Canibais e Reis

Foto: T-shirt I Love Saturated Fat.

Este artigo é quase um duplicado de um recente, mas nunca é demais destacar esta série de artigos do nosso amigo Stephan que, de facto, numa estonteante e cristalina série sobre a Hipótese Lipídica, como que faz o funeral desta hipótese, tornando muito claro que o que interessa aqui não é a quantidade de lípidos/colesterol, mas sim o potencial oxidativo/ aterogénico a eles associado. Estes artigos obviamente inocentam de vez as gorduras saturadas, injustamente condenadas por décadas de investigação selectiva quando, na realidade, os culpados por doença cardiovascular sempre foram os amidos/açúcar e a frutose! Ou você julgava que era absolutamente por acaso que os diabéticos possuem cerca do triplo de risco cardiovascular?!

The Diet-Heart Hypothesis: Oxidized LDL, Part II
The Diet-Heart Hypothesis: Oxidized LDL, Part I
The Diet-Heart Hypothesis: Subdividing Lipoproteins
MRFIT Mortality
The Diet-Heart Hypothesis: A Little Perspective
The Diet-Heart Hypothesis: Stuck at the Starting Gate

No que respeita a estes artigos, aqui vai um "best-of" das melhores passagens:

"The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack. I’m not going to spend a lot of time on the theory in relation to dietary cholesterol because there really isn’t much evidence to debunk in humans. As far as I can tell, most diet-health researchers don’t take this theory seriously anymore because the evidence has simply failed to materialize. Dr. Walter Willett doesn’t believe it, and even Dr. Ancel Keys didn’t believe it."

"The inevitable conclusion is that if saturated fat influences total cholesterol or LDL concentration at all, the effect is modest and is dwarfed by other factors."

"Now that we’ve seen that the first half of the diet-heart hypothesis– that dietary saturated fat and cholesterol elevate serum cholesterol and low-density lipoprotein (LDL)– is false, let’s take a look at the second half. This is the idea that elevated serum cholesterol causes cardiovascular disease, also called the "lipid hypothesis".

"If you’re 80 or older, and you have low cholesterol, it’s time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there’s no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group."

"Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn’t a great predictor of heart attacks in the general population. "

"Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is high LDL (particularly LDL particle number), low HDL and high triglycerides."

"Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality."

"It’s important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor’s office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids."

"Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear, but is associated with a lower risk of heart attacks. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It’s important to remember that the primary sources of carbohydrate in the modern Western diet are wheat and sugar. Are the blood lipid patterns that associate with heart attack risk in Western countries partially acting as markers of wheat and sugar intake?"

"his is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins."

"oxLDL is formed when the lipids in LDL particles react with oxygen and break down. This happens specifically to the unsaturated fats in LDL, because saturated fats, by their chemical nature, are very resistant to oxidative damage. Polyunsaturated fats are much more susceptible to oxidative damage than saturated or monounsaturated fats. Linoleic acid (the omega-6 fatty acid found abundantly in industrial seed oils) is the main polyunsaturated fatty acid in LDL. "

"LDL is packaged with antioxidants in the liver, primarily vitamin E and coenzyme Q10 (CoQ10), to prevent its oxidation*. However, the more time it spends in the blood, the more likely it is to exhaust its antioxidant store and become oxidized. Also, the smaller the LDL particle, the more likely it is to become trapped in the vessel wall and become oxidized there."

"oxLDL has turned out to be a very sensitive marker of cardiac risk, surpassing traditional markers like LDL, HDL, and triglycerides in most studies to date. Since the discovery of sensitive assays that detect oxidized LDL drawn directly from patient blood, a number of studies have been published supporting its ability to detect atherosclerosis (plaque buildup in the arteries), heart attack risk and even the metabolic syndrome."

"It’s time to cross the threshold from markers of heart attack risk to causes of atherosclerosis. Regular, non-oxidized LDL has few properties that would make it a suspect in atherosclerosis. It’s just a little particle carrying cholesterol and fats from the liver to other organs. As soon as it oxidizes, however, it becomes pro-inflammatory, immunogenic, damaging to the vessel wall, and most importantly, capable of transforming immune cells called macrophages into foam cells, a major constituent of arterial plaque."

"Multiple lines of evidence suggest that oxidized LDL plays a dominant role in atherosclerosis. Not only is it associated with cardiovascular risk, there’s also a large body of evidence suggesting it actually directly contributes to it. In the next post, I’ll describe how you can modify your level of oxidized LDL using diet."

"People often think of colorful fruits and vegetables when they think of antioxidants, but vitamin E and CoQ10 are found in both plant and animal foods. Fruits and vegetables are generally not good sources of these fat-soluble antioxidants. Good sources include organ meats, nuts, pastured butter, avocados and red palm oil. The body also manufactures CoQ10 itself."

"The diet-heart hypothesis, the idea that dietary saturated fat and cholesterol raise blood cholesterol and thus increase heart attack risk, is a half-century embarrassment to the international scientific community. It requires willful ignorance of the fact that saturated fat does not increase total cholesterol or LDL in humans, in the long term. It requires a simplistic view of blood lipids that ignores the potentially harmful effects of replacing animal fats with carbohydrate or industrial seed oils. Worst of all, it requires selective citation of the literature on diet modification trials."

"I have to conclude that if dietary saturated fat and cholesterol play any role whatsoever in cardiovascular disease, it’s a minor one that’s trumped by other factors. Industrial seed oils and sugar are likely to play an important role in cardiovascular disease."

Fonte: Whole Health Source.