Orthomolecular Treatment of Schizophrenia

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T h e

OrthomolecularTreatment ofSchizophrenia:A Primer for Cl inicians

by Jo na tha n E. Prousky N D FRSHThe anadian ollege of Naturopathic Medicin

IntroductionSchizophrenia affects one to

two percent of the population.This disease is characterized by acombination of perceptual changes(e.g., hallucinations) and thoughtdisorder (e.g., delusions).' Theseaberrant mental states, which canlead to psychotic behavior, causea tremendous amount of emotionaland psychological suffering.The cause of schizophrenia isthe subject of much debate. It isconsidered a biochemical disease,although certain genetic factorsmost certainly play a role.

The majority of scientistsand psychiatrists subscribe tothe dopamine excess theory ofschizophrenia - that too muchdopamine is largely responsiblefor the symptoms of psychosis.However, since 1952, Dr. AbramHoffer, the founding father oforthomolecular medicine, hasresearched, published, andexpanded upon the adrenochrometheory of schizophrenia. '- He andhis colleagues, Drs. Osmond andSmythies, came to this theory bystudyin gand rese arching the effectsof substances such as mescaline,lysergic acid diethylamide (LSD),and amphetamines - all of which

can cause a clinical syndrome innormal individuals that would beclinically indistinguishable fromschizophrenia.

Hoffer noticed that mescalinehad a similar chemical structureto that of adrenaline, and sinceboth can be converted toindoles in the body, the potentialschizophrenic toxin might be anindole derivative of adrenalinewith similar neurochemicalproperties to that of mescaline orLSD. He eventually deduced thatthe schizophrenic toxin was anoxidized derivative of adrenalineknown as adrenochrome. Since theearly 1950s. Hoffer's adrenochrometheory has been validated due tothe following findings:

• that adreno chrom e and its close

relatives - dopaminochrome(from dopamine) andnoradrenochrome (fromnoradrenaline) - are present inthe human brain,'^

• that these com pound s probablyinduce a combination ofneurotoxic and mind-mood-altering effect, and' •

• that reducing adren ochro meand its close relatives istherap eutic for the treatm ent ofschizophrenia.''

The majority of schizophrenpatients (about 90%) who receimainstream treatments remaunwell and nonfunctional fthe rest of their lives despireceiving the most advanced druand social services currentavailable.' Estimates of firepisode schizophrenics are a littmore optimistic, reporting that ofive recently diagnosed patientone will recover sufficiently live an almost normal life withomedication or with very low dosof medication.* The eco nomcosts of schizophrenia to socieare enormous, amounting approximately two million dollafor each schizophrenic patient ova 40-year course of the illness.^

In a recent publicatio

examining the economic burdeof schizophrenia in Canada, thdirect and non-direct heath cacosts associated with this diseaswere estimated to be 2.02 billioCan adian do llars in 2004.' addition, when these figures weadded to the high unemploymerate with additional productivitmorbidity, and mortality lossethe estimate reached 4.83 billioCanadian dollars, for a total coestimate of 6.85 billion Canadia

TOWNSEND LETTER - FEBRUARY/MARCH



dollars in 2004. The authors ofthis report arrived at the followingconclu sion: Despite significantimprovements in the past decadein pharmacotherapy, programs,and services available for patientswith schizophrenia, the economicburden of schizophrenia in Canadaremains high.

The purpose of the report is tohighlight the problems with thestandard medical treatment ofschizophrenia and to demonstratethat the addition of orthom olecuiarmedicine provides patients withthe best opportunity of living areasonable quality of life. Commonorthomolecular t reatments arereviewed, including summariesof relevant clinical studies andprescribing information. Four

patient cases are described toshow the reader the potentialbenefits of this appro ach , as well asthe difficulties with this approachwhen certain essential treatmentcomponents are lacking.

Standard edical Treatment ofSchizophrenia

Schizophrenic patients willremain ill and less capable ofengaging in a normal quality of life

as long as their treatments involveonly standard medical treatments.Standard treatments use powerfulatypical anti psych otic dru gs (APDs)such as aripiprazole, clozapine,olanzapine. quetiapine, andrisperidone. These drugs primarilyact on dopamine receptors withinthe central nervous system andreduce symptoms of the diseaseby abo ut 15-20%. Add itionalmedications are often prescribed

to control the Parkinsonian/extrapyramidal symptoms (e.g.,involuntary movements, tremors,and rigidity) that can result fromtheir use.

When they were first introduced,the atypical APDs were thoughtto produce less Parkinsoniansymptoms. However, recentresearch has demonstrated that,at high dosages, the atypical

APDs pose the same risks for thedevelopment of Parkinsoniansymptoms as do the older APDs.The majority of schizophrenicpatients are also providedwith a supplementary cocktailof medications consisting ofbenzodiazepines, ant idepressants ,and, sometime s, additional atypical

APDs.Schizophrenic patients taking

one or two of the atypical APDsare at high risk for brain damage,cardiac arrhythmias, diabetesmellitus, sedation, sexualdysfunction, akathisia, and weightgain.'- Often patients experiencea vague dysphoria from theirmedications, a sense of uneasethat something isn't quite right.**Hoffer has written extensively

about the side effects causedby the atypical APDs, which hecalls th e tranquilizer psycho sis.This occurs when patients aretaken from a psychotic state (withsymptoms that are best describedas hot ) to a new med icatedpsychotic state (where they nowdisplay symptoms that are bestdes cribe d as cold ).'-'

Hot symptoms denote extremechanges in personality (e.g.,

paranoid delusions, auditoryand/or visual hallucinations) andbehavior (e.g., agitation and/orsuicidal tendencies) that attract theattention of friends, relatives, and/or coworkers. Patients displayinghot symptoms typically receive themedical care they need becausetheir symptoms are so obviousand abnormal. Cold symptomsare a medicated and dampenedversion of the hot symptoms. Even

though schizophrenic patients areeasier to manage while on atypicalAPDs, when their symptomsbecome cold, they fare no better.They remain debilitated by thistranquilizer psychosis and will beunable to live a normal quality oflife unless they are lucky enough toreceive adjunctive orthomoleculart rea tments .

Orthomolecular Treatment ofSchizophrenia

Orthomolecular substances arfound naturally in the human bodyand include amino acids, essentUifatty acids, minerals, and vitaminsTo effectively use orthomoleculaisubstances, it is necessary thathey be prescribed in the correc

amounts, which typically meanthe use of optimum therapeutidosages that are individualized tosuit each schizophrenic patientThe main orthom olecular strategiethat are required for the effectivtreatment of schizophreniinclude; (1) dietary and lifestyladjustments; (2) vitamin B3 (niacinor niacinamide); (3) vitamin C(ascorb ic ac id); (4) zinc and v itaminB6 (pyridoxine); (5) selenium: and

(6) omega-3 essential fatty acids.

Dietary and Lifestyle djustments

All processed foods, refinedsugars, and stimulants (e.g., caffeineand black tea) should be avoidedStrict avoidance of common foodallergens (e.g., milk, dairy, wheatcorn, and eggs) should be highlyconsidered since about 50% of alchronic cases of schizophreni

are caused by unrecognized foodallergies.'^ A combination of a baddiet, poor lifestyle behaviors, andcommon food allergens increase.the production of adrenalinand consequently increases thiproduction of adrenochrome iischizophrenic patients. '^ '

The ideal diet for the majoritof schizophrenic patients shouldbe high in protein and fat and lowin carbohydrates. Such a diet ha

been clinically proven to correchypoglycemia, increase ththe rap eut ic effectiveness of vltamiiB3, and reduce schizophrenisymptoms.'' Cigarette smokinijalcohol consumption, and the usof mind-altering substances (e.g.hashish and marijuana) must bavoided. Continued use of suchsubstances will significantlyinterfere with the effectiveness othis approach.

WNSENO LETTER FEBRUARY/MARCH 2007



Schizophrenia

Vitamin B3(Niacin or Niacinamide)

To reduce the productionof adrenochrome, Hoffer and his

team decided upon the methylacceptor vitamin B3 (eitherniacin or niacinamide). Thisvitamin had previously been usedin to treat pellagra (a diseaseclinically indistinguishable fromschizophrenia) , and it had relevantbiochemical properties.'- Hofferand his team researched the

metabolism of adrenaline. Theyknew that the reaction involvingnoradrenaline to adrenalinerequired the addition of one

methyl group. Vitamin B3 was

known to function as a methylacceptor. Hoffer's team thoughtthat an optimum dose of niacinmight decrease the amount of

noradrenaline that would be

converted to adrenaline. Sinceadrenoch rome w as thought to be anoxidized derivative of adrenaline,vitamin B3 could help to reducethe quantity of adrenochromeby limiting the production of

adrenaline.

Hoffer and his team alsodiscovered an additional bio-

chemical property of vitaminB3 that would help to explain its

therapeutic efficacy. Vitamin B3 Is aprecursor to nicotinamide adeninedinucleotide, which is present in

both oxidized (NAD) and reducedforms (NADH) in the body. In the

brain, adrenaline beco mes oxidizedand loses one electron to become

oxidized adrenaline. If enoug h NAD

and NADH are available, then the

oxidized adrenaline is reconvertedto adrenaline. These back-and-forth processes continue to occurin the presence of sufficient vitam inB3 coenzymes. However, in the

absence of enough NAD and NADH,the oxidized adrenaline loses an

additional electron and becomes

adrenochrome. This last reaction isirreversible and presumably occursin much greater concentrations in

the schizophrenic brain.

Another potential mechanismfor Vitamin B3 has to do withrecent postmortem findings of

sch izop hre nic brain tissues. *In this report, an upregulationof the enzyme tryptophan 2,3

dioxygenase (TD02) was foundamong schizophrenic pat ients but

not among the controls who wereexamined. The brain tissues of the

schizophrenic patients showedsignificant elevations of kynurenine(1.9 fold, p = 0.02), TD02 mRNA (1.7

fold, p^O.049), and the density of

TD02-positive white matter glialcells (p=0.01). In schizophrenia,the TD02 enzyme was foundto be upregulated, causing an

over-production of pathwayintermediates (e.g., kynurenine).

This upregulation might be

responsible for the evolution of

some schizophrenic symptoms.Instead of linking this upregulationto some defective factor in the

TD02 gene, the authors suggestedthat it might be du e to a diminishedniacin effect - possibly the result of

depressed production or reducedsignal transduction via the niacinreceptor. They recommendedthat niacin or its congeners are

Table 1 Summary of the

Treatment Number

Placebo 9

Niacin 10

Niacinamide 11

Days in

Hospital

63

60

72

First Clinical Study

Number on

Eiectroconvulsive

Treatment ECT)

6

7

7

Using Vitamin B3

Number Sent

to Weyburn

Mental Hospitai)

0

1

2

Number

Well

3

8

9

Adapted from; Hoffer A. Vitamin 8 3 Schizophrenia. Discovery. Recovery. Controversy. Kingston, Ontario:Quarry Press. Inc,;1998:51, These findings were first reported in: Hoffer A. Osmond H Callbeck MJ. Kahan 1.

Treatment of schizophrenia with nicolinic acid and Nicotinamide, J Ctin Exp Psychopath. 1957:18 131-158. 1

necessary regulators of thbiochemical pathw ay and should bcapable of restoring homeostasAlthough these findings are veimpo rtant an d relevant, they are nnovel. In 1973, Hoffer hypothesizthat there are defects in th

metabolism of t ryptophan and th

such defects or deficiencies in th

ensuing reactions would cause back-up of indole metabolites the precursor chain. '^ He furthhypothesized that such defecwould lead to an underproductiof NAD.

The first report on t

therapeutic use of vitamin B3 f

sch izo ph ren ia wa s pres en ted in 19at the Saskatchew an Comm itton Schizophrenia. At this meetineight cases were presented, eacde m on stra tin g favorable effecfrom giving one to ten grams (g)

vitamin B3 and, in the majority <cases, equal amounts of vitamin CAfter a more involved pilot studof 29 patients also demonstratexcellent therapeutic responses vitamin B3,' the first double-blinplacebo-controlled experimein psychiatry was undertaketo assess whether or not thvitamin was effective. The studwhich began in 1952 but was n

published until 1957, involved acute schizophrenic pat ients w

were each randomized to placebniacinamide, or niacin. '- They w egiven 1 g three times daily for

days, and then followed for om

year. After the year, the patiengiven vitamin B3 with the standat reatments at that time had mo

than double the recovery ra(80%) compared to patients the placebo group (33 ). Tablesummarizes the findings from thinitial clinical study.

Other clinical studies soofollowed that involved mo re patienand longer treatment durationThe g oals were to valid ate the initifindings and ascertain if there we

other benefits and therapeuteffects from the administratioof vitamin B3. In 1955, Hoffer an

his team reported on their resu



involving 171 patients: 73 patientsreceived vitamin treatment withniacin or niacinamide and wereompared to 98 patients havingeceived standard treatment (i .e. , combination of ECT. insulinubcoma, and psychotherapy). '

(Table 2 summarizes thesefindings.) They conc luded , When

used in adequ ate dosag es, nicotinlcacid and nicotinamide materiallycontributed to the recovery ofschiz oph renic patients. VitaminB3 reduced the nu mber of suicidesto zero and imposed much lessof a burden upon the health caresystem, since less patients in thevitamin group were sent to themental hospital and subsequentlyspent less time in the mentalhospital upon admission.

In their second double-blind,placebo-controlled experiment,Hoffer an d h is team use d only niacinand placebo.'^ The study lasted 33days and involved 82 patients (43in the placebo group and 39 in theniacin group). (The results of thisstudy are summarized in Table 3.)As can be seen, vitamin B3 onceagain contributed significantly tothe recov ery of acute schizoph renicpatients.

Other parameters wereevaluated and reported by Hofferand his team including the numberof patients readmitted, the numberof readmissions, the number ofpatients well or much improved,and the number of patients whowere considered cur ed. ' ' This

data involved the following groupsof pa tients : (1) those w ho only tookvitamin B3 while in the h ospital andnot in the community; (2) patientswho did not take vitamin B3 whenin the hospital but did take thevitamin when in the community; (3)patients who took vitamin B3 whenin the hospital and community; and

(4) patients who never took vitamin

Schizophrenia

when in the hospital and in thecommunity.

Hoffer followed patients from1953 to 1960 and published a totalof six double-blind, randomizedcontrolled clinical trials. All these

trials confirmed the positive effects

The results of this review dem onstrated

that pa tients who had taken vitam in B3

fared much better than patients who were

not given the vitam in.

B3. The results demons trated that

patients in the community whowere taking niacin (groups 2 and3) had more community years thatwere free of read miss ions com paredto patients not taking vitamin B3(gro ups 1 and 4): 91% ver sus 62%of the community years free ofreadmissions. The entire niacingroup (group 3) was readmitted 38times for 67 readmissions (averagewas 64 days per patient), and thiswas much better than the placebo/

non-niacin group (group 4) thatwas readmitted 36 times for 81readm issions (average was 47 daysper patient), Once all the data wascombined, the results revealed thatthe most five-year cures and bestt reatment responses were amongthe patients who took vitamin B3

that vitamin B3 had up on th e

recovery of acute schizophrenicpatie nts an d verified that th e use ofthis vitamin substantially reducedpatients' reliance upon the healthcare system.- Hoffer even followedpatients who were being treated byother psychiatrists from October1. 1955 to December 31. 1962.' Theresults of this review demonstratedthat patients who had takenvitamin B3 fared much b ette r thanpatients who were not given the

vitamin. The patients on vitamin B3had fewer hospital readmissionsrequired hospitalization for fewedays, and had no suicides.

In terms of treating chronicschizophrenic patients, Hoffer'early studies did not show a

Group

Treatment

Comparison

(Adapted from :

Group

Placebo

Niacin

Number

73

98

Table 2. Effects of Vitamin

Mean Days Number

in Hospital63

50

63 Against Standard Treatment

Sent to Mental Hosp itai

After Treatment7

47

Hoffer A. Niacin Therapy In Psychiatry Springfield, IL: Charles C Thomas: 1962:108.)

Table 3. Results from the Second

Number

43

39

Mean Number thatAge Received ECT

31.9 21

30.3 15

Double-Blind Controllec

Mean Number of Daysin the Hospital

73.8

72

Mean Days

in Mental Hospita23 4

319

Exper imen t

Number of

ll Suicides0

4

Not ImprovedImproved (Percentage Improved

25

8

18(41.9 )

31 (79.5 )

(Adapted from: Hoffer A. Niacin Therapy In Psychiatry Springfield, IL: Charles C Thomas; 1962:42-46.)

WNSEND LETTER - FEBRUARY/MARCH 2007



Schizophrenia

favorable response among chronicschizophrenic patients who wereill longer than one year. However,when Hoffer reviewed this problemmore substantially, he discoveredthat the treatment duration was

not long enough to have producedadequate results. Chronic patientsrequired v itamin B3 trea tm ent forfive or m ore yea rs in order to deriveobservable benefits. ' -' In one studyinvolving 32 chronic patients,all the patients failed to respondto vitamin B3 after two y ear sof use. Nineteen of the patientsdiscontinued the vitamin, and theremaining 13 patien ts co ntinuedwith the vitamin treatment. Datawas obtained for the years, 1956-1957, 1958-1959. 1960-1961, 1962-1963. and 1964.' Of the patientsnot on niacin, the mean numberof days spent in hospital were 691compared to 79 in the niacin group.Also, the proportion of time spentin the hospital was substantiallyless for the chronic patients whoremained on the vitamin.

In a more recent analysis of 27chronic schizophrenic patients who

had been under treatment for atleast ten years, consistent trea tmen twith vitamin B3 produced thefollowing re sults: 11 patie nts wereable to work: two patients wereable to marry and look after theirfamilies and homes; two patientswere single mothers able to takecare of their children; and threepatients were able to manage theirown businesses.- ' These results areremarkable when one considers

the state of these patients priorto receiving orthomolecular care.The average age of these patientswas 40. The majority of them hadbeen ill for seven years beforethey sought treatment from Hoffer,and all had been unresponsive toprevious t reatm ents.

If one is to look at the enormityof this data, as I have, the onlyreasonable conclusion to be madeis that all schizophrenic patients.

including both acute and chronicpatients, need to be treated withvitamin B3 as quickly as possibleand for the duration of theirlives. Vitamin B3 tre atm en t offerssignificant hope of a reasonablequality of life among patientswho would otherwise remainincapacitated and in and out ofhospitals for the remainder of theirlives.

The starting dose of niacin foradu lts is 1000 milligrams (mg) thre etimes daily. In my opinion, the dailydose needs to be slowly increasedto 4,500-18,000 mg to achieve thebest possible outcome. Patientsneed to be educated about theflushing, heat, itchiness, pruritis,redness, and tingling that theywill transiently experience. These

benign cutaneous reactions usuallybegin 15 minu tes after takingniacin for the first time, and arefirst noticed around the forehead,then descend to the thorax, andsometimes to the feet. Thesereactions typically abate in one totwo hours following the ingestionof niacin. Niacin causes thesecutan eou s reactions by inducing theprod uction of prostag landin D^ inthe skin, leading to vasodilation anda marked increase of its metabolite,9a , UP-PGF2. in th e plasma.-^ Niacinis its own anti-flushing agent, andtaking it regularly depletes the skinof prostagiand in D2 and prev entssubsequent cutaneous react ions. At3,000 mg daily, the flush and othersymptoms will cease to be an issuefollowing the first two to thre e d aysof treatment and will practicallydisappear thereafter. If patientsare not consistently taking thesehigh-milligram doses throughout

the day, they will continuallyre-experience these cutaneousreactions. The concern over livertoxicity is very minor if immediate-release niacin preparationsare used.-'- ' Sus tained -releasepreparations (and likely otherpreparations such as timed- orslow-release ones) can cause livertoxicity and are not recommendedfor schizophrenic patients unless

under close supervision.^^ [n clinical experience, niacin is meffective and better-tolerated thniacinamide for schizophrenSome patients prefer niacinamisince it does not cause flushias well as the other cutaneoreactions. Nausea and dry mouare much more common w

the use of niacinamide than wniacin. The daily dosages niacinamide should not exce6,000 mg, since the likelihood nausea accompanied with vomitiis much greater.-'*

Vitamin Ascorbic Acid)In their early pilot a

controlled clinicai studies. Hofand his team also used vitamC since its powerful antioxida

properties would also diminithe double oxidation of adrenalto adrenochrome and prevent auto-oxidation in critical braareas .- - ' This vitamin is also effective anti-stress nutrient thhelps schizophrenic patiencope more effectively.-' There recent evidence that high-dovitamin C (3,000 mg of sustainerelease daily) is indeed an anstress nutrient, since it was able

subjectively reduce psychologicstress, decrease blood pressurand lower cortisol levels in healtmen after 14 days of use.- A rep oby Smythies described additionroles that vitamin C has upothe brain including the followin(1) its ability to protect NMDreceptors from glutamate toxiciwithin the brain; (2) its antagonisof the effects of amphetamine(3) its enhancement of old

APDs like haloperidol; and (its ability to prevent the autoxidation of dopamine to its toxderivatives.^^ Vitamin C alconserves intracellular glutathioand is likely a redox glutathiocofactor.̂ This is im po rtan t singlutathione S-transferases aimportant enzymes that facilitathe conjugation of glutathione adrenochrome. dopaminochromand noradrenochrome and rend

BEST OF NATUROPATHIC M EDICINEY MARCH



these toxic metabolites non-toxicby the production of unreactiveglutathione conjugates.^' The genefor glutathione S-transferase isdefective in schizophrenia.^ I believethat this defect might be partiallyremedied by supplementation withhigh dosages of vitamin C, whichwould preserve glutathione in its

reduced state and increase theamount of available glutathionethat could be used for the synthesisof the glutathione S-transferaseenzyme.

Vitamin C should be presc ribedat 1,000 mg three times daily andthen eventually increased to thesub-laxative dose. There are reportssuggesting that acute and chronicschizophrenic patients require

m ore of it. In one s tudy , the fractionof urina ry vitamin C was evaluatedin 44 recently hospitalized acuteschizophrenic patients and wascompared to 44 other subjectsserving as the control group.-'-All the subjects were given 1.76g of vitamin C orally and hadtheir urinary levels of vitamin Cmeasured every two hours duringa six-hour collection period. Theschizophrenic patients differedsignificantly from the control groupin their elimination of ascorbicacid. Seventy-six percent of theschizophrenic subjects were lowexcretors, which means that lessthan 17% of the ad ministere d oraldo se of vitamin C was recov eredin their urine samples. This resultwas 2.5 times the incidence of thecontrol group, which demonstratedthat only 30% from this group werelow excretors.

In this same study, the lowexcretors of both groups weregiven additional vitamin C forseven days (approximately 10g) , and urine samples werecollected on the eighth day. In thecontrol group, the low excretorgroup went from 7/16 to 5/16 andremained essentially unchanged.In the schizophrenic group, thelow excretors decreased from 9/11to 3/11, a substantial change. The

authors of this study concluded

that a combination of genetic andnutritional-environmental factorscaus e a higher degree of tissueunsaturation among the acuteschizophrenic patients.

In another study using chronicschizophrenic patients, the plasmaand urinary vitamin C levels of35 schizophrenic patients werecompared to an equal number ofcontrols.'' All subjects were giventhe sa me hospital diet and 70 mgof vitamin C daily for four weeks.Baseline plasma vitamin C valueswere lower in the schizophrenicpatients (p < 0.05), but normalizedto be approximately the same asthe control group values afterthe four weeks of treatment. Themean vitamin C levels as measuredin a six-hour urine collection

were different among the lowexcretors of both groups, andthis difference reached statisticalsignificance (p<0.05) - 15.9 mg forschizophrenics and 39.5 mg for thecontrols, When all thesch izoph renicand control subjects were given aloading test of g of v itamin C afterthe four weeks of 70 mg of oralvitamin C daily, the schizo phre nicpatients continued to excrete loweram ou nts of vitamin C in their u rine

compared to the control values.After the loading test, the plasmalevels of vitamin C were different,with the schizophrenic patientshaving a lower mean value thanthe controls (p<0.05). After onemonth of supplementation with 1g of vitamin C, the plasma levels ofeach group equalized, as did theirsix-hour urinary excretion rates.The authors of this study were inagreement with the hypothesis that

Schizophrenia

schizophrenic patients requirehigher levels of vitamin C than thesuggested optimal ascorbic acidrequirement for healthy hu mans.

Vitamin B Pyridoxine) and

ZincMany schizoph renic pa tients testpositive in the u rine for a com poun dknown as kryptopyrrole, which isassociated with physiological and/or psychological stress.''' Hoffercompiled data from thousands ofpatients and found abnormal levelsof kryptopyrrole in the urine ofdifferent types of psychiatric andnon-psychiatric disorders (Table

4).'

Kryptopyrrole combines ir-reversibly with pyridoxine andthen with zinc, and this creates acombined deficiency syndrome.^^Some common clinical symptomsof patients having high amountsof kryptopyrrole in their systemare white areas in the fingernails,stretch marks on the body, andfemale premenstrual syndrome.Many of the clinical features ofpatients excreting high amounts

of kryptopyrrole resemble those ofschizophrenia.'^ Even though it ispossible to test for this compoundI choose not to do so, and Iprescribe these nutrients to all ofmy schizophrenic patients. Theyare relatively free of side effectsand often help to reduce sym ptomsThe daily dosages that routinelyprescribe are 250 mg of pyridoxineand 50 mg of zinc. ^

Table 4. Psychiatric and Non Psychiatric Groups with

Abnorm al Urine Levels of K ryptopyrrole

Group

Acute schizophrenics

Chronic schizophrenics

All non psychotics

Physically ill patients

Normal subjects

Percentage w ith Abnormal Urine Levels

75

50

25

5

0

Recovered schizophrenics

LETTER FEBRUARY/MARCH 2007



Schizophrenia

Selenium

I recom men d that allschizophrenic patients take 200-400 micrograms (meg) of seleniumdaily. Several published reportsindicate a potential need for thistrace mineral among schizophrenic

patients. In one report. Brownand Foster linked a deficiency ofthis trace mineral to an increased

glutathione peroxidase activity,and ensure the proper productionand action of prostaglandins. Inthat same report, Foster discussedthe relationship between niacinand selenium, in that niacin beinga methyl acceptor might slowdown the metabolism of selenium(since its metabolism involvesmethylation) and prolong its action

in the body. Berry was the first toreport on the potential relationshipbetween selenium and niacin.'* He

Regardless of when the orthomolecular

treatments begin to demonstrate their

effectiveness it Is paramount that

once initiated they are never discontinued.

prevalence of schizophrenia inregions of the United States wherefodder crops had the lowest levelsof selenium.- ' They calculated theselenium-related relative risk tobe 1 77:1 in these areas. Accordingto these authors, some of thebiological consequences ol selen-ium deficiency (i.e., prostaglandinimbalances, viral mutation,excess 12-HPETE production, and

decreased glutathione peroxidaseactivity) might be related to theetiopathology of schizophrenia.They also reviewed additionalevidence of a negative correlationin schizophrenic patients betweenglutathione peroxidase activityand brain damage (i.e., brainatrophy and increased ventricle-brain ratios), which was not foundamong a group of controls. Inanother report, Foster suggested

that selenium might be tried asa treatment for schizophreniasince it protects against freeradical damage and is probablyantagonistic to adrenaline andtherefore to adren och rom e. Healso hypothesized that whensupplementing with essentialfatty acids, selenium is essential,as it would prevent the excessiveoxidation of the fatty acids, restore

reported that a certain sub-typeof schizophrenia might be due toa defective selenium transportprotein and to low levels of thistrace mineral in the body. Niacin'santipsychotic properties, accordingto Berry, are possibly due to itsprolongation of selenium within thebody, which would correct boththe defective transport protein andits deficiency.

Foster also reported on anadditional reason why seleniumwould appear to be useful for thetreatment of schizophrenia.•'•' Henoted some evidence that showedthat the desiccated or pure form ofthyroid hormone achieved bettercure rates for schizophrenia whencompared to untreated patientsand to patients receiving standardtranquilizers. He suggested thatthe t r i iodothyronine componentaccounted for the favorableclinical results, as this hormonewould reverse the toxic effects ofexcess adrenochrome. Since thedeiodinase enzyme that convertsthyroxine to triiodothyroninerequires selenium, he hypothesizedthat an effective treatment protocolshould include both selenium andthyroid hormone.

Omeg a 3 Essential Fatty Acidsfrom Fish DocosahexaenoicAcid and Eicosapentaenoic Ac

Schizophrenia is characteriby lipid membrane abnormalit(a.k.a., the phospholipid me mb rhypothesis) that inclu

abnormal brain phospholiturnover, increased levels phospholipase A2, reduced nia

skin flush response, abnormelectroretinogram, and reduccell membrane levels of omegand omega-6 polyunsaturated faacids.^ ^' Fish oils, particulathe eicosapentaenoic acid (EPcontent (as opposed to docosahexaenoic acid [DHA]), habeen shown to help with both positive (e.g., hallucinations adelusions) and negative sympto(e.g., flat affect, depression, aisolation) of schizophrenia whused as an adjunct to standatreatment. '- The optimal daily doshou ld prov ide at least 2 g of EPA

Treatment StrategiesEven though all the nutrie

just described are essential, tmost important are vitamins and C. I recomm end that theparticular vitamins be given schizophrenic patients initialand the others then added ovseveral months. Of course, succeis invariably dependent on tpatient's willingness to comply athe skill of the presc ribing cliniciaCompliance is a significant isswith all schizophrenic patienAt the beginning of this report.mentioned that one out of five firepisode schizophrenic patienhave a chance at living a nenormal existence. Of the remaini

four, only one patient will compwith his medications; one patiewill not take his medicatiocontinuously due to side effecand the remaining two patienwill be lost to follow-up.^ Thneed to be informed that theorthomolecular t reatments aequally as important as are theantipsychotic medications. Resuare sometimes seen after the fir

TOWMSEND LETTER FEBRUARY/MARCH



two mon ths," and sometimes threeto six months are necessary beforeclinical benefits are observed.*'For chronic patients having hadschizophrenia for five or moreyears, the necessary t reatmenttime is at least five years beforebenefits are noticed. Regardlessof when the orthomolecular

treatments begin to demonstratetheir effectiveness, it is paramountthat, once initiated, they are neverdiscontinued. Medications shouldlikewise not be discontinued but,with the coo peration of the pa tient 'spsychiatrist, can be reduced veryslowly over the course of manymonths to several years oncethe orthomolecular t reatmentsare helping. Abrupt cessation ofatypical APDs will cause a relapse,

as will too much of a decreaseor too early of a decrease inmedication. The orthomolecularapproach requires a t remendousamount of patience from theprescribing clinician, since resultstake a long time to materialize.Likewise, schizophrenic patientsand their respective families and/or caregivers need to have thenecessary patience and motivationto stay the course.

easuring Patient Progress andPrognosis

Once orthomolecular t reatmentsare started, how is the clinicianable to monitor his/her patients'progress? Hoffer has publisheda practical system that can beused to determine how a patientis responding to orthomoleculartreatmen ts.- ' He has four me asure sof recovery:

1. Freedom from signs andsymptoms (1 point)

2. Ability to get on rea son ably wellwith family (1 point)

3. Ability to get on reasonably wellwith the community (1 point)

The ability to work at a job orto be productive in the sam emanner as before the illness

struckPatients who have never beenengaged in some ty pe of job orproductive work can be judgedby their ability to perform anyuseful work. (1 point)

Patients are categorized as"well" if they have achieved 4points, "much improved" if theyachieved 3 points, "improved"when they have achieved 2 points,

and "not improved" if they onlyacquired 1 point. I also use aquestionnaire, known as the HODtest (Hoffer-Osmond Diagnostictest for schizophrenia), to monitorand evaluate my patients. Thistrue/false test assesses theoverall intensity of the disease byproviding a total score (TS). TheHOD test also p rovid es sco res forcommon schizophrenic symptomsof perception (PerS), paranoia

(PS), and depression (DS). If apatient achieves a high TS (>30)or a high score (>3) in any of theindividual categories, this wouldindicate pronounced illness. Onceorthomolecular treatments beginto show effectiveness, the scoresdec rease . This test has been shownto be valid in terms of its ability todetect (diagnose) schizophreniaand to assess the severity of the

Schizophrenia

In terms of prognosis, if theorthomolecular program is startedearly in the course of the patients'

disease, they will have greaterchances of recovering. Accordingto Hoffer's eariy placebo-controllecclinical trials and his manypublished clinical reports spanningmore than 50 years, patients canexpect certain prognoses onceorthomolecular t reatments areinitiated.'^ Table 5 indicates theexpected results from the additionof orthomolecular treatments tothe standard approach.

Schizophrenic CasesI have chosen four cases from

my naturopathic medical practiceThe first two cases represent theeffectiveness of this approach. The

latter two cases demonstrate thedifficulties that patients and theirfamilies have with this approachespecially when necessarytreatment components are missingor not sufficiently followed.

C a s e # lThis 24-year-old female first

presented to my private practice onOctober 1, 2005. She was formallydiagnosed with schizophrenia

in March 2005 when she washospitalized for two-and-a-halfmonths due to paranoid ideationthat involved worries aboubeing poisoned, social isolationand withdrawal, and significanimpairments in maintaininghealthy relationships. Prior to heformal diagnosis, she reportedseveral years of intermittenparanoid ideation; she had abuseddrugs such as cocaine, heroin

and methamphetamine, felt thacertain noises were causing heto be crazy, thought she could

Table 5. Expected Results from Orthom olecular Treatments

roup Duration of Treatment Well and Much Improved

Sick one year, or in second or third relapse Up to one year 90%

Sick two to five years Up to five ye ars 73

Sick over five years, but out of mental hospital Five or more years 50

Sick over five years and in mental hospital Five or mo re years 25

LETTER FEBRUARY/MARCH 2007



Schizophrenia

read peop le s mind s, and feltunable to hold down jobs. Duringthe previous six years, she wasenrolled in a geography programat Carleton University in Ottawa,but had to drop out since she couldnot handle the course load. Shehad some boyfriends while livingin Ottawa, but the relationshipsfailed since she became verysuspicious of each boyfriend andthought he was trying to poisonher. She also thought her familymembers were out to poison herand that her mother wanted herdead because she was not Jewish

enough. In November 200,5. shewas hospitalized a second time forsevere auditory hallucinations, butonly for the night and was thendischa rged the next day. At the tim eof my initial consultation, she wasunemployed and unable to pay forher rent and other living expenses.She was living part of the time with

her mother, but would also live inan apartment that was financed byher mother. Although she was notacutely psychotic, she continuedto exhibit schizophrenic symptomssuch as social isolation andfrequent auditory hallucinations.She was taking mg of risperidoneand 30 mg of olanzapine at thattime. Table 6 sumnfiarizes the

patient s respo nse to the adjunctorthomolecular t reatments.

This patient has continuto do exceptionally well. In Ju2006, I wrote to her family docabout the benefits of thyromedication for the treatment schizophrenia (Hoffer, 2001b). Tpatient was prescribed desiccatthyroid and has been taking daily. I also corresp onde d with hpsychiatrist, and in early June 20her olanzapine was reduced to mg daily. As of my last visit wher. August 20. 2006, she remainwell and free of all schizophrensymptoms. Even though her initHOD scores were within normlimits, they must have be

Table 6. Case 1 : Patient's

Consultation Dates

Clinical Presentation

Current Psychiatric

Medications

Orthomolecular

Treatments & Plan

HOD R esultsTS normal <30)

PerS normal <3)

PS normal <3)

DS normal <3)

Category of Recovery

October 1, 2005

Regularly hearing

voices, unable to attendUniversity full-time

taking one course),

antisocial behavior.

watching lots of TV, and

sleeping m ore than 11hours each night.

1 mg of risperidone and

30 mg of olanzapine

daily

3 g of niacin, 3 g of

vitamin C, 250 mg of

pyridoxine, 50 mg of

zinc, 2 teaspoons ofhighly concentrated

fish oil, and 5 mg ofmethylcobalamin. Patientadvised to quit smoking

and cut out all dairy,wheat, and alcohol.

27

4

2

0

Not improved.

Response to Ad junctive

November 26. 2005

More engaged with her

family. Heard voices

one to two nights

during the past month.

Continues to watch lots

of TV, but wants to start

volunteering next week.In the last month, had

pizza once, avoided

all alcohol, and onlysmoked two to three

cigarettes.

Same.

Increased ni cin to 2,000

mg three times daily.

Added a caffeine-free

extract of green tea tohelp with acne. Letter

sent to psychiatrist aboutreducing olanzapine to25 m g daily.

Not Assessed .

Improved.

Orthomolecular Treatments

January 21 , 2006

Psychiatrist approved

the reduction in meds.

Patient no longer

hearing any voices.

is full of energy and

is exercising three

times each week.Quit smoking since

November. Received a

B+ last semester andis enrolled in another

course.

1 mg of risperidone and

25 mg of olanzapine

daily.

Added 200 mg daily of

Ginkgo biloba extract.

Instructed patient to

continue with the current

program. Discontinued

the methylcobalamindue to acne.

13

40

0

Well.

May 27, 2006

Working at a major

Montreal hotel and ha

gained acceptance to

community college fo

hotel management. N

schizophrenicsymptoms.

1 mg of risperidone a

25 mg of olanzapine

daily.

Plan was modified to

include 500 meg of

chromium twice daily.

and herniacin was

increased to 6 500 mg

daily

34

2

0

Well.

TOWNSEND LETTER - FEBRUARY/MARCH



abnormal for her, since she wasvery symptomatic, and her clinicalpicture improved dramatically asthese scores decreased. In August2006, I spok e with the patien t'smother about her daughter'sprogress. The mother said thatthe orthomolecular treatm entshave given her daughter back

her life. Per her moth er's re port,the patient is a lot slimmer, had aboyfriend during the summer, andis working every day and paying allof her expenses including rent andgroceries. She is looking forwardto starting a community college

program in the fall of 2006. and herdisease is clinically in remission.I instructed her to remain onthe current program and to notchange anything without firstconsulting me. She will still haveregular visits with me, but not asfrequently. I expe ct h er to rem ainwell, for she has not had a relapse

since commencing treatment. Shehas many of the essentials of goodresponse, which include a strongdesire to get well, the cooperationof an open-minded psychiatrist,and a very supportive and caringfamily.

Schizophrenia

Case#2This 36-year-old male patient

presented to the Robert SchadNaturo pathic Clinic on May 23.2006 with a chief complaintof schizophrenia. I supervisenaturopathic interns on this clinicalshift, so a fourth-year clinicalIntern and myself evaluated thi.spatient. The patient's goal was toeventually get off his medicationdue to troublesome side effectsof fatigue and weight gain. SinceJanuary 2006, the patient was

Table 7. Case 2: Patient's

Consultation Dates


Current PsychiatricMedications

Orthomolecutar

Treatments & Plan

HOD Results

TS (normal <30)PerS (normal <3)PS (normal <3)

DS (normal <3)


May 23, 2006

Very talkative.

disorganized speech,and thought blocking.Described hisschizophrenia as some

type of gift from God.Also believed that therewere supernaturalbeings and angels

following him andlooking after his

well-being. Describedvarious instances of

seeing supernatural

beings that no one elsecould see.

450 mg of clozapine

daily.

None prescribed.

Not assessed.

Improved.

Response to Adjunctive

May 30. 2006

Expressed strongdesire to get off his

medications. Verydrowsy and sleeping

ten to 12 hours eachday. Complained ofmuscular contractions

around his head, which

he felt was due to themedication. Believedthat he has clairvoyant

abilities.

Same.

1,000 mg of both niacinand vitamin C threetimes daiiy. Omega-3

fatty acids providing

a daily dose of 3 600mg of EPA and 1,800mg of DHA. Given anintramuscular injection

of vitamin B12 (5,000

meg).

32

1122

Improved.


July 25, 2006

Hearing fewer voices

than the previous visits.Continues to be tiredand fatigued m ost of thet ime, which he feels isdue to the me dication. Is

sleeping ten to 12 hours

each day. More coherentspeech and less thought

blocking.

Same

2,000 m g of niacinthree times daiiy.Vitamin C the same as

before. Ginkgo biioba

extract at 240 mgdaily. Added 250 mg ofpyridoxine and 50 mg

of zinc.

5

101

Improved.

August 15, 2006

Continues to experience

fatigue. His voices arestill present, but remainas per the last visit.Continues to be veryinteractive with coheren

speech and less thoughblocking.

Same.

Given an intramuscular

injection of vitaminB12 (1,000 meg). Letter

sent to patient s

psychiatrist requestinga m inor decrease in his

medication to 425 mg

daily.

Not assessed.

Improved.



Schizophrenia

on clozapine at a daily dose of450 mg. He was required to getblood tests every two weeks dueto the potentially life-threateningagranulocytosis. Previously, hehad been resistant to a number

of antipsychotic medications that

included loxapine, quetiapine,olanzapine, and risperidone. Hewas also given lorazepam in thepast, but was no longer taking it.His most recent hospitalizationswere in January and March of2006. He was considered a chronicpatient since his schizophreniahad lasted more than five years,

but the year of his initial diagnosis

could not be ascertained due to patien t s difficulties with timelinDuring the initial interview, he wvery talkative, had disorganizspeech, and demonstrathought blocking. He described schizophrenia as some type of gfrom God. He also believed tthere were supernatural bein

and angels (which he could s

Table 8. Case 3: Patient's

Consultation Dates


Current Psych iatric

Medications

OrthomolecularTreatments Plan

HOD ResultsTS normal <30)

PerS normal <3)PS normal <3)DS normal <3)


August 30, 2004

Thought blocking,

difficulty concentrating.

difficulty answeringroutine questions,

and comprehension

problems. Reported

constant auditory

hallucinations,and some visual

hallucinations. Veryanxious, restless andvisibly diaphoretic

20 mg of olanzapine

daily, 0.5 mg of

clonazepam twice daily,1 mg of apobenztropinedaily, 37.5 mg ofvenlafaxine, and aninjection of 40 mg

flupenthixol every 2weeks.

1,000 mg ofniacinamide three

times daily, 1,000 mg ofvitamin C three times

daily, 2 teaspoons ofliquid fish oil 2,100

mg of EPA and 1,500mg of DHA), 50 mg ofzinc, and 250 mg ofpyridoxine.

Not assessed.

Not improved.

Response to Adjunctive

September 18. 2004

Patient was morepositive and motivated

compared to theinitial visit. Reported

some muscle tension

in his neck. Was

encouraged to remain

on all the prescribedsupplements.

Same.

Niacinamide was

reduced to 1,000 mgtwice daily. Was also

prescribed 500 meg of

chromium three timesdaily, to help with the

hypertriglyceridemia.weight gain, anddysinsulinemia

associated with the

use of atypical APDs.He was given anintramuscular injection

of 5 mg of folic acid and

1,500 meg of vitaminB12.

50

1010

1

Not improved.


October 16. 2004

Auditory hallucinations

have stopped- no longer hearing

death threats in his

head. Reduced theniacinamide to 1,500

mg daily. Anxiety

has decreased, and

patient exhibited bettereye contact. Less

diaphoretic than theinitial visit.

Same.

Patient instructed tostay on all supplements.Was given an

intramuscular injection

of 5 mg of folic acid and1,500 meg of vitaminB12.

Not assessed.

Not improved.

November 13, 2004

Patient reported

smoking less. Living

in new group home,

and has more privacyIs volunteering as asalesperson. Auditor

hallucinations continuto be absent. Anxiety

and diaphoresis have

not worsened since tlast visit.

1 mg of risperidone abedtime in addition to

the other medications

Niacinamide wasdiscontinued. 1.000 mof niacin three times

daily was prescribed.Given an intramusculinjection of 5 m g of foacid and 1.500 meg ovitamin B12.

36

645

Improved.

TOWNSEND LETTER- FEBRUARY/MARCH



following him and looking afterhis well-being. He lived with hisparents who were doing whateverthey could to make his life asproductive and comfortable aspossible. Table 7 summarizes thepatient 's respon se to the adjunctiveorthomolecular t reatments.

This patient has not been on theorthomolecular program for a longtime. Since my initial consultation,he has shown a positive responseby having fewer auditoryhallucinations. This change was alsoreflected by the decreases in hisTS and PerS HOD score s. To derivethe most benefits, he will needto remain on the orthomolecularprogram for at least five years, butthe duration of his life would bepreferable. Although his Categoryof Recovery did not chan ge inthis short time, he showed modestimprovements and was able tocomplete his examination for aplumbing license. I believe he hasa very good chance of recoveringsince he has the necessarycomponents for favorable response(e.g., a supportive and caringfamily, proper psychiatric care, andorthomolecular t reatment) .

Case#3This 30-year-oId male patient

presented to my office on August30, 2004. He reported that hisschizophrenic symptoms beganwhen he wa s 15 ye ars old. At thattime, he was having paranoidthoughts that involved abductionand death threats. For the nexteight years, his symptomsprogressively worsened, and by

1997. he was h aving con stan t visualhallucin ations. In that sam e year, hehad a difficult time dealing with theend of a relationship with a woman.He was hospitalized in Decemberof 1997 and has been hospitalized15 additional times, with the latestone occurring in March 2004. In

1998, the patient was formallydiagnosed with schizophrenia. Atmy initial consultation, he reportedhaving trouble thinking clearly

and difficulty an.swering routine

questions. He sweated profuselyduring the visit and frequentlydrank water from a large waterbottle. He was having constantauditory hallucinations andoccasional visual hallucinations. Hedescribed himself as an antisocialperson. He was living in a group

home for mentally ill patients,but purposely kept his distancefrom the other residents. He was

Schizophrenia

he was finally able to engagein some type of regular work.His HOD sco res reflected the seclinical improvements as well. His Category of Rec overy wen t from not improved to improved in

under three months of treatment.Sadly, from the early part of

December to February 2005, the

The orthomolecular approach requires a tremendousamount of patience from the prescribing clinician

since results take a long time to materialize. Likew iseschizophrenic patients and their respective families and/

or caregivers need to have the necessary patience andmo tivation to stay the course.

not exercising regularly and wassmoking 12-15 cigarettes daily. Hewas last employed in 2000 as abus boy, which involved washingdishes and cleaning up, but thisonly lasted a few months. Hisgoals were to eventually get off hismedications, to experience fewerside effects, to live independently,and to work. He also reportedhaving anxiety, difficulty breathing,light sensitivity, a feeling of notbeing grounded, and problems w ithinvoluntary movements. Table 8summarizes the pat ient 's responseto the adjunctive orthomoleculartreatments.

On November 25, 2004, aletter was sent to the patient'spsychiatrist. After reviewing theletter, the psychiatrist discontinuedthe antipsychotic injection, the

risperidone, and the venlafaxine.The patient remained on the samedoses of apobenztropine andclonazepam, but the olanzapinewas increased to 30 mg daily.He was also pres cribe d 50 mg offluvoxamine daily. Overall, theaddition of the orthomoleculartreatments allowed this patient tobe more positive and motivated,to be less anxious, and to exudemore confidence. His auditoryhallucinations disappeared, and

patient was very inconsistent withthe orthomolecular t reatmentsand even did some drugs for afew weeks during the Christmasholidays. He had a significanrelapse that caused a return of hisprevious symptoms, including theconstant auditory hallucinations.

In each visit with me, thpatient expressed a dislike for hisliving situation. He lived in threedifferent residences during the sixmonths of active orthomoleculatreatment . On numerous occasionsI expres sed concern abo ut hiliving situation with each of hispar ents . I explained to his pare ntsthat this treatment would workbest if their son were providedwith a decent place to live, privacysecurity, nd encouragement tfollow through with the treatmentsI recomm ended that the patient livwith one of them for at least threto six m onth s, after w hich, he wouldlikely learn to comply on his ownNeither parent would allow him tolive at their respective places oresidence. I also discussed therelationship between nicotine andvitamin B3, in that smoking red ucethe clinical effectiveness of thvitamin. Unfortunately, the patienwas unwilling to quit smoking



Schizophrenia

despite my encouragement. Asof August 2006, the patient isliving in his fourth group home,is unemployed, smokes at leastone-half a pack of cigarettes daily,

is symptomatic, and is no longeron any of the orthomoleculartreatments that I prescribed.

Case #4

A 17-year-old female presentedto my office in January 2006 with achief complaint of psychosis. Hersymptoms began in February 2005when she refused to go to highschool. She informed her parentsthat she had been the victim of

bullying and harassment from otherstudents. Her parents enrolled her

in an adult learning program sothat she would not need to attendclasses during the day. Then shebegan to isolate herself from herfamily. She even blasted the musicon her portable headset so thatshe would be unable hear anyone.She complained of bad thoughts

and started to hear voices from hermom's purse. She became paranoidthat there were recorders andmonitoring devices documentingher every move. Finally, in June2005, she asked her mother forhelp and was taken to the localhospital for evaluation. Althoughthe diagnosis of schizophrenia wasnever mentioned, she was told thatshe had had a psychotic episode.She was placed on risperidone

and quetiapine, but discontinuedthese medications since they

Table 9. Case 4: Patient's Response to Adjunctive


Consultation Dates

Clinical P resentation

Current Psychiatric

Medications

Orthomolecular

Treatments & Plan

HOD Results

TS normal <30)

PerS normal <3)

PS normal <3)

DS normal <3)


January 7. 2006

Auditory hallucinations,

paranoid ideation, thought

blocking, shaking, and

restlessness.

10 mg of olanzapine and 1

mg of apo-haloperidoldaily.

1,000 mg of niacinamide

three times daily. 1,000mg of vitamin C three

times daily. 2 teaspoons

of liquid fish oil 2,100 mg

of EPA and 1,500 mg of

DHA), and 1,000 meg of

B12 sublingually daily. Shewas given an intramuscular

Injection of 5,000 meg of

B12. following blood serum

B12 and TSH tests. Patient

instructed to take the HODtest.

Not assessed.

Not improved.

March 4, 2006

No change in symptoms.

TSH normal. Serum vitamin

B 1 2 w a s 1 4 5 p m o l / L i n

the possibly B12 deficient

range).

lOmgofo lanzapineand mg

of apo-haloperidol daily.

Niacinamide was

discontinued. Switched to

1,500 mg of niacin three

times daily. Added 2,500 mg

of glycine at bedtime to help

with sleep, 100 mg of B6, 50

mg of zinc, and 240 m g of

Ginkgo biloba extract.

7614105

Not improved.

did not control her symptomHer psychiatrist then prescrib10 mg of ola nz ap ine and 1 nof apo-haloperidol daily. Whshe finally came to my office fa consultation, her medicatiregiment had not changed, bneither had her symptoms. Scontinued to hear voices constanthad difficulty focusing and wworried about being monitorand followed all the time. She hgained about 15 pou nds sinstarting the medications. Tablesummarizes the patient's responto the adjunctive orthomolecult reatments .

One week after the March 4visit, her parents took her off bopsychiatric medications despite m

instructions to the contrary. Frothe second week in March to Aprthe patient's condition continuto decline. spoke to the patiefather and reiterated to him thnot enough time had elapsed sincommencing the orthomolecultreatments. I explained to hithe connection between fooallergies and schizophreniSince the patient had extremsugar cravings and would eat

much sugar as she could possibconsume, we decided to eliminaall sugar from her d iet. A few dalater, I received a telephone caHer father was amazed. Whthe patient was off sugar, she wpractically normal. The momeshe resumed eating sugar, all hpsychotic symptoms returneHowever, the patient was unwillito give up sugar and was unabto apprehend the connectio

between sugar eliminatioand less psychotic symptomEventually, she discontinueall the nutritional treatmenand opted to try clozapine as last resort. As of April 2006, tpatient was started on clozapinand has done reasonably weAlthough she continues to havpsychotic symptoms, the auditohallucinations are much motolerable than before. She is ab

to attend a special high scho



each day and has even tnodifiedher diet to include more fruitsand vegetables. 1 personallyworry about her future, since she

has opted to not resume any of

the adjunctive orthomoleculart rea tments .

The patients cited in the first

two cases continue to do well sinc ethey both have all the componentsfor a successful respo nse to

t reatment: (a) shelter; (b) decency,understan ding, sup port, safety, and

privacy; (c) psychiatric treatment;and (d) orthomolecular t reatment . 'All these components are equallyimportant . If one component is

missing, the chances of successare diminished. In Case 3, the

patient did not have adequateshelter and was not able to receivesupport, safety, and privacy in

the various group homes in whichhe lived. He lacked the guidancefrom one caregiver to ensure thathe remained consistent with his

psychiatric and orthomolecularme dication s. In Case 4, the patientwas not on the orthomolecularapproach for a sufficient pe riodof time. She was also unwilling to

give up refined sugar when I was

actively treating her, even thoughher response to sugar significantlycontributed to her psychosis.Thus, patients who are receivingall of these necessary components(Cases 1 and 2) show moreimprovements than patients who

do not (Cases 3 and 4).

ConclusionAs clinicians we need to offer

restorative care to patients who

suffer with schizophrenia, asevere and often chronic mentalillness. If the information in thisreport is reviewed carefullyand implemented, I believe thatmany schizophrenic patients willimprove substantially and achievea reasonable quality of life. Somemight improve so much that theyachieve clinical remission. Sincenot enough clinicians utilizeorthomolecular treatments with

schizophrenic patients, this author

hopes that many of you will do

so and continue the exceptionaland important work of Dr. AbramHoffer.

AcknowledgementsWritten consent was obta ined fromthe four patients for publication of

this report. The author would like to

thank Dr. Abram Hoffer for reviewingthis report, Mrs. Erynn Marcus for her

thorough editing, and Mr. Robert Sealeyfor his expert editing and sui^jjestions.

Schizophrenia

Notes1. Hofler A. Vitamin B-3 & Schizophrenia

Discovery. Recovery, Controversy KingstonOntario : Quarry Pres s, Inc., 1998;28-76.

2. Hoffer A. Adventures n Psychiatry. The

Scientific Memoirs of Dr. Abram Hoffer, KO

Publishing Inc. Caledon. ON, 2005:50-99.3. Smythies .IR. Endogenous neuroloxln

relevant to schizophrenia. J R Soc Med1996:89:679-680.4. Smythies JR. Oxidative reactions an

schizophrenia: a revlew-d[8cussion.5c/»zop/(Re s 1997:24:357-364.

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Schizophrenia

Smytliles JR. The adrenochrome hypothesisof schizophrenia revisited. Neurotox Res.

6. Hoffer .\. The adrenochrome hypothesis andpsy ch iatr y. yOr;/)omo/Aferf. 1999:14:49-62.Hoffer A, Heatini Scliizophrenia. Toronto.Ontario: CCNM Press Inc. 2()(>4;7-21.

8. Horrnb ii; D. The Madness of Adam and Eve.Lotidrm. England: Corgi Books, 201)l;149-151.9. Hoffer A. Treating chron ic schizop hrenic

pat ients . J Orthomol Med. 2002:17:25-41.10. Goeree R, FarahatI F. Burke N, et ai. The

economic burden of schizophrenia in Canadain 2004. Curr Med Res Opirt. 2005;2]:2017-2028.

Rochnn PA, Stukel TA. Sykora K. e t a l. Atypicalant ipsychotks and Parkinsonism. Arch InternMed 2005:165:1882-1888.Prou.sky JE, Hayinan R, Orlhomolecular andbotanical t reatments to help alleviate theside effects o( alypicai antipsychotic dru^s. JOrihomolMed 200( : 21:17-3;).Hoffer A. Atypical aiiti-psyctiotics crea tedependency disorders . J Orthomol Med

2004:I9:: -iO.Hoffer A. Orlhoniolecuiar psychiatry Intheory and practice. Townsend LeII Doctors

7.

11

12

13

M

15

16

Hoffer A. Of amb ulant sciiizophren ics withvitamin B3and relative hypoglycemic diet. JOrf/jomo/,V/et/i<W9:14:23-27.Miller CL, Llen.os IC. Dulay JR. Weis S.Upreguiatlon of the initiating step of thekynurenine pathway in postmortem anter iorciitgulate cortex (rom individuals withschizophrenia and bipolar d isorder. BrainRes. 2006:1(173-1074:25-37.

17. Hofler A. Mechanism of action ol nicotinicacid and iiicotinamide In the t reatment ofschizophrenia , in iiawitlns D. Pauling L, eds.Orthomolecular Psydiialry. San Francisco, CA:W.H. Freeman And C ompany; 1973:202-262.

18. Hoffer A. Niacin Therapy In Psychiutry.Springfield, Illinois: Charles C Thomas .1962:35-71.

Hoffer A. Chronic sch izophrenic pat ientstreated ten years of more. J Orthomol Med1994:9:7-37,Morrow JD, Parsons WG. Roberts LJ.Release o( markedly increased quanti t iesoi prostaHltindin U2 in vivo in humansfuilowing the administration ot nicotinic acid.Prostaglandins. 1989:38:263-274.

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2L Holfer A. Vitamin B-li and schizophrenia .Townsend Lett Doctors Patients. 2O0l;213:20-23 .

22 . Paterson ET. Vitamin B3 and liver toxicity.Townsend Lett Doctors Patients. 2001:207:23.

23. Mullen CE, Greenspan JK, Mitchell MC.Fulminant hepatic faiiure after ingestion o\sustained-release nicotinic acid. Ann InternMed 1989:111:253.255.

24 . Hoffer A. Vitamin B-3: niacin and its am ide .Townsend Lett Doctors Patients. 1995:147:30-39.

25 . Hoffer A. Oxidation re duc tion and th e brain. JOrthomol Psychiatr 1983:12:292-301.

26 . Brody S. Preut R. Schornmer K, SchurmeyerTH. A randomized controlled trial of highdose ascorbic acid for reduction of bloodpressure , cort isol . and subject ive responsesto psycholoyical stress. Psychopharmacology.CBerl) 2002:159:319.324 .

27. Smythies JR. The role of a sco rba te in brain:Therapeutic implications. J R Soc Medi996:89:24I.

28. Meister A. (JIutattiione, ascorba te, and cellularprotect ion. C ancer Res. l994:54:i969S-1975S.

29 . Baez S. Segura-Aguilar .1, Widerslen M,Johansson A-S. Mannervik B. Glutathionetransferases catalyse the detoxification

o( oxidized metabolites (o-quinones)of catecholaniines and may serve as anantioxidant system preventing degenerativecellular processes. Biochem J. 1997:324:25-28.

31). Pauling L, Robinson AB. Oxiey SS. et al.Results of a loadinfj test of ascorbic acid,niacinamide. and pyridoxine in schizophrenicsubjects and controls . In. eds. Hawkins I),Pauling L. Orlhomolecular Psychiatry. SanFrancisco, CA: W.H. Freeman And Company:1973:18-34.

31. Suboticanec K, Fohiegovic-Smalc V.Korbar M, ol al. Vitamin C sta tus in chronicschizophrenia . BinI Psychiatry. 1990:28:9.'J9-966.

32 . Jackson JA. Riordan HD. Neathery SS. MayerK. Urine pyrroles revisited, J Orthomol Med

2000:15:47-48.33 . PfeiKer C, l.aMola S. Zinc and manganese

In the schizophrenias . J Orthomol Med.1999:14:28-48.

34. Brown JA. Foster HD. Schizophrenia: Anupdate of the selenium deficiency hypothesis.JOrihomolMed 1996:11:211-222.

35 . Foster HD. The biochemical t reatment ofschizophrenia revisited. J Orthomol Med.1999:14:110-112.

36 . Berry T. An alter nati ve e.'<planatlon of thepsych otropic effect of niacin in schizophre nia.J Orthomol Med. 1994;9:58.

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.17, Foster HI). Schizoph renia, thyroid ho rmoand selenium. J Orthomol Med. 2002:17:55

38 . Fenton WS, Hibbelln J. Knable M. Essenfattyacids. lipid membrane abnormalitie.s,the diagnosis and treatment of schizophreBiol Psychiatry 2000:47:8-2 .

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41. Hawkins D, Orthomolecuiar psychiatreatment of schizo phrenia . In. eds. HawD. Pauling L, Orthomolecular Psychiatry. Francisco, CA: W.H. Freeman And Comp1973:631-673.

42 . Neziroglu F. The relationship amthe Hoffer-Osmond Diagnostic Test, Minnesota Multiphaslc Personality inventand Independent clinical diagnoses. J Psydwl. 197.5:31:430-433,

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Orthomolecular Treatment of Schizophrenia