First anniversary of RALP, my PSA has crept up from 0.02 to 0.04 (GS 4+5=9, pT3b). During this period, I was taking monthly tests except during the recent lock-down when there was a 3.5 months gap. Prior to the latest test I didn't take any medicine or supplement, statines included, for 8 days. Analyzing my test results I found an unbelievably high correlation of PSA to the triglycerides count as computed from cholesterol, i.e. 5*(Total - HDL -LDL). The correlation coefficient of 97.8%, (R^2=0.956) is very HIGH. Furthermore, accounting for the quantization errors of the PSA, (0.02, 0.03, 0.04) one even can suspect a perfectly linear relation. Another interesting finding was that the PSA to time correlation is, by a very small margin, in favour of linear than exponential occurrence. By wishful thinking this can play-down suspicions for a typical BCR, where the exact opposite is the rule.
I searched and found this paper:
"Serum Lipid Profile and Risk of Prostate Cancer Recurrence: Results from the SEARCH Database", 2014, cebp.aacrjournals.org/conte... concluding to:
"Conclusions: Elevated serum triglycerides were associated with increased risk of prostate cancer recurrence. Cholesterol, LDL, or HDL were not associated with recurrence risk among all men. However, among men with dyslipidemia, elevated cholesterol and HDL levels were associated with increased and decreased risk of recurrence, respectively."
My case seems to disagree with the above claim regarding total-C (cor. coef. of 89.6%), but shares a very weak agreement with HDL by a negative cor. coef. of -9.3%.
My imminent project is to try lowering total-C (having the wrong gene) and especially triglycerides in order to see if spotted correlation is maintained, that is, can stop the advancement of PSA. Will let you know in time.
Thanks, When I was at the 0.02 mark I was also taking an Ω3 supplement (180 EPA/120 DHA). Then read about its possibly negative effect on PCa (2014 study) and stopped it.
I have started it again now just to test. The consensus is that it lowers the triglycerides.
As to the PCa side of things there have been two subsequent studies (2017 and 2019) disputing earlier findings. Medical studies are like financial analyses. All eventualities are covered!
I see TG as a proxy for blood sugar, and it makes sense there is a correlation to BCR since PCa feeds off glucose and higher insulin levels are associated with higher IGF-1 growth factor. I have persistently high LDL around 135 and TC around 200, but through diet and exercise maintained TG around 70. I’ve been able to lower TC by periodically taking niacin. I found LDL though is tough to lower, one thing that did help was removing sources of trans-fats like natural peanut butter. Oddly when I tried an all-legume diet, LDL shot up 20 points.
As I have written I have the gene for hypercholesterolemia. I have been following my stubborn cholesterol for almost 4 decades. I was very surprised to find out, just after RP, that it went to an all times minimum. Now it is going up.
I am keeping niacin as plan B. Were you taking the slow release version (flush free)? I read that it is more prone to liver damage as compared to 3 times per day of the fast absorption one.
I just take the straight 50 or 100mg tablets at bedtime with water. I do this for about three weeks and retest. If TC>200, I take it for another two weeks and retest. Usually, the first round lowers TC about 10%. One other thing I found that helps is to not eat anything about 3 hours before bedtime as I’ve heard the body makes most of its cholesterol during sleep. Yes, my numbers dropped right after Brachy to all time lows, TC to 180 and TG to 44. I attribute it to the fasting leading up to the procedure.
There should be a typical servo system active there in. Production, demand and a governor to stabilize the loop. I am anxious to see whether I can tweek it somehow.
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Testosterone Therapy Does Not Increase the Risks of Prostate Cancer Recurrence or Death After Definitive Treatment for Localized Disease
Here we go.......
