20 minutes ago, Colinboko said:

29 minutes ago, guitarman01 said:

yea thats the same antibody and yes it different then the muscle achr antibody.
Ganglionic Neuronalbeing the key term.

I'll certainly try to get this tested soon. I get so nervous asking my doctor for crazy shit like this because I look like a perfectly healthy 21 year old, even though I'm dying on the inside from all these symptoms. But at the end of the day like my mom always says... they're YOUR doctor. They should never laugh at you for wanting a certain test done.

depending on what doctor you're asking they might not be familiar with this test. I would be prepared to give them the exact test code and name of the test from mayo's test catalog. Babis had to try like hell to get this test with 10 different doctors. I got lucky because my doctor didnt even know what the hell I was ordering when I called it in.

I would strongly relate it to accutane and new studies finding it can trigger autoimmune diseases in susceptible individuals. You could stretch the truth a little bit and just say numerous people have tested positive for the ganglionic antibody in this test post tane and have seeked out treatment at mayo clinic. Whatever you have to say to at least get this test. if abnormal a person will take the results to mayo for further investigation, so your doctors dont feel like they have to deal with it. Something along those lines.

I would just say, you have to get me this test, I have to know.

15 minutes ago, guitarman01 said:

depending on what doctor you're asking they might not be familiar with this test. I would be prepared to give them the exact test code and name of the test from mayo's test catalog. Babis had to try like hell to get this test with 10 different doctors. I got lucky because my doctor didnt even know what the hell I was ordering when I called it in.

I would strongly relate it to accutane and new studies finding it can trigger autoimmune diseases in susceptible individuals. You could stretch the truth a little bit and just say numerous people have tested positive for the ganglionic antibody in this test post tane and have seeked out treatment at mayo clinic. Whatever you have to say to at least get this test. if abnormal a person will take the results to mayo for further investigation, so your doctors dont feel like they have to deal with it. Something along those lines.

I would just say, you have to get me this test, I have to know.

Now you said you tested positive right? Does your doc know? Are you going to make any attempts at treatments?

7 minutes ago, Colinboko said:

Now you said you tested positive right? Does your doc know? Are you going to make any attempts at treatments?

Yes i'll be going to mayo as soon as they get back to me. I would be shocked at this point if they turned me down. my doc was absolutely clueless about this test. I dont know if she even was aware of possible implications even though it stated right on the test results. She mailed me the result and i faxed it to the neurology dept at mayo in rochester.

4 hours ago, cnb30 said:

On a lighter note,sometime either after ECT, or while on effexor, my head pressure went awayso if your main goal is getting rid of that, it's doable.

You had electro shock therapy? Again is this a psychiatrist or Nero psychiatrist giving you these tests/treatment? They put you to sleep for the ECT?

27 minutes ago, guitarman01 said:

Yes i'll be going to mayo as soon as they get back to me. I would be shocked at this point if they turned me down. my doc was absolutely clueless about this test. I dont know if she even was aware of possible implications even though it stated right on the test results. She mailed me the result and i faxed it to the neurology dept at mayo in rochester.

You would or wouldn't be shocked? You have physical proof now. Don't let them turn you down..

1 hour ago, guitarman01 said:

5 hours ago, cnb30 said:

On a lighter note,sometime either after ECT, or while on effexor, my head pressure went awayso if your main goal is getting rid of that, it's doable.

You had electro shock therapy? Again is this a psychiatrist or Nero psychiatrist giving you these tests/treatment? They put you to sleep for the ECT?

I had ECT after being in the psych ward for weeks. I literally had no choice at that point. And yes, of course I was put to sleep. What kind of sadistic doctor keeps someone awake for ECT?

Also, I just wanted to say I noticed a huge difference after taking B12 and B6. My only concerns are wheter or not there is a way to be able to permaneantly fix this issue, so I don't have to spend $20 every other week to buy happiness in a bottle from Kroger. Atleast it's vitamins so I feel safer about taking them than supplements.

Professor & patients paper on the solvable biological challenge of ME/CFS: reader-friendly version
(I believe this also relates to accutane)

Introduction

ME/CFS is similar to multiple sclerosis, diabetes or rheumatoid arthritis in terms of the proportion of people affected (about0.2% to 1%),[Edited link out], andquality of life. However, the recentNational Institutes of Health (NIH)andInstitute of Medicine reportsshow that biomedical research and funding have been pitifully limited.

We hope that the NIHsincreased focus on ME/CFS, announced by Director Francis Collins, will attract many more researchers and more resources, but even with the scant funding so far, ME/CFS researchers have already generated promising leads.

In our paper, we suggest the key elements of a coordinated research programme and we call on the wider biomedical research community to focus on this condition.

Biological questions

Patients desperately need treatment, so treatment studies appear to be a good place to start. Researchers can stumble across possible treatments, as Dr ystein Fluge and Professor Olav Mella appear to have done when they noticed that B-cell-targeting cancer medications alsohelped ME/CFS patients: this eventually led them to conduct a large multi-centre clinical trial of rituximab for ME/CFS.

But generally its hard to develop treatments until researchers understand what causes an illness, so trying to understand what causes ME/CFS is a key priority.

Drawing on the experience of our lead author, Professor Jonathan Edwards, inunderstandingthe mechanism behind rheumatoid arthritis and itsapplicationto treatment (rituximab therapy), we use a broad systems approach.

This means that we consider how various parts of our complex biology interact with each other and with things in the environment, such as viruses, bacteria and toxins, in a big system.

One important possible cause of illness can consist of stochastic (random) factors. Stochastic factors are very important in cancer, where random mutations in DNA accumulate over time, and sometimes, by sheer bad luck, those mutations happen in particular series of genes that drive cells towards becoming tumours.

But the potential role of such random factors in diseases other than cancer is often ignored, though they play a role in rheumatoid arthritis too, where random generation of antibodies, and more bad luck, leads to auto-antibodies that attack the body (see box).

This could also apply in ME/CFS, either leading to auto-antibodies (which could explain the apparent success of rituximab, which wipes out antibody-producing B-cells) or some other mechanism driven by random factors.

Epidemiology the study of who gets what illness, when and where also provides several clues as to what aspects of the system may be involved in ME/CFS. The most striking is the high proportion of women with the condition typically 75%.

And there is evidence that people are most likely to fall ill with ME/CFS attwo stages in life adolescence and mid-adulthood suggesting people might be particularly vulnerable to triggers of ME/CFS at certain ages.

ME/CFS can run in families, and sometimes the illnessstarts with an infection(occasionally during an epidemic). Examples are the Epstein-Barr virus (EBV, which can cause glandular fever), Ross River virus and the bacteriumCoxiella burnetii,which causes Q fever.

It seems possible that either prolonged infection or long-lasting exposure to damaging environmental factors such as toxins, together with stochastic factors, could upset our bodies ability to regulate themselves and shift us from a stable, healthy state into astable, dysfunctional, diseased state thatkeeps us sick.

The fact that some people do improve substantially, either spontaneously or following treatment, supports the idea of a shift to a dysfunctional state rather than one of permanent damage.

Notable research findings that give clues to mechanisms include the following.

(i) Two lines of evidence that highlight an abnormal reaction to exercise

• Physiological performance in ME/CFS patients isworse on the secondof a two-day maximal exercise test, despite objective evidence showing that patients are making the maximum possible effort on both days, while healthy controls and patients with various other illnesses can repeat their performance on the second day.
• Moderate exercise leads tosubstantial changes in the gene expressionof receptors that sense small molecules produced by exercise in ME/CFS patients, but not in controls or patients with multiple sclerosis.

(ii) Evidence that implicates the immune system

• There have beenrepeatedbutvariablefindings of problems with natural killer cells, which play a key role in fending off viruses and attacking cancerous cells.
• There is some unconfirmed evidence that particular versions of genes are linked to ME/CFS, includingsomecytokines(the immune systems messenger molecules) andhuman leucocyte antigens(HLA).HLAmolecules help the immune system distinguish the bodys own proteins from those made by invaders such as viruses and bacteria.
• For patients whose illness began with glandular fever, there are changes in the way the immune systems B and T cellscontrol EBV reactivation. (Almost everyone is infected by EBV, which causes glandular fever in some people, and our immune system has to work throughout our lives to control the infection.)
• Brain scans indicate bothactivation of microglia(the brains immune cells) andstructural changesin the brain, and this implicates the brain as well as the immune system.

(iii) Evidence that the autonomic nervous system is involved

• Autonomic problems arecommonin ME/CFS patients, such as orthostatic intolerance, in which standing up triggers symptoms including fainting that are relieved by lying down.

Crucially, these findings have not been replicated robustly enough to provide firm anchor points for further research. Lack of funding may have been an important reason for this, and perhaps also the use of ill-defined or varied groups of patients in the research. In this context, it is interesting that Dr Mady Hornigs team found that levels of cytokines in blood plasmadiffer between ME/CFS patientswho have been ill for fewer than three years, and those ill for longer.

Potential models

Our paper highlights several different models as potentially useful frameworks to understand and study ME/CFS. All of them take a broad systems-analysis approach, assuming that a hit and run event could have knocked patients regulatory systems into a new, diseased pattern.

Searching for a new microbial trigger may be productive, though no particular microbe seems associated with the illness.

The central problem for any model is to explain the ongoing physiological disturbance.

This, together with the symptoms of cognitive and other global problems, such as pain and fatigue, suggest that its likely that the central nervous system plays a key role, plus or minus the immune system. Both systems have extremely complex regulatory systems and so both are strong suspects. The autonomic system, which controls subconscious processes such as breathing, circulation and digestion, is another possibility.

Some researchers have suggested that general metabolic abnormalities including problems with energy metabolism might bekey. There are some intriguing findings such asthosefrom Professor Julia Newtons group, but its hard to explain how cells or mitochondria throughout the body would simultaneously acquire abnormalities. Its more likely that such abnormalities result from problems with control mechanisms for body-wide systems.

Three general models seem most interesting and each one is defined in broad terms that may apply to several different specific mechanisms.

Model 1. The brain is responding normally and symptoms are due to ongoing abnormal signals from the body

The signals could be cytokines being produced as the result of long-term problems with the immune system problems that could be caused by autoimmunity, or even low-grade chronic infection.

The finding that 67% of patients improved with rituximab therapy, which depletes the immune systems B-cells, needs confirming but indicates that problems in the immune system could be driving symptoms. Likewise, the gene-expression changes and the abnormal physiological response to exercise also suggest the body is responding abnormally. Tworesearchgroupsare currently looking at the gut microbiome as the possible ultimate source of the abnormal signals.

Model 2. Signals from the body are normal, but an ongoing problem with the brain leads to it responding abnormally to create symptoms

For example, a hit-and-run initial infection could lead to ongoing activation of microglia even after the infection has cleared, and the activated microglia could then cause the brain to over-react to normal signals coming from the body.

Immune activation in the body caninfluence the microgliain the brain, with the sickness response a biologically-driven set of symptoms inresponse to infection, such as depression, loss of appetite and sensitivity to pain as a stereotypical example (which overlaps with ME/CFS symptoms). Microglia have been implicated in several neurological disorders as well as in animal models offatigue, and a recent study using brain scans indicated activated microglia in ME/CFS patients.

Model 3. There are ongoing problems in neural pathways that lead to distorted signalling

This could be due to abnormal levels of neurotransmitters as seen in Parkinsons disease, or problems with thephysical pathwaysthemselves, either in terms of structural changes to the central nervous system after an acute infection or injury, or changes in how it is regulated.

These three broad theoretical models might overlap, with different models applying in different subgroups of patients. However, its quite possible that all models share a common biological pathway that causes exertion intolerance, as well as some other symptoms. The models are a start and need testing, but show that there are several possible ways of understanding the illness physiologically that are well worth exploring further.

Suggestions for progress

Identifying the biological basis of ME/CFS wont be easy but, with several promising findings, there is a real opportunity to make progress towards treatments based on understanding the disease. Several areas seem particularly promising to study:

• The brain. As so many symptoms are likely to originate in the brain, brain scanning has great potential to provide direct evidence of whats going wrong. This includes usingPET scans, which use tracer molecules injected into the body to light up key cells, such as microglia. Also, MRI scans reveal brain structure, and functional MRI scans look at thebrain in action.
• Immunology. Research has thrown up evidence of shifts in cytokine patterns, and abnormalities in natural killer cells and in how the immune system controls EBV more work is now needed to understand what mechanisms underpin these findings. Recent discoveries of auto-antibodies against nerves and their receptors in several neurological diseases, and interestingsimilar findingsin ME/CFS, make this another lead worth pursuing. (Since we wrote our paper, Dr Avindra Nath, who heads up the NIHs in-house study, has said he will belooking for auto-antibodiesusing a comprehensive new approach pioneered in his lab.)
• Asautonomicsymptoms, such as problems on standing up, are prominent in ME/CFS, further investigation of the autonomic/endocrine systems could reveal what mechanisms are driving these problems.

We also suggest ways to improve how research is done, to get better, more reliable results:

• A broader approach. Studies can be more effective, and generate more insight, by bringing together academics and physicians from different fields and studying more aspects of the illness simultaneously (such as measuring cytokines, gene expression and natural killer cell function at the same time).
• Making sure samples truly represent the population of patients. Patients who make it to specialist clinics are often different from patients who dont (this isnt just an issue for ME/CFS). And research groups use different clinical criteria, and apply them in different ways, so some results might not replicate simply because researchers are studying different types of patients. This is particularly likely if there are several subgroups of patients, with different researchers having a different mix of subgroups in their samples. Future large-scale genetic studies will also need to be representative of the patient population. Recruiting patient groups who accurately reflect the full ME/CFS patient population, capturing any different subgroups, will help researchers probe mechanisms driving ME/CFS. The same representative groups will help generate robust comparisons with other diseases.
• Replicationis essential to establish which findings are robust so that researchers can build on sound foundations. One way to make replication easier would be to set up a system to exchange samples between research groups around the world. Samples should be blinded so researchers wouldnt know if a sample was from a patient or a control until the sample had been tested. Using a group of patients who are representative of the population of ME/CFS patients would also increase the odds of successful replication.
• Stress testing. As post-exertional problems are central to the illness, testing how exercise affects anything from cognitive performance to cytokine levels may provide new insights. (Again, since we submitted our paper, the NIH has announced its study which is built around exercise tests, measuring countless factors both before and after exercise.)

• Data presentation and sharing. Data should be presented in a way that allows exploration of subgroups for example, by showing individual data points, instead of just averages. (Our paper didnt include an example of this, but the excerpt below, from a graph from the 2015 rituximab trail for ME/CFS, includes individual data points. It shows how the usual summary statistics the average, and the 95% confidence interval, in blue, indicates the range within which the true population average is likely to lie mask big variation in the underlying data. This variation can sometimes reveal distinct subgroups, hidden by the use of simple averages.) All data, even unpublished or from studies that found no effect, should be available for meta-analyses, which combine data from several small studies to give a more reliable overall result.

Conclusion

In summary, the current outlook for patients is poor. We still dont know for sure what drives the illness, although the brain certainly seems to be involved. There may well be subgroups with different underlying diseases requiring different treatments. We urgently need much more biomedical research into ME/CFS to provide hope for better treatments.

On 6/30/2017 at 12:08 PM, cnb30 said:

I had ECT after being in the psych ward for weeks. I literally had no choice at that point. And yes, of course I was put to sleep. What kind of sadistic doctor keeps someone awake for ECT?

Also, I just wanted to say I noticed a huge difference after taking B12 and B6. My only concerns are wheter or not there is a way to be able to permaneantly fix this issue, so I don't have to spend $20 every other week to buy happiness in a bottle from Kroger. Atleast it's vitamins so I feel safer about taking them than supplements.

glad to hear your doing better. you could maybe look into b12 shots as well. One study I read showed it was more capable of raising b12 in the CSF. they're fairly cheap at this blood draw place near me at 20 dollars a shot. Maintenance would prob be once a month.

On 6/30/2017 at 12:36 PM, guitarman01 said:

Professor & patients paper on the solvable biological challenge of ME/CFS: reader-friendly version
(I believe this also relates to accutane)

Introduction

 

ME/CFS is similar to multiple sclerosis, diabetes or rheumatoid arthritis in terms of the proportion of people affected (about0.2% to 1%), [Edited link out], andquality of life. However, the recentNational Institutes of Health (NIH)andInstitute of Medicine reportsshow that biomedical research and funding have been pitifully limited.

 

We hope that the NIHsincreased focus on ME/CFS, announced by Director Francis Collins, will attract many more researchers and more resources, but even with the scant funding so far, ME/CFS researchers have already generated promising leads.

In our paper, we suggest the key elements of a coordinated research programme and we call on the wider biomedical research community to focus on this condition.

Biological questions

Patients desperately need treatment, so treatment studies appear to be a good place to start. Researchers can stumble across possible treatments, as Dr ystein Fluge and Professor Olav Mella appear to have done when they noticed that B-cell-targeting cancer medications alsohelped ME/CFS patients: this eventually led them to conduct a large multi-centre clinical trial of rituximab for ME/CFS.

But generally its hard to develop treatments until researchers understand what causes an illness, so trying to understand what causes ME/CFS is a key priority.

Drawing on the experience of our lead author, Professor Jonathan Edwards, inunderstandingthe mechanism behind rheumatoid arthritis and itsapplicationto treatment (rituximab therapy), we use a broad systems approach.

This means that we consider how various parts of our complex biology interact with each other and with things in the environment, such as viruses, bacteria and toxins, in a big system.

One important possible cause of illness can consist of stochastic (random) factors. Stochastic factors are very important in cancer, where random mutations in DNA accumulate over time, and sometimes, by sheer bad luck, those mutations happen in particular series of genes that drive cells towards becoming tumours.

But the potential role of such random factors in diseases other than cancer is often ignored, though they play a role in rheumatoid arthritis too, where random generation of antibodies, and more bad luck, leads to auto-antibodies that attack the body (see box).

This could also apply in ME/CFS, either leading to auto-antibodies (which could explain the apparent success of rituximab, which wipes out antibody-producing B-cells) or some other mechanism driven by random factors.

Making antibodies by random events and the problem of bad luck

Humans can make billions upon billions of different antibodies, each recognising a different molecule, but we do this with only hundreds of antibody genes. How?

The body hasa remarkable abilityto mash up the small number of different antibody sub-genes into a vast set of new combinations, and does this throughout our life.

Critically, this gives us the ability to produce antibodies even against bugs we (or our ancestors) have never encountered before. However, because its a random process, inevitably some of the antibodies, known as auto-antibodies, will end up being able to attack our own bodies. Normally, the body destroys these before they can do any harm.

Sometimes, due to bad luck, the gene-mashing that is responsible for a continued fresh supply of new antibodies can throw up auto-antibodies capable of evading destruction and these can attack the body, leading to diseases such as rheumatoid arthritis.

Epidemiology the study of who gets what illness, when and where also provides several clues as to what aspects of the system may be involved in ME/CFS. The most striking is the high proportion of women with the condition typically 75%.

And there is evidence that people are most likely to fall ill with ME/CFS attwo stages in life adolescence and mid-adulthood suggesting people might be particularly vulnerable to triggers of ME/CFS at certain ages.

ME/CFS can run in families, and sometimes the illnessstarts with an infection(occasionally during an epidemic). Examples are the Epstein-Barr virus (EBV, which can cause glandular fever), Ross River virus and the bacteriumCoxiella burnetii,which causes Q fever.

It seems possible that either prolonged infection or long-lasting exposure to damaging environmental factors such as toxins, together with stochastic factors, could upset our bodies ability to regulate themselves and shift us from a stable, healthy state into astable, dysfunctional, diseased state thatkeeps us sick.

The fact that some people do improve substantially, either spontaneously or following treatment, supports the idea of a shift to a dysfunctional state rather than one of permanent damage.

Notable research findings that give clues to mechanisms include the following.

(i) Two lines of evidence that highlight an abnormal reaction to exercise

• Physiological performance in ME/CFS patients isworse on the secondof a two-day maximal exercise test, despite objective evidence showing that patients are making the maximum possible effort on both days, while healthy controls and patients with various other illnesses can repeat their performance on the second day.
• Moderate exercise leads tosubstantial changes in the gene expressionof receptors that sense small molecules produced by exercise in ME/CFS patients, but not in controls or patients with multiple sclerosis.

(ii) Evidence that implicates the immune system

• There have beenrepeatedbutvariablefindings of problems with natural killer cells, which play a key role in fending off viruses and attacking cancerous cells.
• There is some unconfirmed evidence that particular versions of genes are linked to ME/CFS, includingsomecytokines(the immune systems messenger molecules) andhuman leucocyte antigens(HLA).HLAmolecules help the immune system distinguish the bodys own proteins from those made by invaders such as viruses and bacteria.
• For patients whose illness began with glandular fever, there are changes in the way the immune systems B and T cellscontrol EBV reactivation. (Almost everyone is infected by EBV, which causes glandular fever in some people, and our immune system has to work throughout our lives to control the infection.)
• Brain scans indicate bothactivation of microglia(the brains immune cells) andstructural changesin the brain, and this implicates the brain as well as the immune system.

(iii) Evidence that the autonomic nervous system is involved

• Autonomic problems arecommonin ME/CFS patients, such as orthostatic intolerance, in which standing up triggers symptoms including fainting that are relieved by lying down.

Crucially, these findings have not been replicated robustly enough to provide firm anchor points for further research. Lack of funding may have been an important reason for this, and perhaps also the use of ill-defined or varied groups of patients in the research. In this context, it is interesting that Dr Mady Hornigs team found that levels of cytokines in blood plasmadiffer between ME/CFS patientswho have been ill for fewer than three years, and those ill for longer.

Potential models

Our paper highlights several different models as potentially useful frameworks to understand and study ME/CFS. All of them take a broad systems-analysis approach, assuming that a hit and run event could have knocked patients regulatory systems into a new, diseased pattern.

Searching for a new microbial trigger may be productive, though no particular microbe seems associated with the illness.

The central problem for any model is to explain the ongoing physiological disturbance.

This, together with the symptoms of cognitive and other global problems, such as pain and fatigue, suggest that its likely that the central nervous system plays a key role, plus or minus the immune system. Both systems have extremely complex regulatory systems and so both are strong suspects. The autonomic system, which controls subconscious processes such as breathing, circulation and digestion, is another possibility.

Some researchers have suggested that general metabolic abnormalities including problems with energy metabolism might bekey. There are some intriguing findings such asthosefrom Professor Julia Newtons group, but its hard to explain how cells or mitochondria throughout the body would simultaneously acquire abnormalities. Its more likely that such abnormalities result from problems with control mechanisms for body-wide systems.

Three general models seem most interesting and each one is defined in broad terms that may apply to several different specific mechanisms.

Model 1. The brain is responding normally and symptoms are due to ongoing abnormal signals from the body

The signals could be cytokines being produced as the result of long-term problems with the immune system problems that could be caused by autoimmunity, or even low-grade chronic infection.

The finding that 67% of patients improved with rituximab therapy, which depletes the immune systems B-cells, needs confirming but indicates that problems in the immune system could be driving symptoms. Likewise, the gene-expression changes and the abnormal physiological response to exercise also suggest the body is responding abnormally. Tworesearchgroupsare currently looking at the gut microbiome as the possible ultimate source of the abnormal signals.

Model 2. Signals from the body are normal, but an ongoing problem with the brain leads to it responding abnormally to create symptoms

For example, a hit-and-run initial infection could lead to ongoing activation of microglia even after the infection has cleared, and the activated microglia could then cause the brain to over-react to normal signals coming from the body.

Immune activation in the body caninfluence the microgliain the brain, with the sickness response a biologically-driven set of symptoms inresponse to infection, such as depression, loss of appetite and sensitivity to pain as a stereotypical example (which overlaps with ME/CFS symptoms). Microglia have been implicated in several neurological disorders as well as in animal models offatigue, and a recent study using brain scans indicated activated microglia in ME/CFS patients.

Model 3. There are ongoing problems in neural pathways that lead to distorted signalling

This could be due to abnormal levels of neurotransmitters as seen in Parkinsons disease, or problems with thephysical pathwaysthemselves, either in terms of structural changes to the central nervous system after an acute infection or injury, or changes in how it is regulated.

These three broad theoretical models might overlap, with different models applying in different subgroups of patients. However, its quite possible that all models share a common biological pathway that causes exertion intolerance, as well as some other symptoms. The models are a start and need testing, but show that there are several possible ways of understanding the illness physiologically that are well worth exploring further.

Suggestions for progress

Identifying the biological basis of ME/CFS wont be easy but, with several promising findings, there is a real opportunity to make progress towards treatments based on understanding the disease. Several areas seem particularly promising to study:

• The brain. As so many symptoms are likely to originate in the brain, brain scanning has great potential to provide direct evidence of whats going wrong. This includes usingPET scans, which use tracer molecules injected into the body to light up key cells, such as microglia. Also, MRI scans reveal brain structure, and functional MRI scans look at thebrain in action.
• Immunology. Research has thrown up evidence of shifts in cytokine patterns, and abnormalities in natural killer cells and in how the immune system controls EBV more work is now needed to understand what mechanisms underpin these findings. Recent discoveries of auto-antibodies against nerves and their receptors in several neurological diseases, and interestingsimilar findingsin ME/CFS, make this another lead worth pursuing. (Since we wrote our paper, Dr Avindra Nath, who heads up the NIHs in-house study, has said he will belooking for auto-antibodiesusing a comprehensive new approach pioneered in his lab.)
• Asautonomicsymptoms, such as problems on standing up, are prominent in ME/CFS, further investigation of the autonomic/endocrine systems could reveal what mechanisms are driving these problems.

We also suggest ways to improve how research is done, to get better, more reliable results:

• A broader approach. Studies can be more effective, and generate more insight, by bringing together academics and physicians from different fields and studying more aspects of the illness simultaneously (such as measuring cytokines, gene expression and natural killer cell function at the same time).
• Making sure samples truly represent the population of patients. Patients who make it to specialist clinics are often different from patients who dont (this isnt just an issue for ME/CFS). And research groups use different clinical criteria, and apply them in different ways, so some results might not replicate simply because researchers are studying different types of patients. This is particularly likely if there are several subgroups of patients, with different researchers having a different mix of subgroups in their samples. Future large-scale genetic studies will also need to be representative of the patient population. Recruiting patient groups who accurately reflect the full ME/CFS patient population, capturing any different subgroups, will help researchers probe mechanisms driving ME/CFS. The same representative groups will help generate robust comparisons with other diseases.
• Replicationis essential to establish which findings are robust so that researchers can build on sound foundations. One way to make replication easier would be to set up a system to exchange samples between research groups around the world. Samples should be blinded so researchers wouldnt know if a sample was from a patient or a control until the sample had been tested. Using a group of patients who are representative of the population of ME/CFS patients would also increase the odds of successful replication.
• Stress testing. As post-exertional problems are central to the illness, testing how exercise affects anything from cognitive performance to cytokine levels may provide new insights. (Again, since we submitted our paper, the NIH has announced its study which is built around exercise tests, measuring countless factors both before and after exercise.)

• Data presentation and sharing. Data should be presented in a way that allows exploration of subgroups for example, by showing individual data points, instead of just averages. (Our paper didnt include an example of this, but the excerpt below, from a graph from the 2015 rituximab trail for ME/CFS, includes individual data points. It shows how the usual summary statistics the average, and the 95% confidence interval, in blue, indicates the range within which the true population average is likely to lie mask big variation in the underlying data. This variation can sometimes reveal distinct subgroups, hidden by the use of simple averages.) All data, even unpublished or from studies that found no effect, should be available for meta-analyses, which combine data from several small studies to give a more reliable overall result.

Conclusion

In summary, the current outlook for patients is poor. We still dont know for sure what drives the illness, although the brain certainly seems to be involved. There may well be subgroups with different underlying diseases requiring different treatments. We urgently need much more biomedical research into ME/CFS to provide hope for better treatments.

glad to hear your doing better. you could maybe look into b12 shots as well. One study I read showed it was more capable of raising b12 in the CSF. they're fairly cheap at this blood draw place near me at 20 dollars a shot. Maintenance would prob be once a month.

"Dysfunctional state rather than one of permanent damage"

totally agree with that

7 hours ago, TrueJustice said:

Topamax is for epilepsy correct??

It's for treating seizures, how on earth did you get this may I ask?

It is also FDA approved for the prevention of migraines , which is rare for epilepsy meds. You take a much lower dose for this purpose.

3 hours ago, guitarman01 said:

Yes i'll be going to mayo as soon as they get back to me. I would be shocked at this point if they turned me down. my doc was absolutely clueless about this test. I dont know if she even was aware of possible implications even though it stated right on the test results. She mailed me the result and i faxed it to the neurology dept at mayo in rochester.

let me know if you get too mayo, as I was married too a doctor and I still have their denial letter!!!! can you say B.S

On 6/28/2017 at 2:59 PM, guitarman01 said:

I got my thyroid ultrasound from my ent. Just got the results. Normal. I also had a scope. Didn't notice anything significant. Except a dryness and lack of or thick saliva that could exasperate irritation.

I have had homocystine tested numerous times. It's been normal. Glutathione I don't believe is a standard test you can order from a doctor.

Just now, hatetane said:

Are none of you at all interested in the autistic protocol?
Have any of you even research autism recovery?
I am not saying it is a cure all but for many the recovery is miraculous.
https://www.greatplainslaboratory.com/articles-1/2015/11/13/a-new-generation-of-organic-acid-testing-pushing-the-limits-of-detection-with-new-technology

12 hours ago, Colinboko said:

12 hours ago, guitarman01 said:

yea thats the same antibody and yes it different then the muscle achr antibody.
Ganglionic Neuronalbeing the key term.

I'll certainly try to get this tested soon. I get so nervous asking my doctor for crazy shit like this because I look like a perfectly healthy 21 year old, even though I'm dying on the inside from all these symptoms. But at the end of the day like my mom always says... they're YOUR doctor. They should never laugh at you for wanting a certain test done.

Just a shame you have to ask - doctors don't have a clue - they should be advising you on what tests are needed.

Moving into my second week of taking Glutathione daily, absolutely nothing unfortunately- I'll continue because I believe you should try things for about 5 weeks. Would like to hear from others who might be trialling it..

I was hoping for less fatigue, less light sensitivity, less dryness, better sleep each night, no more teeth grinding, less depression, more energy, the disappearing of eye floaters, compensation in the form of a massive payout for last 20 years of misery, less sweating, thicker fuller hair, less unwanted hair on shoulders, less stiffness in joints, no more brainfog, I could go on.....

perhaps others will get better results?

Hi, I have recently been on a search to find some sort of solution to the treacherous affects from accutane, reading about 200 of the 500 pages on here and I have still have not come across any sort of proven solution to the problems that arise from accutane. Once upon a time, I was a young charismatic and intelligent but acne ridden young man but after going on accutane I have been a shadow of myself and am just looking for a way to go back to my old self again. The two questions that I have are, how close are we to understanding what causes these long term side effects and what is the closest that we have come to finding a cure for these symptom. Even Kevin Pezzi who seems to be the internet's most intelligent and knowledgeable person on the subject didn't have any sort of solution to the issue so I don't expect a whole lot. From what I have heard hemp oil is the closest thing to a solution to the issue. It's amazing to think we have made this many posts trying to find a solution to post isotretinoin problems when we don't even know what the mechanism of action is.

1 hour ago, Taneraped said:

Hi, I have recently been on a search to find some sort of solution to the treacherous affects from accutane, reading about 200 of the 500 pages on here and I have still have not come across any sort of proven solution to the problems that arise from accutane. Once upon a time, I was a young charismatic and intillengent but acne ridden young man but after going on accutane I have been a shadow of myself and am just looking for a way to go back to my old self again. The two questions that I have are, how close are we to understanding what causes these long term side effects and what is the closest that we have come to finding a cure for these symptom. Even Kevin Pezzi who seem's to be the internet's most intelligent and knowledgeable person on the subject didn't have any sort of solution to the issue so I don't expect a whole lot. From what I have heard hemp oil is the closest thing to a solution to the issue. It's amazing to think we have made this many posts trying to find a solution to post isotretinoin problems when we don't even know what the mechanism of action is.

The only person I recall to have returned 100% to their pre accutane state was ehohel when he was put on a prednisone taper. I think we are truly dealing with a modulation of the immune system in some sort of way. What that exact modulation entails I'm not so sure. But we will find out. I feel like we progress. Slowly but surely

48 minutes ago, Colinboko said:

2 hours ago, Taneraped said:

Hi, I have recently been on a search to find some sort of solution to the treacherous affects from accutane, reading about 200 of the 500 pages on here and I have still have not come across any sort of proven solution to the problems that arise from accutane. Once upon a time, I was a young charismatic and intillengent but acne ridden young man but after going on accutane I have been a shadow of myself and am just looking for a way to go back to my old self again. The two questions that I have are, how close are we to understanding what causes these long term side effects and what is the closest that we have come to finding a cure for these symptom. Even Kevin Pezzi who seem's to be the internet's most intelligent and knowledgeable person on the subject didn't have any sort of solution to the issue so I don't expect a whole lot. From what I have heard hemp oil is the closest thing to a solution to the issue. It's amazing to think we have made this many posts trying to find a solution to post isotretinoin problems when we don't even know what the mechanism of action is.

The only person I recall to have returned 100% to their pre accutane state was ehohel when he was put on a prednisone taper. I think we are truly dealing with a modulation of the immune system in some sort of way. What that exact modulation entails I'm not so sure. But we will find out. I feel like we progress. Slowly but surely

How long has it been for you personally, and to what percent do you feel like you have recovered? Personally it has been 5 years and I feel like I have recoverd 10-20%.

1 hour ago, Colinboko said:

The only person I recall to have returned 100% to their pre accutane state was ehohel when he was put on a prednisone taper. I think we are truly dealing with a modulation of the immune system in some sort of way. What that exact modulation entails I'm not so sure. But we will find out. I feel like we progress. Slowly but surely

I am not trying to pain in your sides (honestly, sorry), but if that is the standard we are using for recovery, then you can count the time I felt extremely normal for 8 hours after taking (prescribed) amphetamine salts. IBS completely cleared (even in the absence of going to the bathroom), brain fog eliminated, zero social withdrawal symptoms, no allergies, highly reactive to music, libido completely restored to my pre-teen levels, etc. Yes, it seems to address almost every single problem, but that doesn't mean dopamine deficiency is at the root of my problem. Potentially, I was just experiencing a mild euphoria.

What about all of the people whose depression goes in remission after staying awake for 36 hours? This (acute sleep deprivation) is a well-documented rapid-acting antidepressant, right up there with Ketamine. Scientists have been studying this phenomenon for years trying to understand how we can put "acute sleep depression" in a pill, but we cannot. Regardless, having a positive reaction to acute sleep deprivation doesn't mean too much sleep is at the root of our problem.

What about people who have a positive reaction to fasting for days at a time? Does that mean food allergies are at the root of the problem? Not necessarily; fasting can induce euphoria in just about anyone. There are many other mechanisms at play that make fasting beneficial, but feeling good while fasting can potentially say NOTHING about food allergies. Or perhaps it can; we don't know. But that's precisely the point of all of these examples. We must separate short-term responses from long-term responses. A number of post-Accutane users have talked about the (acute) wonders of various compounds. Other examples include high-dose testosterone and various stimulants. Whether one is sick or healthy, a very positive response would only be expected to those things.

So how can we so easily extrapolate our (completely predictable) reactions to said compounds/protocols to assume the mechanism that is wrong with us? Point being, we'll know if something really helps when people are getting sustainable results, outside of the expected acute good response.

Circling back to prednisone, athletes speak to how prednisone makes them feel good.As I mentioned before, the stuff is banned by certain organizations because it is so powerful. A positive reaction could easily happen to a healthy person or a sick person; it doesn't necessarily indicate something significant. If suddenly a bunch of post-Accutane users are helped by the stuff in a multi-faceted fashion long-term, that's wonderful. I would be happy to witness this outlier event. It would be nice to see something that finally breaks the usual response pattern of these other protocols/compounds! Just be careful, as the drug has brought on nasty long-term reactions in others before. Also, if I didn't make it clear, please note that prednisone is definitely not the only thing that has helped a post-Accutane user acutely. We also see things like alcohol hangovers (1, 2, 3), hemp related stuff, fasting, testosterone, stimulants, etc.

No snarkiness intended. I only want what's best for us.

22 minutes ago, ACCUiTy_drANE said:

I am not trying to pain in your sides (honestly, sorry), but if that is the standard we are using for recovery, then you can count the time I felt extremely normal for 8 hours after taking (prescribed) amphetamine salts. IBS completely cleared (even in the absence of going to the bathroom), brain fog eliminated, zero social withdrawal symptoms, no allergies, highly reactive to music, libido completely restored to my pre-teen levels, etc. Yes, it seems to address almost every single problem, but that doesn't mean dopamine deficiency is at the root of my problem. Potentially, I was just experiencing a mild euphoria.

What about all of the people whose depression goes in remission after staying awake for 36 hours? This (acute sleep deprivation) is a well-documented rapid-acting antidepressant, right up there with Ketamine. Scientists have been studying this phenomenon for years trying to understand how we can put "acute sleep depression" in a pill, but we cannot. Regardless, having a positive reaction to acute sleep deprivation doesn't mean too much sleep is at the root of our problem.

What about people who have a positive reaction to fasting for days at a time? Does that mean food allergies are at the root of the problem? Not necessarily; fasting can induce euphoria in just about anyone. There are many other mechanisms at play that make fasting beneficial, but feeling good while fasting can potentially say NOTHING about food allergies. Or perhaps it can; we don't know. But that's precisely the point of all of these examples. We must separate short-term responses from long-term responses. A number of post-Accutane users have talked about the (acute) wonders of various compounds. Other examples include high-dose testosterone and various stimulants. Whether one is sick or healthy, a very positive response would only be expected to those things.

So how can we so easily extrapolate our (completely predictable) reactions to said compounds/protocols to assume the mechanism that is wrong with us? Point being, we'll know if something really helps when people are getting sustainable results, outside of the expected acute good response.

Circling back to prednisone, athletes speak to how prednisone makes them feel good.As I mentioned before, the stuff is banned by certain organizations because it is so powerful. A positive reaction could easily happen to a healthy person or a sick person; it doesn't necessarily indicate something significant. If suddenly a bunch of post-Accutane users are helped by the stuff in a multi-faceted fashion long-term, that's wonderful. I would be happy to witness this outlier event. It would be nice to see something that finally breaks the usual response pattern of these other protocols/compounds! Just be careful, as the drug has brought on nasty long-term reactions in others before. Also, if I didn't make it clear, please note that prednisone is definitely not the only thing that has helped a post-Accutane user acutely. We also see things like alcohol hangovers (1, 2, 3), hemp related stuff, fasting, testosterone, stimulants, etc.

No snarkiness intended. I only want what's best for us.

No I know! I didn't mean a cure. I guess just relieving symptoms. I apologize.

But I do think all of these things are working in way that is certainly more than just a "mild euphoria". Look at CFS sufferers who get put into remission by using it enough at the right doses... idk...

1 hour ago, Colinboko said:

3 hours ago, Taneraped said:

Hi, I have recently been on a search to find some sort of solution to the treacherous affects from accutane, reading about 200 of the 500 pages on here and I have still have not come across any sort of proven solution to the problems that arise from accutane. Once upon a time, I was a young charismatic and intillengent but acne ridden young man but after going on accutane I have been a shadow of myself and am just looking for a way to go back to my old self again. The two questions that I have are, how close are we to understanding what causes these long term side effects and what is the closest that we have come to finding a cure for these symptom. Even Kevin Pezzi who seem's to be the internet's most intelligent and knowledgeable person on the subject didn't have any sort of solution to the issue so I don't expect a whole lot. From what I have heard hemp oil is the closest thing to a solution to the issue. It's amazing to think we have made this many posts trying to find a solution to post isotretinoin problems when we don't even know what the mechanism of action is.

The only person I recall to have returned 100% to their pre accutane state was ehohel when he was put on a prednisone taper. I think we are truly dealing with a modulation of the immune system in some sort of way. What that exact modulation entails I'm not so sure. But we will find out. I feel like we progress. Slowly but surely

Nah there was that guy who did the liver flush videos on YouTube I followed that and wasted my time and money over a year - may have cleaned my liver up a bit but prob not because after doing 5 or so and then doing blood test/ultrasound last year I got diagnosed with a fatty liver - fucken great isn't it after all that hard work!!

Good luck to whatever that guy's name was, if all he had to deal with was cleaning up his liver post tane than he should consider himself very lucky, I call bullshit though on some of these people claiming to be totally cured, weren't there others who talked up the whole "cannibas oil" thing as the ultimate cure - if I'm not mistaken some of them are still on the forum, so cured??....I think not.

2 hours ago, Colinboko said:

No I know! I didn't mean a cure. I guess just relieving symptoms. I apologize.

But I do think all of these things are working in way that is certainly more than just a "mild euphoria". Look at CFS sufferers who get put into remission by using it enough at the right doses... idk...

I am sure there is more to it than "euphoria," depending on the compound/protocol we are talking about. I was just cautioning against extrapolations made from an acute reaction to a drug, as that can lead to erroneous conclusions. I see it a lot on health forums in regards to stimulants. That's probably how "dopamine deficiency" came to be so prevalently self-diagnosed. XD Good luck on your endeavor. I genuinely hope you find some answers. That is very interesting something as profound as CFS responds to it. Good point indeed.

2 hours ago, TrueJustice said:

Nah there was that guy who did the liver flush videos on YouTube I followed that and wasted my time and money over a year - may have cleaned my liver up a bit but prob not because after doing 5 or so and then doing blood test/ultrasound last year I got diagnosed with a fatty liver - fucken great isn't it after all that hard work!!

I am so sick of hearing about liver flushes, and this just validates it. Sorry to hear about your experience. Every time I ask a liver flushing advocate to come forward with evidence it does something worthwhile for the body, I get nothing. The excuse explaining why it has no research behind it (i.e., it is "natural" and "not sponsored by big-pharma") further makes me skeptical. A number of NATURAL, unpatentable substances have robust research backing their efficacy. There is no reason something as well-known as liver flushing shouldn't have tons of studies supporting its use too, if it truly works. Honestly, post-Accutane sufferers have enough trails to follow. I find it reprehensible that some people try to distract us (all chronically ill people, for that matter) with gimmicky protocols with no basis in science. I obviously cannot speak to everyone's intentions, but I've seen my fair share of deceptive marketing.

4 hours ago, Taneraped said:

Hi, I have recently been on a search to find some sort of solution to the treacherous affects from accutane, reading about 200 of the 500 pages on here and I have still have not come across any sort of proven solution to the problems that arise from accutane. Once upon a time, I was a young charismatic and intillengent but acne ridden young man but after going on accutane I have been a shadow of myself and am just looking for a way to go back to my old self again. The two questions that I have are, how close are we to understanding what causes these long term side effects and what is the closest that we have come to finding a cure for these symptom. Even Kevin Pezzi who seem's to be the internet's most intelligent and knowledgeable person on the subject didn't have any sort of solution to the issue so I don't expect a whole lot. From what I have heard hemp oil is the closest thing to a solution to the issue. It's amazing to think we have made this many posts trying to find a solution to post isotretinoin problems when we don't even know what the mechanism of action is.

I'd go one step further and say why was this drug ever approved in the first place when the mechanism of action was unknown???....,total insanity and corruption of the highest level, but this unfortunately is what we have to put up with in this day and age, you've only got turn the tv on to see men doing corrupt bullshit all around the world - never learning from past mistakes or owning up to anything.

No wonder there's uprisings everywhere, people have had enough!!!

ACCUiTy, what are taking these days for brain fog?

What supplements have you ceased taking over say last 3-4 months?

1 hour ago, TrueJustice said:

ACCUiTy, what are taking these days for brain fog?

What supplements have you ceased taking over say last 3-4 months?

Based upon multiple trials of adding and subtracting supplements from my regimen, I can confirm Acetyl-l-Carnitine (1 gram) and Ashwagandha (generic extract: 470 mg, 1.5% Withanolides) help my brain fog significantly when taken consistently. Brain fog has been very manageable lately. I don't have any idea if root causes are being addressed with these supplements. I just know Ashwagandha boosts thyroid and testosterone (which Accutane depletes) and Carnitine assists in mitochondrial functioning (and Accutane depletes Carnitine levels). Still, I do not know exactly why these help. Both substances do several other things.

Anyway, it's the anhedonia, social withdrawal, and emotional numbness that continues to be a struggle. And as my brain fog has died down I better see how anhedonia is a distinct issue. Intermittent caffeine use continues to help me, and is one of the handful of things I have ever taken capable of touching my anhedonia. Anyway, here is a list of everything I have been taking the past few months: Methyl B12, Folate, D3, fish oil, (through real fish), Pregnenolone, Carnosine, Tianeptine Sulfate, Co Enzyme Q10, Magnesium Citrate (for IBS), Ashwagandha, Acetyl-l-Carnitine, Caffeine.

Mentally, I don't notice a darn thing from Pregnenolone, Carnosine, Co Enzyme Q10, B12, Folate, D3, or fish oil. I simply take them for long-term health benefits. I no longer take low dose Naltrexone, Agmatine, Sarcosine, or Lion's Mane. LDN was traded for Tianeptine, which has better mood brightening effects. The rest needs to be re-evaluated (I guess).

I am due for a full testosterone and thyroid panel (TSH, T3, T4) this week. Hoping to either A) Put the hormone angle to rest or B)Find something to treat. If hormones are out of whack, of course supplementation can only go so far! Recently read an article saying how T3 can be added to help cognitive symptoms and depression in those who have hypothyroidism. Many doctors don't even look at T3, let alone prescribe it.

Thx ACCUiTy!!

Do you have any desire to take Phosphatidyl Choline specificaly?
I thought the video on that looked really encouraging?

Also, what's your take on general blood flow post tane, something that could account for many of our problems? I don't have to go get tests to know that mine is altered, I've only got to glance at my legs which are covered in varicose veins to know there's a problem with blood flow, this could extend to the brain and be part of the brain fog scenario too!!