Hi Taurus~Yes, POTs is associated with MS, as the following study confirms.
Auton Neurosci. 2013 Jan;173(1-2):65-8. doi: 10.1016/j.autneu.2012.11.009. Epub 2012 Dec 14.
Postural orthostatic tachycardia syndrome associated with multiple sclerosis.
Adamec I, Lovrić M, Zaper D, Barušić AK, Bach I, Junaković A, Mišmaš A, Habek M.
“…The results of this study suggest that POTS is associated with MS.”
POTs is a symptom of autonomic dysfunction, which is common in MS.
In the following study the researchers found that “ninety percent” of the MS patients tested had symptoms related to autonomic dysfunction.
Autonomic dysfunction in multiple sclerosis: correlation with disease-related parameters.
Gunal, D.I., N. Afsar, T. Tanridag, S. Aktan. 2002. Eur Neurol. 48(1):1-5.
“…Ninety percent of the patients had symptoms related with autonomic dysfunction…Both parasympathetic and sympathetic functions were impaired…”
Researchers in the following study stated that autonomic dysfunction causes significant disability in patients with MS and that autonomic symptoms such as abnormalities of bladder, bowel, and sexual function have been well documented in previous studies.
Autonomic nervous system function in multiple sclerosis.
McDougall AJ, McLeod JG
J Neurol Sci 2003 Nov 15;215(1-2):79-85
“Autonomic dysfunction causes significant disability in patients with multiple sclerosis (MS)…Abnormalities of bladder, bowel and sexual function have been well documented in previous studies…Autonomic symptoms were common in MS patients…which were associated with increased MS severity…”
Patients with MS have autonomic dysfunction due to an inabilty to produce the neurotransmitters that regulate the autonomic nervous system.
The action of the two branches of the autonomic nervous system is mediated by two neurotransmitters. They are adrenaline and acetylcholine. Adrenaline is the predominant sympathetic neurotransmitter, whereas acetylcholine acts in the parasympathetic periphery.
Adrenaline is derived from dopamine, and dopamine is derived from phenylalanine and tyrosine.
The parasympathetic neurotransmitter is acetylcholine. Acetylcholine is derived from choline. Vitamin B12 and folate are required for the
synthesis of choline before becoming acetylcholine.
In the following study on autonomic dysfunction and MS the researchers discovered that catecholamine levels were significantly lower in active MS patients than in those with stable disease. In the human body the most abundant catecholamines are adrenaline, noradrenaline, and dopamine; all of which are produced from phenylalanine and tyrosine. Adrenaline is the autonomic nervous system sympathetic neurotransmitter.
Autonomic dysfunction in multiple sclerosis is related to disease activity and progression of disability.
“Autonomic dysfunction is frequently observed in patients with multiple sclerosis (MS)…Median catecholamine levels were significantly lower in `active' MS patients than in those with stable disease…”http://msj.sagepub.com/content/7/5/327.abstract
In the following study the researchers found that MS patients had lower acetylcholine (ACh) levels in their cerebrospinal fluid and serum (blood) than normal controls. Acetylcholine is the autonomic nervous system parasympathetic neurotransmitter. In an additional study the researchers found there was literally “no acetylcholine” in the cerebrospinal fluid of the MS patients tested.
Int J Mol Sci. 2012; 13(10): 12656–12664.
Relation between pro-inflammatory cytokines and acetylcholine levels in relapsing-remitting multiple sclerosis patients.
Marcella Reale,1,* Federica de Angelis,2 Marta di Nicola,1 Elisabetta Capello,3 Maria di Ioia,4 Giovanna de Luca,4 Alessandra Lugaresi,4 and Ada Maria Tata2,*
“… ACh levels were lower in CSF and serum of RR-MS patients compared to levels of control subjects…”
Free acetylcholine in the cerebrospinal fluid after brain operations.
“…In 15 of the patients no acetylcholine could be demonstrated in the cerebrospinal fluid; this group included all cases of multiple sclerosis…”
Patients with MS are unable to properly bind and transport vitamin B12-this is why there is a lack of acetylcholine. Here are a few studies on this.
Vitamin B12 metabolism in multiple sclerosis.
Reynolds, E.H., T Bottiglieri, M. Laundy, R.F. Crellin, S.G. Kirker. 1992. Arch Neurol.
“…Patients with MS had significantly lower serum vitamin B12 levels…than neurological and normal controls…There is a significant association between MS and disturbed vitamin B12 metabolism… The cause of the vitamin B12 disorder and the nature of the overlap with MS deserve further investigation.”
In the next study the researchers stated they suspect the vitamin B12 deficiency in MS may be due to problems with binding and/or transport. In addition, the researchers concluded that further studies of vitamin B12 metabolism, binding, and transport in MS are indicated, as they feel this may offer clues to the understanding of MS.
Multiple sclerosis associated with vitamin B12 deficiency.
Reynolds, E.H., J.C. Linnell, J.E. Faludy. 1991. Arch Neurol. 48(8):808-11.
“…A vitamin B12 binding and/or transport is suspected. The nature of the association of multiple sclerosis and vitamin B12 deficiency is unclear but is likely to be more than coincidental. Further studies of vitamin B12 metabolism, binding, and transport in multiple sclerosis are indicated, as these cases may offer a clue to the understanding of a still mysterious neurologic disorder.”
Patients with MS also lack the essential amino acid phenylalanine. Phenylalanine is needed to produce the other neurotransmitter, adrenaline.
J Neurol Neurosurg Psychiatry. 1979 July; 42(7): 640–641.
Plasma and cerebrospinal fluid tryptophan in multiple sclerosis and degenerative diseases.
F Monaco, S Fumero, A Mondino, and R Mutani
“…Tryptophan and competing neutral amino acid levels were found to be diminished in the plasma of patients with multiple sclerosis and degenerative diseases…Tryptophan, leucine, isoleucine, valine, tyrosine, and phenylalanine were all diminished in the plasma of patients with multiple sclerosis…”
Phenylalanine is needed to produce dopamine also. Phenylalanine>Tyrosine>Dopamine>Adrenaline
So, we would expect to see a lack of dopamine in patients with MS.
In the following study the researchers found reduced levels of dopamine in MS patients and concluded their results suggest the involvement of dopamine in the pathogenesis of depression in MS.
Zh Nevrol Psikhiatr Im S S Korsakova. 2012;112(2 Pt 2):34-40.
The role of dopamine in the regulation of the interaction between nervous and immune systems in multiple sclerosis.
Orlova EV, Pashchenkov MV, Davydovskaia MV, Klimova SV, Khozova AA, Mugutdinova BT, Boĭko AN
“…The results suggest the involvement of dopamine in the pathogenesis of depression in MS as assessed by dopamine and its metabolites levels.”
Patients with MS lack the enzymes that digest proteins. These enzymes are called protease and they also bind and transport vitamin B12. The lack of these enzymes would clearly explain the missing essential amino acids and the inability to properly metabolize vitamin B12 and therefore, the resulting low dopamine, adrenaline, acetylcholine, and autonomic nervous system dysfunction. Here is a study from Mayo on protease and MS.
In the following study from Mayo College of Medicine the researchers stated that an “array of studies” implicate protease in multiple sclerosis pathogenesis.
Curr Top Microbiol Immunol. 2008;318:133-75.
The multiple sclerosis degradome: enzymatic cascades in development and progression of central nervous system inflammatory disease.
“An array of studies implicate different classes of protease and their endogenous inhibitors in multiple sclerosis (MS) pathogenesis based on expression patterns in MS lesions, sera, and/or cerebrospinal fluid (CSF). Growing evidence exists regarding their mechanistic roles in inflammatory and neurodegenerative aspects of this disease…”
The following study concludes that these pancreatic enzymes are “essential” for the transport and absorption of vitamin B12. When the study authors speak of ‘R’ proteins they are referring to proteins produced by the salivary gland that are thought to protect vitamin B12 as it travels through the digestive tract.
Cobalamin malabsorption due to nondegradation of R proteins in the human intestine. Inhibited cobalamin absorption in exocrine pancreatic dysfunction.
Marcoullis G., Y. Parmentier, J.P. Nicolas, M. Jimenez, P. Gerard. 1980. J Clin Invest.
“In vivo studies demonstrate that the pancreatic enzymes and the ionic environment in the upper gastrointestinal tract are essential determining factors for transport and absorption of cobalamin in man…These findings confirm the suggestion that the formation of unabsorbable cobalamin complexes may be the reason of impaired vitamin absorption in exocrine pancreatic insufficiency…”