Sugar Intake, Cholesterol, and Liver Metabolism: Rethinking Cardiovascular Risk

Have you ever been told your cholesterol is high even though you eat very little fat? Or followed advice to cut fats, only to find your blood results barely change? If so, you’re not missing something.

Cholesterol is often treated as the villain, yet biologically it is a vital molecule. It stabilises cell membranes, supports hormone production, enables bile synthesis, and plays an essential role in brain and nervous system function. Importantly, most cholesterol is produced by the body itself, not absorbed from food.

So why does cholesterol rise? In many cases, the answer lies not in fat intake, but in carbohydrate metabolism and insulin signalling. Frequent sugar intake leads to repeated insulin spikes. Elevated insulin drives the liver to convert excess glucose into fatty acids and triglycerides. These are packaged into very-low-density lipoproteins (VLDL) and released into the bloodstream.

As VLDL particles are metabolised, low-density lipoproteins (LDL) appear. Under conditions of chronic inflammation, oxidative stress, or micronutrient deficiency, LDL particles become more vulnerable to oxidation. Oxidised LDL is the form most strongly associated with endothelial damage and plaque formation. In this context, cholesterol is not the problem, it is the messenger, reflecting metabolic strain.

One test that helped me understand this more clearly was the Glycan Age test. It assesses patterns of protein glycosylation, which closely reflect chronic inflammation and biological ageing. Lower glycation indicates better metabolic regulation and lower inflammatory load. My results suggested a biological age closer to 40, despite being in my fifties. This reinforced the idea that reducing glycation and inflammation, rather than avoiding fat, supports healthier cardiovascular signalling.

This naturally raises a broader question. Are we really meant to fear every slice of cake? Or is the issue the background metabolic environment, constant sugar exposure, insufficient recovery, ongoing low-grade inflammation? Pleasure itself is not the problem. Context, frequency, and metabolic resilience matter far more than rigid restriction.

Traditional medical systems echo this view in their own language. In Traditional Chinese Medicine, elevated cholesterol-like patterns are often linked to Liver Qi stagnation and internal dampness, states associated with impaired flow, emotional stress, overconsumption of sweet or rich foods, and reduced metabolic movement.

Ayurveda describes a similar process through imbalance of Meda Dhatu, the body’s lipid tissue, often driven by weakened Agni and excess sweetness in the diet. In both systems, the liver is central: when transformation and clearance slow down, accumulation follows. The solution is not suppression, but restoring movement, digestion, and metabolic clarity.

From a modern perspective, this aligns closely with liver physiology. The liver synthesises cholesterol, converts it into bile acids, and clears lipid remnants from circulation. When it is burdened by excess sugar, alcohol, toxins, or chronic inflammation, cholesterol handling becomes inefficient.

Rather than obsessing over lowering cholesterol numbers, a more meaningful question is what metabolic stress the liver is responding to, and how that environment can be gently corrected. Cholesterol does not act in isolation, it responds to digestion, energy production, and inflammation. Which of these might deserve attention first?