cholesterol, statin, sugar

Sugar Changes Your Cholesterol

Cholesterol is a massive topic. However, it is not the sole cause of heart disease.

Naturally, the question then becomes, why is the focus on cholesterol so intense?

We can measure it

As I described in a detailed whitepaper “Avoiding Insulin In Type 2 Diabetes”, blood sugar is the sole focus for most in the medical community who manage this disease state. Giving insulin lowers blood sugar. However, insulin orchestrates a host of growth-related signals, including lipid synthesis. Unchecked growth can lead to cancer even though blood sugar goes down by increasing insulin.

We easily measure cholesterol and often find it in plaques contributory in cardiovascular pathologies. Then, we prescribe statins to lower cholesterol (mainly “bad”  LDL Cholesterol or LDL-C) – to the tune of billions of dollars annually spent.

Guess what though?

LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature”


A big bomb to drop for sure, and I plan on adding cholesterol as a topic in the whitepaper series to unpack the details.

For now though, how does sugar factor in?


Lipoproteins transport cholesterol (and a few other passengers) around the bloodstream since cholesterol is not water soluble. LDL is low-density lipoprotein, HDL is high-density lipoprotein.

Sugar Changes Proteins

We know sugar changes other proteins in the body. For example, in diabetes, we measure in the lab HbA1c (hemoglobin A1c) as a proxy for average blood sugar over the past 3 months. Another name for this test is glycosylated hemoglobin. 

“Formation of linkages with glycosyl groups, as between D-glucose and the hemoglobin chain to form the fraction hemoglobin AIc, the level of which rises in association with the elevated concentration of D-glucose in blood concentration in poorly controlled or uncontrolled diabetes mellitus”.2

Basically, sugar attaches to and modifies proteins. At normal exposures to sugars, all is well. However, at excessive sugar levels, increased glycation occurs leading to Advanced glycosylated end products (AGE).

AGE is the result of years of accumulated glycated damage to molecules that are not replaced regularly but have a low turnover rate. The primary examples are the matrix protein complexes and chromosomal DNA, which are subject to irreversible corruption that can cause genetic mutation

Sugar changes lipoproteins

So, I admittedly used cholesterol in the post title because if I put lipoproteins, not everyone would relate that to cholesterol. You are now an expert though!

Lipoproteins are also influenced by excessive sugar.

A great study demonstrated this comparing 200 patients diagnosed with myocardial infarction caused by coronary atherosclerosis as case group and 230 healthy individuals as a control group. They analyzed and contrasted the levels of blood lipid and glycosylated lipoprotein (those modified by sugar | G-LDL, G-HDL) between the different groups.

Here is a great quote from the study:

“In recent years, the role of glucose metabolism in the development of atherosclerosis has received more and more attention. On the one hand, hyperglycemia can directly act on vascular cells. It can promote the combination of modified lipoprotein and macrophage scavenger receptors to form foam cells which could promote the formation of atherosclerosis. On the other hand, hyperglycemia can cause nonenzymatic reactions of glucose with longer‐lived molecules, resulting in stable early glycosylation products. Then, they undergo a series of rearrangements, dehydration, and cleavage reactions to produce stable glycation end products, including G‐LDL, G‐HDL, and other glycosylated proteins. Glycosylated lipoprotein also promotes lipoprotein oxidation. LDL and HDL with glycosylated or oxidative modification cannot be combined with normal receptors due to structural changes. Modified lipoproteins can only intake cells through the scavenger receptor and cannot downregulate scavenger receptor expression The modified lipoprotein can continuously ingest cells through the scavenger receptor, cause cholesterol accumulation, and eventually result in the formation of atherosclerosis.4

Synopsis: those with heart attacks had higher levels of sugar-changed lipoproteins. It wasn’t the cholesterol levels. And these modified proteins precipitated the accumulation.

Take away

Don’t stop your statin just yet, that should always involve the doc.

However, this is empowering information. 

Reducing blood sugar levels improves cardiovascular health. Reducing carbohydrates (especially those that are highly processed – espescially grains) and anything with added sugar is a great start.

If you can couple that with not being exposed to artificial cholesterol reduction (and associated consequences – will explain in future posts) via statins, you experience a total win-win.

Especially since low cholesterol is associated with a higher risk of mortality.

Changes in cholesterol levels in either direction to low cholesterol or persistently low cholesterol levels were associated with higher risk of mortality. Particularly, spontaneous decline in cholesterol levels may be a marker for worsening health conditions.

Association of change in total cholesterol level with mortality: A population-based study
Su-Min Jeong5

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