What a Single Fatty Meal Can Do to Our Arteries

Oct12 Fatty Meal copy.jpeg

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This 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.

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. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how 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. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, 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, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has 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:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. 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. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! 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. My video Olive Oil and Artery Function addresses less refined fats like extra virgin olive oil,.

For more on angina, see the beginning of my 2014 annual talk--From Table to Able: Combating Disabling Diseases with Food--and How Not to Die from Heart Disease.

Another consequence of endothelial dysfunction is lack of blood flow to other organs. Check out Survival of the Firmest: Erectile Dysfunction and Death and Atkins Diet: Trouble Keeping It Up.

Fat in the bloodstream can also impair our ability to control blood sugar levels. Learn more with What Causes Insulin Resistance?, The Spillover Effect Links Obesity to Diabetes, and Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Finally, for more on how diet affects our arteries, check out Tea and Artery Function, Vinegar and Artery Function, and Plant-Based Diets and Artery Function.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

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What a Single Fatty Meal Can Do to Our Arteries

Oct12 Fatty Meal copy.jpeg

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This 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.

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. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how 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. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, 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, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has 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:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. 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. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! 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. My video Olive Oil and Artery Function addresses less refined fats like extra virgin olive oil,.

For more on angina, see the beginning of my 2014 annual talk--From Table to Able: Combating Disabling Diseases with Food--and How Not to Die from Heart Disease.

Another consequence of endothelial dysfunction is lack of blood flow to other organs. Check out Survival of the Firmest: Erectile Dysfunction and Death and Atkins Diet: Trouble Keeping It Up.

Fat in the bloodstream can also impair our ability to control blood sugar levels. Learn more with What Causes Insulin Resistance?, The Spillover Effect Links Obesity to Diabetes, and Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Finally, for more on how diet affects our arteries, check out Tea and Artery Function, Vinegar and Artery Function, and Plant-Based Diets and Artery Function.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Original Link

Pills vs. Diet For Erectile Dysfunction

 

 

 

 

 

 

 

 

Don’t Pop Pills For Erectile Dysfunction. Help Your Heart, Instead

Erectile dysfunction is the recurrent or persistent inability to attain and/or maintain an erection in order for satisfactory sexual performance. It is present in up to 30 million men in the U.S. and approximately 100 million men worldwide. The U.S. has less than 8% of the world’s population, yet up to 30% of the impotence? We're #1!

But hey, we’ve got red, white, and blue pills like Viagra. The problem is that the pills just cover up the symptoms of vascular disease and don’t do anything for the underlying pathology. Erectile dysfunction and our #1 killer, coronary artery disease, are just two manifestations of the same disease: inflamed, clogged, and crippled arteries, regardless of which organ it affects (See Survival of the Firmest: Erectile Dysfunction and Death).

Atherosclerosis is considered a systemic disorder that uniformly affects all major blood vessels in the body. Hardening of the arteries can lead to softening of the penis because stiffened arteries can’t relax, open wide, and let the blood flow. Thus erectile dysfunction may just be the flaccid "tip of an iceberg" in terms of a systemic disorder. For two-thirds of men showing up to emergency rooms for the first time with crushing chest pain, their penis had been trying to warn them for years that something was wrong with their circulation.

Why does it hit the penis first? Because the penile arteries in the penis are half the size of the coronary artery in our heart. So the amount of plaque we wouldn’t even feel in the heart could clog half the penile artery, causing symptomatic restriction in blood flow. That’s why erectile dysfunction has been called “penile angina.” In fact, by measuring blood flow in a man’s penis we can predict the results of his cardiac stress test with an accuracy of 80%. Male sexual function is like a penile stress test, a “window into the hearts of men.”

Forty percent of men over age forty have erectile dysfunction. 40 over 40. Men with erection difficulties in their 40s have a 50-fold increased risk of having a cardiac event (like sudden death). I said before that various things increase heart disease risk by 20% or 30%. That’s nearly 5000%, leading the latest review to ask, “is there any risk greater?” That’s because it’s not so much a risk factor for atherosclerosis as atherosclerosis itself. A man "with erectile dysfunction (even if he doesn’t have cardiac symptoms) should be considered a cardiac patient until proven otherwise."

Erectile dysfunction is considered to be a cardiac equivalent; it’s a marker of the coronary artery one likely already has. Thus, there’s more to treating ED than establishing an erect penis; it offers an opportunity for reducing cardiovascular risk. The reason even young men should care about their cholesterol is because it predicts erectile dysfunction later in life, which in turn predicts heart attacks, strokes, and a shortened lifespan.

Thankfully, Our Number One Killer Can Be Stopped. Check out my video on Eliminating the #1 Cause of Death. More background can be found in Arterial Acne and Blocking the First Step of Heart Disease.

Related videos include: 50 Shades of Green and Pistachio Nuts for Erectile Dysfunction.

Previous videos on the subject include:

A similar relationship appears to exist for female sexual function as well. See my video: Cholesterol and Female Sexual Dysfunction.

-Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death and More Than an Apple a Day.

Image Credit: sea turtle / Flickr

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