I was listening to the podcast of Ben Greenfield (author of Beyond Training) and was finding everything somewhat interesting until I came across a specific segment where he links coffee to high LDL! This was something I had never heard before.
It all happens around the 38:10 mark. The theory goes something like this:
Coffee contains ‘cafestol’ and ‘kahweol’ which are compounds called diterpenes. These are found specifically in the oils of coffee beans.
According to Ben, “It hijacks this receptor in your intestinal pathway and in particular where it acts upon is your liver” to inhibit bile acid synthesis. At this point I’m not clear if it acts directly on the intestines, directly on the liver, directly on both, or whatever.
This will be a good stopping point to review bile acid basics.
Bile Acid Basics
Bile acid is a dark green substance that your body uses to help digest fats.
It is created in the liver, stored in the gall bladder, and released into the small intestine when a fatty meal is ingested. Its primary function is two fold: (1) to help digest and absorb all the fat in the meal and (2) serve as the primary method for the body to get rid of cholesterol.
The liver uses cholesterol to make bile. There are of course multiple steps in between, using at least 17 different enzymes (the most important of which is CYP7A1), but the gist of it is that the liver takes cholesterol and converts it into bile.
Once bile reaches the last segment of small intestine known as the ileum, approximately 95% of it is reabsorbed back into the blood stream. The 5% that is excreted is the reason poop is brown. This excreted bile acid is the primary method the body uses to get rid of cholesterol.
The reabsorbed bile is then sent back to the liver where it is then re-excreted.
This relationship between the small intestine and the liver in the movement of bile is termed, ‘enterohepatic circulation.’ Entero – meaning small intestine and hepatic – meaning liver.
Back to Ben Greenfield
Ben says that the effects of the diterpenes may be why so many people drinking Bulletproof Coffee have such high levels of LDL and triglycerides.
Paper filtered coffee and Aeropress coffee manage to filter out the cafestol and kahweol from the coffee.
Ben then goes into how Bulletproof Coffee is supposed to work on your brain… and how this can complicate things:
When you drink bulletproof coffee, like one of the things that you’re doing, when you’re putting MCT oil and butter, and stuff like that in the coffee, is you’re enhancing the ability of these fat-soluble compounds, the diterpenes to cross the blood brain barrier and cause some of that cognitive performance enhancing effect that bulletproof coffee can cause. And so, you kind of have this paradox between raising levels of cholesterol significantly and suppressing bile-acids synthesis and your ability to digest fats, and increasing your cognitive performance. So, it’s a real catch 22.
Another issue Ben brings up that can confound things is that arabica coffee has lower mycotoxins compared to robusta coffee. So it seems like the choice is either arabica coffee (low mycotoxins but high cafestol) or robusta coffee (lower cafestol but higher mycotoxins). Hmm…
He does propose a solution for the Bulletproof coffee drinkers though who want the cognitive benefits of the Coffee + MCT oil + Grass-fed butter, but don’t want the LDL elevating effects of the diterpenes:
- Use a paper filter
- Decrease the amount of MCT oil + Grassfed Butter
- Add in bile acid supplements like Thorne Betaine HCL and Pepsin digestive enzyme or ox bile.
A deeper look into the research…
Ok. After going over all of this… naturally I had to see what else I could find out there.
Well, the fact that cafestol and kahwiol can increase LDL is confirmed by this Harvard Health newsletter, although they don’t go into the mechanism.
This Science Daily article goes much further into the mechanism and I suspect served as one of the main sources of Ben’s information, since lines like:
Cafestol, a compound found in coffee, elevates cholesterol by hijacking a receptor in an intestinal pathway critical to its regulation
are almost verbatim to how Ben explains it.
In any case I was still curious about the mechanisms so I found the original research article, which fully explores the mechanism using lots of gene knockout mice.
In this in vivo mouse study they describe how in the normal situation, bile acids stimulate the Farnesoid X receptor (FXR) in intestinal cells to produce something called Fibroblast growth factor 15 (FGF15), which then goes to the liver and suppresses CYP7A1 expression. Remember CYP7A1 from above? The most important enzyme in the conversion of cholesterol to bile acid.
This is sort of like the body’s way of self regulating the amount of bile it produces. If the liver generates too much bile, more of it will reach the small intestine, which will then activate the FXR on intestinal cells, leading to increased release of FGF15, which reaches the liver and suppresses expression of CYP7A1. This then ultimately decreases the hepatic production of bile acid.
Cafestol actually was found to be a strong stimulator of FXR…. which then kicks off that whole cascade ending in the decreased hepatic conversion of cholesterol to bile.
So… if the body loses it’s main route of cholesterol excretion… cholesterol in the body starts to build up. This increased build up of cholesterol then down-regulates LDL receptor expression by the liver. Sorry to introduce yet another character in this long chain…
Ok, so LDL Receptors: if you imagine LDL particles floating around the blood as baseballs, LDL receptors act like catchers mitts on the surface of the liver. The more LDL receptors the liver has, the more baseballs it catches out of the blood stream, hence a lower LDL.
Therefore, if cafestol can ultimately lead to the decreased expression of LDL receptors (via FXR, FGF15, CYP7A1 etc.), it can lead to an increase in serum LDL.
If you’d like to learn more about this, you can read this study from study from 1997 by some of the same authors, exploring this mechanism on cultured rat cells.
So if anyone ever comes up to you and asks: can coffee raise LDL?
You can answer with a definitive YES, and go into a long winded explanation of how!
I feel like reading about this introduced me to a whole lot of vocabulary that wasn’t even on my radar before. Words like arabica, robusta, diterpine, cafestol, kahwiol, farnesoid, fibroblast growth factor, and CYP7A1 have now entered my brain.
One interesting quote in the science daily article by one of the authors was that:
…consuming five cups of French press coffee per day (30 milligrams of cafestol) for four weeks raises cholesterol in the blood 6 to 8 percent.
According to this author it seems like you would need to drink quite a bit of coffee just to raise cholesterol 6-8%. I mean, with a hypothetical LDL of 150 mg/dL, drinking 5 cups of coffee per day for four weeks would only raise it 12 mg/dL to 162 mg/dL. Not quite the stratospheric levels we see in folks like me who go keto.
Still… even though the coffee I drink utilizes paper filters in the k-cups (see above), it may be a worthwhile experiment to cut out all coffee for a month or two and see how that affects my cholesterol numbers.