I dont think anyone would ever in a million years of thought PC and CFS can be caused by the same thing.
Except maybe for those of us who have ME/CFS and have had prostate problems?
I thought the presentation was excellent. It makes such a difference to actually see and hear this data being discussed at mainstream medical conferences.
It also raises a lot of questions for me :
I think we picked him up right that anyone can contract XMRV - not just those with the RnaseL etc mutation suggesting that the 4% estimated prevalence in the wider population may be correct but likely to grow.
Presumably then, only those with the mutation develop pathology in the form of PC, ME/CFS or other?
It also suggests that all males with ME/CFS (who presumably have the RnaseL mutation) are at risk of developing prostate cancer in response to androgens.
What is confusing is that there has been discussion here about the often reported male/female ratio of those with ME/CFS versus autism and the hypothesised protective effect of androgens.
Many males with ME/CFS report androgen deficiencies even to the point of developing gynomastia. In my own case I've seen total T decline from 25nmol/l to 7.5 (normal all age range approx 10-30nm/l) and my apparently prostate related problems (slight pain, difficulty urinating etc) co-incided with low T and have now largely resolved.
While it was reported that XMRV is androgen sensitive (androgens stimulting growth, replication and oncogenes) it has also been reported that XMRV replication also responds to cortisol and thrives in a high cholesterol environment. Given that all steroid hormones are derived from cholesterol there may be a number of pathways through which cholesterol can impact.
While the talk referred to Testosterone and DHT, they have very different characterisics and DHT has long been blamed for benign prostatic hyperplasia. As we (males) age, less testosterone tends to be produced, and less remains free (biologically active) becoming increasingly converted to DHT or aromatised to estrogen. DHT is many
times more powerful than testosterone but is not active in T target tissues such as lean muscle tissue. Instead it tends to endow us with such attractive features as enlarged prostate, male pattern baldness, ear hair etc.
steroid hormones stimulate XMRV to replicate in all target tissues
causing ME/CFS. However, it is only the very powerful DHT that stimulates XMRV in prostate tissues causing initially BPH and eventually PC. Maintaining the balance of free testosterone against DHT may still be protective?
On a lighter note :
"One piece of information that stuck in my mind with regards the cancer part of the talk is that it mentions that frequent ejaculation is important in helping to stave off prostate cancer. I can think of a few rude names that type of therapy may get called."
I'd like to suggest that it should be named after the man who has done so much to popularise the notion of "Chronic Fatigue"
Step forward Professor ...... Jerkoff!