The phenomenon of postprandial angina was described over 200 years ago: chest pain that occurs after a meal, even if you’re just sitting down and resting. The question is, why? It could be intuitively attributed to redistribution of blood flow away from the heart to the gut during digestion; however, such a mechanism could not be demonstrated experimentally. We now know the problem appears to be within the coronary arteries themselves.
The clue came in 1955, when researchers found they could induce angina in people with heart disease just by having them drink fat. This is what was happening in their bloodstream in the six hours after the meal. This is a graph of so-called lactescence, which means milkiness. Their blood became increasingly milky with fat over the next five hours, and each of the ten attacks of angina was found to occur about four-and-a-half to five hours after the fatty meal, right when blood milkiness was at or near its peak. Here’s the curve after a nonfat meal, same bulk and calories, but made out of starch, sugar, and protein. And no anginal pain was elicited in any of the patients they tested after the ingestion of the nonfat meal.
How could just the presence of fat in the blood affect blood flow to the heart? To understand that, we need to understand the endothelium: the inner lining of all of our blood vessels. Our arteries are not just rigid pipes, they are living breathing organs that actively dilate or constrict. Depending on what’s needed, they thin or thicken the blood, release hormones, and it’s all controlled by the single inner layer, the endothelium, making it the body’s largest endocrine organ, the largest hormone-secreting organ, weighing a total of three pounds all gathered up, with a combined surface area of 700 square yards.
We used to think the endothelium was just an inert layer lining our vascular tree, but now we know better. The endothelium is directly involved in peripheral vascular disease, stroke, heart disease, diabetes, insulin resistance, chronic kidney failure, tumor growth, metastases, venous thrombosis (blood clots), and severe viral infectious disease. Dysfunction of the vascular endothelium is thus a hallmark of human disease.
Researchers found that low-fat meals tend to improve endothelial function, and high-fat meals tend to worsen endothelial function. And this goes for animal fat, as well as isolated plant fats—sunflower oil, in this case.
But, maybe it’s just the digestion of fat rather than the fat itself? Our body can detect the presence of fat in the digestive tract and release a special group of hormones and enzymes to deal with it. So, researchers tried feeding people fake fat. The real fat deprived the heart of blood; the fake fat didn’t. But maybe our body is smart enough to know the difference?
This is the study that really nailed it. They tried infusing fat directly into people’s bloodstream through an IV, so the brain wouldn’t know if you’re eating fat or not. And indeed, within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. This decrease in the ability to vasodilate coronary arteries after a fatty meal, just when you need it, could explain the phenomenon of after-meal angina in patients with known coronary artery disease.
This effect could certainly help explain the findings in Low Carb Diets and Coronary Blood Flow. What about so-called healthy fats like extra virgin olive oil? That’s the subject of my next video: Olive Oil and Artery Function.
For more on angina, that’s the topic I started my 2014 year-in-review talk with: From Table to Able: Combating Disabling Diseases with Food.
Another consequence of endothelial dysfunction is lack of blood flow to other organs. Check out: Survival of the Firmest: Erectile Dysfunction and Deathand Atkins Diet: Trouble Keeping It Up
Fat in the bloodstream can also impair our ability to control blood sugar levels.