IN REVIEW

Epidemiology of Schizophrenia
1 2
Heinz Häfner , Wolfram an der Heiden

Objective: To characterize the epidemiology of schizophrenia.

Method: Narrative literature review.
Results: Each year 1 in 10 000 adults (12 to 60 years of age) develops schizophrenia. Based on a restrictive and precise
definition of the diagnosis and using standardized assessment methods and large, representative populations, the
incidence rates appear stable across countries and cultures and over time, at least for the last 50 years. Schizophrenic
patients are not born into ecological and social disadvantage. The uneven distribution of prevalence rates is a result of
social selection: an early onset leads to social stagnation, a late onset to descent from a higher social status. The main
age range of risk for schizophrenia is 20 to 35 years. It is still unclear whether schizophrenia-like late-onset psychoses
(for example, late paraphrenia) after age 60 should be classified as schizophrenia either psychopathologically or
etiologically.
In 75% of cases, first admission is preceded by a prodromal phase with a mean length of 5 years and a psychotic prephase
of one year’s duration. On average, women fall ill 3 to 4 years later than men and show a second peak of onset around
menopause. Consequently, late-onset schizophrenias are more frequent and more severe in women than in men. The sex
difference in age of onset is smaller in cases with a high genetic load and greater in cases with a low genetic load. Type
of onset and core symptoms do not differ between the sexes. The most pronounced sex difference is the socially negative
illness behaviour of young men.
Conclusions: Among the factors determining social course and outcome are level of social development at onset, the
disorder itself (for example, genetic liability, severity of symptoms, and functional deficits), general biological factors
(for example, estrogen), and sex- and age-specific illness behaviour.

(Can J Psychiatry 1997;42:139–151)

Key Words: schizophrenia, epidemiology, incidence, prevalence, ecology, symptomatology, age at onset, gender
differences

O ne hundred years of research efforts have failed to pro-

duce biological indicators specific to a diagnosis of
schizophrenia. Studies on schizophrenia morbidity, therefore,
continue to rely on descriptive case definitions, and the qual-
ity of their results depends on the diagnostic definitions used.
In a historical analysis, Dohrenwend (1) distinguished 3
periods of epidemiological studies in psychiatry. According
to his methodological standards, only the last period, begin-
ning around 1980, has produced valid and transnationally
1
Director, Schizophrenia Research Unit, Central Institute of Mental Health,
Mannheim, Germany.
2
Senior Scientist, Schizophrenia Research Unit, Central Institute of Mental
Health, Mannheim, Germany.
Address for correspondence: Dr H Häfner, Durchwahl 17 03-726, J 5,
Mannheim 68159 Germany
Can J Psychiatry, Vol 42, March 1997
139
comparable findings. The standards include a precise, opera-
tional case definition, the collection of comprehensive data
on all “cases” from a sufficiently large, statistically well-
documented population, symptom assessment by transcul-
turally standardized instruments, and computerized diagnosis
independent of the interviewer. The World Health Organiza-
tion (WHO) “Determinants of Outcome” study (2) was the
first to satisfy nearly all of these requirements at each study
site in the determination of the incidence of schizophrenia (12
centres, 10 countries). Recently, Thornicroft and Johnson (3)
have added a further methodological standard that calls for
the assessment of met and unmet needs for care in psychiatric
surveys.
Ecological Epidemiology
With their ecological Chicago study, Faris and Dunham
(4) began an important chapter in the epidemiology of schizo-
phrenia. The authors found the highest first-admission rates
140 The Canadian Journal of Psychiatry
for schizophrenia in the inner city, characterized by social
disintegration and low-standard housing. The lowest inci-
dence was on the outskirts of the city, in high-standard
residential areas. In the wake of their study, similar zonal
distribution patterns were reported from several American
cities, but also from Oslo, Norway (5), Nottingham, United
Kingdom (6), and Mannheim, Germany (7). In Mannheim,
the incidence of schizophrenia was reassessed 10 to 15 years
(8) and 22 to 23 years (9) later. Parallelling the city’s stable
socioecological structure, the ecological distribution pattern
of first-admission rates for schizophrenia proved stable.
Besides the uneven ecological distribution of the rates,
individuals with schizophrenia at first admission are usually
found to be personally and socially disadvantaged as well.
Dohrenwend and Dohrenwend (10) found the highest rates in
the lowest social class in 5 out of 7 first-admission studies,
and Eaton (11) found the same in 15 out of 17 studies. In a
later metaanalysis of studies on the topic, Eaton and others
(12) calculated a ratio of 3 to 1 for the risk of schizophrenia
between the lowest and the highest of 3 social classes.
Social Drift versus Social Causation
Although time and cause were unclear, the social gradient
provided the impetus for a causal link between severe social
disadvantage and schizophrenia onset (10,13,14). The social-
drift hypothesis—social decline after illness onset—merely
explained the uneven social distribution of prevalence rates.
Since first admission or first contact, at that time, was taken
as the operational definition of the onset of the disorder, any
social consequences of the emerging disorder were not
considered.
Retrospectively studying individual ecological mobility
before first admission, Dauncey and others (15) found that the
ecological disadvantage observed in schizophrenic patients
at first admission had emerged, on average, 5 years before.
The ecological selection is brought about by a tendency of
individuals later admitted with a diagnosis of schizophrenia
to remain during the premorbid period in decaying housing
areas, while their healthy and socially more successful peers
move on from these areas into better neighbourhoods. Similar
conclusions were drawn by Wiersma and others (16) using
Dutch data.
On the basis of the national Norwegian case register,
Ödegaard (17) early pointed out that people with schizophre-
nia tend to cluster in rapid-turnover and low-status jobs prior
to their first admission. He implicated premorbid schizoid
personality traits in the explanation.
It seems that at least a part of the social disadvantage
involved in schizophrenia emerges before first admission.
The question of it already being present in the patients’
parents was investigated by Goldberg and Morrison (18) in a
methodologically sound intergenerational study in London.
They demonstrated, for schizophrenic men, that the lack of
upward social mobility emerges after birth. In another study,
conducted by Turner and Wagenfeld (19) in New York, the
fathers of schizophrenic men showed slightly lower social
statuses compared with controls, but this result is probably
Vol 42, No 2
attributable to the selection of a socially disadvantaged study
population, that is, first admissions to state mental hospitals.
Meanwhile, 3 large studies of birth cohorts from Great Britain
(20,21) and Northern Finland (22) followed into the age of
risk for schizophrenia have demonstrated that schizophrenic
patients are not socially disadvantaged at birth.
Dohrenwend and others (23) tested the alternative hy-
pothesis of social causation versus social selection in a metho-
dologically sophisticated study in Israel. They found
compelling evidence for the social selection hypothesis in
schizophrenia, in contrast to the risk for major depressive
disorder in women or substance abuse in men.
Hence social causation does not appear to play an essential
etiological role in schizophrenia, as is also indicated by the
fairly similar morbidity risk in all the populations investigated
(2).
Prevalence
Prevalence is a product of incidence and length of illness.
Length of illness is determined by various factors, for exam-
ple, variation in the life expectancies of the populations
studied, excess mortality after disease onset, and varying
proportions of symptom-free cases due to differences in treat-
ment, so that comparisons of prevalence rates across studies
are difficult. Prevalence rates are primarily used as an indica-
tor of the morbidity of a given population and its need for
care.
Table 1 lists selected prevalence studies of schizophrenia
and their results according to the following criteria: 1) studies
published in 1980 or later, 2) population studies or suffi-
ciently representative utilization studies (for example, case
registers).
For the reasons stated above, the marked variation in the
total rates cannot be interpreted as reflecting differences in
the morbidity of the populations under study. The point versus
period prevalence rates differ only minutely which, as pointed
out by Eaton and others (24), is accounted for by the primarily
chronic course of the illness involving only slight annual
excess mortality.
The dependence of the study results on the diagnostic
definition is reflected in the fact that only 30% of a repre-
sentative sample of first-admission cases (N = 276) assigned
to a broad clinical diagnosis of schizophrenia according to
ICD-9 (295, 297, 298.3/4) (the ABC schizophrenia study
sample) qualified for a DSM-III diagnosis of schizophrenia
(25). The lifetime prevalence rate of 1.5% reported from the
Epidemiologic Catchment Area study (26) is probably too
high. A possible reason is that the assessments were
conducted by lay persons using instruments of low
discriminative power (27). The most precise estimates of the
lifetime risk so far, though only up to the fifth decade of life,
have been reported from the British birth cohort study (28).
The directly assessed cumulative prevalence until age 43 was
0.63. Assuming that the share of late-onset schizophrenias in
the total schizophrenic morbidity is fairly low (15%), this
figure presumably represents a fairly close estimate of the true
March 1997 Epidemiology of Schizophrenia 141

Table 1. The prevalence of schizophreniaa

Prevalence per 1000
Authors Country Period population Age correction
Babigian (98) USA 1 year 4.1 Yes
Bamrah and others (99) UK 1 year 7.5 No
Bebbington and others (100) UK Point 10.9 Yes
Ben-Tovim and Cushnie (101) Botswana 1 year 5.3 No
Bland and others (102) Canada Lifetime 0.3 No
Blazer and others (103) USA 6 months 6.0 to 11.0 No
Burnam and others (104) USA 6 months 3.0 to 6.0 No
Canino and others (105) Puerto Rico 6 months 15.0 No
Cheung (106) China 1 year 1.9 to 4.7 Yes
Dilling and Weyerer (107) Germany Point 3.9 No
Folnegovic and Folnegovic-Smalc (108) Croatia 3 months 1.5 to 5.1 No
Freeman and Alpert (109) UK 1 year 6.8 No
Halldin (110) Sweden 1 year 6.0 No
Hodiamont and others (111) Netherlands Point 7.3 Yes
Hwu and others (112) Taiwan Lifetime 3.1 No
Lee and others (25,113) Korea Lifetime 3.1 to 5.4 No
Lehtinen and others (114,115) Finland Point 1.3 No
Lin and others (116) China Point 4.2 Yes
Mavreas and Bebbington (117) UK Point 13.0 No
Murphy and Taumoepeau (118) Tonga 1 year 0.9 to 1.3 No
Myers and others (119) USA 6 months 6.0 to 11.0 No
Nandi and others (120) India Point 2.2 Yes
Shen and others (121,122) China Point 1.8 Yes
Sikanerty and Eaton (123) Ghana Point 1.1 No
Temkov (124) Bulgaria Point 2.8 Yes
Vasquez-Barquero (125) Spain Point 5.6 No
Walsh (126) Ireland Point 9.8 No
Weissman and Myers (127) USA Point 4.0 No
Widerlöv and others (128) Sweden Lifetime 0.7 to 5.0 No
Zimmerman-Tansella and others (129) Italy 1 year 1.3 No

a
Abridged version of a compilation by Warner and de Girolamo (36), supplemented by own review of literature.

cumulative lifetime prevalence as based on the ICD-9
diagnosis 295.
The prevalence rates for old age probably need to be
adjusted. It is still unclear how many of the delusional disor-
ders of the old and the very old can be subsumed under the
diagnosis of schizophrenia and, thus, be considered part of
the prevalence and incidence of schizophrenia in these age
groups (29). The reason is that attempts at a precise empirical
distinction at the psychopathological level have failed.
Incidence
As stated, incidence rates are the key indicator of morbid-
ity risk. Their distribution patterns across geographic, cultural
and social units, family membership, age, and sex also
provide some external criteria for testing the validity of a
diagnosis (30) and for formulating etiological and pathoge-
netic hypotheses.
Since the onset of schizophrenia is a comparatively rare
event, the accurate assessment of incidence figures is faced
with considerable practical and methodological problems.
This is especially the case when age distributions are studied
or risks for certain age groups are estimated. To ensure
accuracy, the following preconditions should be fulfilled: 1)
the population at risk must be sufficiently large, geographi-
cally stable, and statistically well documented to provide
exact data on age, sex, and social status for the denominator
in the calculation; 2) the study sample must be representative,
that is, comprise all the cases fulfilling the diagnostic criteria
during the study period; 3) the study sample must be large
enough to cover the whole age-of-risk range for schizophre-
nia; 4) the cases should be entered in the study as soon after
onset as possible in order to keep recall deficits, postonset
deaths, and other distorting effects to a minimum; 5) onset
must be defined and its occurrence determined precisely. The
common administrative definition of onset, first admission to
hospital or first psychiatric contact, is flawed by uncertainty
about the duration of the time period of illness preceding that
event. The more precise, but still artificial, definition of a
“diagnostic onset” (the time point when a set of diagnostic
142 The Canadian Journal of Psychiatry
criteria is fulfilled for the first time), proposed by Pogue-Geile
(unpublished observation), is an acceptable basis for rough
estimates of the incidence. If, however, the intention is to
determine the time point or age of onset precisely, both the
prodromal phase and the development of illness before the
diagnostic criteria are met must be taken into account.
An ideal approach to studying incidence would be a pro-
spective birth cohort design with cross-sectional assessments
at short intervals. A prospective birth cohort design is adopted
in studies of the offspring of schizophrenic mothers, but for
cost reasons, the cross-sectional assessments are carried out
at lengthy intervals. Moreover, the incidence rates calculated
for these high-risk groups do not provide any information on
incidence in the population at large. Birth cohorts of general
populations were studied retrospectively by Fremming (31)
in Denmark and for over 70 years by Helgason (32) in Iceland,
but the number of 34 or 36 cases of schizophrenia is too low
for calculating age-specific risks. The British birth cohort
study (28) provided population-based first-admission rates
for schizophrenia until age 43 years, but did not produce data
on the age distribution of onset.
Only in a minority of cases is the onset of schizophrenia
marked by conspicuous symptoms. In three-quarters of the
cases, the first psychotic episode is preceded by a prodromal
phase of several years’ duration, during which nonspecific
symptoms predominate. The psychotic prephase, too, fre-
quently evolves unnoticed by others, at least for some time
(33). This means that schizophrenia is currently diagnosable
only after it has started to produce psychotic symptoms and
is perceived by the patient himself or herself or by others. Its
onset and all associated variables, such as age distribution of
the morbidity risk, must therefore be determined retrospec-
tively by suitable methods.
The problems involved and possible solutions have been
discussed by Maurer and Häfner (34) in the context of the
standardized interview developed to address them: Instru-
ment for the Retrospective Assessment of the Onset of
Schizophrenia (IRAOS) (35). The interview was designed to
produce data on prodromal signs, symptoms, functional im-
pairment, social disability, and objective social development
from 3 sources and on the basis of a time matrix, which
enables accurate timing by means of anchor events.
Population studies are impractical because of the low
morbidity risk. A 2-stage design should be used, therefore,
that is, one which identifies all incidence cases of nonaffec-
tive psychosis from all the clinical records of a large, defined
population over the course of one or 2 years. For this method
to be accurate, however, the lifetime likelihood of schizo-
phrenic patients coming into contact with the mental health
services of the catchment area must be close to 100%. This
percentage, depending on the availability and cost of mental
health services, is bound to decline with time because of the
growing proportion of patients with schizophrenia treated by
general practitioners. An additional search for incidence
cases not in contact with mental health services can improve
Vol 42, No 2
epidemiological validity, especially in developing
countries (2).
At the second stage, standardized interviews are adminis-
tered to the index population obtained through the initial
screening. The operational accuracy of the diagnosis and all
the other design variables ensured, onset is then assessed
retrospectively.
Comparative Epidemiology
Table 2 is based on a review by Warner and de Girolamo
(36) but restricted to studies published after 1980. Rates
calculated with populations not corrected for age are so
indicated. The incidence rates range from a minimum of 0.07
to a maximum of 7.1. Tempting though it would be to explain
these differences as secondary to regional heterogeneity of
environmental or genetic factors, the studies should first be
compared for their methodological standards.
In the WHO “Determinants of Outcome” study (2), all
patients were assessed for psychopathology with a semistruc-
tured interview, the Present State Examination (PSE) (37).
The PSE is supplemented by a computer algorithm, known as
CATEGO, that can be used at several levels of classification.
The patients are allocated to 1 of 9 descriptive CATEGO
classes, depending on the prevailing symptomatology as, for
example, S+, representing central schizophrenic conditions
(thought intrusion and delusions of control), P (paranoid
symptomatology), or O (other psychoses).
The results from 7 countries are illustrated by data for 8
study sites, depicted in Figure 1 in sections II and III. For
comparison, section I gives the rates from 8 selected national
studies. The transnational variability of the incidence rates
decreases as the stringency of studies increases. The national
studies show the greatest variation in methodology, for exam-
ple, diagnostic definitions and case findings. In the interme-
diate section, annual incidence rates for a broadly defined
diagnosis of schizophrenia (ICD 295 or CATEGO S, P, and
O), based on the same sample as in section III, show less but
still considerable variation, whereas in section III, based on a
restrictive and highly reliable diagnosis of nuclear schizo-
phrenia (CATEGO S), no significant differences can be seen,
the annual rates varying around 10/100 000.
Incidence rates of the same size in all populations and
cultures studied render a substantial role of cultural, social,
or climatic factors in the morbidity risk for schizophrenia
inconceivable.
Zubin (38) tried to explain this unusual epidemiological
pattern by assuming that schizophrenia is the common final
pathway arising from a great number of causes. Another
common disorder with an almost identical age-corrected in-
cidence throughout the world is dementia in old age (39,40),
which shows a clear-cut causal heterogeneity, but largely
identical symptoms.
Age at Onset
In the majority of studies (age of risk beyond 60 years
unconsidered), the mean age at first contact or first admission
March 1997 Epidemiology of Schizophrenia 143

Table 2. The incidence of schizophreniaa

Incidence per 1000
Authors Country Diagnosis population per year Age correction
Babigian (98) USA Clinical diagnosis 0.94 No
Bamrah and others (99) UK ICD 0.19 No
Bates and van Dam (130) Canada Clinical diagnosis 0.10 Yes
Der (76) UK Clinical diagnosis 0.09 to 0.16 No
Dilling and others (131) Germany Clinical diagnosis 0.48 Yes
Eagles and Whalley (75) Scotland ICD 0.12 to 0.20 Yes
Folnegovic and others (132) Croatia ICD 0.27 No
Giel and others (133) Netherlands ICD 0.11 No
Häfner (1996, unpublished observations) Germany ICD 0.16 No
Hagnell and others (134) Sweden Clinical diagnosis / PSE-CATEGO 0.24 Yes
Jablensky and others (2) Denmark Clinical diagnosis / PSE-CATEGO 0.07 to 0.18 No
Jablensky and others (2) India Clinical diagnosis / PSE-CATEGO 0.09 to 0.35 No
Jablensky and others (2) USA Clinical diagnosis / PSE-CATEGO 0.09 to 0.16 No
Jablensky and others (2) USSR Clinical diagnosis / PSE-CATEGO 0.12 to 0.28 Yes
Jablensky and others (2) Japan Clinical diagnosis / PSE-CATEGO 0.10 to 0.21 No
Jablensky and others (2) UK Clinical diagnosis / PSE-CATEGO 0.14 to 0.24 No
Jablensky and others (2) Ireland Clinical diagnosis / PSE-CATEGO 0.09 to 0.22 No
Krasik and Semin (135) USSR Clinical diagnosis 0.08 to 0.23 Yes
Krupinski (1983, unpublished observations) Australia — 0.18 Yes
Munk-Jørgensen (42) Denmark Clinical diagnosis 0.07 to 0.11 No
Ninuallain (136) Ireland Clinical diagnosis / ICD / PSE-CATEGO 0.37 No
Eaton (137) India — 0.58 No
Shen (121,122) China Clinical diagnosis 0.11 Yes
Tien and Eaton (138) USA DSM 1.0 to 7.1 No

a
Abridged version of a compilation by Warner and de Girolamo (36), supplemented by own review of literature.

lies between 25 and 35 years for men and women (41,42). In women. On the basis of first admissions with a clinical
the ABC schizophrenia study (43), mean age at onset diagnosis of schizophrenia to other British registers and to the
according to different definitions as assessed by the IRAOS Dutch national case register, van Os and others (45) recently
interview (35) was 24.0 years for the first sign of the disorder, found an increase from about 10/100 000 in the age group 60
25.5 years for the first negative symptom, 29.0 years for the
first positive symptom, 30.1 years for a first peak of positive
symptoms (climax of the first psychotic episode), and 30.3
years for the first admission to hospital.
Late-Onset Schizophrenia and Late Paranoid Psychoses
The question whether first episodes of schizophrenia also
occur beyond age 60 is still unclarified. A great obstacle to
epidemiological studies of nonaffective functional psychoses
in old age is not only the diagnosis but also the fact that neither
psychiatric nor general medical services nor population
studies guarantee access to all the cases with paranoid or
schizophrenic symptoms. This is why the results from recent
studies continue to vary considerably.
Harris and Jeste’s (44) review of European studies on
late-onset schizophrenia, as well as national Danish
case-register data (41), showed a decrease in first-admission
rates after age 60 based on a clinical diagnosis of schizophre-
nia. In contrast, applying the more restrictive DSM-III-R
Figure 1. Incidence rates from selected national studies and the
diagnosis of schizophrenia, Castle and Murray (29), who
WHO “Determinants of Outcome” study per 100 000
rated Camberwell register data for 1965 to 1984, demon-
population, aged 15 to 54 (both sexes), and for a “broad”
strated a considerable increase in old age, particularly in and “restrictive” definition of schizophrenia.
144 The Canadian Journal of Psychiatry Vol 42, No 2

Table 3. Studies on the psychopathology of late-onset schizophrenia

Author
Fish 1960 (47)
Kay and Roth 1961 (139)
Harris and others 1988 (140)
Pearlson and others 1989 (51)
Howard and others 1993 (53)
Mayer and others 1993 (52)
Yassa and Suranyi-Cadotte
1993 (141)
Jeste and others 1995 (142)
Sample
All 41 “paranoid states”
> 60 years admitted in 1957,
including 9 late-onset and 7
early-onset schizophrenia
(cut-off 60 years)
99 admissions > 60 years
diagnosed with “late
paraphrenia”
5 cases aged 56 to 67 years
with “late-onset
schizophrenia” (first and
readmissions)
54 late-onset (> 45 years)
versus 54 early-onset (young)
versus 22 early-onset
(elderly); first and
readmissions
134 late-onset (> 45 years)
versus 336 early-onset cases;
first admissions
130 first admissions 40 to 63
years versus 126 first
admissions 18 to 23 years
20 late-onset schizophrenia
(> 45 years) versus 7
“paraphrenia” versus 13
“late-onset paranoia” (first
and readmissions)
25 late-onset schizophrenia
versus 39 early-onset
schizophrenia versus 35
normals
Type of study/assessment
Case notes, partly personal
examination
Case records and clinical
assessment
Case study
Rating of case records
Rating of case records
Evaluation of systematic clinical
assessment
Clinical assessment
Clinical and neuropsychological
assessment
Symptomatology in Risk factors for late-onset
late-onset schizophrenia schizophrenia
No specific schizophrenia Paranoid personality traits
syndrome
Auditory hallucinations and Female gender, deafness,
“many typically personality disorder, few
schizophrenic symptoms”; relatives
systematic and fantastic,
usually persecutory
delusions; rare incoherence
of thought
Bizarre (persecutory) —
delusion, auditory
hallucinations, visual
hallucinations, paranoid
subtype
More visual, tactile, olfactory Sensory impairment,
hallucinations, more diversity schizoid premorbid
of hallucinations, more personality, female gender,
persecutory delusions; less living alone
affective flattening, fewer
thought disorders
Persecutory and organized Female gender
delusions; third person
running commentary;
auditory hallucinations
More depression; more Female gender
symptoms of autonomic
nervous system, less
psychosocial impairment
Late-onset schizophrenia: Female gender (all
bizarre delusions, auditory diagnoses); no increased
hallucinations; paraphrenia: sensory deprivation
nonbizarre delusions;
late-onset paranoia:
nonbizarre delusions, organic
conditions
Paranoid subtype, better —
work adjustment

to 74 to 19/100 000 in the group 75 and over in England and
Wales and to 25/100 000 for those aged 90 and over in the
Netherlands (Figure 2).
There are, however, ongoing controversies whether
early-onset and late-onset schizophrenia are different or
similar disorders and which delusional disorders of the eld-
erly should be included with late-onset schizophrenia and
which of them classified separately as, for example, late
paraphrenia, paranoid psychoses, or merely persistent delu-
sional syndromes. Behind the question of a valid diagnosis is
the issue of the underlying etiologies or, at least, of the
similarities or differences of symptoms and course (46–50).
Studies focusing on the differentiation of delusional syn-
dromes in later life are reviewed in Table 3. Final conclusions
are difficult to draw because of methodological limitations:
all of these studies employed small convenience or treatment
samples (44,47). Often first-episode cases as well as readmis-
sions were included or no information was given on this issue.
In none of the recent studies attempting to distinguish
between primary paranoid disorder and schizophrenia in old
age at the symptom level in sufficiently large study
populations did the methods adopted produce a clear-cut
empirical demarcation (44,51,52).
The main risk factors for paranoid disorders in old age are
cognitive and sensory impairment (44,53), whereas in
early-onset schizophrenia, signs of delayed development,
including cognitive impairment, predominate. It is therefore
reasonable to assume that in early-onset and very late-onset
schizophrenia, respectively, disordered or delayed brain de-
velopment and degenerative processes of the brain, in both
instances ranging from mild to moderate in severity, are the
key risk factors. The reaction pattern of schizophrenia or
paranoid psychosis as a common final pathway shows clear-
cut psychopathological similarities but also some age-related
differences in both periods of life (54).
Sex Differences in Age at First-Ever Onset and Lifetime
Risk
As early as 1909, Kraepelin observed that women with
dementia praecox, when hospitalized for the first time, were
several years older than men. In their review of 53 studies,
March 1997 Epidemiology of Schizophrenia
Figure 2. Annual first-contact rates of nonaffective psychosis at age
60+ (based on administrative data).
Figure 3. Mean age values at 5 definitions of onset until first admis-
sion. First-episode sample of schizophrenia, broad defini-
tion (N = 232).
Angermeyer and Kühn (55) found that women at first admis-
sion and frequently also at onset, which has been defined and
ascertained in different ways, were older than men. Figure 3,
taken from the ABC schizophrenia study and based on a
representative sample of 232 first-episode cases, shows a
significant age difference of about 3 to 4 years for all defini-
tions of onset. The pooled data of the WHO “Determinants of
Outcome” study revealed a mean age difference of 3.4 years
(56).
A comparison of the distribution patterns of onset for men
and women on the basis of ABC study data showed that onset
for males started to increase somewhat earlier and more
steeply and, after a pronounced peak in the age group 15 to
145
25 years, steadily fell. Female onsets were slower to increase,
reached a lower peak somewhat later in life and, after decreas-
ing, peaked again, but less markedly in the age group 40 to
45 years. In first-admission rates, a peak would be expected
to occur about 5 years later, which we were able to demon-
strate on first-admission rates from the Danish national case
register (Häfner and others 1996, unpublished observations).
The distribution pattern published by Castle and others (57),
based on Camberwell case-register data over 20 years, also
displayed a second peak of female onsets just prior to
menopause.
Loranger (58), Seeman (59), Lewine (60), and Seeman and
Lang (61) have previously suggested that the sex difference
in age at onset might be accounted for by a protective effect
of estrogen. Animal experiments have shown that acute and
long-term estrogen applications actually reduce dopaminer-
gic behaviour by attenuating the sensitivity of central D2
receptors (62,63). Estrogen effects on serotonin receptors at
the neurochemical and the molecular level (gene expression)
have been reported by Sumner and Fink (64) and on glutamate
receptors by Woolley and McEwen (65). In a controlled
clinical study of schizophrenic and depressive women with
normal menstrual cycles, Riecher-Rössler and others (66)
showed that, when estrogen levels were at their peak, schizo-
phrenic and nonspecific symptom measures were signifi-
cantly reduced but depressive symptoms were unaffected in
both diagnostic groups of women.
The sex difference in age of onset, however, disappears in
cases with a high genetic load, as shown by DeLisi and others
(67), Leboyer and others (68), and Albus and Maier (69),
whereas in the definitely nonfamilial cases of Albus and
Maier’s sample, the onset-age difference grew to 5.7 years.
Evidently, the protective effect of estrogen is the more likely
to prevail, the lower the genetic liability. In addition, patients
of both sexes with a high genetic load seem to develop
schizophrenia at a relatively young age (69).
The lifetime risk for schizophrenia until age 60 appears to
be the same for men and women. In earlier studies in the
United States, higher lifetime incidence rates for men pre-
dominated, in part because of the age cut-off of 45 years in
the DSM-III diagnosis, in part because of the samples
recruited from public mental hospitals with higher
proportions of male patients. The use of criteria representing
more stringently defined schizophrenia (for example, dura-
tion criterion in DSM-III and DSM-IV) seems to yield a
significantly more disparate male-to-female ratio (70). Ham-
brecht and others (56) have recently discussed the methodo-
logical pitfalls that explain the predominance of men in some
studies, for example, an underrepresentation of primarily
female late-onset cases.
A cumulative depiction of the incidence rates for men and
women in 5-year age bands until age 59 from the ABC study
shows that the cumulative incidence, a good indicator of the
lifetime risk as based on an ICD-9 295 diagnosis of schizo-
phrenia is practically the same for both sexes at 13.2/100 000
for men and 13.1/100 000 for women. Men clearly consume
146
Table 4. Symptomatology at first admission: CATEGO syndrome
scores and total score by 3 age groups (N = 232)
Onset agea in years
Syndrome 12 to 20 21 to 35 36 to 59
DAH 11.2 10.3 10.1
BSO 8.7 7.8 7.4
SNR
9.6 6.7 6.6
NSN 16.3 15.5 13.3
Total score 45.9 40.4 37.7
a
Onset defined by first psychotic symptom.
their lifetime risk more rapidly than women do, but from age
30 to 35 on, the rates for women approximate and finally meet
those for men.
Temporal Trends
Considering the even distribution of morbidity across
countries and cultures (see Figure 1), great variation over
historical time is unlikely. This is a difficult assumption to
verify, however, because it requires the registration and diag-
nosis on a fairly identical basis of all cases from a large,
statistically well-prepared population over a long period con-
trolling for demographic changes.
The belief that schizophrenia did not exist before the 18th
century (71) is extremely unlikely to be true, and so is the
conviction that its incidence has increased with the bourgeon-
ing population in the 19th and 20th centuries (71–74). De-
creases of 40% to 50% in the first-admission rates for
schizophrenia from the mid-1960s to about the mid-1980s
were recently reported by Munk-Jørgensen (42) from Den-
mark, Eagles and Whalley (75) from Scotland, and Der (76)
from England and Wales. Der’s interpretation of the findings
as true morbidity trends triggered a critical debate in The
Lancet and the European Archives of Psychiatry and Clinical
Neuroscience. The main point raised was that the number of
available hospital beds and first admissions for a few other
diagnoses, such as affective psychoses and neurotic disorder,
also fell by approximately the same amount in these countries
over the same period (77,79). Strömgren (78) and Kendell and
others (80) also pointed out that the diagnosis of schizophre-
nia had become more restrictive during this period.
Warner and de Girolamo (36), referring to repeated, cross-
sectional investigations with the same methodology at some
study sites over the period in question, found stable,
age-corrected rates. Only 3 longitudinal studies fulfilled the
requirements mentioned for the investigation of long-term
morbidity trends in schizophrenia (17,81,82). They were
conducted on case-register data for Norway, Iceland, and the
state of Victoria, Australia. The longest period was covered
in the Australian study, in which a retrospective application
of operationalized diagnoses to random samples of case re-
cords was used. All of these studies found fairly stable rates,
indicating that temporal changes in schizophrenia morbidity
currently or in the recent past must be considered unlikely.
The Canadian Journal of Psychiatry Vol 42, No 2
Clinical Epidemiology
Clinical epidemiology aims at generally valid conclusions
ANOVA from clinical samples. The precondition is that study samples
P < 0.7 are representative of the disorder in question or at least of a
P < 0.4 defined subtype. The diagnostic definition should not include
P < 0.003
any course criteria, such as the 6-month criterion in DSM-III
and DSM-IV, which is bound to lead to a biased selection in
P < 0.08
the sample and thus to distorted results. Some epidemiologi-
P < 0.03 cal aspects of a disorder with an irregular, episodic course
also require comparisons at an identical stage of illness to
avoid confounds from different duration of illness (83). This
requirement has been fulfilled only recently in primarily
first-episode studies (43,84).
Symptomatology of the First Episode across the Life Cycle
Early-onset schizophrenia (under age 21) and very early-
onset schizophrenia (under age 14) are characterized by dis-
organization and a high frequency of poorly differentiated
and nonspecific symptoms, severe conduct disorders, and
functional impairment: the more prominent these symptoms,
the younger the patients are at onset (85,86). The sex distri-
bution of early-onset schizophrenia shows a slight predomi-
nance of males in most studies, but the opposite has been
demonstrated in other studies. The studies, mostly based on
first-contact samples at child psychiatric institutions, how-
ever, usually do not include admissions after age 18. For this
reason, some young male cases of schizophrenia may be
missed because their asocial behaviour brings them into con-
tact with social and youth guidance services as well as juve-
nile courts before reference to mental health services (87).
Testing the conclusion drawn from several studies—that
early-onset schizophrenias are more severe than late-onset
schizophrenias—investigators from the ABC schizophrenia
study, on the basis of PSE and CATEGO syndrome scores
(37), found that the PSE total scores were significantly lower
for late-onset patients, men and women taken together. As
shown in Table 4, the result was accounted for to a lesser
extent by the specific symptom scores DAH (delusional and
hallucinatory syndromes) and BSO (behaviour and speech),
and primarily by the 2 nonspecific scores SNR (specific
neurotic syndromes) and NSN (nonspecific neurotic syn-
dromes). The implication of this finding is that the greater
severity of early-onset schizophrenia is primarily attributable
to a higher frequency of symptoms not specific to psychosis.
A comparison of the symptom scores in early- and late-
onset schizophrenia (< 21 years versus ≥ 40 years) by sex
yielded different age trends for men and women. On 4 out of
8 symptom dimensions, late-onset men scored significantly
lower than early-onset men. For late-onset women, not a
single indicator was significantly more favourable and one,
the SANS global score, was more unfavourable in late-onset
women (Table 5).
This means that the milder symptomatology in late-onset
schizophrenia as a whole was accounted for by men alone,
while the total scores for late-onset women did not decrease,
and the SANS score, measuring negative symptoms, even
March 1997 Epidemiology of Schizophrenia 147

Table 5. Sex differences in symptom scores at time of first psychotic episode—early versus late onseta
Men Women
Symptomatology Early (n = 28) Wilcoxon Late (n = 9) Early (n = 21) Wilcoxon Late (n = 24)
DAH 12.1 0.02a ↓5.7 10.0 0.95 10.5
BSO 8.6 0.29 7.3 8.9 0.44 7.9
SNR 10.7 0.11 7.3 8.2 0.42 7.1
NSN 18.9 0.03b ↓11.4 13.0 0.58 13.8
Total score 50.3 0.02b ↓31.8 40.0 0.80 39.2
SANS 9.3 0.29 6.6 6.7 0.08c ↑9.5
PIRS 10.7 0.26 8.4 9.8 0.73 10.5
DAS-M 3.0 0.06c ↓1.8 1.9 0.61 1.8

a
Age at first psychotic symptom < 21 years versus ≥ 40 years.
b
P ≤ 0.1.
c
P ≤ 0.05.
Arrows mark the direction of the age difference.

increased in comparison with early-onset cases. In keeping
with the estrogen hypothesis (58–60,62,88), we assume that
this finding resulted from the waning protective effect of
estrogen—responsible for the delay in onset and the milder
early symptomatology in women. In the premenopausal
period, this would explain the higher frequency and severity
of schizophrenias developed by women at this age. The
protective effect of estrogen lacking, men develop relatively
severe cases at a young age, but relatively milder cases with
growing age of onset.
Age and Sex Differences in Illness Behaviour
A series of studies has consistently reported a higher
frequency of conduct disorders, especially asocial and crimi-
nal behaviours, and of substance abuse in schizophrenic men
(89). The WHO “Determinants of Outcome” study (2) also
found more first admissions triggered by acts of violence in
men than in women (22.2% versus 13.9%) (56).
In the ABC schizophrenia study, comparisons by sex, age
not taken into account, did not reveal any significant differ-
ences in the core symptoms. As stated by Goldberg and Gold
(90) with respect to neuropsychological test results in first-
episode patients, the disorder itself appears to be fairly similar
in men and women. The most pronounced sex difference
emerged in behavioural items, such as self-neglect, reduced
interest in a job, social withdrawal, and deficits of communi-
cation, which were all significantly more frequent in men
(Table 6). The socially negative items in men showed the
highest frequency before age 25 and the lowest frequency
after age 35.
Considering that population studies have shown conduct
disorders, antisocial and violent behaviour, and substance
abuse to be significantly overrepresented in men from puberty
to early adulthood (91), it is more plausible to classify this sex
difference in schizophrenia as illness behaviour rather than as
a direct expression of the illness. This presumes that the
socially negative behaviour of young males, also reflected in
a deficient compliance with care provision, has an unfavour-
able impact on outcome (92).
By using syndrome scores derived from the systematic
Arbeitsgemeinschaft für Methodik und Dokumentation in der
Psychiatrie (AMDP) symptom check list (93), the main items
of which are identical with the PSE, we compared a large,
consecutive, first-admission sample of schizophrenic patients
(n = 1109) from the Mannheim-based CIMH in the years 1978
to 1992 by 5-year age bands across the total age range (> 15
to ≥ 75). Neither significant sex differences nor age trends
were found in any of the schizophrenic and affective syn-
drome scores.
At the level of single symptoms, the majority showed only
little variation with age. Only very few symptoms showed
highly significant and pronounced age differences: as illus-
trated in Figure 4, based on 5-year age groups from 15 to 19
years until 75 to 79 years, all the percentages of cases present-
ing systematic and paranoid delusions increased linearly with
age across the total age-of-onset range. Systematic delusions
showed a sixfold increase from 7% in the youngest age group
to 44% in the oldest group. Goodness of fit tests (linear logit
model) demonstrated highly significant linear increases or
decreases in frequency in logits with age.
Unlike the delusional symptoms, the key symptoms of
“incoherence of thought” and “disordered sense of self,”
indicators of the disorganizational syndrome dimension par-
ticularly frequent in early-onset schizophrenia (85,87), de-
creased linearly over the entire age range. These 2 trends are
probably attributable to developmental factors and, again, are
not expressions of the basic psychophysiological process of
the disease. This means that the level of cognitive and per-
sonality development at the onset of the disorder is reflected
in symptoms (85,94,95). As the increase in paranoid and
systematic delusions indicates, the cognitive and coping abili-
ties of personality at more mature stages of personality devel-
opment become more differentiated and increasingly stable,
thus reducing the disorganizing effect of the psychosis on
overall mental functioning.
Like the socially negative illness behaviour of young
males, the age trends in the leading positive symptoms—
148 The Canadian Journal of Psychiatry Vol 42, No 2

Table 6. Gender differences in symptomatology at first admission and during early course
(ABC Schizophrenia First-Episode Sample, N = 232)
Symptom Males (%) Females (%) P(χ2)a
Cross-sectional at first admission (PSE, PIRS, SANS, DAS)
Behaviours:
Overadaptiveness/conformity 5.8 14.9 0.029
Behaviours more frequent in men:
Self-neglect 38.1 18.0 0.001
Deficits of free-time activities 81.9 54.1 0.001
Deficits of communication 76.4 50.7 0.001
Reduced interest in a job 68.3 31.3 0.002
Social disability (overall estimate) 84.7 62.7 0.002
Loss of interests 58.1 39.5 0.005
Deficits in personal hygiene 36.5 19.5 0.005
Social inattentiveness 48.0 31.3 0.012
Cumulative prevalence during early course (IRAOS)
Behaviours more frequent in women:
Restlessness 79.6 92.7 0.003
Behaviours more frequent in men
Drug abuse 39.8 21.0 0.002
Alcohol abuse 31.5 16.9 0.009
Reduced activities in free time 74.1 55.6 0.003

a
The table gives results only for those items (out of the total of 303 items of PSE, PIRS, SANS, DAS, and IRAOS) in which (for alpha-correction) a significant gender difference
was validated with at least a statistical trend (P < 0.10) in both randomly split subsamples.

Eugen Bleuler (96) regarded them as “secondary” symp- morbidity risk, and the distinction of empirical subtypes of
toms—but not in the negative symptoms, illustrate the extent schizophrenia.
to which personality development, together with genetic and
probably also environmentally determined brain processes, The knowledge available allows some fairly reliable con-
influences the clinical expression and probably also the clusions about the epidemiology of schizophrenia, however:
course of the disorder. This issue was recently raised by the average age-corrected morbidity risk for schizophrenia of
Galdos and van Os (97) with reference to the fact that fully a restrictive definition is 0.1/1000 population per year, with
elaborated positive symptoms, such as paranoid and
systematic delusions, require a certain degree of cognitive
maturity and education, for example, knowledge of the sys-
tems included as explanatory principles in the delusions. The
interaction of disease and development is likely to become
one of the key topics for future schizophrenia research and to
help build a bridge between genetic, epidemiological, and
personality research.

Discussion

The epidemiology of schizophrenia is still faced with a

series of unsolved methodological problems, making conclu-
sive interpretations and meaningful comparisons difficult.
Among these problems are the definition of the diagnosis by
conventional criteria, the variability of illness courses despite
the similarity of psychopathological symptoms, and the het-
erogeneity of the study populations. The difficulties resulting
from nonrepresentative study populations or from a failure to
check the findings against alternative interpretations are
reflected in the controversy produced by the reports of de-
creasing first-admission rates for schizophrenia from the mid-
1960s to the 1980s in some regions. Equally controversial
issues are the similarity or difference of age at onset in men
and women, the association between social class and the Figure 4. Psychotic symptoms with significant age trends.
March 1997 Epidemiology of Schizophrenia
a range from 0.07 to 0.14/1000. It is unlikely that cultural,
social, or ecological factors play a crucial part in the etiology
of schizophrenia.
Schizophrenia is primarily a disorder of adolescents and
young adults. The mean age at first contact with mental health
services is 25 to 35 years for both sexes together. In three-
quarters of first-episode cases, the first psychotic symptom is
preceded by a prodromal period of 6 years on average.
Negative and nonspecific symptoms emerge, on average, 5
years earlier than positive symptoms. Both symptom catego-
ries show an exponential accumulation until the climax of the
first episode and disappear altogether or at least partly after
that. Irrespective of how onset is defined, women fall ill 3 to
4 years later than men. The age distribution of onsets for
women shows a second peak in those aged 40 to 45 years.
Despite the difference in age of onset, the core symptoms and
almost all the other actual disease variables do not differ
between the sexes. A pronounced difference is the predomi-
nance of socially negative behaviour and substance abuse in
young male patients, but this finding very likely reflects age-
and sex-specific illness behaviour and is not a direct expres-
sion of the disorder.
Overall, the onset of schizophrenia is determined by vari-
ous factors—genetic and general biological (for example,
estrogen)—and these same factors, interacting with age- and
sex-specific behaviour and level of development at onset,
influence the clinical expression and social course.
Clinical Implications
• Incidence rates of schizophrenia appear stable across countries,
cultures, and over time.
• Given a narrow definition of schizophrenia, the annual inci-
dence rates vary around 1 in 10 000.
• On average, women fall ill 3 to 4 years later than men, probably
because of a protective effect of estrogen.
Limitations
• Comparisons among studies are difficult because of differential
standards in methodology.
• It is still unclear whether schizophrenia-like late-onset psycho-
ses should be classified as schizophrenia.
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Résumé

Objectif : Caractériser l’épidémiologie de la schizophrénie.

Méthode : Analyse documentaire narrative.
Résultats : Chaque année, un adulte sur 10 000 (âgé entre 12 et 60 ans) est atteint de schizophrénie. Lorsqu’on utilise
une définition restrictive et précise du diagnostic, des méthodes d’évaluation normalisées et des populations larges et
représentatives, on constate que les taux d’incidence semblent être demeurés stables, d’un pays et d’une culture à l’autre
ainsi qu’au fil des ans, et ce depuis au moins 50 ans. Les malades schizophrènes ne viennent pas au monde socialement
défavorisés, ni défavorisés quant à leur milieu. La répartition inégale des taux de prévalence est le résultat de la sélection
sociale : l’apparition précoce de la maladie mène à une stagnation sociale alors qu’une apparition tardive entraîne une
diminution du statut social. La principale zone d’âge, pour ce qui est des risques de schizophrénie, se situe entre 20 et
35 ans. On ne sait pas encore si les psychoses d’allure schizophrénique à début tardif (comme les paraphrénies tardives),
qui se déclarent après l’âge de 60 ans, devraient être classées comme des schizophrénies, que ce soit au plan
psychopathologique ou étiologique.
Dans 75 % des cas, la première hospitalisation est précédée d’une phase prodromique d’une durée moyenne de 5 ans
et d’une préphase psychotique d’un an. Chez les femmes, la maladie se manifeste généralement 3 ou 4 ans plus tard que
chez les hommes et une deuxième période d’apparition élevée coïncide à peu près avec la ménopause. Les schizophrénies
à début tardif sont donc plus fréquentes et plus graves chez les femmes que chez les hommes. Les différences entre les
sexes quant à l’âge d’apparition de la maladie sont moindres lorsque le fardeau génétique est élevé et elles sont plus
grandes lorsque le fardeau génétique est faible. Le mode d’apparition et les principaux symptômes de la maladie sont
similaires chez les deux sexes. Les différences les plus marquées entre les sexes se situent au niveau du comportement
socialement négatif dû à la maladie, qui est observé chez les jeunes hommes.
Conclusions : Parmi les facteurs qui déterminent l’évolution sociale et l’issue figurent le niveau de développement social
au moment de l’apparition de la maladie, le trouble lui-même (par exemple le fardeau génétique, la gravité des
symptômes et les déficits fonctionnels), les facteurs biologiques généraux (par exemple, l’oestrogène) et les comporte-
ments pathologiques spécifiques au sexe et à l’âge.