Saturated fat causes heart disease? Bollocks, says Kendrick!

Quick! If your doctor or dietitian still says you should eat a low-fat diet for your heart’s sake, find another one. In the final of a two-part series, Scottish GP Dr Malcolm Kendrick explains why so many doctors and dietitians dish up junk about cholesterol.

And why everything the experts have been telling you about saturated fat, its impact on LDL, and its impact on CVD is – frankly – ‘complete bollocks’. Scroll down for a link to his full blogs. – Marika Sboros

By Malcolm Kendrick

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 the liver then absorbs.

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.

Simplifying the jargon

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.’

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 the body synthesizes are saturated fats and only saturated fats. Thereafter, 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.

Click here to read:  Don’t just swallow whole what doctors say about statins!

 

A conundrum to solve

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 you replace saturated fats with polyunsaturated fats? Well, researchers have shown this 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, polyunsaturated fats, from plant oils replaced saturated fats. Plant oils contain 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?

Tacit acceptance

The authors of this Medscape article – again heavy on jargon – tacitly accept it: 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.’

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 70 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.

‘The good and the bad cholesterol’

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.

Click here to read: Teicholz: how low-fat diets can kill you

 

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 per cent, meaning that it seemed to have a more positive effect on cholesterol-related health than olive oil.’ 

It is worth pointing out that this was the largest study of the kind ever. 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. The BMJ has also since published it.

Best way to find the answers

Equally, I can see no reason why the BBC would have any desire to bias the conclusions in any direction.

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.

Click here to read: Why coconut oils is so good for hearts, minds

 

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.

Risky thinking

It is always, of course, risky to base your thinking and conclusions on what you know 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 is possible to disentangle it, 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.

• This article first appeared on Dr Malcom Kendrick’s Blog
• Part 1: LDL fat heart puzzle: Kendrick soves it!
• Follow me on Twitter @MarikaSboros
• Like my Facebook Page
• Sign up for Foodmed email alerts