Chris Kresser interviews Chris Masterjohn on cholesterol and heart disease.
Chris Masterjohn has a PhD in nutritional sciences studying how diet and nutrition works on a physiological and biochemical level.
Extremely good detailed description of current thinking and analysis of past studies.
* the history of the cholesterol-heart disease connection
* misconceptions around diet vs. lipid hypothesis
* finding middle ground between cholesterol skeptics and proponents of the lipid hypothesis
* the LDL receptor and familial hypercholesterolemia and what they can tell us about cholesterol and CHD in normal populations
* what is a “normal” cholesterol? what can anthropological studies tell us about this?
* are lipoprotein particle size tests accurate? what’s the best way of determining particle size?
* why do some people have high cholesterol (TC & LDL) after adopting a Paleo/WAPF diet? is this something to be concerned about?
* The role of cholesterol in heart disease
* What to do – or not do – about high cholesterol
* The thyroid-LDL connection and why iodine matters
* Are goitrogenic foods inhibiting your thyroid function and raising your cholesterol?
* The telltale sign you need more carbs
A good summary of everything I have learned so far including LCHF, metabolism and slow burn exercise.
The whole video is interesting in parts, but the really interesting part is the science from approx 1hr 2m for about 25mins.
It explains how and why a few mins of slow-burn, muscle failing training works better then an hour of aerobics. Good explanation of cell metabolism too.
The Q&A after that is good too.
Blood test results quote 4 key numbers: total, HDL, Triglycerides, LDL.
Values are in mmol/l (UK) or mg/dl (US).
To convert mg/dl of HDL or LDL cholesterol to mmol/l, divide by 39.
To convert mg/dl of triglycerides to mmol/l, divide by 89.
The LDL value is not measured. It is calculated from the other values using the Friedewald equation.
LDL = Total - HDL - 0.45 * Trig
This is a good approximation as long as Trig
LDL = TC/1.19 + TG/1.9 – HDL/1.1 – 1 (mmol/L)
Also, from "Wheat Belly":
A: If LDL particles are small, the equation underestimates LDL.
B: If LDL particles are large, the equation overestimates LDL.
C: If diet changes LDL from mostly small to mostly large, calculated LDL will appear to go up when real value is going down.
(C is a mathematical result of A and B, but need to understand why A and B are true)
And from NCBI/PubMed
Don't panic if blood test shows increased LDL
In general, it seems that with standard lab tests, the LDL value can be unreliable.
There are 5 important lipoproteins, in decreasing order of size and increasing density. (The more fats, the more they float, the lower the density)
Transports trigs direct from gut to liver, adipose, cardiac and muscle tissues, where trigs are unloaded (by lipase) and the remnant returns to the liver.
VLDL - Very Low Density Lipoprotein
The "triglycerides" on the blood test results.
30-80nm - made by liver - contains trigs and cholesterol.
Are converted to either large or small LDL.
As VLDL encounters HDL and LDL in blood it donates a trig and receives a cholersterol molecule in return.
IDL - Intermediate Density Lipoprotein
VLD that has lost its trigs but retained its cholesterol is smaller and known as IDL.
LDL - Low Density Lipoprotein
Large LDL (>25.5nm)
Safe. Too large to interfere with arterial wall cells. Recognised easily by receptors on liver and recycled.
Lifespan 3 days.
Small LDL (< 25.5nm)
Dangerous. Small enough to cause atherosclerosis. Not so readily recognised by liver receptors.
Taken up by inflammatory white blood cells (macrophages) that reside in the wall of arteries -> plaque.
25% more likely to oxidise then large LDL. Oxidised LDL more likely to cause plaque.
8x more susceptible to endogenous glycation - glycated LDL more likely to cause plaque.
High carbs increases formation of small LDL and higher blood glucose increase glycation.
Lifespan 5 days.
If large and small LDL produced at same rate, small LDL count will increase because they last longer (2 more days).
LDL has only one apolipoprotein B100 protein so a blood test for apo-B count will measure LDL count.
LDL begin large then exchange cholesterol for trig (with VLDL) then deposit trig (lipase) and become small.
Removes cholesterol from arteries and transports it back to liver.
Higher levels of HDL are good indicator of cardiovascular health, but raising levels does not improve health (it's an effect not a cause).
An excess of VLDL (trigs) -> more trig/chol exchanges with LDL -> more small LDL.
With trig level > 1.5, 80% of people develop small LDL.
Anything that increase the liver's production of VLDL and/or increase the trig content of VLDL is a risk for atherosclerosis.
Carbs, especially wheat, consumption increases insulin levels which triggers "de novo lipogenesis" in the liver, effectively turning carbs into trigs (VLDL).
Visceral (mostly belly) fat stores trigs and exports trigs into the blood causing liver to generate more VLDL.
The information below is taken from the following sources:
1. Wheat Belly, William Davis MD
2. The Great Cholesterol Con, Dr. Malcolm Kendrick