J Alzheimers Dis. 2018;64(2):363-366. doi: 10.3233/JAD-180266.
Itzhaki RF1,2, Lathe R3.
1 Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford, UK.
2 Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester, UK.
3 Division of Infection and Pathway Medicine, University of Edinburgh, Little France, Edinburgh, UK.
Herpes Virus => deactivates the Vitamin D Receptor => Less Vitamin D to Tissue => Disease
Candidate solutions include
1) Treat Herpes
2) Increase the activation of the Vitamin D receptor (resveratrol, etc,)
3) Give massive doses of vitamin D
- Herpes (Cytomegalovirus) downregulates the vitamin D receptor by 8X – Jan 2017
- Herpes virus infection while pregnant increases Autism risk by 2 X (Vitamin D not mentioned) – Feb 2017
- Many Infectious diseases (virus) treated and prevented by Vitamin D – review July 2009
- Vitamin D can inhibit enveloped virus (e.g. Corona, Herpes, Zoster, Epstein, Hepatitis, Ebola) – March 2011
- Resveratrol gets vitamin D to cells even if poor vitamin D receptor
- Hypothesis:Vitamin D Epstein-Barr interaction increases MS risk – Sept 2011
- Epstein-Barr is similar to HPV1
- Multiple Sclerosis much more likely if poor Vitamin D Receptor – several studies
Three articles have very recently appeared that are of especial relevance to the causes of dementia and its potential treatment.
The first two (Tsai et al., published in PLoS One in November 2017
- 10.1371/journal.pone.017159 PDF online
Chen et al., published in the January/February 2018 issue of Journal of Clinical Psychiatry
demonstrate an increased risk of subsequent senile dementia (SD) development in patients with acute varicella zoster (herpes zoster) infection.
These articles present data highly relevant to the third, and most important, paper-by Tzeng et al., published online in the journal Neurotherapeutics at the end of February 2018
. These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. It should be stressed that no investigations were made on subjects already suffering from SD, and that those treated were the few rare cases severely affected by HSV. Nonetheless, antiherpetic medication prevented later SD development in 90% of their study group. These articles provide the first population evidence for a causal link between herpes virus infection and senile dementia.