Athletes who have been through major medical procedures know the frustration of trying to interpret doctors’ conclusions in the context of continuing to train and compete. As a coach who believes health is the foundation of performance, it drives me crazy how little useful information you get about your own health from providers.
I don’t consider this the direct fault of medical providers. Due to insurance reimbursement constraints, they are given so little time with you and are under such enormous pressure to be authoritative and decisive with you that they just can’t be thorough. The reality of health care is that most of our health measures are imperfect indicators of activity in the body. None of our health measures are infallible. No one health measure can be predictive on its own. So you have to know how to interpret the data.
This is part one of a series explaining what your health numbers actually measure. We’re starting with the elephant of health numbers: cholesterol.
The first thing to understand is that we don’t even measure your actual cholesterol!
If you want a one-page guide summarizing the numbers in your typical annual blood test, get it here.
If you already have the guide (or just want to know about the misnomer that is “cholesterol” on that blood test), read on!
The public narrative around cholesterol is an absurdity. Poorly structured research decades ago then interpreted by sensationalist media funded by grain companies did us all a massive disservice. Buckle up for a long explanation.
Definitions of “Cholesterol” Numbers
Lipids are fat molecules (triglycerides and cholesterol) and proteins bound by an electrolyte (most often phosphate). Every cell in our body needs protein to open gates in the cell wall or walls of sub-structures (sort of like passthrough windows at a short-order restaurant). Cells use cholesterol directly and break down triglycerides into energy (ATP) for cell processes.
Lipoproteins are vehicles for transporting lipids in our blood stream. Lipids themselves stick to things and can become toxic in high concentrations, so lipoproteins package them up for safe transit.
When you get a cholesterol measurement, it measures HDL, LDL, and VLDL. Those refer to lipoproteins: high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL). The “density” component of that name describes density of protein compared to the volume of each carrier. None of these measures actually counts units of cholesterol in your blood.
HDL has many units of protein, some quantity of cholesterol, and a proportionately small quantity of triglycerides. It has an overall high ratio of proteins to fats. It’s like a Frontier flight: a large number of paying passengers and workers with very few pieces of baggage.
LDL has a much smaller overall ratio of proteins to fats. This is a United flight that takes 45 minutes to deplane because each passenger has a lot of baggage.
VLDL has lots and lots of lipids for each unit of protein. But this is not bad, because VLDL is a UPS plane: all useful packages (cholesterol + triglycerides) to be transported yet very few people (protein).
How cholesterol-related molecules work together
Your cells need cholesterol for repair (and hormone production) and need triglycerides to extract energy. Your liver is the storage depot for those lipids, so it releases them for use around the body. Neither fat can just float along in your bloodstream by itself and both need proteins to open the correct gates through cell walls anyway, so those fats get packaged up with proteins, then carried along in a lipoprotein vehicle. Initially, that vehicle has lots of fats and a few proteins.
When the lipoprotein arrives to a cell, protein opens the gate, then gets back on the bus. Triglycerides get off the bus to go into the cell to be used for important activities. The bus leaves the cell to either deliver triglycerides to other cells or to return to the liver to pick up more of them. As triglycerides exit the bus, the *proportion* of protein-to-fat on the bus shifts to a higher value. So VLDL becomes LDL becomes HDL simply because triglycerides get off the bus while protein stays.
Here’s where things get interesting:
HDL is headed back to your liver to pick up more lipids (typically triglycerides), presumably because your cells need more energy to do their jobs. HDL is very buoyant in the bloodstream because it doesn’t carry much fat, so it rarely crashes into things or gets stuck on arterial walls. It’s like a flyer bus that only travels in the HOV lane on a calm highway. That’s why there’s no observable risk to increasing the number of empty buses headed back to depot. It’s somewhat inefficient, but not dangerous.
VLDL is on its way to cells. It has to make frequent, sudden stops. Like a New York UPS truck driven by a new hire, that means it’s always at risk of hitting something or getting detoured in traffic. The first trip of the day tends to go without issue, but each subsequent trip (stopping at more cells to unload triglycerides, the process which changes this molecule from very low-density to low-density) increases the likelihood of a delay or a wreck.
How the cholesterol transport system falls apart
When your liver releases far too many triglycerides (like if it’s saturated with them because of excess glucose in your bloodstream or if you have a liver disease), it doesn’t only call for buses or UPS trucks anymore. Those are high-occupancy vehicles (for packages of triglycerides at least), so they are a bit slow and they are always busy. Instead it starts contracting Uber Eats drivers – lots of smaller vehicles with less-trained drivers. Basically, this “contract” LDL gets called back to depot before it has unloaded all of its triglyceride packages simply because it can travel faster, so can shuttle the small loads.
But LDL is crash-prone and gradually decays (like a delivery car too active to get regular maintenance). So LDL can stick in places along your arteries and around your organs. Because not enough LDL is making it back to the liver to shuttle triglycerides, your liver releases hormones which demand your body create more lipoproteins.
Those new lipoproteins were “hired” to make up capacity in the lipid shuttling job, so new VLDL becomes LDL as it unloads triglycerides but never loses enough lipids to become HDL. More cars on the road; fewer new buses. Except the whole reason your body made more cars was because some cars were getting stuck on the road (like during a snowstorm, they are clogging up the shoulders). So the road (your artery) is getting narrower at the same time there are more cars (LDL) attempting to drive on it.
Packages (triglycerides needed for energy) get delivered more slowly, so cells demand energy faster (triggering hunger signals). You feel desperately hungry, so you overeat (often with carbs because you feel ravenous). Stuffing yourself beyond your immediate energy needs causes excess glucose in your bloodstream that your liver needs to store as triglycerides, except it’s already pumping out all the triglycerides that it can…
You can see the vicious cycle you’re caught in at that point.
What “cholesterol” measures really mean
We monitor LDL because when it trends upward, it is an early indicator that things are going wrong in the system. Intervention might be treating the liver (rare) or it might be managing lifestyle factors (common). There has to be some intervention because LDL count doesn’t go up without a strong signal from the body.
Higher HDL is not “good” for you. It’s simply not-obviously-bad.
Higher LDL doesn’t mean anything on its own. Upward-trending LDL is indicative of something going wrong in your metabolism.
Increasing LDL and high/increasing triglyceride count are strong indicators of your risk for metabolic and heart diseases because they mean your body is congested with fat-energy and unable to use it all.
Since your actual cholesterol count was never measured, your cholesterol numbers tell you nothing at all about that particular lipid. But these two facts may disturb you:
- dietary cholesterol intake has no correlation to actual blood cholesterol values.
- low-fat diets (which are often high-carb diets) associated with “heart healthy” eating tend to make lipoprotein and triglyceride numbers worse over time.
This is because inflammation and high blood sugar are intimately related…and commercialized “heart healthy” eating involves highly-addictive, sugar-laden, processed packaged foods. I’ll cover blood glucose, insulin, and hunger triggers in another piece. Read Strong Medicine by Chris Hardy and Marty Gallagher if you want a deep dive.
Get the free guide to your health numbers here for a printable, 1-page summary of what your blood test metrics actually mean.