Search below url for term "mannose"
Do you think I should be taking resveratrol too? Also, I like your idea of tagging for increased search-a-bility. Is there a more appropriate place to discuss 'cases' such as I? Seems my questions are getting more tangential and I don't want to distract from the main topic of this thread.
Yes, D will transfer visitor stories to their own threads to keep everything organized.
There is a lot to explain and summarize about our perspective on metabolic treatment. Usually we keep plowing forward and do not maintain detailed summaries of what we have learned along the way which does make things more difficult for those new to the site to be orientated. So here's a broad summary to give you the highlights.
Cancer is a metabolic disease.
This is the unrefutable truth that we have learned over the last 5 years of our cancer journey.
The fundamental essence of cancer is its metabolic behavior. Almost all of the leading figures in cancer research have acknowledged this reality and were actually quite strong metabolists: It is hardly reasonable to believe otherwise. My suspicion is that if we were to jump in a time machine and go back 80 years, Warburg (the Nobel prize winner in Medicine) would know exactly what we were talking about. In fact, this is exactly the line of argument that he took at that time. Warburg was not amused by incompetents; I do not believe that he would be amused by the incompetence that has been demonstrated over the last few decades. There does not seem to have been a conceptual breakthrough in all the intervening years that changes the fundamental biochemistry of cancer and the logical path forward to a cure.
Without having to read a tiresome discourse, what is the answer? How can cancer be effectively treated? The one sentence answer is: Apply metabolic stress (a lot of metabolic stress).
This statement cannot be realistically refuted. Roughly, selectively shut off OXPHOS (at subunit 1, 2, 3, 4, and or 5); selectively shut off glycolysis; selectively add oxidant stress; selectively deplete ATP, NADH ... ; selectively apply stress to cancer's pH balance; stress the MCT transporters, stress GSH processing, stress glycolysis after the investment phase, ... This observation cannot be argued. Any disagreement simply represents a profound lack of understanding of what cancer is. Applying the above strategy would without question cure cancer.
We have seen this basic game plan applied too many times to count. It is the goto strategy.
The problem of course is that it is a somewhat empty argument if the above items are not readily achievable. Selectively stressing the metabolic machinery of cancer has been a challenge. Glycolysis is a 4 billion old primitive machine that is deeply conserved in cancer. OXPHOS though is a complex machine that can be easily disabled (Think peanut butter on your hard drive; takes no talent to break a complex machine. Much more difficult to defeat a Neanderthal mano a mano (glycolysis)).
What is the best understanding as of now as to how to apply this metabolic stress successfully?
OXPHOS
- There are a number of extremely powerful high cancer selective OXPHOS inhibitors that have demonstrated extreme anti-cancer effects.
These include:
- E260 This shuts off OXPHOS subunit 1 selectively in cancer cells. The protein that they discovered in the cancer cell subunit 1 was specific to cancer. Somewhat surprisingly this treatment by itself was not able to cure cancer in mice. Yet, adding in glycolytic stress with a ketogenic diet had substantial anti-tumor effects.
https://www.nature.com/articles/s41467-017-00832-w
- mito-Honokiol These mito drugs demonstrate truly profound anti-cancer effects. The simple logic here is that the drug is attached to a charged molecule that drags it into cancer cells and to its mitochondria. The electrical potential in cancer cells is larger than other cells so there can be selectivity on the order of ten fold according to the Nernst equation. Mito-Q is a drug in this class that underwent some clinical testing and is now available as a nutritional supplement. These mito drugs are massively powerful. They accumulate in cancer cell mitochondria up to 1000 times more than in the plasma. In the mouse study there was a very large safety margin applied yet the treatment was still highly effective. mito-HK blocks subunit 1 causing blockage of the NADH processing, causing ROS generation etc.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6137433/
- mito-metformin A fairly similar profile as mito-HK (targets subunit 1 etc.)
https://www.ncbi.nlm.nih.gov/pubmed/31191823
- mito-phenformin
and others.
- There are some other selective OXPHOS inhibitors such as methylglyoxal, though they can have a variety of complex cell interactions. The above OXPHOS inhibitors seem to be quite specific and extremely effective.
(I'll discuss the somewhat trickier question of glycolysis in a future post.)
The above treatments and many others that we have encountered for all of these years have demonstrated time and time again the extreme power of dual metabolic strategies: by definition selectively shutting off OXPHOS and glycolysis (or applying stress at other metabolic pressure points) at the same time will produce extreme anti-tumor responses. None of us who have been here for a while can be surprised at the success of the syrosingopine and metformin combination: I wasn't. Given the mode of action involved it would not be plausible for it not to be effective (the only stipulation involves the effective dosing levels.)
Once you lock into this logic, you can see it being applied almost everywhere. The entire playing field suddenly appears in view. The syrosingopine and metformin combination is yet another example of many many highly similar other treatments. When you fully recognize how pervasive the approach is you will realize that the metabolic treatment approach is beyond reasonable discussion: It has not generated a few marginal or sporadic successes, but many thousands.
We have seen the OXPHOS - glycolysis strategy used so many times over the many years that we have begun offering our own suggestions for what would likely be effective. At the very least the body of research evidence has established beyond any doubt that these approaches are highly effective at least in mice models (though there are also many many published reports in humans as well). The remaining hurdle which can be formidable is actually gaining access to these treatments.
(Below figure is mito-DCA with its positively charged lead group to drag the DCA molecule to the cancer cells mitochondria.)
Ray, I really like your monitoring of glucose and ketone levels. I have advocated that all cancer patients be monitored 24/7 for these biomarkers. There is (at the least such a monitor for glucose, possibly ketones). I also looked around and saw a lactate model that was used in the high performance cycling community. This would be another one that should be recording 24/7. These three values really are the core metabolic biomarkers that patients should be obsessed with. You want to drive glucose down. Glucose is not an essential nutrient; in fact it is what feeds cancer. One of the highly intriguing anti-cancer strategies suggests targeting it. Even engaging in endurance athletics can rapidly drive down glucose levels. Notably this is treatment strategy used at cancer clinics. Endurance athletics also drives up lactate levels (temporarily) which can have anti-cancer effects (I will discuss this in a future post.) This is where lactate monitoring is important. One needs to guard against lactic acidosis, yet often there is no ongoing real time measure of lactate levels. It makes no sense to me. One idea that we have talked around on forum is possibly depleting lactate levels by limiting glucose. Lactate becomes converted to glucose, so I have thought that one might simply draw down the excess lactate that are a prominent feature of cancer. Lactate is actually a central feature of cancer and there are endless problems that are caused by high lactate levels. Carefully monitoring these levels around the clock would allow people to engage in biomarker biofeedback. This could be a helpful anti-cancer strategy.
Thanks @jcancom.
On my phone so sorry about the brevity. On my way to get PET scan results and talk to my oncologist now. Fingers crossed things are goodish!
To monitor my levels I use urinalysis sticks. Mine are durui 14 parameter ones and they include ketone and glucose though are probably not very accurate. I would like to make an app to record the levels using phone cameras but I'm finding it hard to find time for that (the idea is much more than that though, you'd also snap each meal and image recognition would try to figure out what you ate and record that too,and the whole thing would be encrypted by users fingerprints, I also want to build in data release capabilities).
I'll read as much as I can from your hints later. At the moment I don't know whether I'll be getting chemo in a few hours or not! I've been visiting the porcelain a bit too much lately.
Kind regards,
Ray.
J, long time ago I decided to be a flexible moderator and let people speak where and as they want. Sometimes it gets crazy but I think I should not stand against nature, but let it happen and work with it. I also enabled the forum option so that everyone can start-up own topic. I also agreed to create dedicate posts for visitors on the Blog space https://www.cancertreatmentsresearch.com/category/visitor-story/, where I can post the visitor story and others can react on that, giving more attention to a specific story/need. In this context, I let anyone chose what they like. Otherwise in this platform I do not have the functionality to move around each comment. I can only move the whole topic to another Forum section. Comments can only be edited or deleted. So everyone should think and chose where they want to post their comments. I will not interfere with that. Thanks for understanding.
Thanks for the info. Welcome to this forum where we all benefit from everyone else's inputs. Welcome to Ray also.
I am convinced that Metformin sustained, extended or slow release, whatever you want to call it, is more efficacious, less troublesome and more sustainable over the long run that the instantaneous release. It has been proven in diabetes but there is no evidence in cancer treatment that I know of. See this:
Sustained release metformin stays longer in the body and may have fewer side effects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006121/
https://www.healthline.com/health-news/why-so-many-people-with-diabetes-stop-taking-metformin#1
I may be wrong but I am under the impression that the metformin StevenK takes is a version of the extended-release tablet, possibly Synjardy XR.
What you are quoting that 1 mg of syro may be enough to fight cancer stem cells might be correct. However, it seems to specify "killing stem cells of cancer". The way I read this is that it would be enough only as a prophylactic measure in healthy persons or persons in cancer remission. I doubt that it would be effective against an established cancer, especially the heavy cancer burdens shared by most members in this forum. So, I would not try to treat with just 1 mg of syro because you might actually breed syro resistance in your cancer cells instead. But I cannot prove it either way.
Yes, SteveK is taking extended release metformin. I will have to order it online.
I searched the .pdf of the 2018 syro/metformin research paper for "stem" or "stem cells", no results.
I believe the combo is targeting tumor cells, not stem cells.
I apologize if the first part of this post gets repeated. I thought I had posted it already but I can’t see it in so I think it did not go through.
Inconsistent mechanisms.
I understand the drugs and substances we take to treat cancer must be not only compatible with each other to avoid serious side effects but also consistent in their mechanisms of action so as to achieve their intended purpose.
In this context I have these practical questions that may come up during the use of syro+metformin.
A- Are vitamins B3 and the Ks to be avoided?
The Basel study found that
“High NMN and NAD+ concentrations were needed to counter the effect of syrosingopine-metformin treatment but nevertheless, both NMN and NAD+ were able to restore ATP levels after syrosingopine-metformin treatment.”
“ATP levels can be partly restored by exogenous NAD+ or the NAD precursor NMN”
“NAD+ levels can be artificially increased by supplementation with quinones, such as vitamin K2 (menaquinone).”
“ATP levels are partially restored in a dose-dependent fashion by exogenous vitamin K2”
“Vitamin K2 partially rescues ATP production in syrosingopine-metformin-treated cells.”
“NAD+ and NMN are unable to prevent cell death after 48 hr of syrosingopine-metformin treatment”
“Exogenous vitamin K2 gives a temporary boost in NAD+ levels that transiently supports glycolysis despite syrosingopine-metformin treatment. The rescue is short-lived due to the depletion of exogenous vitamin K2 and the absence of NAD+/NADH-regenerating mechanisms”
1- What do you people think regarding supplements that contain vitamin K of any kind, vitamin B3, niacin, nicotinic acid, nicotinamide, or their derivatives by any names (NAM, NMN, NAD, NAD+ or vitamin V) while taking syro and metformin? Should there be a concern that they might reverse or reduce these drugs anti-cancer effects?
I imagine that high dose supplements should be avoided. But how about multivitamin pills and foods with high contents in any of them such as natto? Are they also risky or are the amounts they contain so small that they should not matter? Should they not be taken daily so as to avoid cumulative risks?
B- Are antioxidants to be avoided?
I read that one must avoid using drugs that fight cancer by causing ROS in the cancer cells while at the same time taking anti-oxidants that counter ROS and may rescue the dying cells.
I read that Metformin’s “Inhibition of complex I is expected to increase superoxide production by mitochondria, enhance formation of other ROS, leading to oxidative stress and potential DNA damage.”
This seems to indicate that the syro+metf regimen does depend to some extent on ROS and so the addition of anti-oxidant substances to it might hinder its anti-cancer effects.
1- Any thoughts?
2- If my suspicion is correct, should all antioxidants, including Vit C, resveratrol, etc. be avoided or just large doses?
We want to make the treatment as strong and effective as possible. On the other hand, we need to keep in mind that the syro+met regimen is a long-term proposition, not a one month treatment. Thus, avoiding all sorts of vitamins and supplements might weaken the patients’ bodies and make them less capable to fight the cancer.
Thanks for your feedback
Best luck, Ray!
I listen frequently to The Drive and Found My Fitness podcasts. These matters are often discussed. Much of it I don't understand. I can however dig out links to the podcast episodes I think most relevant if people would like that?
Of course GgE, I could not stand against sharing info as long as people share links and they do not have to upload large files on the website. But thank you for asking.
Addressing one of your questions, next to ATP depletion, one of the "side effects" of mito inhibitors is related to the facst that they induce incomplete electron transfer to oxygen that can lead to the formation of reactive oxygen species. This adds additional pressure on the cell. As a result, I would avoid the addition of strong anti-oxidants in combo with mito inhibitors such as Metformin.
Kind regards,
Daniel
Dan, you were asking for info on the half-life data for syrosingopine. I could not find it for syrosingopine. But I found it for its mother compound, reserpine at
https://www.drugs.com/pro/reserpine.html where it says:
“Reserpine, like other rauwolfia compounds, is characterized by slow onset of action and sustained effects. Both cardiovascular and central nervous system effects may persist for a period of time following withdrawal of the drug.
Mean maximum plasma levels of plasma concentrations after a single dose of 0.5 mg of Reserpine, administered as two 0.25 mg tablets or as an aqueous solution, peaked after 2.5 hours. The mean peak level was approximately 1.1 ng/ml. The two formulations were found to be bioequivalent. Absolute bioavailability of Reserpine, as established by comparison to an intravenous dose, has been reported to be approximately 50%.
Reserpine is extensively bound (95%) to plasma proteins. Reserpine is almost completely metabolized in the body, and only about 1% is excreted as unchanged drug in the urine. No definitive studies on the human metabolism of Reserpine have been made. After oral administration, an initial half-life of approximately 5 hours is followed by a terminal half-life of the order of 200 hours. Plasma levels may be measurable 14 days after a single dose. The clinical significance of the long terminal half-life is unknown.”
Also, per http://www.inchem.org/documents/pims/pharm/reserpn.htm
“6.3 Biological half-life by route of exposure.
Reserpine can be described using a two compartmental pharmacokinetic model. The elimination half-life ranges from 45 to 168 hours in plasma. Because of binding to red blood cells, the terminal elimination half-life is longer when whole blood levels is measured, and has been reported to be 386 hours. (Maass, et al, 1969) The half-life is longer in patients with renal insufficiency. Zsoter and associates (1973) observed that the elimination half-life was significantly prolonged in patients with creatinine clearance values of less than 10 mL/min.”
Reserpine is easier to buy. However, when paired with metformin Reserpine only had a small fraction of the anticancer effect that syro has in the Basel study, being close to zero for some cancer types if I remember it right.
The type of syrosingopine that had the highest effect in the mice study seems to be the derivative F3-syro while another derivative, SyroD was totally ineffective. However, I don't know if F3-syro has been tested in humans or if the alibaba vendor has it available for sale.
FWIW
Picked up my scales this morning, they do seem to be a real bargain.
I got back from a day of 3 chemo infusions (irinotechan, cetuximaub and 5FU and have a pump home with me for 2 days). This is after my short chemo break which didn't get me back to 100% if I'm honest. The scan results were good though but I need to study them (after I translate them).
My CEA level has drop significantly for the first time in a long time, basically since my operation on 3rd Dec 2018 I believe. Crossing as many digits as I can without risking cramp!
There is so much to write about cancer!! There needs to be a 24/7 Jcancom feed for all the cancer updates that I need to report. I can only give brief snippets of my various investigations.
To start, consider the dosing curve in the figure below (top left) from the 2016 combination article. It is fairly remarkable that even with an over ten fold shift in the molarity needed for a 50% reduction of tumor burden in the cell line with metformin the combo of syrosingopine and metformin still does not seem an overly powerful metabolic combination, as the dosing range for effective treatment would appear to be difficult to achieve.
Truly effective metabolic treatments, as we saw with 3-Bromopyruvate, can create tumor destruction within about 15 minutes. This is in fact one of the great advantages of metabolic therapy: one can quickly choose alternatives if a metabolic approach is not effective. Such a treatment modifier strategy could be applied to the syrosinopine and metformin combination, so that ineffective treatment could be replaced with an alternative.
The below figure also illustrates for me probably one of the most common mistakes that people will make when applying alternative treatments to their cancer care; namely, they will apply treatments at the dosing level of the flat plateau areas. With metformin dosing below 0.5 mM is entirely ineffective. I suspect that the length of survival tens of millions of cancer patients has been negatively influenced by not appreciating the importance of this observation.
When under treatment, you want to be on the near vertical ski run ~2 mM for metformin and 0.03 mM for phenformin. This is of course completely self-evident, though the ball-park numbers that I provided in a previous post suggested that the phenoformin dosing was way back on the plateau at ~1 micromol. This would seem a hopelessly inadequate dose to use. What you need is to be in the region of the dosing curve where when you reel in line you feel the tension; the treatment needs to use sufficient dosing that it is binding to actual therapeutic results. From what I have roughly calculated this does not seem to be true in the syrosingopine and phenformin combination. In fact, it appears clearly untrue for syrosingopine or phenformin individually as well. Phenoformin might be about 30 fold below a truly effective dose, and syrosingopine might be upwards of an order of magnitude off the central part of the shalom. If this is true then even additive benefit from two treatments near the top of the plateaus on the left of the dosing curves below would not be expected to give overly powerful results.
Much of the scientific literature reports such results, even when it can be highly deceptive. For many it would not be immediately obvious that the dosing is more to the left than to the middle of the curves even after a ~15 fold enhancement by adding in syrosingopine. I would suggest that research should include examples of the more powerful OXPHOS inhibitors (and others). For example, mito-metformin, mito-phenformin and mito-honokiol could shift the blue curve dramatically to the left even without syrosingopine. mito drugs can efficacy by 2 or 3 orders of magnitude. A thousand fold enhancement in efficacy would greatly change the treatment power available. The mito-Honokiol article found that even monotherapy at a minimal dose was therapeutically binding. That is, even mito-HK monotherapy at a dose far below any side effects (~20 fold below any side effects) was in the therapeutically active region where the blue and red lines move almost straight down.
One highly practical implication of the above discussion is that posters on the forum could investigate for themselves where on the dosing curve they were. For example, what one could imagine doing is fixing a dosage of syrosingopine and then adjusting the dose of metformin (etc.) to see the treatment effect (this would be an ideal time for a lactate monitor, though perhaps even daily biomarker could be adequate (?)). One might start at a dose an order of magnitude below the expected maximum dose and see the shape of the curve. One could imagine performing a series of such experiments with a range of syrosingopine doses. One would then have a series of side by side curves illustrating where there might be some pull in the line. This would be a highly useful exercise to consider pursuing. It is all too likely that some people might fruitlessly try to push beyond maximum doses even when unaware to them the dosing curves indicated that this would have minimal clinical effect.
As I noted in my previous post, OXPHOS is a complex machine that is relatively easy to break. 500 million years ago I am sure it was the greatest and best ever, though such complexity exposes it to a range of strategies to inactivate it.
The mito- drug class directed specifically at OXPHOS is half the solution to cancer. Having the ability to manipulate ROS generation, NAD+ recycling, ATP creation with subunit 1, etc. with binding control has to have a powerful anti-cancer treatment effects. Thus, manipulating dose in the region of vertical decline of cell viability would provide tumor control even with monotherapy.
One drug in this class is mito-Q. A small phase 1/phase 2 clinical trial was conducted in a neurodegenerative illness using a dose of 80 mg for a year without generating concerning side effects. With this and possibly a few other smallish clinical trials, the product was launched on the market as a nutritional supplement. Significantly the rough human equivalent dose of mito-HK is ~3 mg which corresponds to clinical activity in mice models of cancer as a monotherapy. Even more importantly is the fact that in the neurodegenerative context, one might assume that there would be no specific advantage in targeting the drug to the cells of interest. All human cells would have a similar exposure to the drug.
However, this is very different from the context of cancer. In cancer, the difference in electrical potential between cancer cells and normal cells means that cancer cells have an effective exposure ten times greater than normal cells. Thus, one might suspect that there would be more of a safety margin if one were to treat with mito drugs in cancer than in most other illnesses.
It would still be comforting to have yet more built-in safety. For example, perhaps the mito drugs could be formulated in chitosan or as a prodrug to make the specificity even more exacting.
This post has noted the under-dosing that often is reported in the literature and the expected result of not having binding therapeutic power. However, the next generation of extremely powerful OXPHOS inhibitors ( especially mito-HK, mito-met- and mito-phen) offer the opportunity of single agent treatment power. The description of the synthesis of mito-HK is given in the supplementary file (Document S1) starting on page 13. The next supplementary file Table S2 is also of high interest. It provides a comprehensive list of human genes and the fold differences in the tumor versus normal cells' gene expression. Several glycolytic and other relevant genes are noticeably downregulated for example GAPDH, LDHA,GLO1,HKII etc. Such information might be used to therapeutic effect. Some of these gene changes are very large for example ALDH1A1 is upregulated by 15 (log2) in tumor cells. Whoa! SLC38A1 is downregulated by 7.4 (log 2). Hmm, that certainly makes one think of the potential of mito-HK.
The results from the Turkish clinic using a metabolic approach have been very impressive. It is difficult to see what if any rebuttals could be given for the below metastatic lung cancer patient series. One realistically would not expect median survival any where over 3 years, though the results beat such estimates even given the inclusion of those with substantial metastatic disease. Retrospective comparison groups typically survived less than 1 year. Even more notably is that those with ECOG status 0-1 appeared to do especially well in comparison with ECOG 2-3 (though the numbers involved were very small).
The treatments that were used included metabolically supportive chemotherapy, hyperthermia, hyperbaric oxygen and ketogenic diet. This is a fairly low intensity metabolic regimen and yet the results were quite impressive. It can be imagined that even better results could be achieved if more metabolic stress were added. Given the non-standard nature of the treatments it should also be noted that some of the patients were known to have not fully complied with the ketogenic diet, so there is some amount of actually underreporting the benefits.
It should be obvious by now that metabolic approaches do have evidence based legitimacy in the treatment of cancer. In fact, it is reasonable to suggest given the extremely strong results reported at the Turkish clinic that in some respects it is now at the leading edge of practical cancer therapy even while using fairly basic treatment approaches. It is by combining several non-toxic treatments that such results become possible.
Interestingly after reading about this type of hyperthermia I found a more recent type of hyperthermia treatment that might also be of use. This newer research has found that even increasing ambient temperature up to 30 C can have anti-cancer effects. At this temperature the immune system can become more active. There are various approaches to hyperthermia including local, whole body, ambient (30C), nanoparticle, infrared etc. that would be worthwhile to explore further.
Concerning metformin and antioxidants combinations. Is this a problem with active disease only or also in prevention (NED situations)? And how about METABLOC + Metformin combination? It seems to work and ALA is a strong antioxidant though also an aerobic glycolysis inhibitor (if I´m not mistaken).
Here are some links to the podcasts I mentioned.
Peter Attia's "The Drive" podcast:
NAD is discussed on https://peterattiamd.com/davidsinclair2/
also on an "Ask me anything", which non-subscribers can only hear previews of https://peterattiamd.com/ama09/
An update on cancer research in general: https://peterattiamd.com/keithflaherty/
Dr Rhonda Patrick's "Found my fitness" podcast:
NAD+, Nicotinamide Riboside, and Nicotinamide Mononucleotide: https://www.foundmyfitness.com/episodes/nad-nr-nmn
Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & More: https://www.foundmyfitness.com/episodes/david-sinclair
(If you get a craving for something sweet on a keto diet this might help, I followed the recipe and it was good, next time I'll use more lemons) Low-Carb Lemon Tart Dessert (High Citrate & Choline): https://www.foundmyfitness.com/episodes/lemon-tart
Sauna Use as an Exercise Mimetic for Heart and Healthspan: https://www.foundmyfitness.com/episodes/sauna-heart-presentation
How To Increase Sulforaphane in Broccoli Sprouts by ~3.5-fold: https://www.foundmyfitness.com/episodes/sfn-maximize
Best regards,
Ray.
Since I had a lot of chemo yesterday I would like to go to the sauna for some hyperthermia treatment but having a pump attached prevents it 🙁
Thanks for those links. I listened to one he did with Dr. Dominic D'Agostino, from 7/18, I think. About 2.5 hours of good discussion, including cancer.
Dr.Dom relates a story of self experimentation with hypoglycemia, based on Dr. George Cahill's work from 1970. He says he got to talk with him before he passed on.
His glucose reading was so low the meter couldn't measure it, but he was safe with ketones. Dr. Peter did something similar but it was scarier. I don't think he had ketones. Insulin in one vein, glucose in another. I think he was trying to measure his insulin sensitivity.
Shirley had her monthly follow-up with the oncologist today. Her CA15-3 rose another 12 points, now at 126. At least it's still linear. Have only been on the syro/met combo for ten days. Praying for better numbers next month.
They are giving us a "courtesy" low dose prescription for metformin, but it's quick release. I got them to change it to ER, but the pharmacy won't fill it, saying it's not approved by our insurance. Then I looked online and saw Walgreens wants over $2k for it. Online searches show greedy drug companies are patenting generic drugs. Will have t o check out the BuyPharma site...
$2K is nonsense. Insurance denial also. You may want to read this website's page on insurance denial at https://www.cancertreatmentsresearch.com/for-us-patients-a-way-that-may-help-to-overcome-the-medical-insurance-denial/
Thank you, I'll save that for another time.
Apparently Walmart has a $4 drug plan:
https://www.goodrx.com/blog/the-walmart-4-generic-prescriptions-list/
I called our oncologist to have the prescription sent to our closest Walmart...
Shirley had her monthly follow-up with the oncologist today. Her CA15-3 rose another 12 points, now at 126. At least it's still linear. Have only been on the syro/met combo for ten days.
Are you dealing with an estrogen + progesterone positive, HER-2 negative ductal carcinoma to the bones only?
I don't know the type, except that it feeds on estrogen. She is on Letrozole and just started Faslodex and Exgeva.
She has bone mets in her back, spine, ribs, hips, and thighs. The radiologist that did the biopsy in 5/18 told her "You have multiple lesions, too many to count, at least a hundred. There are more now.
What is infinity times two?
it feeds on estrogen
A side benefit may be that Metformin seems to lower estrogen (estradiol) production
At her monthly follow-up yesterday, the oncologist's PA said she is a miracle. She said she should be in a lot more pain with all the lesions. Other than being in a wheelchair, you wouldn't know she is sick. She looks beautiful, and her mobility is increasing.
Did she get by any chance get any antibiotics between her second PET scan and her third scan seven months later when she showed progression?
I think she did, as she had a root canal in the early part of that period.
I have doxycycline on order.
I think she did, as she had a root canal in the early part of that period.
https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.23622
“even a single antibiotic treatment in healthy individuals contributes to the risk of resistance development and leads to long-lasting detrimental shifts in the gut microbiome.”
Thanks a lot for the info gge!
I think, for syro,we really need to contact one of the authors of a recent paper on Syro (regardless if it's cancer related on not) and ask for what they know about the pharmacokinetics.
