Well, I got my bloodwork done yesterday and my ALC continues to go down. It has dropped from 43.2 to 25.4 since starting using the Cordyceps in tea, and 9 points since my last test. My hemoglobin went up and my platelets stayed steady after rising a lot in my last test. I don’t profess to know why it works, it just does. There is about 15 others that are also seeing dramatic results. I’m just sharing my experience and not trying to convince anyone of anything, I just want to share because think this is miraculous! I assume???? that the codycepin probably encourages apoptosis in the lymphocytes??
I wish everyone a happy new year!!
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Stanandvan
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I’m just waiting for Neil to come in with the studies he’s already relayed to the group 😅
I also dabbled in cordyceps (more for exercise benefits and beta-glucans), and the research I’ve seen where cordycepin (the active component of cordyceps) was beneficial was for myeloid—not lymphoid—cell lines. And I believe those studies were in vitro.
Bottom line is it’s hard to attribute the ALC drop to the cordyceps (although that’s wonderful news!).
On the other hand, just because it hasn’t yet been studied for CLL doesn’t mean it isn’t effective from an anecdotal perspective.
Keep in mind too that for 0.3% of CLL patients with a somatically hypermutated IGHV, the beta-glucan in these mushrooms may accelerate CLL growth .
Yes, although the drop in my ALC is directly attributed to the timing of starting the Cordyceps. Also, there’s about 15 of us that are having the same results.. yes, there’s also no definite proof, but seems something is going on for sure..
Could be. I’m staying on cordyceps until I run out of my current supply (a couple months worth). I have an SLL presentation which means my blood work is within normal ranges and my cells are in my nodes and spleen.
My next scan will be in the spring. Will be interested to see if cordyceps has any impact on node and spleen size. I take turkey tail as well.
Thanks for your encouraging update. I wondered how you and others trying cordyceps were going. Maybe something is going on, but the odds are highly against this, given what we do know. However, it's definitely worth investigating in far greater detail, so let's fill in as much of the missing information as possible and list some guiding principals, keeping in mind the introduction of this review article; Cordyceps – A traditional Chinese medicine and another fungal therapeutic biofactory?(2008)
Too much about Cordyceps is unsubstantiated. This literature is written to sell so-called medicines to potentially vulnerable people with serious diseases. On the other hand, there is convincing scientific information that indicates significant pharmacological properties which are worth assessing (see Table 1)
As dumbsaintmind noted, all mentioned studies were in vitro studies of myeloid, not lymphoid cell lines as I detailed previously: healthunlocked.com/cllsuppo... CLL is the most commonly diagnosed adult Non-Hodgkin's (B-cell) Lymphoma, which happens to express as a leukaemia unless you have the SLL expression. Therefore we lack relevant information on the possible mechanisms by which cordyceps might work on B cell lymphomas, specifically CLL, i.e. DNA mutational changes, cellular pathways; up and down regulations/inhibitions and so on. Even with a laboratory developed BTK targeted therapy, there are lots of off-target effects, which later generation BTKi drugs have improved on - see accompanying graphic. With a natural substance, there will be a whole range of potential factors that might cause apoptosis, as mentioned in these TCM supporting papers from Korea and and China.
Cordycepin induces cell cycle arrest and apoptosis by inducing DNA damage and up-regulation of p53 in Leukemia cells (2015)
Growth inhibition of U937 leukemia cells by aqueous extract of Cordyceps militaris through induction of apoptosis (2005)
(The U-937 myeloid pro-monocytic model cell line was used in both papers)
Cordyceps militaris is a traditional herbal ingredient, which has been used for patients suffering from cancer in Oriental medicine. In the present study, we investigated the biochemical mechanisms of anti-proliferative effects by aqueous extract of C. militaris (AECM) in human leukemia U937 cells. It was found that AECM could inhibit cell growth of U937 cells in a dose-dependent manner, which was associated with morphological change and apoptotic cell death such as formation of apoptotic bodies and DNA fragmentation. We observed the down-regulation of anti-apoptotic Bcl-2 expression and proteolytic activation of caspase-3 in AECM-treated U937 cells. However, AECM did not affect the pro-apoptotic Bax expression and activity of caspase-9. Furthermore, Western blotting and RT-PCR revealed that AECM treatment caused a dose-dependent inhibition of cyclooxygenase-2 and prostaglandin E2 accumulation. Taken together, these results indicated that the anti-proliferative effects of AECM were associated with the induction of apoptotic cell death through regulation of several major growth regulatory gene products such as Bcl-2 family expression and caspase protease activity, and AECM may have therapeutic potential in human leukemia treatment.
Does anyone see the irony of encouraging the use of an untested substance, which a study paper claims works by causing mutations and then up-regulating p53, when the CLL world has moved on from chemo treatments that work by causing DNA damage while still recommending staying untreated in watch and wait as long as possible, despite access to now proven better targeted therapies?
Importantly, if cordyceps does cause mutations in myeloid leukaemias, it's likely to do so in other body cells, so there's a risk of secondary primary cancers. That's where we need to have functional TP53. No-one with mutated TP53 or 17p del CLL should take cordyceps, because they could be causing harder to treat CLL clones. Also, there would theoretically be a higher risk of secondary primary cancers, because of how CLL inhibits our T cell surveillance of body cells turning cancerous.
Dumsaintmind's warning about fungal beta glucan is more important than the 0.3% figure might indicate. That figure is from one study, so is likely to vary depending on the study location, as it could be influenced by environmental exposure and genetic background of study participants. See; A mutated B cell chronic lymphocytic leukemia subset that recognizes and responds to fungi
Firstly, congratulations on stating the absolute changes in your ALC. This is what we need - quantitative data, such as records of absolute counts and date taken. Unfortunately, statements such as "hemoglobin went up" and "platelets stayed steady after rising a lot", "15 others that are also seeing dramatic results" are far less helpful. Let's keep the information scientific! Members who wish to share their experiences can do so by providing information in their bio - shortcut link healthunlocked.com/profile/... or plots of their blood counts or other relevant information in posts/replies.
That your haemoglobin has improved might be important - it could indicate that your CLL bone marrow infiltration has lessened, or it could just be part of the normal variation in your reported haemoglobin result due to other factors, including equipment calibration for which I've seen reproducibility figures of +/-0.1 to +/- 0.3. So in the worst case scenario, it's possible for a reported haemoglobin result to vary from say 14.0 to 14.6 when testing the same blood sample.
I would encourage everyone interested in how their blood counts are changing to use a spreadsheet, such as this one provided by the CLL Society, to record their counts.
"..white blood cell counts and overall cholesterol levels were among the most variable.
:
In addition, the researchers noted that, although they controlled subjects’ eating and physical activity, data from blood samples collected earlier in the day were sometimes significantly different from samples taken from the same subjects later in the day."
Blood Tests - accuracy and precision; why trends are important
Below I've attached the analysis of the off target effects of 5 different targeted BTKi drugs, for which we now have data from many thousands of CLL patients. (I hit the 7,000 character limit in my reply above.) The advantage provided by proven pharmaceutical drugs, is that just one active ingredient (which might have been identified in a cordyceps variety, for example, is analysed for how it works and the structure modified to improve the desired effect at a lower dose, while minimising off-target effects. Other changes may be made to provide resistance against digestion, improved absorption through the gut wall, longer half-life by changing how it is metabolised by the liver and so on.
With a natural substance - just as is reported in the many cordyceps studies, there are going to be a range of possible biological effects which will vary from person to person. Anyone taking a natural substance in the hopes of changing their health, should first check for potential interactions with what else they are taking and then keep a health diary to record any changes in their health. With CLL, we need to look at how the total tumor is changing, both in magnitude and distribution. Are the spleen and nodes shrinking or growing? What's happening with other blood counts, primarily haemoglobin and platelets as you are monitoring. How are the other noted biological effects of the substance impacting your overall health?
You are effectively doing a phase 1 trial - the most risky type of trial. The quality of what you are taking won't be as well quantified as what is used in clinical trial studies, so take care and keep your doctor and CLL specialist informed of what you are doing.
Neil
Varying off target effects of different BTK inhibitors; circle size indicates magnitude
"The advantage provided by proven pharmaceutical drugs, is that just one active ingredient (which might have been identified in a cordyceps variety, for example, is analysed for how it works and the structure modified to improve the desired effect at a lower dose, while minimising off-target effects." - reading about the side effects of chemo and the targeted therapies many report on this forum, I wonder whether drinking cordyceps tea causes similar. Months long diarrheas and terrible headaches? The advantage of the novel drugs is clear, the disadvantage is that they cost an arm and a leg, unfortunately.
It would be interesting to know whether drinking cordyceps tea is reducing the count of healthy lymphocytes too, or selectively targets monoclonal ones.
Neil, my hemoglobin went from 134 in August to 138 in October to 143 in December. My platelets went from 156 in August to 194 in October to 178 in December. I started during the tea after my blood test in August.
Hi Lovely67, I follow a pretty strict protocol, I never boil. I use freeze dried Cordyceps. I grind them in a small coffee grinder, and steep them in 8 ounces of water for 15 minutes at 176 degrees. I then pour into a cup and drink the tea and eat the residual Cordyceps. I use 1 gram of Cordyceps twice daily. It acts tastes very good. The steeping at that temp supposedly unlocks the most cordycepin., as does grinding them. This is just what I do from what I’ve read. I have tried many things to try and slow the proliferation of lymphocytes, lots of different supplements etc, change in diet, lots of exercise. I think that those changes have made me healthier, but this is the only thing that has worked for me in lowering my lymphocyte count. I acknowledge that we are all different and what works for one may not work for another, I’m just trying to share my experience.
That's a most interesting result. Any chance to find out the ratio between your healthy and monoclonal B cells? With higher ALC numbers most of the ones eliminated will sure be monoclonal but as the number gets lower the difference could show. In short: does this work like chemo or does it target monoclonal cells preferentially?
Hi LeoPa, interesting question and I won’t pretend to know the answer. I will discuss with my hematologist when I meet with him to see if there is a test that can determine that.
Stanandvan and LeoPa, an immunophenotyping blood test reports the number of B and T leukaemia cells as well as the number of monoclonal B, or in in our case CLL cells.
The only drug or substance that targets CLL without also targeting healthy B cells that I know of is Cirmtuzumab, an ROR-1 inhibitor drug, but sadly, it didn't prove that successful when trialled. To achieve this level of selectivity, the active ingredient needs to target something found only in the cancerous cells and that's extremely difficult, as you can see from the plots I provided above, for 5 different BTK inhibitors that were specifically engineered to be highly selective for BTK. healthunlocked.com/cllsuppo...
"Studies with ROR1-specific mAbs have confirmed that surface ROR1 is expressed by CLL cells, but not by normal B lymphocytes,10,22,23 including normal CD5 B cells.10"
It's interesting to look at the impact of drugs used to treat CLL on healthy B cells at different stages in their life cycle. The degree to which they are susceptible, varies with the amount of target expression. For example, CD20 expression is pretty well limited to B cells. Thankfully the anti-CD20 monoclonal antibodies (rituximab and obinutuzumab) tend to spare pro-B lymphocytes and plasma cells, with CD20 down regulated at the point of differentiation into plasma cells. Of note, despite CD20 only being dimly expressed on B cells, it still works very, very well.
Wow, I never heard about that one.Thank you for the links.
The approach, to find something targetable on the cancer cell surface and go after it makes sense.
Why wasn't it very successful? They say it was well tolerated, no dose dependent toxicity. Was the method of going after the target not good enough? Can it be improved?
BCL-2 inhibits apoptosis, inhibit BCL-2 and apoptosis ramps up again.
The EGCG trial achieved something similar, but did it better. It was selective, no off target effects.
If the EGCG was not consumed but infused, would it have hurt the liver less?
I documented the failure of ROR-1 in my YABTKi post.
Only patients with MCL or DLBCL showed antitumor activity. "Among patients with CLL (n=7), follicular lymphoma (n=3), RTL (n=1), or marginal zone lymphoma (n=1), we did not see antitumor activity. "
Where did you heard that "EGCG was selective, no off target effects". It has been shown to have some activity in at least 12 different types of cancer, so why wouldn't it have off target effects?
I guess I jumped to the conclusion because they did not report atrial fibrillation, blood pressure problems or any other effects that would indicate such. The activity in other types of cancers is a plus.
Suppose EGCG somehow helps restoring or speeding up apoptosis. Healthy cells would unlikely to be affected because they have no problem with it. Cancerous cells would thus be the only ones benefitting from it.
Thanks for the ROR clarification.
Seems like the method of targeting the ROR wasn't good.
If it's a distinctive feature of CLL cells, a better mab is needed.
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Richters Biopsy Update
Just a little update :)
Update.
BRUKINSA UPDATE
