Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.
A new study shows that alcohol related cerebellar degeneration can trigger gluten sensitivity in certain genetically susceptible individuals.
Celiac.com 11/04/2013 - The mechanisms of cerebellar degeneration associated to prolonged and excessive alcohol intake remain unclear. Additional or even alternative causes of cerebellar degeneration are often overlooked in suspected cases of alcohol-related ataxia.
A team of researchers recently set out to investigate the prevalence of gluten-related serological markers in patients with alcohol-related ataxia, and to compare the pattern of brain involvement on magnetic resonance imaging between patients with alcohol and gluten ataxias.
The research team included Stuart Currie, Nigel Hoggard, Matthew J. R. Clark, David S. Sanders, Iain D. Wilkinson, Paul D. Griffiths, and Marios Hadjivassiliou.
They are variously affiliated with the Academic Unit of Radiology at the University of Sheffield, and with the Department of Gastroenterology, and the Department of Neurology of Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, United Kingdom.
For their study, the team used a retrospective review of patients attending an outside clinic to identify patients diagnosed with alcohol and gluten ataxias.
The team recorded HLA genotype and serological markers of gluten-related disorders. They also conducted cerebellar volumetry, MR spectroscopy and voxel-based morphometric analyses on the patients and compared the results to matched control data.
Results from 904 registered patients showed 104 patients with alcohol ataxia, and 159 patients with gluten ataxia. The data also showed that 61% of the patients with alcohol ataxia, and 70% of the patients with gluten ataxia had HLA DQ2/DQ8 genotype compared to just 30% of people with healthy local blood donors.
Interestingly, 44% of patients with alcohol ataxia showed antigliadin antibodies compared to 12% in the healthy local population and 10% in patients with genetically confirmed ataxias. None of the patients with alcohol ataxia and antigliadin antibodies had celiac disease, while 40% in patients with gluten ataxia had celiac disease.
Patients with alcohol ataxia who had antigliadin antibodies showed patterns of structural brain abnormality that were different from gluten ataxia, but were the same as those common in alcohol ataxia.
The results show that alcohol related cerebellar degeneration can trigger gluten sensitivity in certain genetically susceptible individuals. Such sensitivity might be caused directly by the cerebellar impact of alcohol, but factors other than duration and amount of exposure to alcohol may also be responsible for the resulting sensitivity to gluten.
Further study is needed to nail down the exact mechanisms at work here, but this is certainly an interesting study.