I've got Gleason 3+4 PCa, PMSA PET, 3T MRI, CT Bone Scan show nothing outside capsule, but 31 PSA (Age 53). Have Robotic Prostatectomy scheduled in a couple months. Done tons of research and the area I'm most "unsure" of is CAMs (Complimentary Alternative Medicines). From what I've gathered, Lycopene & Sulforaphane have showed early promise in clinical results (there's one combination trial with mice that showed combo worked best.)
However there's also been evidence in recent years is taking too many antioxidant supplements can actually help cancer grow. However my take is that non Provitamin-A antioxidants such as these are generally "safe" compared to the studies finding Vitamin A & E can be counter-productive to preventing cancer. But in my case the horse has already left the barn (with prostate at least.)
There's also the question of, could these supplements actually accelerate the same process that PCa cells go through to eventually get around ADT? My understanding is that the effect on Testosterone levels is minimal compared to ADT and these supplements work by affecting the "Androgen Axis" and upregulate Nrf2 which is a very different mechanism than what ADT does. So I'm assuming there's much more potential upside than downside in taking these supplements for those with PCa.
With that being said, it appears that tomato paste is the way to go for Lycopene (2 tablespoons a day?) I decided, since it's cheap to also take one 10mg lycopene supplement although studies show it's really the actual tomato product that works, not the supplements. I'm trying to get in the 30-45 mg/day Lycopene range (I also eat things with tomato/tomato sauce for dinner probably a couple times a week.)
Sulforaphane, as others point out, the only recent human study used 60mg. There's really no date I can find on any other dose. So know one really knows the minimum effective dosage. 60mg in good quality supplement form is pretty pricey. I was thinking just eat a cup of broccoli (raw or steamed) at least every other day and take 1 or 2 Broccomax capsules (17.5mg/35mg) and if Sulforaphane does really make a difference, that should be enough?
My goal is that if the RARP is not curative, I can try my best to slow the progression (delay biochemical recurrence and metastasis) giving the max amount of time for other newer more effective treatments to develop.
Wondering people's opinions on Lycopene/Sulforaphane regimen using a combination actual product + supplemental use of supplements? Also wondering anyone who took these things for several years after PCa diagnosis if they had any degree of confidence that actually made any difference?
As PCa patients, it's common for us all to get multiple 2nd opinions from Urologists and Oncologists. I think Molecular Biologists specializing in CAM research might bring important information to the table.
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The one thing to remember about CAM supplements is they lose their efficacy just like standard treatment drugs. So, as one supplement fails, discard it and find another to replace it. You will find lots of supplements it research on this form.
This seems logical from a general common sense perspective but can you reference any data that supports that specific to Lycopene and Sulforaphane? I guess an argument could be made to cycle between the two to "keep the cancer guessing" so to speak.
"I look at many supplements like lycopene not as something that will "cure" cancer. It is a substance that is found in tomato products that when consumed on a regular bases over the long term (decades) is beneficial to cancer patients."
It is part of a cancer healthy diet. I would not expect a reaction to my PSA, just one more thing I do for myself. I eat a lot of tomato based dishes.
The only kinds of trials worth the paper they are printed on are randomized clinical trials (RCTs). Lycopene has been tested in two randomized clinical trials( RCTs):
In the Pro-Diet RCT, PSA levels did not differ between lycopene or green tea groups at 6 months:
Another small RCT on men with pre-cancerous diagnosis concluded that it was "associated with a higher incidence of PCa at re-biopsy and expression of microRNAs implicated in PCa progression at molecular analysis. The use of these supplements should be avoided"
The second study you referenced, Lycopene was combined with Selenium and GTCs . I've read studies attributing Selenium alone and GTCs alone to having adverse effects regarding PCa but not Lycopene. So that study cannot say whether it was the Lycopene, Selenium, GTCs or combination that caused the result. The answer may be in whether or not Selenium and GTCs upregulate Nrf2 like Lycopene does. If they don't, then it's highly likely the Selenium and/or the GTC component was responsible for the negative outcome.
Lycopene studies are mixed as far as post PCa diagnosis effects. I am not aware of any study involving humans and Lycopene only that showed adverse effects (other than skin starting to turn orange from too much of the red pigment LOL). Otherwise results are mixed, some with no effect and some with positive effects (longer PSA doubling time, etc) There is wider evidence with a stronger consensus it has a preventative effect of PCa occurring in the first place but for those of us here, that is inconsequential at this point.
"selenium supplementation did not reduce prostate cancer risk in men with baseline low selenium status but selenium supplementation in men already replete with selenium from dietary sources increased their risk for aggressive prostate cancer. "
Realistically, no one here is aware of and has read every single study about everything to do with PCa and I don't pretend to be an exception. The more good information people can point out the better, the point of having a discussion.
I've since noted that raw broccoli has around 100 mg Sulforaphane per 1.5 cups on average (in raw mature or unsprouted broccoli, it has about 44 to 171 milligrams of sulforaphane per 100 grams of mature broccoli) The bioavailability of raw is about on par with the best supplements, around 35%. Cooked is way lower (1/10th of raw, unless you add mustard seed which makes cooked 5 times more bioavailable if I remember correctly). If the goal is to consume 60 mg dose of Sulforaphane a day (per the French Study), considering they used Prostaphane which is supposedly 70% bioavailable = 45mg bioavailable, you'd need to ingest 128 mg sulforaphane of raw broccoli or 3 cups. (Although I've seen 1.5 cups recommended in some articles.)
But the study you referenced with the Lycopene+Selenium+GTC supplement reinforces my original concern about too many antioxidant supplements potentially being a bad thing. This leaves one stuck deciding about risk/reward ratios. It seems it basically boils down, at least on this particular subject, to each individual's own semi-educated guess based on data which so far unfortunately has not built a consensus one way or another as far as I can tell.
I am frankly a bit surprised that, given the prevalence of PCa, the research isn't further along in the area of CAMs. But I probably shouldn't be surprised, considering they aren't as popular in Western Medicine and Pharmaceutical companies that have the resources to power large trials aren't interested in selling natural supplements.
Thanks for showing me that small (n=26) and very short-term (3 weeks!) RCT. I don't think there are others, but I may be wrong.In that none, there was no statistically significant difference in the PSA change.
I actually have read every important RCT about prostate cancer. Because I know about levels of evidence I (and you) can safely ignore studies that are of lower levels of evidence when there are already higher level of evidence studies. So many "studies" are just written for junior doctors in teaching hospitals to get published ("publish or perish"), and as far as patients are concerned, aren't worth the paper they are printed on. Every time I raise this issue with medical fellows, they just shrug and say, "but that's how it works, Allen." Caveat emptor!
As you say, Sulforaphane requires some of the heat-sensitive enzyme myrosinase in order to be bioavailable. I always recommend eating a raw broccoli floret along with the cooked cruciferous vegetable. zThe nice thing about enzymes is that they don't get used up biochemically, so even a little goes a long way.
Agree on all points. Thanks to this site, I’ve become aware that the cooked cruciferous route I took for many years was missing the myrosinase. So now I add raw broccoli (dipped in hummus — really quite tasty), raw cauliflower, radishes and/or cole slaw to most meals of the day, including those with the cooked veggie.
TA, I'm curious how an RCT can be reliably conducted with any food product. Wouldn't both groups need to consume exactly the same diet except for the nutrient being studied? Otherwise, it seems many factors could be affecting the outcome.
That's the miracle of randomization! As long as food consumption is on average about equal in both groups (and with a big enough,sample size, they always will be) all those other factors are averaged out. For example, if group A is given sulforaphane pills and Group B is given a placebo, if there are big eaters of cruciferous veggies in group A, there are also going to be big eaters of cruciferous veggies in group B. The same holds for any other food item that is consumed within the population. Randomization assures that a person is just as likely to wind up in Group A as Group B.
In several large studies, men with high selenium levels were at greater risk of being diagnosed with aggressive prostate cancer or dying from prostate cancer.
Here's an article titled "Selenium, lycopene and GTC—a case of 'chemopromotion'" from Nature Reviews Urology commenting on that trial.
Although the study sample size was relatively small, the results are comparable to those from the large SELECT trial. “Taken together, the findings suggest that (at least) selenium might increase the risk of prostate cancer,” warns Gontero.
RE: GTCs
A trial of oral green tea extract in patients with solid tumors reported that drinking 7 to 8 Japanese-style cups (equal to 3 ½ to 4 cups U.S.) of tea consumed 3 times a day for 6 months was a safe dose.
I can't remember the study I read about GTCs (too much at least) being potentially harmful. Could have been that study with it combined with Lycopene and Selenium. Seems GTCs may be "safe."
RE: Lycopene there's no studies referenced regarding trials with cancer patients. Just that FDA has not approved use of Lycopene as a treatment.
In my opinion it's all about Nrf2 upregulation which Sulforaphane and Lycopene both do. But then it begs the question is too much or too early Nrf2 upregulation bad in the long run regarding PCa progression? Does it just make the cancer become more resilient quicker in exchange for a short term benefit?
Oh, for those interested in these two supplements, I just remembered one study I read that sort of put my mind at ease on the Lycopene+Broccoli safety. Yes it's mice, but the main point is it didn't show a worse instead of a better outcome.
"A new University of Illinois study shows that tomatoes and broccoli--two vegetables known for their cancer-fighting qualities--are better at shrinking prostate tumors when both are part of the daily diet than when they're eaten alone."
The thing I still wonder is ADT has essentially the same end effect but then it eventually stops working as the cancer adapts. So are we just accelerating the inevitable that the cancer will adapt to therapies that affect the androgen matrix?
Your PSA is very high. You most probably already have metastatic prostate cancer. Maybe you scans don't show it. Scans usually don't show micromets when the mets are smaller than 4mm. You need a good oncologists. I personally would start ADT as soon as possible and then in 2 months or so chemotherapy. Lot of people have bone mets even with PSA 4. I understand that you would like to heal yourself without all of these. It is better to overreact than to hope that you will be fine without chemotherapy an ADT. Go to Dana Farber or to some teaching hospitals in California or in NY. Better if you start treating early. Here is a link about chemotherapy. urotoday.com/journal/everyd...
THe PSA > 20 does technically put me in high risk, however the 18F PMSA-1007 PET Scan I had much more sensitive than MRI, down to 3mm. So we won't know about micromets until the post-surgery pathology report comes back. The published nomogram I've used that takes into account T stage, primary and secondary gleason, PSA, and a few other things shows a 1.7% chance of upgrading to distant metastasis (bone) and 4.5% chance of lymph node involvement.
Your recommendation is the complete opposite of George71 . Based on my research, I really don't think any Urologic Oncologist would put me on ADT or Chemotherapy based on my initial PSA alone. There would need to be some post-surgery test results to trigger that and even so, I believe @George71 is correct in that ADT (and from what I read, Chemotherapy) really doesn't have that significant of an effect on the overall PCa survival (a few months typically.)
There is a trial, I think in Australia that is giving patients one or two Lu-177 PSMA Radioligand treatments prior to prostatectomy mainly to investigate actual dosages given to the tissues but it could also shed light on if neoadjuvant Radioligand therapy could be curative when the cancer is at an early stage but currently it is only approved by the FDA for MRPC and like many of the other drugs, only extends survival around 3-5 months if I recall.
Advances over the coming years in Immunotherapy, mRNA Vaccines, and Radioligand treatments could improve these treatments to becoming curative for some patients or at least have a more significant benefit on extending survival.
Do you have a Medical Oncologist? Is your PSA rising?
I was told by my GP when I tested with the PSA 20 back in November 2017 that I may have infection and he wanted to treat me with antibiotics. I myself new that I have a cancer. I had neurological symptoms. My GP recommended Magnesium supplements for my neurological symptoms.
I went to another GP and that GP said that my sciatica will improve in 6 months. Just don't walk up the hill he said.
So I went to a third GP and she sent me to the CT of my spine in April 2018 and I was diagnosed inside 2 days with metastatic prostate cancer. My PSA was 50. The other GPs still had the opinion that I just have an infection (did not know my bone scan results).
I also did not start ADT until my PSMA PAT scan in July 2018. I ended up with Degarelix in July 2018. My sciatica was much better in 7 days.
My PSA was 50 when I was diagnosed. My PSA was 70 when I had my biopsy and was 100 when I started ADT (Degarelix) after my PSMA PAT scan.
Now I still have my prostate. Last PSA was 0.44. My PSA was 20 in November 2017 when I started to have neurological symptoms. In April 2018 I was officially diagnosed with PSA 50. With PSA 70 i had my biopsy of the prostate (4+3) and with PSA 100 I started ADT (Degarelix).
No. That's part of what they looked at in the Hussain trial. They found that castration resistance occurred at the same time, whether the patients used iADT or cADT.
In the TOAD trial, which looked at early vs. delayed use of ADT, the early users were non-metastatic and used IADT. They found that the early users became castration resistant after the later users.
All the mHSPC trials found the same thing - that early use of advanced hormonal agents delays castration resistance.
The effect on tumor load is much stronger than the effect on selective adaptation.
You might find this discussion by a sulforaphane researcher interesting. Note his comment about taking sulforaphane if you have cancer/metastases at the 00:40:29 mark... "It may not be wise to take Sulforaphane or go heavy on Broccoli"youtu.be/-PNGxNzogOY
I look at many supplements like lycopene not as something that will "cure" cancer. It is a substance that is found in tomato products that when consumed on a regular bases over the long term is beneficial to cancer patients.
If I read your Bio above correctly, you had a PSMA scan that showed nothing outside the prostate gland. Although 31 is a high PSA -- surgery or radiation may get it all. I would be very careful to not start ADT or Chemo unless or until warranted or necessary... they rarely cure anyone -- and in many cases accelerate the cancer spread.
My thoughts exactly based on all the information I read about ADT. See if the surgery is curative first, then, radiotherapy if not with maybe a very short course of ADT during and after RT (4 months) to maximize the effects of the RT but not get the cancer too far long the adaptation to ADT path.
This one from back in 2003 isn't an RCT - the Abstract is vague on the methods so I'm not sure if this was in vitro or in vivo, sounds like it was in vitro. But it is basically advocating the "two much of a good thing is actually bad" philosophy on cancer and antioxidant supplementation. I question the practical significance of in vitro only studies. They are basically a starting point for determining if further in vivo trials. You have to pay for the full report. It is in contradiction to the small human RCT done Omer Kucuk released the year prior emphasizing my point, what happens in the lab under a microscope can be very different than the outcome in a human. A lot of it cold be dose dependent. I would imagine in vitro studies you are exposing a small number of cells (relative to an actual tumor in a human) to a large ratio of the compound that may practically be the equivalent of megadoses of the compound in a human.
Decided to search for Lycopene in the clinicaltrials.gov database to see what is ongoing or about to complete or released results that are not widely published. Most are all preventative but found another one for the +Lycopene treatment column. I had to hunt around for another article that references this study as even the Abstract is not obtainable without an institutional login to Wiley or others.
"Lycopene significantly decreased the growth of cells in a dose-dependent manner when cells were incubated for 24, 48, 72, or 96 hours (F = 3.150, 11.27, 54.51, and 297.5, respectively; P <.05). The growth inhibitory effect of lycopene on human prostate cancer cells observed in this study suggests a possibly important role for lycopene as an antioxidant in human prostate cancer; however, investigations of other mechanisms are warranted."
Seems the jury is still out but there appears to be more evidence thus far of a neutral or positive effect as opposed to a negative effect.
In my opinion the best thing you could start doing is take one Avadart daily. At the outset I talked to 8 nationally known specialists and got 8 widely differing opinions .
I am 6 years post surgery that was supposed to get it all -- but they found 4 of 10 lymph nodes and Gleason 8 or G 9 depending on who I am to believe.
My post surgery PSA was 0.03 -- PSA went to 0.8 in less than 8 months ! -- started Avadart as per my urologist and Snuffy Meyers video and PSA doubling time increased to 20 months. (currently PSA is1.7 -- 6 years post surgery)
I take one Avadart daily and weekly (T)estosterone cyp injections to keep my T levels up around 500 to 600)
low T and high DHT ratio may actually be what triggers PCa in the first place. There is a time to take ADT -- but in my opinion -- not until it is absolutely necessary -- ADT can increase mutations, cause CRPC and help PCa spread... not to mention increased muscle wasting, bone loss and dementia.
There is evidence that trying to kill every PCa cell with ADT (after failed surgery or radiation) brings on CRPC by stressing the cancer cells to mutate, become more aggressive and spread. Currently there is no cure for metastatic PCa -- overly aggressive treatment just to try and reach an undetectable PSA may be what speeds up the mutation process and cancer growth . Why not try slowing the growth (ie. doubling time) . If one can slow the doubling time to a year or a year and a half or longer they will likely outlive it.
Instead of trying to get to a PSA of zero for a year or 2 and have it explode ... why not try to slow the process with healthy lifestyle changes and proven treatments that don't cause the cancer to mutate or try to find alternate workarounds which is what happens more often that not with ADT... 70 years of ADT results is proof enough that PCa treatment is sorely lacking. They have 4 or 5 different types of ADT and they all result in the same thing... If they worked very well no one would be looking for anything else.... If you have an infection you take penicillin ... it works ! .. you don't go looking for something else.
This is anecdotal but there are a couple of guys that post on here that have achieved extended time in remission and are still hormone sensitive. They are taking a number of supplements and other substances that are not part of SOC.
Are they just lucky?
Would their PCa not have progressed if they had done nothing additional?
It is hard to know but I think it bears watching by the rest of us that are earlier in the process.
That was my gig (but saved weekends for myself). I was a mainframe computer programmer who maintained various applications for financial institutions. I also dealt with mergers and acquisitions for these companies,,,, (thank goodness I embezzled from them). I am now a retired "dinosaur".....
Based on exhaustive searching and reading and discussions like this, this is what my current conclusions are:
1. Lycopene & Suolforaphane are likely "safe" especially as long as you aren't taking MEGA doses. Antioxidants that are not Provitamin-A (don't convert to retinol) appear to be "safer" than those that are Provitamin-A sue to evidence of Vitamin A & Vitamin E promoting cancer, whereas I see no similar clinical evidence for Lycopene and Sulforaphane promoted any cancer (given the latter is relatively new on the scene.) Dr. Fahey, in the video john_in_pa posted in my opinion is making a very broad general warning about overuse of antioxidants in general without any data that confirms Sulforaphane can have a negative effect. I have scoured and scoured Pubmed and the Internet and there's nothing indicating Lycopene or Sulforaphane exacerbate any form of cancer, let alone PCa. To the contrary, all findings are either no significant benefit or significant benefit (including the most common form of cancer: lung cancer.) As noted earlier, the one study showing negative effects with Lycopene was combined with high amounts of Selenium which HAS been shown to have potentially negative outcomes regarding PCa.
2. Lycopene supplements are not very useful. Information I've uncovered, and this seems true with many plant-based compounds, that there really is only strong evidence of Lycopene benefits when consuming tomato products, with tomato sauce and tomato paste having the most Lycopene. Aiming for 30mg/day seems like a good target but not more than 45mg.
3. You should try to get your Sulfurophane from raw vegetable product instead of supplements, or at least from a combination of raw vegetable and well formulated supplements. Again, in general, it's widely viewed that the beneficial effect of many of these compounds is attributed to a synergy between the particular compound and other phytochemicals in the plant/vegetable. This is the case with Lycopene, maybe less so with Sulforaphane, but seems the "wise" approach on Sulforphane is to not go the supplement only route. It's frustrating though that other than the French Study using 60mg, there's no other evidence on the optimal dose of Sulforaphane to achieve the most benefit.
4. The risk/potential reward ratio appears to be very low on Lycopene+Sulforaphane from the viewpoint of accelerating PCa mutation to more aggressive forms and regarding ADT resistance (I think Dr. Fahey was mainly just covering his butt in case later research proves otherwise.) If my primary treatment is not curative, looking at existing evidence, and considering the big picture that PCa is not (yet) curable after recurrence after the primary treatment, I think the risk if any, is minimal long-term, compared to the possible reward being prolonging biochemical recurrence, increasing PSA doubling time, etc. In other words, I don't see in the future an authoritative statement that "you wouldn't have died so soon if you hadn't eaten so much tomato sauce and broccoli!"
5. As far as Sulforaphane supplements go, I believe the French Study used Prostaphane which had some type of French Regulatory approval and is proprietary but claims to be much more bioavailable than supplements like Broccomax. Not cheap, but I'm not going to grow my own sprouts. It is now available in the US under the brand name Broq. Seems like it may be worth the extra cost over the other supplements, especially considering I'm going to augment my Sulforaphane intake with raw Broccoli and thereby can take less of the supplement. I'm always a little skeptical though on some of these supplement claims of being 2X more potent, etc. But the lab results look pretty legit. Only problem is to match the French Study you'd have to take 6 capsules meaning one $60 bottle is 10 days worth costing $6/day. (Guess that's only a little more than getting your fancy coffee drink at Starbucks each day.) In my experience most shoppers on Amazon gravitate to the cheapest products hence why it has relatively fewer reviews (in addition to not being available very long.) This is not the type of product I would consider Amazon reviews very useful information though.
Note that the lab reports show Broccmax (popular) having about 1/9th the bioavailability of Prostaphane. That's a bit hard to believe but assuming that data is correct the bioavailable equivalent of 60 mg Prostaphane would be 31 Broccomax caps if my math is correct.
I've read that John Hopkins also confirmed its greater bioavailability. I think I ran across the whole paper (without paying) but can't remember where I found it.
This is the problem that I have with a lot of published studies. They vary in all ways. There’s all kinds of things to watch for when looking at them.healthunlocked.com/advanced...
You find that people search and then come across a promising study. There’s all kinds of conflicts of interests, suspect testing, missing data. Worse is, it looks credible and scientific. The issue is, people generally will not know what they are looking at and decide to try something like a supplement for example.
Some people may experience a positive effect. The issue is though, you cannot attribute any study result being down to a single variable. There are millions upon millions of variations of inputs. Anything can cause some effect.
Best you can do is try something and measure your progress. You can measure your psa for anything you try. Sure attempt to read some study and try it out of you like. But I wouldn’t rely on other peoples anecdotes or a single thing as some panacea as your best hope. I’d personally consider looking at a more holistic approach. Improve your diet, exercise, sleep, less stress and measure that. What I do personally is target inflammation. This is strongly associated with cancer. Exercise and diet seem like a good way to start.
FWIW, I tried both those and it didn’t have any affect at all. There’s no harm in trying though.
You’re right about tomato paste for lycopene. You can even get double concentrated. For sulforaphane, search for Rhonda Patrick. She recommends freezing broccoli sprouts. The freezing breaks the fibers open to maximize the amount of sulforaphane.
I agree with a lot you're saying and it jives with the main theory that Dr. Michael Gerger seems to operate with (author of the book "How Not To Die" which I haven't read yet but seen some of his videos) which is, the most effective approach is really aiming for obtaining synergy from combining multiple concurrent strategies: diet high in fruits & vegetables, low in animal protein + high amount of exercise, etc.
I'm not surprised you didn't see a significant change in your PSA experimenting with Sulforaphane supplements. Yet it is still of interest to people here, especially newcomers like myself. That French study with the 60mg of Prostaphane is encouraging but there's really not a significant enough amount of other evidence to really draw any conclusions. Like you have eluded to, it really boils whether you want to give it a try or not and in this particular case probably end up spending $180/month for 6 months taking 6 Broq caps a day to see if it makes a difference. I suppose maybe if I was past primary treatment and dealing with additional, expensive treatments, that's a drop in the bucket related to overall health care costs even with low-deductible Gold or Platinum level PPO insurance.
I'll do pretty much anything within reason though if it might lower the chance of micrometastases.
For those interested in Sulforaphane, I was able to get my head around the Sulforaphane supplement fiasco. In reviewing what I've concluded, a lot of the supplements have Glucosinolate on the label which is only partly made up of Glucoraphanin, which combined with a small amount of Myrosinase is 30% bioavailable Sulforaphane. If you wanted to mimic the French Study of 60mg Prostaphane, that's 6 Broq caps or a little over $6/day. At 70% bioavailability you are getting 42mg bioavailable Sulforaphane.
There's a trademarked substance called "Truebroc" used in some supplements. Ultrabroc shows 115mg of Truebroc being equal to 115mg "Sulforaphane Glucosinolate." But Glucosinolate is not equal to Glucoraphanin which was what was determined in the study to have 30% bioavailable Sulforaphane.
Oncoprotect ES has 769mg Trubroc which they equate to 100mg Glucoraphanin. That means something that has 100mg Glucosinolate (aka Truebroc) has 13% Glucoraphanin! At 30% bioavailability, Oncoprotect ES has 30mg bioavailable Sulforaphane or about the equivalent of 4 Broq capsules (at 70% bioavailable.) So it's about 1/3 the cost of Broq per mg bioavailable Sulforaphane! ($1.33/cap vs 4X $1.08/cap = $4.32)
This is an example of how poorly regulated supplements are. No supplement that does not use stabilized free Sulforaphane should be allowed to put the word Sulforaphane on the ingredient label but most all do and call it Sulforaphane Glucosinolate when it's just Glucosinolate, a term that encompasses more than just Glucoraphanin, the PRECURSOR to Sulforaphane. Not Sulforaphane itself. So something containing 100mg "Sulforaphane Glucosinolate" is about equal to 4.5 mg bioavailable Sulforaphane (100mg X 13% X 30% = 4.5mg)
The lab result from Broq purports only 0.56 mg Sulforaphane in Oncoprotect ES. But if you look at the result closely, first, it says 489mg a capsule not 798 Truebroc+2 Myrosinase = 798. And it also says "product without enzyme addition" so this is some old form of Oncoprotect that didn't have 796mg Truebroc nor the Myrosinase enzyme that converts Glucorphanin to Sulforphane. Nor does it account for the fact Myrosinase is in the human gut. They just mixed these products with water and in this case without the Myrosinase so of course very little is going to convert to Sulphorphane.
In addition was able to contact Dr. Jed Fahey (retired) from John Hopkins that did the study on bioavailability that Broq links to! He's recommended several supplements in his podcast and he replied that he doesn't endorse Broq.
Hey, whatever happened to allspice, remember that? University of Miami did some paper on it,then it fizzled out. There also was a big deal made about noscapine a couph medicine from Europe. I took this stuff , then gave up after it ran out. I was doing conventional treatment so I had no way of knowing if it did anything.
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