by Dr. Malcolm Kendrick
“Explanations exist; they have existed for all time; there is always a well-known solution to every human problem — neat, plausible, and wrong.’ H.L. Mencken.
Of all the flaws of the human mind, the number one must be the overwhelming desire to find simple, easy to understand answers – to everything. I think this is why my favourite film of all time is Twelve Angry Men. It was a stage play first:
- A black youth is accused of killing his father. The evidence that is presented by the prosecution seems utterly overwhelming. A unique knife is used for the murder, one that the youth was known to carry. He was seen leaving the apartment after shouting ‘I’ll kill you’ and suchlike. Most importantly, however, he was a young black youth, and young black youths are widely considered to be the sort of person who do such things. In the film, prejudice presses down heavily on most of the jurors. Some of them, it is hinted, would have found him guilty no matter if there had been any evidence, or not. Here we have all the worst aspects of human decision making on show. Confirmation bias, prejudice, gathering together only the evidence that supports a case, the desire to ‘get on with it’ and not hang about listening to people who just want to make things complicated.
In my mind, for many years, I have changed ‘black youth’, into the word ‘cholesterol’ as I watch the ‘heart disease jurors’ in action. A suspect was found, fitted up, put on trial and found guilty by people who were just desperate to get on with it. At the very first congressional meetings on dietary guidelines, any attempts to wait until there was sufficient evidence, were railroaded.
‘When the US government introduced “Dietary Goals for the United States”, they did not have unanimous support. The guidelines, which urged the public to cut saturated fat from their diet, were challenged by a number of scientists in a Congressional hearing. The findings were not based on sufficient evidence, they argued.
They were ignored. Dr. Robert Olson recounts an exchange he had with Senator George McGovern, in which he said: “I plead in my report and will plead again orally here for more research on the problem before we make announcements to the American public.” McGovern replied: “Senators don’t have the luxury that the research scientist does of waiting until every last shred of evidence is in.’1
Senator McGovern might as well have said. ‘Listen son, we know that saturated fat raises cholesterol and causes heart disease, we don’t need any damned evidence.’ Of course, they didn’t have any evidence at all. None. But they still managed to find saturated fat and cholesterol guilty. Some people would call this proper leadership. Make a decision and go with it.
I would call it monumental stupidity.
As you can see I am stepping back in this blog to look at saturated fat – again. Because I am going to share some thinking with you, which I have not really shared before. Some of you will know that I am a ‘first principles’ kind of guy. I take very little at face value, and I am certainly highly critical of accepted wisdom: I usually translate it, in my mind, into accepted stupidity.
So, I am going to try and explain to you that saturated fat cannot raise blood cholesterol levels. By which I mean low density lipoprotein levels (LDLs) as this is the substance which someone or another ended up calling ‘bad’ cholesterol. It is the lipoprotein that is thought to cause CVD.
However, LDL is not cholesterol, it never was. We do not have a blood cholesterol level – but we are seemingly stuck with this hopelessly inaccurate terminology for all time.
Anyway, the idea that saturated fat raised cholesterol was driven by Ancel Keys in the late nineteen forties. The first point to make here is that, when Keys first started his anti-fat crusade, no-one knew that there was such a thing as LDL. You took a blood test, gathered together all the lipoproteins you could find (good, bad, and indifferent) and measured them all. Quite what they were measuring is a good question.
Despite this rather important gap in his knowledge, Ancel Keys was able to create an equation to exactly predict the effect of saturated and polyunsaturated fatty acids in the diet on serum cholesterol levels.
Change in serum cholesterol concentration (mmol/l) = 0.031(2Dsf − Dpuf) + 1.5√Dch
[Where Dsf is the change in percentage of dietary energy from saturated fats, Dpuf is the change in percentage of dietary energy from polyunsaturated fats, and Dch is the change in intake of dietary cholesterol].
This became the accepted wisdom. You could believe, given the apparent precision of this equation, that he did some proper research to prove it was true. Frankly, it seems bloody unlikely, as the equation contains the ‘change in dietary cholesterol’ as a key factor in raised blood cholesterol levels. It is now accepted that cholesterol in the diet has no significant impact on blood cholesterol levels. Keys even knew this himself.
To quote him from a paper in 1956:
‘In the adult man the serum cholesterol level is essentially independent of the cholesterol intake over the whole range of human diets.’
In 1997 Keys wrote this:
“There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.” Ancel Keys, Ph.D., professor emeritus at the University of Minnesota 1997.
More recently, the fact that cholesterol in the diet has no impact on ‘cholesterol levels’ or CVD was reaffirmed. In 2015, the Dietary Guidelines Advisory Committee in the US, having reviewed all the evidence made this statement:
“Cholesterol is not considered a nutrient of concern for over-consumption.” 2
This was even supported by the likes of Walter Willet and Steven Nissen:
‘Nutrition experts like Dr. Walter C. Willett, chair of the Department of Nutrition at Harvard School of Public Health, called the plan a reasonable move. Dr. Steven Nissen, chair of cardiovascular medicine at the Cleveland Clinic, told USA Today “It’s the right decision. We got the dietary guidelines wrong.’3
Anyway, Keys had started out with a hypothesis that cholesterol in the diet raised cholesterol levels in the blood but discarded it after feeding eggs to volunteers (eggs contain more cholesterol than any other food) and finding that their cholesterol level remained stubbornly unchanged.
Undaunted, he did what no scientist should ever do. He simply changed the hypothesis. The nutrient of concern was no longer cholesterol, it was saturated fat. So, what is it about saturated fat that can raise LDL? I wanted to know the exact, proven, mechanism.
We start with the certain knowledge that the body is exceptionally good at keeping all substances in the blood under strict control. If the level of something rises too high, mechanisms are triggered to bring them back under down, and vice-versa. The entire system is known as homeostasis.
Thus, if saturated fat intake really does cause LDL levels to reach damaging levels, it must be overcoming homeostasis, and breaking metabolic and physiological systems. How does it do this?
To try to answer this question we should look at what happens to saturated fat when we eat it. The first step is that it binds to bile salts in the bowel. Bile salts are a form of mildly adapted cholesterol, synthesized in the liver and released from the gall bladder. Without bile, fat cannot be absorbed well, if at all, and simply passes through the guts and out the other end.
The absorbed saturated fat is then packed into a very large lipoprotein (known as a chylomicron). Once a chylomicron is formed it travels up a special tube, called the thoracic duct, and is released directly into the blood stream. It does not, and this is important, pass through the liver.
Chylomicrons then travel around the body and are stripped of their fat, shrinking down until they become about the size of an LDL. At which point they are called chylomicron remnants. These are absorbed back into the liver – using LDL receptors – and are then broken down into their constituent parts.
Therefore, a small amount of fat that you eat will end up in the liver. However, the vast, vast, majority will go straight from the guts to fat cells (adipose tissue). Whereupon they are stored away for later use.
In fact, this is the fate of all types of fat: saturated, polyunsaturated, or monounsaturated. There is nothing unique about saturated fat in the way that it is absorbed and transported around the body. Anyway, as you may have noticed, none of this has anything to do with LDL whatsoever. Nothing. Ergo the consumption of saturated fat, or any fat, can have no direct impact on LDL levels.
I suppose the next question to ask is simple. Where does LDL come from? LDL is created when VLDLs (very low-density lipoproteins) shrink down in size. VLDLs are the type of lipoproteins that are synthesized in the liver, then released into the bloodstream. They contain fat and cholesterol and, as they travel around the body, they lose fat and become smaller and smaller, until they become an LDL -which contains proportionately more cholesterol.
Almost all LDL molecules are removed from the circulation by LDL receptors in the liver. They are then broken down and the contents used again. Some LDL continues to circulate in the blood, and cells that need more cholesterol synthesize an LDL receptor to bind to LDL molecules and bring the entire LDL/LDL receptor complex into the cells.
Just to re-cap. Saturated fat (any fat) is absorbed from the gut and packed into chylomicrons. These travel around the body, losing fat, and shrink down to a chylomicron remnant – which is then absorbed by the liver. There is no connection between chylomicrons and LDL.
Instead LDL comes from VLDL. VLDLs are made in the liver, they contain fat and cholesterol. VLDLs leave the liver, travel around the body and lose fat, shrinking down to become an LDL.
As the only source of LDL is VLDL, this leads to the next obvious question. What makes VLDL levels rise? Well, it sure as hell isn’t fat in the diet. What causes VLDL levels to rise is eating carbohydrates. The next quote is a bit jargon heavy but worth including.
‘De novo lipogenesis is the biological process by which the precursors of acetyl-CoA are synthesized into fatty acids [fats]. In human subjects consuming diets higher in fat (> 30 % energy), lipogenesis is down regulated and extremely low; typically < 10 % of the fatty acids secreted by the liver. This percentage will increase when dietary fat is reduced and replaced by carbohydrate.’4
To simplify this as much as possible. If you eat more carbohydrates than your body needs, or can store, the liver converts the excess (primarily fructose and glucose) into fat in the liver. This process is called de novo lipogenesis (DNL) The fats that are synthesized are saturated fats, and only saturated fats. Once synthesized they are then packed into VLDLs and sent out of the liver.
In short, if you eat fat, the VLDL level falls. If you eat carbohydrates the VLDL level rises. Which is pretty much what you would expect to see.
Moving the discussion on, as VLDLs are the only source of LDL. you now have a conundrum to solve. How can you connect saturated fat intake to a rise in LDL levels, when saturated fat consumption reduces VLDL synthesis? What is the mechanism? The mechanism does not exist!
You could counter by saying, what of the many studies that have shown a fall in LDL when saturated fats are replaced by polyunsaturated fats? Well, this seems to have been shown often enough for me to believe it may even be true.
The explanation for this finding is most likely the fact that, in these studies, saturated fats were replaced by polyunsaturated fats, from plant oils. Plant oils contains stanols (the plant equivalent of cholesterol).
Stanols are known to lower LDL levels, see under Benecol and other suchlike ‘low fat’ spreads. Because stanols compete with cholesterol for absorption there is an impact on the ‘measured’ LDL levels. What this means, in turn, is that the studies that demonstrate a lower LDL, with a reduction in saturated fat consumption, fall foul of the two variables problem.
Namely, if you change two variables in an experiment at the same time, you cannot say which of the variables was responsible for the effect you have seen. Was it the reduction in saturated fats, or the increase in plant stanols, that lowers LDL?
This is all tacitly accepted in this Medscape article – again heavy on jargon: ‘Saturated Fat and Coronary Artery Disease (CAD): It’s Complicated.’
‘In a meta-analysis of over 60 trials, higher intakes of saturated fat were associated with increases in both LDL-C and high-density lipoprotein cholesterol (HDL-C) and decreases in triglyceride levels [VLDL}, for a net neutral effect on the ratio of total cholesterol to HDL cholesterol.
Although saturated fats increase LDL-C, they reduce the LDL particle number. Total LDL particle number quantifies the concentration of LDL particles in various lipid subfractions and is considered a stronger indicator of CV risk than traditional lipoprotein measures.
As for stearic acid, the allegedly non-cholesterol-raising fat, while it appears to lower LDL-C relative to other SFAs, one analysis concluded that it raised LDL-C, lowered HDL-C, and increased the ratio of total to HDL cholesterol in comparison with unsaturated fatty acids. And this is one of the confounders of much nutrition research—observations about a given nutrient are highly dependent on what you compare it to.’5
Which is a long-winded way of saying that everything we have been told about saturated fat, its impact on LDL, and its impact on CVD is – frankly – complete bollocks. And if it is complete bollocks, the Keys equation – which has driven all research in this area for seventy years – is also bollocks.
In truth, all possible combinations of LDL going up, down, and staying the same have been found in dietary studies. But I would like to focus on the most recent study. It formed the basis of an episode of a programme called ‘Trust me I’m a doctor’, on the BBC. Researchers studied the impact of different types of saturated fat on LDL and HDL levels.
‘For the experiment, the team recruited nearly one hundred volunteers, all aged over fifty. They were split into three groups and every day for four weeks each ate fifty grams of coconut oil (about two tablespoons), or fifty grams of olive oil – an unsaturated fat already known to lower bad LDL cholesterol – of fifty grams of butter.
This amount of coconut oil contains more than forty grams of saturated fat, twice the maximum recommended daily amount for women, according to Public Health England, but is the level previous research has revealed is necessary to show measurable changes in blood cholesterol over a four-week period.
Before the experiment, all the volunteers had their bad LDL and good HDL cholesterol measured, as well as their height, waist, blood pressure, weight and body fat percentage. Four weeks later, these tests were repeated.
The group who ate butter saw their bad LDL levels rise by about ten per cent, as expected. But the olive oil and coconut oil saw no rise in bad LDL – despite coconut oil having more saturated fat than butter.’
Even more surprisingly, while butter and olive oil both raised good HDL cholesterol by five per cent, coconut oil raised it by a staggering fifteen percent, meaning that it seemed to have a more positive effect on cholesterol related health than olive oil.’ 6
It is worth pointing out that this was the largest study of the kind ever to have been done. This may surprise you, but in many nutritional studies the number of subjects is often in single digits. In case you are thinking we can simply ignore a study done by the BBC, it was carried out to high standards, and has since been published in the BMJ. Equally I can see no reason why the BBC would have any desire to bias the conclusions in any direction.7
What they found was that coconut oil, containing the highest percentage of saturated fat, had absolutely no impact on LDL. But it did raise HDL (so-called ‘good’ cholesterol) by 15%. Which is no surprise. If VLDL goes down, HDL goes up. And in this experiment they kept everything else the same, but just added saturated fat. A single variable.
Anyway, the thing that interests me most, and the reason for writing this particular blog is that I have come to the realisation that the best way to find the answer to a scientific question is to immerse yourself in the science. I would like to believe the published research, because it would be lovely if you could look at a study and believe it to be correct/true/unbiased. But that is no longer possible, most especially in the connected fields of heart disease, and nutrition.
‘It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgement of trusted physicians or authoritative medical guidelines.” Marcia Angell – long-time editor of the NEJM.
‘The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue…science has taken a turn towards darkness.’ Richard Horton – editor of The Lancet.
‘The poor quality of medical research is widely acknowledged, yet disturbingly the leaders of the medical profession seem only minimally concerned about the problems and make no apparent efforts to find a solution.’ Richard Smith – long time editor of the BMJ.
It is always, of course, risky to base your thinking and conclusions on what is known about the basic science. New facts can come along to upend your thinking at any time. However, with mainstream medical research in such a corrupt mess, I do not know how else to do it. The basic research tells us that there is no mechanism whereby saturated fat can raise LDL levels, and the research, such as it can be disentangled, appears to fully support this.
I looked at this blog again, and again, and I thought: Why did I write it…for sure? I wrote it because I wanted to make you aware of three things. First, how powerful a thought can be. Saturated fat raises the LDL level, and how difficult this is to shift. The power of a simple idea.
Secondly, so that you can see that the truth is out there. It is not to be found amongst the experts in the field. It cannot be found by reading the research, or the guidelines. But it is out there, if you look hard enough.
Third, the mainstream just will not change its mind. A recent conference in Switzerland, organised by the BMJ, and others, tried to discuss the dietary guidelines and the role of Saturated fat. I was invited, but did not go, as I was working. Zoe Harcombe went, and wrote a blog about it.8 As she wrote about the conclusion of the conference:
‘At the recent Swiss Re/The BMJ Food for Thought conference, the closing speakers tried to find some agreement on dietary fat guidelines…
Fiona (Fiona Godlee, editor of the BMJ) started with: “The point about saturated fat is: the evidence is now looking pretty good, but the guidance hasn’t shifted… there doesn’t seem to have been an enormous ‘mea culpa’ from the scientific community that we got it so wrong. That does surprise me.”
Salim replied: “We got brainwashed by a very questionable study, called The Seven Countries Study, many years ago and it was ingrained in our DNA and generations of us were brought up with that… Somebody said that you need to wait for guidelines committees to die before you can change the guidelines committees”!
Fiona then said: “Maybe one outcome of this meeting would be for this meeting to say ‘that’s gone now’, the science has changed. Am I right Salim? Am I right Dariush? It seems to be that should be an outcome of some sort from this meeting.”
Alas, the UK guidelines committee shows no signs of such change, let alone the ‘mea culpa’ that Fiona suggests might be in order.’
Original posting can be found on Dr. Kendrick's blog https://drmalcolmkendrick.org/2018/07/03/why-saturated-fat-cannot-raise-cholesterol-levels-ldl-levels/