Dr. Jay Goldstein's Rapid Remission ME/CFS Treatments.

[Sidereal]

Regarding ketamine, what was deemed crazy dangerous practice when Goldstein said it is now deemed the single most promising therapeutic advance ever in psychiatry because some douchebags from the NIH and ivory towers in America said it works for many people with refractory depression like nothing else ever tried. These days the situation is not as dire as in Goldstein's times. There are apparently office psychiatrists who administer IV ketamine in major cities though they'll probably first want you to try several toxic antidepressant drugs and combos before being willing to administer it.

 

[bertiedog]

Very interesting indeed. I take it you meant to write that the brain showed hyperperfusion after a successful treatment, rather than hypoperfusion. That is to say, the treatment led to increased blood flow to the brain.

This makes me think that vasoconstriction in the brain could be a key disease-maintaining factor in ME/CFS. And as I speculated in my above post, it could be that endothelial nitric oxide synthase (eNOS), which generates the nitric oxide that dilates the blood vessels, is down-regulated in ME/CFS, leading to chronic hypoperfusion in the brain,

What you have written above makes me think there must be sub groups because I am completely the opposite. Vasodilators are the last thing I need because they will every time give me horrendous migraines and my legs feel horrible and weak, like water running down a stream and I will sweat constantly and my hr and bp will go way too high.

I do suffer with POTS which is controlled by low dose betablocker and occasional Fludrocortisone plus extra salt so maybe those of us who have this problem are a different sub group.

(Also I am fortunate in that I have good cognitive function until I do too much physically when it falls apart but recovers after 30 minutes of using my oxygen concentrator. I also take dessicated thyroid containing T3 and replacement steroid for my adrenal insufficiency plus co-enzyme Q10 and carnitine fumerate and suppplemets to help methylation amongst others which all have a positive effect.. With all these on board I can feel very well and for instance I managed 9500 steps which is exceptional for me but the previous week when I had a severe throat infection which needed Azithromycin, I could only manage half that number and felt very ill and weak. Today I have no PEM whereas at the end of the day at the races yesterday, I was in horrible pain in my back, my legs were so weak I could hardly stand and my shoulders ached but with the oxygen, meds/supplements, today I have some recovery.

Pam

 

[JPV]

Here's a better version of Goldstein's "Decision Tree" that I got off of the Wayback Machine's cache of his website...

 

[Thomas]

@zzz thanks for that post regarding the resurrection cocktail ingredients. I was trying to piece it together also, but had only read BBTB and haven't started Tuning the Brain yet due to inability to read much at this point of my illness.

It's unfortunate that the two most effective treatments listed by Dr. Goldstein (Lidocaine and Ketamine) are also the most difficult to obtain. And even if you do get a local doctor to agree to it, the administration protocol of the IV is very specific as well. And of course, both drugs can't be ordered online to the best of my knowledge.
There's a local pain clinic here that offers IV Lidocaine and Ketamine for treatment-resistant neuropathic pain so I'd really have to do some arm twisting to my family doc to agree to refer me.

Also, I'm Canadian and can't find any source of over the counter chlorzoxazone. And I can't seem to find a source online either. Do you have any further info on how I can obtain it?

 

[JPV]

Also, I'm Canadian and can't find any source of over the counter chlorzoxazone. And I can't seem to find a source online either. Do you have any further info on how I can obtain it?

You can try United Pharmacies.

 

[Hip]

Great find on that Goldstein decision tree, @JPV. The whole of Dr Goldstein's website appears to be archived and viewable on the Wayback Machine.


Goldstein's Decision Tree And Profiling Drugs

I understand that the purpose of Goldstein's use of profiling drugs in his decision tree is to ascertain which receptors are dysregulated in a given ME/CFS patient. The profiling drugs are shown in the central column of the decision tree (the decision tree in this post above).

Each of Goldstein's profiling drugs targets and agonizes a particular receptor, and the profiling drug is used to find out how well that receptor is working.

If you feel either better or worse on a particular profiling drug, Goldstein says it indicates you have a dysregulation in the receptor the profiling drug targets.

Specifically, I am guessing that if you feel better on a profiling drug, it means your associated receptors are under-stimulated, so you would need to boost them (and this is done using the drugs listed in the boxes pointed to by the brown arrows in the decision tree).

Conversely, if you feel worse on a profiling drug, it means your associated receptors are over-stimulated, so you would need to inhibit them (and this is done using the drugs in the boxes pointed to by the turquoise arrows).

Does that sound right to you, @zzz?

More details of some of the drugs listed in the boxes in the left and right-hand columns of the decision tree can be found on this page and this page of Goldstein's website.



One thing I am not sure about: in Dr Goldstein's decision tree diagram, the titles of the boxes in the left and right-hand columns include both receptor types (namely norepinephrine alpha 1&2, dopamine, NMDA/glycine receptors) along with drugs (namely benzodiazepines and ketamine).

I was a bit confused by this at first, but I then I realized that what I think Goldstein is implying with benzodiazepines is the GABA-A receptor (the receptor benzodiazepines act on), and what he is implying with ketamine is the NMDA receptor (the receptor that ketamine antagonizes).

But then if that is the case, and ketamine just represents the NMDA receptor, why has Goldstein also got a another box entitled glycine/NMDA?

So I am not entirely clear on this decision tree diagram as yet.



An overview is given in this article by Ben Galvin on Goldstein's website on how the decision tree works:

The receptor profiling procedure involves giving the patient a series of drugs, each of which acts on a known set of receptors. The patient's responses to these drugs are then used to determine which receptors may be dysregulated.

For example, if a patient's symptoms improve after taking the drug amantidine, we can reason that at least one of the receptors which Amantadine interacts with is dysregulated. A quick search of the medical literature reveals that amantidine is known to excite dopamine receptors (so amantidine is a dopamine agonist) and inhibits ketamine receptors (so amantidine is also a ketamine antagonist). Further study of the literature allows us to compile a list of drugs which are similar to amantidine in the sense that they are either dopamine agonists (for examples of these drugs see the second box on the right, below), or ketamine antagonists (the third box on the left, below). It is probable that one of these drugs would further reduce the patient's symptoms.

If, on the other hand, amantidine made the patient's symptoms worse, we would look for drugs which act the opposite of amantidine - we would be looking for drugs which are either dopamine antagonists (the second box on the left, below), or ketamine agonists (the third box on the right, below). Again, it is probable that one of these drugs would reduce the patient's symptoms.

If the patient has no response to amantidine, we gain little information and must move on to the next drug in the series.

Currently eight different drugs are used by Dr. Goldstein for receptor profiling. Each was chosen either because its effect on receptor function is well understood, or because the drug is particularly useful in treating Chronic Fatigue Syndrome.

The diagram below collates the basic information that Dr. Goldstein uses to find a patient's receptor profile. For a given profiling drug, begin by finding its name in the center column. If symptoms improve after taking the drug, the brown arrow starting on the right leads to a group of drugs which should improve the patient's symptoms. If symptoms worsen, the blue arrow starting on the left will lead to an appropriate group of drugs. Dr. Goldstein has many agents compunded into eye and nose drops, as well as rapidly-achting transdermal gels.

Note that in the above, the correct spelling should be amantadine rather than amantidine.

I am not sure why in this the above text the term "ketamine receptor" is used. This is not a standard name for any receptor. Ketamine does have effect on the NMDA receptor: it antagonizes this receptor. But receptors are named after agents that agonize them, not antagonize them.

 

[MeSci]

Always bear in mind that not everything is known about any drug, and people vary enormously in their responses to things, so although the profiling drugs are relatively well-understood, there will probably always be responses that give the wrong impression, or of course someone may feel well or ill for a different reason.

So although the protocol appears very well thought-through, there may still be a fair amount of trial-and-error.

 

[Sidereal]

But then if that is the case, and ketamine just represents the NMDA receptor, why has Goldstein also got a another box entitled glycine/NMDA?

The NMDA receptor is quite complicated with different binding sites. Ketamine binds to a different site than glycine does and they produce somewhat different effects. This schematic should make things clearer:

https://www.cnsforum.com/upload/imagebank/download/hrl_rcpt_sys_NMDA.png

So although the protocol appears very well thought-through, there may still be a fair amount of trial-and-error.

Absolutely. Goldstein discussed this problem in Tuning the Brain. He says that the algorithm is an aid to treatment but it's by no means bullet-proof. He found that it increased odds of treatment success far above pure trial-and-error but it wasn't 100% accurate.

 

[Hip]

The NMDA receptor is quite complicated with different binding sites. Ketamine binds to a different site than glycine does and they produce somewhat different effects. This schematic should make things clearer:

https://www.cnsforum.com/upload/imagebank/download/hrl_rcpt_sys_NMDA.png

Nice diagram of the NMDA receptor in your link.

I am still not clear though why Goldstein is separating ketamine in one pair of boxes from glycine/NMDA in another pair of boxes.

 

[JPV]

The NMDA receptor is quite complicated with different binding sites. Ketamine binds to a different site than glycine does and they produce somewhat different effects. This schematic should make things clearer:

https://www.cnsforum.com/upload/imagebank/download/hrl_rcpt_sys_NMDA.png

Thanks, if I understand it correctly, that diagram seems to help explain why MG is potentially such a powerful NMDA blocker.

 

[zzz]

First, I want to mention that in my previous post where I gave the details of Dr. Goldstein's Resurrection Cocktail, I mentioned the use of thyrotropin-releasing hormone, but did not include it in the final formula. I have edited the post to fix this.

It's unfortunate that the two most effective treatments listed by Dr. Goldstein (Lidocaine and Ketamine) are also the most difficult to obtain. And even if you do get a local doctor to agree to it, the administration protocol of the IV is very specific as well. And of course, both drugs can't be ordered online to the best of my knowledge.

Ketamine can't be reliably ordered online because it is a scheduled drug, and not allowed to be imported into the U.S. Therefore, none of the reputable online pharmacies sell it. There are a number of places that claim to sell ketamine, but they come and go, and it seems that most of them are scams. Either they never deliver anything, or what they deliver is not ketamine. I don't believe it is safe to try to order ketamine over the Internet, even though a few people appear to have gotten lucky occasionally.

Lidocaine is a completely different story. It is permitted to import lidocaine into the U.S. to the same extent it is permitted to important any other nonscheduled drug for personal use. As for where to get it, Goldpharma is a good place to find many unusual drugs, and sure enough, they have this version of lidocaine, which would probably be most suitable if you were following Dr. Goldstein's protocol.

But how do you administer it? IV administration is tricky and requires considerable training and practice even for professionals. And IV self administration is extraordinarily difficult. Errors here can result in medical emergencies and even death. For this reason, administration by a qualified medical professional is strongly recommended for reasons of safety and efficacy. On one hand, you can find YouTube videos showing you how to do IV self administration. But watching these videos does not guarantee that you will be able to develop the experience and skill to do these procedures safely.

There's a local pain clinic here that offers IV Lidocaine and Ketamine for treatment-resistant neuropathic pain so I'd really have to do some arm twisting to my family doc to agree to refer me.

Twist that arm, and twist it hard! I think that that's by far your best and safest approach. But you really need to get the clinic to use Dr. Goldstein's protocol, as otherwise you risk not only adverse drug reactions, but you risk losing the ability to have these drugs ever help you again.

Also, I'm Canadian and can't find any source of over the counter chlorzoxazone. And I can't seem to find a source online either. Do you have any further info on how I can obtain it?

If you're in Canada, you're in luck. You can buy Acetazone Forte (which is chlorzoxazone plus acetaminophen) online from Well.ca for $9.79 for 30 tablets. Acetazone Forte has 250 mg of chlorzoxazone, which is half that of Parafon Forte; you can double the dose and still stay well within the safe daily limit of acetaminophen intake. Well.ca will not ship Acetazone Forte outside of Canada, unfortunately.

The cheapest source of chlorzoxazone that I know of is NorthWestPharmacy.com, where you can get 100 tablets of generic chlorzoxazone (500 mg each) for $35.39. This is about a sixth of what online sites typically charge. However, you need a prescription at this pharmacy.

I understand that the purpose of Goldstein's use of profiling drugs in his decision tree is to ascertain which receptors are dysregulated in a given ME/CFS patient. The profiling drugs are shown in the central column of the decision tree (the decision tree in this post above).

Each of Goldstein's profiling drugs targets and agonizes a particular receptor, and the profiling drug is used to find out how well that receptor is working.

If you feel either better or worse on a particular profiling drug, Goldstein says it indicates you have a dysregulation in the receptor the profiling drug targets.

Specifically, I am guessing that if you feel better on a profiling drug, it means your associated receptors are under-stimulated, so you would need to boost them (and this is done using the drugs listed in the boxes pointed to by the brown arrows in the decision tree).

Conversely, if you feel worse on a profiling drug, it means your associated receptors are over-stimulated, so you would need to inhibit them (and this is done using the drugs in the boxes pointed to by the turquoise arrows).

Does that sound right to you, @zzz?

Yes, I think that's a good summary.

One thing I am not sure about: in Dr Goldstein's decision tree diagram, the titles of the boxes in the left and right-hand columns include both receptor types (namely norepinephrine alpha 1&2, dopamine, NMDA/glycine receptors) along with drugs (namely benzodiazepines and ketamine).

I was a bit confused by this at first, but I then I realized that what I think Goldstein is implying with benzodiazepines is the GABA-A receptor (the receptor benzodiazepines act on), and what he is implying with ketamine is the NMDA receptor (the receptor that ketamine antagonizes).

But then if that is the case, and ketamine just represents the NMDA receptor, why has Goldstein also got a another box entitled glycine/NMDA?

As @Sidereal indicated, many of these receptors are quite complex, with different binding sites that do very different things. For example, benzodiazepines are not actually GABA agonists, contrary to what many people believe, but are positive allosteric modulators of the GABA-A receptor. That is, they enhance the effect of GABA-A agonists. Benzodiazapines bind to various alpha subunits of the GABA-A receptor. So when Goldstein refers to benzodiazepine agonists, he is referring to drugs that specifically enhance the effects of this type of positive allosteric modulator. A benzodiazepine antagonist, in Goldstein's terminology, would be a drug that decreases or nullifies the effect of benzodiazepines; such a drug may or may not have an effect on the rest of the GABA receptor. Flumazenil is an excellent example of a benzodiazepine antagonist. It binds to the same alpha subunits of the GABA-A receptor that other benzodiazepines do, but it is a neutral allosteric modulator as opposed to a positive allosteric modulator like the commonly used benzodiazepines. As a result, it displaces other benzodiazepines from these binding sites while having no effect on other GABA agonists. This makes Flumazenil an excellent agent for tapering off benzodiazepines, and there are clinics that use Flumazenil to get people who are addicted to benzodiazepines completely free of them within a week. This requires a tightly controlled dose of Flumazenil administered frequently via IV, and as you might imagine, such treatments are quite expensive.

I am not sure why in this the above text the term "ketamine receptor" is used. This is not a standard name for any receptor. Ketamine does have effect on the NMDA receptor: it antagonizes this receptor. But receptors are named after agents that agonize them, not antagonize them.

Again, this is just another example where the term "ketamine receptor" is being used as a shorthand for "the ketamine binding site on the NMDA receptor".

I am still not clear though why Goldstein is separating ketamine in one pair of boxes from glycine/NMDA in another pair of boxes.

Glycine is somewhat unique in its role in the NMDA receptor. Technically, the glycine binding site is known as the glycine co-agonist site, as this site needs to have a glycine molecule bound to it in order for NMDA agonists such as glutamate to be fully effective. Drugs that block that glycine co-agonist site are in effect indirect NMDA antagonists. But as each binding site on the NMDA receptor has a somewhat different effect, drugs that block the glycine co-agonist site have a somewhat different effect than other NMDA antagonists. And the role of glycine here explains why although glycine is an amino acid that usually has a calming effect, in some people it can have an excitatory effect, as its role in filling the glycine co-agonist site of the NMDA receptor can predominate.

Thanks, if I understand it correctly, that diagram seems to help explain why MG is potentially such a powerful NMDA blocker.

Yes; magnesium appears to be the single most potent NMDA antagonist, which makes it a very powerful drug for treatment of ME/CFS. However, people's sensitivity to magnesium varies widely, depending on how hypersensitive their NMDA receptors have become through the course of the illness. For people with extremely hypersensitive receptors, very low doses of magnesium must be used at first, or else the hypersensitivity of the receptors will result in CNS depression effects. As the low doses of magnesium gradually reduce the hypersensitivity of these receptors, the dose of magnesium can gradually be titrated up until a full therapeutic dose is attained. Such a dose, which is most effective when done through IM or SC injections, can have a profound effect on a wide variety of ME/CFS symptoms. If injections are unavailable, magnesium via nebulizer is the second most effective delivery system.

 

[RustyJ]

For people with extremely hypersensitive receptors, very low doses of magnesium must be used at first, or else the hypersensitivity of the receptors will result in CNS depression effects.

I hope this is not too far off topic... I experienced this a couple of weeks ago when I doubled my dosage of Mg. However, I also reduced a proton pump inhibitor and a H2 antagonist at the same time. I later discovered that these medications deplete magnesium, so I may have been increasing the effective Mg dosage by much more than 2x.

I got very depressed and backed off the Mg when I read about CNS depression in this thread. I have recovered somewhat.

I have googled this but only found one less than satisfactory study. Do you have a more appropriate reference, as I want to continue to increase Mg?

 

[Soporificat]

Are any of you going to try Goldstein's approach? Does anybody know of ANY doctors who treat according to Goldstein's ideas?

It's all so tantalizing, but as someone with no chemistry/medical background, and a full-sized case of ME/CFS brain, I feel hopeless about trying it myself. I would probably end up killing myself by accident.

 

[JPV]

Such a dose, which is most effective when done through IM or SC injections, can have a profound effect on a wide variety of ME/CFS symptoms. If injections are unavailable, magnesium via nebulizer is the second most effective delivery system.

I'm experimenting with a combination of Magnesium Threonate and Transdermal Magnesium Oils. Too early to tell how effective it is. I think I may have been taking too much, compared to your recommendations, so I'm going to back off a bit for now.

 

[Thomas]

@zzz @Hip how long are you guys trying a treatment before determining its effectiveness and whether or not you will continue to take it as part of your protocol?
Do you play around with dosages if you had a negative response to a certain medication. For example, I took my first 300mg dose of gabapentin this afternoon (I had high hopes for this drug) but didn't have a very positive response. I got extra fatigue and then quite agitated. I'm wondering if I should lower the dose(perhaps 300mg was too high), give it more time, or trash it altogether and move on to the next drug.

I've read BBTB and am halfway through TTB and it seems Goldstein wouldn't give a drug a second chance. But then sometimes it appears that he would. I'm curious what you would do in this instance?

As an aside, I will be skyping with Dr. Hyde tomorrow and I intend on asking him about Dr. Goldstein's current state of health and whether correspondence with him is at all possible.

Thanks!

 

[Hip]

@Thomas
Speaking for myself, I tend to try a given treatment multiple times, with different durations of treatment, and sometimes different dose levels.

So for example, I might initially try a drug or supplement at a cautious low dose for just one day. I try to observe any effects, good or bad. If there are no bad effects on that day or in the subsequent few days, I might starting taking the drug again a few days later, and take it for a slightly longer period, say for 4 days. Again, I try to observe any effects, good or bad for the duration of the 4 days, and also try to notice if these effects disappear after the 4 days are over and I stop the drug.

It is often when you start or stop a treatment that you tend to most notice what the benefits and side effects are. This is because we quickly get used to the effects of a treatment, and start to consider them to be normal. It's only during a change, when you start and stop a drug, that you most notice the effects it provides. That's why I tend to start and stop a drug a lot when I am testing it.

After the 4 day trial, if things seemed promising, I might do a longer trial of several weeks. Then again after those few weeks, I will stop for a week or two, and take stock, and again try to observe any changes in symptoms, good and bad, during the transition to both starting and stopping.

Finally, if I really think the drug is offering some useful benefits, I will start taking it on a long term basis, for many months. But even during this long term period, I will sometimes stop taking the drug just for a short period of say week or two, just to see if what happens. If I start feeling worse in one or more of my symptoms when I briefly stop, then it gives me confidence that the drug is still offering benefits, and that it is therefore a good idea to keep taking it.



The only exception to this multiple testing is when a drug or treatment leads to unpleasant mental side effects. I have tendency towards several psychiatric conditions, including generalized anxiety disorder, depression, anhedonia, and mild psychosis. Although I have most of these under control / eliminated, they can easily reappear for a day or two as side effects to drugs that don't agree with me.

I once did a trial of a very obscure opioid compound called dermorphin (see this thread). I got very good results that appeared very quickly, within 12 hours, but after several days I had a episode of mild psychosis, which I always find very unpleasant, so in spite of the significant benefits I noticed from dermorphin, I have yet to pluck up the courage to take it again.



I tend to try many drugs and supplements each year. I tend to weave the testing of 2 or 3 at the same time. For example, I might try one drug for 4 days, and then while I am giving that one a break, the next week I might try a different drug, with a few days washout period in between.

I do this to try to be efficient, as there is never enough time, and there is only one of me to test on.

 

[Navid]

Question for Goldstein people:

Fentanyl and hydrocodone are the only 2 drugs that make me feel better....take away pain, give ma a tiny tiny boost of energy and take away sickness feeling....from this knowledge, is there a next avenue I can research to find something that would give me some energy and refreshing sleep...what receptors are the fentanyl and hydrocodone positively affecting. other opiates DO NOT have the same positive affect.

We all know that Dr. Goldstein is no longer practicing and is in fact ill himself....are there any other Dr's in the US who understood what he was doing and follow his practices.

I am not really seeing any Docs right now and am at a complete standstill in treatment ideas after having tried: antibiotics, antivirals, methylation and many other protocols with no success at all.

Despite my lack of any positive progress in a decade I still believe there MUST be something that can help me regain some functionality.

Thanks : )

 

[zzz]

I hope this is not too far off topic... I experienced this a couple of weeks ago when I doubled my dosage of Mg. However, I also reduced a proton pump inhibitor and a H2 antagonist at the same time. I later discovered that these medications deplete magnesium, so I may have been increasing the effective Mg dosage by much more than 2x.

I got very depressed and backed off the Mg when I read about CNS depression in this thread. I have recovered somewhat.

I have googled this but only found one less than satisfactory study. Do you have a more appropriate reference, as I want to continue to increase Mg?

It's important to understand that CNS depression (central nervous system depression) is completely different from the mood disorder known as depression. CNS depression means that the activity of the central nervous system is depressed; i.e., there is less activity than there should be. Some of the typical manifestations of this are very weak muscles, trouble breathing, and excessive drowsiness or sleepiness. If CNS depression becomes excessive, it can lead to coma and even death.

A depressed mood can be an indication of a magnesium deficiency; it never occurs from too much magnesium. A depressed mood can result from medications that deplete magnesium. However, if you increase your magnesium intake substantially without increasing potassium, you can suffer from depression that is one of the effects of hypokalemia (low potassium). So if increasing magnesium leads to depression, you probably need more potassium.

Magnesium deficiency is pretty much endemic among people with ME/CFS, and it is possible that your remaining depression may be at least partially due to this. Gradually augmenting your magnesium intake may be helpful, as long as you supplement your potassium as well.

Are any of you going to try Goldstein's approach? Does anybody know of ANY doctors who treat according to Goldstein's ideas?

I've been using Dr. Goldstein's methods since last summer, with gradually increasing success. Unfortunately, it takes a lot of work to learn these methods well enough for them to be very effective. No doctors are currently using Dr. Goldstein's approach; even in his time, he was the only one to use it.

It's all so tantalizing, but as someone with no chemistry/medical background, and a full-sized case of ME/CFS brain, I feel hopeless about trying it myself. I would probably end up killing myself by accident.

It's true that it can be dangerous to use Dr. Goldstein's methods if you don't understand them. Please send me a PM if you're interested in knowing some of the approaches that could be helpful for you.

I'm experimenting with a combination of Magnesium Threonate and Transdermal Magnesium Oils. Too early to tell how effective it is. I think I may have been taking too much, compared to your recommendations, so I'm going to back off a bit for now.

The key to using magnesium therapy successfully is to start out at a dose that has no side effects, and then titrate up slowly, either to higher doses of the same form of magnesium or to more potent forms. Always wait until the side effects completely disappear before titrating up. Also, be sure to supplement properly with potassium; at larger doses of magnesium, some calcium supplementation may be necessary as well. It's important to know what the side effects of too much magnesium are, as well as the side effects of too little potassium or too little calcium.

@zzz @Hip how long are you guys trying a treatment before determining its effectiveness and whether or not you will continue to take it as part of your protocol?

It depends on the treatment. Generally, I will only ditch a treatment quickly if I have a reaction that I know either won't go away with time or is potentially dangerous, and I am already at a low dose. Although my regimen for trying out medications is not as highly organized as @Hip's, I try to give medications as much of a chance as possible, especially if it seems that they should work. Sometimes they just take a while. For example, I was on Hydergine for several months before it kicked in, but when it did, it gave me a major energy boost.

Do you play around with dosages if you had a negative response to a certain medication. For example, I took my first 300mg dose of gabapentin this afternoon (I had high hopes for this drug) but didn't have a very positive response. I got extra fatigue and then quite agitated. I'm wondering if I should lower the dose(perhaps 300mg was too high), give it more time, or trash it altogether and move on to the next drug.

In the case of gabapentin, Dr. Goldstein recommends a dose of 100 to 300 mg 3x/day. I started out with one dose of 100 mg, and it did absolutely nothing. I gradually built up to 100 mg 3x/day, and it has turned out to be one of my two most beneficial drugs from Dr. Goldstein. One reason I continued with it is that it's his #1 oral drug.

I've read BBTB and am halfway through TTB and it seems Goldstein wouldn't give a drug a second chance. But then sometimes it appears that he would. I'm curious what you would do in this instance?

When you first read Dr. Goldstein's books, they seem incredibly technical and dense. Later on, it becomes clear that although he's included a lot, he's also left out a lot, due to space and time limitations. He expects the intelligent reader to read between the lines (even though it's hard enough to read the lines themselves at first). So you see various things in his books that seem to be contradictory, such as whether or not he would give a drug a second chance. As you get to understand his methods more, it becomes clear that one answer applies in some cases, while another answer applies in others. I've gradually been seeing that his books are merely an outline of his methods. Like any outline, they may seem unreasonably terse. But as you understand them more, the details begin to fill in.

The reason Dr. Goldstein usually gave drugs only one shot is that typically his patients were in town for only a few days, and he had to get them better (or mostly so) within that time frame. This explains his rapid use of drugs. He would often go through up to seven drugs in a day, building on the effects of drugs that worked, and reversing the effects of drugs that didn't by using other drugs. He knew far more about how to do this than anyone else, then or now.

Although we have neither Dr. Goldstein's knowledge nor skill, we have one advantage that he usually didn't: time. We can give drugs more time to work, try them in different doses, etc. With Dr. Goldstein's long term patients, he often did the same. There are hints of this here and there in his books.

In your case, I'd try going back to gabapentin at 100 mg once a day, and then work up to 3x/day slowly. That may be all you need. If you can't tolerate 100 mg, it may be worthwhile opening the capsule and trying less.

As an aside, I will be skyping with Dr. Hyde tomorrow and I intend on asking him about Dr. Goldstein's current state of health and whether correspondence with him is at all possible.

I appreciate your doing this, and I would be very interested indeed to hear the answer.

Fentanyl and hydrocodone are the only 2 drugs that make me feel better....take away pain, give ma a tiny tiny boost of energy and take away sickness feeling....from this knowledge, is there a next avenue I can research to find something that would give me some energy and refreshing sleep...what receptors are the fentanyl and hydrocodone positively affecting. other opiates DO NOT have the same positive affect.

Dr. Goldstein described how opiates were effective for a certain subset of his patients, but he didn't describe any differences in opiate receptors, nor did he indicate why some opiates might be more effective than others.

We all know that Dr. Goldstein is no longer practicing and is in fact ill himself....are there any other Dr's in the US who understood what he was doing and follow his practices.

Unfortunately, no.

Despite my lack of any positive progress in a decade I still believe there MUST be something that can help me regain some functionality.

There certainly is, and I would encourage you in that belief. Certainly, Dr. Goldstein's resurrection cocktail worked on patients at least as sick as you. Of course, the question is who would you get to administer such a treatment? Fortunately, the whole cocktail is usually not necessary; either the ketamine or lidocaine portion is usually enough to get someone on their feet. If you have a doctor who is prescribing fentanyl and hydrocodone for you, there should be a way to get one of these treatments done. IV lidocaine is certainly a far more benign treatment than opiates, and Dr. Goldstein found that it was usually far more effective as well.

I'll follow up more in an email with you tomorrow, but I really think you should be able to make a significant improvement here.

 

[Thomas]

@zzz and everyone else reading this, I actually had the pleasure of speaking with Dr. Goldstein (DG for now on) himself this afternoon. During my skype call with Dr. Hyde I expressed my (and our) admiration for DG's work and tireless effort in treating his patients (I also expressed our frustration at the lack of the ME/CFS scientific community in adopting his theories), and how I would be thrilled to converse with him.

Dr. Hyde then called DG's wife, who put him in touch with DG. Hyde asked him if he would take my call, which he said he would. But Dr. Hyde went ahead and said I would be calling him immediately (which I wasn't happy about as I was already in a PENE state from having been on skype with Hyde for an hour and wouldn't have enough time to craft what I wanted to say). Regardless, I called right away.

I have good news and bad news. The bad news is that DG is in very poor health and is currently in a nursing home unable to stand up or speak much and suffering from an early stage of a type of dementia and heart problems. Hyde would not disclose exactly what it was but he said it was bad.

The good news is that I was able to cheer DG up very much by calling him and expressing the ME/CFS's patient population's gratitude for his work, and thanked him for writing down his theories for people to follow (and hopefully researchers too -- although he told me not to hold my breath for that one). I must admit that he spoke very slowly and with a slight slur and it took him a few seconds after a question to be able to begin answering it. And his insights were very much limited although he was able to elaborate slightly. He did mention that his treatments were all trial and error and that you simply had to find the right combination. He said IV's worked best if you can someone to administer them regularly. He said if you got a bad reaction to a drug it was most likely not worth fiddling around with it anymore, and that if you didn't get a response to most oral medications that day or within a few days of taking it regularly, you should probably move on to another.

He referenced the chart posted above (the one from Tuning the Brain) as a good guideline but could not tell in advance what would work for what. I could tell that after several minutes of conversation he was beginning to fade and I felt bad and didn't want to take up too much of his time. Of course, I didn't get a chance to ask him any of the 100 questions that popped into my mind AFTER the call ended as is so classic with me. I should have confirmed the ressurection cocktail, discussed NE in greater detail, and ask what his favourite drugs were right before retirement etc. I probably should have asked if there was a manuscript of Brain Static, the book he never completed.

If there are any really important or specific questions that you think should be asked that could drastically assist in helping us get better quicker by assisting in navigating through his protocol, let me know and I will try and call him again. He said I could in a couple weeks, but also asked not give out his phone number.

All in all he was a delightful person to speak to and I feel so bad that such a great person had such a rough career because of the stupidity of selfish regulatory boards and manipulative patients. And sorry if I didn't provide any new information but I felt the need to make conversation with him before peppering questions at him out of respect.

That's the update. Cheers.

 

[Hip]

The good news is that I was able to cheer DG up very much by calling him and expressing the ME/CFS's patient population's gratitude for his work, and thanked him for writing down his theories for people to follow (and hopefully researchers too -- although he told me not to hold my breath for that one). I

Nice one, Thomas. It's great to hear that you managed to cheer Dr Goldstein up by passing on the ME/CFS patient community's gratitude to him.