by Mark Hyman
The take-home message here: Saturated fats lower inflammation when consumed with a low-carb, high-fiber, omega-3-rich diet. And lowering inflammation is key to healing and weight loss.
Does Saturated Fat Cause Strokes?
One study of 60,000 people in Japan showed that higher intakes of saturated fat led to a reduced risk of stroke.27 So based on this study we should be recommending saturated fat to reduce heart disease risk and stroke, not warning against it.
SATURATED FATS AND CARBOHYDRATES
As we’ve reviewed, the saturated fats you eat don’t increase blood levels of saturated fats. Doubling or even tripling saturated fat in your diet has no impact on saturated fat in your blood. It’s the carbs that spike your blood levels of saturated fats. Many studies confirm that blood levels of saturated fat (palmitic, stearic, and palmitoleic acid) are significantly correlated with the development of type 2 diabetes28 and heart disease.29 But these fats in the blood are not coming from the fat you eat. They are produced by the liver in response to the carbs in your diet.
A group of researchers from Ohio State University did a very elegant study that tested this idea in a group of overweight pre-diabetic people.30 They gave the study participants six different diets, each three weeks long. In the first part of the study, they increased the amount of carbs, starting at 50 grams a day and going up to 350 grams a day, and decreased the saturated fat. In the other part of the study they increased the saturated fat and reduced the carbs. There was no difference in blood levels of saturated fats despite a doubling of saturated fat from 46 to 84 grams a day. Only when the participants got to the high-carb part of the study did the researchers find higher levels of saturated fats in the blood, specifically palmitic acid.
The liver formed these bad fats even when the participants lost weight. So it was carbs, not fat, that raised the levels of saturated fat in the blood. These well-done studies show over and over again that in the face of low-carbohydrate diets, saturated fats are harmless and may be beneficial.
Another interesting study found that saturated fats consumed in a low-carbohydrate diet had no impact on blood cholesterol levels or profile, but in a high-carb diet, they made things worse.31 So we should skip the bread and eat the butter. At least our cholesterol would improve.
I’ve put thousands of patients on a high-fat, low-carb diet and have seen for myself beneficial changes in all the important known risk factors for heart disease, including overall cholesterol profile, blood sugar, insulin, inflammation, liver function, hormones, and belly fat.
SATURATED FATS AND CHOLESTEROL
The obsession with cholesterol and LDL in particular as the only thing that drives heart disease is completely misguided. Why are we all so focused as doctors and patients on LDL? Simple. There is a multibillion-dollar drug industry behind the number one selling class of drugs on the market: statins. And the main effect of statins is to reduce LDL (bad cholesterol), which turns out not to be the most important thing in preventing heart disease. More on statins in a minute. First, let’s dispel one of the biggest myths we have in medicine today: the connection between cholesterol and heart disease.
Saturated Fat Facts
They have not been linked to heart disease, despite more than half a century of this belief and billions of dollars of research.
They actually improve your overall cholesterol profile in the face of a low-carb diet by lowering triglycerides, raising HDL, and decreasing the small, dangerous LDL particles.
They are a problem only in the face of a high-carb, low-fiber, omega-3-fat-deficient diet.
They seem to be neutral or improve inflammation in many studies.
When compared with higher-carb low-fat diets, higher-fat and saturated-fat diets do better in improving every single risk factor for heart disease (and promoting weight loss).
Some dietary saturated fats (from dairy) may reduce the risk of heart disease.
Blood levels of certain saturated fats are associated with heart disease, but it is carbs that increase those blood levels of saturated fat, not the saturated fats we eat.
The fact that saturated fat raises cholesterol is the biggest reason we have vilified meat and butter. The logic went that if high blood cholesterol causes heart attacks, and saturated fat raises cholesterol, then reducing saturated fat in the diet should reduce heart attacks and death. Sounds sensible. Except for one thing. The overwhelming body of research doesn’t support this.32
We need a little biochemistry lesson here to understand cholesterol metabolism in the body. Hang in there with me; this is super important.
Most of the cholesterol floating around your blood is made in the liver. The liver gets triggered to produce fat and cholesterol in response to sugar and carbs. This is called lipogenesis. Everyone who has taken a biochemistry course knows this (or should know it); it is basic science. But somehow this fact has been completely ignored by most doctors and scientists studying cholesterol.
High-carb diets increase the production of triglycerides, lower the good cholesterol (HDL), and increase the number of LDL particles.33 They also reduce the size of your cholesterol particles, or the small LDL particles.34 It’s not the LDL that’s bad, but the small LDL. This kind of lipid profile is called atherogenic—in other words, it causes atherosclerosis, or hardening of the arteries, the very thing at the root of heart disease, stroke, and many cases of dementia. If you reduce fat, you may lower LDL (bad cholesterol), and that may seem like a good thing, but in fact it is a bad thing. Lower cholesterol is not always better cholesterol.
Shifting your diet from fat to carbs shifts you from light, fluffy, harmless LDL particles to small, dense, dangerous ones. In one study, a low-fat diet was compared to a higher-fat diet of exactly the same number of calories. The low-fat (high-sugar and refined-carb) diet led to dramatically higher triglycerides in both thin and overweight people.35 In another analysis of more than sixty studies, researchers found that increasing saturated fats in the diet raised both LDL (which is not bad if it is large particles) and HDL while lowering triglycerides and increasing LDL particle size.36 All these changes are beneficial, not harmful. In fact, it isn’t the typical LDL value (which is the weight of your cholesterol measured in milligrams per deciliter) that correlates with heart disease at all. It is the LDL particle size and number.37
The LDL number your doctor measures is simply the weight of LDL in your blood (in milligrams per deciliter). Think of it as a box that weighs a certain amount. Inside that box there can be many small golf balls (small, dangerous LDL particles), or a few large, light beach balls (large, benign LDL particles). Most doctors never measure that, but that is what is most correlated with heart disease. Doctors should order the NMR (nuclear magnetic resonance) lipid test, offered by LabCorp or the Cardio IQ test offered by Quest Diagnostics. It puts your cholesterol in a mini MRI machine to examine the number and size of the particles. The other cholesterol tests should be left in the twentieth century. Demand the NMR lipid or Cardio IQ test instead!
You can have the exact same LDL value (130 mg/dl), which is the weight, but it can be made up of many dangerous small particles (pattern B) or a few large, light, fluffy particles (pattern A).38
The main factor that stimulates your liver to produce these small, dense cholesterol particles and to produce many of them is sugar and refined carbs. It seems hard to believe that we got the whole story wrong for more than half a century, but it is true. It is sugar, not fat, that is the big driver of heart disease (as well as stroke, obesity, type 2 diabetes, and dementia). In fact, our whole effort to reduce heart disease by lowering LDL (bad cholesterol) by reducing saturated fat and prescribing statin drugs has had unintended consequences.
Cholesterol… the Hero?
Think cholesterol is the enemy? Think again!
Cholesterol is a fatty substance produced by the liver that is necessary for thousands of bodily functions. The body uses it to help build your cell membranes and to cover your nerve sheaths as well
as much of your brain. It’s a key building block for hormone production; without it you would not be able to maintain adequate levels of testosterone, estrogen, progesterone, and cortisol. Even more important, without it, you would die. In fact, people with the lowest cholesterol as they age are at highest risk of death. Under certain circumstances, higher cholesterol can actually help to increase life span.
In terms of cholesterol, the type of fat that you eat is more important than the amount of fat. Trans fats or hydrogenated fats and refined vegetable oils (omega-6 PUFAs) promote abnormal cholesterol, whereas omega-3 fats from fish and monounsaturated fats found in nuts and olive oil actually improve the type and amount of cholesterol your body produces.
In reality, the biggest source of abnormal cholesterol is not fat at all—it’s sugar. The sugar you consume converts to fat in your body. And the worst culprit of all is high-fructose corn syrup. Consumption of high-fructose corn syrup, which is present in sodas, juices, and processed foods, is the primary nutritional cause of most of the cholesterol issues we doctors see in our patients. Fructose is a problem because when ingested in high amounts (without the associated fiber found in whole fruit) it turns on the cholesterol production factory in your liver, called lipogenesis.39
A study published in the American Journal of Clinical Nutrition looked at the impact that sugar intake has on cholesterol. The researchers carried out a meta-analysis of thirty-nine randomized controlled trials on sugar intake. Overall, it showed that people who ate higher amounts of sugar had significantly higher levels of triglycerides and LDL and total cholesterol. This effect occurred even if there was no change in weight with higher-sugar and carb diets. In other words, it was not weight gain that made the cholesterol worse; it was sugar.
So the real concern isn’t the amount of cholesterol in your blood, but the type of fats and sugar and refined carbohydrates in your diet. Of course, many health-conscious people today know that total cholesterol or LDL is not as critical as the following factors or numbers:
Your levels of HDL (good cholesterol) vs. LDL (bad cholesterol) (HDL ideally greater than 60 mg/dl)
Your triglyceride levels (ideally less than 100 mg/dl)
Your ratio of triglycerides to HDL (ideally less than 1:1 or 2:1)
Your ratio of total cholesterol to HDL (ideally less than 3:1)
Another concern is whether or not the cholesterol in your blood is rancid or oxidized. If it is, the risk of arterial plaque is real. Rancid or oxidized cholesterol results from oxidative stress and free radicals, which trigger a vicious cycle of inflammation and fat or plaque deposits under the artery walls. This can occur more often when consuming omega-6 fats because they are unstable and more easily oxidized. Cholesterol is like the body’s Band-Aid, and when there is inflammation it tries to patch things up. That is the real danger: When small, dense LDL particles are oxidized, they become hazardous by starting the buildup of plaque or cholesterol in your arteries.
It is fine to enjoy dietary cholesterol from the right type of fat in any amount because it has no impact on your blood cholesterol or heart disease risk. In Europe, Australia, Canada, New Zealand, Korea, and India, there is no upper limit on the amount of cholesterol considered safe in the diet, and America is finally catching up. The 2013 American College of Cardiology/American Heart Association Task Force on Practice Guidelines did not recommend lowering total fat, only saturated fat.40 And they completely gave up on decades of advice to reduce dietary cholesterol, which had us all eating tasteless egg white omelets and avoiding shrimp and lobster. In fact they noted that dietary cholesterol had no impact on blood cholesterol. In about 25 percent of people it raises the LDL (bad cholesterol), but it also raises the HDL, or good cholesterol, resulting in a neutral effect on your cholesterol profile.41
The government’s own 2015 Dietary Guidelines Advisory Committee (DGAC) Report also did not make any recommendations to lower total fat content, only saturated fat. And for the first time since the guidelines were established in 1980, dietary cholesterol was exonerated: “Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum cholesterol, consistent with the conclusions of the AHA/ACC (American College of Cardiology/American Heart Association Task Force) report. Cholesterol is not a nutrient of concern for overconsumption.”42
I love that: “not a nutrient of concern.” What an unceremonious death for the tarnished reputation of dietary cholesterol!
THE BIG BUSINESS OF STATINS
Drug company marketing has convinced us all that statin drugs are God’s gift to humankind and that they are essential to lower your risk of heart attacks and death. Think about how many feel-good commercials and magazine ads you’ve seen for cholesterol-lowering drugs. But do statins live up to all the hype? What does the science really prove?
Most doctors now know that inflammation and oxidative stress are the biggest causes of heart disease, not cholesterol. A landmark paper in the New England Journal of Medicine43 lays out the science of why inflammation, not cholesterol, is the root cause of atherosclerosis. It explains how macrophages (white blood cells) are driven into the walls of your arteries to protect you against rancid or oxidized cholesterol. They soak up the toxic oxidized or rancid cholesterol (not all the cholesterol), and that is what causes the plaque that clogs your arteries and leads to heart attacks. It turns out that the reason statins have any effect at all is not because they lower cholesterol, but because they lower inflammation and also act as antioxidants. So they do have some benefit, but there are a lot better ways to reduce inflammation and get antioxidants with many fewer side effects!
However, a recent study found that using statins did not lead to lower heart attacks or death. In 2011, a group of Swedish researchers looked at the relationship between statin prescriptions and heart attacks in their country. They found that between 1998 and 2002, the rate of statin use among Swedish men and women between the ages of forty and seventy-nine roughly tripled. Yet this had no impact on the corresponding rate of heart attack incidence or mortality. Stunning, isn’t it? A tripling of statin use and no impact on heart disease! This is not a randomized trial, and just shows a correlation, but it still worries me.
Roger Williams, a twentieth-century American biochemist who discovered vitamin B5, once said something about research that rings true: “There are liars, damn liars, and statisticians.” We see prominent ads on television and in medical journals for statins that report a 36 percent reduction in the risk of having a heart attack. But we don’t look at the fine print. What does that really mean, and how does it affect decisions about who should be using these drugs?
Before I explain that, here are some interesting findings to ponder about cholesterol and statins:
If you lower bad cholesterol (LDL) but have a low HDL (good cholesterol) there is no benefit to statins.44
If you lower bad cholesterol (LDL) but don’t reduce inflammation (marked by a test called C-reactive protein), there is no benefit to statins.45
If you are a healthy woman with high cholesterol, there is no proof that taking statins reduces your risk of heart attack or death.46
If you are a man or a woman over sixty-nine years old with high cholesterol, there is no proof that taking statins reduces your risk of heart attack or death.47
Aggressive cholesterol treatment with two medications (Zocor and Zetia) lowered cholesterol much more than one drug alone but led to more plaque buildup in the arteries and no fewer heart attacks.48
Older patients with lower cholesterol have a higher risk of death than those with higher cholesterol.49
Countries with higher average cholesterol than America, such as Switzerland and Spain, have less heart disease.
Recent evidence shows that it is probably the ability of statins to lower inflammation that accoun
ts for the benefits of statins, not their ability to lower cholesterol.50
About 20 percent of people who take statins have side effects, including muscle damage and pain,51 neurologic problems, memory issues,52 sexual dysfunction,53 and more.54
Statins have been linked to a dramatically higher risk of diabetes. In one study of almost 26,000 healthy people, those taking statins to prevent heart attacks were 87 percent more likely to get type 2 diabetes.55 In another randomized controlled trial of 153,840 women, those who took statins were 48 percent more likely to get type 2 diabetes.56 Large reviews of all the studies show about a 10 percent increased risk. But if all the people who are currently advised to take statins did so, that would mean we would have another 4 to 5 million diabetics in the country!
Winston Churchill said—and I am paraphrasing—that men occasionally stumble over the truth, but most of them pick themselves up and hurry off as if nothing happened. This is precisely what happened with a dramatic study published in 2009 in the American Heart Journal, which found that 75 percent of patients admitted to hospitals with heart disease had normal cholesterol levels.57 The authors looked at 231,836 hospital admissions from 541 hospitals, accounting for 59 percent of all heart attack admissions in the country from 2000 to 2006. A very big sample! They assessed cholesterol levels within the first 24 hours of admission. Their findings were shocking. About 75 percent had normal LDL (bad cholesterol) levels (under 130 mg/dl) and more than 50 percent had “optimal” LDL levels (under 100 mg/dl). For those who argue that this means we need to lower LDL benchmarks even further, the study also found that more than 17 percent had LDL levels below 70 mg/dl.