The Great Cholesterol Myth (16 page)

The real action is with polyunsaturated fats.

Remember, polyunsaturated fats, which are primarily found in vegetable oils, are the very ones we’ve been admonished to include more of in our diets. When lard was slammed back in the early part of the twentieth century, the health dictocrats started their cheerleading effort for vegetable fats. (The first major beneficiary of this all-out campaign to make vegetable fats synonymous with “healthy” fat was actually the trans fat–laden Crisco, the most popular vegetable shortening of its time.) Even now, most people believe that substituting vegetable oil for animal fats is universally a good thing.

But is it always?

Let’s, as they say, go to the videotape.

Polyunsaturated fats as a whole are divided into two subcategories: omega-3 fatty acids and omega-6 fatty acids. (For those who’ve always wondered what the heck an “omega” is anyway, you can think of the terms
omega-6
and
omega-3
as real estate terms; they’re simply descriptions of the location of certain chemical structures—called double bonds—within the fatty acid. An omega-3 has its first double bond at the third carbon atom in the chain, while omega-6 has its first double bond at the sixth carbon atom in the chain. Now, for our purposes, you can promptly forget all that and just concentrate on what these two types of fatty acids—omega-3s and omega-6s—actually do in the body.)

Omega-6s, as mentioned, are found primarily in vegetable oils and some plant foods. Omega-3s are found primarily in fish, such as salmon, and certain animal foods, such as grass-fed beef, as well as in some plant foods, such as flax and flaxseed oil. So far, so good.

Here’s where it gets tricky.

Both inflammatory and anti-inflammatory hormones, known as
eicosanoids
, are made in the body from polyunsaturated fats. (And to answer the inevitable question, yes, we actually need both. Inflammatory compounds are a necessary part of the immune system and play a big part in the healing process when you have a wound or other type of injury.)

Omega-6s are the precursors to the inflammatory compounds in our body—they’re the building blocks the body uses to make these inflammatory hormones (specifically
series 2 prostaglandins
). And omega-3s have the opposite function: The body uses omega-3s as building blocks for the anti-inflammatory compounds (known as
series 1 prostaglandins
and
series 3 prostaglandins
).

A ton of research has established that the ideal ratio of omega-6s to omega-3s in the human diet is somewhere between 1:1 and 4:1. This seems to be the best balance to keep inflammation in check and everything running smoothly. It’s the ratio found in the diets of both hunter-gatherers and healthy indigenous societies where heart disease is rare.
¹⁸

But the ratio of omega-6s to omega-3s in Western diets is anywhere from an astonishing 15:1 to an even more astonishing 20:1 in favor of omega-6s.
¹⁹
If you think of the inflammatory and anti-inflammatory hormones as two armies that work together in the body to create balance in the body, that means we’re overfunding the inflammation army by 1,500 to 2,000 percent!

Our extraordinarily high intake of vegetable oil has another unintended consequence, and one that may have a profound effect on cardiovascular health. To understand it, though, you have to take a short excursion into the world of omega-3 fatty acids. (Trust us, it’s a short and easy trip.)

You see, there are actually three omega-3 fatty acids—ALA (
alpha-linolenic acid
), EPA (
eicosapentaenoic acid
), and DHA (
docosahexaenoic acid
). The only one
that is “essential” in the diet is ALA, which is found in green, leafy vegetables and in flaxseeds, chia seeds, perilla seeds, and walnuts. That doesn’t mean the other two aren’t important. In terms of their overall effects on human health, the other two are probably
more
important than ALA. The reason the other two—EPA and DHA—aren’t considered “essential” is that scientists use the word
essential
in a different way than regular people use it in ordinary conversation. In this context,
essential
simply means that it’s something the body can’t make, so you have to get it from your diet. Your body can make EPA and DHA, so technically they’re not classed as “essential.” Because the body can’t make ALA, however, it’s considered an “essential” omega-3.

But the fact that the body can make EPA and DHA from ALA doesn’t mean it does a particularly good job of it. It converts the ALA from the diet into EPA and DHA using enzymes and a complicated series of operations known as
elongation
and
desaturation
, the success of which is influenced by many different factors, including the amount of inflammatory omega-6’s in the diet. Even under the best of circumstances, only a small amount of ALA successfully gets converted into the very critical EPA and DHA.

Omega-6s and omega-3s compete for the same enzymes, and when omega-6 intake is very high, it wins the competition by default. A high intake of omega-6 reduces the conversion of ALA into EPA and DHA, which might be another reason why high omega-6 diets contribute to heart disease.
¹⁹
So not only are those omega-6 fatty acids pro-inflammatory on their own, but they also reduce the body’s ability to produce two of the most anti-inflammatory substances on the planet: the omega-3s EPA and DHA. It’s a double whammy, and your heart is the loser.

No, the omega-6s that have been the darling of the high-carb, low-fat movement, the vegetable oils we’ve been told to use instead of animal fats—the very vegetable oils that “saturate” (no pun intended) our diet through their incorporation into virtually every baked, fried, and processed food available in the supermarket, the very vegetable oils that restaurants proudly boast of
using because they’re so “healthy”—are actually turning out to be as bad as, or worse than, the original saturated fats (such as lard) that they replaced, just as margarine turned out to be far worse than butter.

The vegetable oils we’ve been told to use instead of animal fats are actually turning out to be as bad as, or worse than, the original saturated fats (such as lard) that they replaced, just as margarine turned out to be far worse than butter.

For example, the primary omega-6 fatty acid—linoleic acid—has been shown to increase the oxidation of LDL cholesterol, thus increasing the severity of coronary atherosclerosis.
²¹
One research study showed that a diet enriched with linoleic acid increased the oxidation of the small, nasty LDL particles, precisely the cholesterol particles that are most dangerous and most involved in the formation of arterial plaque.
²²
Omega-6s even inhibit your body’s ability to fully incorporate the EPA you get from fish or fish oil supplements into the cell membranes, which is meaningful because EPA is the omega-3 that has the most profound effect on the heart.
²³

Published values for omega-6 intake closely track observed coronary heart disease death rates for all sorts of populations worldwide.
²⁴
And in the famous MRFIT study, subjects with the lowest ratio of omega-6 to omega-3 (i.e., those with the lowest intakes of omega-6 relative to their omega-3 intakes) had the lowest death rate.
²⁵

At this point you may well be wondering why low-fat, high-carb diets work at all when they do work. If saturated fat is not the bad guy we thought it was, and if carbohydrates aren’t always the good guys, why is it that some of these high-carb, super-low-fat programs seem to work sometimes?

Glad you asked, because we have a theory about that.

Although many people may believe that extremely low-fat diets work because they cut out saturated fat, we suspect the real benefit comes from reducing omega-6s. Omega-6 is the predominant fat we consume, and as we’ve seen, we consume way too much of it. When we follow a very low-fat diet we consume less of it, which automatically lowers the pro-inflammatory to anti-inflammatory ratio. The fact that saturated fat is lowered is actually incidental.

In addition, those famous low-fat, high-carb diets, such as those promoted by McDougall, Ornish, and Esselstyn, are remarkably low in sugar. The carb content may be high, but they’re not the carbs most people are gorging on. The carbs in these high-carb diets tend to be vegetables, fruits, and a smattering of starches, such as beans and brown rice. And although some of the starches may be high-glycemic (such as potatoes), they don’t contain a ton of fructose (as do most processed carbs and virtually all packaged goods). Fructose is the most metabolically dangerous of the sugars, and it is a very minor player in any of the low-fat, high-carb diets that are successful. We suspect that when very low-fat, high-carb diets work at all—and they frequently don’t—they work because of these three dietary factors: fewer inflammatory omega-6s, fewer high-glycemic carbs, and much less fructose or sugar. We believe that whatever benefits might sometimes accrue from extremely low-fat, high-carb diets could be easily achieved by simply reducing sugar and processed
carbs, eliminating trans fats,
in
creasing omega-3s, and
de
creasing omega-6s. Reducing saturated fat and dietary cholesterol intakes has virtually nothing to do with it.

Besides, what is the mechanism by which saturated fat could cause heart disease? In 2008, the distinguished biochemist Bill Lands attempted to answer this and other related questions about conventional dietary advice in a closely argued review (complete with 231 scientific references) that was published in the scientific journal
Progress in Lipid Research
.

Here’s what Lands had to say about saturated fat and heart disease:

“Advice to replace saturated fat with unsaturated fat stimulated my early experiments in lipid research. It made me ask by what mechanisms could saturated fats be ‘bad’ and unsaturated fats ‘good’ . . . Fifty years later, I still cannot cite a definite mechanism or mediator by which saturated fat is shown to kill people . . . The current advice to the public needs to identify logical causal mechanisms and mediators so we can focus logically on what food choices to avoid.”
²⁶

When it comes to the theory that saturated fat kills people, Lands was essentially challenging his researcher colleagues to “prove it.”

And they haven’t.

CHAPTER 6

STEPHANIE SENEFF ALWAYS WANTED TO BE A BIOLOGIST.

For as long as she can remember, she has been fascinated by how things work, particularly how living things work. She wanted to know how frogs jump, how grasshoppers breathe, how cells communicate, how the heart talks to the brain, all of which scientists study in detail, frequently by spending hours a day peering into a microscope. She was interested in systems, and to her the human body was the most fascinating system of all. So she was more than a little delighted when, after high school, she was accepted into the biology program at MIT.

After completing her B.S. in biophysics, she entered the MIT Ph.D. program and spent a year working under Professor Harvey Lodish in the laboratory headed by future Nobel Prize winner David Baltimore.

But there was a problem.

After a year in Baltimore’s lab, Seneff realized two things. One, she wasn’t really cut out for the isolation required by a life in the lab, and two, she wanted to start a family. So she quit the Ph.D. program.

But she didn’t quit MIT. “In those days,” she told us, “you could get a job as a programmer with no prior experience. I got a job at MIT Lincoln Laboratory, where I lucked into a group of pioneers in the fledging field of computer speech processing.”

Voilà. Seneff found a home, a perfect blend of her two great interests—biology and computer dialogue systems. She went on to earn a Ph.D. in electrical engineering from MIT, ultimately publishing more than 170 papers and becoming one of the world’s leading experts in blending biological systems with computer intelligence. (It was her pioneering work in the field of voice recognition and computer systems that led to commercial applications such as SIRI, the virtual assistant built into the iPhone, which has an uncanny ability to recognize what you say to it and execute voice commands.

Then something happened: Seneff’s husband was diagnosed with heart disease.

His doctor put him on a high-dose statin—four times the usual dose—and told him it was imperative that he stay on it. “If you go off this, or even reduce the dosage, I can no longer be your doctor,” his physician told him.

Almost immediately, the side effects started. He developed debilitating shoulder problems; muscle aches and weakness (he could no longer open drawers or jars); cognitive and memory problems; and depression, something he had never experienced before.

We all know what we do when we first get a diagnosis, or are prescribed a medication we’re not familiar with, or begin having a bunch of unexplained symptoms or side effects: We go on the Internet, which is exactly what Seneff did.

Except Seneff, as you can probably imagine, is no ordinary Googler. She applied her not inconsiderable, methodologically precise skills as a researcher to the task at hand and proceeded to try to learn everything there was to learn about cholesterol, heart disease, and statin drugs. She had no agenda, other than to help her husband get well. She had not spent four years in medical school being subtly influenced by the drug companies, had not been a consultant to the pharmaceutical industry, had not been visited daily by a charming crew of pharmaceutical company reps spinning studies—paid for by those same pharmaceutical companies—that tout the unabashed benefits of their products. And she had not been paid hefty fees by those same pharmaceutical companies (like Dr. Sinatra had) to give “educational” lectures on behalf of their products (lectures that are little more than marketing tools disguised as scholarship).