Understanding the cholesterol story
There has been confusion for decades about dietary cholesterol and the risk it may pose for cardiovascular disease (CVD). You can check out my prior posts on 7 ways to optimize cholesterol and statins – should you take them for some of the current thinking concerning this.
Dr. Rhonda Patrick, PhD, is a researcher and scientist, as well as creator of foundmyfitness.com, which is her website where she posts podcasts and videos as well as reports. I am linking to a video below posted on Dr. Patrick’s YouTube channel in which she interviews Dr. Ronald Krauss, Senior Scientist and Director of Atherosclerosis Research at Children’s Hospital Oakland Research Institute, Adjunct Professor in the Department of Medicine at UCSF and in the Department of Nutritional Sciences at UC Berkeley, and Guest Senior Scientist in the Department of Genome Sciences of Lawrence Berkeley National Laboratory. Dr. Krauss has done extensive research into cholesterol and heart disease risk and has recently collaborated in developing one of the more cutting edge LDL particle size tests.
The Basics of Cholesterol in the Arteries
Cholesterol is manufactured in the liver to deliver fatty acids known as triglycerides to cells throughout our body. We can get cholesterol from dietary sources, however it has turned out that after many studies we cannot find a significant effect of the amount of dietary cholesterol on the level of cholesterol in the blood. Translation: Eat all the cholesterol you want, your body will likely react by just not manufacturing as much of it as a result.
Cholesterol leaves the liver into the blood circulation as Very Low Density Lipoproteins (VLDL) carrying its load of triglycerides to the body. Additionally the liver manufactures and releases High Density Lipoproteins (HDL) – commonly known as the “Good Cholesterol”, although it really does not carry much cholesterol to start with. HDL interacts with VLDL particles to unload their triglycerides for delivery to cells, and it also scavenges unused cholesterol from cell surfaces (such as arterial walls) to be taken back to the liver and recycled.
The VLDL then transitions as its load decreases to large bouyant LDL particles, known as Pattern A particles, which continue the transport and delivery of their triglyceride load, and then also takes excess cholesterol back to the liver for recycling. However, a certain portion of these Pattern A LDL particles are not efficiently sensed by LDL receptors in the liver and continue to circulate, losing more of their triglyceride cargo and becoming smaller and denser.
The smaller and denser they become, the harder they are to remove from the blood and the more likley they are to penetrate the arterial wall, become lodged there, oxidize, and start the formation of arterial plaque. This leads to a condition known as Atherogenic Dislipidemia, which when present is the highest correlation marker we have for CVD risk. This condition is typically indicated by low levels of HDL, high levels of small dense Pattern B LDL, and high levels of triglycerides. This is also one of the reasons the HDL to Triglyceride ratio is one of the best predictors of CVD risk.
Statin use for CVD risk
Statins work by increasing the LDL receptor activity in the liver and lowering the overall level of LDL, both Pattern A and B. Unfortunating they work much better at lowering Pattern A LDL, which is the one which is beneficial and not a risk, and only do a marginal reduction of the Pattern B LDL which remains as a risk factor.
It is believed that the same results can be achieved through diet, exercise, and a generally good lifestyle profile, but unfortunately the studies just do not exist to be able to prove that. The nature of nutrition studies is that they are very complicated, very large and very expensive, and the funding has just not been there to do these studies. I will say for what it is worth, in my personal N=1 experiment diet and exercise were very successful – see my post on My Wellness Screening and Blood Testing for the numbers.
Unfortunately, statins do have adverse side effects on muscle metabolism and also a tendency to lead to diabetes – diabetes development occurred in about 12% of all patients and as many as 30% to 40% of female patients. The current recommendations go way too far in recommending these statins as a preventative measure, we should be much smarter about when we have a proven risk that can be helped before taking them.
It would make more sense to screen with the standard test, and then if we have AD profile numbers in the results which indicate increased risk, we can then consider particle testing to determine true risk. Particle testing is becoming less costly and better standardized and once doctors become better educated on the issue this testing may be used much more extensively.
Other issues discussed in the interview
Additionally the interview has extended sessions on chronic inflammation and the role it plays in this entire process of CVD risk, as well as an extended discussion on some of the dietary aspects. On the diet front, Dr. Krauss discusses the fact that we now understand saturated fat is not the villain we once thought, that added sugar to the diet is likely the prime culprit behind higher cholesterol levels due to destroying the feedback loop which regulates VLDL production in the liver, and that while refined and processed carbohydrates may be dangerous for other reasons – such as inflammation, weight gain and diabetes – we do not have adequate study data to link them to directly to CVD risk.
This is a very long video, about an hour and twenty minutes. However, if you want to know the cutting edge thought on cholesterol and CVD risk, it is well worth the time to watch. I have had to be somewhat simplistic in my explanations above, and I encourage you to compare them to the more educated comments given in the video.