Saturated fat is not the major issue - Malhotra

Saturated fat is not the major issue

BMJ 2013; 347 doi: http://dx.doi.org/10.1136/bmj.f6340 (Published 22 October 2013)

Cite this as: BMJ 2013;347:f6340

Let’s bust the myth of its role in heart disease

 

Scientists universally accept that trans fats—found in many fast foods, bakery products, and margarines—increase the risk of cardiovascular disease through inflammatory processes.1 But “saturated fat” is another story. The mantra that saturated fat must be removed to reduce the risk of cardiovascular disease has dominated dietary advice and guidelines for almost four decades.

Yet scientific evidence shows that this advice has, paradoxically, increased our cardiovascular risks. Furthermore, the government’s obsession with levels of total cholesterol, which has led to the overmedication of millions of people with statins, has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia.

Saturated fat has been demonised ever since Ancel Keys’s landmark “seven countries” study in 1970.2 This concluded that a correlation existed between the incidence of coronary heart disease and total cholesterol concentrations, which then correlated with the proportion of energy provided by saturated fat. But correlation is not causation. Nevertheless, we were advised to cut fat intake to 30% of total energy and saturated fat to 10%.”3 The aspect of dietary saturated fat that is believed to have the greatest influence on cardiovascular risk is elevated concentrations of low density lipoprotein (LDL) cholesterol. Yet the reduction in LDL cholesterol from reducing saturated fat intake seems to be specific to large, buoyant (type A) LDL particles, when in fact it is the small, dense (type B) particles (responsive to carbohydrate intake) that are implicated in cardiovascular disease.4

Indeed, recent prospective cohort studies have not supported any significant association between saturated fat intake and cardiovascular risk.5 Instead, saturated fat has been found to be protective. The source of the saturated fat may be important. Dairy foods are exemplary providers of vitamins A and D. As well as a link between vitamin D deficiency and a significantly increased risk of cardiovascular mortality, calcium and phosphorus found commonly in dairy foods may have antihypertensive effects that may contribute to inverse associations with cardiovascular risk.6 7 8

One study showed that higher concentrations of plasma trans-palmitoleic acid, a fatty acid mainly found in dairy foods, was associated with higher concentrations of high density lipoprotein, lower concentrations of triglycerides and C reactive protein, reduced insulin resistance, and a lower incidence of diabetes in adults.9 Red meat is another major source of saturated fat. Consumption of processed meats, but not red meat, has been associated with coronary heart disease and diabetes mellitus, which may be explained by nitrates and sodium as preservatives.10

The notoriety of fat is based on its higher energy content per gram in comparison with protein and carbohydrate. However, work by the biochemist Richard Feinman and nuclear physicist Eugene Fine on thermodynamics and the metabolic advantage of different diet compositions showed that the body did not metabolise different macronutrients in the same way.11 Kekwick and Pawan carried out one of the earliest obesity experiments, published in the Lancet in 1956.12 They compared groups consuming diets of 90% fat, 90% protein, and 90% carbohydrate and showed that the greatest weight loss was in the fat consuming group. The authors concluded that the “composition of the diet appeared to outweigh in importance the intake of calories.”

The “calorie is not a calorie” theory has been further substantiated by a recent JAMA study showing that a “low fat” diet resulted in the greatest decrease in energy expenditure, an unhealthy lipid pattern, and increased insulin resistance in comparison with a low carbohydrate and low glycaemic index diet.13 In the past 30 years in the United States the proportion of energy from consumed fat has fallen from 40% to 30% (although absolute fat consumption has remained the same), yet obesity has rocketed.

One reason: when you take the fat out, the food tastes worse. The food industry compensated by replacing saturated fat with added sugar. The scientific evidence is mounting that sugar is a possible independent risk factor for the metabolic syndrome (the cluster of hypertension, dysglycaemia, raised triglycerides, low HDL cholesterol, and increased waist circumference).

In previous generations cardiovascular disease existed largely in isolation. Now two thirds of people admitted to hospital with a diagnosis of acute myocardial infarction really have metabolic syndrome—but 75% of these patients have completely normal total cholesterol concentrations.14 Maybe this is because total cholesterol isn’t really the problem?

The Framingham heart study sanctified total cholesterol as a risk factor for coronary artery disease, making statins the second most prescribed drug in the US and driving a multibillion dollar global industry. In the United Kingdom eight million people take statins regularly, up from five million 10 years ago. With 60 million statin prescriptions a year, it is difficult to demonstrate any additional effect of statins on reduced cardiovascular mortality over the effects of the decline in smoking prevalence and primary angioplasty.15

Despite the common belief that high cholesterol is a significant risk factor for coronary artery disease, several independent population studies in healthy adults have shown that low total cholesterol is associated with cardiovascular and non-cardiac mortality, indicating that high total cholesterol is not a risk factor in a healthy population.16 17 18

A recent “real world” study of 150 000 patients who were taking statins showed “unacceptable” side effects—including myalgia, gastrointestinal upset, sleep and memory disturbance, and erectile dysfunction—in 20% of participants, resulting in discontinuation of the drug.19 This is massively at odds with the major statin trials that report significant side effects of myopathy or muscle pain in only one in 10 000.

A meta-analysis of predominantly industry sponsored data reported that in a low risk group of people aged 60-70 years taking statins the number needed to treat (NNT) to prevent one cardiovascular event in one year was 345.20 The strongest evidence base for statins is in secondary prevention, where all patients after a myocardial infarction are prescribed maximum dose treatment irrespective of total cholesterol, because of statins’ anti-inflammatory or pleiotropic (coronary plaque stabilising) effects. In this group the NNT is 83 for mortality over five years. This doesn’t mean that each patient benefits a little but rather that 82 will receive no prognostic benefit.21 The fact that no other cholesterol lowering drug has shown a benefit in terms of mortality supports the hypothesis that the benefits of statins are independent of their effects on cholesterol.

Adopting a Mediterranean diet after a heart attack is almost three times as powerful in reducing mortality as taking a statin. The recently published PREDIMED randomised controlled trial was stopped early after it showed that in high risk people the Mediterranean diet achieved a 30% improvement over a “low fat” diet in terms of cardiovascular events.22

Pharmacotherapy can assuage the symptoms but can’t alter the pathophysiology. Doctors need to embrace prevention as well as treatment. The greatest improvements in morbidity and mortality have been due not to personal responsibility but rather to public health. It is time to bust the myth of the role of saturated fat in heart disease and wind back the harms of dietary advice that has contributed to obesity.

Notes

Cite this as: BMJ 2013;347:f6340

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Read the complete article here.

Read also - Top heart doctor: Unprocessed fatty foods may actually be good for you

Watch this excellent video on saturated fat and heart disease. http://www.abc.net.au/catalyst/stories/3876219.htm
Here are some quotes from the video:

Dr Johnny Bowden
"Sugar is far more damaging to the heart than fat ever was, and we're beginning to see this now. So, this focus on cholesterol has been incredibly destructive because we haven't looked at these real promoters of heart disease - inflammation, oxidative damage, sugar in the diet, and number one with a bullet - stress."

Dr Johnny Bowden
"Margarine is the perfect example of the stupidest nutritional swap-out in history. We had this trans fat-laden crappy manufactured product that we were eating because we were so phobic about saturated fat and cholesterol."
Dr Stephen Sinatra
"To switch to polyunsaturated fats with the vegetable oils, that's horrific advice. The polyunsaturated fats, the vegetable oils, these omega-6 oils, are inflammatory because they're very prone to oxidation."

Dr Stephen Sinatra
"It took decades to really entrench this myth. It's probably going to take a few more decades to get us out of this myth. But to vilify saturated fats I think is one of the worst things the medical profession has done."
Dr Ernest Curtis
"I'd love to see the medical establishment saying, 'Whoops, we were wrong'. That's not going to happen. Frankly, that generation is going to have to die off, and perhaps the generation coming up can do better."

Triglycerides: Mother of Meddlesome Particles - Davis

Triglycerides: Mother of Meddlesome Particles



Triglycerides are a crucial risk factor for coronary plaque growth, even at levels previously thought to be normal. Dr. Davis discusses why and how this oft-neglected factor can be harnessed to strengthen your program.

While the world obsesses over cholesterol, a potent stimulator of plaque growth is frequently ignored—triglycerides. A subject of controversy in past, the data are now clear: triglycerides spawn unwanted lipoprotein particles that trigger plaque growth. Track Your Plaque members are advised that control of triglycerides is essential to everyone’s plaque control program.

Triglyceride control is crucial if you are interested in gaining control over coronary plaque. Triglycerides should be brought under control at the start of your program. If you are experiencing plaque growth (increasing heart scan scores), seriously reining in triglycerides should be considered.

How important are triglycerides?

 

For years, the relationship between coronary heart disease and triglycerides remained muddled by the confounding effects of low HDL. In other words, increased triglycerides tend to occur alongside low HDL. This caused many to dismiss the importance of triglycerides. To make matters even murkier, high triglycerides in some situations generated high risk for heart disease, while in others it appeared unrelated to heart disease, even when markedly elevated (in the thousands!).

Thanks to the evolving science of lipoproteins, the issues are crystallizing. One important fact has emerged: triglycerides are a critical risk factor for coronary plaque growth, even at levels previously thought to be normal. Yes, high triglycerides frequently occur with low HDL, but they also behave independently. High triglycerides are a common cause of heart disease, even in people with low or normal cholesterol values. It is crucial that you (and your doctor) pay close attention to triglycerides if you are to succeed in controlling your plaque. We urge Members to make triglyceride control a priority in their program.

 

Where do triglycerides come from?

 

The liver produces a particle called “very low-density lipoprotein”, or VLDL, packed full of triglycerides. The higher your triglycerides, the more VLDL you will have. Sometimes triglycerides are increased due to genetic factors. More commonly, triglycerides are high due to excess weight, indulging in processed carbohydrates, and resistance to insulin (metabolic syndrome).

VLDL is like that bad kid on the block you want your kids to avoid. VLDL particles in the blood come into contact with LDL and HDL particles and they’re never quite the same. When a LDL or HDL particle meet VLDL, the triglycerides of VLDL are passed on. The result: LDL and HDL become bloated with triglycerides. Triglyceride-loaded LDL and HDL are a ready target for a set of enzymes in the blood and liver that reconfigure these particles into smaller versions, small LDL and small HDL. Recall that both small LDL and HDL are highly undesirable particles that stimulate plaque growth.

Although “official” (ATP-III) guidelines suggest that triglycerides over 150 mg are undesirable, we regard any value over 60 mg as high. An ideal level for an intensive Track Your Plaque approach is <45 font="font" mg.="mg.">

 

How will I know if I have this pattern?

 

On a conventional cholesterol panel, increased triglycerides and low HDL are tip-offs that excess VLDL are available to contribute to coronary plaque growth. At what triglyceride level does this cascade begin to take effect and create this collection of particles? Levels of 45 mg/dl or greater. In the Track Your Plaque program, we aim for zero plaque growth or reduction, and so we target triglyceride levels of 60 mg/dl or less.

You’ll notice that low HDL and increased triglycerides are also patterns that characterize the metabolic syndrome. In our experience, over 50% of adults show at least some of the characteristics of the metabolic syndrome. In our society of inactive, sedentary lifestyles and packaged, processed foods, metabolic syndrome is rampant. That means increased triglycerides from VLDL are also running rampant. The result: a 3 to 7-fold increase in risk for heart attack. Eliminating the metabolic syndrome is another battle we need to fight to conquer plaque. (See Shutting Off the Metabolic Syndrome.)

 

How can triglycerides be reduced?

 

Our triglyceride target of 60 mg or less dramatically reduces triglyceride availability. Without triglycerides, LDL and HDL can’t be processed into undesirable small particles. Among the strategies we use to reach our triglyceride target of 60 mg or less:

• Fish oil—The omega-3 fatty acids in fish oil are our number one choice for substantially reducing triglycerides. Fish oil, 4000 mg per day, is a good starting dose (providing 1200 mg EPA+DHA); higher doses should be discussed with your physician, though we commonly use 6000–10,000 mg per day without ill-effect. Flaxseed oil, while beneficial for health, does not correct lipoprotein patterns. Consider a concentrated fish oil preparation (e.g., Omacor™, a prescription preparation, or “pharmaceutical grade” preparations from the health food store) if you and your doctor decide a high dose is necessary.
• Weight loss to ideal weight or ideal BMI (25). If achieved with a reduction in processed carbohydrates, the effect will be especially significant. Exercise will compound the benefits of weight loss, triggering an even larger drop in triglycerides.
• Reduction in processed carbohydrates—especially snacks; wheat-flour containing foods like breads, pasta, pretzels, chips, bagels, and breakfast cereals; white and brown rice; white potatoes. The reduction of high- and moderate-glycemic index foods is the factor that reduces triglycerides. High triglycerides are therefore a pattern that develops when someone follows a low-fat diet. For this reason, we do not advocate low-fat diets like the Ornish program. Reducing your exposure to wheat-containing snacks and processed foods is an especially useful and easy-to-remember strategy that dramatically reduces triglycerides.
• Elimination of high-fructose corn syrup—This ubiquitous sweetener is found in everything from beer to bread. High-fructose corn syrup causes triglycerides to skyrocket 30% or more.
• Niacin in doses of 500–1500 mg is an effective method of reducing triglycerides. Niacin also raises HDL, increases large HDL, reduces the number of small LDL particles, reduces VLDL, and modestly reduces total LDL. The preferred forms are over-the-counter Slo-Niacin® and prescription Niaspan®, the safest and best tolerated. Immediate-release niacin (just called niacin or nicotinic acid on the label) can also be taken safely, provided it is taken no more frequently than twice per day. Total daily doses of >500 mg should only be taken under medical supervision. Avoid nicotinamide and “no-flush niacin” (inositol hexaniacinate), neither of which have any effect whatsoever.
• Green tea—The catechins (flavonoids) in green tea can reduce triglycerides by 20%. Approximately 600–700 mg of green tea catechins are required for this effect, the equivalent of 6–12 servings of brewed tea. (Tea varies widely in catechin content.) Nutritional supplements are also available that provide green tea catechins at this dose. The weight loss accelerating effect of green tea may add to its triglyceride-reducing power.
• The thiazolidinediones (Actos®, or pioglitazone, and Avandia®, or rosiglitazone), usually prescribed for pre-diabetes or diabetes, can reduce triglycerides by 30%; Actos may be more effective than Avandia in this regard. However, these agents are accompanied by weight gain.
• The fibrate class of prescription drugs (fenofibrate, or Tricor®, and gemfibrozil®, or Lopid) reduce triglycerides 30–40%, i.e., almost as effectively as fish oil.

The evil influences of VLDL and triglycerides are therefore erased from your risk profile by achieving the Track Your Plaque target of triglycerides 60 mg/dl or less. One or more of these strategies are usually required to bring your triglycerides to target. 

        William Davis, MD


Selected references:

Packard CJ. Understanding coronary heart disease as a consequence of defective regulation of apolipoprotein B metabolism. Curr Opin Lipidol 1999; 10:237–244.

Otvos J. Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy Clin Cardiol 1999;22 (Suppl II) II-21–II-27.

Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol 1998;81(4A):18B–25B.

Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem 1995;41(1):153–158.