So, they told you that you have high cholesterol, put you on the statins, and now you’ve lost your memory, and your sex drive, and were told to ditch the butter and use canola oil instead?
Read on, as the myth of cholesterol is busted and the real cause of heart attacks is revealed.
(Adapted from ‘The Great Cholesterol Myth’ by Jonny Bowden and Stephen Sinatra, with thanks!)
What’s a fat?
Fat is the collective shorthand name given to any big collection of smaller units called fatty acids. There are three families of fatty acids: saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids. There’s actually a fourth class of fatty acids called trans fats too: those are the man-made Frankenstein fats, such as canola oil, which is extracted and refined using very high heat and petroleum solvents (such as hexane), then refined, degummed, bleached and deodorized using even more chemicals, since it stinks. Canola oil is found in the Oatly oat milk the vegetarians love so much under the name of ‘low erucic acid rapeseed (LEAR) oil’.
Saturated fats are primarily found in animal foods (meat, cheese, butter, eggs) and, less often, in certain plant foods, such as coconut, coconut oil, and palm oil. They tend to be solid at room temperature (think butter) and soften when warm.
Unsaturated fats, such as vegetable oils, damage easily and form carcinogenic compounds (free radicals) when heated. Hence lard is a better option for frying than vegetable oils are.
The popularised belief that the consumption of saturated fats causes atherosclerosis by raising cholesterol levels is erroneous when one begins to examine the facts closely, hence it is not just enough to recommend someone to increase their intake of monounsaturated fatty acids to prevent heart attacks and strokes. To sum it up, the biggest culprit is sugar, not fat, and by moving to a low-fat diet, wherein the fat has been replaced by highly processed carbohydrates (anything that comes in a package, e.g. cereals, pasta, minute rice etc.) with a high glycaemic index, which quickly and dramatically raises your blood sugar, one is more likely to develop insulin resistance, obesity and atherosclerosis leading to a heart attack.
Saturated fats have been wrongfully demonized in the 1960s based on an American physiologist Ancel Keys’ The Seven Countries Study, in which he hand-picked data from the available 22 countries to fit his preconceived hypothesis, that there is a direct connection between dietary fat, and heart disease. (Keys had access to food consumption data from 22 countries, but he chose to use data from only 7 of those, namely: Italy, Greece, the former Yugoslavia, the Netherlands, Finland, the United States, and Japan).
Other researchers analysing the data from all twenty-two countries found that the correlation between fat, cholesterol, and heart disease literally vanished. One of the researchers who questioned Keys was a British doctor named John Yudkin from the University of London. He actually found that the strongest association with coronary heart disease was sugar.
Every time we eat, insulin is produced. Excess insulin which is not used up by physical activity gets stored in the fat cells. High levels of insulin can narrow the artery walls. Insulin also damages kidneys, it makes the kidneys hold on to salt, which in turn makes them demand more water. Increased sodium retention results in increased water retention. More water means more blood volume, and more blood volume means higher blood pressure. 70% of people with hypertension have insulin resistance.
British physician Malcolm Kendrick, M.D., re-examined the same data available to Keys and quickly discovered that if you simply chose different countries, you could easily prove that the more saturated fat and cholesterol people consumed, the lower their risk of heart disease. Keys was a member of the nutrition advisory committee of the American Heart Association, so despite the flaws in his study, he managed to get his theories officially incorporated into the 1961 American Heart Association dietary guidelines, where they have influenced government policy on heart disease, fat consumption, and cholesterol for decades. Long story short, since that study low fat diets became government policy in the US and the food industry begun to churn out low-fat versions of every food imaginable, replacing missing fat with tons of sugar and processed carbs, both of which are far more dangerous to heart than fat ever was.
The demonisation of saturated fats is intrinsically tied to the demonisation of cholesterol, as the main culprit in the development of atherosclerosis. Every medical book in the world will further help to popularise this belief, since behind it are the Big Pharma and Big Food billion $ industry interests.
So, let’s talk about what cholesterol is and does then.
Cholesterol is an essential molecule without which there would be no life, so important that virtually every cell in the body is capable of synthesizing it. Among its other duties, cholesterol is a major structural molecule, a framework on which other critical substances are made. Were we able to somehow remove all its cholesterol, the body, would, in the words of Shakespeare, “melt, thaw and resolve itself into a dew.” And that’s not to mention that we wouldn’t have bile acids, vitamin D, or steroid hormones (including sex hormones), all of which are cholesterol-based.
Cholesterol is transported in the blood attached to carrier proteins, and these protein-cholesterol complexes are called lipoproteins. Their densities now describe these lipo-proteins: HDL (high-density lipoprotein), LDL (low-density lipoprotein), VLDL (very-low-density lipoprotein), and a number of others. Some of these lipoproteins are considered good (HDL) and others bad (LDL). The small, dense, type B LDL has been labelled as the true risk factor for heart disease.
Problem is, this small, dense type B LDL is worsened by the very diet those promoting the lipid hypothesis have hailed for decades as the best diet to prevent heart disease: the low-fat, high-carbohydrate diet. Turns out that fat, especially saturated fat, decreases the amount of these small, dense LDL particles while the widely recommended low-fat diet increases their number.
The opposite of the small dense LDL (subtype B) are large fluffy LDL particles (subtype A), which are not only not harmful but are actually healthful. But the LDL–lowering drugs lower those, too. A recent study showed that of almost 140,000 patients admitted to the hospital for heart disease, almost half of them had LDL levels under 100 mg/dL (100 mg/dL has been the therapeutic target for LDL for the past few years).
Saturated fat raises cholesterol, but it raises overall HDL cholesterol and the good part of LDL cholesterol (LDL-A) far more than it raises the bad part of LDL cholesterol (LDL-B). There is no evidence that supports a direct relationship between saturated fat and heart disease.
· Cholesterol is the parent molecule for sex hormones (estrogen, progesterone, and testosterone) as well as vitamin D and bile acids needed for digestion.
• The only time cholesterol is a problem is if it’s oxidized (damaged).
• Damaged or oxidized LDL cholesterol sticks to the lining of the arteries and begins the process of inflammation.
• The true cause of heart disease is inflammation.
• Inflammation is initiated by damage from free radicals (oxidative stress).
• The concept of “good” and “bad” cholesterol is outdated.
• There are several types of LDL (“bad”) cholesterol and several types of HDL (“good”) cholesterol.
• It is far more important to know whether you have a pattern A or pattern B LDL cholesterol profile than to know your total amount of LDLs.
· A cholesterol level of 160 mg/dL or less has been linked to depression, aggression, cerebral haemorrhages, and loss of sex drive.
The most important subtypes of LDL are subtype A and subtype B. When most of your LDL is of the “A” type, you’re said to have a pattern A cholesterol profile. When most of your LDL is of the “B” type, you’re said to have a pattern B cholesterol profile. Knowing you have a “high” LDL level is pretty much a useless piece of information unless you know how much of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least).
Fat raises LDL cholesterol, but it raises the big, fluffy, harmless particles (producing the desirable pattern A profile) and lowers the nasty little BB gun–pellet LDLs (type B) that actually do cause heart disease. Sugar, in contrast, has the opposite effect, increasing the number of really bad LDL molecules (producing the harmful pattern B profile) and decreasing the number of harmless ones. On top of that, high levels of sugar and insulin damage those nasty little LDL particles, making them far more likely to start the process of inflammation.
Sugar
Regular sugar (sucrose) is 50 percent glucose and 50 percent fructose.
Fructose and glucose are metabolized in the body in completely different ways. They are not identical. Glucose goes right into the bloodstream and then into the cells, but fructose goes right to the liver. Research has shown that fructose is seven times more likely to form the previously mentioned artery-damaging AGEs (advanced glycation end products). Fructose is metabolized by the body like fat, and it turns into fat (triglycerides) almost immediately. “When you consume fructose, you’re not consuming carbs,” says Robert Lustig, M.D., professor of paediatrics at the University of California, San Francisco. “You’re consuming fat.” Fructose is the major cause of fat accumulation in the liver, a condition known technically as hepatic steatosis but which most of us know as fatty liver. When you deposit fat in the liver, that’s when you become insulin resistant.
High-fructose corn syrup (HFCS) was first invented in Japan in the 1960s and made it into the American food supply around the mid-1970s. It had two advantages over regular sugar, from the point of view of food manufacturers. Number one, it was sweeter, so theoretically you could use less of it. Number two, it was much cheaper than sugar. Low-fat products could be made “palatable” by the addition of HFCS, and before long, manufacturers were adding the stuff to everything. HFCS hides in our food under following names:
Maize syrup, glucose syrup, fruit fructose, crystalline fructose, glucose-fructose, corn sugar.
Unsaturated fats
Unsaturated fats are divided into mono- and polyunsaturated fats. Monounsaturated fat is the fat that’s predominant in olive oil (as well as in nuts and nut oils, such as macadamia nut oil).
Both inflammatory and anti-inflammatory hormones, known as eicosanoids, are made in the body from polyunsaturated fats. Omega-6s are the precursors to the inflammatory compounds in our body — they’re the building blocks the body uses to make these inflammatory hormones (specifically series 2 prostaglandins). But the ratio of omega-6s to omega-3s And omega-3s have the opposite function: The body uses omega-3s as building blocks for the anti-inflammatory compounds (known as series 1 prostaglandins and series 3 prostaglandins). in Western diets is anywhere from an astonishing 15:1 to an even more astonishing 20:1 in favour of omega-6s. Research has established that the ideal ratio of omega-6s to omega-3s in the human diet is somewhere between 1:1 and 4:1. This seems to be the best balance to keep inflammation in check and everything running smoothly. It’s the ratio found in the diets of both hunter-gatherers and healthy indigenous societies where heart disease is rare.
There are actually three omega-3 fatty acids — ALA (alpha-linolenic acid), EPA (eicosapentaenoic acid), and DHA (docosahexaenoic acid). ALA (found in leafy green vegetables, flaxseeds, walnuts and chia seeds) is called ‘essential’, since it can not be made by the human body.
Omega-6s and omega-3s compete for the same enzymes, and when omega-6 intake is very high, it wins the competition by default. A high intake of omega-6 reduces the conversion of ALA into EPA and DHA, which might be another reason why high omega-6 diets contribute to heart disease. The primary omega-6 fatty acid — linoleic acid — has been shown to increase the oxidation of LDL cholesterol, thus increasing the severity of coronary atherosclerosis.
Statins
Once the Big Pharma has managed to convince you that your cholesterol level is high and scare you into thinking of imminent death due to a heart attack or stroke, you’ll be prescribed statins. There are 5 types of statin available on prescription in the UK:
- atorvastatin (Lipitor)
- fluvastatin (Lescol)
- pravastatin (Lipostat)
- rosuvastatin (Crestor)
- simvastatin (Zocor)
Cholesterol is synthesized in the liver through a pathway called the mevalonate pathway, also known as the HMG-CoA reductase pathway. The HMG-CoA reductase enzyme is the one directly responsible for initiating the manufacture of cholesterol, and it is this enzyme with which the statin drugs interfere. (Statin drugs are technically known as HMG-CoA reductase inhibitors.)
The mevalonate pathway produces cholesterol, but it is also responsible for the production of coenzyme Q10, one of the most vital nutrients for the heart. Cutting off the mevalonate pathway at the root also blocks or lowers the production of nuclear factor kappa B (NF-kB) and disrupts the activities of pathways that regulate the production of tau proteins, dolichols, and selenoprotein.
The brain absolutely depends on cholesterol for optimal functioning. Although the brain makes up only about 2 percent of the total weight of the body, it contains 25 percent of the body’s cholesterol. Cholesterol is a vital part of cell membranes in the brain, and it plays a critical role in the transmission of neurotransmitters. Lipitor is known to have caused transient global amnesia (TGA)- loss of short-term memory and an inability to form new memories. There is a famous case of an astronaut, Duane Graveline, who was put on Pfizer’s Lipitor and experienced 2 episodes of TGA, the first one lasting for 6 hours, the 2nd for 12 hours, even though the dose had been reduced by a half. Graveline became a critic of the use of statins once he learned that there were hundreds of other people who had experienced TGA following administration of statins. He also discovered that other side effects included elevated liver enzymes, muscle wasting, sexual dysfunction, and fatigue.
While on statins, the production of CoQ10 is hampered, resulting on a reduced serum levels of this vital coenzyme that helps to convert food into energy and is a powerful antioxidant. Statins also dial down the production of NF-kB (nuclear factor kappa B)- a regulator of innate immunity. Also, research has shown that LDL cholesterol itself is able to inactivate more than 90% of the worst and most toxic bacterial products. In short, statins can make you lose your memory, impair your cognitive functioning, lower your serotonin levels and make you depressed, as well as lower your immune response to evading pathogens. On top of that, it will mess up your love life as well.
Cholesterol is a precursor to sex hormones, lowering it with statins will also lower your level of testosterone, oestrogen and progesterone. A quick search of research papers on the subject will try to downplay the effect, and blame some statins, while saying that others have no effect, yet you’re welcome to make up your own mind and try via empirical evidence if you fancy being a test bunny with erectile dysfunction or you can read a book by a French doctor called Michel de Lorgeril, called Cholesterol and statins: Sham science and bad medicine.
I could go on and on about statins and heart health, but most likely the reader has run out of patience by now. Health can not be bottled or injected. Health is in our heads, lifestyles, wholesome environments and in healthy family patterns.
