Are statins and omega-3s incompatible? - Davis

Are statins and omega-3s incompatible?
Posted on June 18, 2013 by Dr. Davis

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

 2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association’s advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

 –Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)

–Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)

–Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don’t have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.

 - See more at: http://blog.trackyourplaque.com/2013/06/are-statins-and-omega-3s-incompatible.html

DHA: the crucial omega-3 - Davis

DHA: the crucial omega-3  

Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:


□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam’s Club Triple-Strength, Costco, Nature Made, Nature’s Bounty, as well as prescription Lovaza. (That’s right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.

By Dr. William Davis
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Read the complete article here.

Effects of n-3 fatty acids on major cardiovascular events in statin users

These statistics seem to show that omega-3 are better at secondary prevention than statins.

Effects of n-3 fatty acids on major cardiovascular events in statin users and non-users with a history of myocardial infarction

1. Simone R.B.M. Eussen1,2,
2. Johanna M. Geleijnse3,
3. Erik J. Giltay4,
4. Cathy J.M. Rompelberg2,
5. Olaf H. Klungel1 and
6. Daan Kromhout3,*

Abstract

Aims Recent secondary prevention trials have failed to demonstrate a beneficial effect of n-3 fatty acids on cardiovascular outcomes, which may be due to the growing use of statins since the mid-1990s. The aim of the present study was to assess whether statins modify the effects of n-3 fatty acids on major adverse cardiovascular events in patients with a history of myocardial infarction (MI).

                    

Methods and results Patients who participated in the Alpha Omega Trial were divided into consistent statin users (n = 3740) and consistent statin non-users (n = 413). In these two groups of patients, the effects of an additional daily amount of 400 mg eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA), 2 g α-linolenic acid (ALA), or both on major cardiovascular events were evaluated. Multivariable Cox's proportional hazard models were used to calculate adjusted hazard rate ratios (HR_adj). Among the statin users 495 (13%) and among the statin non-users 62 (15%) developed a major cardiovascular event. In statin users, an additional amount of n-3 fatty acids did not reduce cardiovascular events [HR_adj 1.02; 95% confidence interval (CI): 0.80, 1.31; P = 0.88]. In statin non-users, however, only 9% of those who received EPA–DHA plus ALA experienced an event compared with 18% in the placebo group (HR_adj 0.46; 95% CI: 0.21, 1.01; P= 0.051).

Conclusion In patients with a history of MI who are not treated with statins, low-dose supplementation with n-3 fatty acids may reduce major cardiovascular events. This study suggests that statin treatment modifies the effects of n-3 fatty acids on the incidence of major cardiovascular events.

                    

ClinicalTrials.gov number: NCT00127452.

Key words

• n-3 fatty acids
• Eicosapentaenoic acid
• Docosahexaenoic acid
• α-linolenic acid
• Cardiovascular diseases
• Statins
• Lipids

• Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2012.

Why fish stomps flax as a source of omega-3

May 5, 2010 in Food & Nutrition, Myths & Truths

 

I want to thank everyone for sending in their questions and voting on the next topic. The good news is that there’s a lot of interest in all of the topics I’m researching right now. The bad news is that there was no clear winner.

 

I’ve decided to go ahead with the series on fish and fish oil, but I may write about thyroid and diabetes simultaneously. I’m also going to experiment with shorter (although I’m clearly breaking that rule here), but more frequent, articles. Hopefully these will be easier for me to write and for you to read.

Finally, stay tuned for the first episode of The Healthy Skeptic audio podcast, coming up next week. I’ll be interviewing Stephan Guyenet, Ph.D, on the subject of obesity and weight regulation. Stephan is a senior fellow at the University of Washington studying the neurobiology of body fat regulation. He’s also the author of Whole Health Source, which is one of my favorite health related blogs.
Before we get into talking about the benefits of fish consumption, or how how much fish or fish oil you should eat, it’s probably a good idea to start with a basic review of the omega-3 fatty acids.

Essential Fatty Acids 101

A fatty acid is a chain of carbon, oxygen and hydrogen atoms with a carboxyl group on one end. Fatty acids are classified on the basis of how many carbon atoms are in the chain, as well as how many double bonds exist within the molecule.

Fish contain a variety of fatty acids, but the ones that are believed to confer the majority of the benefits are the long-chain omega-3 fats eicosapentanaenoic acid (EPA) and docosahexaenoic acid (DHA). These omega-3 fats are found exclusively in seafood and marine algae.
As you can see from the chart below, it is also possible for the body to synthesize EPA and DHA from the short-chain omega-3 alpha-linolenic acid (ALA). ALA is found in plant foods such as flax, hemp and pumpkin seeds and walnuts.

Click thumbnail for a larger version

However, research clearly indicates that the conversion of ALA to EPA and DHA is extremely limited. Less than 5% of ALA gets converted to EPA, and less than 0.5% (one-half of one percent) of ALA is converted to DHA.

A common misconception, especially amongst vegetarians and vegans, is that our need for EPA and DHA can be met by consuming flax oil and other plant sources of ALA. But the conversion numbers above clearly indicate that this isn’t the case.

Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline. (ref) So unless they are supplementing with an algae-derived source of DHA, it is likely that most vegetarians and vegans are deficient.

This is significant because researchers now believe that the majority of the health benefits we get from dietary omega-3 fats come from the longer chain derivatives (especially DHA, as I will explain below).

Is DHA essential?

In fact, some researchers have proposed that DHA is essential. When scientists label a nutrient as “essential”, they they’re not just saying that it’s “very important”. In the context of nutrition essential means that the nutrient cannot be synthesized in the human body, and must be derived from dietary sources.

According to today’s nutrition textbooks, there are only two essential fatty acids, omega-6 linoleic acid (LA) and omega-3 alpha-linolenic acid (ALA). It is believed that as long as these fats are present in the diet, all of the longer-chain omega-3 and omega-6 derivatives can be synthesized in the body.

As I pointed out above, while this is theoretically possible, in reality the conversion doesn’t work well. This is true even for healthy people, but it’s especially true for those with nutrient deficiencies, because the conversion of ALA to DHA depends on zinc, iron and pyridoxine.

The bioavailability of iron in plant sources is poor compared to animal sources, so iron deficiency is common in vegans and vegetarians. This is another reason why they tend to be poor converters of ALA to DHA.

Several other observations support the hypothesis that DHA is essential:

• DHA content in the tissues of all mammals is very similar despite widely varying intakes of omega-3 fatty acids. ¹
• DHA and AA, but not other omega-3 or omega-6 fatty acids, are selectively transferred across the placenta (PDF).
• 60% of the dry matter of the brain is lipid, and DHA and AA are the most abundant fatty acids of brain phospholipids (PDF)
• DHA status in newborns is much lower in those receiving formula with LA and ALA, than in those receiving milk or formula with pre-formed DHA (PDF)

It is possible that the primarily carnivorous diet of our ancestors, which ensured a consistently high dietary intake of DHA and AA, precluded the need to evolve efficient conversion mechanisms.

In other words, since we were eating a lot of meat and fish with pre-formed DHA and AA, our bodies didn’t need to be experts at converting ALA and LA in plants to DHA and AA. It is far easier for the body to assimilate pre-formed DHA and AA than it is to synthesize them from precursors.

What about EPA? Isn’t it essential too?

EPA is another long-chain omega-3 fatty acid that is conventionally believed to be responsible for the benefits of fish consumption.

EPA is often referred to as “anti-inflammatory”. However, according to this report on essential fatty acids by Masterjohn, EPA’s effect seems to be more of an interference with the metabolism of omega-6 arachidonic acid (AA) than the performance of any essential role itself.

Take a look at the chart again that I linked to in the beginning of the post. The fatty acids in blue boxes are less inflammatory, and those in pink boxes are more inflammatory. The chart shows that AA is used to synthesize prostaglandins that cause inflammation (indicated by the pink box on the chart). Because it has the same number of carbon atoms, EPA competes with AA for the enzymes that metabolize it. Since the prostaglandins made by EPA are less inflammatory than those made by AA (indicated by the blue box), EPA is often referred to as “anti-inflammatory”.

But while EPA is certainly less inflammatory than AA, it doesn’t make sense that the body would require an essential fatty acid just to block the inflammatory effects of of another fatty acid.
By contrast, DHA is used to synthesize compounds that play an active role in resolving inflammation. EPA only makes these compounds in the presence of aspirin (PDF). EPA is thus likely to simply be a byproduct of compromised DHA synthesis.

What does this mean to you?

Putting all of this information together yields the following conclusions:

1. DHA is the most important of the omega-3 fatty acids, and is primarily responsible for the benefits we get from consuming them.
2. DHA is likely to be essential, which means that you must consume it in the diet to prevent disease and ensure optimal function.
3. The conversion of plant sources of ALA, such as flax seed oil, to DHA is poor in healthy people and even worse in people deficient in certain nutrients. Vegans and vegetarians are especially prone to be poor converters of ALA to DHA.
4. If you’ve been buying flax oil in the hopes that it will help, you’d be far better off putting that money towards some fish or fish oil capsules.

Dietary changes over the past century have lowered the DHA status to a state of subclinical deficiency in many people. Countless studies show that this deficiency is at least in part to blame for the rising incidence of cardiovascular disease, inflammatory disease, mental and psychiatric disorders and suboptimal neurodevelopment.

DHA is not the only reason to eat fish, which is also rich in selenium and vitamin D. However, DHA is likely to be the primary reason why populations that eat fish on a regular basis have consistently been shown to healthier than those that don’t. We’ll discuss this further in the next article.

1. Jones PJH, Kubow S. Lipids, Sterols, and their Metabolites. In: Shils ME, et al., eds. Modern Nutrition in Health and Disease: Tenth Edition. Baltimore, MD; Philadelphia, PA: Lippincott Williams & Wilkins (2006) pp. 92-122.

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http://chriskresser.com/why-fish-stomps-flax-as-a-source-of-omega-3

Fish oil: The natural triglyceride form is better

Posted on February 2, 2011 by Dr. William Davis

If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol “backbone,” is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).
Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza–nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis–is the ethyl ester form. That’s not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.
Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al.

Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations – ethyl esters, free fatty acids and re-esterified triglycerides – with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.

(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)

Eur J Clin Nutr 2010 Nov 10.

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al.

Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.

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Read the full article here.

5 Steps You Can Take To Reduce Your Heart Scan Score

By William Davis,MD

CT heart scans are booming in popularity. With over 300 scanners nationwide,
over one million Americans have now been scanned since the introduction of this
technology 10 years ago.

In some cases, lives have been saved. People with high scores (e.g., over
1000) can end up with lifesaving procedures like bypass surgery or stents.

But what about the majority of people who don't have a life-threatening
score?

Too often, people in this very large group are prescribed a cholesterol drug
and patted on the back with advice to cut the fat in their diet. According to
several recent studies, that's a recipe for failure. Do nothing, and you can
expect your score to increase 30% per year. Take a cholesterol drug and cut your
fat, and you can still expect your score to grow 30% per year!

Surely there's a lot more you could do to gain control over your score.

Here's our list of 5 easy yet crucial steps you can take that tip the odds in
your favor that you will not just stop your score from increasing, but perhaps
even reduce it.

1. Take fish oil

Fish oil is among the few breakthrough discoveries of the past 20 years that
has altered the course of cardiovascular illness, slashing risk of death, heart
attack, and stroke. The mis-guided advice of the 1980s that polyunsaturated oils
were healthy has left us appallingly overloaded with omega-6 fatty acids, and
omega-3 supplementation from fish oil has become increasingly important.

The 11,000-participant GISSI-Prevenzione trial brought any remaining
naysayers to their knees. Participants taking fish oil experienced 30% reduction
in cardiovascular death and an astounding 45% reduction in sudden death.

Fish oil provides anti-inflammatory benefits, plaque-stabilizing effects, and
corrects many genetic and acquired causes for heart attack. Fish oil helps
correct the triglyceride and small LDL abnormalities triggered by metabolic
syndrome, the collection of pre-diabetic abnormalities now afflicting 59 million
Americans. Fish oil also accelerates clearance of abnormal fat particles in the
blood that persist after eating. All of this adds up to a dramatic reduction in
cardiovascular "events" and greater control over coronary plaque. In our heart
disease reversal program, we start with 4000 mg of standard fish oil capsules
per day provide 1200 mg of omega-3 fatty acids, EPA + DHA.

2. Take vitamin D

Imagine over half the adults in the U.S. were toothless and had open skin
sores covering their bodies from vitamin C deficiency, or "scurvy. Well, that's
the situation, though less graphic, with vitamin D. Deficiency is rampant in the
U.S., particularly in northern climates where sun exposure is in short supply
for long periods. It's not uncommon even in southern climates, given indoor
workplaces and lifestyles. Vitamin D deficiency has been implicated in
osteoporosis, prostate and colon cancer, hypertension, multiple sclerosis, and
heart disease.

The higher your heart scan score, the more likely you are deficient in
vitamin D. Consider taking a minimum of vitamin D 1000 units per day. Even
better, have your doctor check a blood level (25-OH-vitamin D3) and the dose can
be adjusted accordingly. In our heart disease reversal program, most women
require 2000 units per day, most men 3000 units per day to achieve the desirable
blood level of >50 ng/ml.

3) Boost your HDL cholesterol to 60 mg/dl

Raise this simple value to 60 mg/dl or greater, and you will have
accomplished a huge improvement in a whole constellation of health effects.

This is because HDL is a gauge of many things: body weight, your body's
ability to respond to insulin, potential for hypertension, and the presence of
hidden causes of heart disease, especially the dreaded small LDL. The higher
your HDL, the less likely other undesirable phenomena are present. HDL is the
blood particle that is responsible for regression, or shrinkage, of plaque. The
more, the better.

Boost HDL by losing excess weight, reducing processed carbohydrates like
breads and breakfast cereals, exercise, 4-8 oz of red wine per day, and fish
oil. Raise it even further by considering niacin (vitamin B3), 500-1000 mg.
(Discuss niacin use with your doctor.)

4) Have a colorful lifestyle

Deeply colored foods are rich in flavonoids, naturally-occurring substances
that pack broad, powerful health effects and include blood pressure-reducing and
anti-inflammatory benefits.

Add more deeply colored foods to your day, especially blueberries,
pomegranates, plums, black grapes, spinach, green peppers, and red wine. Drink
green tea whenever possible. Use cocoa powder (unsweetened) in your protein
shakes or add a daily two-inch square of dark chocolate. Add capers, fresh basil
and other herbs to your salads and dinner dishes. All are rich in
naturally-occurring flavonoids, destined to become health champions of the 21st
century. Among their myriad benefits, flavonoids are natural artery relaxing
agents and add another healthy dimension to your heart scan control program.

5) Substitute raw nuts for unhealthy snacks

Dump the chips, pretzels, and crackers. Replace them with raw almonds,
walnuts, and pecans. (Not "party mix", "honey-roasted", mixed nuts, etc., all no
better than other unhealthy snacks.) Raw and whole (unshelled) are the keys,
bought bulk in most supermarkets or health food stores. This simple substitution
reduces LDL cholesterol 20 points, reduces blood sugar, reduces small LDL,
raises HDL, and boosts your energy level. Don't sweat the fats--the
monounsaturated fat in raw nuts are the source of much of the benefit.
One-quarter to one-half cup per day provides maximum benefit.

Stopping your heart scan score from increasing may be among the most powerful
ways to sharply reduce, perhaps even eliminate, risk for heart disease in your
lifetime. There's no single strategy that guarantees you stop your heart scan
score from increasing―it's all your efforts combined, followed consistently over
time.

Dr. William Davis is a cardiologist and expert in reversal of heart disease. He is author of “Track Your Plaque: The only heart disease prevention program that shows you how to detect, track, and control coronary plaque.” Dr. Davis also makes his book, “What Does My Heart Scan Show?” available for free at www.trackyourplaque.com. Article Source: http://EzineArticles.com/?expert=William_Davis,MD

Article Source:
http://EzineArticles.com/297354

Why the Low-Fat Diet is Stupid and Potentially Dangerous

Be it known there is controversy in this subject. Here is a scholarly, well written and well documented article that bears scrutiny. Verify what he says and if, as he states, the evidence is significant, act on it. Note that the last 1/3 of this article is composed of references so please do your Due-Diligence. Though it's a bit long I believe it is worth the read. Else I would not have posted it in its entirety.

Here is a quote from near the end of the article. "NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part."
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Why the Low-Fat Diet is Stupid and Potentially Dangerous

Anthony Colpo, February 23, 2006.
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.

Such stupidity makes my head spin…

First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.

My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that wouild have made lipid-phobes like Ornish and Pritikin proud.

For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.

My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!

Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.

Basically, I felt like crap!

It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.

When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"

While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!

Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!

Why the Low-Fat Diet is a Big Fat Fraud

One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
   1) Directly slashing your intake of important vitamins and fatty acids;
   2) Reducing the absorption of crucial fat-soluble vitamins;
   3) Decreasing the absorption of important minerals.

You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!

The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).

The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.

Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!

Absorb This!

Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).

When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).

The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)

Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.

Making a Bad Situation Worse

The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).

The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.

Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.

It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).

A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).

Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!

Low-Fat, Low Omega-3

Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.

Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)

So what has this all got to do with low-fat eating? Everything!

Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).

Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).

When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).

Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!

Speaking of scrambled brains…

Nature's Anti-Depressant: Fat!

Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!

In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.

The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.

The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!

Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.

Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)

Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.

The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape

For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).

Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.

The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)

Fatless Shrugged

It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser. Low-Fat Diets Lower Testosterone

Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.

Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.

So too can low-fat diets.

Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).

Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).

It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.

Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune FunctionDiet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.

Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).

In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).

It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).

For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.

The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).

There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!

Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.

After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!

Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).

After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).

If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.

It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.

So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?

I truly doubt it…

If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.

The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg'dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.

In Search of the Elusive 'Negative Fat Intake'!

The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!

The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!

But the Japanese Eat a Low-Fat Diet…Don't They?

Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)

If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).

OK, So What About the Mediterranean Diet?

A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!

Oops!

Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).

Conclusion

I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!

The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.



References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.

To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, and defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.

NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com

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