University of Oxford New study finds even moderate alcohol consumption may increase brain damage, potentially through iron overload. MEEOM’s® Pivotal Breakthrough Made In Alcohol Addiction Treatment. The Famous 3 Month Alcohol Free Treatment Solution. @New Formula!
Alcohol consumption, including at low levels, was observationally associated with higher brain iron in multiple basal ganglia regions. There was some evidence supporting a causal relationship between genetically predicted alcohol consumption and putamen and hippocampus susceptibility, although this did not survive multiple testing correction. Alcohol was associated with both higher liver iron, an index of systemic iron load, and genetically predicted AUD associated with genetically predicted serum iron markers. Brain iron accumulation in drinkers was only partially mediated via higher systemic iron. Markers of higher brain iron (higher susceptibility) were associated with poorer executive function and fluid intelligence and slower reaction speed.
The accumulation of iron in the brain we observed in moderate drinkers overlaps with findings of an observational study in AUD. Higher putamen and caudate iron levels were described in a small study of males with AUD (n = 20) [1]. These individuals were drinking substantially more than our sample—a mean of 22 standard drinks per day (>37 units daily). In contrast, we observed associations in those drinking just >7 units per week. A recent phenome-wide association study of quantitative susceptibility in the same dataset reported significant associations in basal ganglia regions with higher frequency binge drinking [2]. Regional heterogeneity in iron concentrations is well described although the aetiology is not understood [3]. The basal ganglia, including the putamen [4], have some of the highest iron concentrations in the brain and suffer the greatest age-related increases [5]. Interestingly, we found significant alcohol-age interactions with susceptibility, suggesting that alcohol may magnify age effects on brain iron. We are mindful however that within UKB, changes with age could represent a cohort effect. In this sample, associations with susceptibility and T2* measures were observed at lower alcohol intakes in females. In haemochromatosis, females are relatively protected against the clinical manifestations of iron overload through menstrual blood loss. The majority of our included sample, however, (70%) was postmenopausal and menopause status did not alter alcohol–brain iron associations. Sex differences in alcohol metabolism therefore may be responsible. These findings do not support current UK “low risk” drinking guidelines that recommend identical amounts for males and females. We found some support for a causal relationship between alcohol consumption and susceptibility in the putamen and hippocampus, and between AUD and putamen susceptibility in MR analysis. Although these associations did not survive multiple comparisons correction, they are in the same direction as the highly significant observational associations. Associations between genetically predicted alcohol and susceptibility in other regions were not significant. We suspect this results from our limited power to detect small associations despite the sample size, given that the genetic instruments explain less than 1% of the phenotypic variation in alcohol consumption. Furthermore, weak instrument bias, in the direction of the null, may be contributing. Using UKB for our calculations, about one third of SNPs we used to instrument alcohol consumption had F statistics <10.
Our MR results provide evidence for a causal role of AUD in increasing serum iron and transferrin saturation, a sensitive marker of iron overload. While genetically predicted alcohol use was not significantly associated with ferritin, this mirrors findings in early haemochromatosis, where ferritin levels can be normal and transferrin saturation is the earliest marker of iron overload.
To our knowledge, this is the largest study of moderate alcohol consumption and multiorgan iron accumulation. It is also the first study to use MR to investigate causality of alcohol on serum and brain iron.
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References1. Juhás M, Sun H, Brown MR, Mackay MB, Mann KF, Sommer WH, et al. Deep grey matter iron accumulation in alcohol use disorder. Neuroimage. 2017;148:115–22. doi: 10.1016/j.neuroimage.2017.01.007. pmid:28065850
2. Wang C, Martins-Bach AB, Alfaro-Almagro F, Douaud G, Klein JC, Llera A, et al. Phenotypic and genetic associations of quantitative magnetic susceptibility in UK Biobank brain imaging. Nat Neurosci. 2021.
3. Ramos P, Santos A, Pinto NR, Mendes R, Magalh?es T, Almeida A. Iron levels in the human brain: a post-mortem study of anatomical region differences and age-related changes. J Trace Elem Med Biol. 2014;28(1):13–7. doi: 10.1016/j.jtemb.2013.08.001. pmid:24075790
4. Mcallum EJ, Hare DJ, Volitakis I, Mclean CA, Bush AI, Finkelstein DI, et al. Regional iron distribution and soluble ferroprotein profiles in the healthy human brain. Prog Neurobiol. 2020;186:101744. doi: 10.1016/j.pneurobio.2019.101744. pmid:31870805