How the TV bout Sugar vs. Fat was rigged

Just how accurate and informative was BBC2’s Horizon program on Wednesday that aimed at scientifically answering the question: which is more deadly: Eating lots of sugar or lots of fat? The format was to feed two doctors who were also identical twins – Alex and Chris – unlimited amounts of one or the other. Alex got a low carb/high fat diet while Chris followed the traditional low fat/high carb diet with added the sugar.

Officially the result was an undramatic draw. Neither is to blame for making us sick and overweight individually. It’s only when they join forces do the twins become evil – think ice cream or glazed donuts. In fact the program’s headline message was the familiar, but still welcome, advice to avoid most processed food.

Dieticians don’t understand the diet

But few viewers will have been left in any doubt that as a lifestyle choice the low carbohydrate diet is a bad thing. This is a highly misleading conclusion for reasons that will become clear. A charitable explanation would be that those setting up the experiment didn’t understand how this diet actually works or how the body responds to it.

Less charitably it might be that the 40-year-old low fat diet lobby is very influential and has been under considerable attack recently from those who point out that demonising fat isn’t supported by good evidence and that there are good reasons why feeding people a heavy diet of carbohydrates can lead to metabolic problems.

So HealthInsightUK asked some of our expert contacts and contributors to give us their response to the program.

Hannah Sutter writes…

No one would want to be on Alex’s diet, certainly not any of the people I know who regularly eat like this and report great results. The aim of going on a really low carb diet is to reach the point where the body switches from using glucose (from carbohydrates) for fuel to being able to burn fat in the muscles. Fat gets released from the fat stores (why this diet is good for losing weight) which the liver uses to make compounds called ketones that the brain can use for energy.

Alex did poorly compared with Chris on two key trials – a test of his thinking skills and how well he could sprint up hill on a bike. He lost more weight at the end but half of that was supposedly protein that his body had turned into carbohydrates to make up for the ones missing in his diet.

But Alex wasn’t on a ketogenic diet which meant that these supposedly “scientific” comparisons were deeply misleading.

To drop your carbs low enough be become ketogenic you have to limit your cheese intake because it has quite a lot of sugar. But Alex was given unlimited diary by the dietician Amanda Ursell. This is no surprise as Ms Ursell has no expertise in low carb high protein ketogenic diets.

Wrong and misleading

Someone who understood the ketogenic diet would also have increased the amount of protein available because it is well known that the body breaks down muscle for carbohydrate unless there is enough protein in the diet. So the starting point was not only wrong but misleading. We were not comparing two bodies being fuelled by different energy sources. If Alex had been producing ketones he might well have had the energy available to power his brain in the thinking test.

This fundamental misunderstanding about low carbs and ketones showed up most clearly in the cycling test. A number of clinical trials have shown it takes about 6 weeks for a body, to become ketoadaptive, (ie to perform as well on fats as on glucose) and you need to exercise in that time help the process. Not only was Alex probably not ketotic, but had only been on the diet for a few weeks and had done no exercise.

But even a properly ketoadapted athlete would have used glucose as a power source for a sprint because the ketogenic diet comes into its own in endurance sport. The external expert was fundamentally wrong when he told the twins you cannot burn body fat for energy. This is exactly what happens when you are in ketosis and my top athletes use fat burn to deliver top results.

The tests, along with the rest of the program were more about entertainment than proper science. So it was particularly infuriating when Alex, on camera, dismissed Dr Robert Lustig’s “Insulin Hypothesis” that explains the toxic nature of sugar, for not being supported by robust science. Having read his book I can say that it is a lot more robust than this naff, poorly constructed and deeply misleading study for the BBC.

We eat less and still we are fatter

Equally unimpressive was Dr Susan Jebb who was asked to comment as an expert. In her calm and very assured manner she tells the audience that her studies have shown that no extreme diet makes any difference to health and that to lose weight we should simply eat a little less and move a little more.

It sounds convincing but Dr Susan Jebb has never carried out a proper study into a high fat ketogenic diet and she believes that saturated fats cause heart disease, even though the evidence is very weak. What’s more I have yet to find any published peer reviewed clinical trial that shows exercise has any influence on serious weight loss.

The icing on this high carb cake of misinformation is that there is no peer reviewed published clinical trial that shows that eating a bit less will have any real impact on serious weight loss. In fact, according to official government statistics, as a nation, we eat less today and do more exercise than we did 10 years ago but we are fatter than ever.

Hannah Sutter

Hannah Sutter

Hannah Sutter was a lawyer for 17 years before becoming involved in the low carb diet and obesity. See her book ‘Big Fat Lies’. She runs a specialist service for people wanting to use the diet to reverse obesity, treat diabetes and for general wellbeing. Clinical trials are being run on her range of completely natural low carb high protein foods.


Editor: Jerome Burne |

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  • You can get a handle on Ms Ursell’s viewpoint at – she’s a carb queen. The low carb guy should have had expert advice from Volek, Phinney, Noakes et al. He was in modest ketosis with ketones visible on a flipchart in the cycling segment at 0.5 and below, hardly optimum.

    I was annoyed by the reference to “muscle loss” when a BodPod does not measure this – only body fat and fat free mass (FFM). The loss of FFM could have been largely water, but it was made out to be a big problem of muscle loss.

    The OGTT at the end gave predictably poor results in the low carber who had not had any carbs for a month – Quelle Suprise ! Don’t we know already that taking carbs for three days ahead of an OGTT is required to get a sensible result.

    Susan Jebb published a paper in the mid 90s pointing out that UK calorie intake had declined while obesity tripled in 20 years, yet she still expects us to believe it’s all about eating a bit less and moving a bit more. She is an epidemiologist though, and probably drives by only looking in the rear view mirror.

    • Hmmm. Peter Attia eats lots of cheese, and he’s in ketosis…

      • Editorial

        There are obviously a lot of unknowns or at least uncertains here. Any more clarification on this very welcome.

        • I agree – far too many variables for this ‘experiment’ to give accurate results, as demonstrated by numerous and differing reviews by health experts. I had my own frustrations (, but ultimately it was the misinformation that is all too often put out there for a public wanting of information that will help them lose weight and be able to sustain it. It is human nature to hear what you want to hear! As a nutritionist, I still think the best way forward is to retrain eating habits which can only be achieved once sugar addiction has been conquered. Robert Lustig’s research supports this thoroughly. That means avoiding processed foods with hidden sugars. Otherwise it is like giving a heroin addict a few shots a day and still expecting them to rationalise and make sensible lifestyle choices!

          Whilst the scientists are debating the science, surely the most important issue here is to deal with the food manufacturers. The buck surely stops with them – the correlation of obesity/diabetes to the development of the processed food industry is clear. Publicly procrastinating over unclear science and broadcasting mixed, inaccurate messages is not going to halt the rise in diabetes/metabolic syndrome and its related health risks.

      • Yeah that bit caught me, I’m ketotonic and eat a lot of cheese.

        I’m UK perhaps US cheese generally comes with added sugar? Or perhaps I’m missing something.

  • A useful analysis but still a little wide of the mark regarding what was wrong with the allegedly high fat diet. In fact the protein levels were too high, not too low. We know that the US twin had had weigh problems in the past so it’s highly likely that to sustain ketosis he would need fat levels at 70% or more of total calories, especially if his cortisol levels were raised. My work with obesity shows time and again that we need a high fat low carb diet and not a high protein low carb diet for the weight to come off as desired and muscle mass to be preserved. The nutritionist gave herself away when she said ‘no one eats a slab of butter’, revealing her bias that she just couldn’t bring herself to design a genuinely high fat diet due to her attachment to the flawed ‘healthy carbs’ hypothesis. I would have expected to see avocado, olive and seed oils, coconut and macadamias included and emphasised on this diet. Frustrating. I’d love to have that sort of budget and a brief to educate.

  • Not Alex – Xand is his name

  • I agree with Dawn in that there are many ketogenic diets which range from high fat through to simply very very low carb and each person can have quite different reactions. Over the past 7 years we have managed and provided food for literally thousands of people following a ketogenic low carb diet and for some cheese can throw them out of ketosis quite easily due to their sensitivity to lactose while for others the issue is actually protein as it can trigger a significant insulin response. I cannot say what was affecting Xand on the diet but I am sure that the advice he was getting from Amanda would have been lacking in real expertise as I happen to know she has no expertise in this type of dieting.

    • Nice to hear from you Hannah. You’re right, getting it right for individuals is more of an art than a science and we agree that they chose the wrong nutritionist for the task.

      • HI
        You are so right about the US cheese and in the UK hard cheeses should be sugar free. Naturally soft cheeses do contain lactose. We have learnt over the past 9 years to strongly recommend a limit of just 40-50grams of cheese a day whilst people are in their first month of ketosis as this seems to guarantee the best results for most although as Dawn says, it is an individual journey. I was not convinced that Xand was in proper ketosis and I suspect that might be down to a number of factors which may include the cheese and the protein levels. The programme was set up to be anti low carb because the programme organiser chose not to appoint Zoe or John to be the nutritionist with Xand which would have been the professional choice.

  • American cheese appears to generally contain a couple of grams of sugar per 100g, but UK cheese, virtually zero.

  • The carb content of cheese is interesting..

    The hard cheddar I eat is 1.3g per 100… Hardly a lot of sugar!

  • Again interesting comments from those who sell low carb products and books – conflict of interest strikes me!

    • Editorial

      Yes the conflict of interest is a tricky one. I suppose in some utopian world there would be disinterested experts in universities or other research foundations who had security of tenure, good salaries, no commercial links and tested drugs, vitamins, diets and all all other health related products and approaches and provided doctors and patients with perfect and unbiased advice.

      We are of course a long way from that certainly as far as drugs, are concerned – take a look at the post on this site about drug companies regarding side-effects as a commercial secret. It is also the case that decades of low fat advice has generated shelffuls of products and that companies producing carbohydrate-based products fund a considerable amount of research; another of our posts on the government SACN committee responsible for issuing guidelines on carbohydrate consumption (SACN or sack ‘em) reports on extensive commercial interests among committee members which seems to have skewed their judgement.

      So what do you do if you are an expert in some area not funded by large companies – such as the low carb approach or a nutritionist who finds vitamins and other supplements helps patients? What if there is no one producing quite the product that you have researched and found beneficial? Do you give it away?

      If you are a consumer how do you decide on product/treatments when vested interests abound? My own feeling is that, as with most other things in life where you have to make decisions based on imperfect information – best household products to buy, best bank, best school, best partner – you make a judgement on a variety of inputs – the opinion of people you respect, what your own research reveals, what you can gauge about the trustworthiness of the person or organisation and so on.

      I would suggest that when the realisation of commercial interest strikes that is the start of a process rather than the end

  • There’s another big point about this. The chap on the non-carb diet was considerably heavier than his brother. Given that being identical twins they would have a similar power output, the heavier one is at a big disadvantage climbing as power to weight ratio is what matters doing that. That’s why all the great cycling climbers are really light.
    Box Hill is 400ft. of a climb. Now I have in my head at all times (I’m a keen cyclist) that a pound will delay you half a minute in a 2000 ft climb, therefore it will delay you 6 seconds on Box Hill. I reckon from their BMI’s that the US chap is about 20lb heavier than his brother.. That’s two minutes of a difference. Going hard that is around the gap you would expect.

  • ” you have to limit your cheese intake because it has quite a lot of sugar”

    Where does this come from? Cheese has 1% CHO in general. It contains no or virtually no sugar!

    Pity: it detracts from an otherwise excellent article.

    • I could be wrong but I imagine Susan Jebb is not a doctor. There’s something you have to realise about such people (People in high positions with academic power). If they hold contrary opinions to others of similar ilk etc., they may be totally wrong.
      It is said that she once said that there wasn’t a shred of evidence for the efficacy of the Atkins diet. I don’t know if she did or not but…
      Not being a doctor is a bit of a disadvantage to seeing the full clinical picture IMO. I’m a retired doctor but when I saw the doctor with the beard tell the protein doctor that the diet was giving him early diabetes, from what I know about Atkins etc., I was absolutely sure that this was wrong. It just could not be. His problem (the doctor’s) was that he absolutely nothing about the Atkins diet, something which is true about most doctors. I’ve known about it for years and its beneficial effects but only started it properly myself recently. It’s going to be hellishly difficult to persuade the lovers of the wonderful all-singing all-dancing NHS that the NHS apart from a few visionaries who are considered bats, is batting on the wrong wicket with a tennis racket and a bowling ball.

  • I watched the programme, thinking it didn’t make sense – for example, if it’s not good for you to burn fat , then how on earth can anyone lose weight!- and that the diets they showed were ridiculously extreme. Thank you for explaining so lucidly the things that puzzled me.

  • I am a type 2 diabetic and when the “expert” told one twin that his low carb diet was causing insulin resistance and had made him pre-diabetic I could not believe my ears. I have successfully controlled my diabetes and returned my blood measurements to normal entirely through a low carb diet without drugs.
    I can only assume that they used a one-off measurement to justify a statement so contrary to logic and the experience of very large numbers of successfully controlled diabetics.
    I shudder to think how many pre diabetics may have taken this programme as authority to eat high sugar diets in future.

    • This raised sugar is normal adaptation to ketosis. I emailed scientist involved and only got defensive bullshit back. They are a scientific disgrace.

  • “This raised sugar is normal adaptation to ketosis.”

    Dr Lee,

    Are you able to give us a bit more insight on this, what physiological responses accompany lipolysis and/or ketosis and what hormones are driving them?

    One might anticipate a shift in metabolic balance from glucosis to lipolysis/ketosis might provoke a downwards trend in HbA-1C. Are such expectations correct, or might it take longer for Hba-1C results to begin to normalise?

    Their reaction is normal, btw, they begin defensive and quickly become completely mute.

    • I don’t know, but Google ketosis, hyperglycaemia/hyperglycemia, raised blood sugar etc. and you’ll get somewhere.
      I’m retired and it’s been a long time since I looked after patients though I did get a Membership in Medicine before doing Histopathology. I’ve always kept abreast of this stuff though, because the mystery interested me.
      I imagine that HbA1c is going to come down because even though the resting glucose can be a bit raised, there will be no peaks.
      Certainly that is a universal finding in all the trials I’ve read of this diet!
      I don’t know how long it will take to come down. It’s a reflection of the average over three months, apparently, so the anwer must be a good bit.

      • The capacity to gain weight and to store surplus energy as fat at the usual adipose sites is a process which confers evolutionary advantage in many species, but the advantage is commuted when conditions change, the quality or quantity of food available changes, and it becomes expedient for the creature to begin burning some of the fat reserves it has gained. Robert Atkins was quite right, a tendency to gain weight, has to be commuted to a tendency to lose it, and ‘in the wild’ hormones respond to cues, and the altered balance of hormones permits a switch in emphasis from glucosis to lipolysis and ketosis. In the modern human living in the modern world the cues tend to ensure hormones keep the metabolic balance leaning to glucosis, and this becomes an impediment to lipolysis and ketosis.

        So I am with you Dr Lee.

        High levels of insulin bar the way to lipolysis and ketosis; so encouraging levels of insulin to fall is good, and anything that may encourage cortisol to fall or normalise may be deemed good too, and one should be wary of over-consuming proteins and invoking gluconeogenesis. We are surrounded by a lot of eventualities that bear witness to the reality that a great many people over-consume carbohydrates and could afford to eat less, while the evidence that compels people to go low-fat isn’t half as reliable as they have us believe.

        But I was thoroughly intrigued by your direction that raised sugar would be a normal accompaniment to ketosis.

        I did as you suggested and punched terms into a search engine. I am wiser, a couple of useful results came up, but sadly not the confirmation or explanation I was seeking.

          • Brilliant! Truly. Thank you.

            Now armed with that link and the directions offered within it I can get more acquainted with the prospects, and one of the great benefits of blog and comment is that others can take up if they wish.

            Actually I have just (today) had a medical examination to rule out that the episodes of feeling faint, or twice blacking out briefly, could be attributable to underlying issues and not entirely the result of a rhinovoirus (cold-like) that has been a persistent nuisance sine 15th Jan.

            It’s a while since I last gave bloods for analysis, but in the intervening period (and mostly over the last twelve months) I have lost as much as twelve kilos in weight. I take that as an indication that the pathway to lipolysis and ketosis has been opened up, and has been done so by going low carb and intentionally high fat.

            So while I don’t care two hoots for what the lipid profile test will report, I am kinda hoping it reflects a better balance, but I am itching to learn the results of the HbA1c.

  • I finally got around to watching this Horizon episode in full, and actually I didn’t find it as contentious as I found it disappointing. It is available on the BBC iPlayer until March 3rd for those who may not have seen it.

    My principle disappointment centres around the conventional experts represented by Dr Richard Mackenzie, a lecturer and research specialist in metabolism, Amanda Ursell, a nutritionist, and Dr Susan Jebb.

    Each of these ‘experts’ could be described as belonging to the ‘cholesterol faithful’; meaning they subscribe to a groundless hypothesis that saturated fat in the diet raises cholesterol in the blood, and raised cholesterol causes heart disease. It is a commonly held believe amongst members of the medical profession, nutritionists, and people seeking funding for research, so Messrs Mackenzie’s, Ursells and Jebbs views on fats are in keeping with the vast majority of the herd, but that have very little exposure to the fats. Cholesterol is not the atherogen that Dr Ancel Keys made it out to be when he fashioned his hypothesis, and the bit about saturated fat thet he then bolted on was mere fantasy upon his part. This dictates that much of what Mackenzie, Ursell, and Jebb have come to consider to be true is riddled with the bias the trust in a false hypothesis brings. They find it difficult to debate saturated fat with an open mind.

    I don’t think the contrasting diets were described too well in their detail, but each seemed a bit extreme. And while brother Xand was said to be on a low-carb / high-fat diet, he was directed to include MUFAs and PUFAs from certain sources, saturated fat seemed off-limits, and if anything his diet seemed to be higher in protein perhaps, than it might have been in fat. There wasn’t any real doubt about Chris, his diet was undeniably high carb.

    I always thought risks of developing type II diabetes were compounded by over-consuming refined and readily digestible carbohydrates, and my experience has been that I achieved alleviation from symptoms by excluding vegetable oils and margarines rich in omega-6 PUFAs, and by cutting back upon those carbs. Indeed once I learned reals fats like butter and cream, and the native fats that come with cut of meat, could be included in the diet risk free, management of type II diabetes came a whole lot easier. An added bonus was I began to lose weight too; around 16 kilos in all, and without counting a single calorie. So the discussion towards the end involving Mackenzie and Xand that in one month he was well advanced to becoming significantly insulin resistant and type II diabetic simply jarred with me. I mean, where has this new tendency to implicate fats in diabetes (and Alzheimers) come from?

    Then there was the weight loss, and Xand had done well, but Mackenzie took the edge off that claiming that half of the loss was visceral fat but half was from muscle mass. Even if the programme makers and advisers were daft enough to advocate a no-carb diet for Xand on no account was Xands diet no-carb, although as low-carb diets go it may have trended to quite low, but Xand was not starving himself, and his diet supplied enough protein for gluconeogenesis to arise and to convert some proteins to glucose. No, Xand could well have been trending to the metabolic mode that is lipolysis and ketosis (fat burning) but the pressures upon his metabolism to venture to starvation mode and begin dismantling lean muscle to meat energy needs would not seem that great to me. I think Mackenzie slipped in an Easter egg here, and if you didn’t know an Easter egg is cartographers term for the insertion of a deliberate error.

    The program could have opened up the hormonal discussion to better effect. How much and how frequently a person eats is not a conscious choice, it is signalled by an array of hormones that act in concert and bear upon each other and in which cortisol, insulin, and ghrelin are leading examples. Appetite is not under conscious control, though what we may elect to eat may be. Dr Lustig gave value for money. It’s the insulin, stupid! In order to gain weight, sequester fat, two prime co-factors are needed, a plentiful supply of glucose to the blood, and raised levels of insulin to command that glucose of synthesised into fat and that those synthesised fats are received by the fats cells at the usual adipose sites. In order to lose weight the trafficking of fats to adipose sites must be reversed, and reversal requires a fall in the levels of insulin.

    Both Chris and Xand had relative tall aspect ratios and modestly athletic physiques, but stripped down to their boxers they did look a bit apple shaped around their middles, with waists, midriffs, buttocks and thighs that looked to me as if they could afford to shed some (I still have some way to go, btw). Each of them displayed evidence that the cofactors needed for the sequestration of body fat had been present for some years before their involvement in the programme.

    The calories count but there is no need to count the calories. The composition that makes up the calories counts for more because it is composition that bears upon hormones and thus restores the natural processes that permit natural self regulation of appetite. If cortisol and/or insulin are exposed to influences that has them running high, and if carbohydrates are plentiful metabolism enters summer mode and remains there. Summer mode is preparation for winter when food and sugary carbs become scarce, The pressure in summer mode is to carry on eating despite you’ve met the quota for the day, because added calories are needed for conversion to fat as part of the preparations for winter. Winter mode favours a metabolic balance whereby lipolysis and ketosis are permitted, and that energy stashed as body-fat gets to released to advantage.

    Many a modern human endures metabolism operating in perpetual summer mode simply because modern life and modern choices provide the cues all year round, and takes on the shape and measurements that result.

    Neither diet seemed to bear much on either of the twins cholesterol test results, but the irony seemed entirely lost on the two GPs and Mackenzie.

  • .. .. very little exposure to the facts.

    .. relatively tall aspect ratios ..


  • “COMA back in 1984 openly admitted: “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.””

    You do realize that the reason they would never do such a trial is that it would put people’s lives in jeopardy and is therefore not ethical to do?

    • Editorial

      Interesting. Are you saying that is what Coma believed or what you believe?

      • I read somewhere that that was the reason for the statement. It made sense to me.

        • What doesn’t make sense is directing a whole nation to cut down saturated fat without supporting evidence. Comma and now SACN are responsible for the “Balanced Diet” which pushed every food producer in the UK to remove saturated fats as far as they could from their food. Period. This direction has caused no end of problems for the vast majority of our population. It is true that it is impossible to get ethical approval for a trial increasing saturated fats – I happen to know this from personal experience but that ethical permission is not forthcoming because of bodies like SACN and others who have decided without clinical trials that saturated fat is bad for us. I am certain that it would be possible to get a trial approved showing a further reduction of sat fat…I have to say that in my humble opinion the buck stops with SACN and its predecessor – COMA. They are supposed to be an independent body of experts reviewing the science..Ha bloody ha.

          • I don’t get the ‘without supporting evidence’ bit. There are hundreds of trials connecting saturated fat with coronary heart disease. Look it up yourself.

          • Not only is there NO evidence for it, but the one bit of evidence on which it was based was fraudulent. Ansel Keys’ paper.
            Tests done in Framinham on a huge scale could not show ANY effect of dietary lipid on blood lipid.

          • Such a good point Garry. Indeed in 2011 a WHO funded review of all the apparent evidence connecting saturated fats with heart disease concluded in black and white that there was no connection between the intake of sat fats and coronary heart disease. The study was carried out by the team at Harvard lead by Frank Hu.

          • “Not only is there NO evidence for it, but the one bit of evidence on which it was based was fraudulent. Ansel Keys’ paper.”

            I’m aware of the accusations made against Ancel Key’s paper(s) and I’m also aware that they falsely confuse data taken from different studies many years apart to make it seem he cherry picked his data.

            What do think they find inside an atherosclerotic lesion? It’s cholesterol.

          • “Such a good point Garry. Indeed in 2011 a WHO funded review of all the apparent evidence connecting saturated fats with heart disease concluded in black and white that there was no connection between the intake of sat fats and coronary heart disease. The study was carried out by the team at Harvard lead by Frank Hu.”

            I believe you are talking about the study carried out by Patty W Siri-Tarino, Qi Sun, Frank B Hu, and Ronald M Krauss.

            ie This one
            Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease

            Patty Siri-Tarino led the study.

            It turns out not to have been done very well at all. Jeremiah Stamler was very critical of their findings and approach.
            Diet-heart: a problematic revisit

            Easier and much clearer to understand is this guy

            It turns out there is plenty of evidence connecting saturated fats with heart disease when you look at the individual studies. The meta study was seriously flawed in its conclusion.

    Take a quick look at this if you want the very latest view on saturated fats and heart disease – published in the BMJ

  • Q:“What do think they find inside an atherosclerotic lesion? It’s cholesterol.”

    A: Cholesterol is a highly ubiquitous and highly functional biochemical, not just in human biology and physiology, but throughout a great swathe of biology itself. Broadly speaking cholesterol is not a constituent found in species that photosynthesise (mere sterols are), but cholesterol is the one sterol that the species that metabolise their energy cannot do without. There are lots of biochemicals found in athersclerotic tissues, and in arterioosclerisis some are hard and calciferous. Cholesterol is to be found within and within the membranes of every cell in the body. Although the liver is cholesterol central the greater majority of cells and cell types can synthesis cholesterol too. Why? Because cholesterol is a ubiquitous and vital biochemical in the physiology of species that are mobile and have some perception of the nature of their surroundings, Cholesterol in the synapses helps them perceive and navigate their surroundings.

    Q: How is cholesterol so functional and expedient in one moment and toxic in the next?
    A: It isn’t.

    Q: What is arteriosclerosis, and what induces it?
    A: Arteriosclerosis is what results when the cells in and around the endothelial layer of the arterial wall cease to behave as they once did and should. Something compels these cells to begin behaving badly. Given the placement cholesterol enjoys in biology are you still convinced cholesterol is the agent that induces this altered behaviour? I’m not. In 1974 Hideshige Imai et al published a write up of an experiment not unlike Anitchkovs from 1913. They added cholesterol and oxidised cholesterols to the feed fed to several species of mammals in a trial. Anitchkov and Imai each proved it is possible to induce atherosclerosis by adding an atherogenic agent to the diet. The level of care introduced into the design of their trial proved that cholesterol is not at atherogenic, while oxidised cholesterols are atherogenic.There are three possible derivatives of oxidised cholesterol. Cholestane triol is the most potent atherogen amongst the oxycholesterols. Dr Ancel Keys was misled by a confounding error in the work of Anitchkov and his chums.

    Q: Where did saturated fat enter the equation?
    A: Once Keys had mistaken the effects of oxycholesterols on Anitchkovs rabbits and attributed them to cholesterol itself he had a truly inspired thought. In the complete absence of any evidence he considered saturated fat in the diet would raise peoples cholesterol. It was pure speculation on his part. When challenged for evidence he went in search of some. He found some that was not at all standardised in any way. He had data points available on 22 countries. When he wrote his paper(s) he cherry picked either six or seven data points that fitted his highly suspect theory. Keys, and the diet-heart hypothesis he founded, was/is highly fraudulent. To subscribe to it should be seen as conspiracy to defraud. In the BBC Horizon broadcast the extreme diets of either twin did not impact upon their cholesterol numbers.

    Q: What is known about atherogens and atherogenesis?
    A: In the late 1960s a young pathologist was beginning a distinguished career. His name was Dr Kilmer McCully. McCully was the man who spotted a possible connection between homocysteine and atherosclerosis and arteriosclerosis. Homocysteine is an amino acid, but you won’t find it in the proteins that make up your diet. Homocysteine is a breakdown product of another amino acid called methionine. McCully soon established homocysteine is an atherogen, and he soon established that under the right conditions homocysteine is managed by the body and spirited harmlessly away. However there are circumstances under which levels of homocyteine may rise. Raised levels of homocysteine turn out to be very reliable risk factors for atherosclerosis. But as yet that does not commute to understanding the beginnings of atherogenesis.
    Here’s something Dr Kilmer McCully wrote on the topic some as the hypothesis developed:
    “Homocysteine catalyses oxidation of low-density lipoprotein in the presence of ferric ions in vitro. Cholestane triol is highly atherogenic cholesterol oxide that is produced by oxidation of low-density lipoprotein within the arterial wall. These and other observations led to the proposal of altered mitochondrial function in arteriosclerosis promoted by hyper-homocysteinemia” (elevated levels of homocysteine).
    [Homocysteine and Vascular Disease (Developments in Cardiovascular Medicine) by Killian Robinson and K. Robinson (30 Apr 2000) ]
    I’ll translate: Homocysteine is a potent oxidsing agent. On contact with a molecule of cholesterol homocysteine induces oxidation, resulting that cholesterol is converted to a molecule of oxycholesterol. Cholestane triol may result as a feature of this contact. In keeping with some aspects of contempoary theory it mat be considered that LDL is the faction of lipoprotein that may expose cells of the endothelium to the atherogenic stress conveyed by oxycholesterols and cholestane triol. We’d expect that all lipoproteins including chylomicrons may be capable of harbouring oxycholesterols and thnsporting them. However the life-cycle of a lipoprotein and the significance of size dictates that any oycholesterols that afflict the endothelial layer and induce atherogenisis will conform to our description and definiction of LDL. In the eyes of Dr McCully and other proponents/adherents of homocysteine theory cholesatne triol has the cells in the area express themselves diferently resulting in compromised integrity of tissues that we witness as atherosclerotic plaques.

    Q; Is there anything else?
    A: Yes, homocysteine levels are sensitive to levels of cortisol and stress. Hence if the mind can perceive a notional axis involving cortisol, homocysteine, and oxycholesterols (CHO axis) then the several (multifactorial) lifestyle and environmental risk factors for CHD can actually be linked, via intelligent discussion, either to oxycholesterol, to homocysteine, or to their potential to raise cortisol. In reality I do not think the whole oxidative stress aspect is so discrete as the notion of the CHO axis may suggest. In other words other ‘routes’ capable of conveying oxidative stress may feed into that, but ultimately it may appear that oxycholesterols are the specific biochemicals capable of getting to the scene of the crime and capable of inducing altered behaviour. It is worth reading into.

    Saturated fat doesn’t affect our cholesterol, and if it did it wouldn’t matter. According to the analysis of actuary Garth Lane no study undertaken to standards that satisfy the Bradford Hill criteria has ever proven a statistically significant link between saturated fat and heart disease. Why would it when it was deceit from day one?

    McCullys book, ‘The Homocysteine Revolution’ is worth read. Aspects are very good, while some aspects look a little dated in the light of how the theory has developed since. He has written and edited more recent work on the topic.

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