How does saturated fat mechanistically raise "cholesterol"?

(Bob M) #1

It is commonly believed that saturated fats can affect “cholesterol” values, such as total cholesterol or LDL or HDL:

See this for instance:

My problem with this is that I cannot find anything that tells me mechanistically how this is supposed to work. Why, for instance, is there a different effect for stearic acid (18:0) as compared to palmitic acid (16:0) (where 18, 16 indicate the number of carbon atoms and the zero effectively means it’s saturated)?

Logically, this does not make sense to me.

And Malcolm Kendrick agrees:

So, does anyone know what the supposed mechanism is, by which saturated fat affects cholesterol levels?

(Michael - When reality fails to meet expectations, the problem is not reality.) #2

Thanks for the links! I think Kendrick explains it pretty well. There is no such mechanism.

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.

In my opinion, Ancel Keys created (maybe not entirely alone) a zeitgeist that dietary saturated fat was the problem. He fudged and cherry picked data for the so-called ‘Seven Countries Study’, from a total of 23 countries, most of which did not support his thesis, so he ignored them.

No correlation/causation between dietary saturated fats and cholesterol and CVD was ever established! Keys and his supporters just shouted loud enough long enough to convince a bunch of scientifically ignorant politicians. Once the table was tilted the medical/scientific people went along for the funding. Just like the current ‘climate’ non-science bullshit. The few who protested and told everyone else this was sheer speculation were simply ignored, shut out of funding or belittled/shouted down.

Why different SFA have different effects remains to be determined. Hopefully, now that we’re finally beginning to emerge from the dark ages, someone(s) will try to determine why.

(Todd Allen) #3

Some believe saturated fat reduces the receptors for LDL uptake in the liver.

I don’t know how it is working but I’ve had good results raising my cholesterol since making a habit of eating a breakfast of raw egg yolks beat into warmed coconut oil often served with beef liver. Perhaps it is just coincidence but I had been on a cholesterol plateau for a year with my LDL stuck in the mid 100s and since making the dietary change it’s come up rapidly to the mid 200s.

(Bob M) #4

Interesting. Right now, I’m testing a high saturated fat diet with some carbs (mashed potatoes today) on the days I work out.

I may have to try your test one day, though, because I have “low” LDL.

At some point, I’ll have to get a cholesterol test done to see what if anything my “high” saturated fat has done. The problem is that those values are so variable, it’ll be hard to tell what’s up.

(Bob M) #5

I hear you. The thing is that palmitic acid, since it supposedly raises LDL/TC, is verboten. No one will do studies with it. Or there are very few.

It’s like the low fat diet: when all you do is test one thing, you get the results you want (or you explain away the results you don’t want, or you hide them).

(Michael - When reality fails to meet expectations, the problem is not reality.) #6

Yes, it would be scientifically very interesting to understand why 18 carbon atoms has a different metabolic effect than 16 carbon atoms. I suppose we’ll have to wait until a lot more old guys die off to find out.

#7

I find it interesting the fear of saturated fats, and the push of “healthy whole grains” onto people. Thing is, if you eat too many grains they are converted to 100% saturated fat by the liver. By comparison, grass fed beef is almost 1/2 monounsaturated. So they say don’t eat red meat because of the saturated fat! But they are getting more saturated fat eating the carbs instead! Not that saturated fat matters though.

(Bob M) #8

Technically, there’s a slight difference in the formula to see whether a fat cell would be insulin sensitive or resistant:

Basically, it hinges on the 2 carbon difference.

So stearate (C18) is 0.486

Palmitate (C16) is 0.484

But this has nothing to do with cholesterol.

@Jennifer1 Yeah, I always thought “reducing saturated fat” was short-hand for “reducing red meat intake”, since red meat has a slightly higher saturated fat content. This was way before cocoa/cacao, coconut, etc., came to be popular.

(Michael - When reality fails to meet expectations, the problem is not reality.) #9

I seriously wonder just how much difference 2 thousandth can make. So if there’s a significant difference in metabolic effect, I would suspect it’s due to something else, or something else in addition.