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Re: Substance Abuse and CMT

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Mark,

Look atThe Many Faces of Addiction - one CMT person's story in there.

http://www.mda.org/publications/Quest/q114subabuse.html

As for peer reviewed medical research and literature:

The Damaging Effect of Alcohol in Charcot-Marie-Tooth Disease by Dr. Victor

Ionasescu (April 1989)

The close association of alcoholism and peripheral nerve disease has been

appreciated for many years . In a study of 1030 alcoholics admitted to Boston

City Hospital, 92 (9%) proved to have peripheral nerve disease (Victor, M and

, RD: The Effect of Alcohol on the Nervous System. Res Publ Assoc Res

Nerve Dis 1953, 32:526).

In the background of patients with alcoholic neuropathy, two features are

invariably present: the abuse of alcohol, usually severe in degree and of many

years' duration, and dietary deficiency. The diets of these patients were

conspicuously low in meat and fish, cereals and fresh fruits and vegetables.

The essential pathologic alteration in alcoholic neuropathy is a degeneration of

the peripheral nerves. Both myelin and axons are destroyed, the latter probably

earlier and to a greater extent than the former. More recent studies definitely

indicated that segmental demyelination is a rare finding in alcoholic neuropathy

and axonal degeneration is the basic histologic abnormality. The clinical

picture varies considerably. In its mildest form, the neuropathy is virtually

asymptomatic, the presence of peripheral nerve disease being disclosed only on

neurologic examination.

The neuropathic signs in these asymptomatic cases consist of thinness and

tenderness of the leg muscles, loss of depression of some reflexes and an

inconstant impairment in the perception of painful and tactile stimuli over the

feet and shins. If alcoholic patients are examined electrophysiologically, a

certain proportion will show impairment of peripheral nerve function before the

clinical signs of neuropathy can be detected. The majority of alcoholic patients

with involvement of the peripheral nerves have symptoms - weakness, tingling,

numbness, and pain of the feet and hands. These symptoms are usually insidious

in onset and slowly progressive.

Charcot-Marie-Tooth (CMT) neuropathy is characterized by weakness of the feet

and hands, foot deformities, including permanently flexed " hammer " toes, and

unusually high arches and some loss of sensation in the limbs.

The disease is inherited in different ways: autosomal dominant, autosomal

recessive or X-linked. The motor symptoms (weakness) and the pathology (nerve

degeneration) resemble very much the alcoholic neuropathy. The main distinctions

are: a) presence of foot deformities, B) absence of mildness of sensory symptoms

such as tingling, numbness and pain of the feet and hands.

Recently, we became aware that some of our CMT patients have an excessive daily

intake of alcohol (more than three glasses of wine per day). We compared the

neurologic signs in the few alcoholic and the large group of non-alcoholic CMT

patients. The numbers of alcoholic CMT patients is small and does not allow

statistical analysis. However, it is obvious that the alcoholic CMT patients

have more severe weakness and/or sensory symptoms than the non-alcoholic CMT

patients. Close questioning of two alcoholic CMT patients disclosed that there

was a sudden worsening of

symptoms after alcohol daily intake on a background of chronic and relatively

mild neuropathy. These findings should not surprise us. The abuse of alcohol is

more damaging for CMT nerves which already show a degeneration secondary to the

undetermined genetic defect.

In conclusion, alcoholic drinks should be forsaken entirely or strictly limited

if you have CMT.

also

Alcohol Clin Exp Res. 2007 Dec;31(12):1953-62.

Molecular and cellular events in alcohol-induced muscle

disease.

Fernandez-Solà J, Preedy VR, Lang CH, -Reimers E,

Arno M, Lin JC, Wiseman H, Zhou S, Emery PW, Nakahara T, Hashimoto K,

Hirano M, Santolaria-Fernández F, González-Hernández T, Fatjó F,

Sacanella E, Estruch R, Nicolás JM, Urbano-Márquez A.

Alcohol Unit, Hospital Clinic, University of Barcelona, Spain.

Alcohol consumption induces a dose-dependent noxious effect on

skeletal muscle, leading to progressive functional and structural

damage of myocytes, with concomitant reductions in lean body mass.

Nearly half of high-dose chronic alcohol consumers develop alcoholic

skeletal myopathy. The pathogenic mechanisms that lie between alcohol

intake and loss of muscle tissue involve multiple pathways, making

the elucidation of the disease somewhat difficult. This review

discusses the recent advances in basic and clinical research on the

molecular and cellular events involved in the development of alcohol-

induced muscle disease. The main areas of recent research interest on

this field are as follows: (i) molecular mechanisms in alcohol

exposed muscle in the rat model; (ii) gene expression changes in

alcohol exposed muscle; (iii) the role of trace elements and

oxidative stress in alcoholic myopathy; and (iv) the role of

apoptosis and preapoptotic pathways in alcoholic myopathy. These

aforementioned areas are crucial in understanding the pathogenesis of

this disease. For example, there is overwhelming evidence that both

chronic alcohol ingestion and acute alcohol intoxication impair the

rate of protein synthesis of myofibrillar proteins, in particular,

under both postabsorptive and postprandial conditions. Perturbations

in gene expression are contributory factors to the development of

alcoholic myopathy, as ethanol-induced alterations are detected in

over 400 genes and the protein profile (i.e., the proteome) of muscle

is also affected.There is supportive evidence that oxidative damage

is involved in the pathogenesis of alcoholic myopathy. Increased

lipid peroxidation is related to muscle fibre atrophy, and reduced

serum levels of some antioxidants may be related to loss of muscle

mass and muscle strength. Finally, ethanol induces skeletal muscle

apoptosis and increases both pro- and antiapoptotic regulatory

mechanisms.

I have not found any studies or research ever on Coke, Meth, etc and CMT,

Addiction Medicine and CMT, or others. You can find information in our message

archives about people's use of marijuana for their CMT.

Gretchen

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Of course, Ionasescu in 1989 was writing about substance ABUSE with

regard to alcohol. The consumption of alcohol was removed from the

neurotoxic list by the CMTA website, dating the removal as early as

2004. The myopathies discussed here are related to people who give

their lives to alcohol, not the CMT'er who drinks in moderation or

only socially. The caveat is that alcohol, affects balance and

coordination-something we are always striving to maintain.

Dennis

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