Men’s Health and Eat this, Not that – bad science at its worst!
“Swap cheddar for edam and Snickers for Flakes and you could lose two stone in a year” screamed the Daily Mail article headline on 11 January 2012.
The claim comes from a study “by the team behind Men’s Health magazine”. As you will be able to see from the link, the article lists 21 items and suggests that you swap one for the other. Examples include:
- Have crunchy nut cornflakes instead of Special K honey clusters to save 54 calories;
- Have half a Tesco simply peperoni pizza instead of half a Tesco cheese feast deep crust pizza to save 40 calories;
- Have a Flake instead of a Snickers to save 161 calories. You’ve got the idea.
The 21 items add up to a saving of 2,205 calories. The article then says that – if you save these each week you could lose two stone in a year!
Here’s the maths – 2,205 * 52 weeks = 114,660 calories. It is then wrongly assumed that one pound = 3,500 calories and so 114,660 is divided by 3,500 to assume that 32.76lbs would be lost in a year. The calorie theory (as this 3,500 assumption is known) is also supposed to be about fat lost alone. Hence, if you believe the theory, people should lose 32.76lbs in fat alone and more on top in lean tissue (sadly) and water – approximately 15% on top – so nearer 38lbs in total.
Here are a number of ways in which this is stupider than a very stupid thing!
1) One pound does not equal 3,500 calories. See here to save me duplicating the summary. Write to Men’s Health/The Daily Mail and demand evidence for this formula – can they succeed where seven UK public health and obesity organisations failed?
2) You will not lose 1lb for each deficit of 3,500 calories (and nor will you gain 1lb for each surplus of 3,500 calories). See here to save me duplicating the summary. The figure of an average of 11lb vs an expected 100+lbs has been confirmed in a few recent studies. This shows the sources of some of the 11lb examples. Hence you may lose a tenth of what you expect – in this case approximately 3-4lb – not 30-40lb!
3) Assuming that every deficit of calories is matched to the single calorie by the body giving up the equivalent in body fat is beyond absurd and yet it is assumed by this article and 99% of people working in the field of weight loss.
a) The body has to be in the biochemical state that it can break down body fat and this won’t happen if glucose is available in the bloodstream, or stored as glycogen, to use for fuel instead.
b) The body can and does adjust. If we put 100 fewer calories in to the body, it can adjust both our basal metabolic activity for the day and/or our energy used above the basal metabolic rate for that day. Put in 100 fewer calories and the body can just cross “keeping you warm” or “building bone density” off the’todo’ list for that day; the body can also make you tired and slow you down so that you use up 100 fewer calories being active. To assume that the body cannot and does not adjust at all – let alone by a single calorie, I’m sorry but there’s no other way to put this – is totally naive and stupid.
4) A calorie is not a calorie – as Jequier’s thermogenesis work showed (Eric Jequier, “Pathways to Obesity”, International Journal of Obesity, (2002).) Jequier found that the thermic effect of nutrients (thermogenesis) is approximately 6-8% for carbohydrate, 2-3% for fat and 25-30% for protein. Hence any 100 calories eaten is no longer 100 calories the minute it enters the body. Men’s Health would need to adjust for every macro nutrient for every food compared and even then points 1, 2, 3 and 5 here render the whole study nonsense.
5) Some calories have a job to do. Fat and protein calories to be precise. Let us say our average man needs 2,605 calories a day (as the government has decided), if he exercises 1-3 times a week, the Harris Benedict Equation tells us that approximately three quarters of these calories will be for basal metabolic needs (the BMR) and a quarter for energy/activity over and above this. The BMR needs fat and protein. Hence approximately 1,900 calories are needed for the BMR and approximately 700 on top of that for other activity for the day. This means that Mr Average needs to eat 1,900 calories in the form of (quality) fat and protein and 700 in the form of carbohydrate (or fat – fat can equally be used for energy – protein can too, but it’s less efficient).
So, back to Men’s Health, if our person eats 8.8 Snickers, at 296 calories each this will deliver the 2,605 daily calorie intake. If Mr Average eats 8.8 Flakes instead – they have ‘saved’ 1,416 calories and Men’s Health assumes that this will deliver a weight loss of 1lb for every time two and a half times that this 1,416 saving is made (3,500 calories). This is nonsense. Mr Average only needed 700 carb calories (he actually needed zero, as he could have fueled on fat, so I’m being generous). Empty junk confectionery calories can do nothing to build bone density, fight infection, repair cells (BMR) etc. Hence, eating Snickers, Mr Average consumed 1,900 effectively useless calories, which can only be stored as fat and thereby make him fat. With the Flakes, Mr Average still consumes more carbs than he needs and still gets fat. Mr Average also gets sick by the way - with either option – Men’s HEALTH!
The final point to make is that virtually every food on this “Eat this, Not that” list is complete junk – the tuna in water is the only decent product out of 42 products. Tuna doesn’t come naturally in vegetable oil! Men who care about their health shouldn’t even get lamb from Tesco – they should get grass grazed quality lamb from their local butcher. Pizza, processed ham, oven chips, confectionery, Quavers, Discos, Mr Kipling rubbish, Magnums, Vienettas have no place whatsoever in a health diet – for men or women.
If you want to lose weight – eat real food and nothing but real food – meat, fish, eggs, veg, salad, dairy products should be the staples and then nuts, seeds and fruits in season in moderation. Grains – ‘whole’ or otherwise – are just glucose with a few or very few vitamins and minerals. Animal foods will always beat a starchy carb in any nutrition contest.
Why trying to ‘burn off’ food is a waste of time
On 30 Dec I tweeted: “All these people ‘walking off’ indulgence make me laugh – I’d have to walk to Bristol & back (54 miles) to counter a Duchy Xmas pudding!” “Oh & that doesn’t deduct the BMR calories I would have used anyway so make that to Bath and back!”
Here’s the maths!
One fairly small (5 inch diameter) Duchy Original Christmas pudding contains 2,839 calories (313 per 100g)
We live 27 miles from Bristol. This site tells me that a 110lb person would use up 1,482 calories in 9 hours walking 27 miles at 3 miles per hour. Hence I have to walk there and back to ‘use up’ over 2,800 calories.
However – and this is something I only realised writing this blog that all calories burned calculators include the Basal Metabolic Rate. Hence, I would need to allow for what I would have been doing had I not been walking to Bristol and deduct this – because, by walking, I have only burned additional calories. If I had been writing for 9 hours instead, I would have used 808 calories, so, walking to Bristol would use 2,000 calories.
Just as well that none of this calorie stuff amounts to very much. If you want to be fit – be active; if you want to be slim – don’t eat Christmas Pudding!
Weight Watchers New Year’s Day advert
Weight Watchers are running one of the longest adverts on British television, simultaneously on commercial channels, between 6.30pm and 7pm on January 1 2012. The advert was announced in the media so that coverage could start before the advert.
The advert (three minutes and 10 seconds long) is fronted by Alesha Dixon who has never had a weight problem in her life, but wrote the song for the advert. The cost of the New Year’s Day ad alone is estimated to be £15 million – to make the advert and to air it.
I open my book “The Obesity Epidemic: What caused it? How can we stop it?” with the following passage:
“In a study of formerly obese people, researchers at the University of Florida found that virtually all said that they would rather be blind, deaf or have a leg amputated than be obese again (Ref 1). That is the extent of our desire to be slim and yet two thirds of people in the UK, USA and Australia are overweight and one quarter obese. Why?”
People do so desperately want to be slim and I would encourage people to try anything (safe and healthy) that will work. However, the evidence does not support the claim that calorie deficit diets work. Indeed we have known the following since Stunkard and Hume quantified the failure rate in 1959:
“Most obese persons will not stay in treatment for obesity. Of those who stay in treatment, most will not lose weight, and of those who do lose weight, most will regain it.” Stunkard and McLaren-Hume’s own statistical study showed that only 12% of obese patients lost 20 pounds, despite having stones to lose, only one person in 100 lost 40 pounds and, two years later, only 2% of patients had maintained a 20 pound weight loss. This is where the often quoted “98% of diets fail” derives from. (Ref 2)
The Mail article about the New Year’s Day advert ends with this sentence: “The company launched its ProPoints weight-loss plan last year and in just 12 months its one million members in the UK have lost more than 11million pounds between them.” The maths is easy – one million members losing c. 11 million pounds between them means an average 11 pounds per member – in one year.
The famous calorie formula (which I show to be wrong at every level here and here) claims that, if we create a deficit of 1,000 calories a day (which is approximately the goal with Weight Watchers) we should lose 2lbs per week (7*1,000 = 2*3,500). And – that should be fat lost alone. More should be lost on top in water and, sadly, lean tissue/muscle. Hence, the precise weight loss for every single person, who stuck to weight watchers for the year before this advert, should be 104lbs in fat and approximately 15% more in water/lean tissue – i.e. 120lbs in weight. The actual weight loss was 11lbs per person – less than one tenth of what ‘should’ have happened.
This 11lb number keeps popping up. In a study funded by Weight Watchers and conducted (appallingly in my view) by a government body – The Medical Research Council (MRC) – it was found (for a fee of “almost £1 million” Ref 3) that dieters doing Weight Watchers lost an average of 11lbs in a year. (The link to the blog gives full details of this study and links to the original data from the MRC study).
When I wrote to seven UK government and obesity organisations (National Institute of Clinical Excellence (NICE), National Health Service, Department of Health, National Obesity Forum, Association for the Study of Obesity, British Dietetic Association and Dieticians in Obesity Management) asking from whence the calorie formula came (the 3,500 theory) and asking for proof that it was true, the only study that was sent back to me was this one:
The NICE document Management of obesity: Full Guidance, December 2006 was offered as proof of the formula. Table 15.14 in this document contains results of one study of 12 people, given a deficit of 600 calories a day, where the outcome was “a change of approximately -5 kg (95% CI -5.86kg to -4.75kg, range -0.40 kg to -7.80 kg) compared with usual care at 12 months. Median weight change across all studies was approximately -4.6 kg (range -0.60 kg to -7.20 kg) for a 600 kcal deficit diet or low-fat diet and +0.60 kg (range +2.40 kg to -1.30kg) for usual care”.
So, let me understand this, the people on the 600 calorie-a-day deficit (the NICE recommendation) were 5 kilograms (11 pounds) lighter than those not doing this “at 12 months.” Applying the basic maths formula, these 12 people should each have lost 600*365/3,500 = 62.57 pounds of fat. Not an ounce (of fat) more or less. AND, there should have been no range of results – everyone should have lost exactly the same (that’s what happens with a mathematical formula). The least anyone lost (let’s put it all into pounds) was 0.8 pounds and the most anyone lost was 17.2 pounds. Even the highest weight loss was 45 pounds lower than it should have been. This is also all about fat – we haven’t even started looking at muscle or water loss. This is also a study of 12 people. There are 1.5 billion overweight people in the world and we can’t prove a formula using 12 of them.
The other bit that the advert won’t tell you is the well documented regain with calorie deficit diets – the 98% failure rate – known about for at least 50 years. In the Weight Watchers funded study – the press release omitted to mention that regain was starting to show at approximately 9 months (see slide 8).
There is an excellent and exceptionally useful review presented in the Journal of the American Dietetic Association (2007). (Ref 4) Marion Franz and seven colleagues performed a systematic review of 80 weight loss studies, grouped into eight different categories, including only those trials with a one-year follow-up. The studies were all from the period January 1997 and September 2004. 26,455 participants were enrolled in the studies. At the one-year follow-up, the attrition rate was 29% across the studies. Overall attrition was 31% at study end regardless of follow-up timing. The graph of results is shown in this thread in our club here. Notice, again, the regain at 6-9 months in all calorie deficit methods (the post explains the anomaly for the now withdrawn Sibutramine – the dark brown line).
Hence the evidence confirms that you are most likely to lose less than a tenth of what you expect – less than a pound a month over time, not 2lbs a week. You are also highly likely to start regaining at around six months. My book “Stop Counting Calories & Start Losing Weight” explains why.
If you have been doing calorie deficit diets (Weight Watchers, Slimming World, Rosemary Conley etc) for some time and are either a) not at your natural weight or b) one of the ‘lucky’ 2%, but finding you have to starve and obsess about food to stay there – you need to try something different. There is a way to lose weight and keep it off, without cravings or hunger and without feeling deprived. It is super healthy – focused on giving you optimum nutrition and no empty calories/processed food. You will understand why you have craved food in the past and how to ensure that you never do so again.
If you’ve been doing calorie deficit diets for some time and are not where you want to be and are planning to continue – you are mad! The definition of madness is doing the same thing again and expecting a different result. Come and see what the people losing weight and keeping it off are doing – it’s called The Harcombe Diet. Oh, and by the way, you have a good chance of losing 11lb in the first week or two and going on to lose a lot more and keeping it off.
References:
Ref 1: Colleen S.W. Rand and Alex M. C. Macgregor, “Successful weight loss following obesity surgery and the perceived liability of morbid obesity”, International Journal of Obesity, (1991). (The study results are presented in the summary of this book).
Ref 2: Stunkard A. and M. McLaren-Hume, “The results of treatment for obesity: a review of the literature and report of a series”, Archives of Internal Medicine, (1959).
Ref 3: http://www.thesundaytimes.co.uk/sto/news/uk_news/Health/article359154.ece The Sunday Times 1 August 2010.
Ref 4: Marion J. Franz, Jeffrey J. VanWormer, A. Lauren Crain, Jackie L. Boucher, Trina Histon, William Caplan, Jill Bowman, Nicolas Pronk. “Weight Loss Outcomes: A Systematic Review and Meta-Analysis of Weight Loss Clinical Trials with a Minimum 1-Year Follow-Up”, Journal of the American Dietetic Association, (2007).
The low down on alcohol & weight loss
This post is about alcohol. It was written for people following The Harcombe Diet, so references to Phase 2, Candida, Food Intolerance, Hypoglycaemia and ‘cheating’ may not be familiar to everyone. However, the information about the carb, calorie and composition of the different types of alcohol should be interesting and useful for anyone trying to integrate alcohol into their weight loss plan.
Introduction
Remember alcohol is still is still ‘a cheat’ in Phase 2 – no alcohol is recommended regularly while you’re still trying to lose weight. The recommendation for red wine to be the one you cheat with if you do have alcohol is because is ticks the health benefits box and is OK for insulin. Red wine has well documented antioxidant benefits (related to the polyphenol, reservatrol), although avoiding oxidants (smoking, chemicals, processed food, stress) in the first place would be a much better idea. Red wine is the only recommended fluid to consume whilst eating (even water washes away natural digestive juices and should be drunk between, not with, meals).
Below is a list of common alcoholic drinks with their carb and calorie contents and any relevant notes for The Harcombe Diet. The calorie information is only of interest, as it can give a guide as to how sweet a drink is. Other than that, calories are just fuel – we don’t care much about them. The carb information is more interesting, as this is going to indicate how much you are going to wake up your pancreas, to produce insulin, with each particular drink. For example, brandy and whisky are practically zero carb and are therefore not bad drinks at all from an insulin perspective. (Unlike beer which can have 13g of carb for a 12oz glass, stout 20g and a shot of Amaretto can have a whopping 42 grams of carbohydrate).
However, distilled sprits are much higher in alcohol content – which introduces another hormone issue. Alcohol inhibits the operation of glucagon, which is a hormone that naturally elevates blood sugar, so drinking high alcohol drinks is likely to give you the munchies. Whisky is grain based (usually barley), which won’t be great for anyone wheat intolerant and any varieties of brandy that are not distilled from wine (e.g. the fruit brandy like calvados) can be sweet. All sorts of other things need to be considered when you move away from real food.
Ingredients in common alcoholic drinks:
Beer is a fermented, hop flavoured, malt sugared liquid whose chief ingredients are water, malt, hops & yeast. (Malting is a process of bringing grain to its highest point of possible soluble starch content. This forms ‘maltose’– a sugar – which is then metabolised into alcohol by the yeast).
Lager (from the German word “lagern” which means to store) is just beer kept in a cold dark place for thirty days or more.
With beer and lager, therefore, you are risking all three conditions discussed in The Harcombe Diet. You can be feeding Candida with the sugar and yeast, feeding Food Intolerance with grains and feeding Hypoglycaemia with the carb and sugar content.
| Beer (12oz) | Carbs | Calories | Notes |
| Regular beer/lager | 13g | 150 | e.g. Heineken, Stella, Budweiser |
| Light beer | 4.5g | 116 | e.g. Bud light, Miller Lite – will usually say “Light”, “Lite” or “ultra” |
| Ale | 7g | 126 | e.g. bitters, milds, golden ales and old ales – the pub’s own pint on draught is in this category |
| Stout | 20g | 178 | e.g. Guinness |
Wine is primarily made from grapes which end up in a highly concentrated form (i.e. refined fruit). White wine is made from the fermented juice of grapes stripped of their seeds and skins. Red wine is made from the fermented juice of grapes with the skin and pips included – it is less refined, therefore. It is also slightly lower in sugar content. It contains more reservatrol – a plant anti-oxidant – than white wine. Wine is one of the best drinks to cheat with on The Harcombe Diet – either the occasional glass of red wine (the drier the better) with a main meal or a white wine spritzer as a long drink if you are out socialising.
| Wine (5oz) | Carbs | Calories | Notes |
| Dry white | 3g | 130 | e.g. Chardonnay, Sauvingnon Blanc |
| Medium dry | 5g | 118 | e.g. Reisling, Chenin Blanc |
| Dry red | 4g | 114 | e.g. Pinot Noir, Cabernet Sauvignon |
| Red Bordeaux | 4.5g | 116 | |
| Red Burgundy | 5.5g | 120 |
Champagne is made in the same way as wine – but then more yeast is added and it’s left to ferment in the bottle a second time, producing carbon dioxide (fizz). It’s also not too bad a cheat with The Harcombe Diet, but it can be ‘more-ish’, so do watch how much you drink.
| Champagne (5oz) | Carbs | Calories | Notes |
| Dry Champagne or Sparkling Wine | 4.5g | 116 | |
| Sweet Champagne or Sparkling Wine | 10g | 138 |
Liqueurs are essentially highly concentrated, highly fermented drinks, where a greater proportion of the water has been removed during the fermentation process making a much denser (and more alcoholic drink). Here is an example of the making of a specific liqueur, so that you can get an idea of what happens:
How Tequila is made: The agave plant is responsible for tequila, and all tequila is made in Mexico. Agave plants are harvested as large thick trunks; the spiny leaves are hacked off with machetes, and the plants are trucked to special hot houses where they begin the fermentation process. The plants are then cut up and the juices are fermented before moving on to their final form. Tequila is sold in a variety of styles – each is dramatically different, making the different types of tequila almost totally different liquors. The longer an aged tequila stays in the barrels the darker the colour and stronger the flavour becomes.
| Liqueurs (2.5 oz. serving) | Carbs | Calories | Notes |
| Amaretto | 42g | 266 | Almond based – not suitable for nut allergy |
| Bailey’s | 18g | 170 | Watch out if lactose intolerant |
| Campari | 20g | 178 | |
| Coffee Liqueur (e.g. Kahlua) | 40g | 258 | Watch out if lactose intolerant |
| Cointreau | 25g | 198 | |
| Creme de Menthe | 35g | 238 | |
| Grand Marnier | 17g | 166 | |
| Kirsch | 15g | 158 | Cherry Liqueur |
| Ouzo/Sambuca | 28g | 210 | This contains essential oils from star anise, which give the Liqueur a strong anise flavour. The oils are added to sugar and other flavouring. |
| Tequila | 0g | 160 | Pure tequila has no carb content. When it is drunk as Tequila sunrise or mixed with other liquids, the carb content of the added liquids will count. |
| Triple Sec | 27g | 206 | Triple sec (meaning “Triple distilled”) is a strong, sweet and colourless orange flavoured liqueur. It is made from the dried peel of oranges found on Curacao, an island in the Caribbean. Curacao, Grand Marnier and Cointreau are popular triple sec’s. The above entries for Grand Marnier and Cointreau show how varieties can differ in carb content and sweetness. |
Distilled Spirits are also highly concentrated, highly fermented drinks, where a greater proportion of the water has been removed during the fermentation process making a much denser (and more alcoholic drink). Here is an example of the making of rum:
How Rum is made: Rum is generally made from molasses (a syrupy byproduct of the processing of sugar cane or sugar beets into sugar). However, some rums are made from raw sugarcane juice. Rum is mostly made in the Caribbean and South America, and is usually aged in wooden barrels depending on the style. Like tequila, rum can be either aged or not. And, like tequila, the longer the rum ages in the charred oak barrels, the darker and stronger the taste. Light rums are sweet and do not have much flavour, while darker rums have aged longer and have much bolder taste.
Whisky & Gin are grain based (barley, oats or wheat) and generally contain sugar in addition. Vodka used to be distilled from potatoes but is more typically grain based today. Rum has sugar cane as its key ingredient.
With distilled spirits, therefore, you are risking all three conditions discussed in The Harcombe Diet. You can be feeding Candida with the sugar and grains, feeding Food Intolerance with grains (especially any with wheat) and affecting Hypoglycaemia with the carb and sugar content.
| Distilled Spirits (1.5oz servings) | Carbs | Calories | Notes |
| Brandy | 0g | 98 | Brandy is a spirit distilled from red wine, so it has a high concentration of anti-oxidants. |
| 80 proof Gin, Vodka, Rum, Whisky | 0g | 98 | |
| 90 proof Gin, Vodka, Rum, Whisky | 0g | 111 | |
| 100 proof Gin, Vodka, Rum, Whisky | 0g | 125 |
The End!
For the record – the real truth about dried fruit
There is a column on the Health page in You Magazine on 18th December 2011 – The truth about dried fruit. It is the latest in a series of columns intended to give some snappy and informative facts about foods and to dispel some myths. To date we have done the truth about butter, water, green tea, chocolate and now dried fruit.
The final bullet in the snippet is entitled “Coeliac readers” and says “Coeliac readers may want to know that YOU testers voted Genius gluten-free mince pies “absolutely delicious”. £2.19 for four, at selected supermarkets. Find your nearest one at geniusglutenfree.com (tel: 0845 874 4000)” The credit “By nutritionist Zoe Harcombe” immediately follows this apparent endorsement.
I did not know that YOU testers had been polled, let alone what they had voted. I had never heard of Genius or their products. I have no idea or interest how much they are or where you get them from. I never said any of these words and never would. Anyone who knows me knows that I abhor conflict of interest and will never endorse any product or even accept any advertising on any of my sites – no matter how lucrative this would be.
After seeking to understand how this happened, I have received an explanation and an apology.
I have looked at the genius web site as a result of this shock upon opening the magazine this morning and here are the ingredients for this gluten-free mince pie concoction:
Gluten Free Pastry: [Maize Starch, Vegetable Oils, Vegetable Margarine; (Vegetable Oil, Water, Salt, Emulsifier; (Polyglycerol esters of fatty acids), Flavouring, Colours; (Annatto, Curcumin)), Water, Sugar, Dextrose, Whey Powder, Whole Egg Powder, Modified Potato Starch, Stabilisers; (Guar Gum, Xanthan Gum), Raising Agents; (Sodium Bicarbonate, Disodium Diphosphate), Rice Flour].
Mincemeat (49.6%) : [Sugar, Sultanas, Bramley Apple Puree; ( Bramley Apple, Preservative; (Acetic Acid)), Currants, Humectant E422, Vegetable Suet; (Palm Oil, Sunflower Oil, Rice Flour), Modified Maize Starch, Orange Zest, Mixed Spice, Raisins, Lemon Zest, Orange Oil]
Sugar Topping: [Glucose, Maize Starch, Vegetable Oil].
OMG! That is truly gross. My recommendation, never having heard of these fake foods before, is don’t touch them with a barge pole. If you even know what all those ingredients are, you’re a step ahead of me.
My original article filed by the way was as follows:
What’s the deal with dried fruit & Christmas?
Fresh fruit is not naturally available in winter, so festive cakes and puds are traditionally based on dried fruit.
Is it healthy?
There are some useful nutrients in dried fruit – carotene, iron, potassium – but there are richer and less sugary sources for all vitamins and minerals.
What’s the sugar issue?
Dried fruit is approximately 30% water and 70% sugar. Different dried fruits have different proportions of glucose and fructose, but you’re essentially eating sucrose (table sugar) with a mild vitamin tablet.
Is this unique to dried fruit?
All fruit is a mixture of glucose and fructose, but dried fruit is especially dense, having lost water. You wouldn’t eat a dozen apricots, but you could easily eat the dried equivalent.
What’s the best way to enjoy it?
Ideally with real food and not in puds or pies. A handful of raisins with nuts, or cheese and dried apricots will be delicious, nutritious and the protein can help mitigate the sugar load.
24,000 diabetes deaths a year ‘could be avoided’
This news story broke on 14 December 2011. There are 2.3 million diabetics in the UK. The vast majority (c. 90-95%) are type 2 diabetics – all will be explained below. The remainder are type 1 diabetics.
A recent (the first ever) audit on patient deaths from diabetes notes that approximately 70-75,000 diabetic patients die each year and it is estimated that approximately one third of these deaths could be avoided with better care of their condition.
This post is about the different types of diabetes, insulin non-production, insulin sensitivity, fat storage, insulin and obesity. It covers the issues related to diabetes, insulin and obesity and is intended to provide an understanding for why people are not keen to take medication for diabetes and why we could far better manage diabetes and avoid much of the incidence of diabetes if only we would return people to eating the real food that we ate before we had epidemics of obesity and diabetes – animals, vegetables and fruits in season, nuts & seeds where available. No cereals, no ready meals, no fortified margarines – none of the heinous products making us fat and sick.
Diabetes Type 1 & 2
Rosalyn Yalow and Solomon Berson are credited with having taken Sir Harold Himsworth’s distinction between what we now know as type 1 and type 2 diabetes (Ref 1), and demonstrating that type 1 diabetes was an insulin-deficient state, whereas patients with type 2 diabetes had substantial amounts of insulin in the blood and could be classified as insulin resistant (Ref 2). Type 1 diabetes can therefore be simplistically described as the type where the pancreas does not release insulin at all. In type 2 diabetes the pancreas is effectively releasing too much insulin and yet this still fails to regulate blood glucose levels normally, as cells have become resistant to insulin. This is a critical distinction and helps to explain why this Yalow and Berson study remains one of the most cited articles from the Journal of Clinical Investigation.
It follows that type 1 diabetes requires the administration of insulin and type 2 diabetes can be managed through medication to help optimise the insulin available and to help overcome insulin resistance. Both types of diabetes, I would argue, could be far better managed through diet, and I actually fail to see how type 2 diabetes can manifest itself in the absence of carbohydrate. Obesity in diabetics would be far less common if we adopted the low-carbohydrate principles from the nineteenth century, before the discovery of insulin in 1921, openly shared by William Banting in 1869 (Ref 3).
Insulin, obesity & diabetes
In their 1965 article (Ref 4), Yalow and Berson teamed up with Seymour Glick and Jesse Roth to review the relationship between insulin, obesity and diabetes. They opened with “Here we summarize several well established observations: A relatively high percentage of adult-onset diabetics (Ref 5) are obese and were so long before the onset of clinical diabetes. Diabetes occurs far more frequently in obese than in nonobese subjects. Obese patients without diabetes exhibit impaired glucose tolerance with abnormally high frequency.” With no claims of causation in any direction, the authors are merely observing associations between diabetes, obesity and insulin resistance. At the end of a rigorous study of blood glucose levels and insulin responsiveness in all permutations of lean and obese, diabetic and non diabetic people, their conclusion was as follows: “Thus, there is some degree of insulin insensitivity in obesity without diabetes and a greater degree of insensitivity in diabetes without obesity. When the two conditions coexist, insensitivity is greatest and results in the highest insulin concentrations if pancreatic reserve is adequate.”
This confirms that obese people are more likely to have type 2 diabetes and, even if not diabetic, they are more likely to display insulin sensitivity. Those who are both diabetic and obese are likely to be the most insulin resistant of all. The causation is likely circular, as obesity increases the person’s chance of developing type 2 diabetes and the accompanying insulin resistance makes obesity more likely. The subject of fat storage is very interesting to compare in type 1 and type 2 diabetes.
Type 1 diabetes
The first life event to trigger my interest in the subject of weight, insulin and carbohydrates was my brother developing type 1 diabetes when he was aged 15 and I was 13. As is classic in the onset of the condition, he lost approximately 20 pounds in a similar number of days (the condition took an inexplicably long time to diagnose, given the classic nature of the symptoms). His ‘energy in’ had undoubtedly increased – as he was sending me to the corner shop to buy litre after litre of sugary fizzy drinks. His ‘energy out’ undoubtedly decreased, as he seemed unable to move from his armchair. Having shared this story a number of times – the most common response is curiosity about any possible violation of the laws of thermodynamics – how could energy in go up and energy out go down and a human lose so much weight?
When type 1 diabetes occurs, sugar is lost in the urine. Indeed, diabetes means ‘sweet urine’ in Greek and diabetes is diagnosed by testing for sugar in the urine. At the 2010 Wales obesity conference Dr. Jeffrey Stephens a diabetologist, estimated that glycosuria (literally weeing out sugar in the urine) may account for 500 calories a day. That still doesn’t allow the first law of thermodynamics alone to explain the notorious weight loss in the sudden onset of type 1 diabetes. We seem more interested in calorie reconciliation than thinking about possible implications for obesity. I was always more interested in what this told us about the role of insulin in weight and weight loss.
What we observe, at the onset of type 1 diabetes, is, essentially, a human body incapable of storing fat in the absence of insulin. As soon as the condition is diagnosed we (unforgivably in my view) advise the person to eat carbohydrate at every meal and administer insulin regularly and the ability to store fat resumes. Invariably the person then struggles to avoid obesity for the rest of their life.
Type 2 diabetes
Conversely, just as onset type 1 diabetics, before diagnosis, are unable to store fat, type 2 diabetics are masters at this. Pre-diabetic individuals are often efficient ‘fat storing machines’ while insulin resistance is developing and before they are officially diagnosed with type 2 diabetes. Whereas the onset of type 1 is sudden and dramatic, type 2 diabetes can emerge over time and remain undiagnosed for months, even years. Any insulin resistant type 2, diagnosed or otherwise, would be well advised to avoid carbohydrates, as this is the one macronutrient that they cannot handle. Instead, we advise all citizens, diabetic or non-diabetic, to base their meals on starchy foods and to eat little and often and we maintain an excellent fat storage environment in so doing.
Insulin, fat storage & getting fat
Edgar Gordon wrote in the Journal of the American Medical Association (JAMA) 1963 “It may be stated categorically that the storage of fat and therefore the production and maintenance of obesity cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin. Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.” (Ref 6)
There are enough journal articles and medical references connecting insulin and weight to keep an obesity researcher engaged for years on this subject alone. The conclusion of all references, however, is that insulin leads to weight gain (and, therefore, by inference, that carbohydrate leads to weight gain). Nothing illustrates this better than medical journal forums seeking ways to encourage diabetics (especially young females) to take their insulin, because the doctors know that the diabetics know that insulin makes them fat.
The audit recently undertaken confirmed that the most at risk group was women aged 15 to 34 with diabetes. They were nine times more likely to die than non-diabetics of the same age. That’s because they know that insulin makes them fat and young women, particularly, don’t want to be fat. The solution is to lessen the intake of the macro nutrient that requires insulin to be administered – carbohydrates – but we do not advise this. Instead – we tell diabetics that this is a role model for healthy eating. It is, in fact, a recipe for making more diabetics and making current diabetics fat and sick.
The weight gain resulting from insulin is so well known that, as far back as 1925, Wilhelm Falta began using insulin to treat underweight adults and anorexia (Ref 7). The weight loss at the onset of type 1 diabetes is equally long known and remarkable. The non diabetic person can produce the same fattening effect of administering insulin by eating carbohydrates frequently and causing the pancreas to release insulin. The impact of insulin on weight is irrefutable and substantial, as we will also see in the next section on medication.
Diabetes & medication
The large-scale studies, such as the diabetes control and complications trial (DCCT) in patients with type 1 diabetes and the United Kingdom prospective diabetes study (UKPDS) in patients with type 2 diabetes, have quantified the weight gain resulting from the administration of insulin. The DCCT was a prospective trial involving 1,441 patients with type 1 diabetes randomised to either an intensive (three to four insulin injections/day or insulin pump) or conventional (one to two insulin injections/day) treatment protocol (Ref 8). At the nine year follow up, approximately 30% of men and 35% of women, receiving the intensive insulin dosage, were five points higher on their BMI scale. Men and women on the more conventional dose still gained weight, but far less. The study quantified the average (mean) weight gain as 4.75 kilograms greater for the three to four injections a day group.
The UKPDS study had 3,867 participants, newly diagnosed with type 2 diabetes (Ref 9). They were randomly assigned to either an ‘intervention’ group, with insulin or alternate drug treatment, or to a ‘managed through diet’ group. Weight gain over the 10 year study was a mean of 6.5 kilograms. Weight gain was significantly higher in the insulin/drug group (mean 2.9 kilograms) than in the diet group. Furthermore, of the drug treatment options, patients assigned insulin had a greater gain in weight (4.0 kilograms) than those given chlorpropamide (2.6 kilograms) or glibenclamide (1.7 kilograms). (The latter two named drugs are from the family of medication called sulphonylurea. They act to stimulate the release of insulin from the beta cells in the pancreas, thus trying to optimise any insulin that can be ‘squeezed out’ from the body more naturally than insulin administration).
The Glasgow report (Ref 10) presented numerous other studies confirming the same observed weight gain with the administration of either insulin or sulphonylureas. The latter produced lower weight gain than insulin, but gain none the less.
The weight gain with insulin is immediate and sustained, as the Yki-Jarvinen 1992 study showed, with a mean gain of 1.8 kilograms to 2.9 kilograms in 12 weeks with two injections and multiple injections respectively. Similarly the Yki-Jarvinen 1997 study, carried out over a one year period, showed a mean weight gain of 5.1 kilograms with 2-4 injections per day. All of these studies were done for management of type 2 diabetes, not type 1.
The people taking sulphonylureas fared better than those taking insulin, but still recorded notable weight gain. The largest weight gain, over a one year period, for a sulphonylurea, was a mean of 3.6 kilograms recorded by Marbury (1999) for glipizide (Ref 11).
Conclusion
The BBC article linked to in the opening line says of diabetes: “It means their bodies cannot use glucose properly. If they do not manage it, they can develop potentially fatal complications like heart or kidney failure.” This is a useful, if simplistic, description of both types of diabetic – “their bodies cannot use glucose properly.”
Q) So, how does the body get exposed to glucose? A) From our public health dietary advice:
- “Base your meals on starchy foods” (glucose);
- “Eat five-a-day” (glucose and fructose);
- Eat less fat” (which means that carbohydrate as a proportion, if not absolute amount, in the diet must increase – more glucose).
Insulin makes us fat. Glucose demands that insulin be released, so glucose makes us fat. Carbohydrates break down into glucose (and fructose) – fructose goes straight to the liver to be turned into fat and glucose stimulates and insulin response to make us fat. Medication for dealing with the complications of not being able to “use glucose properly” makes us fat. What doesn’t make us fat is the real food that the government tells us to eat less of – meat, fish, eggs and dairy products.
I hope that the government realises the consequences of their dietary advice before we make any more diabetics, let alone record the deaths of those we have already made.
References
Ref 1 : Sir Harold Himsworth, “Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types”, The Lancet, (1936).
Ref 2: Rosalyn Yalow, Solomon Berson, “Immunoassay of endogenous plasma insulin in man”, Journal of Clinical Investigation, (1960).
Ref 3: William Banting, “Letter on Corpulence addressed to the public”, (1869).
Ref 4: Yalow R.S., Glick S.M., Roth J., Berson S.A.,“Plasma insulin and growth hormone levels in obesity and diabetes”, Annals of the New York Academy of Sciences, (1965).
Ref 5: “Adult onset” was the common terminology used for type 2 diabetes at the time of the 1965 article. Type 1 diabetes similarly used to be called juvenile diabetes, as it manifested itself in children, adolescents or young adults. Type 1 and 2 are the favoured terms nowadays, not least because we are observing new cases of type 1 diabetes in middle aged people and, extremely worryingly, type 2 diabetes in children. The vast majority, 90-95%, of diabetics have type 2 diabetes.
Ref 6: Edgar Gordon, “A new concept in the treatment of obesity”, The Journal of the American Medical Association, (1963).
Ref 7: Wilhem Falta, Endocrine diseases including their diagnosis and treatment, (1923).
Ref 8: DCCT Research Group, “Influence of intensive diabetes treatment on bodyweight and composition of adults with type 1 diabetes in the Diabetes Control and Complications Trial”, Diabetes Care, (2001).
Ref 9: UKPDS Group, “Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes”, The Lancet, (1998).
Ref 10: W.S. Leslie, C.R. Hankey and M.E.J. Lean, “Weight gain as an adverse effect of some commonly prescribed drugs: a systematic review” QJM, (June 2007).
Ref 11: Marbury T., Huang W.C., Strange P., Lebovitz H., “Repaglinide versus glyburide: a one-year comparison trial”, Diabetes Research and Clinical Practice, (1999).
“Divorce rate for over-60s surges”
So screamed the Daily Mail headline on 19 November 2011.
“Britain is seeing a boom in ‘silver separations’”, read the first line.
I wonder if they do with other headlines what they do with drug and disease headlines?
The article soon gave some numbers – 11,500 over-60s were granted a divorce in 2009. It takes a 30 second google search to get a recent enough figure for the number of over-60s in the UK. An article from August 2008 says: “The Office for National Statistics revealed that 13,262,256 people were 60 or over in mid-2007 – up from 12,928,071 the previous year.” So, the 2009 numbers are almost certainly higher still, but let’s go with the 2008 known number.
11,500/13,262,256 is 0.086% – not even one tenth of one percent. Not even 1 in over a thousand over-60s got a divorce in 2009. This was up 4% on the previous year said the Daily Mail article – not quite a surge really is it? That means that there were 0.083% of over-60s divorcing in 2008 and then 0.086% in 2009.
Hardly “Hold the front page” now eh?!
England’s Obesity Strategy (not)
On Thursday 13 October, 2011, the Department of Health issued this press release, optimistically called “Government calls time on obesity.” The government has done anything but.
We need to remember that the UK health service was devolved in 1999, with England, Scotland, Wales and Northern Ireland managed separately from this point forth. Hence, this Department of Health announcement was for England only.
On 15 March 2011, the Department of Health issued a press release on what they call “The responsibility deal.” The government believes that partnering with the food and drink industry “can be the most effective way of tackling some public health objectives.” The purpose of the food and drink industry is to sell as much food and drink as possible. The government believes that we need to be consuming less food and drink to lose weight. How these aims can be compatible, therefore, baffles me.
The pledges announced in the March press release include:
- Calories on menus from September this year;
– Reducing salt in food so people eat 1g less per day by the end of 2012;
– Removal of artificial trans-fats by the end of this year;
– Achieving clear unit labelling on more than 80 per cent of alcohol by 2013;
– Increasing physical activity through the workplace; and
– Improving workplace health.
We know that putting “Smoking kills” and “Smoking will harm your unborn child” on cigarette packets makes no difference, so why would putting a calorie number on food make any difference? It won’t and we know already that it won’t – here is an article about a study done in the British Medical Journal to prove this.
The October ‘new’ news
Health secretary, Andrew Lansley, and England’s Chief Medical Officer, Professor Dame Sally Davies, launched the ‘new’ proposals, but there really was only one thing new:
1) Davies called for everyone to be more honest about their eating and drinking habits – so, not only are we greedy and lazy, we are now liars too!
2) We have been told to “slash” five billion calories a day. If the population of England approximates to 50 million people, that’s 100 fewer calories per person per day. No knowledge whatsoever of the difference between calories has been demonstrated with this headline grabbing number.
3) Astonishingly – this was the only new bit – the Scientific Advisory Committee on Nutrition (SACN) – advised that the recommended daily calorie intakes for both men and women should be raised. We are told to eat less, but our intake guidelines should go up? Davies tried to explain this by saying – our daily intake should be raised but we are still eating more than this, so we still need to cut back. This is confusing at best and ludicrous at worst. I do not think that we should be raising calorie recommendations in the midst of an obesity epidemic. Not because the obesity epidemic is about calories (because it isn’t), but because it sends the wrong message. If health were going to suffer by not raising these calorie limits then raise them – but at a completely different time, so as not to confuse the public. However, I am far from convinced that anyone’s health would suffer if we did not raise calorie limits – health is about what we eat and the vital nutrients that we consume – not the amount of petrol we put in our tank. Putting petrol in a diesel car is the worst thing we can do to a vehicle. Putting sugar, transfats and empty calories in a human body is equally harmful.
The calorie intakes, just for the record, have been increased from 2,550 to 2,605 for men and a whopping 1,940 to 2,079 for women.
The chair of the SACN working group, Alan Jackson, has declared interests in Nutricia (a specialised unit of Danone food company) and Baxter Healthcare (see page 32). The full list of members of the energy requirements sub committee is on p19 of that link. Ian Macdonald has declared interests with Mars Inc, Mars Europe, Unilever, Nestle and Coca-Cola – just what we want on a Scientific Advisory Committee on Nutrition! Andrew Prentice, also on the group, ‘only’ has connections to Tanita Scales and Danone. His wife, however, (see p34) has the most extraordinary list of declared interests: Beveridge Institute for Health and Wellness, Diabetes UK, Institute of Brewers & Distillers, Milk Development Council, Optimal Performance Ltd, The Rank Prize Funds, Tanita UK Ltd, World Cancer Research Ltd, Weight Watchers UK Ltd, B Kassardjian Fund – Zurich, Dee Caffari Ltd, Mars, BBC, Rosemary Conley Diet & Fitness Club, National Trust, Coca Cola, Outsights, Nestle, Emap, Kelloggs, Almond Board California, Nunwood Consulting, Pepsico, GlaxoSmithKline, British Institute of Sport, The Pelican Buying Co, National Institute of Nutrition and J Sainsbury. Go girl!
The bottom line
The bottom line is that the English government thinks that people just need to eat less and do more and they will lose weight. As I detail at length in my book The Obesity Epidemic this has been Plan A for more than three decades and we have continued to get more and more obese. We have known since Benedict’s 1917 study that eating less leads to short term weight loss and then regain to beyond the starting weight. This was confirmed in the definitive eat less experiment – the Minnesota Starvation Experiment - initial weight loss, followed by regain plus 10%. At least 9 out of 10, if not 19 out of 20, of the personal consultations that I do start with the explanation “I didn’t really have a weight problem until I went on my first diet. I lost weight, regained and more. I went on another diet, lost weight, regained and more.” When they say ‘diet’, my clients mean a calorie deficit diet – the eat less/do more that the government thinks will get us out of this mess.
Here’s an interesting statistic for you:
The MAFF (Ministry of Agriculture Fisheries & Food) National Food Survey tells us that we were eating 2,290 calories per person per day in 1975 and, by 1999, this had fallen to 1,690 calories per person per day. If we apply the 3,500 calorie formula (notwithstanding that this formula is also wrong, but it’s the one that government and all calorie advisors rely upon), to the change in annual average calorie intake, all other things being equal, we should have lost an average of 62.6 pounds per person during this period. Instead obesity rose nearly ten fold during this time.[i]
The DEFRA (Department for Environment, Food & Rural Affairs) report notes the continual decline in calorie intake. The Family Food Survey for 2001-02 comments on the short term: “Energy content of the household food supply has decreased considerably over the last 5 years.” The Family Food Survey for 2002-03 notes the same trend over the longer term: “Average energy intake per person in the UK is unchanged in 2002-03 compared with the previous year, although it has been declining since 1964.”[ii]
The Food Standards Agency (FSA) web site also acknowledges the above conundrum, “Since the 60s we’ve been consuming fewer calories from household food (this doesn’t include eating out). However, there are an increasing number of people who are overweight or obese. The reasons for this are not clear.”[iii]
We need to eat better, not less. We need to return to eating real food, not the empty calories dominating the eatbadly plate. We need to eat naturally produced meat, fish, eggs, dairy products, vegetables and salads to ensure that our bodies can use the calories that we eat for our basal metabolic needs. We absolutely cannot afford to eat the empty sugar and flour calories, which we are eating.
World Health Organisation data tells us that the average UK citizen consumes 38 kilograms of sugar per year.[iv] Statistics from the Flour Advisory Bureau note that UK per capita flour consumption reached 74 kilograms in 2008/9.[v] This represents a few calories short of 1,150 per person per day from those two ingredients – when did that become a healthy balanced diet?
What the government should have done
I set out in Chapter 16 of The Obesity Epidemic what should be done to reverse the obesity epidemic. Here are the headlines:
1) Tear down the eatbadly plate from every surgery, hospital and school in the country and never allow it to be shown again. Tell people to eat real food from now on and nothing but real food. If nature provides it – eat it; if food manufacturers provide it – don’t. That’s the only healthy eating food message that the government needs to have to start to reverse the obesity epidemic.
2) Ban trans fats. In the unlikely event that we were bold enough to ban sugar, trans fats and sweeteners, this one step would be sufficient to reverse the obesity epidemic (whether such bans are necessary is a matter for debate). Trans fats should be singled out for an immediate ban (as has happened in Denmark and Switzerland). The National Heart Forum summed up their position on trans fats in the opening to their paper calling for a ban on these substances: “Industrially produced Trans fats (IPTFAs) are harmful to health, they have no nutritional benefits and there is no known safe level of consumption.”[vi]
3) Fiscal policy (taxation). I cannot conceive of any government having the courage to ban sugar, trans fats and sweeteners. Hence, if we lack the leadership qualities to ban nutritionally void substances, the minimum that we need is a deterring and punitive tax on each of them. We need to be very specific about the targets. In May 2009 Dr. Tim Lobstein called for a ‘fat tax’,[vii] while talking about junk food and pizza. The reiteration of the notion that ‘fat is bad’ is incessant. We must stop this forthwith. Here is a blog on the October 2011 Denmark fat tax and how misguided this is. The target of fiscal measures needs to be processed foods and no real food should ever be demonised again. Again, although this step may not be necessary, it would be sufficient and we are almost expecting the impossible from our populations to tell them to avoid processed food while the food manufacturers are simultaneously promoting BOGOF’s (Buy One, Get One Free) on biscuits, cakes, confectionery and all the things that we need help to resist. David Kessler’s book, The end of overeating, gives full details of what humans are up against in terms of food industry tactics.[viii]
Taxation would merely be a return to previous public policy, albeit from centuries ago. Adam’s Smith’s The Wealth of Nations (1776) noted “Sugar, rum, and tobacco are commodities which are nowhere necessaries of life, which are become objects of almost universal consumption, and which are therefore extremely proper subjects of taxation.” Just under one hundred years later, the sugar tax was repealed. If sugar is not banned, the tax needs to be reinstated.
The objective of such taxation should primarily be to reduce consumption, but any revenue generated can have an added benefit of subsidising real food and/or the health services that are impacted by such consumption. Using sugar as an example, I would put a minimum 100% (double the price of the product) tax on any product containing non naturally occurring sugar (any added ‘ose’).[1] This would immediately discourage food manufacturers from adding sugar, completely unnecessarily, to ham, cottage cheese, tins of chick peas, kidney beans and other healthy products. I would put at least a 200% tax on any product where all sugars added together are the majority of the composition of the product. For any product (e.g. children’s sweets) where the entire product is essentially sugars (with a bit of crushed animal innards, gelatine, for bonding), we should multiply the current price by four or five fold. The proceeds from taxes on sugar, trans fats and sweeteners should subsidise real food for people who are currently least able to afford it. We cannot hope to solve an obesity epidemic when we can buy ten doughnuts or one cucumber for the same price.
Other fiscal measures should be considered. Corporation tax can be raised on companies that make processed food and lowered, or eliminated, on companies that provide completely unadulterated natural food. The local butcher must become the provider of choice for meat, not McDonald’s. Today, I can buy one pound (454 grams) of grass fed steak for the same price as a regular cheeseburger and medium fries and mayo chicken and a McFlurry original and a medium drink and a double cheeseburger.[ix] This is not conducive to healthy eating – particularly in the sections of our population who can least afford, and most need, real food. Kessler details some of the most contemptuous examples of fast food: “One of the signature hamburgers at Hardee’s is called the Monster Thickburger, which famously contains 1,420 calories and 108 grams of fat.” “Yet even that pales in comparison to a slice of Claim Jumper’s Chocolate Motherlode Cake … 2,150 calories a slice”. (Note the use of the word ‘mother’ to imply approval). Such inhumanity to man should be met with an “Inhumanity Tax”. It’s not far away from manslaughter, if you are familiar with the legal definition.
If this sounds extreme, how does “90% of today’s children being overweight or obese by 2050” sound?[x] And, why would this be considered extreme? I am merely suggesting that we return to eating what we used to eat before we got too obese to function as human beings.
England has one of the worst obesity epidemics in the world. Thanks to the conflict of interest and ignorance of the English government, they now have one of the worst obesity strategies in the world. Relying on the profit motivated organisations that want us to eat ‘fake’ food instead of real food, to lead a return to the real food that would signal their demise, is naive at best and fatal at worst.
[1] As an example, fructose in a whole apple is fine, as this is the form in which nature intended us to eat fructose. Fructose added to sweeten other products is not necessary.
[i] I calculated this mathematically year on year and analysed the average calorie intake for 1975 and then that for 1976 and used the 3,500 calorie formula to work out what the average person should have gained/lost between these two years and repeated this for each year between 1975 and 1999 to calculate the overall number of pounds that should have been lost on average. The overall number was calculated cumulatively, as some years people should have gained weight and most should have produced weight loss – all according to the calorie theory.
[ii] http://www.defra.gov.uk/evidence/statistics/foodfarm/food/familyfood/index.htm
[iii] http://www.eatwell.gov.uk/healthydiet/seasonsandcelebrations/howweusedtoeat/ changingtastes/
[iv] http://www.whocollab.od.mah.se/expl/globalsugar.html
[v] http://www.fabflour.co.uk/content/1/31/facts-about-bread-in-the-uk.html
[vi] http://www.heartforum.org.uk/Policy_Consultations_2093.aspx
[vii] http://www.medindia.net/news/British-Expert-Calls-for-Fat-Tax-on-Unhealthy-Foods-to-Save-Children-51144-1.htm
[viii] David Kessler, The end of overeating, published by Rodale, (2009).
[ix] Rump steak was £14 per kilo (£6.36 per pound) and McDonald’s had the first five items listed for 99p and the double cheeseburger listed at £1.29 (June 2010). http://www.mcdonalds.co.uk/food/saver-menu/saver-menu.mcdj?dnPos=0
[x] One of the forecasts of the Foresight Report: “Tackling Obesities: Future Choices” (October 2007).
Denmark Fat Tax
In March 2003, Denmark became the first country in the world to introduce laws to severely restrict consumption of trans fats. This has been reported as a ban on trans fats, but the law is on ingredients rather than final products and the limit was placed at 2% of fats and oils to be used for human consumption. i.e. no food that humans may eat can contain more than 2% trans fats. Given that there is no limit deemed safe for human consumption, this would still allow traces of these ‘Franken-Fats’ to get into the human body where they cannot be metabolised. It was however, a bold move and one followed by Switzerland (April 2008) and New York City (for restaurants – enforced in December 2006 to take effect from July 2008) but sadly not adopted worldwide.
Such a progressive move by Denmark has been followed by the astonishingly regressive move – adopted in October 2011 – to tax foods containing a certain level of saturated fat. The magic number has randomly been set at 2.3% – foods above this level of saturated fat (by weight) will be taxed at the rate of 16 Danish Kroner per kilogram of saturated fat.
Time Magazine helpfully gave us some examples of what this will mean for standard food items: On October 1st “The average price of a half-pound package of butter increased by 2.5 krone (or 45 U.S. cents). A pound of cheese rose from 34.5 krone ($6) to 36 krone ($6.50). And don’t even think about lard. In a single day, the cost of a half-pound block of pork fat skyrocketed from 12 krone ($2.15) to 16 krone ($2.85) — a 35% increase.”
What are fats?
Fats, commonly known as lipids, consist of a wide group of organic substances that are not soluble in water. In simple terms, fats are chains of carbon atoms (chemical symbol C) with hydrogen atoms attached (chemical symbol H) and they have a COOH group at one end (carbon, oxygen, oxygen and hydrogen). There are two groups of fats in which we have a nutritional interest – saturated and unsaturated. Within the unsaturated category, there are two further types – monounsaturated and polyunsaturated fats.
Saturated fats are the most stable fats (this is merely a statement about chemical structure). They have all available carbon bonds filled with (i.e. saturated with) hydrogen. Saturated fats are solid at room temperature. Interestingly, when our glycogen (storage form of glucose) capacity is full, the liver turns the excess glucose (from carbohydrates) into fat in the liver and it turns it into saturated fat. If saturated fat is bad for us, this could be the first example of the human body, in normal circumstances, trying to kill itself. Breast milk is also high in saturated fat, so did evolution also design us to kill our offspring? I have my own views on this; I’ll let you develop yours.
Unsaturated fats, quite simply, have pairs of hydrogen atoms missing. Monounsaturated fats have one double bond in the form of two carbon atoms ‘double-bonded’ to each other and, therefore, lack two hydrogen atoms. Mono means one and hence, with monounsaturated fat, there is one double bond. Monounsaturated fats tend to be liquid at room temperature (but solid at fridge temperature) and are the next most stable fat. The best known monounsaturated fat is oleic acid, the main component of olive oil. Oleic acid is also found in the oils from almonds, pecans, cashews, peanuts and avocados.
On the web site “margarine.org.uk” (described on the site as “the mouthpiece of the margarine and spreads industry”), unsaturated fats are described as follows: “In unsaturated fats, some of the carbon atoms are joined to others by a double bond and, therefore, could accept more hydrogen atoms.”[i] They could accept more hydrogen atoms. Isn’t that just a wonderful way of saying they are missing some hydrogen atoms (and are therefore less stable)?
Normally poly means many, but, in the case of polyunsaturated fat, it can mean only two. Polyunsaturated fats have two or more pairs of double bonds and, therefore, lack four or more hydrogen atoms. Polyunsaturated fats are liquid at room and fridge temperature. The two polyunsaturated fats found most frequently in our food are double unsaturated linoleic acid, with two double bonds, also called omega-6; and triple unsaturated alpha-linolenic acid, with three double bonds, also called omega-3. (The omega number indicates the position of the first double bond. If the double bond is three carbon atoms along from the right hand end, this is an omega-3 fat. If it is six carbon atoms from the right hand end, this is an omega-6 fat. The logic comes from the Greek alphabet, which goes from Alpha to Omega – like we go from A to Z). Omega-3 and omega-6 fats are called “Essential Fatty Acids” because the body cannot make them, so it is essential that they are consumed.
It is not widely known that all fats and oils, whether of vegetable or animal origin, are a combination of saturated, monounsaturated and polyunsaturated fat. Coconut oil has the highest saturated fat content of all foods at 92% saturated, 6% monounsaturated and 2% polyunsaturated. Lard is 41% saturated, 47% monounsaturated and 12% polyunsaturated. Olive oil is 14% saturated fat, 75% monounsaturated and 11% polyunsaturated. The above are 100% fats, so we can usefully compare their composition as percentages. Butter has a significant water content and a trace of protein, so 100 grams of butter has 51 grams of saturated fat, 21 grams of monounsaturated fat and 3 grams of polyunsaturated fat.[ii]
We simply cannot eat “saturated fat” – no such food exists in isolation in nature. A healthy human, who only eats real food as provided by nature can only reduce intake of saturated fat by reducing intake of all fats. An unhealthy human, who eats things that man makes, can reduce saturated fat intake and have this artificially ‘replaced’ by man-mad Franken-fats and/or carbohydrates – both substantially worse for us than nature’s real fats.
The role of Fat
Fat is utterly vital for human health – dietary fats serve four key purposes:
1) They provide the essential fatty acids (EFA’s);
2) They are the carriers of the fat soluble vitamins A, D, E and K;
3) They supply the most concentrated form of energy in our diets;
4) They help make our diets palatable. Food with little or no fat can be quite tasteless and sometimes difficult to digest.
Fats are crucial for every aspect of our wellbeing as they form the membrane (protective wall) that surrounds every cell in our bodies. Excluding water, our brains are approximately 60% fat (lipids in fact, including cholesterol).[iii] Fats also play a crucial role in cushioning vital organs, as some people have tragically found out when fat (and lean tissue) has been lost suddenly on a very low calorie diet. Put simply, with the right fats and enough of them our cells are strong, without them they are weak and prone to attack.
Let us look at these four key roles in more detail.
1) Starting with the EFA’s, good sources of the essential fats are as follows: omega-6 is provided by meat, eggs, avocado, nuts, whole grains and seeds and their oils (sunflower seeds, rapeseeds and pumpkin seeds as common examples). Omega-3 is found in meat, fish and fish oils – salmon, halibut, shark and swordfish being particularly valuable sources.
Omega-6 deficiency may cause: growth retardation; eczema-like skin conditions; behavioural disturbances; arthritis-like conditions; liver and kidney degeneration; excessive water loss through the skin accompanied by thirst; drying up of glands; susceptibility to infections; wounds fail to heal; sterility in males; miscarriage in females; heart and circulatory problems; dry skin and hair; dry eyes and hair loss.
Omega-3 deficiency may cause: growth retardation; dry skin; behavioural disturbances, tingling sensations in arms and legs; weakness; impairment of vision and learning ability; high blood pressure; sticky platelets; tissue inflammation; mental deterioration and low metabolic rate.
Both lists present a compelling case for ensuring adequate consumption of essential fats.
2) Moving on to the four fat soluble vitamins – A, D, E and K. (We can become blasé about the role of vitamins and minerals in the body. It may be interesting to read the following lists with the mindset – would you personally like to have any, or all, of the following functions impaired and can you be sure that you eat the foods necessary to deliver these vital nutrients?)
- Vitamin A has many functions within the body. It is needed for our sight, cell function, skin, bones, growth, reproduction, blood formation and to fight infection. Vitamin A is particularly important for pregnant women and growing children. Deficiency in vitamin A can lead to: sight conditions generally and night blindness particularly; growth and reproductive impairment; increased susceptibility to infections; and rough, dry, scaly skin. Retinol is the pure form of vitamin A – the form used most easily and readily by the body. This makes for a memorable connection between retinol, the retina of the eye and the role vitamin A plays in sight.
There is much debate as to whether plants can provide adequate vitamin A, or whether it needs to be consumed in an animal product. We can say the following with certainty: a) only animal products contain retinol; b) plant sources of vitamin A come in the form of carotene, which requires conversion within the body into retinol; c) even with Beta-carotene, the carotene most easily converted into retinol, there is substantial loss such that the conversion ratio is at best 6:1 (“The accepted 6:1 equivalency of beta-carotene to preformed vitamin A must be challenged and re-examined in the context of dietary plants”);[iv] d) not every person is capable of converting carotene to retinol “Diabetics and those with poor thyroid function cannot make the conversion. Children make the conversion very poorly and infants not at all”[v] and e) carotenes are converted by the action of bile salts and very little bile reaches the intestine when a meal is low in fat. Our grandparents put butter on their vegetables for good reason. We can confidently assert, therefore, that animal food generally, and liver particularly, are the best sources of vitamin A.
- Vitamin D is critical for the absorption of calcium and phosphorus. Vitamin D is increasingly being studied in nutritional journals and its possible role in cancer prevention is being explored. Deficiency in vitamin D can lead to tooth decay, muscular weakness and a softening of the bones (rickets), which can cause bone fractures or poor healing of fractures.
Vitamin D is found naturally in oily fish (for example herring, halibut, catfish, salmon, mackerel and sardines) and unnaturally in fortified breakfast cereals. Vegetarians would need to eat 26 medium eggs each day (1,634 calories) to get 10 micrograms of vitamin D – considered an “adequate intake”. Mushrooms, which have been exposed to sunlight, are the only conceivable option for vegans. Over two kilograms of such mushrooms would need to be sourced and eaten daily to deliver 10 micrograms of vitamin D. Ideally, but not an option for vegans, these would need to be consumed with butter to make them ‘bio-available’ to the body.
- Vitamin E is a generic term for a family of fat soluble vitamins active throughout the body. We are learning more about the different forms of vitamin E and more of them are being found to have unique functions. The key role of vitamin E is as an antioxidant. The oxygen that we need to breathe can make molecules overly reactive and this can damage cell structure. This imbalanced situation involving oxygen is called oxidative stress. Vitamin E helps prevent oxidative stress by working together with a group of nutrients (including vitamins B3, C and selenium) to prevent oxygen molecules from becoming too reactive. Vitamin E protects the skin (cells) in much the same way as it protects other cells. We hear little about the possible heart protection role of vitamin E, yet it acts as an anti-blood clotting agent and it maintains healthy blood vessels.
Deficiency in vitamin E can lead to dry skin, poor muscular and circulatory function, damage to red blood cells and blood vessels and an inability of the white blood cells to resist infection.
Vitamin E is found naturally in seeds, nuts and oils that derive from these. Hence, we don’t need to eat animal foods to obtain vitamin E, but we do need to consume fats. Sunflower seeds are one of the best sources of vitamin E and they have 51 grams of fat per 100 grams of product.
- Vitamin K has a number of important functions, such as its role in blood clotting and wound healing. Vitamin K is very important for the health of our gut and it is being destroyed with the high modern consumption of anti-biotics, leaving humans prone to imbalance in the gut flora and concomitant illness. Deficiency in vitamin K complicates blood clotting and can manifest itself in nose bleeds, bleeding gums, heavy menstruation or even blood in the urine or stools. A propensity to bruise can also be a sign of vitamin K deficiency.
Vitamin K comes in two forms: K1 and K2. K1 is found in plants, green leafy vegetables particularly, and is also called phylloquinone. Vitamin K2 is found in animal foods. K2 is also known as menaquinone and comes in different forms – MK-4 through to MK-10 (the ‘MK’ comes from a phonetic abbreviation of MenaKwinone). Meat is a primary source of MK-4. Eggs and calcium rich hard cheese are particularly good sources of MK-7, 8 and 9. The Rotterdam Study[vi] concluded: “Intake of menaquinone was inversely related to all-cause mortality and severe aortic calcification. Phylloquinone intake was not related to any of the outcomes. These findings suggest that an adequate intake of menaquinone could be important for CHD prevention.” I share this as another example of the animal form of fat soluble vitamins being the most useful – in the context of current public health advice steering us away from these nutritious foods.
3) The fact that fat supplies the most concentrated form of energy in our diets is used against this macronutrient in today’s modern, obese environment. It is argued in our calorie obsessed world that we should avoid fat because of its calorie content. There are two ironies here:
a) Man would not be here today without the energy supplied by fat (predominantly from animals, but also from nuts) during evolution and particularly during the ice age and in regions of the earth where vegetation was not available. At 80-90% water and containing only approximately four calories per gram, humans would simply not have been able to get enough vegetation to survive. (If any ancient berry approximated to, say, a wild strawberry in nutritional content, Neanderthals would have needed over three kilograms of berries to provide 1,000 calories).
b) The second irony is that fat cannot make us fat – only carbohydrate can do this. The glycerol backbone, which turns fat particles into a triglyceride (the form in which adipose tissue is stored), is produced in the presence of glucose and insulin – the environment created following the consumption of carbohydrate.
4) In this carbohydrate consuming/calorie avoiding world, we have lost the awareness of the palatability and unique satiety of fat. 100 grams of a well known brand of cereal, marketed to slimmers, contains rice, wheat (whole wheat, wheat flour), sugar, wheat gluten, defatted wheat germ, dried skimmed milk, salt, barley malt flavouring, and a number of added vitamins to give the product nutritional value. This brand has 76 grams of carbohydrate and 379 calories per 100 grams of product. Most people could eat 100 grams of this with relative ease. (I work with people who commonly binge on cereal). Try to eat 300 grams of “pork chop, boneless, raw lean and fat” – calculated by the USDA database as having slightly fewer calories than the cereal and no carbohydrate content. It will be substantially more filling, and therefore more difficult, to eat the meat than the cereal.
What Denmark now needs to tax
So, Denmark has started down the road of destroying human health. People who eat real food will be penalised for all fat consumption, as they cannot reduce saturated fat consumption in isolation. People who eat fake food will be able to increase their consumption of man-made, bleached, deodorised and emulsified alternatives to real fats and/or their consumption of fattening carbohydrates.
However, I wonder if Denmark knows which foods contain more than 2.3% saturated fat?
From the extremely useful United States Department of Agriculture -all-foods database, we can find the following:
Meat
- Beef, Porterhouse steak, raw, trimmed to 1/8″ fat (USDA reference = URMIS 2145) will be taxed; Beef, Sirloin, lean only (URMIS 2244) won’t be. Hence humans will be encouraged to eat an unnaturally high ratio of protein to fat – taxing (excuse the pun) the liver and our vitamin A requirement further.
- Pork chop, boneless, raw, lean and fat escapes tax with 1.5% saturated fat. However, Pork, fresh, loin, top loin (chops), boneless, separable lean and fat, raw [America's cut chops, Pork top loin chops, Strip loin chops, URMIS #3369] will be taxed at 2.5% saturated fat. Again – the fact that pork has far more unsaturated than saturated fat seems to have escaped the wisdom of Danish-powers-that-be. Somewhat amusingly, the notoriously ‘low fat’ meat, favoured by fat phobics, venison, will be taxed: Venison, game meat, deer, ground, raw has 3.4 grams of saturated fat per 100 grams of product. Interestingly, venison is the only meat thus far that I have been able to find with more saturated than unsaturated fat. Not that one fat is better or worse than the other – all real fats are vital – but just to dispel nonsense that we have been told.
Fish
- Fish – that ‘heart healthy’ oily fish, which we are encouraged to eat – will likely be taxed. The less nutritious white fish likely won’t be. Mackerel has almost twice the saturated fat of our boneless pork chop above. Again – the polyunsaturated fat ‘darling’ of dietitians will suffer for being in the same food as something with more than 2.3% saturated fat content. Damn nature for putting all the fats in all the foods!
Eggs
- Eggs, although only one third saturated fat and with the main fat being that so-called super fat “mono-unsaturated” – will be taxed. That’s a tax on a product containing omega-3 and omega-6, complete protein and a phenomenal range of vitamins and minerals – the closest a vegetarian will get to a super-food.
Dairy products
- Cheese, with the vital vitamins A and D (the UK currently gets approximately 50% of the minimum vitamin A requirement and barely 25% of the paltry vitamin D requirement) and an abundance of the crucial minerals calcium and phosphorus, as well as zinc, will be taxed heavily. That’s osteoporosis set to continue its relentless rise and rickets in children set to continue.
- Milk – if you want the fat-free nonsense, with the delivery mechanism for the fat soluble vitamins removed – no tax. If you want the ‘full fat’ version (still only c. 3-4% total fat) the saturated fat content could get close. Those dairy farmers had better to be able to measure this one to the gram or ml – it’s going to be touch and go!
Nuts, Seeds & Fruit
- Sunflower seeds will be taxed, at 4.5 grams of saturated fat per 100 grams of seeds. The 18.5 grams of monounsaturated fat and the 23.1 grams of polyunsaturated fat in sunflower seeds get ‘taxed’ indirectly by association. At a whopping 33mg of vitamin E per 100 grams of product, sunflower seeds are unbeatable for vitamin E. This is the body’s natural anti-oxidant, so we are taxing a unique natural anti-oxidant that would help with heart and blood health.
- Any nuts – prepare to pay highly for the natural fats and terrific amounts of nutrients in nature’s gold nuggets in a shell.
- Avocado just escapes at 2.1% saturated fat. Olives are also dangerously close at 2% saturated fat.
Real fats
Butter is not the only real fat that will be taxed. That ‘superfood’ of the Mediterranean diet, olive oil, is 14% saturated fat – 9 times that of our boneless pork chop. That will get a hefty fine on its claimed healthful benefits. Sunflower oil ditto. Lard, mostly unsaturated fat (60% infact – not many people know that) will also get clouted, despite this being (like butter) one of the most stable, and therefore safe, fats to cook with.
I think that’s covered real foods – meat, fish, eggs, dairy products, nuts, seeds & fruit and real fats. Vegetables and sugary fruits are the only real foods to escape this Danish madness. I have deliberately not mentioned any manufactured foods because I couldn’t care less about any of them. Tax them out of reach. Heck – ban the horrors – but don’t attack nature’s real foods when the real culprits are those made by man.
A final thought
My passion is obesity. All I care about is how we can reverse this horrific epidemic that we inflicted on our fellow humans. I am convinced that our change in dietary advice (USA 1977 and UK 1983) was responsible for the concomitant obesity epidemic.
I open my book The Obesity Epidemic: What caused it? How can we stop it? with the following quote from the UK document (Proposals for nutritional guidelines for Health Education in Britain (1983))
“The previous nutritional advice in the UK to limit the intake of all carbohydrates as a means of weight control now runs counter to current thinking and contrary to the present proposals for a nutrition education policy for the population as a whole… The problem then becomes one of achieving both a reduction in fat intake to 30% of total energy and a fall in saturated fatty acid intake to 10%.”
And so started the obesity epidemic…
The data in the UK National Food Survey is extremely comprehensive, to the point of including detail on both macro and micronutrients. The information on macronutrients says that we consumed 51.7 grams per person per day of saturated fat in 1975 and 28.1 grams in 1999. The food examples in the data tables support this – all fat, butter, meat, whole milk and eggs – real foods and sources of saturated fat – are down. Dramatically in some cases – we eat half the number of eggs that we used to and one fifth of the butter and whole milk.
During the time, in which we all but halved saturated fat intake in the UK, obesity increased from 2.7% for men and women in 1972 to 22.6% for men and 25.8% for women in 1999.
Fat doesn’t make us fat – only carbs can do that. Theoretically, biochemically and empirically, the evidence is irrefutable. Although not to the Danes apparently. They have shown themselves to be a few rashers short of a packet.
[i] http://www.margarine.org.uk/whatisfat-types.html#unsaturated
[ii] United States Department of Agriculture nutritional database. www.nutritiondata.com
[iii] McIlwain, H. and Bachelard, H.S., Biochemistry and the Central Nervous System, Edinburgh: Churchill Livingstone, (1985). Estimates the composition of the brain to be (approximately) 78% water, 10-12% lipids, 8% protein, 2% soluble organic substances, 1% carbohydrate and 1% inorganic salts.
[iv] Solomons, N. W. and J. Bulux. “Plant sources of provitamin A and human nutriture.” Nutrition Review, July 1993.
[v] Sally Fallon and Mary G. Enig, “Vitamin A”, (March 2002).
[vi] Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC, “Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study”, The Journal of Nutrition, (November 2004).
Eggs & Prostate Cancer
Yet another story came out over the past few days trying to demonise a real food. The Daily Mail ran the story “Eating just THREE eggs a week ‘increases chance of men getting prostate cancer’”
I have the following points to make:
1) Association vs causation:
This study makes the usual and unforgiveable mistake of assuming that association means causation. To give an example, we can observe that people in the bath may be singing. This means that we could say singing may be associated with being in the bath. However, we can no more say that bathing causes singing than we can say that singing causes bathing!
If the study had measured sock colour, these men may also have worn blue socks – would the headline then be “wearing blue socks increases the chance of men getting prostate cancer?” Yes, it really is as daft as that. To jump from observed association to causation and risk is the most outrageous bad science and yet studies do it every day and the media amplifies it every time.
2) How risk is calculated:
Notwithstanding that association can say nothing about risk or causation, here is how ‘risk’ is calculated between two studies… If in one study people ate no eggs and 1 in 100,000 people died and in another study people ate eggs and 2 in 100,000 people died – they will say “Eating eggs doubles your risk of dying”. They always ignore the denominator (the bottom number in the equation – in these cases the study size). The second group still only had a 1 in 50,000 chance of dying full stop and yet the headline tells you you’ve got twice the risk – this is indefensible scare tactics.
The summary of the original research article is here. The study followed 27,607 men over a 14 year period from 1994 – 2008.
The study looked at the 3,127 men initially diagnosed with what is called “non-metastatic prostate cancer” (“non-spreading” or localised prostate cancer) and then reviewed those who went on to develop, as they called it “lethal prostate cancer”. (I assume “terminal” would be a word we would more typically use). The findings were “we observed 199 events during 306,715 person-years”. That’s an incidence rate of 0.0649%. That’s a 1 in 1,541 incidence. To put this in perspective, our chance of dying in a car crash was put at 1 in 200 .
The summary stated: “Men who consumed 2.5 or more eggs per week had an 81% increased risk of lethal prostate cancer compared to men who consumed less than 0.5 eggs per week (HR: 1.81; 95% confidence interval (CI): 1.13, 2.89).”
There are three things wrong with this:
i) The completely unjustifiable leap from association to risk must be reiterated. For researchers to claim “increased risk” from an observed association is simply not valid. This is the kind of food survey that Harvard Public Health use in studies like this (if not the same one). This shows how many foods are being studied, in how many different quantities, relying on subject recall of what they have eaten – and that’s just the food, let alone other lifestyle factors – smoking, exercise, stress, location, marital status, financial circumstances etc.
ii) The study is claiming that in amongst the overall incidence of 0.0649%, those people eating 2.5 or more eggs per week had almost ‘double the chance’. As an example, those eating more than 2.5 eggs a week could have had a 0.09% incidence rate and the 0.5 egg group could have a 0.05% incidence rate (there’s a difference of 81% between those two percentages and the overall incidence can still be 0.0649%). Can you see the absolutely tiny number behind the 81% risk massive headline?
PLUS – this is critical and irresponsible not to have highlighted – after the number 1.81% the 95% confidence interval is given as 1.13 to 2.89. What this means is – the researchers are 95% confident that the observed differences between the higher and the lower egg consumption were somewhere in a range between 13% and 189% – that’s one heck of a range. This means that they cannot even establish an association within a fourteen fold range, let alone make a claim of 81% with any degree of accuracy.
iii) There is a very good NHS review here. This suggests that the NHS have obtained a full copy of the report (not just the summary) and they have been able to see that “Men who consumed more red meat or eggs tended to exercise less and have a higher BMI, and were more likely to smoke and have a family history of prostate cancer.”
Do you wonder if smoking, exercising less, having a higher BMI and having a family history of prostate cancer was more relevant that any egg consumption?!
Why would so called researchers mislead the public in this way? Academics have egos and they want their ‘research’ widely published and talked about. The headline “Smoking causes cancer” is not new; “Obesity causes cancer” has been said before (whether correct or not is immaterial – it’s not new news). How about “Family history of prostate cancer increases your risk of getting cancer” – hardly surprising. So, pick the one headline that would be new. “Wearing blue socks increases the chance of getting prostate cancer?” That would be new – but absurd, so let’s pick the one vague association that will get the Daily Mail headline – it must be the eggs!
Even if the eggs have any relevance at all – what else could be happening at the same time? Were the egg eating men Paleo dudes, or were they egg and soldier addicts (blame the bread), or egg and brown sauce addicts (blame the sugary gunge), or even egg and bacon addicts who hadn’t selected their bacon carefully enough (blame the processed meat).
3) Cholesterol is vital not evil:
The suggestion from the ‘experts’ that cholesterol could be the cause of harm is laughable. Cholesterol is protective – one of its most important functions is to repair cells – not attack them. The longevity facts associated with high cholesterol are related in major part to the protective benefits that cholesterol has for cancer (cell repair – it should be obvious). My book, The Obesity Epidemic: What caused it? How can we stop it?, has many studies showing the benefits for cancer and cholesterol. The body makes all the cholesterol it needs (cholesterol in food makes no difference), but you never know what survival signals the body could send out. Should the headline have been “men with prostate cancer crave eggs!”?
4) Common sense:
Would nature really put both the essential fats (omega-3 and omega-6), amino acids, complete protein and the most phenomenal range of vitamins and minerals in the tiny, humble egg if it were trying to kill us at the same time? By the way – the reason why eggs contain so much cholesterol is because it takes a lot of cholesterol to make a healthy chicken. It takes a lot of cholesterol to make a healthy human as well!
5) Conflict of interest:
Finally – always follow the money – remember who stands to gain if we demonise eggs – the sugary cereal companies. The Kellogg’s and General Mills who sponsor the American Dietetic Association , to make sure that dieticians are ‘on message’.
Eggs have only recently been exonerated for being harmful for cholesterol even though Ancel Keys, the man who started the war on fat and cholesterol declared years ago “Cholesterol in food has no impact on cholesterol in the blood and we have known that all along”. No sooner have eggs been let out of jail for containing cholesterol – they need to be put back in jail or (heaven forbid) people will start eating eggs again for breakfast and not coco-pops.
Andy and I have just had a three egg omelette each for breakfast. Enjoy whatever real food you guys have!
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