How can you lower cholesterol without resorting to medications? High cholesterol is considered a treatable risk factor for cardiovascular disease such as heart attacks and strokes. There are many nuances to cholesterol which I do not want to get into, but traditionally, the main division has been between Low Density Lipoprotein (LDL) or ‘bad’ cholesterol, and High Density Lipoprotein (HDL) or ‘good’ cholesterol. Many people do not look so closely at total cholesterol anymore, because there is both good and bad factions and therefore, the total cholesterol gives us little useful information.
We also measure triglycerides, a type of fat found in the blood. Fat is stored in fat cells as triglycerides, but also floats around freely in the body. For example, during fasting, triglycerides get broken down into free fatty acids and glycerol. Those free fatty acids are used for energy by most of the body. So triglycerides are a form of stored energy. Cholesterol is not. This substance is used in cellular repair (in cell walls) and also used for to make certain hormones.
One might (mistakenly) think that decreasing dietary cholesterol may reduce blood cholesterol levels. However, 80% of the cholesterol in our blood is generated by the liver, so reducing dietary cholesterol is quite unsuccessful. Studies going back to Ancel Key’s original Seven Country Studies show that how much cholesterol we eat has very little to do with how much cholesterol is in the blood. Whatever else he got wrong, he got this right – eating cholesterol does not raise blood cholesterol.
The next thought was that lowering dietary fat, especially saturated fats may help lower cholesterol. While untrue, there are still many who believe it. In the 1960’s the Framingham Diet Study was set up to specifically look for a connection between dietary fat and cholesterol. Why haven’t you heard of it, before? Well, the findings of this study showed no correlation between dietary fat and cholesterol whatsoever. Because these results clashed with the prevailing ‘wisdom’ of the time, they were suppressed and never published in a journal. Results were tabulated and put away in a dusty corner.
The Tecumseh study divided their subjects into 3 levels of blood cholesterol – low, medium and high. Then, they looked at how much fat and cholesterol each group ate. It turns out that each group pretty much ate the same amount of fat, animal fats, saturated fats and cholesterol. So, what they demonstrated was that dietary intake of fat does not have very much to do with cholesterol at all.
Low fat and extremely low fat diets can lower the LDL (bad cholesterol) slightly, but they also tend to lower the HDL (good cholesterol) so it is arguable whether things improve or not. Actually, we’ve known that for quite some time. For example, here’s a study in 1995, where 50 subjects were fed either a 22% or a 39% fat diet. Baseline cholesterol was 173 mg/dl. After 50 days of a low fat diet, it plummeted to … 173 mg/dl. Oh. High fat diets don’t lower cholesterol either. After 50 days of high fat diets, cholesterol increased marginally to 177 mg/dl.
Millions of people try a low fat or low cholesterol diet without realizing that these have already been proven to fail. I hear this all the time. Whenever somebody is told their cholesterol is high, they say “I don’t understand. I’ve cut out fatty foods”. Well, reducing dietary fat will not change your cholesterol. So, what to do? Statins, I guess?
“A little starvation can really do more for the average sick man than can the best medicines and the best doctors” – Mark Twain
Studies show that fasting is a simple dietary strategy that can significantly lower cholesterol levels.
Now, there are many controversies about lipids that I do not wish to get quagmired in. I’m only going to discuss the conventional view of it. That is, many of the classic studies, such as the Framingham study, have pointed out that there is a correlation between high levels of ‘bad’ cholesterol and cardiovascular disease. The higher the LDL, the more bad things happen.
‘Good’ cholesterol (HDL) shows an inverse relationship. High levels are protective. So the lower the HDL, the higher the risk of CV disease. This association is actually much more powerful than that for LDL, so let’s start here. However, it is clear that HDL is not causally related to CV events. They are only a marker for disease.
Several years ago, Pfizer poured billions of dollars into researching a drug called torcetrapib (a CETP inhibitor). This drug had the ability to significantly increase HDL levels. If low HDL caused heart attacks, then this drug could save lives. Pfizer was so sure of itself, it spent billions of dollars trying to prove the drug effective.
The studies were done. And the results were breathtaking. Breathtakingly bad, that is. The drug increased death rate by 25%. Yes, it was killing people left and right like Ted Bundy. Several more drugs of the same class were tested and had the same killing effect. Just one more illustration of the Correlation is not Causation truth.
What happens to HDL during fasting? You can see from the graph that 70 days of alternate daily fasting had a minimal impact upon HDL levels. There was some decrease in HDL but it was minimal.
The story of triglycerides (TG) is similar. While TGs may be correlated weakly to heart disease, they do not cause it. There were several drugs that reduce TG to a much greater extent than the cholesterol medications, the statins. Niacin was one such example. This drug would increase HDL and lower TG without very much effect on the LDL.
The AIM HIGH study tested whether this would have any benefit. The results were stunning. Stunningly bad, that is. While they did not kill people, they did not help them either. And there were lots lot side effects. So, TG, like HDL is only a marker not a causer of disease.
What happens to TG during fasting? There’s a huge 30% decrease in TG levels (good) during alternate daily fasting. In fact, triglycerides is quite sensitive to diet. But it is not reducing dietary fat or cholesterol that helps. Instead, reducing carbohydrates seems to be the main factor that reduces TG levels.
The LDL story is much more contentious. Certainly, there is a correlation between high LDL levels and CV disease. However, the more important question is whether this is a causal relationship. The statin drugs lower LDL cholesterol quite powerfully, and also reduces CV disease in high risk patients. But these drugs have other effects, often called the pleiotropic (affecting multiple systems) effects. For example, statins also reduce inflammation, as shown by the reduction in hsCRP, an inflammatory marker. So, is it the cholesterol lowering or the pleiotropic effects that are responsible for the benefits?
This is a good question to which I do not have an answer yet. The way to tell would be to lower LDL using another drug and see if there are similar CV benefits. The drug ezetimibe in the IMPROVE-IT trial also had some CV benefits, but they were extremely weak. To be fair, the LDL lowering was also quite modest.
A new class of drugs called the PCSK9 Inhibitors has the power to reduce LDL a lot. The question, though is whether there will be any CV benefit. Early indications are quite positive. But it is far from definitive. So the possibility exists that LDL may play a causal role here. This is, after all, why doctors worry so much about keeping LDL down.
What happens to LDL levels during fasting? Well, they go down. A lot. Over the 70 days of alternate daily fasting, there was about a 25% reduction in LDL (very good). To be sure, drugs can reduce them about 50% or more, but this simple dietary measure has almost half the power of one of the most powerful classes of medications in use today.
In combination with the reduction in body weight, preserved fat-free mass, and decreased waist circumference, it is clear that fasting produces some very powerful improvements in these cardiac risk factors. Don’t forget to add in the reduced LDL, reduced Triglycerides and preserved HDL.
But why does fasting work where regular diets fail? Simply put, during fasting, the body switches from burning sugar to burning fat for energy. Free fatty acids (FFA) are oxidized for energy and FFA synthesis is reduced (body is burning fat and not making it). The decrease in triacylglycerol synthesis results in a decrease in VLDL (Very Low Density Lipoprotein) secretion from the liver which results in lowered LDL.
The way to low ever LDL is to make your body burn it off. The mistake of the low fat diet is this – feeding your body sugar instead of fat does not make the body burn fat – it only makes it burn sugar. The mistake of the Low Carb High Fat diet is this – giving your body lots of fat makes it burn fat, but it will burn what’s coming into the system (dietary fat). It won’t pull the fat out of the body.
Here’s the bottom line for those big-picture, spare-me-the-details kind of folks. Fasting has the following effects:
- Reduces weight
- Maintains lean mass
- Decreases waist size
- Minimal change in HDL
- Dramatic reductions in TG
- Dramatic reductions in LDL
That’s all good. Whether this will all translate into improved cardiac outcomes, I don’t have the answer for you. My guess is Yes.
However, fasting always boils down to this. There’s all these benefits. There’s very little risk. What do you have to lose (other than a few pounds)?
For people worried about heart attacks and strokes, the question is not “Why are you fasting?”, but “Why are you NOT fasting?”
Start here with Fasting Part 1
Continue to Fasting part 17 – Fasting and Hunger
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