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Baptista · 08-30-2012, 09:51 PM

Independently of the treatment one has chosen or been administered, we all will go through a period of recovery which experiences are important to know in advance by the many starting the therapy. In any case, recovery experiences from hormonal treatments are rarely reported and diverse probably because HT is usually administered in combinations with other therapies or because doctors prefer to administer the HT drugs continuously until these fail and the patient becomes an hormone refractory case, therefore with no recovery period to contemplate.

In my case the HT protocol chosen by the uro-oncologist regards for intermittent administration (on/off medication periods) which OFF period leads to recovery before reaching to a “normal” status. This choice is better than continuous, particularly for those suffering nasty side effects from the drugs or from the hypogonadism status the treatment causes.
I also believe that the intermittent approach can prolong the control on the cancer apart of providing a relief from the side effects and return to normal function of other “body parts” affected by the low T levels. This includes avoiding the risks for cardio and diabetes complications.

Nevertheless, it is noted in a recent study that HT on intermittent application is not better than continuous.

In my view the conclusions of the study were based on protocols inconclusive of the whole benefits. They could not assure that patients would recover from their hypogonadism status completely. No testosterone tests were executed but instead preferences were given to a fixed period on/off drugs.
Here is the link to such reference;
http://www.healthboards.com/boards/cancer-prostate/903711-intermittent-hormone-therapy-inferior-continuous-therapy.html

I started HT in November 2010 with a protocol for intermittent administration on mono blockade with 6-month shots of Eligard. The on/off “switch” is controlled through periodical PSA values, testosterone tests (to confirm castration levels) and symptoms. The ON period required remission levels (PSA less than 0.05 ng/ml) for at least 12 months. In my case it took 18 months for the achievement.
The OFF period is expected to last until one gets to a certain threshold PSA value depending on the previous diagnosis/treatment histology of a patient. In my case the threshold is set to PSA=2.5. This is when I will return to the treatment, starting with bicalutamide and leuprolide.

I would like to note that this protocol is recommended by many renowned oncologists, experts on the administration of hormonal therapies in PCa cases.
My doctor commented that I may get different drugs depending on what is available at the time of restarting HT. I am hopeful for a long vacation period (over 5 years) and then start with newer drugs that better address intratumoral activity of cancer cells such as; the antiandrogen enzalutamide (MDV 3100), the CYP17 inhibitor abiraterone (Zytiga), or CYP17 inhibitor orteronel (TAK-700).

You may follow the chronology of my treatment and tests (PSA, etc) in this link;
http://www.healthboards.com/boards/cancer-prostate/879442-i-got-lower-psa.html

Here I want to report on the recent achievements of the treatment which is now at the 3-month mark since starting the OFF-drugs period.
My last test results of August 2012 come as;
PSA =0.02 ng/ml and Testosterone = 0.11 ng/ml (11 ng/dl).

This is a continuation of the remission level (lower than 0.05) while a small increase of testosterone become apparent from >0.1 to 0.11).
I do not know if such is common but the PSA could be expected to be maintained for the still castration levels of T which is lower than 0.3 (30 ng/dl). My body has not yet recovered to normal levels of testosterone. However, symptoms all indicate improvements.

During the ON-drugs period, the side effects were numerous but mild being fatigue the one most annoying. Some effects were present but unnoticed. Now three months since the end of drug’s effectiveness I can identify additional effects that I thought being a cause from other factors.
One example is the rheumatism/arthritis like symptoms which existed in the whole joints but suddenly (two months ago) start disappearing and now have gone completely.
I also feel more energetic (fatigue is down to 2 in a scale of 1 to 10) and the testicles are bigger. The penis continues smaller though. Mood changes are lesser and I sleep longer with lesser wake ups for peeing. I turned to be calmer when confronting people (my wife’s comment) and I am getting thinner but the boobs are still noticeable. Overall I feel much better. I still have occasional hot flashes. Surely the symptoms are all indicative that the “T-factory” (testes) is in operation again.

I feel fortunate for the positive response to the treatment by the cancer and my system. I also have no prostate in place producing serum from benign tissue, which makes the case more impressive.
One note on the drug effectiveness (Eligard-leuprolide acetate); This LHRH agonist has a short half life period of 7 days, therefore the drug’s “power” losses the effect just after the end of the period of effectiveness of the shot (in my case was 6 months). However, what causes the majority of symptoms we experience is the condition on castration due to stoppage of the “factory” (the testes). To start fabricating testosterone, the testes require signalling from the pituitary. This function differs from person to person but many report on periods lasting from two to twelve months. In some cases the system does not recuperate at all subjecting the patient to a permanent condition of hypogonadism. This is scaring and many need TRT treatments.

It is yet too early to confirm success because of the castration levels but the last results are showing that all is working in my favour.

Some guys wishing to get a relief from the symptoms should discuss with their care team on the possibility of going OFF-drugs. However keep it in mind that one may respond differently in each situation.

Good luck to all.

Baptista

(posted in another forum for PCa cases)

Tall Allen · 08-31-2012, 12:01 PM

Hi Baptista,

I'm wishing you the longest possible vacation.

On the issue of continuous vs intermittent ADT, there was published today in the New England Journal of Medicine, the results of a Canadian comparative study among 1,386 men who had failed primary radiotherapy and were assigned to either continuous or intermittent ADT. It showed that intermittent was not inferior to continuous on overall survival, and that there were some quality of life benefits to IADT.
http://www.ncbi.nlm.nih.gov/pubmed/22931259

Together with a dear friend of mine, who is also on IADT, having failed RP, failed RT, pGleason 9, N0 and M0, I've been investigating whether it might be of benefit to try now certain available cancer therapies that are normally only tried later with mCRPC. Our hypothesis is that attacking the cancer on a number of fronts; i.e., a cocktail, while it is still hormone responsive may actually provide a chance at curing it.

He noted that cocktails are used for HIV and many cancers, so why should we wait until our cancers become castrate-resistant before bringing out the big guns? (Most clinical trials only allow men with metastatic castrate-resistant PC.) At the same time, he didn’t want something he took now to preclude taking it or something else later. Using docetaxel, abiraterone, or Provenge now, which probably all have a good shot at being more effective if used earlier in the game, may preclude the use of the next generation of chemo, hormone therapies and vaccine/immune stimulants when they become available for clinical trials. He was looking for something more powerful than nutritional supplements and dietary interventions, which he is doing anyway. We ignored for now the question of whether insurance would pay for it. So we came up with the following requirements:
1. Has a good chance of working with your hormone therapy
2. Available by Rx now, outside of clinical trials
3. Won't interfere with getting on clinical trials or other meds later
Based on those requirements, I came up with several classes of medications that might improve the effectiveness, long-lastingness, and, stands a chance at putting the cancer into remission: angiogenesis inhibitors, somatostatin analogues, Selective Estrogen Receptor Modulators (SERMs), Tyrosine Kinase Inhibitors (TKIs), mTOR Inhibitors, Histone Deacetylase (HDAC) Inhibitors, Metformin, Statins, and COX-2 Inhibitors. I mention only a couple of nutritional supplements that pertain to those categories.

There are some other substances (e.g., HSP blockers. IGF inhibitors, prolactin inhibitors, matrix metalloproteinase inhibitors, Custirsen) that might be useful in a cocktail and are in clinical trials, but I don’t know of any that are already approved.

We showed our investigations, together with all the peer-reviewed references, to his oncologist, Dr. Scholz, who is amenable to trying the cocktail approach. However, we decided to hold that off for now while we try some advanced imaging approaches first in order to determine if his disease is in an oligometastatic stage that may be slowed by SBRT to a few lymph nodes.

If you or others are interested, I will post an extensive explanation of the "good witches brew" that we came up with.

- Allen

livingatlake · 08-31-2012, 05:30 PM

Hu Allen

Please post. I am sure many of us are most interested. Thank you.

Livingatlake

Tall Allen · 08-31-2012, 07:33 PM

It's rather lengthy -- about 10 pages including all the references. Maybe I'll exclude the government references for now, but if in discussions with your oncologist, he would like to see them, let me know. Many of these are quite powerful. They all have drug interactions, contraindications and side effects that should be carefully analyzed. I'm not a doctor and don't recommend any of these -- I'm hoping that it may be a good kickoff to a conversation with your oncologist as it was to my friend's.

Angiogenesis inhibitors

Thalidomide is the oldest, and a newer version, called lenalidomide (Revlimid) may possibly be more effective or have fewer sides. I know Jim has been taking thalidomide. These drugs will make you very sleepy though, which can be a good thing if hot flashes keep you awake. They may also have immune suppressive effects. The hot new one in this category, Tasquinomod, is in clinical trials and will probably get fast-tracked for FDA approval. A previous one, Avastin, did not prolong survival for PC and was disapproved by the FDA for breast cancer.

Somatostatin Analogues

Lanreotide and Octreotide are synthetic versions of somatostatin, the hormone responsible for antagonizing somatotropin (growth hormone). As prostate cancer progresses, the somatostatin receptor is less expressed, allowing the cancer to grow more quickly. It would seem to make a lot of sense to use this sooner rather than later. It is always given with a corticosteroid. A new version called Pasireotide has been approved in Europe.

It’s only a single case study, so I throw it in just as a curiosity, but it seemed to completely cure the advanced hormone-responsive PC of one man:
"Complete response to the combination therapy with androgen blockade and somatostatin analogue in a patient with advanced prostate cancer"
http://www.ncbi.nlm.nih.gov/pubmed/17316966

As an interesting side note, a recent study of over a million people showed an association between height and PC that could not be explained away by other risk factors. Maybe tall guys like me have a surplus of growth hormone:
"Adult height and the risk of cause-specific death and vascular morbidity in 1 million people"
http://www.ncbi.nlm.nih.gov/pubmed/22825588

SERMs (Selective Estrogen Receptor Modulators)

The role of estrogen and estrogen receptors in prostate cancer is very complex. Estrogen is an old therapy and is sometimes still used as a second-line therapy because it acts in the brain to inhibit the production of androgens, called negative feedback. However, estrogen receptor beta (ERβ) is highly expressed in prostate cells, and when activated, it seems to have anti-proliferative properties. ERα may have an opposite effect, so the trick is to activate ERβ without activating ERα, hence the selective ER modulators (SERMs). The estrogen story is even more complex: a person may have damaged estrogen receptors that are unresponsive to ERβ stimulation, or the receptors may disappear -- estrogen receptors diminish as the cancer progresses (the opposite of the androgen receptor). Therefore, it makes sense to use this earlier rather than later in the progression.

Gamma and delta-tocotrienols are thought to enhance ERβ activity. It is available as a pure annatto extract from health food stores and on the internet. It’s important not to try to obtain it from other mixed Vitamin E extracts – even small amounts of alpha-tocopherol seem to suppress absorption of tocotrienols.

Clomiphene is a relatively cheap and effective SERM that may be worth trying. It selectively blocks ERα. Also, soy isoflavones stimulate ERβ, so taking the two together may be a good one-two punch.

I should add about clomiphene that it would not make sense to take it while on Lupron, and could be dangerous with it. Clomiphene blocks the ERα receptor, which in turn controls the negative feedback between steroids and GnRH in the brain. Therefore taking Clomiphene with a GnRH agonist (like Lupron) may cause a runaway super-flare of testosterone production. It should work fine, however, with a GnRH antagonist like Firmagon, or with Casodex plus a 5-ARI.

Here’s something that’s as confusing as it is interesting about all this. There is a drug in clinical trials now called Capesaris that could potentially be used instead of Lupron. It does the opposite of what clomiphene does in the brain -- it is ERα receptor agonist. In the brain, the ERα receptor mediates the negative feedback between steroids and GnRH. That’s why estrogen was given as an old treatment for PC – it shuts down the pituitary signal that stimulates androgen production. Capesaris similarly enhances the negative feedback to GnRH, thus shutting down androgen production. The hope is that it will be less harsh than Lupron or Firmagon. It remains to be seen if its anti-proliferative effect of shutting down androgen stimulation from the brain exceeds its pro-proliferative effect on the ERα receptors in the tumor. If I were a betting man, I'd wager that it slows down the tumor at first, but will stimulate growth of the tumor eventually.

Tyrosine Kinase Inhibitors (TKI)

There are about a dozen different tyrosine kinase inhibitors in clinical trials now for PC, and dozens more for other cancers. They represent the hottest area of cancer research right now. They work by inhibiting certain growth factors within the cancer cell. They are usually used in conjunction with other cancer therapies like hormones and chemo, and they can be combined. The hottest one for PC is called Cabozantinib (formerly XL 184) and seems to clear bone mets almost miraculously in 12 weeks. Exelisis tried to get early FDA approval for it based on relief of bone pain, but the FDA insisted on a demonstrated survival advantage and asked for a lower dose to improve tolerability. It’s in Phase 3 trials now. Several TKIs have already been approved for other cancers, but none yet for PC. Those could potentially be prescribed “off-label.” However, it is possible that using one now may preclude getting one in a clinical trial later. If it were me, I would wait for Cabozantinib approval, which may not take too long if it keeps performing as it has been.

The TKIs that are already approved for other cancers and are in clinical trials now for PC include: Axitinib (Inlyta), Dasatinib (Sprycel), Erlotinib (Tarceva), Gefitinib (Iressa), Imatinib (Gleevec), Sorafenib (Nexavar), Sunitinib (Sutent).

PC uses Interleukin-6 (IL6), an immune cytokine, to protect itself, and IL6 seems to interfere with TKIs. Immunosuppressors like mTOR inhibitors (see below) may suppress IL6 and may work synergistically in a cocktail with TKIs. Corticosteroids, which are usually included in these cocktails, may help also.There is a monoclonal antibody in clinical trials, Siltuximab, designed to suppress IL6.

In addition to stimulating the ERβ and inhibiting angiogenesis, soy isoflavones may also act as TKIs.

mTOR Inhibitors

These target a cancer proliferation protein. Three have already been approved for use in cocktails against other cancers, and are in clinical trials for use against prostate cancer. They could potentially be prescribed now off-label. The approved ones are Sirolimus/rapamycin(Rapamune), Temsirolimus (Toresel), and Everolimus (Afinitor). However, Everolimus failed to show any incremental benefit when used with Casodex in a recent clinical trial. Would it work in conjunction with a TKI and/or an GDACI (see below)? The jury is out on that.

Note: These are all powerful immunosuppressants used to prevent transplant rejection, and may also cause diabetes-like symptoms. Not something to stay on for a long time.

Histone Deacetylase Inhibitors (HDACIs)

Valproic Acid (Depakote) is a well-known anti-epileptic and mood stabilizer that was recently discovered to have powerful anti-cancer effects. It may cause PC cells to differentiate; i.e., lower Gleason grade. It and other HDACIs are in clinical trial against prostate cancer. In lab studies, it had a synergistic effect with Everolimus (see mTOR inhibitors, above).

Metformin

The anti-diabetic drug Metformin seems to have a powerful anti-PC effect. It may only work in conjunction with statins. It’s clinical trials now with statins and with Lupron. Metformin enhances the antiproliferative and apoptotic effect of bicalutamide in prostate cancer.

Statins

Statins may slow down the growth of advanced, high grade androgen-independent PC cells. However, this association has been found only in some epidemiological and retrospective studies, and not all of them. Some researchers believe that health-conscious men are both more likely to take statins and to get PSA tested earlier, which would explain why they show up with less advanced disease. Some lab studies support its role. A large controlled prospective study is underway, using red yeast rice as a statin surrogate; the results may provide a more definitive answer. Meanwhile, there seems to be few downsides and many potential upsides to taking low doses as part of the cocktail.

COX-2 Inhibitors

Although early results in animal models and in small scale trials looked promising, the first large scale, controlled study (the STAMPEDE trial) of celecoxib+hormone therapy vs hormone therapy alone showed no benefit to celecoxib (Celebrex). Whether or not it may have a synergistic effect with other ingredients in a cocktail remains to be seen.

Aspirin (which is a mild COX-1 and -2 inhibitor) and other anti-coagulants like Warfarin were associated with reduced mortality in men who'd been treated with RP or RT in a retrospective analysis published this week. It seems like a reasonable supplement unless their are known sensitivities or contraindications.

Other

I've written in previous posts about how I believe that prostate cancer will only be cured if we look at it as a system of interacting cell types, almost like an ecological niche. If we attack only one cell type, as by androgen deprivation alone, for example, we are sure to cause some other deleterious cell type to take over. I was, therefore, intrigued by an interesting lab study from the University of Rochester (one of my Alma Maters

). They suggest a two-pronged approach.

For the typical androgen-sensitive cancer cell, they suggest an attack with a turmeric/curcumin derivative called ASC-J9. It seems to degrade the androgen receptor without allowing it to find away around the therapy. Interestingly, ASC-J9 is being investigated as an anti-baldness and anti-acne medicine.

For the prostate cancer stem cells, they want to accomplish the opposite: repair and stimulate the non-functional androgen receptor. When the androgen receptor on a stem cell is activated, it encourages the cell to differentiate; i.e., become less cancerous. They propose doing this with two substances. One, called 5-AZA, is in a class of of chemotherapeutic medicines called demethylating agents. It fixes old (methylated) DNA. However, although available (sold as Vidaza in the US), it can have some serious side effects. The other agent they tried against the cancer stem cells is gamma tocotrienol, which activates the ERβ receptor (see SERMs above).

In their lab studies they found that this combo suppressed castrate-resistant cancers.

livingatlake · 08-31-2012, 07:53 PM

Wow! Thank you very much. I am going to print this and keep this for any future reference. Thank you for your time spent on researching all of this and to put this into a very comprehensive manner. I wish you could sit by me as I pick away at all the myriad of info out there and keep me on track

Thanks again

Livingatlake

Baptista · 09-01-2012, 03:20 AM

Allen

I like your post and the way you spell it; “a chance at curing”. What a magical word.
This is positive thinking in rough waters which made me recall the times (15th century) of the great navigators/explorers like Vasco da Gama, Colombo or Fernao de Magalhaes.
I got roots from those (and probably genes) and I am an adventurer.
I would be looking for a cocktail prepared with “brains” and based on facts as the ones you and your friend are pointing at.
Surely I appreciate your explanations about the “brew” and its contents.

Though, I find it intriguing your assertion of castration resistance and the timing of the “cocktail party”. Castration resistant in my view is set from the very beginning but noticed later when the treatment fails (apparent progress of the disease).
In other words, the “brew” should be administered at any time independently of the status of castration resistance. The success in a cure could be expected no matter to when the cocktail party takes place. The important point to consider is that the patient is naïve to the drug even if he has experienced resistance to previous treatments. This is true if the target (inhibitor) is different from the previous one.

In my view, response to a drug stops due to the behaviour of cells that are well prepared to survive any attempt in killing them. Darwin’s principle on “natural selection” can be expected to occur at cells “levels”. This is a justifiable reason to understand behaviourism in adapting to newer environments in cells structure.
I like the newer targeted drugs (on the market or still on the drawing boards) because they better address the problem of the disease through the genes. These are in fact the source of the behaviour of the cells.

If you take into consideration my idea, the brew should include added drugs that make it possible of altering the proteins in specific cells prone to become cancerous. While some attack from the front others close down the escape from the ambush.
Inhibiting a cell of androgens is for me like typing the same key on a keyboard. The resistance is there from the beginning. It may provide control but cure becomes ambiguous.
You may have read already these articles circulating in the net with the titles; “Many drugs are doomed to fail from the beginning; a Darwin’s Principle”, and “Links between Nutrients, Genes and Cancer Spread Documented”.

In any way, we know that chemotherapy is in fact the only possible way of combating cancer because it can reach all parts in the body where those cells are hiding. Success from radical treatments is limited to the parameter of knowing exactly were cancer is located (predefined targets) which modern equipments or techniques still cannot identify totally.
Lots of guessing and no Silver Bullet.

I am thrilled for your endeavour. Advancement in medicine can be felt in procedures like this of yours. Thanks in advance for sharing your ideas.

Regards.
Baptista

Tall Allen · 09-01-2012, 01:03 PM

Baptista,

I quite agree that we must view the cancer as an evolving ecological niche of cell types, each impacting one another. We know that cells send molecular "signals" to one another; a nearby healthy cell may induce a cancer cell to differentiate, whereas as nearby cancer cell may induce a healthy cell to de-differentiate, becoming more stem-cell like (i.e., more cancerous). As you point out, targeting only the androgen-dependent cell population induces adaptive changes in some of those cells. It also kills off some of the androgen-dependent cells (healthy and cancerous alike) which allows for the growth of androgen-independent cells to take over the ecological niche, just as spraying Roundup to get rid of one weed may allow a Roundup-resistant weed to take over.

I was fascinated by the following paper published this week about cancer stem cells. The authors argue that "stemness" (i.e., lack of differentiation) is a dynamic process. They hypothesize that all prostate cancer cells possess stem cell properties and that the "stemness" is modulated by the microenvironment. A key prediction of their model is that to cure prostate cancer, all prostate cancer cells (both those already exhibiting stem-cell like properties and those that haven't yet) should be eliminated at once. Otherwise, the ones that haven't yet will be induced to.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3423925/

This is similar to something I put forward in a recent post where I discussed efforts to mathematically model the cancer as a system of dynamically changing and interacting cell types:
http://www.healthboards.com/boards/cancer-prostate/885192-blood-work-before-iadt-vacation.html
I would add to that the following model by Gatenby and Vincent that argues for a multi-modal approach:
http://www.ncbi.nlm.nih.gov/pubmed/14555711

We all discussed Hussain's presentation at this year's ASCO meeting about how continuous ADT was superior to intermittent ADT in men who had metastatic yet still hormone-sensitive PC. Yet we saw this week that in a Canadian study of men with a recurrence after RT, IADT was not inferior to cADT:
http://www.ncbi.nlm.nih.gov/pubmed/22931259

Perhaps the difference is that the "stemness" of the metastatic disease was already well-established in Hussain's study group and it was too far gone to be slowed by the re-introduction of androgens during the vacations; whereas the Canadian group had more of the non-stem-like cell type that was better maintained during the vacation periods when testosterone was allowed to rise.

If my hypothesis is true, the timing of various therapies will be important in determining their curative power. It may be impossible to restore the ecological balance of cell types once they have progressed (or been pushed by our well-meaning interventions) beyond a certain tipping point.

- Allen

Baptista · 09-02-2012, 05:08 AM

Allen

Thanks for the answer. You have shown in past posts that you are well “educated” over cells interaction and their types. You are the top guy I have come across in PCa dedicated forums discussing about it. I recall exactly your entry where you exposed your theories in the theme of cells types (http://www.healthboards.com/boards/cancer-prostate/885192-blood-work-before-iadt-vacation-3.html#post4914354) and now in regards to stemness stem cells.

In my researches on the subject to cancer cells I read about the confusion

among the scientists regarding stemness. They compared the behavior of such cells as being different so that they would not fall in the same theory that characterize stem cells. Instead they “referenciated” the fact to a unique set of genes expressed in stem cells in charge of doing a particular job
I recall reading about similar stem cells; say the prostate, which are “produced” in different levels. Some would act as a daily handyman ready for action immediately (sort-term stem cells) and others would be spared for a latter precise job (specialist long-term stem cells). All seems to be set by the genes instructions and these may alter if their environment changes, but they are the same type of cell. Or is there where Stemness appears?

I think that your comment regarding “the timing of the various therapies” relates to the various “brews” you comment above. This is what I regard as important of including in the brew other drugs that would address the problematic genes. Without knowing what is regulating or causing cells of becoming cancerous your cocktail party will be subjected to schedules and you may have to “invite” the participants latter to a repeated “gathering”.

I would like to learn more about your experiences.

Best.
Baptista

Inti447 · 09-07-2012, 01:56 AM

Hi Baptista

I`m really glad you`re doing well.

I came across this in a health magazine:- "Ginseng appears to help relieve the fatigue experienced by 90% of people with cancer, according to a study that pitted ginseng capsules against placebo."

Best Wishes

Tall Allen · 10-24-2012, 03:46 PM

I wanted to update on my friend. While he's waiting to get the C11-Acetate PET/CT done next week, he's been taking the gamma-tocotrienol. He said that his PSA doubling rate has been "like clockwork" doubling every month. He said that after one month of taking the gamma-tocotrienol, his PSA velocity has dropped by 40%. He says he's done nothing else differently, so he attributes the improvement only to the supplement.

- Allen

Baptista · 10-25-2012, 02:25 AM

Quote:

Originally Posted by T*** ***en

I wanted to update on my friend. While he's waiting to get the C11-Acetate PET/CT done next week, he's been taking the gamma-tocotrienol. He said that his PSA doubling rate has been "like clockwork" doubling every month. He said that after one month of taking the gamma-tocotrienol, his PSA velocity has dropped by 40%. He says he's done nothing else differently, so he attributes the improvement only to the supplement.

- ***en

Thanks for the update.
Could you ask your friend to get a Total Testosterone (plus a DHT if possible) before the C11 PET/CT?
The results would provide a "clue" to the positive action of gama-tocotrienol, clean of the C11 acetate.

Best
Batista

Tall Allen · 10-26-2012, 12:51 PM

He's on continuous Avodart, so his DHT remains low. His T levels are high and have been high (no change) because he was only on Casodex/Avodart on his last round of hormone treatment. He had a good PSA response (undetectable) from just that combo, although he plans to be Firmagon and Zytiga next time, if there is a next time.

He was delighted that his PSA velocity slowed over the previous month, which he can only attribute to the gamma-tocotrienol.

- Allen

Ocibote · 10-30-2012, 06:11 PM

Very interesting about the gamma tocotrienols. I have been looking for a source of straight gamma tocotrienol. All seem to be mixed either with tocopherols or with other tocotrienols.
Would you be so kind as to inquire of your friend what his source is? I'd really appreciate it.
Many thanks, Ann

Tall Allen · 10-30-2012, 09:36 PM

You can mix the tocotrienols (γ & δ), as long as it's pretty low on alpha-tocopherol (Vitamin E). Apparently, they have to extract it from annatto beans. He uses Unique E brand, but I see there are others made by Nutricology, Allergy Research Group and possibly other brands that you can find at health food stores or online.

Ocibote · 10-31-2012, 07:11 AM

Thanks Tall Allen. Looks like something to try for some. John however is on Lovenox, a blood thinner, and I just remembered that vitamin E may increase bleeding risk. Too bad.
Ann

Tall Allen · 10-31-2012, 10:01 AM

There's been some recent evidence that anticoagulants may have a beneficial effect on PC. In a retrospective study, researchers found that men who took anticoagulants (which included Lovenox (enoxaperin), aspirin and others) had a markedly reduced risk of death from high-risk PC. The 10 year risk was only 4% for those on blood thinners vs 19% for those not taking any. This was only a retrospective study, so the usual caveats apply.

http://www.ncbi.nlm.nih.gov/pubmed/22927523

Perhaps John should ask his cardiologist if he can add the tocotrienol. I have a friend on blood thinners (I seem to have a lot of sick friends. It comes with age, I guess) who regularly monitors his blood with a home machine and adjusts his anticoagulant dosage accordingly.

- Allen

Ocibote · 10-31-2012, 06:14 PM

Thanks Tall Allen. Yes, we are aware of the effect of Lovenox on progression of PC. According to scans, John does not have distant metastases. However he has spread of the disease into the bladder and has blocked ureters too. He had brachytherapy in 2000.

It is certainly a good idea to ask the hematologist about taking gamma tocotrienols. With Lovenox, unlike coumadin, there is not a blood test that is done to check on clotting levels. Apparently the anti-coagulation effect is very consistent based on weight. He is not to take aspirin or Ibuprofen etc but is not restricted in any way in diet and most supps.

At the moment John is having some bleeding problems from bladder. Not uncommon in his situation but more worrisome because he is on Lovenox. He does adjust the amount of Lovenox himself as taught by the nurse practitioner. He has been on Lovenox for 4 years now.

He sees the urologist tomorrow and hopefully we will know more then.

Thanks for your help. Ann

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