Disregarding the discussion as whether to temporarily discontinue or not discontinue in fht efirst place... Purportedly some substances may "mask" PSA. I believe the general rule of thumb is on 5-ARIs like Avodart (Dutasteride) you are supposed to double the PSA reading to get the "real" PSA?
In addition to or instead of 5-ARIs, is there any data out there that confirms how long you should discontinue each substance prior to a blood test to get a more realistic PSA reading? I believe one of the more common supplements believed to mask PSA is curcumin for example.
The other side of the coin is I guess if you are beyond salvage treatment, then you probably shouldn't change what you are taking as you can still see relative changes in PSA levels over time. But the issue is if you are at a point prior to salvage RT, seems to me taking anything that masks PSA may mistakenly cause a false sense of security to delay initiating salvage treatment to a point that is later than optimal.
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jazj
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Fascinating article Tall, guess this is one of the reasons Kishan had me stop any kind of antioxidants during radiation. He said they could interfere with the treatment.
With a half life at the ballpark of 5 weeks it will take months for Avodart to wash out, provided you have been on it long enough to reach steady state. It isn't a surprise that the daily dosage of Avodart is so little (0.5mg) as it stays in the body and builds up gradually for months if not years. I have tested curcumim in me and didn't find any "masking" effect.
There is a misconception that Avodart "masks" PSA. That is not true. It actually reduces PSA values for real. On average, it reduces PSA by 50% in most men.
A recent randomized, double-blind study by Moore et al. (2017) studied the effect of Avodart on PCa tumor size by direct imaging with an MRI machine, and found that (after 6 months of treatment or placebo) that the tumors in men taking Avodart shrunk by 31 % on average, versus the tumors in the placebo group grew by 17%, on average. That's a significant amount of shrinkage, and explains why the PSA decreased when taking Avodart. (Prostate tumors secrete much more PSA than healthy Prostate tissue).
The often-reported statement that you need to "double" the PSA when on Avodart is because of a very large (N>10,000 men) VA study of Veterans that took Avodart (or finesteride, I have to check), and were found later to have a higher incidence of higher-grade PCa. The explanation for this is a "detection bias" that was present.
This sub-group of men had their PSA drop below the screening threshold for ordering a biopsy. Let's say the threshold for doing screening is PSA = 4 for a 60 yr old man. Assume, then , that the man has a PSA = 5. Dropping that by 50 % makes the new PSA = 2.5, which is below the threshold for screening. So, because of this real effect, some fraction of men decided not to get a biopsy, and they eventually ended up with higher-grade PCa down the road. This explanation makes sense, when you think about it.
Because of this "detection bias" effect, some doctors recommend doubling the reduced PSA to get a "true" PSA. This is an OK thing to do, as a "psychological trick" to motivate that person to be screened with a biopsy or MRI. But, the reality is that the measured PSA is a real and true value when otaking Avodart.
Let's consider the example of doing Lupron ADT. Let's assume that Lupron drops your PSA from 10 down to 1. That's a factor of 10 X reduction. No-one is suggesting that you multiply your reduced PSA by 10 to get back to a "true" PSA.
You are perhaps familiar with graphs that show sensitivity vs specificity for a certain method of predicting PCa. It is well known that the absolute value of PSA has poor sensitivity and specificity for predicting PCa (because many other factors affect PSA production, e.g., inflammation, infection, BPH, etc.). What researchers have recent discovered is that the sensitivity and specificity for predicting PCa is enhanced (improved) when men take Avodart. I can send you papers about that. That's Point #1.
Point #2 is that the PSA doubling time is, in general, a more accurate predictor of PCa than the absolute value of PSA. So, combining Points #1 and #2, if you wanted to have the best biomarker predictive ability you would (a) take Avodart, and (2) measure your PSA doubling time. None of this silly "double your PSA to get a "true" value". We're much more informed now.
I take Avodart daily for high DHT. My PSA has dropped by 76% since starting Avodart monotherapy 5 months. (My plan is to do ADT and RT in a few months.) Avodart is not a "cure" for PCa, but it does delay progression of the disease by a significant amount of time.
So, to answer your question, my recommendation is to stay on Avodart, and feel comfortable that you will have a better predictive value using that measurement, compared to no Avodart, especially if you monitor your PSA Doubling Time (PSADT).
As a followup to my previous reply, here is my own PSA history while on Avodart monotherapy.
Now, not every man is a good responder. Approximately 15-30% of men don't respond to Avodart. Reason: unknown.
As I said before, Avodart is not a "cure" for prostate cancer. But, it does delay progression of the disease, shrinks tumors, lowers PSA, is safe, and is a relatively inexpensive drug. Those are all desirable features.
Recent, large, randomized controlled trials (3 of them) have shown that Avodart reduces PCa by 38% on average (range = 23% to 51% reduction), compared to placebo, with no increased incidence of higher-grade PCa.
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