Is “Bad Cholesterol” Really That Bad?
…Inflammation, Not Cholesterol, as the Root Cause
***Feel free to just read the quotes & summaries if you’re in a time crunch!***
When we go to the doctor and get our blood checked, a cholesterol panel is always on the list. We all know the story: eat cholesterol, cholesterol goes up, and high cholesterol causes heart disease. But in the last decade, this story has changed. We now know that butter is ok (thanks TIME magazine for breaking that news in 2014! Let’s just make sure it’s 100% grass-fed), and that yes, we can eat the yolks in eggs. But the story on cholesterol is still evolving.
Currently, a cholesterol panel is the main tool used to assess cardiovascular disease (CVD) risk. We look at total levels, HDL (the “good”) and LDL (the “bad”). This simplified equation was useful 50 years ago when technology and research were just starting to uncover the trends behind CVD, but are outdated today. Cholesterol itself can’t block your arteries, so measuring it won’t give you the full picture of how at risk you are.
How We Really Get Blocked Arteries
Smoking, stress, fried food, high blood sugar or blood pressure, sleep debt, infections, and pollution can all lead to damage to the blood vessels. The immune system sweeps in to fix the tears, a process called inflammation. If we keep damaging them, then the immune system doesn’t stop, and this is chronic inflammation.
Cholesterol comes in to patch it all up, and the cholesterol itself can become damaged, also known as oxidized. Oxidized cholesterol attracts more of the immune system, and we keep patching things up until we have a nice big plaque that can block blood flow. Furthermore, it’s the little pieces of cholesterol that can plug up the holes, big fluffy pieces of LDL don’t do a good job of patching the damage. See how you are not getting a full picture with a simple cholesterol panel?
Studies show that patients with high total LDL (basically think of it as a big box filled with LDL vs. a small box) but low LDL particles (meaning they’re more big and fluffy because less pieces fit in the box) have a lower risk than those with low LDL but higher LDL particles.1 They also show that LDL cholesterol loses its predictive value in those with high blood sugar, low HDL, or elevated triglycerides, which is at least one third of our population.1
SUMMARY: Inflammation is the trigger and oxidized, small-dense LDL is the most likely to build up in plaque. Therefore, an accurate panel would include markers for these 2 components.
Cholesterol Isn’t There to Harm Us
Cholesterol makes up the membrane of our cells and is the building block of our hormones, so there’s nothing inherently evil about it. We need it. In fact, many studies show low cholesterol is correlated with worse health outcomes.
One large study of over 52,000 Norwegians showed that women with a total cholesterol below 193 had just as much heart disease as those over 270. 2 Staying in between this range conferred the most protection. Men in that study also had a U-shaped curve, meaning that the lower cholesterol levels had high risk just like the higher cholesterol levels, with the lowest risk being in the middle of the range. It’s also interesting to note that in women, there was an inverse association between total mortality and cholesterol levels, meaning the lower the levels went the higher the risk of dying. The authors conclude:
If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.
There are many more studies suggesting negative effects from lower cholesterol:
- In men with high blood pressure, cholesterol below 160 made them 3 times more likely to die from a stroke. 3
- A study of almost 7,000 Italian patients in the hospital observed the risk of dying from any cause was double when total cholesterol was below 160, even when compared to the group with cholesterol above 240. 4
- In those over 70, cholesterol below 160 is associated with three times greater rates of depression and two times more deaths unrelated to physical health such as suicide and accidents. 5
- In men aged 40-70, there is a greater risk of depression with cholesterol below 174. 6
- A study of 300 healthy middle-aged Swedish women also found that the lower the cholesterol the more depressive symptoms experienced, especially for cholesterol below 180. 7
- Likewise, in a group of four ethnicities aged 45-84, low cholesterol was associated with depression regardless of age or ethnicity. 8
- A review of the literature shows cholesterol is lower in those with Alzheimer’s and likely plays a role in developing dementia. 9
- A review of the evidence on the effect of age on cholesterol as a predictor of heart disease concludes:
From the data available, it is reasonable to conclude that after the age of 65, increased blood lipids, although still a risk factor for coronary heart disease (CHD), become less pronounced as risk factors and that by 75 years of age their predictive value has disappeared. Indeed, in the very elderly, there is evidence to suggest that high total cholesterol is associated with longevity
This relationship between cholesterol and heart disease is extremely nuanced. We have seen how slightly high cholesterol might be protective in women and the elderly, but what about younger men? This is where the strongest argument for keeping cholesterol below 200 lies. A review of 3 large studies showed in men under age 40, cholesterol above 240 leads to double the risk of heart disease as those under 200. 11
But Don’t Statins Help?
There is no question that statins help to reduce events and deaths, especially in middle-aged people with very high cholesterol (over 260) or who already have CVD.12 But what may be surprising is that they only help about 1 in 100 people taking them. For example, a study of over 10,000 people aged 55 or older found that 9.3% of those taking statins had a cardiac event while 10.4% of those with usual care (no statins) did.13 Furthermore, the all-cause mortality between the 2 groups was essentially the same during the 6 year trial.
There’s even less benefit in those over 65 years of age who have never had a heart attack: rates of heart events between the group taking a statin and the control were about the same, and there was a trend toward higher risk of dying in the group on statins, which increased as they aged.14
Finally, statin use also carries with it the risk of lowering an important antioxidant in the body called CoQ10, muscle or liver damage, diabetes, and side effects if the statin makes your cholesterol too low. So no, statins don’t help all people in all situations as we are led to believe, and might not be significantly more beneficial than plain diet and lifestyle.
So What Should We Have Measured Then?
A little bit ago I told you how CVD is an inflammatory condition. So looking for markers of inflammation is a good place to start! C-reaction protein (CRP) is one such marker of generalized inflammation.
Considering that about half of all heart attacks occur in individuals with normal LDL levels, experts in the field have determined CRP should be included when evaluating one’s risk.15 If more people get disease with higher levels of a marker, that means that marker is much better at predicting who is at risk. Let’s see what the research says:
- A study comparing LDL to CRP (whew this is a lot of letters!) found that those with the highest LDL had 1.5x greater risk of CVD but with the highest CRP they had 2.3x greater risk! It concludes that the 2 markers should both be considered for the best prevention.16
- Women with high CRP were 4.4 times more likely to have a heart event whereas those with the highest LDL were 2.4 times more likely. The relative risk for a high total cholesterol to HDL ratio was 3.4. So both the ratio and CRP are much more predictive than LDL.17
- Adding metabolic syndrome increases prediction of risk even more. Metabolic syndrome is having 3 or more of: high blood sugar or blood pressure, waist circumference, cholesterol, or triglycerides. Having 3 of these means you are likely to have high CRP (equal to or above 3.0) as well, and 3.4 times more likely to have a cardiac event even if CRP is below 3.0. However, if you have both metabolic syndrome AND high CRP, you are 6 times more likely to have an event! This is the greatest predictive formula I’ve seen, and cholesterol isn’t involved at all.18
So Then How Do I Reduce My Risk?
As mentioned above, metabolic syndrome is associated with higher CRP and CVD. Therefore, reducing your blood pressure and fasting glucose, shrinking your waist line, and lowering triglycerides will all help. There have also been many studies on diet and inflammation, and in general they find fruits, vegetables, fiber, antioxidants (the color in fruits, vegetables, beans, herbs, and spices), nuts, fish, and olive oil reduce inflammation and CRP.19 On the other hand, conventional high-fat meat and dairy products, refined grains, and sugar all increase CRP.
Researchers have come up with a food survey that scores participants’ diets and assigns a Dietary Inflammatory Index.20 They have found that a high score increases likelihood of CRP above 3. From their survey, the authors conclude that garlic, onion, tea, ginger, turmeric, and oregano strongly reduce inflammation while saturated and trans fat increase it (can be found in baked goods, hot dogs, hamburgers, fried food, and cheese).
As the saying goes, food is medicine. And you don’t have to worry about muscle or liver damage with this medicine!
SUMMARY: If you are concerned about your risk for heart disease, look at hs-CRP (high sensitivity), or at least total cholesterol to HDL ratio, for a more predictive assessment. Don’t drive cholesterol too low, try diet and lifestyle to get rid of metabolic syndrome, and take CoQ10 if you do have to take a statin.
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References:
1. https://www.ncbi.nlm.nih.gov/pubmed/21981835
2. https://www.ncbi.nlm.nih.gov/pubmed/21951982
3. https://www.nejm.org/doi/full/10.1056/NEJM198904063201405
4. https://www.amjmed.com/article/S0002-9343(03)00354-1/abstract
5. https://www.sciencedirect.com/science/article/pii/0140673693925569
6. https://www.ncbi.nlm.nih.gov/pubmed/10772398
7. https://www.ncbi.nlm.nih.gov/pubmed/9316185
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290355/
9. https://www.ncbi.nlm.nih.gov/pubmed/21402242
10. https://www.ncbi.nlm.nih.gov/pubmed/10999646
11. https://www.ncbi.nlm.nih.gov/pubmed/10891962
12. https://www.ncbi.nlm.nih.gov/pubmed/27905702
13. https://www.ncbi.nlm.nih.gov/pubmed/12479764
14. https://www.ncbi.nlm.nih.gov/pubmed/28531241
15. https://www.ncbi.nlm.nih.gov/pubmed/16239491
16. https://www.nejm.org/doi/full/10.1056/NEJMoa021993
17. https://www.ncbi.nlm.nih.gov/pubmed/10733371
18. https://www.ncbi.nlm.nih.gov/pubmed/12551861
19. https://www.ncbi.nlm.nih.gov/pubmed/24107546
20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925198/
