Inflammation, Metabolism, and the Statin Question 

Rethinking Cholesterol… 

Cholesterol has been turned into a villain, but the science tells a far more complex story. LDL and HDL are not cholesterol at all, statins are not the benign panacea they are marketed as, and the continual lowering of ‘safe’ cholesterol thresholds has expanded the pool of people labelled as patients. The real drivers of vascular damage are inflammation, oxidation, high glucose and high insulin; and cholesterol is often acting as a repair molecule, not a threat. 

Cholesterol is a structural molecule required for life. It forms the backbone of cell membranes, is the precursor to steroid hormones, and is essential for vitamin D and bile acid synthesis. The body manufactures most of its cholesterol internally, tightly regulating levels according to physiological need. This is not the profile of a toxin. It is the profile of a foundational nutrient. 

A persistent misconception is that LDL is ‘bad cholesterol’ and HDL is ‘good cholesterol’. In reality, neither LDL nor HDL is cholesterol. They are lipoproteins which are transport particles that just carry cholesterol, triglycerides, fat‑soluble vitamins, and antioxidants around the body to the point of need. 

LDL delivers cholesterol to tissues that need repair, hormone synthesis, or membrane support. HDL returns excess cholesterol to the liver. Both are part of a dynamic transport system, not independent actors. 

The problem is not LDL itself, but oxidised LDL, a damaged particle created by inflammation, high blood glucose, smoking, and oxidative stress. Oxidised LDL is what the immune system reacts to, initiating arterial inflammation. 

GPs usually tell my patients that cholesterol is the cause of atherosclerosis, and that if they do not take statins they could die of a heart attack. But the evidence shows that inflammation and oxidation are the initiating events. LDL becomes problematic only when oxidised, and this oxidation is strongly associated with high blood glucose, high insulin, smoking, and systemic inflammation. 

In this context, cholesterol often acts as a repair molecule, arriving at sites of endothelial injury to stabilise damaged tissue. Blaming cholesterol for appearing at the scene of inflammation is like blaming firefighters for being present at a fire, just because they are usually on site. 

Over time, recommended cholesterol targets have repeatedly shifted downward and the acceptable ‘safe’ level of cholesterol has been consistently lowered, with guideline committees repeatedly redefining what counts as ‘high’ cholesterol. This lowering of LDL targets creates a moving threshold that brings more of the population into the treatment net. 

More people are labelled as now ‘high risk’, even when their cholesterol levels would have been considered normal a decade ago. And statin prescriptions increase, not necessarily because of worsening population health, but because the definition of risk has broadened. 

Statins do lower LDL, but LDL reduction is not the same as reducing mortality. For people without established cardiovascular disease, the absolute benefit is small. Meanwhile, side effects [muscle pain, fatigue, cognitive effects, and impacts on glucose metabolism] are widely reported. 

An important nuance is that current evidence suggests ApoB-containing lipoproteins are not merely innocent bystanders in atherosclerosis. ApoB [apolipoprotein B] is a structural protein found on LDL and related lipoproteins, and because each particle carries one ApoB molecule, ApoB levels act as a marker of the number of circulating LDL-type particles that may enter and become trapped within damaged arterial walls, particularly in the presence of inflammation and metabolic dysfunction. So, for many individuals, addressing inflammation, diet, metabolic health, smoking, and physical activity offers far greater benefit than just medicating cholesterol transport particles. 

I do not recommend that people simply stop taking prescribed medication, but it can be true that a conversation with a GP about deprescribing or alternatives is not always productive. Many clinicians work under time pressure, guideline pressure, and medico‑legal pressure, and these constraints can make nuanced discussions difficult. No one should discontinue medication without understanding the underlying issues, improving their health at a foundational level, or at the very least taking an active interest in the research and the physiology involved. That said, I cannot leave this subject without recommending herbs for heart health. A growing body of research explores how certain botanicals influence inflammation, oxidative stress, and endothelial function. Several herbs contain bioactive compounds that interact with the same inflammatory and oxidative pathways implicated in vascular injury. 

Turmeric has been shown to modulate NF‑κB signalling and reduce oxidative stress markers in human studies. Ginger demonstrates similar effects, with evidence of improved endothelial‑dependent vasodilation. Rosemary  contains rosmarinic acid and carnosic acid, both potent antioxidants that help limit lipid oxidation.  

Herbs such as hawthorn and garlic have been studied for their ability to support endothelial nitric oxide production, improving vascular tone and reducing the inflammatory burden on vessel walls. Meanwhile, demulcent herbs like plantain leaf and marshmallow root offer mucilage compounds that soothe irritated epithelial tissues, including the delicate endothelium lining blood vessels. 

Vascular health is not about cholesterol numbers but about reducing lifestyle and dietary factors which increase inflammation, oxidative stress, and metabolic strain which are the true drivers of endothelial injury.