Deborah KayBy Deborah KayFebruary 1, 202019 Minutes

TL:DR: Eating cholesterol has very little impact on cholesterol levels in body. Dietary cholesterol is not absorbed and excreted in gut. Most of the cholesterol in body was made by our body. Eating sugar increases production of plasma cholesterol. The addition of fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.


What is cholesterol?

Cholesterol is a waxy lipid (non-water soluble molecule) that is made in the body. 20% of cholesterol is synthesized in the liver and 80% in other cells. It can be found in every cell in the body. Cholesterol is essential to life (to protect our nerves, make cell tissues / hormones): we eat, make, store and excrete it.

Cholesterol exists in 2 forms:

  • unesterified or “free cholesterol” (UC)
  • esterified (CE)

The form of cholesterol determines how we absorb or store it.


Where does cholesterol come from?

  • Exogenous cholesterol – this refers to cholesterol that we eat.
  • Endogenous cholesterol – this refers to cholesterol that we make in our liver and other cells. Most of the time this is sufficient for our body’s needs.


Does eating cholesterol raise your cholesterol levels?

Eating dietary cholesterol has a very little impact on our blood or serum cholesterol levels.

Much of the cholesterol we eat is in the form of esterified cholesterol (CE). It is not absorbed and is excreted by our gut, leaving the body as stool.  For the body to absorb CE, it first has to de-esterify the cholesterol.

Eating more cholesterol (exogenous) is associated with decreased endogenous de novo cholesterol (cholesterol that you make), due to cholesterol homeostasis.

Extensive research has not shown evidence to support a role of dietary cholesterol in the development of cardiovascular disease. In fact, the recommendations of eating less than 300 mg of dietary cholesterol a day has been removed in the 2015–2020 Dietary Guidelines for Americans.


How does cholesterol move around?

Cholesterol is hydrophobic, which means it cannot move in water. It is carried around the water in liproproteins.

Liproproteins are produced in the liver and the intestines.

Lipoproteins = “boats” that carry around cholesterol and triglycerides. Their primary role is to transport triglycerides to muscle tissues that need them for energy (which gets oxidized into ATP).

Cholesterol = “cargo”.


Why do people think that cholesterol bad?

Atherosclerosis occurs when a sterol becomes engulfed in a macrophage in an artery wall.

Atherosclerosis or inflammation in the arteries occur when a apoB containing particle penetrates the endothelium, and gets retained in the subendothelial space, and an inflammatory response occurs, immune cells arrive, and “fixes” the apoB particle in the place.

Insults to the endothelium increases the permeability and the capacity for macrophages to take residence in the “space” in the subendothelium.  When inflammation occurs, it creates more space for more apoB carrying particles to get in and get “stuck”.

The only way sterols are carried in is when they are carried in by an apoB lipoprotein.

apoB lipoproteins can be found in VLDL, IDL, and LDL particle, but 95% of the apoB are in LDL-P.


How do we measure cholesterol levels?

Most doctors use a standard lipid test to measure LDL-C (cholesterol content in low density lipoprotein), HDL-C (cholesterol content in high density lipoprotein) and triglycerides (TG).

Total cholesterol (TC) refers to all the cholesterol molecules (in every single lipoprotein) in a deciliter of your plasma. This metric is assayed (i.e. directly measured). You can also directly measure HDL-C. LDL-C is then calculated based on a formula:

LDL-C = TC – HDL-C – TG/5

(TG/5 is an estimation of VLDL because a VLDL particle has five times the amount of triglycerides and 1/5th the amount of cholesterol).

Proper nomenclature is important – you can’t measure LDL, that’s just the lipoprotein. Tests measure LDL-C or LDL-P.

LDL-C is used as a way to assess risk of atherosclerosis. However, a better way to quantify risk of atherosclerosis is to measure LDL-P (or apoB) as this is the best predictor of adverse cardiac events. You can use apoB number to measure LDL-P because each LDL-P particle only has one apoB.

LDL-C is only a good predictor of cardiovascular risk if LDL-C is concordant with LDL-P.

Measuring C is also not reflective of the flux in the system – how much cholesterol there are in the cells and how much forward or reverse cholesterol transportation (i.e. movement) there is.



LDL-C refers to the amount of cholesterol in the low density lipoprotein. LDL-P refers to the number of LDL particles in a certain volume.

The higher the LDL-P, the higher the risk. If you want to stop atherosclerosis, you must lower the LDL-P number.

LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P.  There is no way to tell if LDL-P and LDL-C are concordant or discordant in patients without measuring both.

Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes (due to over-crowding of boats vs cargo). When someone suffers from metabolic syndrome, there is too much triglycerides in the body so the body has to produce more lipoproteins to carry the “cargo”.

The higher the level of serum triglycerides, the greater the likelihood of discordance between LDL-C and LDL-P (and apoB).

The greater the number (from 0 to 5) of inclusion criteria for metabolic syndrome, the greater the likelihood of discordance between LDL-C and LDL-P (and apoB).

If your “boats” can carry more “cargo”, you will need less “boats”.


How do you measure LDL-P?

Nuclear magnetic resonance (NMR) spectroscopy.


What about HDL?

HDL-P particles carry cholesterol from the subendothelial space back to the liver. (LDL particles carry cholesterol to the muscles and cells.)

HDL-P carry the apoA apoprotein. LDL-P carry the apoB apoprotein.

More HDL particles are good. Smaller HDL-P particles appear to be more protective than larger ones.

A higher HDL-C does not imply more HDL particles. Higher HDL-C levels are often driven by a disproportionate rise in HDL size, not HDL-P.

Therefore artificially increasing HDL-C with drugs isn’t going to fix the problem.

Low HDL-cholesterol and high triglyceride is four times more predictive of myocardial infarction (MI is the clinical term for heart attack), than high LDL-cholesterol.


What should you eat to “lower” your cholesterol risk?

  • Less sugar. Sugar or (sucrose, high fructose corn syrup) increases plasma levels of triglycerides, VLDL and apoB, and reduces plasma levels of HDL-C and apoA-I.
  • Less fructose. Fructose alone, has a similar but less harmful impact as that of fructose and glucose combined (i.e., sugar).
  • Foods such as shrimp and eggs contain a high amount of cholesterol are ok. Neither of them have negative effects on serum cholesterol levels and are actually beneficial in improving cholesterol levels.
  • Foods high in saturated fatty acids, however, may increase the risk of CVD due to the saturated fatty acid content.
  • Some argue that fat is ok, in the absence of sugar and starch.  Fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.
  • Replacing saturated fat (meat, eggs, dairy, cheese) with monounsaturated fat (olive oil, avocado, nuts) is reported to lower LDL-P.



Lipoprotein(a) is an LDL-like particle with additional apolipoproteins bound to it – apolipoprotein(a) and apolipoprotein B.

Elevated LP(a) is associated with increased risk of atherosclerosis, aortic stenosis, and venous thrombosis. If one has high Lp(a) and a bad family history or positive CAC, etc., he should lower all other risk factors (apoB and metabolic parameters like BP, uric acid, homocysteine, etc.) to the extent possible.

An Lp(a) test is one of the five most important blood tests you should ever do, says Dr Attia, and you only need to do it one time.

  • Optimal: <30 mg/dl
  • Borderline: 30-50 mg/dl (mine is 32.3 mg/dl)
  • Increased risk: >50 mg/dl

About 1 in 10 people have an elevated Lp(a), which is the greatest genetic driver of atherosclerosis. This is genetic so lifestyle interventions cannot lower your LP(a).

ADVICE: Anybody that has an elevated Lp(a) must immediately be screened for aortic stenosis, which is about a 2-4x increase in said patients



90-95% of apoB particles are LDL particles. So apoB is basically just another way of saying LDL particle count. The main structural protein that enwraps lipids in our plasma is Apolipoprotein B. ApoB is made in the liver and small intestine. The causal relationship between apoB and atherosclerosis is very strong. Lowering apoB by 50% is good.  ApoB is a marker of all atherogenic particles including, if present, Lp(a). The more apoB particles you have, the more problems you have. Most people with low HDL cholesterol also have high apoB, which is what’s driving atherosclerosis.

  • Optimal: <80 mg/dl
  • Borderline: 80-120 mg/dl (mine is 0.91 g/L)
  • Increased risk: >120 mg/dl

Can take drugs (e.g. PCSK9 inhibitors) or to the lower the amount of lipoprotein, you can to lower the amount of cargo they have to carry. i.e.means lowering triglycerides and lowering cholesterol. To lower cholesterol, you need to reduce the synthesis of cholesterol, or reduce the reabsorption of cholesterol. NOTE: It does NOT include reducing the intake of dietary cholesterol since that features very little into how much cholesterol you have since most of that is not absorbed.


How to test for LP(a), apoA and apoB in Singapore

You can go directly to Quest Diagnostics to do the lipoprotein (a), apolipoprotein a1 and apolipoprotein b blood test.

Most GPs will not have heard of these tests but if you would prefer to do this via a GP so that the GP can interpret the results for you, you can go to Tucker Medical.


Insulin Resistance and LDL

Insulin resistant patients are at higher risk of getting atherosclerotic disease, because they tend to have very high LDL-P and apoB. High triglyceride / HDL cholesterol ratios tend to correspond to high apoB numbers.

Cholesterol in the Brain

Serum (blood) cholesterol has nothing to do with cholesterol in the brain. The brain makes all the cholesterol that it needs. There are no LDL particles delivering cholesterol to your brain. LDL particles do not fit through the blood brain barrier (apoB is too big). apoE is the protein transporter in the brain and this is what moves cholesterol around the brain.



YouTube: Dr Peter Attia: Redressing Dietary Guidelines
YouTube: Dr Peter Attia – An Advantaged Metabolic State: Human Performance, Resilience & Health
YouTube: Dr Peter Attia – The Straight Dope on Cholesterol Slides can be found here.
YouTube: Dr Paul Mason – Ketogenic Diets and Cholesterol
Peter Attia ‘s Website on Cholesterol

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