In my quest to learn more about cholesterol especially given my history of developing paradoxically elevated LDL-C, LDL-P, Small LDL-P and Total cholesterol after eating low carb (here are my most recent blood lipids), I’ve scoured the net wide and far, even venturing deep into strange forums and comment threads… and still haven’t come across any clear answers.

Neither of Jimmy Moore’s books, Cholesterol Clarity nor Keto Clarity provided any clear answers.

I’ve explored the possibility of coffee being a potential source of increased LDL through the effect of diterpenes, and the effect of certain Apo-E genotypes causing this sort of paradoxical reaction (even looking into the Framingham Offspring source material itself).

While one of the more helpful resources I came across was this case presentation and writeup by Dr. Dayspring, I still wanted to know more.

Why does 1/3 of the population who eat low carb develop the sky rocketing levels of cholesterol when the remaining 2/3 demonstrate no change or a dramatic decrease?

In my journeys to the corners of the net to learn more, a few folks directed me to the work of Ivor Cummins, a chemical engineer who developed a deep interest in all things cholesterol (you can read more of his stuff at thefatemperor.com).

They recommended this lecture in particular:

I’ve finally gotten around to taking the time to watch through all 1 hr and 47 minutes of it and took some notes which I will share with you all below.

He does a wonderful job of covering cholesterol metabolism and biochemistry as well as addressing why dietary cholesterol and fat aren’t the problems they’ve been made out to be, when the real culprit is dietary carbohydrate.  All material people who follow my stuff regularly will be familiar with and can be found in Jimmy Moore’s very readable Cholesterol Clarity.

While Ivor does a better job than Jimmy about going into the source research material, he does have a pretty thick Irish accent which I found made the lecture that much more interesting.  The BJJ Cavewife however, who has trouble with accents, couldn’t understand a word!

I got excited at one point when Ivor began addressing the changes in blood lipids seen with a low carbohydrate diet and how dramatic the improvements can be… but was a bit let down because he never addresses the main question that I have, which is why do some folks who eat low carb paradoxically develop high cholesterol…. so I’ll have to continue on with my search!

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Notes from this lecture

Key molecules

• Cholesterol fundamental to life. Cells need it. Hormones need it.
• Important in damage repair system.
• Cholesterol blamed for disease like blaming paramedics at the scene of an accident.
• Triglycerides – comes from diet. Can also be synthesized by body.

Key particles

• Lipoprotein particles. These are needed to transport cholesterol and triglycerides because they are hydrophobic. Lipoproteins packages these cholesterols and triglycerides so they can be transported throughout the body, the outer shell is hydrophilic.
• Lipoprotein particles are like boats, and the triglycerides and cholesterol are the cargo.
• Chylomicron – largest. Contains mostly triglycerides. Packages dietary triglycerides.
• LDL class:
  • VLDL: contains 2:1 trigs to cholesterol. Made in the liver. As it moves through the body, and gets smaller as it unloads is cargo, and becomes LDL. Has a B100 surface protein marker.
  • sdLDL: small dense LDL. This is the bad one. If you have lots of these, it’s indicative of a dysfunctional system. Oxidized LDL also tracks this measurement. Oxidized LDL are the damaged versions and no longer work as they are supposed to.
  • HDL: Does a lot of good work.

Athersclerosis:

• When a sLDL ends up in the vessel wall, your body recognizes this as a problem, and a defensive cell, the macrophage, goes after it and eats it, and becomes a blobby ‘foam’ cell. It looks foamy under the microscope because it gets filled up with all the fatty material.
• And this builds up in the artery wall, building a plaque, and clogging the system.

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How the cholesterol processing system works:

• Chylomicron – created in gut when consuming dietary fat. It takes the cholesterol and triglycerides, mostly triglycerides, and is packaged into chylomicrons, and this goes into the blood stream.
• It goes into they system and docks with muscle cells and fat cells and deposits it into those cells.
• As it gives off its cargo, it shrinks, and becomes a chylomicron remnant, and only survive for around 20 minutes.. These go back to the liver, where they’re recycled.
• For this to work, insulin must be kept low!
• High insulin suppresses fat metabolism, suppresses lipolysis, and causes dysfunction of fat processing.

LDL

• Liver creates VLDL for purposes of transporting cholesterol and triglycerides.
• It goes to muscle and fat cells to deposit its cargo, and becomes an LDL.
• LDL live for a few days before they are taken back up in the liver.
• sdLDL and oxidized LDL (the outer shell of the LDL is damaged by oxygen) track together.
• Glucose is key factor in creating oxidation and inflammation.
• There is poor uptake of the sdLDL and oxidized LDL by the liver.
• There is good uptake however by the macrophage/foam cells in the artery walls.
• This can be reversed though… up to a point.

HDL

• It’s like an empty balloon and it goes around the body picking up cholesterol.
• It gives cholesterol to cells that can’t make cholesterol by themselves (adrenal glands and gonads).
• It also takes back cholesterol excess from other tissues and cells, so that it can be ferried back to other places it can be used.
• HDL can go into the arterial wall, dock with the foam cells, and take up the cholesterol within the foam cells.
• It also has antioxidant action, designed to manage LDL oxidation.
• HDL also transports cholesterol between other LDL particles.
• There has been multiple attempts to increase the amount of HDL pharmacologically, and in a few of these trials, when they have successfully increased the HDL, it also lead to an increase in mortality!

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Risk Factors of Mortality

• Dysfunctional lipoprotein status
  • LDL/HDL Ratio (or better still, ApoB/ApoA ratio)
  • High serum triglyceride levels, larger VLDL particles
  • Small dense LDL and associated LDL Particle count (ApoB)
• Insulin levels and insulin resistance status
• Blood glucose level and HbA1c
• High blood pressure
• Other markers of systemic inflammation
  • GGT, CRP, Serum Ferritin

Total cholesterol as a predictive factor?

• He brings up a study showing that increasing total cholesterol decreases risk of all cause mortality.
• Now, total cholesterol is effectively not considered as a risk factor anymore by leading edge researchers.
• Increased LDL in the setting of a high HDL doesn’t lead to any significant increased risk of heart disease.
• Increased LDL in the setting of a low HDL leads to increased risk.
• Low LDL in the setting of a low HDL also leads to increased risk.
• So it’s the ratio that tells you more.

Serum Triglyceride as a predictive factor

• High triglycerides can be bad.
• However if you have high triglycerides but a good HDL:LDL ratio, then the risk isn’t bad.
• If the ratio is bad, and the triglycerides are high, then your risk really goes up. More mortality.

Serum Insulin as a predictive factor

• Insulin is fundamental to Coronary disease and mortality risk
• Insulin has been grossly underemphasized as a risk factor for decades.
• Triglyceride risk totally outgunned by insulin status here.
• If he could choose only one lab value to know, he would choose insulin!
• When insulin is low, then the triglyceride level doesn’t matter much.

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Serum Insulin and LDL particle count

• Again insulin is key, but significant interaction with LDL particle count (ApoB)
• LDL particle count tracks with small dense LDL
• When insulin is low, even the higher particle count doesn’t matter much!
• When insulin is high, then the particle count becomes a strong risk factor! 11x risk for high particle count and high insulin.

Glucose and HbA1c, as they increase, so does all cause mortality.

Carbohydrates drive blood glucose and insulin.

• Low carb diets improve total cholesterol:HDL ratio, LDL:HDL ratio, serum triglyceride, improve LDL particle diameter, improve HDL,
• Higher fat, higher saturated fat improve HDL, and don’t change LDL too much.
• In population with Small dense LDL and coronary issues, they found that as they reduced carbs from 70% down to 38%, there was a linear reduction in percentage of small dense LDL.
• There are around 30% of people who can tolerate a high carb low fat diet. The remaining 70% people don’t do well, and every risk factor is going to be worse.