Statins do not increase the risk of amyotrophic lateral sclerosis

Statins do not increase the risk of amyotrophic lateral sclerosis

A new study found no association between statin use and an increase in ALS incidence. This result is in line with some previous studies and provides strong evidence that denies the possible association between statin uptake and disease induction.

Amyotrophic lateral sclerosis (ALS) is a paralytic, heterogeneous and progressive disease characterized by the degeneration of both upper and lower motor neurons. Several studies about the effects of statin drugs on the risk of ALS showed contradictory results and evidence for this is inconclusive.

Statins are a division of medicine that can inhibit cholesterol synthesis in initial steps by competitively binding to the
active site of HMG-CoA reeducates enzyme. The effect of statins as first-line agents in the prevention of cardiovascular diseases is supported by clinical shreds of evidence, they do this by controlling the plasma level of lipids. Although these drugs are a type of medicine with a safety profile they are widely used so it has always been serious concerns about their adverse effects that might accommodate their proven beneficial effects.

Hyperlipidemia is always known as a risk factor for the incidence of neurological disorders, but several studies reported adverse effects of statin use. While statins are believed to be a protective factor for neurodegeneration diseases such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, but the studies about statin’s effect on ALS have shown contradictory results. So a meta-analysis on previous studies to clarify the association between statin use and risk of ALS.

The rate ratio and 95% confidence interval (CI) were used for association measures in case-control and cohort studies. After full-text and abstract review, data from 8 studies with a total of 547,622 participants and 13,890 cases of ALS were entered in the present meta-analysis. We combined eight studies using a random-effect model and the RR for drug users among groups was 0.98 (95% CI 0.80–1.20) which indicates no association between statin and incidence of ALS. Also, high heterogeneity was detected across the studies (Q value = 26.62, P = .00; I2 = 72.71%). 

Together all these contrasts upon the possible effect of statins on ALS incidence justify more studies in this subject. In our meta-analysis study, we found no association between statin use and an increase in ALS incidence. This result is in line with some previous studies and provides strong evidence that denies the possible association between statin uptake and disease induction. However, further studies should be conducted to clarifying the exact mechanism of lipid profile and statins in the ALS progression.

Contact: Fardin Nabizadeh

Image: Public domain

Reference: Nabizadeh, F., Balabandian, M., Sharafi, A.M. et al. Statins and risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis. Acta Neurol Belg (2021). https://doi.org/10.1007/s13760-021-01753-8