http://jnnp.bmjjournals.com/cgi/content/full/74/4/495
A friend posted me this link. It is not a new study, it dates back to 2003 but it is quite interesting on the possible link between the petide ß endorphin in MS.
A lot of this backs up the Lucchinetti argument (see my boring post on the annal of neurology article on response to Bartlett).
And of course it also relates to LDN. Maybe someone should show this to the MS society!
Especially interesting is that the lowest levels of endorphin were found in people with PPMS and SPMS. And that increased concentrations were found in individuals taking beta interferon.
Felly
Felly
Endorphin role in MS
Good article. But there sure is a lot of possibility that the endorphin level is a result (as opposed to cause) of someone's MS activity and the subsequent changes in mood and/or lifestyle. For example, what about something a simple as physical activity level - likely decreased with the severity of MS - contributing to the conrtibuting to the endorphin level.
The article is not saying that lower endorphin levels are the cause of MS but rather they play a role in MS. A higher level of endorphin in people with MS may downregulate inflammation. And on the whole that would be a pretty good thing.
What causes the lower levels of endorphin the first place is open to speculation, most certainly the less active you are the more likely your endorphin levels will be lower and there could be a whole host of other reasons. For example stress,depression or too much leptin in the brain. While sex can increase endorphins so maybe people with MS are just not getting enough sex. Well, you know there is only one answer to that folks:-)
Endorphins are neurotransmitters as well as hormones so the interactions are on numerous levels, as the article says 'Clearly, we cannot completely rule out that mechanisms leading to MS progression may influence ß endorphin concentrations'
While there are no perfect candidates for an MS cure I am interested in researching ways to at least attenuate the condition. And LDN is looking like a very interesting option. As my background is in biochemistry it is something I am investigating thoroughly before trying.
Felly
What causes the lower levels of endorphin the first place is open to speculation, most certainly the less active you are the more likely your endorphin levels will be lower and there could be a whole host of other reasons. For example stress,depression or too much leptin in the brain. While sex can increase endorphins so maybe people with MS are just not getting enough sex. Well, you know there is only one answer to that folks:-)
Endorphins are neurotransmitters as well as hormones so the interactions are on numerous levels, as the article says 'Clearly, we cannot completely rule out that mechanisms leading to MS progression may influence ß endorphin concentrations'
While there are no perfect candidates for an MS cure I am interested in researching ways to at least attenuate the condition. And LDN is looking like a very interesting option. As my background is in biochemistry it is something I am investigating thoroughly before trying.
Felly
Well thank you, very nice of you to say so Arron.
I should have emphasised in response to Billf that ultimately it doesn't matter what the cause of lower endorphin levels are the fact higher levels may help mediate the immune system is the information that matters. And it looks like LDN might increase endorphin levels.
I am not yet completely convinced on dosage levels. The only study I have found is with autism which shows LDN does raise endorphin levels (see pubmed extract below). But if I had SPMS or PPMS I wouldn't be hanging around waiting for a clinical trial. What's to lose by trying it?
Felly
Low-dose naltrexone effects on plasma chemistries and clinical symptoms in autism: a double-blind, placebo-controlled study.
Bouvard MP, Leboyer M, Launay JM, Recasens C, Plumet MH, Waller-Perotte D, Tabuteau F, Bondoux D, Dugas M, Lensing P, et al.
Service de Psychopathologie de l'Enfant et de l'Adolescent, Hopital Robert Debre, Paris, France.
The effect of month-long naltrexone (NTX) treatment at a daily oral dose of 0.5 mg/kg/day was contrasted with placebo (PLC) in a double-blind study with conjoint clinical and biochemical evaluations of therapeutic effects. Modest clinical benefits were achieved with both PLC and NTX, with marginally better overall results following NTX, and degree of improvement appeared to be related to plasma chemical profiles. Massively elevated levels of beta-endorphin were observed in all children with assays using C-terminal antibody but not with an N-terminal antibody assay. In addition, 70% of the children exhibited abnormally low levels of adrenocorticotropic hormone, and smaller subsets exhibited elevated norepinephrine (60%), arginine-vasopressin (50%), and serotonin (20%).
The best clinical responders exhibited the clearest normalization of the elevated plasma chemistries, especially in C-terminal-beta-endorphin and serotonin. There was some evidence of therapeutic carry-over effects in both clinical and biochemical measures in those children who received NTX before PLC. The results suggest that NTX only benefits a subgroup of autistic children, who may be identified by the presence of certain plasma abnormalities. These results suggest a possible linkage between abnormal plasma chemistries, especially those related to the pro-opiomelanocortin system, and autistic symptoms.
I should have emphasised in response to Billf that ultimately it doesn't matter what the cause of lower endorphin levels are the fact higher levels may help mediate the immune system is the information that matters. And it looks like LDN might increase endorphin levels.
I am not yet completely convinced on dosage levels. The only study I have found is with autism which shows LDN does raise endorphin levels (see pubmed extract below). But if I had SPMS or PPMS I wouldn't be hanging around waiting for a clinical trial. What's to lose by trying it?
Felly
Low-dose naltrexone effects on plasma chemistries and clinical symptoms in autism: a double-blind, placebo-controlled study.
Bouvard MP, Leboyer M, Launay JM, Recasens C, Plumet MH, Waller-Perotte D, Tabuteau F, Bondoux D, Dugas M, Lensing P, et al.
Service de Psychopathologie de l'Enfant et de l'Adolescent, Hopital Robert Debre, Paris, France.
The effect of month-long naltrexone (NTX) treatment at a daily oral dose of 0.5 mg/kg/day was contrasted with placebo (PLC) in a double-blind study with conjoint clinical and biochemical evaluations of therapeutic effects. Modest clinical benefits were achieved with both PLC and NTX, with marginally better overall results following NTX, and degree of improvement appeared to be related to plasma chemical profiles. Massively elevated levels of beta-endorphin were observed in all children with assays using C-terminal antibody but not with an N-terminal antibody assay. In addition, 70% of the children exhibited abnormally low levels of adrenocorticotropic hormone, and smaller subsets exhibited elevated norepinephrine (60%), arginine-vasopressin (50%), and serotonin (20%).
The best clinical responders exhibited the clearest normalization of the elevated plasma chemistries, especially in C-terminal-beta-endorphin and serotonin. There was some evidence of therapeutic carry-over effects in both clinical and biochemical measures in those children who received NTX before PLC. The results suggest that NTX only benefits a subgroup of autistic children, who may be identified by the presence of certain plasma abnormalities. These results suggest a possible linkage between abnormal plasma chemistries, especially those related to the pro-opiomelanocortin system, and autistic symptoms.
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