Saturday, July 14, 2012

5 Reasons Not to Worry About Your Cholesterol Numbers- Kresser

person relaxing on the beachI do a lot of public speaking. As you might suspect, regardless of the specific topic I’m presenting the dietary recommendations I make are always essentially the same: high-fat, nutrient-dense and low in toxins. Since omega-6 vegetable oils are toxins, when I say high fat I’m talking about saturated and monounsaturated fat. You know this.
But a lot of people I speak to don’t. They fully steeped in 50 years of mainstream propaganda perpetuating the idea that saturated fats cause heart disease – primarily by raising blood cholesterol. So, inevitably, when I stand up in front of a group of people and tell them all to eat lots of saturated fat, I get a question that goes something like this:
But won’t that raise my cholesterol? And won’t high cholesterol give me a heart attack?
I haven’t yet perfected an answer that can dismantle a half century of cultural brainwashing about fat and cholesterol in less than 3 minutes. But I’m working on it.

In the meantime, I usually explain some variation of the following:

Point #1: Eating saturated fat doesn’t raise cholesterol levels in the blood

There’s no convincing evidence that eating saturated fat raises blood cholesterol. Stephan Guyenet spanked that old yarn to the curb in this recent blog post. In short, of all of the studies examining the relationship between saturated fat intake and serum cholesterol, only one found a clear relationship between the two and even that association was weak. The rest found no association at all.

Point #2: Eating cholesterol doesn’t (usually) raise cholesterol levels in the blood

Nor is there evidence that eating cholesterol in the diet raises cholesterol levels in your blood. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

An increase of HDL is a good thing. And as it turns out, so is a boost of the type of LDL that eating saturated fat and cholesterol increases. We now know there are two different types of LDL: small, dense LDL, and large, buoyant LDL. Small, dense LDL is a significant risk factor for heart disease because it’s more likely to oxidize and cause inflammation. Large, buoyant LDL is not a risk factor for heart disease. And guess what? Eating eggs not only increases the benign large, buoyant LDL, but it also decreases the harmful small, dense LDL by 20%. I’ve written more about this here and here, and you can also watch some videos on this topic here.

Point #3: Even if eating saturated fat and cholesterol did raise cholesterol levels in your blood, it wouldn’t matter because “high cholesterol” isn’t a strong risk factor for heart disease.

This is the one that really spins people out. Even if they follow me on the first two points, their eyes tend to glaze over when I mention this one. As Mark Twain used to say:
The history of our race, and each individual’s experience, are sown thick with evidence that a truth is not hard to kill and that a lie told well is immortal.
Nowhere is that more true than with the lie that high cholesterol causes heart disease. It’s so deeply ingrained in our collective consciousness that it’s become an almost unassailable article of faith. That’s why people are so surprised to learn that there’s very little evidence to support the idea.
This point is the current bottleneck in my “3-minute” explanation, because it takes a while to explain why it’s not true. I’ve written about it extensively here, here and here. For the purposes of this brief article, we’ll have to leave it at this: both total and LDL cholesterol – which are the numbers your doctor, the media and everyone else seems to be concerned with – are only weakly associated with heart disease.

If “high cholesterol” were the cause of heart disease, you’d expect it to be a risk factor in:
  1. All populations around the world.
  2. In both men and women.
  3. In people of all ages.
And you’d also expect that lowering cholesterol should prevent heart disease.
Makes sense, right?
Unfortunately for the lipophobes, the cholesterol hypothesis fails on all fronts.
  1. High cholesterol is not a risk factor in all populations. The French have among the highest cholesterol levels in the world, and among the lowest rates of heart disease of any industrialized nation. The Austrians and other European nations are similar.
  2. Women on average have 300% lower rates of heart disease than men, despite higher average cholesterol levels.
  3. The rate of heart disease in 65 year-old men is 10 times that of 45-year old men. Yet high cholesterol is not a risk factor in men over 65. (In fact, men over 65 with low cholesterol (<150 mg/dL) are twice as likely to die from heart disease as those with normal or even "high" cholesterol.)
Finally, more than 40 trials have been performed to see if lowering cholesterol prevents heart disease. In some trials more people got heart disease, in others fewer. But when all the results were taken together, just as many people died in the treatment groups (those who took cholesterol-lowering drugs) as the control groups (those who did not).

Point #4: If you want to worry about your cholesterol numbers, forget about total cholesterol and LDL and pay attention to the ratio of triglycerides to HDL.

In general I’m not a fan of people worrying about their lipid panel numbers at all. Like Dr. Kurt Harris, I think this compulsive testing and re-testing of lipids that has become common in the Paleo community not only isn’t necessary, but may even be harmful. There’s still a lot we don’t know about how these numbers change on a day-to-day basis. What’s more, it’s not always easy to distinguish between cause and effect. Researchers made the mistake of assuming high cholesterol was the cause of heart disease, when in reality it’s much more likely that high cholesterol is a consequence of it.
But for crying out loud, if you’re going to get your lipds tested at least pay attention to the right numbers. And the most important number on a conventional lipid panel is the relationship between triglycerides and HDL. (Divide triglyercids by HDL to get it.) If that number is less than 2, this suggests you have mostly large, buoyant LDL – which is not a risk factor for heart disease. If that number is higher than 3, it suggests you have mostly small, dense LDL – which most certainly is a risk factor for heart disease.

Point #5: Eat good food and don’t worry about the numbers.

But in the end, even that ratio doesn’t matter so much. Why? Because the treatment is always the same! If your TG:HDL ratio is high (bad), what should you do? Eat a high-fat (saturated, of course) diet. This will reduce your triglycerides and small, dense LDL, and increase your HDL. Triple win. And if your TG:HDL ratio is low (good), what should you do? The exact same thing: eat a high-fat diet.

Conversely, replacing saturated fat with carbs, as we’ve been told to do for 50 years to protect ourselves from heart disease, actually contributes to it in three ways: it increases triglycerides and small, dense LDL, and decreases HDL.

Finally, I often get emails from people who’ve switched to a high-fat / Paleo-type diet expressing concern that their LDL and total cholesterol levels have gone up. My response usually has three parts: 1) don’t worry about it, because high total and LDL cholesterol do not cause heart disease; 2) the increase is usually temporary, and may be the result of the body curing itself of fatty liver (a good thing!); 3) don’t worry about it. Doesn’t hurt to remind them.

**Note: if your total cholesterol levels are very high (i.e. above 300 mg/dL), this may be an indicator of a metabolic abnormality or inflammatory process that needs to be addressed. Cholesterol is a repair substance in the body, and persistent elevations beyond a certain threshold may point to an underlying problem that hasn’t been identified.


  1. I don't agree that you should casually ignore high LDL-C. I see that this post was written a month ago. Do you still stand by everything you wrote here?

    What do you say to the genetic evidence that those with hypercholesterolemia (genetically high LDL) have extremely high risk of CVD, while those with hypocholesterolemia (genetically low LDL) hardly ever develop heart disease?

  2. Will
    I appreciate you visiting my blog and taking the time to comment.

    I will admit that within the many sources providing information and recommendations on dealing with cholesterol there is a wide divergence.

    This blog was started out of my personal research due to my own health situation. I began by posting articles I found that seemed to show credible evidence to a side not presented by most in the medical community and in the main stream media. And a lot of the evidence was coming from the same medical journals as the low-cholesterol mongers were using but ignoring. Many highly qualified medical professionals do not agree with the 'lower is better' philosophy in fact it is very credibly disputed. So this blog both chronicls and doccuments some of my findings of 'the other side of the story'.

    And to more directly answer your question, Yes I do stand by what this article states and other articles that I post as credible evidence that the "We Must All Be Taking Statin Drugs To Lower Our Cholesterol" and "Eat Low Fat Low Cholesterol Diet" mantras are false or at least have strong views to the contrary such that the informed must at least consider them when making health decisions. That said, my focus has not at all been on the specific nuance you bring up, that of hypercholesterolemia. I have read articles on that topic but it is not my focus here. So though I stand by what I posted, it may not be specifically applicable to hypercholesterolemia.

  3. Mr. Kresser's first 2 points don't even directly address the title of this post.
    One could also conclude based on research, etc that high cholesterol isn't the ONLY contributing factor to CAD, and even that other factors, if in place, can compensate for high cholesterol effects, but to take his points and conclude it has not contribution is overstated and potentially harmful to some people.
    Research clearly shows that large puffy AND small dense LDL are contributors to CAD, but small dense is relatively worse. But that does not mean large puffy LDL, when in excess (ie particle number vs particle size) makes not contribution. Again, I feel Kresser's blanket statements here are misleading and potentially dangerous.


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