidence of first stroke by age and we can see that in the first period of the study (1995-98), there were 8.4 incidences per 100,000 in the 15-44 age range and 1,933.7 in the 85+ age range. The over 85 year olds were 230 times more likely to have a first stroke than the youngest group in the study. By 2007-10, these incidence rates had fallen to 6.7 for 15-44 year olds and 1,185.2 for the over 85 year olds. That’s still 176 times the incident rate in the oldest vs youngest group.
5) Women have lower incidence of strokes than men in every period of the 16 years studied. And women have higher cholesterol than men. Hence the gender facts render the cholesterol hypothesis invalid for strokes, just as they do for heart disease (women have lower heart disease and higher cholesterol).
The full paper has many useful details on the lifestyle attributes of participants. Are they a current smoker? drinker? do they have diabetes? have they previously had a heart attack?
This additional data can offer an explanation for the decline with one line – smoking. Smoking in white people has declined from 63.5% to 47.2% for 15-54 year olds and from 34.8% to 28.7% in white people over 55 years olds. Smoking in black people has halved from 42.6% to 21.4% for 15-54 year olds and has fallen from 24.9.8% to 18.6% in black people over 55 years old. That’s a halving of the smoking incidence in one case and substantial reductions in all groups.
Why have black people not experienced a lower stroke incidence despite this reduction in smoking? Could the diabetes information offer an explanation? Diabetes has increased five fold in black people aged 15-54 – from 4.3% in 1995-1998 to 21.4% in 2007-10.
The study does not offer these explanations as I do. Their suggestions in the discussion part of the paper are: “The decline in stroke incidence may be partly because of improvements in prevention, combined with an increase in healthy living. A recent study by Marshall et al31 showed antiplatelet and cholesterol-lowering treatment for treating before stroke risk factors had improved significantly from 1995 to 2010 in SLSR, similarly for both white and black patients. We do not have information on the use of these medications among different age groups.”
This is the only hint of something related to statins in the article: the mention that another study showed “cholesterol-lowering treatment… had improved”. I can only assume that this means there was more cholesterol-lowering treatment – it tells us nothing about end outcomes. And, as the SLSR study is quick to point out – we have no idea what meds any of the people in the study were taking. The study also explicitly states that they have no information about cholesterol levels in the stroke register.
And yet The Daily Mail has no doubt that “Wonder drugs cut toll of strokes by 40%”. I cannot put this any other way but to say that it is a lie. It is simply not true. It is disgraceful ‘journalism’.
Replies from the journalists
Jenny Hope also replied quickly (and briefly) to say “Hi Zoe, I spoke to and quoted researcher. Best wishes Jenny”. I sent back by return Dr Wang’s email showing the same bafflement as me as to how The Mail came up with their headline.
14/10/2013 UPDATE – I have filed three complaints with the Press Complaints Commission. If you share my view that these articles breach the first clause of the code – Accuracy – it only takes 5 mins to add your complaint. This may help.
I received a further reply from Jenny Hope (shortly after the PCC complaint was filed):
No, I spoke to Professor Charles Wolfe.
The quotes I used in my story were the following:
‘Professor Charles Wolfe, head of the Division of Health and Social Care Research, King’s College London, one of the three researchers behind the latest study, said declining stroke rates among older people were mainly due to better treatment.
He said ‘This group of people are being managed better, their GPs are prescribing medication for high blood pressure and cholesterol that is helping bring down the stroke rate.
‘It’s an optimistic message although we won’t see a drop in the total number of strokes because we have an ageing population, more people are living longer.’
Stroke rates among black people have remained the same, driven by rising rates of diabetes, partly because they are not a target group for GPs to identify factors that put them at risk.
‘High blood pressure is one of the biggest factors, along with high cholesterol and a sedentary lifestyle.
‘We need to see those at risk who currently miss out because they are thought to be too young for a stroke getting medical checks, advice and where necessary treatment’ he added.’
Prof Wolfe made it quite clear in conversation that blood pressure lowering medication and statins were behind the changing incidence in stroke rates. Obviously Prof MacGregor’s interest lies in declining salt consumption and its predicted effect. But he too gave me the following quote:
‘Statins cut the risk of stroke by 30 to 40 per cent so they have also played a part, but we need to do more.’
As with all research papers like this, it’s a sensible idea to talk to people with the knowledge and expertise in the area to seek their interpretation of the reasons behind findings – especially if the paper does not do so.
Best wishes. Jenny
Many thanks for this but my complaint still stands. This study was not about statins. It makes no mention of statins. It has no information whatsoever on any medications taken by any of the study participants and Professor Wolfe knows that. Prof MacGregor was nothing to do with this study and the linking of his comment with the 40% (relative) reduction from the SLSR study – in white people over 45 – was misleading. Also – did you request the evidence for Prof MacGregor’s claim, albeit unrelated to this study, that statins cut the risk of stroke, as this needs substantiating.
I am a big admirer of your work and am gutted to be having this exchange, as I thought you and The Mail were aware of The Great Cholesterol Con – to quote the work of someone we both know. It is simply not accurate to state “Wonder drugs cut toll of strokes by 40%” – not at all and certainly not as an outcome of this study.
Best wishes – Zoe
To which Jenny replied:
Sorry you’re not happy.
I’m equally a fan of The Great Cholesterol Con – ask Malcolm Kendrick.
However, I’m a reporter. I ask people in a position to know what they attribute the findings of research to and then we print what they say.
I’m equally fine with the fact that you don’t agree with their interpretation.
This is not about me being happy. It is about whether or not the statement “Wonder drugs cut toll of strokes by 40%” can be stated as fact and it can’t.
Update following the Press Complaints Commission investigations
The following amends were made by the newspapers following the PCC investigations:
Ms Zoe Harcombe complained to the Press Complaints Commission that the newspaper had published inaccurate and misleading information in breach of Clause 1 (Accuracy) of the Editors’ Code of Practice. The complainant said that the newspaper had incorrectly stated as a fact that a 40 per cent fall in the number of strokes was due to an increased use of statins. The study which reported the decreased incidence of strokes made no reference to statins.
The complaint was resolved when the PCC negotiated the alteration of the headline of the online article and the publication of the following footnote:
An earlier version of the headline stated that “Statins reduce number of stroke sufferers by 40% in 16 years”. We are happy to make clear that the King’s College London research itself did not attribute the reduction to statins.
Date Published: 06/12/2013
Ms Zoe Harcombe complained to the Press Complaints Commission that the newspaper had published inaccurate and misleading information in breach of Clause 1 (Accuracy) of the Editors’ Code of Practice. The complainant said that the newspaper had incorrectly stated as a fact that a 40 per cent fall in the number of strokes was due to an increased use of statins. The study which reported the decreased incidence of strokes made no reference to statins.
The complaint was resolved when the PCC negotiated alterations to the online article to make clear that the increased use of statins correlated to the decrease in the number of strokes, rather than necessarily causing the decrease. It also published the following footnote:
UPDATE: An earlier version of the headline stated that “Strokes fall by 40 per cent due to increased statin use”. We are happy to make clear that the King’s College London research did not attribute the reduction to statins.
Date Published: 14/11/2013
Ms Zoe Harcombe complained to the Press Complaints Commission that the newspaper had published inaccurate and misleading information in breach of Clause 1 (Accuracy) of the Editors’ Code of Practice. The complainant said that the newspaper had incorrectly stated as a fact that a 40 per cent fall in the number of strokes was due to an increased use of statins. The study which reported the decreased incidence of strokes made no reference to statins.
The complaint was resolved when the PCC negotiated the alteration of the headline of the online article and the publication of the following footnote:
NOTE: An earlier version of the headline stated that “Statins reduce number of stroke sufferers by 40% in 16 years”. We are happy to make clear that the King’s College London research did not attribute the reduction to statins.
Date Published: 14/11/2013
The last word
These amends are somewhat useless after the inaccurate headlines. People will be left with the completely non-evidence based impression that statins had something to do with an observational study, which had nothing to do with statins. I could never get the newspapers unprinted. However, I hope that three newspapers will think a bit more carefully next time before printing dangerously inaccurate and misleading headlines.
I ended this blog suggesting that we all need to demand evidence for the nutritional nonsense that we hear on a daily basis. I also advised not to hold your breath while waiting for the Australian Heart Foundation – or any other organization – to come up with such evidence. Here is why I am so confident that Jessie will be perfectly safe writing to the AHF. This is an argument that she won’t lose …
1) Because the experiment has not been done.
British authorities have been telling us since 1984 – in the document that changed dietary advice for Britain – that the study to assess saturated fat and heart disease has not been done and never will be done:
- “There has been no controlled clinical trial of the effect of decreasing dietary intake of saturated fatty acids on the incidence of coronary heart disease nor is it likely that such a trial will be undertaken.” (COMA, 1984). (REF 1)
When I wrote to the UK Food Standards Agency (FSA) in 2009 and asked them for their evidence against saturated fat – they referred me to a meta-analysis by Truswell (which I dissect in Chapter Eleven of The Obesity Epidemic: What caused it? How can we stop it?) Not only does this Truswell analysis fail to prove any case against saturated fat – it actually opens with the following words:
- “It has been accepted by experienced coronary disease researchers that the perfect controlled dietary trial for prevention of coronary heart disease has not yet been done and we are unlikely ever to see it done.” (Truswell, 1994). (REF 2)
Where have we seen those words before?! And in the letter from the FSA to me in 2009 they also used the same words – just in case I was in any doubt that the experiment had even been done.
- “The ideal controlled dietary trial for prevention of heart disease has not yet been done and it is unlikely ever to be done.” (FSA, 2009). (REF 3)
2) Because the experiment can’t be done
I have yet to find someone who condemns saturated fat who can accurately define it. The UK National Health Service thinks that saturated fat is: fatty cuts of meat; meat products, including sausages and pies; butter, ghee and lard; cheese, especially hard cheese; cream, soured cream and ice cream; some savoury snacks and chocolate confectionery; biscuits, cakes and pastries.
The Dietary Guidelines for Americans list: ice cream; sherbet; frozen yogurt; cakes; cookies; quick breads; doughnuts; margarine; sausages; potato chips; corn chips; popcorn and yeast bread as major sources of saturated fats. The Australian Government “Measure Up campaign” lists fatty processed meats and baked cereal based foods such as cakes, pastries and biscuits as sources of saturated fat, so this is not only a UK error.
Let’s look at the three different categories into which these claimed saturated fats fall:
Category i) baked cereal based foods, biscuits, (quick) breads, cakes, chocolate confectionery, cookies, corn chips, doughnuts, ice cream, margarine, pastries, pies, popcorn, potato chips, savoury snacks, sherbert, yeast bread, (frozen) yogurt. Category i we can call cr@p. It’s junk food. Processed food. I would not be at all surprised if it caused heart disease but it is NOT saturated fat. It is bad for us because of the sugar, flour, vegetable oil and myriad of processed and unpronounceable ingredients. If there is any real fat in any of these fake foods, it will be the healthiest part of the product by a margin.
Category i is a list of fake foods, which are in virtually all cases – mostly carbohydrate. However all of these fake foods contain all three macro nutrients (carbohydrate, protein and fat). Since they contain fat, they contain all three fats (saturated, monounsaturated and polyunsaturated). Every food that contains fat contains all three fats. There are no exceptions. Hence no one is able to say what it is in these foods that may be associated with heart disease. However, as Dr. T. L Cleave said “For a modern disease to be related to an old-fashioned food is one of the most ludicrous things I ever heard in my life.” So suspect the modern ingredients ahead of the real fat, which has sustained humans for 3.5 million years, or look ludicrous!
Category ii) is much smaller - fatty cuts of meat; meat products, including sausages and lard is the UK list and Australia specifies fatty processed meats. Category ii also has a lot of junk food. Processed food. The meat eaters that I know and respect are eating quality meat (and lard) from pasture living animals. We don’t eat processed meat. We do eat fatty cuts of quality meat, but our governments don’t appear to know that meat has more unsaturated than saturated fat – not that one real fat is better or worse than another – that’s why all three fats are in all foods that contain fat – but just to set the record straight. Lard has more unsaturated fat than saturated fat. And, bad as processed meat may be, it’s still more unsaturated than saturated fat.
Category ii also has the same problem as category i – saturated fat cannot be isolated. Much processed meat and definitely processed sausages contain all three macro nutrients again – carbohydrate, fat and protein. Quality meat, which has no carbohydrate, often has more protein than fat. Whether or not carbs are present and whether or not the meat is mainly protein or mainly fat, all three fats will be present. Again – it will be impossible to determine what it is in any of these foods that may be even associated with any illness.
We are left with category iii – the only food group on the planet with more saturated than unsaturated fat is dairy products. Repeat that after me! Butter, ghee, cheese, especially hard cheese, cream, soured cream have more saturated than unsaturated fat. Not that one real fat is better or worse – but just because we need to start using accurate terminology. Dairy products are also an excellent source of fat soluble vitamins – A, D, E and K – the ones that Brits are deficient in, if not Americans and Australians. Dairy products also contain carbohydrate (between a trace and about one tenth of the product composition) and protein and fat. They therefore contain all three fats. No study has been able to isolate saturated fat in dairy products and yet our governments will categorically tell us that it is the saturated fat in dairy, not the protein, not the carbohydrate, not the monounsaturated fat and not the polyunsaturated fat, which is out to get us.
The average Brit eats 39g of butter per week. The average Brit eats 730g of sugar per week. The average Brit eats 1,423g of flour per week (REF 4). That’s over 2 KILOGRAMS of nutritionally pointless sugar and fairly pointless flour – and we have the absurdity to demonise butter!
So now we know the following:
a) The authorities don’t know what saturated fat is. The majority of the products they call saturated fats are processed carbohydrates.
b) No one can isolate saturated fat from monounsaturated fat and/or polyunsaturated fat in the foods listed. In virtually all foods listed, no one can even isolate fat from carbohydrate and protein.
c) As I explain in this paper, the ONLY experiment that can be done to isolate fat involves swapping one oil for another. See section 7. We can swap olive oil out and sunflower oil in and change the proportions of the three real fats. We, however, also change nutrient intake – vitamins E and K. The control experiment, where we change one thing and one thing alone, cannot be done.
If they’re not too busy trying to work out from the first blog how dietary fat can end up in arteries or metamorphosise into LDL, Jessie may well get an attempt at a defense back from the Australian Nonsense Foundation. However our first question back will be – what did you assume saturated fat to be? and our second will be – how did you isolate it?
Now stop holding your breath!
REF 1 – Committee on Medical Aspects of Food Policy, “Diet and Cardiovascular Disease: Report of the Panel on Diet in Relation to Cardiovascular Disease”, (1984).
REF 2 – A Stewart Truswell, “Review of dietary intervention studies: effect on coronary events and on total mortality”, Australian New Zealand Journal of Medicine, (1994).
REF 3 – Letter from the FSA to Zoë Harcombe, (25 September 2009).
REF 4 – See refs 120 and 121 from the obesity book
A super woman called Jessie has been taking on the Australian Heart Foundation just as I have taken on the British Heart Foundation and so has Dr John Briffa. If you want to keep up with these terrific two – they are on twitter as @jessiereimers and @drbriffa.
Jessie started this petition and got enough support to elicit a reply from “Kerry” at the Australian Heart Foundation (AHF). Jessie has blogged on this here and put her own comments alongside the nonsense that she got back from the AHF. These are the questions that I hope Jessie can go back with because we need to stop accepting nonsense with claims that it is evidence based. It’s time to start demanding that the evidence be presented – because we know that it doesn’t exist.
The letter from Kerry/the AHF is below – Kerry’s words are in blue (verbatim) and mine are in red:
Thanks for getting in touch with us so quickly. We recognise that this is a subject that people feel passionately about and clearly it is one that the Heart Foundation and yourself disagree on.
We believe it is fair and reasonable that the Heart Foundation’s position is represented on the petition page.
The Heart Foundation recommends switching from butter to margarine as one way to reduce the amount of unhealthy saturated fat in our diet.
Please provide evidence that saturated fat is unhealthy. Please also explain why all three fats (saturated, monounsaturated and polyunsaturated) are found together in all foods that contain fats. There are no exceptions whatsoever. Why would nature do this if one were bad and another good? (see my paper here)
Our recommendations are based on good quality scientific evidence.
What evidence? You have provided none thus far. Please do so.
The vast body of evidence shows that saturated fat raises bad cholesterol levels, clogs the arteries and increases the risk of heart disease. We need to reduce the amount of unhealthy saturated fat in our diet and replace it with healthier fats.
Again – what evidence? You have provided none thus far. Please do so. By “bad cholesterol levels” you are presumably making the common error of calling a Low Density Lipoprotein (LDL) “bad cholesterol”. It is not even cholesterol, let alone bad. It’s a lipoprotein, which carries protein, triglyceride, cholesterol and phospholipids around the body to do vital repair work.
How can dietary fat clog arteries? Assuming that you eat your food, you don’t intravenously inject it! Please describe the process by which something that we eat can find its way out of the digestive system to clog an artery?
Please read this and then explain how it would even be possible to replace saturated fat with other fats without changing anything else. Even if this were desirable (and it isn’t) – please explain how it is possible.
We believe that the research on the health benefits of coconut oil is inconclusive, but we do know that coconut oil, milk and cream are all high in unhealthy saturated fat.
Again – how is saturated fat unhealthy? Why would saturated fat be in every real food that contains fat (meat, fish, eggs, dairy products, nuts, seeds, avocados, olives) if it were unhealthy? You have provided no evidence thus far. Please do so.
Kerry’s reply then contains more nonsense about the AHF ‘tick’ programme for their endorsements of fake foods like chemically solidified, bleached, deodorized, emulsified, coloured, margarine and then Kerry refers people to these pages of their web site…
For more information, visit:
This page has no evidence for any of the allegations made against saturated fat – hence Jessie has every right to go back and demand evidence for the allegations made. This page also has more nonsense: “Saturated fat is the fat that raises our LDL…” Dr Malcolm Kendrick threw out this biochemistry challenge in his book The Great Cholesterol Con and it has not been answered since (2007). How can saturated fat raise LDL? What is the biochemical process by which this is even possible? Jessie – please demand that the AHF explain HOW this can happen while claiming that it DOES.
This link is just PR nonsense for the AHF tick nonsense. Again – there is no evidence presented whatsoever for the allegations made against saturated fat.
If I said that Kylie Minogue or Russell Crowe were seriously bad for your health, would cause heart disease, clog your arteries, raise some fictitious nonsense called bad cholesterol and that you should avoid them like the plaque they would sue the last penny out of me. Just because saturated fat doesn’t have the ability to defend itself doesn’t mean that those who attack it should get away with their their slander and libel. Jessie, Dr John and I are not the only ones defending real food and the real fats and nutrients contained therein. We all need to demand that the accusers present evidence. Please join us in demanding evidence from every attacker of real fats and real food. Just a word of warning – Don’t hold your breath while waiting for evidence to be presented!
This is a follow up to this post. The original post resulted in a number of comments from angry mums who were appalled at the Netmums’ support for Kellogg’s and the general outrage led to this article in the Mail on Sunday on 22nd September 2013.
The Mail took an interesting (unusual?) angle about one particular mum allegedly being censored by Netmums – saying that her anti-Kellogg’s comments were moderated out whenever she put them on the Netmums site.
The story so far
In the 2008 Kellogg’s annual report they announced in the opening statement “We are aggressively embracing digital media, which affords an efficient, cost-effective way to target specific audiences, providing an excellent platform for developing our brands… In addition, we are successfully building relationships with moms around the world ...”
Targeting ‘moms’ and digital media. Surely an organisation like Netmums would see through that.
Kellogg’s then do some research about breakfast skipping and publish it in the journal of the friend-to-the-fake-food-industry: The British Nutrition Foundation. Members and sustaining members here and here.
The study isn’t about poverty – it’s about breakfast skipping. The bigger story has already been covered – the 10-15 year old girls skipping breakfast because they are dieting.
Another bigger story is that one in three final year primary school children are overweight or obese – may I suggest because of sugary cereals and other fake foods, which have come into the human food chain in the blink of an eye in terms of evolution.
In the first post, I could not believe that Siobhan Freegard could have been naive enough to fall for what had been a Kellogg’s promotion from start to finish.
It turns out that I was the naive one…
Netmums and Kellogg’s have a commercial relationship…
… and have done so for three years. Netmums refused to answer the Mail on Sunday’s question about how much the deal was worth.
And that’s the story. This is a commercial arrangement between two organisations for mutual benefit. Netmums gets money; Kellogg’s gets access to mums to make more money and money makes the world go round.
This was not about Netmums falling for a story about poverty. The Hoyland article was published in 2012 – they’d already been in bed together for two years.
The love-in started in September 2010 with ‘Greg’, the MD of Kellogg’s, getting direct access to mums. If you get a moment – do look at some of the comments. They are a depressing mix of falling for Greg’s invitation to name your favourite Kellogg’s concoction and not seeming to care about the sugar content of children’s cereals to more reassuring challenges about the sugar in the products, the price of Kellogg’s vs. own label, the number of ingredients and clearly peddling the products to children.
Greg’s replies start at #78 and the first comment made is the standard Kellogg’s defence. It was used when the Children’s Food Campaign challenged Kellogg’s about the Coco-pops advert. When I wrote to Kellogg’s to support the Children’s Food Campaign with this particular campaign their reply to me was: “When it comes to sugar, one portion of Kellogg’s Coco Pops has just 10.5g – approximately two teaspoons. To put this into context: a portion of fruit yoghurt contains 20g of sugar and toast and jam has 13g.”
This is their standard reply and Greg knows it. In comment 78 Greg says “Firstly, I thought you might appreciate the facts on sugar. The media coverage of breakfast cereals isn‘t always balanced so I think it‘s important you get the truth. To put things into perspective, a serving of cereal, like Coco Pops and Frosties, contains just two teaspoons of sugar which is less than a fruit yoghurt or jam on toast.”
Don’t try to defend the sugar content because it is indefensible. Compare it to other products that contain sugar to show that it is equally unhealthy – with the implication being that it is equally healthy.
Greg then gets the free rein to say how much calcium is in a serving of Kellogg’s & milk – I think you’ll find that the milk provides the calcium Greg (actually they’ve added calcium to the cereal as well – a high calorie vitamin tablet in effect). They’ve also added other vitamins to cereals because there are none left naturally by the time the sugar and starch have been processed together. And so on…
Give a child a breakfast
Back to the #giveachildabreakfast campaign, because it was this that first attracted my disbelief. Siobhan Freegard defends her position on this here.
Netmums: “With regard to the Give a Child a Breakfast campaign, Netmums – and I personally – chose to become involved in this campaign as we have seen first-hand the rise of families unable to feed their children in the UK…”
Me: This isn’t about poverty. Yes there are children going to school without having eaten breakfast. There are many different reasons for this – not least girls worried about their weight. Netmums should be worried about this. One in three final year primary school children is obese or overweight. Netmums should be worried about this. Netmums and Kellogg’s are quoting statistics for breakfast skipping, engineered by Kellogg’s – the Kellogg’s study was not about poverty.
If this were about poverty Netmums would donate their fee from the Kellogg’s commercial relationship and Kellogg’s would ban their own products from any breakfast clubs because more children could be fed cheaper and better on eggs and oats.
Netmums: “There is no national register for hungry children – so it is easy for authorities and the affluent to assume it isn’t really happening, to look away. But there is a growing pile of authoritative research showing it is a very real problem. I am happy to support a business like Kellogg’s who are investing in further research and, actually doing something to help.”
Me: Now you are being naive. Kellogg’s make breakfast cereals. Breakfast skipping, for whatever reason, can impact their sales and profits. Kellogg’s have a vested interest in coming up with studies to make sure that people don’t skip breakfast – for whatever reason.
Here’s a Kellogg’s PR release, sorry “factsheet”, all about why we shouldn’t skip breakfast. At the end – there’s all that evidence to which you may be referring. I just took the last name on the list – A. P Smith – as it appears quite a few times. Turns out Andrew P. Smith is working in the School of Psychology in Cardiff University. Here’s a paper he published in 2010 all about the benefits of breakfast. Ignore the article – look first at the “Acknowledgements” on page 6 “The present research was carried out with the financial support of the Kellogg Marketing and Sales Company Limited.” I bet it was! This took five minutes – if you’ve got more time, you may like to look at the other ‘research’ being funded by Kellogg’s to try to ensure that breakfast skipping is eliminated.
The ethical response
I was approached in October 2012 as follows – by a dietician (love them!) – to try to help the cereal industry:
I’m a freelance dietitian working on a project to set up stakeholder meetings for the Association of Cereal Food Manufacturers (ACFM) which represents UK breakfast cereal manufacturers.
ACFM are keen to understand how breakfast cereals are viewed by key opinion leaders, such as yourself, and to gather opinions about what they should be doing in future as an industry group. They have also commissioned a literature review and would like to elicit views on the scientific evidence.
I was wondering if you would consent to meet ACFM representatives for an hour at a time and place most convenient for you. You would also be sent a copy of the literature review for comment.
Do let me know if you are agreeable to this in principle. Look forward to hearing from you.
My reply was as follows:
I’m the wrong person to ask here. I will never do anything to help any fake food manufacturer. I loathe fake food associations and the companies they represent. I abhor the shameless way in which they market (in this case) sugary cereal to children, putting their profitability above the obesity epidemic, type 2 diabetes and other things to which they contribute. What I would love them to do in the future as an industry group is to go out of business.
We should be eating eggs for breakfast – not concoctions of sugar and flour, so deficient in natural nutrients that fortification is necessary (and then disingenuously promoted as healthy).
Best wishes – Zoe
If only Netmums had replied similarly.
The alternative title to this post is “How Kellogg’s manipulated mums to get near their children.”
This blog is serious and about something seriously clever. It involves one of the two most predatory companies when it comes to pushing junk on our children – Kellogg’s. Coca-Cola is the other chief culprit.
If I told you that the founder of Netmums would be doing a promotional video, on behalf of Kellogg’s, on the home page of one of their sites, smiling like a paid celebrity endorser to close with: “And if you are buying Kellogg’s – look out for the special pack”, you would think I was joking. I wish…
On Monday 9th September #GiveAChildABreakfast was trending (promoted) on twitter. I was stunned to see that one of the top tweets was from @Netmums: “Please retweet – For every share tweet or watch … Kelloggs will donate a breakfast on your behalf #GiveAChildABreakfast”
Thankfully my tweet was retweeted enough times to become a top tweet to counter this: “PLEASE do not support this #GiveAChildABreakfast disgrace. Allowing a sugar pusher like Kellogg’s access to our children is evil.”
Among 30 or so retweets, I did get some choice replies:
@DaleHarrison92 told me “get a grip you would rather see a child go on an empty stomach than have a bowl of cereal. Not the work of the devil.”
Rachal Winter (@rachal_ava) took a similar line: “get a life they are helping children that’s all that matters! Someone has got to feed these kids!!”
To which I couldn’t resist replying “Um – isn’t that what parents are for?!”
But anyway – helping children or helping Kellogg’s?…
The marketing person who conceived this idea deserves the marketing world equivalent of an Oscar. It is genius.
Organisations that protect children, like the Children’s Food Campaign, exist to counter the power of the likes of Kellogg’s and Coca-Cola. Here’s are a couple of examples…
In early 2010, Kellogg’s launched a campaign trying to get children to consume 35% sugar Coco Pops, not once, but twice a day. “Ever thought of Coco Pops after school?” was the slogan – calculatedly placed on bus shelters where children would be waiting for transport to and from school. Christine Haigh of the Children’s Food Campaign launched a counter campaign: ”It’s outrageous that Kellogg’s, which is a partner of Change4Life, is encouraging children to eat more of their sugary products.”
The Guardian reported in April that 26 people and organisations complained to the Advertising Standards Authority that the advert was irresponsible because it targeted schoolchildren, and encouraged them to eat a snack that was particularly high in sugar. The ASA rejected the complaints, accepting the Kellogg’s argument that although Coco Pops are approximately 35% sugar, there is no current UK or EU definition of “high” as far as sugar content is concerned. I wonder how many of those who complained have fallen for the latest scam?
“Eat football, sleep football, drink Coca-Cola” was the banner adorning the playing field at Bexley Heath School in Nick Cohen’s brilliant 2004 Channel 4 programme on how the fake food industry targets our children. The Cola banner was accompanied by a large Kellogg’s Frosties banner behind the goal posts. In December 2008, the lobby group Sustain and the Children’s Food Campaign published an excellent exposé of ‘educational material’, such as this, produced by the food industry entitled “Through the Back Door.”
Against this backdrop of criticism, the cunning marketer has the idea – if we can create a sob story that children are starving and present Kellogg’s as the white knight that comes to the rescue – maybe these campaigners will stop attacking us? Maybe we can position Kellogg’s as the marvellous saviour of hunger in poverty stricken Britain and then this inconvenient opposition will look really mean trying to stand in the way of a child and their right to a 35% sugar breakfast?
If that marketer could have imagined that they would not only silence most opposition, but that they would have Netmums making videos for them, Heart FM as a radio partner and the Mirror group backing them, they would have barely believed it themselves.
I knew that Kellogg’s had been trying to extend their breakfast clubs since 1997. I didn’t know that this particular campaign is in its third year.
I found that out on the ‘money-can’t-buy’ PR for Kellogg’s on the Netmums site : “Here at Netmums we know that times are tough, and lots of us are struggling financially, but for many families, it’s just the start of their problems. That’s why we’re so delighted to tell you that Kellogg’s is bringing back its Help Give A Child A Breakfast campaign. Now in it’s (sic) third year, this heart warming initiative works with schools to provide breakfast clubs for the most vulnerable children in society, making sure that these kids start the day with full tummies and happy hearts. This year, Kellogg’s hopes to donate 2 million breakfasts to the children and families who need them most, and they need your help.”
“Heart warming” – oh for goodness sake! Wake up and smell the money.
As Netmums’ founder, Siobhan Freegard, explained on the video (please don’t watch it – another sugar injection is given to a child every time you do so – I’ve already condemned one child to 35% sugar Coco-Pops for a day by watching it to write this note.) “Collectively there is something we can do to make a difference. Kellogg’s have pledged 2m breakfasts, through breakfast clubs, through their “giveachildabreakfast” campaign.”
The idea is that UK PLC does Kellogg’s marketing for them. We tweet, Facebook, blog – generally spread the word about how wonderful Kellogg’s are trying to get sugar in children’s tummies – and Kellogg’s then enjoy a terrific, attack-free, promotion until they hit their upper cap of expenditure. The small print is here: “Kellogg’s will target to pledge £400,000 under the GACAB initiative for 2013.” That wouldn’t even get Kellogg’s one two-minute advert during X Factor. As I said – genius marketing.
What about the children who are already getting a great breakfast at home? Those children lucky enough to have mums who know all about real food and healthy eating. Will those children think it’s more fun to attend a breakfast club (a party before school?) and thus start getting Kellogg’s sugary cereal for breakfast instead of the eggs/milk/yoghurt that smart parents would have been feeding them? This Kellogg’s sales strategy is harmful on so many levels.
Every site that covers the giveachildabreakfast [GACAB] campaign positions the issue as follows:
The Kellogg’s campaign home page says: “Sadly, 1 in 7 children in the UK* goes to school without breakfast every day. Together, we can give 2 million kids a better start.”
Netmums says: “It’s hard to believe, but every morning, 1 in 7 children in the UK goes to school without breakfast in their tummies*. For many families, skipping the most important meal of the day isn’t a choice, it’s a necessity. One of the main reasons that lots of kids are starting the day on an empty tummy is sadly due to the increasing number of families in this country who live in food poverty.”
Crikey – no wonder The Mirror Group got involved.
The asterisk takes you to an academic-looking reference: Hoyland et al (2012) Nutr Bull, 37 (3), 232-40, UK Kellogg Report, “No food for Thought. The impact of hunger in UK classrooms 2012″. The original article was not easy to find and the whole thing is not on free view, but here’s the abstract.
65 schools were sampled – 38 primary and 27 secondary – from which 3,311 children aged 5-15 years were surveyed about their breakfast consumption. “The results indicated that 86% of children ate something before school (whether at home, on the way to school or at a school breakfast club). Of the remaining 14% of breakfast skippers, a third reported not eating anything until lunch time. The extent of breakfast skipping was higher in girls than boys, and higher in secondary than primary school pupils.”
This study was not about poverty, family income or whether or not families could provide breakfasts for their children. It was about breakfast skipping for whatever reason. Note the “girls skip more than boys” and “secondary school children skip more than primary.” This study reinforced a much larger study, conducted by The Exeter based Schools Health Education Unit, which surveyed 32,000 10-15 year olds in 2009. This non-conflicted study led to the headline “The girls living on just one meal a day: teens risk health to copy stick thin celebrities.”
Notice also that only a third of the 14% – barely 1 in 20 – doesn’t eat anything until lunchtime. That’s probably those 11-15 year old dieting girls again. Did 10 of the 14% grab a banana or a packet of nuts leaving the house and have this long before lunch time? This is as much (more?) about children valuing sleep more than breakfast and being quite happy to eat something once they’ve woken up. It tells us nothing about poverty-driven breakfast absence in the UK. But don’t let the truth get in the way of a good story.
Would it be better for every boy and girl under 15 to start the day with eggs? Absolutely. Make that every human. However, that’s not what’s on offer here. When the concoction that Kellogg’s is trying to stuff into our children is more sugary than the doughnut they might pick up en route, don’t give me the line that Kellogg’s are trying to do a good thing here.
And if this is about poverty/cost, then a quick check on Tesco groceries tells us that Coco Pops are 36p per 100g; Rice Krispies are 39p per 100g; and Coco Pops Cocorocks (whatever the heck they are) are 68p per 100g. Meanwhile Quaker oats are 20p per 100g and Tesco every day value oats are 8p per 100g. If Kellogg’s really cared – they could spend their £400k marketing budget on the Tesco oats and feed far more children and with zero added sugar.
Before we move on from this study, reiterated ad infinitum as ‘evidence’ for the one in seven positioning, it should be noted that Nutr Bull stands for Nutrition Bulletin (I know – the second word should have stayed abbreviated!), which is a British Nutrition Foundation publication. As a reminder – here are the members of the British Nutrition Foundation and here are the sustaining members. You should be able to spot Kellogg’s in among every other fake food and drink company you can think of.
The last name on a journal paper is usually the supervisor. The last name on this paper is J. L Walton. Click on author information and you will find that Jenny Walton’s organisation is “The Kellogg company, Manchester UK” and the person to whom correspondence should be addressed is firstname.lastname@example.org.
Worse, the first person named on a study does the work. In this case, the first person named is Dr Hoyland, who turns out to be Dr Alexa Hoyland. The author information listed for Dr Hoyland says “Institute of Psychological Sciences, University of Leeds, Leeds, UK.” Do a simple Google search and you find that Dr Hoyland is UK & ROI Senior Nutrition Manager at Kellogg‘s, which seems underhand at best and fraudulent at worse. I then wondered what the second listed reference to Leeds University was – the School of Food Science & Nutrition, University of Leeds, Leeds, UK. Check the logo that hits you on the first search page that you find here.
This story has been created, engineered and manipulated by Kellogg’s from start to finish.
Kellogg’s aren’t just concerned about children skipping breakfast (for whatever reason). When the product you sell is one eaten at breakfast you want to campaign relentlessly to make sure that no one skips breakfast. Apparently 2-30% of men (bit vague) and 24% of women skip breakfast. And how do we know this? Because Kellogg’s tell us. Breakfast skipping harms Kellogg’s profitability – it must be stopped.
Kellogg’s have got previous
One of the reasons that this incensed me so much – and probably the Children’s Food Campaign too – is that people working in the arena of obesity are all too familiar with the tactics of the likes of Kellogg’s and Coco-Cola.
The original eatbadly plate was called The Balance of Good Health. It was launched by the UK Department of Health in 1994. This original version was Kellogg’s branded (The eatbadly plate replaced this in 2007, but the cornflakes clearly shown will still trigger the thought “Kellogg’s” in the minds of most people.) Kellogg’s (and Coca-cola – see the red can on the plate) have managed to infiltrate ‘healthy’ eating messages from the outset.
Kellogg’s are a partner of the American Dietetic Association, as are Coca-cola. Kellogg’s are a major partner of the Dietitians Association of Australia.
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).
Kellogg’s are one of many fake food companies who have associated themselves with The Department of Health, Change4Life programme, managed by the UK National Health Service. The £75 million programme was criticised for the involvement of junk food partners from the outset. Marketing Week noted that Richard Watts, co-ordinator of the Children’s Food Campaign at lobby group Sustain, was concerned that allowing companies to use the Change4Life logo gave companies “tacit support”.
Kellogg’s have been sponsors of the Amateur Swimming Association’s (ASA) awards scheme, with the “Kellogg’s Swimtastic Awards” as a key annual event. This partnership started in 1996 and 15 million children had taken home a Kellogg’s branded award by the mid noughties. The ASA annual report (2004) said, under the heading “Another Grrreat Year”, “It’s been another financially successful year for the Kellogg’s Frosties ASA Awards Scheme… The Annual Awards Gala Dinner, now known as Swimtastic, was held… Tony the Tiger was of course around to lend a helping paw of support to everyone.” Oh love him!
Kellogg’s bottom line
The company’s annual report is a good starting place to understand organisational priorities. The opening statement in the 2008 annual report for Kellogg’s says: “At Kellogg Company, our goal is to drive sustainable and dependable growth by leveraging the talents of our people and the power of our brands, and by fulfilling the needs of our consumers, customers and communities.” Sales in 2008 were nearly $13 billion, making Kellogg’s the world’s leading producer of cereal. More than 1,500 products were marketed in over 180 countries. Kellogg’s “met or exceeded” all growth targets, even during the recession, and the opening statement from the chair and president ends with …”we remain committed to delivering sustainable and dependable growth into the future.”
The word “growth” appears 24 times in the brief opening statement. The word “obesity” appears once in the 98 page report: “Our innovation teams develop nutritious foods that take into account major public health issues, such as diabetes, heart disease and obesity.” In the 2009 annual report, the word growth appears 85 times; the word obesity not once. Why would Kellogg’s sponsor so many different dietary organisations when obesity does not appear to be a subject worthy of mention in the annual reports?
The opening statement admits: “We are aggressively embracing digital media, which affords an efficient, cost-effective way to target specific audiences, providing an excellent platform for developing our brands. We have already tapped the Internet to gain significant brand development traction for Special K, Frosted Flakes, Apple Jacks, Kashi, Rice Krispies, Morningstar Farms and Pop-Tarts. In addition, we are successfully building relationships with moms around the world through Kelloggs.com and KelloggNutrition.com. Our strength in brand building allows us to successfully drive new business opportunities that expand our portfolio and reach more consumers.”
When I shared these growth missions in my obesity book I actually asked the question - I wonder how ‘moms’ feel about being targeted and manipulated in this way?
We now know. They’ll be fronting the campaign!
On 23 August 2013 news headlines were “Red meat could raise Alzheimer’s risk.”
“Iron in red meat could raise the risk of Alzheimer’s” said the Daily Mail actual newspaper. On line we had a fuller headline: “Eating too much red meat could increase the risk of Alzheimer’s: Scientists warn build-up of iron may damage the brain.”
A quick check on line revealed that the story was making global headlines: “Is iron in steak to blame for risk of Alzheimer’s? Study suggests excess red meat bad for the brain” was the story on the Canadian Global News site.
The original article
The original journal article was published online on 21 June 2013 in The Journal of Alzheimer’s Disease. The full title of the article is “Increased Iron Levels and Decreased Tissue Integrity in Hippocampus of Alzheimer’s Disease Detected in vivo with Magnetic Resonance Imaging.”
This catchy title was inexplicably overlooked until a press release was issued on the 20 August 2013, on the main Journal of Alzheimer’s Disease web site, with the more media friendly headline: “UCLA study suggests iron is at core of Alzheimer’s disease.”
I haven’t paid $27.50 to get the full article, but I can confirm that the abstract (summary) of the article makes no mention of meat, or even diet, at all (you can read it for yourself on the link to the original journal article above).
The abstract tells us that the study hypothesised that “with age, iron accumulates in the brain and may contribute to the risk of developing age-related diseases such as Alzheimer’s Disease (AD).” Previous studies of AD have (according to the abstract) shown that an area of the brain called the hippocampus is heavily damaged with AD, while the thalamus seems to be resistant to AD damage.
The study set out to assess iron levels and evidence of tissue damage in the hippocampus and thalamus in 31 people with AD compared to 68 people without the disease. The participants undertook MRI scans to quantify (ferritin) iron levels in the two areas of the brain being studied. The results were that “compared with healthy controls, AD subjects had increased (ferritin) iron in the hippocampus but not in the thalamus.”
The study concluded: “The data shows that in AD, hippocampus damage occurs in conjunction with ferritin iron accumulation. Prospective studies are needed to evaluate how increasing iron levels may influence the trajectory of tissue damage and cognitive and pathologic manifestations of AD.” i.e. we assume that the hippocampus damage and ferritin iron levels are related and further studies are needed to understand how iron levels could be related to tissue damage.
Keywords for the study were “Alzheimer’s disease, chelation, dementia, ferritin, field dependent relaxation rate increase (FDRI), iron, magnetic resonance imagining (MRI), myelin, prevention, treatment.” And that was it. No mention of red meat, diet, ingestion of iron or anything related to the headlines that were to follow.
The press release
The press release is quite a technical introduction to current thinking on Alzheimer’s – that it’s related to two proteins that can disrupt signalling between neurons. This would have the effect of impacting the body’s messaging system and would explain the cognitive impairment observed with Alzheimer’s.
The PR note explained that the study by Bartzokis and his team hypothesised that iron could be a factor and not just these two proteins. Nothing in the continuing copy looks like it would excite the world’s media (“myelin”, “oligodendrocytesm”, “oxidative damage” etc, yawn, yawn). But then we have the wakeup call in the penultimate paragraph:
Bartzokis noted: “The accumulation of iron in the brain may be influenced by modifying environmental factors, such as how much red meat and iron dietary supplements we consume and, in women, having hysterectomies before menopause.”
Red meat! Oh how the media loves a good bit of red meat bashing:
Red meat and cancer
Red meat and diabetes
Red meat and dying and more Red meat and dying.
The mention of red meat and an overlooked study published two months earlier suddenly appears in English newspapers published in Majorca (we picked this up while on holiday) and on Fox News.
The leaps to be made
For red meat to impact Alzheimer’s, as implied, ALL of the following need to hold true:
1) Alzheimer’s sufferers need to ingest and absorb excessive dietary iron from red meat;
2) Dietary iron needs to end up in the hippocampus (and not the thalamus) area of the brain;
3) This iron needs to cause tissue damage;
4) This tissue damage needs to be responsible for Alzheimer’s.
1) Alzheimer’s sufferers need to ingest and absorb excessive dietary iron from red meat.
The study falls at the first hurdle. We don’t even know if the 31 people with Alzheimer’s Disease consumed red meat. They could all have been vegan for all we know.
The study falls at the first hurdle on a population level. The 2011 UK average iron intake was 11.8mg (p28 of the Family Food Survey) The RDI (Reference Daily Intake) for iron is 18mg. There is thus no evidence for iron excess – it is rather iron deficiency that we should worry about.
The researchers could have taken blood iron levels of the participants to see if AD sufferers and/or control people had generally excessive or deficient iron levels. This would have been a crucial piece of information – excessive iron in the blood and in one part of the brain is a very different puzzle to deficient iron in the blood and ‘excessive’ iron in one part of the brain.
The study falls at the first hurdle for another, easily assessable, nutritional reason – red meat is a source of iron, but it is by no means the best source, let alone the only source. Here is iron intake per 100g of the following foods:
- Red meat 1.5mg
- Spinach 2.7mg
- Sardines 2.9mg
- Cocoa powder 13.9mg
The USDA all foods database will tell you that the richest sources of iron are thyme, parsley and marjoram with 124mg, 98mg and 83mg of iron per 100g of product respectively. We use spices in very small quantities, however, so we should continue down the list of highest providers of iron until we find a food that we would consume in 50-100g portions. This turns out to be fortified sugary cereals, with Kellogg’s oat bran flakes having 63mg of iron per 100g of product. That’s 45 times the iron levels of our sirloin steak!
The top 20 sources of iron, according to the USDA bible, are 7 spices, 9 fortified cereals, 2 baby foods and 2 meats – whale and seal. I don’t know about you but I’ve never eaten whale or seal. I have eaten baby food, fortified cereals (thanks mum) and spices. Beef or lamb spleen is the only other meat in the top 50 – baby food makes up most of the places from 21-50. Probably because iron is a pretty vital mineral to ingest.
So why was the headline not “Bran flakes could raise the risk of Alzheimer’s”? or “Baby food could raise the risk of Alzheimer’s.” Or even oily fish or spinach or high cocoa content dark chocolate? The simple answer is that red meat bashing is a media past time and the other products are not demonised in the same way.
Finally, hurdle 1 notes that iron not only needs to be ingested, but absorbed. Iron needs vitamin C for its absorption. Hence someone with high iron intake with insufficient vitamin C intake will have deficient iron levels due to impaired absorption. Someone with moderate iron intake and high vitamin C intake is likely to optimise their blood and body iron levels. How about “Too much vitamin C can cause Alzheimer’s”?!
Back to the four steps, which need to all hold true, to justify the world headlines:
2) Dietary iron needs to end up in the hippocampus (and not the thalamus) area of the brain.
The study did not try to show that dietary intake of iron had accumulated in any part of the body. The original journal article did not even consider dietary sources of iron. Notwithstanding that the study has already fallen at the first hurdle, it also falls at the second.
3) This iron needs to cause tissue damage.
The study does not claim that iron causes tissue damage, so it openly falls at the third hurdle.
The study concludes: “hippocampus damage occurs in conjunction with ferritin iron accumulation. Prospective studies are needed to evaluate how increasing iron levels may influence the trajectory of tissue damage and cognitive and pathologic manifestations of AD.” i.e. we observe iron levels and hippocampus damage together, but studies are needed to see how these could be related.
The opening of the article offers one mechanism: “Although essential for cell function, increased tissue iron can promote oxidative damage to which the brain is especially vulnerable.”
This probably should be the starting point for further research – why are higher levels of iron found in one part of the brain and not another? Are body iron levels higher generally in people with higher levels in the hippocampus? Does iron go to the damaged tissue to repair damage or did the iron cause the damage? There is a wealth of further research to be done before going anywhere near red meat.
Talking about areas for research, the press release said that two proteins, and their impact on neurons, are currently held by “most researchers” to be the cause of Alzheimer’s. A growing number of researchers are calling Alzheimer’s “type 3 diabetes” – the response of the brain to glucose, just as type 2 diabetes is the response of the body to glucose. That would be a worthy area for research.
4) This tissue damage needs to be responsible for Alzheimer’s.
Does Alzheimer’s damage tissue in the hippocampus (and not the thalamus) or does tissue damage in the hippocampus (and not the thalamus) cause Alzheimer’s?
Bartzokis needs to get some Roland Rats or Mickey Mouses and induce the same tissue damage and see if Alzheimer’s develops.
This is the kind of assessment that the media should have done – not just leap four unproven steps and join the red meat attackers.
Dear journalists. Please – I beg you – please don’t be part of the demonisation of the food that we have been eating for the longest time in human development. Surely – if it’s something new you’re after – NOT bashing red meat would be a refreshing change!