How it all started

Dr. Costantini and his team first started using high dose thiamine intramuscularly in two conditions characterized by fatigue as a key symptom and which share symptoms similar to thiamine deficiency: Ulcerative Colitis (2010) and Multiple Sclerosis (2011). The response to treatment not only had a beneficial effect on fatigue but unexpectedly also lead to an improvement of other symptoms. Blood thiamine levels were normal, so the authors concluded that the mechanism by which thiamine worked was not by improving a deficiency status.

Given these observations, the team then turned to neurodegenerative diseases in which fatigue was an important symptom, to test the hypothesis whether fatigue pathogenesis in neurodegenerative diseases was similar and would respond to high dose thiamine. They started with Spinocerebellar ataxia type 2 (2013). Again, not only fatigue but also other symptoms improved. Given these findings, Dr Costantini’s team wondered whether the mechanism by which thiamine acted was targeting the diseases themselves.

In 2013, the team eventually tested this hypothesis in Parkinson’s Disease (PD), as they noted that hereditary Parkinson’s Disease share common genetic features with Multiple Sclerosis.

The remarkable results in PD have been described briefly in Studies on high-dose vitamin B1 in Parkinson’s Disease in this section.

This was the beginning of a large clinical practice experience marked by the administration of high dose thiamine to an estimated over 2,500 Persons with Parkinson’s Disease (PwP), witnessing significant symptom improvement without reports of adverse reactions in most of them. The dose of thiamine had to be titrated to each patient to find the right dose which would at the same time be efficacious and cause no overdose symptoms.

Text author: Sergio Pièche
Page updated - 24/04/23