85

ARE NORTH AMERICAN INDIANS BIOCHEMICALLY

MORE SUSCEPTIBLE TO THE EFFECTS OF ALCOHOL?

Lillian E. Dyck

The abusive use of alcohol i s a prob lem experienced by many

different nat ions and thei r respect ive peopl es, and i t is wellI

known t ha t North American Ind i an s are no ex cept ion. The rat e s

of al cohol i s m among s ome Indi an t r i bes are hi gh , especial ly when

compa red to national, state or provincial stat i s ti cs. As a

c on s e quence , an i ncrea s ed incidence of s oc i al , j udi cial and

health p r ob l ems is common ly experi enced b y Ind i an peop l e .

Because of h i gh rates of a lcohol abuse Bnd bec aus e I ndi ans are a

vi s i ble minor ity , t he general public has developed a vivid ,

stereotyped image of a drunken Indian , one whi ch i s racially

defined and s eldom applied to people of European descen t .

The i mage i s one of an Indian male who drinks to such

excesses t hat he l os es contro l and be co mes aggressive - -sexua l ly

and ot herwise . The drunken Indian becomes crazed , may enter

into phys i cal f ights wi t h o t he r Indi ans or Whit es , may t hrow-up ,

defec a t e or ur ina t e in publ i c, and e vent ua l ly pass out in the2

s tree t o r ot he r inappropriat e place. Wha t many pe op le in the

general pub l i c s eem to ignore or be unaware of, howev er, is that

such beha v i our has become associated with Ind i a ns be caus e of

their vis i bil i ty. In White urban areas, Indi an s look different,

a r e a minori ty an d , there fo r e, a re noticed and remembered . A

Caucasian drunk who behaves in t he same wa y wi l l no t be noticed

to the s ame extent because he is not expected to behave in this

manner and because he i s consi de red t o be t he exc ep t i on rather

than the rule . Consequently , we do not ment a l l y tally up t he

numbe r of Caucasian drunks we s ee , but we do note and remember

the dr unken Ind i an s we encounter. Eve n Indians t hemse lves a r e

l i kely to prac tice s uch selec t i ve perception; howeve r , in this

cas e , the under ly i ng reason is no t because t hey expect their k in

to be unruly drunka r ds but be cau s e they fee l a s ens e of shame

NATI VE STUDI ES REV IEW 2, No. 2 ( 1986) , 85-95.

86

and are keenly awar e t ha t such behav i our is what the White

cul t ure expec t s of them. So ever y examp l e of drunken behaviour

by t heir kin is a noteworthy event to them, too . We do no t lump

all of the ' Whi t es ' togethe r and ex pect them to behave the same

way . Nor do we expe c t t he membe r s of the dominant European­

de rived cultures t o be a he terogeneous group f rom 8 s ocio­

economic point of view, and t herefore, s ome of them can behave

quit e poor ly a ccord ing to s ocial no rms . Yet paradoxically, we

expect the members of the Indian culture t o be a homogen eous l ot

who al l ac t the same way .

As soci ated wi th the idea of a typi cal Ind ian drunk is t he

co ncep t that Ind i ans are somehow i nnately pred isposed to the

effec ts of a l cohol. They are beli ev ed to be more sensitive to

the euphorian t e f f ects of alcohol an d to be less able to contro l

t he i r behaviour whi le unde r i ts i nf luence . In essence , Indians

are thought t o hav e a heredi tary biochemi cal predispos i t i on that

accounts f or t hei r hi gh level of dr i nk i ng. The idea of ge ne t i c

pred i s pos i t i on is ment i oned f r equent l y as one of the possib le

fac tors cont r i but i ng to dr i nk ing l eve l s dis played by I ndi an

peop les. Although this expl an a t i on has been dismi ssed as un­

li ke ly by s ome, i t has not been discounted i n · 8 signi fi cant

volume of publ i s hed research on the t op i c. This paper is ad ­

dressed t o s uc h research .

Alcohol i sm is a probl em ex perienc ed wor l d-wide, an d despite

a vast number of s tudi es , no consensus exists as to wha t factors

caus e an i ndi vi dua l to become a problem dri nker or addicted.

Nor does a un i versal defi ni tion of alcohol ism ex i st . The f ac­

t ors whi ch can infl uence drinking behav i our may be divided into

t hree broad ca t egor i es: psychological , physiologica l and socio­

l ogi ca l f actor s. This paper focuses on the physiologi ca l or

biochemical dime nsions .

A plethora of hypotheses as to why people become problem or

abusive drinkers has been proposed . Thes e r ange f rom de fect s

in sugar me t abol i sm t o t he f ormat ion of narcot ic- l i ke compounds

in susceptibl e individuals . However, t wo avenues of approach

seem mos t promising : f i r s t , studies conc e r ned wi t h the role of

studies

setebc-

87

heredity i n the expression of alcoholism, and s econd,

cent er i ng on genetic or racial differences in alcohol

lism.

While i t is difficult to s eparate genetic and environmental

factors when analyzing the aetiology of alcoholism, a number of

studies have concluded that 8 genetic predisposition to3

alcoholism can occur. When chi l dr en of alcoholic parentage are

raised away from the home environment, their frequency of

alcoholism drops compared to those raised in the home

(alcoholic ) environment. Thus, envi r onment a l factors influence

the development of alcoholism. However, in a Danish study, male

adoptees separated from their alcoholic parents were four times

more likely t o become alcoholic than adoptees from non-alcoholic4

parentage. Similar findings were repor t ed in Sweden . There,

adopted-out sons of alcoholic pa r entage were more likely to be

r egi s t er ed i n the record of the Swedish Temperance Board for5

a lcohol i s m than adopted-out sons o f non-alcoholic parents . De-

spite the problems of adoption studi es, such as il legitimacy of

the adopted ch ildren or the possibility of prenatal damage with

alcoholic mothers, other studies have borne out the findings.

Independent studies in Sweden and the United States compar i ng

the rates of alcoholism among monozygotic (genetically identi­

cal, one fertilized egg split to produce twins ) and dizygotic

(non- i dent i cal, two different eggs fertilized t o produce twins )

twins have shown that the monozygotic twins were more likely to

be simi lar wi th r espect t o a measure of al cohol i sm than wer e6

dizygot i c twi ns. Therefor e, deve l opment of alcohol i s m does

appear to hav e a genetic component.

A rel a ted area of r esearch is concerned wi t h racial

d i f fe r ences in alcoho l metabol i sm. In the body, a l cohol is

broken down or metabol i zed by s peci fic enzymes whos e product ion

i s genetically progr ammed. It has been f ound that the pattern

of al cohol met abol i zing enzymes i s dif f e r ent in Orient a l s and7

Caucas i ans; thus, these t wo races ar e genet i cally divergent

with respect t o these enzymes. Interestingly , t hese enzyme

di ffer ences have been deemed res pons i b l e for t he increased

88

susceptibility of the Japanese to the dysphoric or unpleasant

effects of alcohol. Similarly, more recent studies have

suggested that because the North American Indians may be derived

from t he same gene pool as the Japanese and other Oriental

races, they too should have a greater sensitivity to the

dysphoric effects of alcohol. Sensitivity to these effects

(measured by facial flushing ) was absent in a sample of

Tarahumara Indians from New Mexico, but was present in a large8

percentage of Eastern Cree Algonkian Indians. An individual

who is susceptible to the dysphoric effects of alcohol may

appear to be unable "to hold his/her liquor" and thus might be

thought to be at risk in terms of becoming a problem drinker or

an alcoholic. However, quite the opposite phenomenon has been

observed. It was clearly demonstrated that those Japanese who

are sensitive to the dysphoric effects of alcohol do not become9

alcoholics.

In studies comparing Orientals and Caucasians. it has been

found that alcohol intake caus es significant physical discomfort

for about half of the Oriental subjects. but very little or no

discomfort in most Caucasians. Such discomfort following

alcohol intake acts as a deterrent to further alcohol intake and

ultimately inhibits the development of alcoholism. This

discomfort is characterized by marked facial flushing,

dizziness, increased heart rate and decreased blood pressure.

These effects are due to an accumulation of acetaldehyde . In

ninety to ninety-five per cent of the European population and in

about half of the Japanese population. little or no acetaldehyde

accumulates in the body because it is readily broken down or

effectively eliminated. In contrast. in those individuals who

experience an adverse physical reaction to alcohol intake ( i . e . ,

in about half of the Japanese population and five to ten per­

cent of the European populations ), acetaldehyde does accumulate

in the body.

The metabolism of alcohol in the body is catalysed by a

number of enzymes acting sequentially ( see Figure 1) . Alcohol

metabolism occurs mainly in the liver. The conversion of

B9

FIGURE I

SIMPLIFIED SCHEME OF ALCOHOL METABOLISM

Ethyl Alcohol

jAlcohol Dehydrogenases

a ) typical ADR's

b) atypical ADH's*

(ADH' s)

it was thought that the presence of an atypical ADHseveral types ) caused an accumulation of

by increasing the rate of conversion of alcohol to

Acetaldehyde

[

Acet a l dehyde dehydrogenases CALOR' s)

a ) type I ALDH**

b ) type II ALDH

Acetatet Many enzymes

CO + H 02 2

Acetaldehyde ac cumulation causes dysphoric effects in humans.

*At one time( t he r e areacetaldehydeacetaldehyde.

**Now it has been found that type I ALDH is inactive, orfunctionally absent, in individuals who have an adverse flushingresponse after alcohol intake . Acetaldehyde accumulates inthese individuals because its degradation to acetate has beensignificantly retarded by the absence of type I ALDH.

It was

individuals

90

alcohol to acetaldehyde is catalyzed by alcohol dehydrogenase

(ADR). This enzyme exists in 8 number of physically distinct

forms, or isoenzymes, which vary in their ability to ca t al yse

the conversion of alcohol to acetaldehyde. The ADH isoenzymes

are the major enzymes involved in the first stage of alcohol

metabolism. Two other enzymes, catalase and the mitochondrial

ethanol oxidizing system (MHOS ), can also catalyse the conver­

sion of alcohol to acetaldehyde, but they account for only a

small percentage of alcohol metabolism. The metabolism of

acetaldehyde to form acetate is catalysed by ALDH isoenzymes .

Types I and II are the major ALDH t soenevaes , and under normal

circumstances, type I ALDM is responsible for converting most of

the acetaldehyde to acetate. Under the influence of many other

enzymes, acetate is eventually converted to carbon dioxide and

water.

initially thought that acetaldehyde accumulation in

who flushed after alcohol intake was due to the10

presence of an atypical alcohol dehydrogenase, which would

increase the rate of conversion of alcohol to acetaldehyde (s ee

Figure 1). It is now known, however, that acetaldehyde accumu­

lates in these individuals because the type I acetaldehyde

dehydrogenase which metabolizes, or gets rid of most of the11

acetaldehyde, is inactive or deficient in these individuals.

So, in most Europeans and in non-flushing Orientals, alcohol is

metabolized to produce acetaldehyde, which in turn is metabo­

lized mainly by type I acetaldehyde dehydrogenase. The type II

enzyme is present, but the properties of these enzymes are such

that t he type I rather than the type I I enzyme, degrades most of

the acetaldehyde produced from alcohol . In those individuals

who flush adversely after alcohol intake. the type I enzyme is

inactive . If the inactivity or functional absence of type I

enzyme acts as a deterrent to alcohol intake, one would not

expect this enzyme t o be absent in alcoholics . This is precise-12

Iy what has been found. This enzyme was absent in only three

out of 150 Japanese alcoholics. This contrasts significantly

from a control sample of the Japanese population in which the

91

enzyme would be absent in about 75 of 150 subjects . Therefore,

it appears that those Japanese with a type I enzyme deficiency

are protected from becoming a lcoholic because of the dysphoric

effects that alcohol causes in them . Having said this, however,

one must keep i n mind that the i ncidence of a lcoholism in Japan,

which traditionally has had verr310w rates of alcoholism, has

risen over the last forty years. Apparently other factors can

override this genetic deterrent to alcohol intake .

These enzyme s tudi es are pertinent t o t he present

discussion because such enzyme alterations have been found to be

conf i ned to populations of Mongoloid origin. Since it is

thought that North American Indians are also of Mongol oi d

origin, one might expect them to exhibit a s imi l a r enzyme

pattern . However, the rates of alcoholism amongst many Indian

peoples are high, rather than low, as in Japan. So far only two

reports have appeared concerning the types of acetaldehyde14

dehydrogenase present in Indians. In a sample of forty-six

northern New Mexico Indians, type I enzyme activity was found in

all forty-six ; that is, the enzyme pattern was equivalent to

what has been found in most Caucasians. Consistent with this

enzyme pattern, no adverse effects, such as flushing, were

observed. Similarly , in a study of sixty-three full blood

Indians from Oklahoma, only sixteen percent were found to be

deficient in type I enzyme, and were seen to drink less than

those Indians who had the enzyme, though they drank more than

the Caucasian subjects. Overall then, from these two studies one

can conclude that most of the Indian peoples studied so far

metabolize alcohol in the same fashion as most Caucasians rather

than like the portion of Oriental races who are sensitive to the

adverse effects of alcohol, and hence, rarely become alcoholic .

The idea that North American Indians are more susceptible

to the effects of alcohol may have arisen from some of the early

work compa r i ng rates of alcohol metabolism in Caucasians and in

Indians. While one study showed a slower rate of alcohol

metabolism in Eskimo and Indian males compared to White males,

all subsequent studies reported either no differences or an

92

15increased rate of alcohol metabolism in the Indian subjects.

Thus, it seems highly unlikely that the presumed susceptibility

of Indians to the inebriating effects of alcohol is due to their

diminished ability to metabolize or get rid of alcohol.

Many factors make it difficult to compare rates of alcohol16

metabolism between individuals of the same or different races.

In some of these studies, differences in body weight, body

composition and previous drinking history were not taken into

account. Because there are a number of different types of

alcohol and acetaldehyde metabolizing enzymes and because their

degree of expression varies from one person to the next, widely

different rates of alcohol metabolism are observed between

individuals. Moreover, while moderate alcohol intake can

induce, or stimulate, the formation of other alcohol

metabolizing enzymes, chronic abusive alcohol intake can have

the opposite effect. In addition, the Dutritional status of the

individual plays an important role. Some of the acetaldehyde

metabolizing enzymes are lost after periods of poor nutrition,

but can be regained with the resumption of proper nutrition .

Thus, measurements of the rate of alcohol metabolism are subject

to many variables whose presence or absence may artifactually

cause differences in alcohol metabolism compared to a so-called

control group.

If it does turn out that some Indian peoples have a genetic

aversion to becoming alcoholic, as does a large percentage of

the Japanese race, and if the rates of alcoholism are higher

amongst such Indians than in the Caucasian population, then one

could speculate that these Indians are over-exposed to other

factors which lead to alcoholism. Though a particular group of

Indians may be resistant to developing alcoholism, perhaps they

can still become alcoholic because of the presence of unusually

high levels of environmental stress.

Overall, with respect to physiological or biochemical

factors that contribute to the development of alcoholism, it can

be concluded that genetic factors do play a role as evidenced by

the adoption studies and by the alcohol metabolizing enzyme

studies. The former studies have revealed an undefined genetic

93

predispos i t i on , whi l e the lat t er have r eveal ed a well -def ined

genetic aversion . While we know that an aversion is expressed

primarily in peopl e of Mongoloid origin , we do not know whethe r

a predisposition also occurs in t hese people because t he adop­

t i on studies whi ch r eveal ed t his tendency were done in Europe .

The biochemical studies repor ted so far do QQ1 s upport any

presumed susceptibility of North American Indians to the aver­

si ve ef fects of al cohol t ha t can be attributed to di f ferences in

their metabolism of this drug compared to t ha t of Caucasians.

The development of al coholism is probably polygenic and

infl uenced by many other interact ing fac t ors. By using a

simplisti c approach , we can continue t o find single factors that

vary f r om one culture to anot her and t ha t appear to explain

differing abuse rates, but these fac t ors are not universally

signifi cant. Such approaches tend to emphasize t he di fferences

be tween cultur es , whil e it may be that t he similarities are more

important . Perhaps we are uncons c i ous l y attempting to find a

psychologica l or physiological defi ciency in the alcoholic

( I nd i an and non-Indian ) so that we as a society do not have t o

accept responsibil i ty for the problem. The alcoholic is forced

to accept a l l of the b l ame . Similarly, from a c r os s -cul t ur a l

perspective, perhaps we are saying that cul t ural factors

i nhe r ent in Indi an s ociety are t o blame . This approach is

irrational because it ignores t he fact that alcohol problems are

not confi ned t o In dian s ociety. It i s time we accepted the fac t

t ha t people of al l races and cu l t ures are more l ikely to be come

problem dr inkers or alcoholics when t hey live in condit i ons of

s ocial depri vat i on and ex treme pover ty.

NOTES

1Hugo SoIms , "Al coholism In Europe, tI Annals New York

Academy of Sc iences , 273 ( 1976) 25- 32; Thomas S:-welsner~ J oanC: --Wei be I - Or-liiilooand John Long t "Serious Dri nking , Whit e Man' sDrinking and Tee totalling: Dr1nkin~ Levels and St y l es in anUr ban American Indian Population Journal of Studies onAlcohol, 39 , No.7 ( 1978) , 1166- 1177; -Heport by-reoeration ofSasKatcn ewan In di ans , Alcohol and Drug Abuse Among Treat~I ndi ans in Sas katchewan :-- Neeas Assessmen{ ana- - Recommendat l ons!Qr-QQ~g~ fRegina:- rSIN, I983}.---------- --- ------------- - -

Genetic Aspects of Alcohol ism endQ~eral e~lch.!!!!!:X, 35 (1978 ), 269-

322.

94

2Hugh Brody, Indians on Skid Row (Ot t awa: Information

Canada, 1971)t pp. 35=~I;-8nd-Rea£6er-R65ertson~ReservBt ions aref~r lnQ!~! ( aronta: James Lorimer and Co., 19-,OJ~-pp:-270=2~7

3Albert L. Lehninger, Vi ctor A. McKusick and Patr i cia B.

Santora , "Proceedin~s of the Conference on Genetic an dBi och emIcal Variabil~ty in Response to Al cohol

1" Alcoholism:

Clinical and Experimental Research , 5, No. 3 ( 981J-i-~39=~~I;J-:-n-:-- -Sauiioers-aiia-Roger-WIlliams:-;- "The Geneti cs of A coho I i sm:Is there an inherited sus~ectibility to alcohol-relatedproblems?," Alcohol and Alcohohsm

L18 , No .3 (1983 ),. 189-217 ;

and Stephen B:--TfiacKer,-~cnara- . Veech, Andrew A. vernon andDevid D. Rwtst e i p, "Genetic B1)d Bi ochemi cal Factors Relevant to~~~O~Oli9W4),~§75Q3A~~~l g!ln!£~l ~4 ¥~p~r!~~n!~! B~~~~r£h, 8,

4D.W. Goodwin. et. a l . "Al coho l Problems in Adoptees

Ra ised Apart f ro m Alconolic-S,i ological Parents." ~!:£hiY~~ QfQ~ner!!l r~l£h.!!!!rxJ 28 (1973 ) , 238- 243 .

5M. Bohman. "Some

Criminality, II Archi ves of276 . -------- --

6See L. Ka ij, Alcoholism in Twins : Studies on the Etiology

end Seguelae of A6use -of--XlcohoI--TStocKnolm: --Almguisr--anaWiRseII,--I960 ) ; - aiia-z:- - Hr u6ec- aiia G. S. Omenn, "EvIdence ofGenet i c Predisposi ti on t o Alcoholi c Cirrhosis and Psychosis :Twin Concordance f or Alcoholi sm and its Bi ologi cal End Poi nt sby Zygosity Among Male Veterans

6" Alcoholism: Clini cal and

~~p~rl~ent~l E~§~§!:gh, 5 (1981) , 2 7-215:--------- --- ----- ---

7Ti ng- Ka i Li , William F. Bosron. Werner P. Dafeldeck er

Louis G. Lange , and Bert L. Vall ee, "Isolation of II-alcoho1dehydrogenase of human liver : Is it a de t e rmi nant ofa l coholIsm? It Proceedings of the National Academ.r o f Science(U. S. A.) , ~4, NO~-10-11977 )~-4378-~381T-El.~-Goeade, -S. Elaraaa

A­

and D. P. Agarwal, "Racial fhfferences In Alcohol Sensi ti vi ty:New Hypothesis " Human Genetics, 51 (1979) , 331-334· Dharam P.Agano;s li. Shoji Haraaa:;-aiiir~werner Goedde} "Rac ial Differ encesin Bio ogical Sensit i vi t y t o Et hano l: The Rol e of Al coholDe~y~rogenase and Aldehyde Dehydrogenase Isozymes," Al£Qhol.!sm~Cl InIca l and Ex~rimental Research. 5, No . 1 ( 1981J , l2-1E jJean=Plerre-voi}-War"t15u?g-8nlrRolrBuhler, "Biology of Disease,Alcoholism and Aldehydism : New Biomedical co ncepts t" Laborator~Inves tigation) 50 1 No. 1 ( 1984 ) , 5-15; Kazuyos h i noue~~ana5uFiiKWiaga- -T8..k:ayuJn Kiriyama and Set s uo Komur a, "Accumul ation ofAce tal dehyde in Alcohol-Sensit ive Ja~anese : Rel ation t o Ethano land Acetaldehyde Oxid i zing Capaci ty Alcoh olism: Clinical andEXEerimental Research. 8. No. 3 ( 1984) ~-319=322T-S . -H8raaa~ D:-P:­Agarwal~---H.W:----Goedde s. T~aki B. IshIkawa. "PossibleProtec tI ve Role A~ainst AlcoholIsm tor Aldehyde DehydrogenaseI sozyme Defic i ency I n J apan." The Lance t, October 9. 1982, p.827 . - - - --- - --

8Pet e r H. Wolff "Vasomotor Sensitivity to Alcohol in

Divers e Mongoloid Populations , " ~~rican JQ!!rn!!'! Qf Q~net.i£,§ . 25( 1973) , 193-199

1. Arthur R. Zeiner . AlfOnso Paredes ana-Lawrence

Cowden, "Phys io ogic Responses to Et hano l Among t he TarahumaraIndians . " Annal s of t he New Yor k Academl':' of Sciences, 273 (l976 )151-158. ---- -- - - --- - - - - - -- --- - - - -- --- ---- -

9von Wartburg and Buhler. pp. 5-15 ; Inoue , ~i al .• pp. 319-

95

tovon Wartburg and Buhler, pp. 5-15 ; Bennion and Li, pp .

9-13.

11von Wartburg and Buhl er , pp. 5-15; In oue et al. , pp. 319­

322; Goedde, pp . 331-134; Agarwa l ~! ~l., pp . 12=I6~

12Harada, et ~!.. p. 827.

13See

~!!fl.!~ o fP . Ratan akorm , "As i a an d Problems of Al c oh o lism , "

!h~ ~~~ YQK~ ~~flde~~ Qf §g ien£g§ , 273 (1976) , 33-38 .14

D.K. Rex, W.F. Bosr on, J .E. Smia l ek and T.R. Li, "Alcoholand Aldehyde Dehydrogenase Isoenzymes in a North American IndianPopulation, II Al cQhQl ! s J!l£ Q! i Q!£8! ~d . ~~Eet: il1!~n t!i!l . Be~e~!:£h, 9( 1985) ~ 147-152 ; A.H. Ze~ner , J .M. G1rarQof, ~ N1cfioI s and D..Ione e- Saunt .y " ALDH I Isozyme Defi ci en cy among Nor t h Ame r icanI nd i ans , " Al coholi s m: Clin ical an d Ex~erimental Res ea r ch , 8(1984) , p. 129~------- ---- - --- --- -- --- - - ---- - - - - - - - -

15D. Feens L. Mi x , O. Schaef er , J . A.L. Gi l bert "Et hanol

Met abo lis m i n ~arious Racial Groups I" Canadian Medi cal Assoc i a­t i on J ournal

t105 ( 1971) . 472-475 ; WoII~-pp~ I93=I99; -lynn-J~Bennion-an-a- ing Kal Li , Alcohol Metabolism 1n American Indi an s

and Whites, It New England Journal of Medicine 294 No . I (197 6 ) I

9-13; T. Edwar~Reea~-Harola-Kalant~-Ro5ert J. bibbins, BushanM. Kapur, James G. Rankin, "Alcohol and Acet aldehyde Met ab olismin c auces t ans , Chinese and Amerinds, " Canadian Medical Associa­t ion J ournal, 115 ( 1976) . 851-885 ; John-J~-rarris-anarBen-HOrganJones-;-- "'EUianol Metabohsm in Male American Indians and Whites"Alcohol ism: Clinical and Experimental Research , 2 , No. 1 ( 1978 \ ,77=B1;--Zeine~--AITonso Pareaes~--ana-Lawrence Cowden, pp. 151­158.

16T.M. Brod, "Alcholism as a Ment al Heal th Problem of Nat i ve

Americans6" Arch i ves of General Psychiatry/ 32 (1975) ). 1385­1391 ; K.. tinaros~ "Human-Blooa-Acetalaenyde Levels : with Im­proved Methods . a Clearer Pi cture Emerges),," Al coholism: Clinicaland Expe r imental Research, 6 ~ 1982 ) , 70-·/ 5 ;-R:F~-Tlpton-;--G~T~HeneliBn-ana-J~~~ -~CCroaaen , ' Metabolic and Nut ri tional Aspect sof the Eff ec ts of Ethano l ," Bio chem i ca l Soc iety Transactions, 11( 1983) , 59-61. - ------- --- ----- - ------- - - - - -