Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?
Omega-3 MUST be from fish oil

Omega-3 MUST be from fish oil

Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.


Copyright 2008 William Davis, MD

Comments (14) -

  • Michael

    3/7/2008 2:59:00 AM |

    Anyone have any experience using krill oil, and how does it compare to fish oil?

    As for other forms of omega-3s, isn't flax considered dangerous for men, due to ALA content? There are conflicting studies, but I recall at least one that said ALA caused a rise in the rate or prostate cancer.

  • Zubin

    3/7/2008 3:31:00 AM |

    Is there any way for a vegetarian to replace fish oil and get the same benefits?

  • Missbossy

    3/7/2008 5:01:00 AM |

    I am definitely down with the fact that Fish Oil is vastly superior to Flax Oil. I've seen quite a few people touting flax oil lately so I'm glad you put that to bed.

    Question: You mention recommended doses of EPA and DHA for those with elevated triglycerides. Can you offer any guidance for supplement levels when triglycerides aren't an issue? IE a level for good preventative nutrition? I've looked around and recommendations are all over the shop.

    Thanks.

  • Anonymous

    3/7/2008 12:53:00 PM |

    I've read a few other articles about the differences between fish oil omega-3s and other sources, but this article spells it out very clearly about how those differences apply directly to heart disease. I'll be printing this one for my family. Thanks!

    S

  • Anonymous

    3/7/2008 2:11:00 PM |

    Vegetarian DHA is available. It is cultured from algae. That's where the fish get. EPA may be available now too.

  • Anonymous

    3/7/2008 3:52:00 PM |

    zubin:

    There are vegetarian DHA/EPA supplements made from algae.

  • Liss

    3/8/2008 12:09:00 AM |

    Zubin, when I followed a vegetarian diet I was able to find DHA supplements derived from algae, but EPA is harder to come by.  V-Pure is the only one I found that contained both EPA and DHA.  The capsules are costly, but might be a good option for you if you aren't comfortable taking krill or fish oil.

  • Zubin

    3/9/2008 2:06:00 PM |

    Thanks all, I will look into the algae supplements!

  • Anonymous

    5/12/2008 1:03:00 PM |

    As a newcomer to your blog please forgive me if this topic has been brought up before.
    There is a scathing attack in an article by Ray Peat,a noted Biology professor, on the damaging effects of fish oil.
    A few people have stopped taking fish oil after reading the article.
    Can you please comment?
    http://raypeat.com/articles/articles/fishoil.shtml

  • Anonymous

    7/8/2008 4:05:00 AM |

    http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html
    A Reply to Ray Peat
    on Essential Fatty Acid Deficiency

    By Mary G. Enig, PhD

    Ray Peat, PhD, is an influential health writer who claims that there is no such thing as essential fatty acid (EFA) deficiency. According to Peat, the body can make its own EFAs; furthermore, he claims that EFAs in the body become rancid and therefore cause cancer.

    Unfortunately, Peat does not understand the use of EFA by the human body. He is trained in hormone therapy and his training in fats and oils has been limited to misinformation as far as the polyunsaturated fats and oils are concerned.

    Research on EFAs is voluminous and consistent: EFAs are types of fatty acids that the body cannot make, but must obtain from food. We do not make them because they exist in virtually all foods, and the body needs them only in small amounts. The body does make saturated and monounsaturated fatty acids because it needs these in large amounts and cannot count on getting all it needs from food.

    There are two types of EFAs, those of the omega-6 family and those of the omega-3 family. The basic omega-6 fatty acid is called linoleic acid and it contains two double bonds. It is found in virtually all foods, but especially in nuts and seeds. The basic omega-3 fatty acid is called linolenic acid and it contains three double bonds. It is found in some grains (such as wheat) and nuts (such as walnuts) as well as in eggs, organ meats and fish if these animals are raised naturally, and in green vegetables if the plants are raised organically.

    Essential fatty acids have two principal roles. The first is as a constituent of the cell membrane. Each cell in the body is surrounded by a membrane composed of billions of fatty acids. About half of these fatty acids are saturated or monounsaturated to provide stability to the membrane. The other half are polyunsaturated, mostly EFAs , which provide flexibility and participate in a number of biochemical processes. The other vital role for EFAs is as a precursor for prostaglandins or local tissue hormones, which control different physiological functions including inflammation and blood clotting.

    Scientists have induced EFA deficiency in animals by feeding them fully hydrogenated coconut oil as their only fat. (Full hydrogenation gets rid of all the EFAs; coconut oil is used because it is the only fat that can be fully hydrogenated and still be soft enough to eat.) The animals developed dry coats and skin and slowly declined in health, dying prematurely. (Interestingly, representatives of the vegetable oil industry blame the health problems on coconut oil, not on fatty acid deficiency!)

    In a situation of fatty acid deficiency, the body tries to compensate by producing a fatty acid called Mead acid out of the monounsaturated oleic acid. It is a 20-carbon fatty acid with three double bonds named after James Mead, a lipids researcher at the University of California at Los Angeles who first identified it. An elevated level of Mead acid in the body is a marker of EFA deficiency.

    According to Peat, elevated levels of Mead acid constitute proof that your body can make EFAs. However, the Mead acid acts as a "filler" fatty acid that cannot serve the functions that the original EFA are needed for. Peat claims that Mead acid has a full spectrum of protective anti-inflammatory effects; however, the body cannot convert Mead acid into the elongated fatty acids that the body needs for making the various anti-inflammatory prostaglandins.

    Peat also asserts that polyunsaturated fatty acids become rancid in our bodies. This is not true; the polyunsaturated fatty acids in our cell membranes go through different stages of controlled oxidation. To say that these fatty acids become "rancid" is misleading. Of course, EFAs can become rancid through high temperature processing and it is not healthy to consume these types of fats. But the EFAs that we take in through fresh, unprocessed food are not rancid and do not become rancid in the body. In small amounts, they are essential for good health. In large amounts, they can pose health problems which is why we need to avoid all the commercial vegetable oils containing high levels of polyunsaturates.

    Peat’s reasoning has led him to claim that cod liver oil causes cancer because cod liver oil contains polyunsaturated fatty acids. Actually, the main fatty acid in cod liver oil is a monounsaturated fatty acid. The two main polyunsaturated fatty acids in cod liver oil are the elongated omega-3 fatty acids called EPA and DHA, which play many vital roles in the body and actually can help protect against cancer. Furthermore, cod liver oil is our best dietary source of vitamins A and D, which also protect us against cancer.

    Actually, Peat’s argument that polyunsaturated fatty acids become harmful in the body and hence cause cancer simply does not make sense. It is impossible to avoid polyunsaturated fatty acids because they are in all foods.

    EFAs are, however, harmful in large amounts and the many research papers cited by Peat showing immune problems, increased cancer and premature aging from feeding of polyunsaturates simply corroborate this fact. But Peat has taken studies indicating that large amounts of EFAs are bad for us (a now well-established fact) and used them to argue that we don’t need any at all.

    Finally, it should be stressed that certain components of the diet actually reduce (but do not eliminate) our requirements for EFAs. The main one is saturated fatty acids which help us conserve EFAs and put them in the tissues where they belong. Some studies indicate that vitamin B6 can ameliorate the problems caused by EFA deficiency, possibly by helping us use them more efficiently.

    About the Author
    Mary G. Enig, PhDMary G. Enig, PhD is an expert of international renown in the field of lipid biochemistry. She has headed a number of studies on the content and effects of trans fatty acids in America and Israel, and has successfully challenged government assertions that dietary animal fat causes cancer and heart disease. Recent scientific and media attention on the possible adverse health effects of trans fatty acids has brought increased attention to her work. She is a licensed nutritionist, certified by the Certification Board for Nutrition Specialists, a qualified expert witness, nutrition consultant to individuals, industry and state and federal governments, contributing editor to a number of scientific publications, Fellow of the American College of Nutrition and President of the Maryland Nutritionists Association. She is the author of over 60 technical papers and presentations, as well as a popular lecturer. Dr. Enig is currently working on the exploratory development of an adjunct therapy for AIDS using complete medium chain saturated fatty acids from whole foods. She is Vice-President of the Weston A Price Foundation and Scientific Editor of Wise Traditions as well as the author of Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Bethesda Press, May 2000. She is the mother of three healthy children brought up on whole foods including butter, cream, eggs and meat.

    IMPORTANT CORRECTION

    In the Winter 2004 "Know Your Fats" column we stated that Siberian pinenut oil was a good source of gamma-linolenic acid (GLA). This was indicated from fatty acid analyses performed in Siberia. We have since performed further tests on the oil and found that it does not contain significant amounts of GLA but rather a fatty acid called pinoleic acid, an 18-carbon fatty acid with three double bonds but with the first double bond on the fifth carbon, not the sixth, as in GLA. We are sorry for any inconvenience this may have caused.

    http://www.westonaprice.org/knowyourfats/essentialfattyaciddef.html

  • Arlie

    6/5/2009 4:26:30 PM |

    I'm a 57 year old grandma and have been vegan for over 6 years. I've run 3 marathons since turning 50, but took at 18 month hiatus to care for a grandson.  I was slowly trying to get back into running by starting out with 20 min. jogs and 3 minutes of jumping rope. Last October I developed painful tendinitis in my knee...my M.D. encouraged me to try O.T.C. painkillers (aspirin, acetaminophen, and ibuprofen) and take glucosamine all to no avail...he sent me to a physical therapist who gave me a few exercises said I shouldn't run at all, ever...that he quit running at age 30 and advises walking only. At that point my doctor wanted to prescribe some NSAID and give me a 2nd prescription for something that would allow my stomach to handle the prescription NSAID.   Without my M.D.'s recommendation I went to an acupuncturist for 3 months...no luck there.  Then a few months ago, again without my M.D.'s referral, I went to a chiropractor.  Since I was vegan, he prescribed flax oil, which seemed to help only a little, although the chiropractor said he really thought I would benefit the most from fish liver oil. Yesterday, in desperation, I took fish oil and felt much better.  I'm not pain free yet...but the improvement was quite dramatic.  I'll have to see how it goes.  I was vegan for personal, ethical reasons as opposed to health concerns...so even though this is a bit of a disappointment for me and my veganism...I think I will continue to use the fish oil and see if I benefit further.  By the way I had been taking vegan DHA for years from either "Omega Zen" or "Deva". Many, many years ago I heard that the playwright George Bernard Shaw had to take liver for a B-12 deficiency.  As the story goes someone said to him, "Is that liver you're eating...I thought you were a vegetarian."  Shaw replied "I am, this is my medicine."

  • Anonymous

    2/15/2010 9:11:25 PM |

    Ah, This is exactly what I was looking for! Clears up
    a few misnomers I've read

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  • moseley2010

    12/8/2010 4:40:26 PM |

    I have heard about acai berries and acai berry supplements containing sufficient Omega 3. I found out about this while I was looking for great alternatives for kids. Because for sure, they don't like fish oil supplements as they are huge and smelly, but I also believe they need the Omega 3 and all the good it brings. I found out about acai berry powder with Omega 3. I admit I am almost convinced.

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