“Table 2 details the associations between the use of cholesterol-lowering medications and liver cancer overall. In the adjusted analysis, ever use of cholesterol absorption inhibitors was associated with a reduced risk of liver cancer (OR, 0.69; 95% CI, 0.50–0.95). When examined according to recency of use, past use of cholesterol absorption inhibitors was associated with reduced risk (OR, 0.52; 95% CI, 0.33–0.83), but current use was not (OR, 0.92; 95% CI, 0.59–1.42). An examination of cumulative dose identified no stronger effects at higher doses. In contrast to cholesterol absorption inhibitors, ever use of bile acid sequestrants was associated with increased risk of liver cancer (OR, 5.31; 95% CI, 3.54–7.97), which was most evident for current use (OR, 13.08; 95% CI, 6.98–24.49) and was most pronounced at the lowest cumulative dose (OR, 12.30; 95% CI, 5.42–27.90). No associations were observed between the use of fibrates, niacin, or omega-3 fatty acids in adjusted analyses, overall, by recency of use, or by dose. As anticipated, ever use (OR, 0.65; 95% CI, 0.58–0.74) and current use (OR, 0.61; 95% CI, 0.54–0.69) of statins were associated with reduced risk of liver cancer.”
Query: what is the relationship in human health terms, between APOB levels and cancer risks?
Great question — ApoB (apolipoprotein B) is mostly thought of in the context of cardiovascular disease, but its relationship with cancer risk has been getting more attention recently. Here’s what is known so far:
What ApoB Represents
ApoB is a structural protein present on atherogenic lipoproteins (LDL, VLDL, IDL, Lp(a)), and it essentially reflects the number of these particles in circulation.
Clinically, ApoB levels are a more accurate measure of atherogenic burden than LDL-C.
Evidence on ApoB and Cancer
Epidemiological findings
Large population studies (e.g., UK Biobank, EPIC cohort) suggest mixed associations between ApoB and cancer.
Some studies show higher ApoB associated with increased risk of certain cancers, especially colorectal, breast, and prostate cancers.
Others show inverse or null associations (e.g., lower ApoB linked to higher risk of some cancers, possibly due to reverse causation from cancer-related metabolic changes).
Mendelian randomization studies
Genetic proxies for higher ApoB (lifelong exposure) show increased risks of some cancers, but evidence is weaker than for cardiovascular outcomes.
Importantly, when ApoB-associated genes are adjusted for BMI, insulin resistance, and triglycerides, the direct effect on cancer risk often diminishes → suggesting that metabolic dysfunction may be the real driver.
Mechanistic insights
Hyperlipidemia and tumor growth: Cancer cells require lipids for membranes and signaling; ApoB-containing lipoproteins may supply this.
Oxidized LDL and inflammation: ApoB-rich particles can drive chronic inflammation and oxidative stress, which promotes carcinogenesis.
Metabolic syndrome link: Elevated ApoB often travels with insulin resistance, hyperinsulinemia, and obesity — all strong cancer risk enhancers.
Low ApoB in cancer: Some cancers lower circulating lipids (cancer cachexia, tumor lipid uptake), which can confound observational findings.
Current Understanding
High ApoB → generally increases cancer risk indirectly, through obesity, insulin resistance, and systemic inflammation.
Low ApoB → sometimes observed in advanced or preclinical cancer, but this is likely a consequence of tumor metabolism, not a protective factor.
Independent role: The causal evidence that ApoB itself directly drives cancer is weaker than for cardiovascular disease. ApoB may be more of a biomarker of unhealthy metabolic milieu than a direct oncogenic factor.
Summary:
High ApoB is linked with higher cancer risk, mainly via its associations with metabolic syndrome, chronic inflammation, and lipid supply for tumors.
Low ApoB can sometimes be observed in patients with existing or undiagnosed cancers, reflecting tumor-driven lipid metabolism.
The relationship is bidirectional and complex, with strongest evidence for cancers like colorectal, breast, and prostate.