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  • trichrider
    replied
    Cancer

    CBD exerts antiproliferative/proapoptotic effects (IC50 in the 5–25 ?M range) in several tumor cell lines, including human breast, prostate and colorectal carcinoma, gastric adenocarcinoma, and rat glioma and transformed thyroid cells (478). In human prostate carcinoma cells, CBD induces apoptosis and expression of PUMA and CHOP, two markers of intrinsic apoptotic pathways (194). The production of ROS is at least in part responsible for the antitumor activity of the phytocannabinoid both in vitro (194, 478, 539, 547) and in vivo (800).
    The ability of CBD to inhibit cancer cell viability and proliferation can be reversed in vitro in the presence of blockers of either CB2, TRPV1, TRPM8, cyclooxygenase-2 (COX-2), or PPAR? (reviewed in Ref. 548), and in vivo in the presence of a PPAR? antagonist (713) ( THC???). Furthermore, CBD is able to inhibit cancer cell invasion and metastasis (478, 548, 715). These actions, in highly aggressive human breast cancer cells, are in part mediated by inhibition of epidermal growth factor (EGF), NF-?B, ERK/AKT, and matrix metalloproteinase 2 and 9 signaling pathways (238). CBD also reduces angiogenesis through actions on both tumor and endothelial cells (809) (Figure 1).

    FIGURE 1.

    Schematic representation of the main signaling pathways through which (endo)cannabinoids impact proliferation, apoptosis, migration, and angiogenesis in cancer. Blue arrows indicate pathways initiated by cannabinoid/vanilloid receptor-mediated mechanisms, and red arrows indicate non-cannabinoid/vanilloid receptor-mediated mechanisms. Continuous lines indicate stimulation, and dotted lines indicate inhibition. AC, adenylyl cyclase; CBD, cannabidiol; CBG, cannabigerol; eCBs, endocannabinoids; ER, endoplasmic reticulum; ?9-THC, ?9-tetrahydrocannabinol; PKA, protein kinase A; AKT, protein kinase B; PI3K, phosphatidylinositol 3-kinase; ERK, extracellular regulated kinase; MAPK, mitogen-activated protein kinase; mTOR, mammalian target of rapamycin; ROS, reactive oxygen species; p27/p21, cyclin-dependent kinase inhibitor proteins.


    https://journals.physiology.org/doi/...rev.00002.2016


    ..so if THC antagonizes (imo blocks) sites where CBD might be more effective, then instead of THC blocking the sites responsible for endocannabinoid expression, perhaps a reduction in THC in treatment is required for the CBD to excite immune response in apoptosis and CC proliferation.


    it is shown CBD is anxiolytic, and we all here know or think we know that THC induces paranoia...then reasoning that ingesting THC is anxiogenic and reducing the intake of THC may be a more appropriate treatment for the anxiety.

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  • Guest's Avatar
    Guest replied
    Originally posted by trichrider View Post
    It is now well established that ?9-THC is a cannabinoid CB1 and CB2 receptor partial agonist and that depending on the expression level and coupling efficiency of these receptors it will either activate them or block their activation by other cannabinoids. Further research is now required to establish in greater detail the extent to which the in vivo pharmacology of ?9-THC is shaped by these opposing actions both in healthy organisms, for example following a decrease in cannabinoid receptor density or signalling caused by prior cannabinoid administration, and in animal disease models or human disorders in which upward or downward changes in CB1/CB2 receptor expression, CB1/CB2-receptor-coupling efficiency and/or in endocannabinoid release onto CB1 or CB2 receptors have occurred in cells or tissues that mediate unwanted effects or determine syndrome/disease progression. The extent to which the balance between cannabinoid receptor agonism and antagonism following in vivo administration of ?9-THC is influenced by the conversion of this cannabinoid into the more potent cannabinoid receptor agonist, 11-OH-?9-THC, also merits investigation.
    Turning now to CBD, an important recent finding is that this cannabinoid displays unexpectedly high potency as a CB2 receptor antagonist and that this antagonism stems mainly from its ability to induce inverse agonism at this receptor and is, therefore, essentially non-competitive in nature. Evidence that CB2 receptor inverse agonism can ameliorate inflammation through inhibition of immune cell migration and that CBD can potently inhibit evoked immune cell migration in the Boyden chamber raises the possibility that CBD is a lead compound from which a selective and more potent CB2 receptor inverse agonist might be developed as a new class of anti-inflammatory agent. When exploring this possibility it will be important to establish the extent to which CBD modulates immune cell migration through other pharmacological mechanisms. There is also a need for further research directed at identifying the mechanisms by which CBD induces signs of inverse agonism not only in CB2-expressing cells but also in brain membranes and in the mouse isolated vas deferens.
    Important recent findings with ?9-THCV have been that it can induce both CB1 receptor antagonism in vivo and in vitro and signs of CB2 receptor activation in vitro at concentrations in the low nanomolar range. Further research is now required to establish whether this phytocannabinoid also behaves as a potent CB2 receptor agonist in vivo. Thus, a medicine that blocks CB1 receptors but activates CB2 receptors has potential for the management of certain disorders that include chronic liver disease and also obesity when this is associated with inflammation. The bases for the ligand and tissue dependency that ?9-THCV displays as an antagonist of CB1/CB2 receptor agonists in vitro also warrant further research. In addition, in view of the structural similarity of ?9-THCV to ?9-THC, it will be important to determine the extent to which ?9-THCV shares the ability of ?9-THC, and indeed of CBD, to interact with pharmacological targets other than CB1 or CB2 receptors at concentrations in the nanomolar or low micromolar range. It will also be important to establish the extent to which CB1- and CB2-receptor-independent actions contribute to the overall in vivo pharmacology of each of these phytocannabinoids and give rise to differences between the in vivo pharmacology of ?9-THC or ?9-THCV and other cannabinoid receptor ligands such as CP55940, R-(+)-WIN55212 and SR141716A.
    Finally, cannabis is a source not only of ?9-THC, CBD and ?9-THCV but also of at least 67 other phytocannabinoids and as such can be regarded as a natural library of unique compounds. The therapeutic potential of many of these ligands still remains largely unexplored prompting a need for further preclinical and clinical research directed at establishing whether phytocannabinoids are indeed ‘a neglected pharmacological treasure trove' (Mechoulam, 2005). As well as leading to a more complete exploitation of ?9-THC and CBD as therapeutic agents and establishing the clinical potential of ?9-THCV more clearly, such research should help to identify any other phytocannabinoids that have therapeutic applications per se or that constitute either prodrugs from which semisynthetic medicines might be manufactured or lead compounds from which wholly synthetic medicines might be developed.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/



    so it appears that THC AND CBD can be antagonists to binding CB1 AND CB2 receptor sites...which is news to me. they may also inhibit endogenous agonists re immune cell receptor.
    Yep, and yet Weez said his PSA didn't drop under JUST THC extract tx, but rather after he had added the CBD tincture/oil.

    That caused me to wonder if there was either some sort of saturation reached, that stopped the THC from being as effective, or the issue Weez raised, re. tolerance to the THC/cell apoptosis, and the 'tougher' cancer cells no longer responding to cannabinoids in general.

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  • trichrider
    replied
    It is now well established that Delta9-THC is a cannabinoid CB1 and CB2 receptor partial agonist and that depending on the expression level and coupling efficiency of these receptors it will either activate them or block their activation by other cannabinoids. Further research is now required to establish in greater detail the extent to which the in vivo pharmacology of

    Delta9-THC is shaped by these opposing actions both in healthy organisms, for example following a decrease in cannabinoid receptor density or signalling caused by prior cannabinoid administration, and in animal disease models or human disorders in which upward or downward changes in CB1/CB2 receptor expression, CB1/CB2-receptor-coupling efficiency and/or in endocannabinoid release onto CB1 or CB2 receptors have occurred in cells or tissues that mediate unwanted effects or determine syndrome/disease progression. The extent to which the balance between cannabinoid receptor agonism and antagonism following in vivo administration of Delta9-THC is influenced by the conversion of this cannabinoid into the more potent cannabinoid receptor agonist, 11-OH-Delta9-THC, also merits investigation.


    Turning now to CBD, an important recent finding is that this cannabinoid displays unexpectedly high potency as a CB2 receptor antagonist and that this antagonism stems mainly from its ability to induce inverse agonism at this receptor and is, therefore, essentially non-competitive in nature. Evidence that CB2 receptor inverse agonism can ameliorate inflammation through inhibition of immune cell migration and that CBD can potently inhibit evoked immune cell migration in the Boyden chamber raises the possibility that CBD is a lead compound from which a selective and more potent CB2 receptor inverse agonist might be developed as a new class of anti-inflammatory agent. When exploring this possibility it will be important to establish the extent to which CBD modulates immune cell migration through other pharmacological mechanisms. There is also a need for further research directed at identifying the mechanisms by which CBD induces signs of inverse agonism not only in CB2-expressing cells but also in brain membranes and in the mouse isolated vas deferens.
    Important recent findings with ?Delta9-THCV have been that it can induce both CB1 receptor antagonism in vivo and in vitro and signs of CB2 receptor activation in vitro at concentrations in the low nanomolar range. Further research is now required to establish whether this phytocannabinoid also behaves as a potent CB2 receptor agonist in vivo. Thus, a medicine that blocks CB1 receptors but activates CB2 receptors has potential for the management of certain disorders that include chronic liver disease and also obesity when this is associated with inflammation. The bases for the ligand and tissue dependency that Delta9-THCV displays as an antagonist of CB1/CB2 receptor agonists in vitro also warrant further research. In addition, in view of the structural similarity of Delta9-THCV to Delta9-THC, it will be important to determine the extent to which Delta9-THCV shares the ability of Delta9-THC, and indeed of CBD, to interact with pharmacological targets other than CB1 or CB2 receptors at concentrations in the nanomolar or low micromolar range. It will also be important to establish the extent to which CB1- and CB2-receptor-independent actions contribute to the overall in vivo pharmacology of each of these phytocannabinoids and give rise to differences between the in vivo pharmacology of Delta9-THC or Delta9-THCV and other cannabinoid receptor ligands such as CP55940, R-(+)-WIN55212 and SR141716A.
    Finally, cannabis is a source not only of Delta9-THC, CBD and Delta9-THCV but also of at least 67 other phytocannabinoids and as such can be regarded as a natural library of unique compounds. The therapeutic potential of many of these ligands still remains largely unexplored prompting a need for further preclinical and clinical research directed at establishing whether phytocannabinoids are indeed ‘a neglected pharmacological treasure trove' (Mechoulam, 2005). As well as leading to a more complete exploitation of Delta9-THC and CBD as therapeutic agents and establishing the clinical potential of Delta9-THCV more clearly, such research should help to identify any other phytocannabinoids that have therapeutic applications per se or that constitute either prodrugs from which semisynthetic medicines might be manufactured or lead compounds from which wholly synthetic medicines might be developed.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/



    so it appears that THC AND CBD can be antagonists to binding CB1 AND CB2 receptor sites...which is news to me. they may also inhibit endogenous agonists re immune cell receptor.

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  • Guest's Avatar
    Guest replied
    Originally posted by trichrider View Post
    this, and Weezard suggesting it works until it doesn't, is why i posted about CBD being an antagonist to THC...it occupies the sites where THC may bind and reduces effectiveness of other drugs that may/might also bind there.
    i have no clue whether or not it contributes to the tight chest/anxiety issue or if the CBD does either. would be interesting and most likely helpful to source some research regarding levels of antagonistic efficacy of CBD to THC.
    i'll look into the black mirror for answer...
    sorry about your bad news Wezzard.
    Thanks trich.

    And I'd read about CBD (initially I had posted it as THC AND CBD, but it was CBD, I think), interfering in the processing of a variety of drugs, per Galvano's post and the reading.

    I think the tight chest experience I was having lies at least partly at the feet of an over-active auto-immune system, cast into full self-defense mode, and seeing every thing as an opponent. I don't like the thought of going into surgery with that feature, but it is changing a bit for the better, so...

    I'm still eating fresh sauce with ^ lycopene, 2-4 oz. of broccoli sprouts each day, for the sulforaphane, (edit: sticking to the whole-plant-based diet, as well), and the THC/CBD, though upon reading Weez's report last night, I had dropped my CBD intake to half, and with 50mg/ml, I'm not at a .5ml AM and PM, and thinking of dropping that by half for at least one of those doses.

    I'm tossing every bit of ammunition I have at it, on the hope that the items don't inhibit each others' effectiveness.

    I am resigned to the reality that there wil be some loss of some function in either course of formal treatment, and like Weez, I am heading in soon (I hope), maybe this next week, for another PSA, A1C, and lipid draw, to chart any progress, as well as having sent an inquiry to the surgeon this AM, asking where the labs in the chart came from, as the PSA doesn't reflect the labs I last saw, so raised some questions.
    Last edited by moose eater; 01-30-2021, 23:21.

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  • trichrider
    replied
    Originally posted by moose eater View Post
    Sorry to read of the back-steps, Weez.

    It's not my thread. I started it, and commandeered the frequency of posts, but I think that any input of value for treating prostate cancer, and even some others, ought to be welcome here.

    There are so many components to this thing, from the initial shock (long gone for you), the maps of treatment, and following success or failure at that stage, then into later battles, and some finding the tenacity of this stuff, while others catch a break and go on, yet many always worried when it's coming back.

    I admire your facing into the wind and taking time to use this as an opportunity for research. Seriously..

    I sent you a PM with my thoughts re. cause and effect relationships, and it might be more broad than I initially began to write, once I thought about it.

    I think adjusting the THC to a greater dose, and/or decreasing the CBD, if what Galvano posted (and I read similar elsewhere) has merit, and CBD can slow down the processing of (some) other compounds or drugs in the liver.

    Is your CBD decreasing the effects of your THC? No clue, other than what's been posted or read.


    this, and Weezard suggesting it works until it doesn't, is why i posted about CBD being an antagonist to THC...it occupies the sites where THC may bind and reduces effectiveness of other drugs that may/might also bind there.
    i have no clue whether or not it contributes to the tight chest/anxiety issue or if the CBD does either. would be interesting and most likely helpful to source some research regarding levels of antagonistic efficacy of CBD to THC.
    i'll look into the black mirror for answer...
    sorry about your bad news Wezzard.

    Leave a comment:


  • Guest's Avatar
    Guest replied
    Last night, as we reviewed more recent data, and realized that, at least looking a generic research, for those in my stage of cancer (reportedly a T1C now, though looking at the PSA they based that on, I think I need to make some more corrections to records now; not uncommon at all for anyone who has ever requested to view their records), for EBRT & brachy seeds, versus radical prostatectomy, with unilateral nerve-sparing tx, there is a fairly consistent problem or outcome with erectile dysfunction on both paths, and lesser issue with urinary incontinence with radiation.

    Going with the surgeon's initial reports, based on HIS clinic's data, 90% probability (for the entire group) of no urinary incontinence (or a 10% chance of having urinary incontinence to some measurable degree), and a 25% chance of being able to experience a spontaneous erection (or 75% chance -against- that outcome), without adding some sort of tx. specifically geared toward ED.

    My younger son initially sticking to the words of the local urologist; if you want to be able to have the majority of options remaining should the cancer return, then go with surgery, as you can still do EBRT later. <paraphrased>.

    My wife's input last night was that there's all sorts of things that need to be done, whether it's adventures with our youngest son, or building her sauna, finishing other projects, etc. She said, "You don't need an erection for any of those things."

    She added that the loss of the ability to have spontaneous sex can be overcome, but that it affects me far more than her, due to differences in requirements for sexual activity <men's needs, versus the needs of a woman, as far as what leads to sexual satisfaction>, therefore, concluding that this is more something that concerns my ability or disability, but that it is only -one- aspect of life, not all of life..

    We discussed both unwelcome, but possible outcomes, as also being tied to age in general, among men. That eventually, copping a woody or not having any leakage, simply become wishes for many older men, so if it doesn't provide what I'd like via either procedure, I'm only a bit ahead of many men in general.

    Consolation prizes and truth, all rolled into one.

    At that point, it at least enters the thought process that I/we really don't need to move on this right away... except metastases is a path that leads to misery, for the last numerous years preceding succumbing, and the quality of life in that phase is not to even be discussed as an option or attractive image to look forward to.

    So, I will phone the nurse/scheduler for the radio-oncologist, and see if the 1 question I've received an answer to, is the limit for post-appt. questions, or if there's another message, and if need be, schedule another consultation, if that is what it requires to get the remaining questions answered. Though it seems as though the more thorough answers and descriptions of the larger issue have come from the surgeon.

    And at this point, a first post-appt list of questions not answered elsewhere, is in order, to send to the surgeon..

    The surgeon has already told me the procedure with him was conditional, or tentative, based on my first speaking with the radio-oncologist Doc, as the surgeon is "concerned he might disappoint me in the outcomes, based on what I want to see occur." Our interpretation of that statement is that they are worried that if I don't find acceptance of my outcomes after surgery, they fear I might sue them. Not based particularly on anything threatening of that sort I've uttered to them, but simply the expectations or hopes of the patient; me.

    On another level, radiation would require 2 trips down for prep and implanting of the seeds, then EBRT for 5 weeks (likely in Seattle), meaning another 38 days away from familiar settings, loved ones, etc., versus my decision that if surgery is the decision, even if I stay the additional time post-op, to make extra sure there's no post-procedure complications, infections, etc., I'm gone 1 time for all of about 10 days. In that way, logistics are a part of this as well, only in as far as a support group (my immediate 2 family members) is truly important; familiar setting and related greater calm, if calm is a word that can be used (sometimes it can't lately), are very important factors.

    That's the status. Yes, we're closer to making the decision. No, there are few outcome criteria that wave the giant green flag. And my wife is right; there's a lot of things here for me to take care of, that don't require a spontaneous erection, but they do require me to be here, alive, ambulatory, etc..

    -------------------------------------------------

    Fitting cynical humor, a 'la a tune and video...

    Kurt Vile

    'Loading Zones'

    https://www.youtube.com/watch?v=7mbh...fkN-8&index=27

    Life's gonna' cost us all something. How much, is the question.
    Last edited by moose eater; 01-30-2021, 19:27.

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  • buzzmobile
    replied
    Originally posted by Weezard View Post
    So, what do you folks think?

    Aloha,
    Weeze
    I think your continuing to add to this thread is a good thing. I'm 10 years behind you, but I'm not trying to catch up. I hope that there are 10 more in my future.

    I'm gonna have to get a grip and start thinking, objectively.
    What are your thoughts now, Weeze?

    Leave a comment:


  • Guest's Avatar
    Guest replied
    Originally posted by Weezard View Post
    Howzit, y'all?

    I promised to post my PSA test here.
    As you can imagine, I was expecting great news so I pushed for an early test.
    This is not the case.

    Last 2 tests were a rollercoaster. Went from 21.6 ng. to 6.94. In a 9 month period.
    That seemed too good to be true. And, in fact, it was.

    I asked for a second test.
    That came in at 22 ng..

    An increase of only 0.4 ng. in 9 months.
    Thought it was due to the addition of CBD.
    So, I pushed for another test at 4 months.

    It had jumped to 29 ng. in that short a time!
    That's a doubling rate of about 13 months!
    If this keeps up I'm looking at <10 years.

    Hmm, when I think about it, no big deal. I'm pushing 78 now.
    I'm definitely going to beat the averages.

    There's a slim chance that this lab is not to be trusted.
    Would make finding proper dosage a crap shoot.

    There is also the chance that cannabis works well, until it doesn't.
    This happens with other treatments.

    The cancer cells that are less effected just naturally become the majority.

    I'm gonna have to get a grip and start thinking, objectively.
    So, I'm asking for input.
    Any and all thoughts are welcome.

    No wanna hijack M. E.s thread, so will move this to a new thread if it gets busy.
    So, what do you folks think?

    Aloha,
    Weeze
    Sorry to read of the back-steps, Weez.

    It's not my thread. I started it, and commandeered the frequency of posts, but I think that any input of value for treating prostate cancer, and even some others, ought to be welcome here.

    There are so many components to this thing, from the initial shock (long gone for you), the maps of treatment, and following success or failure at that stage, then into later battles, and some finding the tenacity of this stuff, while others catch a break and go on, yet many always worried when it's coming back.

    I admire your facing into the wind and taking time to use this as an opportunity for research. Seriously..

    I sent you a PM with my thoughts re. cause and effect relationships, and it might be more broad than I initially began to write, once I thought about it.

    I think adjusting the THC to a greater dose, and/or decreasing the CBD, if what Galvano posted (and I read similar elsewhere) has merit, and CBD can slow down the processing of (some) other compounds or drugs in the liver.

    Is your CBD decreasing the effects of your THC? No clue, other than what's been posted or read.
    Last edited by moose eater; 01-30-2021, 11:38.

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  • sdd420
    replied
    Originally posted by Weezard View Post
    Howzit, y'all?

    I promised to post my PSA test here.
    As you can imagine, I was expecting great news so I pushed for an early test.
    This is not the case.

    Last 2 tests were a rollercoaster. Went from 21.6 ng. to 6.94. In a 9 month period.
    That seemed too good to be true. And, in fact, it was.

    I asked for a second test.
    That came in at 22 ng..

    An increase of only 0.4 ng. in 9 months.
    Thought it was due to the addition of CBD.
    So, I pushed for another test at 4 months.

    It had jumped to 29 ng. in that short a time!
    That's a doubling rate of about 13 months!
    If this keeps up I'm looking at <10 years.

    Hmm, when I think about it, no big deal. I'm pushing 78 now.
    I'm definitely going to beat the averages.

    There's a slim chance that this lab is not to be trusted.
    Would make finding proper dosage a crap shoot.

    There is also the chance that cannabis works well, until it doesn't.
    This happens with other treatments.

    The cancer cells that are less effected just naturally become the majority.

    I'm gonna have to get a grip and start thinking, objectively.
    So, I'm asking for input.
    Any and all thoughts are welcome.

    No wanna hijack M. E.s thread, so will move this to a new thread if it gets busy.
    So, what do you folks think?

    Aloha,
    Weeze
    Dang Weeze sorry buddy. What about adding in some mushrooms like turkey tail or Chaga etc. Try to double that 10 years. I just want to support you and wish you the best. Peace sdd420

    Leave a comment:


  • Weezard
    replied
    Howzit, y'all?

    I promised to post my PSA test here.
    As you can imagine, I was expecting great news so I pushed for an early test.
    This is not the case.

    Last 2 tests were a rollercoaster. Went from 21.6 ng. to 6.94. In a 9 month period.
    That seemed too good to be true. And, in fact, it was.

    I asked for a second test.
    That came in at 22 ng..

    An increase of only 0.4 ng. in 9 months.
    Thought it was due to the addition of CBD.
    So, I pushed for another test at 4 months.

    It had jumped to 29 ng. in that short a time!
    That's a doubling rate of about 13 months!
    If this keeps up I'm looking at <10 years.

    Hmm, when I think about it, no big deal. I'm pushing 78 now.
    I'm definitely going to beat the averages.

    There's a slim chance that this lab is not to be trusted.
    Would make finding proper dosage a crap shoot.

    There is also the chance that cannabis works well, until it doesn't.
    This happens with other treatments.

    The cancer cells that are less effected just naturally become the majority.

    I'm gonna have to get a grip and start thinking, objectively.
    So, I'm asking for input.
    Any and all thoughts are welcome.

    No wanna hijack M. E.s thread, so will move this to a new thread if it gets busy.
    So, what do you folks think?

    Aloha,
    Weeze

    Leave a comment:


  • Guest's Avatar
    Guest replied
    Oh.. The good news today, other than most of us are still here, is that the 4 sticky cards ('sensor cards', since their obscene price increase) have no flyers on them. So I can assume that what ever I THOUGHT I saw in the recovering moms box, was either something with no real interest in cannabis, or its died since, or they're laying eggs, or I was seeing peripheral images that weren't really there.

    Either way, cool.

    As far as which plant will get to become the next batch of medicine, one member had advised they liked the Satori for the effect, and I'll go along with that for at least a part of a run of medical for extraction. Also considering one of the White Lotus, but want to do some more reading re. others' perceptions and any analysis of potency and cannabinoid array I might find.

    Headed to read myself to sleep now. Bedtime cancer treatment stories.

    Leave a comment:


  • Guest's Avatar
    Guest replied
    I'm sensing from one of the recent Docs, that my OCD-generated or heightened 'need to know' in order to manage my choices and risks, is over the top, compared to many other patients.

    I have been given the set of answers & data I posted the other day, from the radio-oncologist. I'm not necessarily confident in some of those numbers, especially in light of some of the missing answers that have now been submitted 2x's or more.

    I suspect it's possible that my OCD and neediness, (and the panic initially expressed in the presence of the surgeon), as well as asking direct questions that might be difficult to answer concisely, makes me a bit of a leper where more generic patients are concerned. And I think it's an error, maybe irreversible at this point(?) to distance or create friction with persons to whom one is going to be trusting their life... literally.

    So we're reading through a STACK of the most recent and credibly-sourced research we can find (preferably nothing older than 2017), and vetting data given by the 2 Docs who hold the highest esteem thus far.. But I have found myself wondering if my neediness in recent past, has maybe brought about a sort of hand-off and 'blue-sky and sunshine' going on with one of them.

    Don't know, but can examine, assess, etc.

    Spoke the other evening, at length, with an 85-yr. old gent who had brachy seed tx., with no external radiation beam tx., about 20 years ago or so. He was 65 when he received his tx. He stated that shortly after the Palladium seeds and hormone suppression tx took maximum effect, he had difficulty maintaining his normal stream of urine. He stated the shrinking of the prostate had essentially 'throttled' or 'choked' the urethra, and restricted flow.

    He also stated that for 3 years post-brachy seeds, his ability to maintain an erection and engage in sex was fairly normal, but that at the 3-year mark, that ability began declining, and by 6 years post-procedure, he couldn't spontaneously experience an erection. He was obviously disappointed by this.

    I asked if anyone had offered him testosterone tx for this, as it had been mentioned to me by one of the current specialists. He said, "no."

    My in-depth research, reading studies and data, is muddying the water more than it is clarifying it at times, I'm not especially certain that I'm a 'welcome' patient, and I don't want to be unconscious while being viewed as less than deserving. Everything matters at this point.

    So I and my wife are headed upstairs to read some more, and see if any of the 2 primary paths reach out and slap me in the forehead this evening.

    Called the COVID-19 hotline to clarify that I was eligible for the earlier set of C-19 vaccinations as a result of comorbidities, acknowledging my ambivalence re. the vax, just in case I need to travel again for treatment in the near future, and it seems I was misinformed.

    Co-morbidities are not a determining factor at this time, for the State to accelerate anyone's status for eligibility to receive the vax, but I was assured that when the next set of eligible folks come up, and there's more vaccine, I'm in that group. In theory, some time between the end of February and the 1st of March (*Meanwhile the news stated there's a 1-shot vax coming out, maybe.. Cool).

    Notable stress about TOO MANY stops during the town trip this AM, so I ate a smaller half of the new Rx for Ativan .5mg, and between that, and the sinus strips to keep my shnoz as open as possible under my mask, and plenty of hydration before departure, I was mostly cool as a cucumber.. Up until more boundary violations by less than thoughtful, or persons in town.

    Instead of lashing out in the tenor of last confrontation, I simply said, "6 ft. or I'm apt to become hostile." but stated in a more calm, and serious voice. Which I think actually gets their attention better, and, ironically, sends the message more clearly that you meant EXACTLY what was said.

    Checked my near-antique EpiPen last night, as it had been years since I examined the expiration date, and with the way my auto-immune system is going haywire lately, I figured I ought to know what I have in the arsenal. The pen I have expired in Spring of '05. Oops.

    So there was some research done, and it was pretty clear that Epi Pens that are 3-7 years past expiration date, often have close to 90% of their original potency. That was the oldest that was tested in the research I read. So I likely have SOME amount of protection in my almost-16 years outdated Pen, and a friend is assisting in getting me a much more recent one. Likely the same friend who provided this one, 16 years ago.

    There you have it; clear as mud. I'm off to do some more (sometimes depressing) research. Doesn't look like there's always a -huge- difference in outcomes for EBRT and brachy seed tx, versus robotic radical prostatectomy.

    Perspective: https://www.cancer.org/cancer/prosta...ie%20from%20it.

    Jim Morrison & the Doors

    'Five to One'

    https://www.youtube.com/watch?v=3tHPsphg9xc
    Last edited by moose eater; 01-30-2021, 05:58.

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  • Guest's Avatar
    Guest replied
    Originally posted by sdd420 View Post
    https://youtu.be/ynYi6MWJcV0
    Stay positive
    Stay strong

    One of my favorite bands

    Thank you, sdd. You are a gem among gems. Thank you. For everything. I owe you, and hope to repay you with something special or unique one day.

    GD

    'Dear Mr. Fantasy' & 'Hey Jude'

    Foxboro, Mass., July 2, 1989

    https://www.youtube.com/watch?v=QwaK...g-wuwo&index=6

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  • Guest's Avatar
    Guest replied
    Originally posted by buzzmobile View Post
    These Days

    Safe travels, moose eater.

    Damned old SOOT!
    That was the departing tune (Gregg Allman, Laid Back Lp, 'These Days') that played all night when I left SW Michigan under a bit of duress, in about 1976. We had a party at a friend's home in the ghetto, and that Lp played most of the night.

    Later on, I would catch a ride at -53 f. in a 1958 Ford medium shorty school bus, named Maybelline (as in Chuck Berry's "Why can't you be true".. and it was appropriate, per later in this story) with a couple lads from Palmer Alaska, in front of what used to be McCrae's Truck Stop (now a Petro-Can station), about 7 miles south of Whitehorse, Yukon Territory, Canada, about 3 days before Christmas, 1977, headed back to the Upper Peninsula of Michigan by thumb, via Wisconsin and Minnesota, visiting along the way.

    The young men from Palmer had that same Gregg Allman Lp, playing on cassette.

    We kept warm with the wood stove installed in the bus, and the next day, when the pressure plate blew out, about 10-20 miles south of Teslin, Yukon Territory, we slowly parted paths... them finding a qp of Lumbo on-board they didn't realize they had, making the chocolate cake that one of their mom's had sent them on the road with, all that much tastier.

    I learned to never wear tight leather hiking boots in the cold of arctic winter, no matter how good the hand-knitted wool socks were. Tight boots compress wool, and you WILL freeze your feet. And it does hurt badly, contrary to the nonsense some spew about that issue.

    There's some SOOT in there, buzz. There truly is. Truly.

    I found this the other day, and was blown away. Rural setting, rehearsal sessions in a sound studio that appears to be in the woods some where, with a cumulative or joint effort by members of the Jefferson Airplane, CSN&Y, Jerry Garcia, Joni Mitchell, and more. Things I've never heard before, and that left a mark.

    Gerry Garcia & David Crosby

    The Perro Sessions, 1971

    https://www.youtube.com/watch?v=WELR...t_radio=1&t=68

    Take care. And keep the fish frightened of you, but not so much they won't attack your lure.
    Last edited by moose eater; 01-30-2021, 05:14.

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    Guest replied
    Originally posted by Galvano View Post
    If you don't already know beware that CBD could interact with other drugs.
    CBD is metabolized by cytochrome P450 enzymes in the liver (inhibiting them), the same enzymes are responsible for the metabolization of 50-60% of other drugs, so other drugs could remain in circulation longer than expected.

    https://thecbdinsider.com/knowledge-...-interactions/
    https://www.healthline.com/health/cb...now#the-basics

    Best wishes
    Thank you. I had read something similar, re. CBD potentially slowing the processing of some drugs through the liver, and wondered about a residual build-up. Your post echoes this.

    I ceased the Hydroxyzine the other day (4-5 days ago), had one minor effort by the rash to reappear, and with a minor dose of 1% Hydrocortisone (light-weight, over-the-counter) cream, it tucked tail; hasn't recurred.

    More irritating is the area on my right hand, where I poured the CBD and solvent concoction into the decanter, apparently thoroughly soaking my right hand for a sufficient duration of time, and scratching the bejesus out of it. 6-mil nitrile gloves next time, for sure.

    I've contemplated that it might have been the perfect storm, and bears the results of both the effects of the suspect CBD in the solvent (and anything that might be on/in that), and the reaction that I assume came about from the antihistamine/sedative they gave me that's been quit since.

    But your insight re. the possible issues with CBD are very helpful.

    Unfortunately, I can't formally discuss this with any of my healthcare providers at this time; some due to indiscretions, and some due to clinic policies.

    So reading is what we're doing a lot of these days, and I get really sleepy on a GOOD day, when I read a lot.

    But thank you. Sincerely. I am intending to get to the links you shared. Soon.

    Take care.
    Last edited by moose eater; 01-30-2021, 06:13.

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