HOPE FOR ALS/HND ANO MS

Thie week j'g'ALS'

week.

(Amyotrophic Lateral sclerosis)/'Hororneurote digease. (MND)

to, *t experience, thie condition is associated with severe B group vitamin defiencies, esPeci'rrY Bl, 86, 83 and hi-gh intake of these is necessary to have normar levelg and levels shoutd be monitored unril the iltake oE these is sufficient not, to have lor blood levers. rn some ALs patients, in ny experience (20 patientsl, 83 may have to be over two gram of Niacinarnide to prevent low BJ or perlagra which can cause paralysis and bulbar pafsy - in6!ility to 5walt6ur, tark and later, breathe as
seen i-n ALS.

eensitivl.ties.

with 8l (thiamine) up to 500mg to ?00mg may be regur-ired to stop low 81 (beri beri). lli'th 86. up to one gram or 1250rng may be necessary to have normal bLood levels. Should Bl or 86 of 83 be Ieft low, any of these can res*It in paralysis per se severe vitamin and trace erement deficiencj-es in the condition appear to be due to severe food and chemical sensitivity/intolerance to cowrs mi.Jk. gruten conEairdng grains ( wheat' fY, oats' corn, barley/malt, slillg!, buckwheat) and legumes./beans - all of which can. caus sovere malabsorption state for nutrients. ALS patients are rise to lslarry avoid these foods - reactions to these c.ul be assessed by arlergiste using the BCFT (cytotoxic test| for de,layed, reactions to food. and, chemical

rn Hs uhich hag anti-nerve antibod.ies and anti-myelin antibodies this ig crearly an autoimmune disease' {white gp]ls attack the persons own neurorogical tissueg). rn MS and other patients with anti-nerve and anti-myprin anlibodies that do not have, HS. these high antibody titres/levels can be reversed to negaLive off cow's milk and gluten contairdng grains and in certaio pati-ents the HS is held, i_n check. rn Ms the fractions of gLuten contairri-ng grails is not gluten and not the gflalrss parE of gLuten qarlsd a]-pha-gliadin. rn the cow's mil-k the fractions that are neurotoxic are not alpha-casein, alpha-lactalbumin or beta-lactoglobrr.tis (causing juvenile diabetes in some chirdrenl because antibodies to these fractions of cow,s miLk and gtuten containing grains.are negative u5sally in us patients. Also when all are positive. anti-nerve and- anti-myerin antobodies are not seen, irr my experience with hundreds of patients with anti-nerve antibod,ies, etc. The most tikely explanation of, ttris is that in HS. - rnuch slual I gs fractj.ons of cor I s milk than the above and s 6al r gs fracLions of gluten containing graine than gtuten and arpha-gliadin are neurotoxic damaging myaril and nervoug tissue in MS. lf allgrgic to the bigger fractions then the smel'lsg/neurotoxic fracLions cannot be reJ-eased to cause anLi-nerve and anLi-mye,Lia antibodies. However ALS patients do not get MS and vice versa. They appear mutuarry excrusive.

ALS patients do not have anLi-nerve and anti-myelin antibodiee, in my exporlonco but are 5fill highly Al!ergic/intolerant to cow's milk and gluten containing grains. Usu..lry ant-ibodies to gluten, alpha-gliadin (of wheatl and alpha-casein, alpha-lactalbumin, beta-lactoglobrr'lin (of cow's mil,k) are negative. Even smaller fracti,ons than these seen in t{S are likely to be causing the neurological damage in ALS/MND e g damage to anterior born cells {in the spinal cord degeneraLion of which cdilses paralysis ). Is ALS/MND a.Lso an autoimrnune disease like l.lS? And thus like MS, can antibodies to neurological tissue be reversed and remj.sgion re6ult as a conse9uence ? Researclr overseas shows ALS/HND patients have antibggies to cMl ganglioside neurological 5)LrLissue. Now in A,u5!r'aliE, I have shown cal out of tt*ee patienrs looked at. had anterior hottt cell antibodies - new findings as far as I am auare. This suggests tt is an autoimmune disease and thulf notentially able to be halted with diet and nutrienta. In Australia, ALS/MND patients can have blood tests to measure anti.bodies both to GMI gandL.oside antibodies and to anterior horn cetl antibodies - costing only Sf0 each (at this stage. called health screenlng). one swa'llow does not make a summer, however, if many other palients also have anterior horn ceIL antibodies and GMI ganglioside antibodies. this cor.rl.d confirm ALS rearly ie an autoimmune disease and should be tre,ated with dietary irte,nwentisn yhich helpe SLE patients, coeU.ac disease patients, HS palients, etc. If patients with ALS/I'IND sish to confirm if they have anterior horn cell antibodier t GHI ganglioside antibodies positive,, then the AtS Socj.ety or I can give detaife of where'the 3 mls of clotted blood can be sent for testing. Hopeft'l'ly ALS/MND pdtients wi1r. h6vs these tests done to see how ofEen these teata show positive and can they be reversed to negative off cowrg mjJk, gLuten containj.ng grains and idsnlry also legumes and beans and if so, ig the progression of the i'tlness slowed down or slopped. Hopef Illy, next yeaE for ALS/MND Week. the nurnber of paLients positive for these two antibodies to their neurological tissues can be discussed and whether off Lhe foods I have suggested together with adeguate Bl, 83, 86, etc not to be low in these in serurn, this approach has helped other ALS/ MND paLients to halt the.ir disease or greaLly slow down its progress with reversal of these ant:ibodj.es to negaLive.

,|fu e"j Dr. Chrie H

Reading'

10 Ian Avonue lioRTH cuRt cuRL

2099