Side effects of methadone

https://www.ncbi.nlm.nih.gov/pubmed/32060760

Safety aspects of opioid-naïve patients with high-grade glioma treated with D,L-Methadone: an observational case series.

from the abstract:

"Twenty-four patients were included. All patients were opioid-naïve and received D, L-Methadone from their general practitioners. Sixteen patients experienced side effects. The median dosage when side effects began to occur was 15.8 mg/ 24 h. Fatigue and mood changes were reported most frequently (14 of 24 patients). Five patients had severe side effects related to relatively high doses. In all cases, symptoms resolved after cessation or dose reduction. Our results show that D/L M intake lead to frequent occurrence of side effects in opioid-naïve patients especially when not handled with caution and close supervision. Patients, their relatives, their GPs and neuro-oncologists need to be informed about the broad spectrum of side effects in order to thoroughly counsel glioma patients."

Cocktail review after 1 year

Dear community,

I'd like to revise my husband's cocktail after 1 year of doing this protocol. He is at 14.5 months from diagnosis and has just started his 12th cycle of TMZ and just got his 3rd excellent MRI saying that the main part of the thalamic tumor is barely visible at the moment (which was the bigger concern of the two tumor sites) and the frontal one is still non-enhancing. 

Although he is methylated, I attribute the good results to the cocktail approach or at least to the synergy between the chemo and the cocktail because the first MRI after radiochemotherapy showed progression and it couldn't be pseudo progression, at least not on the frontal site because only the thalamic site was involved in the treatment. 

We're reaching the 1 year mark of supplementation with the following: 

Fluoxetin 40 mg

Chloroquine phosphate (Delagil) 250 mg (he already stopped taking it)

DCA  500 mg 2 times a day for a patient who is sadly weighs only 55-58 kg these days

Silymarin 630 mg

Celebrex 400 mg

The rest of the meds were added later on gradually. 

In your opinion, is it good to stick to the cocktail if it's working because we don't know what elements are working or after a year would it be wiser to make some changes in the regimen to disturb the tumor?

Does it make sense to take Celebrex if there's no edema and we are 1 year from radiation therapy?

I'm thinking about replacing DCA with the ALA + HCC protocol. 

Sorry if it was discussed before but is LDN an antagonist to methadon? Can the ALA + HCC protocol be effective without LDN? Combining this protocol with ketogenic diet is not an option for us because he has a sweet tooth and these days his main calorie intake is from fruits and baked goods which makes me frustrated big time but I can't help it, he lost so much weight. 

I'm not sure if we can use 800 mg of ALA 2 times a day instead of RLA 800 mg 2 times a day or should we double the dose of ALA considering that ALA is just 50% RLA.   

What's the longest period of time that a patient can take DCA? My husband is on a fairly low dose although he noticed considerable neuropathy on several occasions when we ran out of methadone for one day. Since it has painkiller effects I suppose that the neuropathy is continuous but methadone may conceal DCA's side effects. So I suppose that after a year we should address this problem and make at least a longer break of DCA.

Since his seizure he is on 300 mg of valproate acid 3 times a day, too. Considering that it became a necessity to take an AED I see reason to maybe replace fluoxetine with LITHIUM and so he would be taking almost the whole CLOVA cocktail. He's been on cimetidine 800 mg since last Sept./Oct. I'd like to exclude olanzapine because I read terrible things about its side effects but this way he is already taking 3 of the 4 medicine of the CLOVA cocktail anyway. 

By the way, at first, he was prescribed the same amount of sodium valproate in the A&E but the NO changed it to valproate acid later on. I know that those two are in the same family but can be any difference between their tumor-fighting properties?

I read here an older comment that stated that a patient's NO advised against taking Silymarin and valproate together because valproate is metabolized by the liver and Silymarin flushes it out. Is it a true statement in your opinion? I'm not sure if we can keep that in the cocktail. 

Cimetidine: I suppose it's advisable to take it together with TMZ. In our case it will be 24 cycles if he can tolerate it on the long term. So should he continue it for an additional year?

If stopping with DCA, Celebrex, chloroquine, he will only take a few prescription drugs (metformin, fluoxetine or lithium, alfacalcidol, D,L methadone and of course the anticonvulsant) and it seems a bit scary that natural supplements will be predominant. 

Do you recommend to add anything to this list at this stage of the disease?

Thank you for your inputs in advance! I think I would be a complete nerve-wreck if this blog did not exist. 

Need suggestions to incorporate supplements in my mom's cocktail(GBM Patient)

Hi folks,

My mother(Age 47) was diagnosed with glioblastoma(IDH1/2 -ve, Methylated) in September 2017, and it has left me devastated ever since. She has completed her 6 weeks of radiation/chemo and her first cycle of 5/23 temozolomide. Her next cycle of temozolomide starts 5 days from now. I stumbled upon this blog just a week back, and have found this to be immensely helpful and resourceful.

I need help from you guys on what else should I incorporate in my mom's cocktail. Following are the supplements that are present in her cocktail per day already:

Metformin: 500 mg
Boswellia Serratta: 4000 mg
Resveratrol: 400 mg
Fish Oil: 3600 mg DHA+EPA + 400 mg of other omega 3 fatty acids
Curcumin with piperine: 5000 mg
Longvida: 400 mg
Quercetin: 5000 mg
Melatonin: 20 mg
Selinium: 200 mcg
Vitamin ADK supplement with 5000 IU Vitamin D3
Ashwagandha: 500 mg
Garlic: 6 cloves
Ginger: 6 cloves
Dendritic cell therapy: On the cards
Cannabis oil: Dropped because it was suppressing her WBCs

She is also on ketogenic diet and has done about 2 weeks of hyperbaric oxygen. We are looking at two more weeks of hyperbaric oxygen.

I'm looking for more supplements that are good adjuvants to temozolomide/standalone good adjuvants that I should definitely include in my mom's cocktail. It'd be great if you guys could help out in more supplements that I should include, I'm finding it very hard to self medicate my mom. Basis Ben Williams' book and reading several blogs, the following supplements have repeatedly been catching my attention:

1. DCA
2. Chloroquine
3. Care oncology clinic protocol(Metformin + Doxycline + Mobendezole + Atorvastatin)
4. Ruta 6 + Calceria Phos(Not sure if it is a good idea to use while on chemo)
5. Methadone
6. Veramapil
7. Low Dose Naltrexone
8. Disulfiram
9. Perilyl Alcohol
10. Methadone
11. Celebrex

She is already taking a total of 50 meds per day and I think she can take only 10-15 more. Would be great if you can help me from above list/any other supplement that should definitely be a part of her cocktail.

Thank you in advance!

Levi's cocktail update & pretty good MRI at 8 months

Luckily my husband (who is MGMT methylated, wild type and has a multifocal tumor) got a quite promising MRI report today after a slight progression in late August following radiation therapy. We need to wait for the NO's opinion till 12/18 but it's clear for us that this is good news because the report contains words like regression (both in the thalamic and frontobasal areas), reduced T2 signaling, reduced edema. 

The only negative statement mentions increased rCBV at some parts of the frontobasal tumor. Good results were not so surprising since he is doing very well. He basically slept through the 2 months after radiation therapy but now he is is back to normal. His only deficiency is left-side peripheral vision loss due to surgery. 

Since my previous post we made some changes to his cocktail. Thanks to a nice blog member's guidance my husband started to take D,L methadone a month ago. He will reach the therapeutic dose (2 x 35 drops) soon. It didn't have enough time to make a difference yet so I chalk the fairly good MRI results up to the cocktail approach. I hope that the next MRI in late February / early March will be even better thanks to methadone. 

With mebendazole, we try to follow Care Oncology's protocol so after the 3 months course of mebendazole which he we'll complete within days we'll alternate it with minocycline (instead of doxycyclin). Somebody stated on a forum that mebendazole and minocycline do the same job. I suppose mebendazole isn't the strongest part of our cocktail considering its bioavailability and the fact that he takes way less than the dosage used in clinical trials. So maybe it would be wiser to choose minocycline on the long term. What do you think, dear fighters & relatives, should we pick the substitution alternative or should we favour minocycline? If so, which one would be better, 100 mg or 200 mg? I have concerns about putting all our eggs in one basket. Maybe if the current cocktail works we can keep up with it, otherwise what will we have left in case of a progression if we blow all our ammunition now?

Current cocktail:

- TMZ 280 mg (5th cycle completed)

Tried to increase it to 380 mg for one cycle but BP dropped to 40,000 so it turns out that he can tolerate only 280 mg.

Morning, on an empty stomach: 

1,5 g PSK mushroom

250 mg EGCG (500 mg on TMZ days + fresh green tea)

1000 mcg sulforaphane from dried broccoli sprouts (2000 mcg on TMZ days)

2000 mg Fish Oil

250 mg vitamine C

D,L methadone 25 drops 

0.5 liter of beetroot-carrot-apple-orange juice ( I don't really believe that it can help but at least it's delicious.) I used to make fresh pomegranate juice daily but then I read that it can increase the concentration of corticosteroids so we stopped it. 

After breakfast:

Curcumin 1000 mg

Fluoxetine 40 mg

Alfacalcidol 2.5 mcg 

Metformin 500 mg 

After lunch:

mebendazole 100 mg / minocycline 100 mg

methylprednisolone 16 mg (I hope it'll be reduced after the next meeting with the NO) 

cimetidine 2 x 200 mg 

During the afternoon & evening 

cimetidine 1 x 200 mg

silymarin 630 mg (I increase it on TMZ days to 850 mg but just like everybody else I'm just guessing with the dosage)

celebrex 400 mg

metformin 500 mg (1500 mg on TMZ days in total) 

DCA 500 mg x 2 + 500 mg B1, 2 weeks on, 1 week off

This means 15.6 mg/ kg. He was on 500 mg x 3 / 20.4 mg/ kg for several weeks, parallel with his Temodal cycle increased to 380 mg but it caused neuropathy in his hands and feets and balance issues so we decreased DCA to 15.6 mg/ kg and symptoms disappeared. I'm not sure if it was Temodal or DCA because both of them were decreased after these issues. Now, we try DCA without B1. We'll see...

After dinner:

Chloroquine (Delagil) 250 mg (Only every other day since he takes cimetidine.) 

Selenium 200 mcg

cup of tomato juice as Lycopene source

Before bedtime:

D,L methadone 25 drops 

melatonin 20 mg 

PSK 1.5 g

cimetidine 1 x 200 mg

- Omeprazole 40 mg x 2 (2 days before and 2 days after TMZ days) 

Information on DCA and methadone

Hello all,
I'm looking for information on DCA. My dad was diagnosed with an inoperable glioblastoma in December 2015. He's doing pretty well at the moment and we're happy with his treatment. But we want to be prepared for the worst case and that's why I'm interested in DCA.
We live in Germany and as many other cancer patients my dad is taking methadone as part of his cocktail. That's also my main concern because I couldn't find any information on whether methadone and DCA can be combined (I read that you need to be careful with cannabinoids which could be problematic as methadone uses the same receptors). My dad's tumor was stable for a year and then started shrinking in December 2016. As you can imagine we're extremely happy and don't want to omit any of the drugs he's taking at the moment:
- Temodar (still on 5/23)
- methadone
- Optune TTF
- dexamethasone  (tapering 0,5 mg)
- Omega 3
- Vitamin D
- Levetiracetam
- Coriolus versicolor (PSK)
- broccoli sprouts
- Eliqius (blood-thinner)
If you have any information on the combination of DCA with our cocktail, please let me know. I'd also like to know whether you really have to be careful with the dosage in brain tumor patients. I read some really scary stories online, they said that the combination of DCA and caffeine was dangerous.
Thanks a lot!!

Looking for help with our cocktail

Hi everyone,
I'm new to this blog and would love to get some advice. My dad was diagnosed in December 2015 with a glioblastoma. Unfortunately it's inoperable because of it's location (corpus callosum). I've just read Ben William's book and I think it's very sensible to try the cocktail approach. He finished radiation plus Temodal and is now in his 5th cycle of Temodal. After the 6th cycle he'll be switched to metronomic Temodal. He also takes:
- dexamethadone 4mg/day
- D-L-methadone 1,75ml/2x day
- Heparine injections because of a thrombosis
- Keppra 500mg/2x day
He is also using Optune TTF. But there's more that we want to do. I'm very interested in DCA but worried if it might interact with the methadone. From what I've read online, he should start on a low dose and without caffeine as brain tumor patients can't seem to tolerate a higher dose. Do you think that we should give it a try? I think it's pretty hard to get...
Additionally we're considering the following:
- PSK
- Melatonin plus Aloe Vera (again I'm worried because of the methadone as it makes him really tired)
- Fish oil (Omega 3)
-CoQ10
It would be so helpful for us if you could give u your advice!
Thank you so much
Steffi

Temodar... Hospice... What to do...

Hi -

Dad has declined.  Last week we had lots of activities, and I think it was too much for him.  Tuesday was our 3rd dose of Nivolumab, Wednesday was a visit with the NO (a 5-6 hour ordeal roundtrip), and Thursday we had our Optune hat arrive.  Dad removed it 6 or so times that night before Mom gave up for the time being.  Dad has been sweating much more than ever before and had difficulty holding his head upright at the NO's office, Mom had to cradle his head.

Just this week his breathing is laborious and he had a bit of a rattle, but the rattle seems to have gone away.  He is now sleeping and has been all day.  His blood oxygen is only 85% - which is a drop from our usual 97-98%.  Otherwise his vitals seem good.

Our background:  Dad had 1 round of Temodar last Sept/Oct during radiation, became impaired (couldn't walk, speech worsened), local Oncologist assumed the Temodar wasn't working and switched us to Avastin.  In hindsight, his tumor did not progress and the radiation was hitting the motion strip of his brain - it is entirely possible that he DID respond to the Temodar, and that the symptoms were due to the radiation.  NO at UCLA said that as the tumor did not progress this is likely.

Late May, after 6-7 months of Avastin as a monotherapy, (+ cocktail including DCA, etc) Dad's tumor had it's first increase.  Another local Oncologist said we could revisit Temodar since we never tried the maintenance dose.  Dad received 1 round of the 5 day Temodar - it was well tolerated.  While this was going on our application for Nivolumab was approved.  The Onc then said to stop Temodar and just do the Nivolumab (this was not a NO, just a regular Onc).

We then saw our NO and started the process of getting an Optune hat.  The NO weighed in and said that we could try Temodar + Optune, in addition to the Nivolumab, but wanted to wait a month until Dad's had time with the Optune so as not to change too much at once and have so much toxicity in Dad's system.

Dad won't wear his Optune. I am thinking of maybe trying the Temodar on a metronomic dose schedule, as we happen to have some from a friend.  The NO didn't give us any yet.

You are all as aggressive as me, and I value your collective opinions.  Would you go ahead and give the Temodar on a metronomic dose?  I honestly believe if we don't he will not make it til next week.  If we do, he might still perish but will I be harming him?  Is there any chance it can help him?  I have verapamil, celebrex, disulfiram, copper, everything to make the Temodar more powerful.  I don't want to have regrets about 'not trying' but I also don't want to regret making him sick (if it will) or making his last days horrible.

What would you do...   Dad was on board with absolutely everything early on.  Now he can't communicate so we can't ask him.  Is metronomic Temodar unbearable?  Does anyone have personal experience with it?  Are we too far gone?

Love to all.
Annie

Methadone a possible addition to the cocktail?

             BioFabNet Telemedicine BW                        

Hi Stephen and all

I came across this article about methadone from a Belgian  blog GBM patient who is using Methadone as a part of his cocktail and doing well, he is also doing immunotherapy etc so as usual you can never be sure what is working. There is some interesting research regarding GBM and Methadone in the article below.  The article is mainly about leukaemia but does include some GBM investigations near the end. I wonder if Methadone works along the same lines as Noscapine? Below is a link to the blog.

http://www.slideshare.net/pjmuller/glioblastoma-go-for-the-cocktail-approach

1. Methadone the last step to becoming an anti-cancer drug

Methadone – the last step to becoming an anti-cancer drug

It all began several years ago with a surprising discovery in the laboratory. Claudia Friesen, a chemist at Ulm University, discovered that leukaemia cells that were exposed to methadone died within a relatively short period of time. Seven years on and many papers later, what was once a rather exotic substance is now undergoing clinical testing in cancer patients.

Dr. Claudia Friesen has been extremely interested in anti-cancer drugs ever since she studied chemistry at Heidelberg University. She has been with the University Hospital in Ulm since 1998 and when she joined Professor Erich Miltner’s group at the university’s Institute of Legal Medicine in September 2007, she started to look more closely at potential drugs for cancer treatment, with a particular focus on drugs with a cytotoxic effect. She made rapid progress and only three months after starting her investigations, Friesen made a groundbreaking discovery that she has been working on ever since.

Surprising death in the test tube

Cancer researcher Claudia Friesen found that methadone is a promising new potential therapy for leukaemia. © Pytlik/BioRegionUlm

When Friesen and her team tested methadone in leukaemia cells, they were surprised to find that methadone effectively killed leukaemia cells in a comparatively short time; until now methadone has usually only been used for managing severe pain and as an anti-addictive preparation for use in patients with opioid (e.g. heroin) dependence. At the time of Friesen’s discovery, little was known about methadone and its mechanism of action. What was known was that it exerts its analgesic effect by binding to opioid receptors and that tumour cells express many opioid receptors on their surface.
Friesen and her team found that methadone induced apoptosis in leukaemia cells, a finding that Friesen was able to deduce from the presence of typical membrane-enclosed vesicles outside the cancer cells. It goes without saying that Friesen was aware that the process of apoptosis is often defective in cancer cells, and is the reason why such cells grow in an uncontrolled manner. The excitement of the hunt had got its hold on her.
In 2008, Friesen published her findings and caused quite a stir in the scientific and non-scientific press, probably because her findings were unusual in the context of mainstream cancer research. The binding of methadone to opioid receptors on cancer cells induces apoptosis, i.e. programmed cell death; the process is triggered by protein-degrading enzymes (caspase 9 and 3), which quickly sweep obstacles such as Bcl-xL and XIAP (X-linked inhibitor of apoptosis protein) out of the way. Moreover, methadone does not have any toxic effects on healthy, non-leukaemic blood cells.
Friesen and her team discovered that the binding of methadone to an opioid receptor leads to the activation of inhibitory G-proteins. These inhibit the enzyme adenylate cyclase, which in turn leads to the downregulation of cyclic adenosine monophosphate (cAMP). This improves the effectiveness of anti-cancer drugs in treating cancer. 

Opioid receptors and cell death

Opioid receptors appear to play a key role in the induction of cell death, but little is yet known about them. They are found in the brain and spinal cord of mammals including humans, and bind to endogenous and exogenous opioids such as methadone. They have seven transmembrane-spanning domains and are usually found in areas involved in pain control and regulation of emotional response. Methadone binds to μ receptors.

Cancer cells carry a large number of opioid receptors on their surface. Healthy cells only carry a few. The more opioid receptors a cell has, the easier it is to trigger its death. A cancer cell that has a particularly large number of opioid receptors can be driven to suicide by methadone alone. Unfortunately, as Friesen has found, most tumour cell types do not carry enough opioid receptors for methadone to be effective on its own. However, she has also found that cells with a median density of opioid receptors can be driven to suicide by exposing them simultaneously to methadone and cytostatic drugs, which increases the drugs' cytotoxic potential.

Ex vivo experiments with patient cancer cells and human cancer cell lines confirmed the apoptotic effect of methadone (“the speed with which cell death occurs depends on the type of tumour”), and animal models were used to confirm the results in vivo. The scientists tested the effect of methadone in combination with a chemotherapeutic drug in mice bred to have human leukaemia and found that the tumour stopped growing, and did in fact shrink and disappear completely.

Mutual increase in cytotoxic potential makes the clinical application of methadone more likely

But this was not the only thing Friesen and her team discovered. They also observed a phenomenon that has brought their findings closer to clinical application (Friesen 2013). When methadone binds to opioid receptors, cancer cells not only take up greater amounts of the anti-cancer drug than without methadone, they also reduce the efflux of the drug. In addition, the anti-cancer drug used leads to an increase in the number of opioid receptors that are expressed on the cancer cell surface, with the result that more methadone can bind. In other words, methadone and the anti-cancer drug mutually increase their cytotoxic potential. Friesen has already shown this “dual synergism” for several substance classes with a cytotoxic effect (e.g. platinum complexes, anthrocyclines).

Friesen strongly believes that the mutual increase of the agents’ cytotoxic potential improves the therapeutic outcome: significantly lower amounts of cytostatic drugs would be required, which in turn would reduce the number of adverse drug effects. Methadone also has the potential to sensitise resistant cancer cells to anti-cancer drugs and give ‘untreatable’ patients another chance of treatment with a better outcome.

Even cancer stem cells capitulate in vitro

Glioblastoma cells survive treatment with an anti-cancer drug. © Friesen/University Hospital Ulm

Recently, Friesen’s research group (Friesen 2014) has once again come up with findings that highlight the positive effect of methadone in the treatment of cancer. The researchers found that methadone breaks chemo- and radioresistance in leukaemia cells expressing opioid receptors and sensitises leukaemia cells for doxorubicin treatment, and hence apoptosis.
Unexpectedly, Friesen and her team also succeeded in doing the same with glioblastoma stem cells. This project was supported with funds from German Cancer Aid. Glioblastoma is the most common malignant brain tumour in adults and has a bad prognosis. It cannot currently be cured.

Methadone can break the resistance of glioblastoma cells to anti-cancer drugs and induce apoptosis. Apoptosis leads to a typical granular cell shape. © Friesen/University Hospital of Ulm

There have already been a few clinical cases that substantiate Friesen’s findings. For example, Friesen knows of a cancer patient who was no longer responding to conventional chemotherapies and was given palliative chemotherapy in combination with methadone. The combined administration of methadone and anti-cancer drug led to a strong reduction in tumour volume. The administration of methadone therefore appears to have led to the sensitisation of tumours cells. Some of the patient’s tumours even disappeared completely. It goes without saying that methadone has dramatically increased the patient’s quality of life.
Despite undergoing several chemotherapies, another cancer patient nevertheless developed liver metastases. Eventually, the combined administration of anti-cancer drug and methadone led to the destruction of the metastases. A patient from Florida, USA, with small-cell lung cancer contacted Friesen to tell her that he was given methadone to relieve cancer pain and has survived for 12 years instead of the predicted six months. Friesen has also received reports of successes from Westphalia-Lippe where palliative doctors prescribe methadone as standard for the treatment of peritoneal carcinomatosis.

Ulm University Hospital to initiate clinical trial

In the meantime, the scientific world is becoming less sceptical about the use of methadone in cancer treatment. Friesen reported on the observed effects of methadone at the German Cancer Congress earlier this year. Something that seemed unthinkable seven years ago, will become reality in 2014: Professor Thomas Seufferlein, medical director in the Department of Internal Medicine I at Ulm University Hospital, in cooperation with Professor Ralf-Dieter Hofheinz, head of the TagesTherapieZentrum at the Interdisciplinary Tumour Centre at the Mannheim University Medical Centre, will continue Friesen’s work and carry out a clinical trial with the aim of providing evidence that methadone, when given in combination with an anti-cancer drug, acts as a chemosensitiser or resistance breaker in patients undergoing conventional chemotherapy.

The clinical trial will also include patients who barely or no longer respond to conventional chemotherapies. The study design is not yet ready, but it is planned to include a broad range of patients with different types of tumours. The trial has the major goal of improving the effect of anti-cancer drugs and the quality of life of cancer patients.

A new helper for conventional cancer therapy?

Despite all positive results achieved so far, Claudia Friesen knows that the use of methadone in the treatment of cancer patients has its limits. The effect of methadone will depend on the dose used and on the condition of the patient treated. Nevertheless, it would be considered successful from the patient’s perspective if methadone was shown to improve upon conventional cancer treatment.

Although the use of methadone as an anti-cancer drug has already reached the clinical trial stage, Claudia Friesen will continue to have plenty of work to do and she is planning to focus specifically on the molecular processes that are ignited in tumour cells when methadone binds to opioid receptors. Understanding these processes might help scientists to elucidate how methadone is able to effectively trigger cellular apoptosis.

<sup>References:

Friesen, C. et al.: Methadone, Commonly Used as Maintenance Medication for Outpatient Treatment of Opioid Dependance, Kills Leukemia Cells and Overcomes Chemoresistance, Cancer Research 2008, 68, 6059-6064.
Friesen, C. et al.: Cell death sensitization of leukemia cells by opioid receptor activation, Oncotarget 2013, 4, 655-690.

Friesen, C. et al.: Opioidrezeptoraktivierung verstärkt Effektivität von Chemotherapeutika, Ärztliches Journal Onkologie, 4, 2013, 26-27.

Friesen, C. et al.: Opioid receptor activation triggering downregulation of cAMP improves effectiveness of anti-cancer drugs in treatment of glioblastom Cell Cycle 2014, 13:10, 1560–1570.</sup>

 

Methadone

Dear all,

after several very positive cases of GMB treated with methadone hydrochloride in Germany, even our NOs began to believe in this stuff. It was not easy to get it, but today my husband took his first 5 drops. :)
The idea is to take methadon with metronomic Temodal... 
Other than that, he has a fast deterioration right now... Hope this stops somehow. 

Best,
Katja