A discussion on whether decaf would have similar effects was deleted while I wrote this up. TLDR: I suspect dark roast decaf would.
While caffeine's adenosine receptor antagonist activity appears to reduce neural inflammation[1] and block β-amyloid neurotoxicity[2] , with potential benefits in dementia prevention, I suspect the benefits seen in this discussion's study are from the melanoidins produced by roasting, which activate Nrf2 and inhibit NF-κB[3] . Other Nrf2 inducers reduce DNA double strand breaks[4] , as are detected by the comet assay of this discussion's study.
FWIW, I drink 4-5 cups of dark-roast caffeinated coffee brewed through paper filters (to remove the LDL elevating cafestol & kahweol) daily. This is the sweet spot suggested by dozens of papers I've read on coffee health effects.
Unfiltered coffee, such as through a French press, can raise blood cholesterol by 5-15% in otherwise healthy adults. On mobile so cannot source. FYI I drink nespresso everyday at my desk, and not to sound like a corporate shill but that shit is the bomb diggity.
Everyone knows cholesterol is separated into LDL (bad) and HDL (good) cholesterol. Current research is far more advanced than that and has identified that LDL has small and large LDL. Of those, the small LDL is worse, and of the small LDL, Lp(a) is the worst blood lipid that we know of.
Do we know what type of LDL is being increased with these coffee byproducts?
Edit: After finding the proposed mechanism, I'd guess that we are raising large LDL by drinking coffee, but I don't like guessing.
I found this, which happens to be pretty good.
I'll keep this as simple as I can while remaining thorough.
When we worry about cholesterol, we are worrying about heart disease and stroke. This is caused by a process called atherosclerosis, which is often times referred to as the hardening of the blood vessels. The process can cause an increase in pressure, a vessel blockage, or even rupture. This happens when LDL (bad cholesterol) flows through your blood and enters the wall of the blood vessels. Once inside the LDL it becomes oxidized by a free radical. This triggers your immune system to recruit white blood cells into the area. The white blood cells enter the blood vessel wall and 'eat' the oxidized LDL. So far this is all normal and happens to everyone all the time. Your body then processes the oxidized LDL by pulling it out with HDL, and then the rest of the inflammatory process breaks down and is removed. No harm no foul.
In atherosclerosis your body cannot keep up with the removal of oxidized LDL because you either have too much of it, not enough HDL, or usually both. It's also possible that you could have genetic issues with your immune system, although this isn't fully understood. Then you start creating a buildup known as a plaque. The larger the plaque, the harder your blood vessels get, and the larger it gets, the more it wants to grow.
The large type of LDL (type a) is much less likely to enter the vessel walls and become oxidized. The small type of LDL (type b) is much more likely, with most people believing small LDL is almost the sole force behind atherosclerosis buildup, because of the small types ability to pass through the vessels wall and the large types inability to do so.
Large LDL is increased when you eat things like saturated fats. Small LDL is increased when you eat excess carbohydrates that are processed into fat. Lp(a) is a small molecule inside of you that is very similar to small LDL and is controlled by your genetics. It's usually much higher in people of African descent, and can also be altered both up and down by several liver disorders. Lp(a) is 4 times more likely to correspond to heart disease than LDL levels, but thats still just a correlation. Increased large LDL without increased small LDL has so far been shown to not increase heart disease significantly, or at all. There's a correlation to high triglyceride levels and small LDL, however thats not fully understood yet either.
There is also a couple types of HDL, one of which is active and one of which is much less active.
To lower small LDL, eat less excess simple carbohydrates that will be turned into fat if the energy is not burned. I do not advocate removing carbohydrates completely unless you have very specific health conditions to require it. There is evidence that your body requires a certain amount of carbohydrates for the immune system to work properly, including most importantly the ability of your body to regulate against cancer formation. Uncontrolled diabetes is especially bad in regards to small LDL formation. Exercising has also been shown to both lower total LDL and alter the composition of LDL more towards the less harmful large LDL. Exercising also alters the composition of HDL more towards the more active type, while increasing total HDL. Different cholesterol lowering drugs do different things to your lipid profile, and not all effect the bad LDL as much as the next. The only thing proven to lower Lp(a) is niacin, but its not a drug that is tolerated well by everyone. If you are being treated for increased cholesterol, get a more specific diagnostic test than the typical blood test and match your treatment to what you need.
This is why I continuously advocate against fad diets. We are still finding out a lot about our bodies all the time, and it almost always comes back to the same thing. Everything in moderation, and exercise is extremely important for most systems in your body.
Fun fact: Lp(a) still has no known function even though we produce it genetically. It only shows up in asian/african monkeys and humans which means it probably developed at some point not too long ago to counteract some environmental factor we don't have to deal with anymore, such as a disease. There are other theories as well which are just as interesting to a nerd like myself.
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