Download - Racism and Hypertension
AMERICAN JOURNAL OF HYPERTENSION 1
STATE OF THE ARTnature publishing group
Racial disparities in hypertension (HTN) continue to be a pressing problem in the United States. There is consistent evidence that black Americans are more likely than white Americans to develop HTN. Prevalence rates for black adults range from 30.6 to 40.5%; whereas the rates for white range from 24.4 to 29%.1–5 There is also evidence of racial dispari-ties in blood pressure (BP) control (control rates: blacks 44.1–65.2%; whites 55.6–86.3%),5–9 although not all studies have found race differences.10,11
These disparities exist despite the fact that black Americans are more likely to be aware of their HTN12 and in some cases are more likely to receive treatment for HTN than are white Americans.7,8 Even when black Americans are as or more adherent to antihypertensive treatment than are whites6,13 disparities in BP control are manifest. To address the high prevalence of HTN among black Americans, it may be useful to identify other variables, including different psychosocial
stressors, that might serve as potential individual-level and environmental risk factors that disproportionately affect black Americans, and to understand the ways in which these vari-ables may operate to increase HTN prevalence.
Racism has been hypothesized to serve as a psychosocial stressor contributing to the excess rates of HTN among black Americans.14–18 The goal of this review is to provide a detailed evaluation of the evidence linking individual/interpersonal, internalized, and institutional racism to HTN and to known risk factors for HTN, including obesity, fitness, and alcohol use, as well as psychosocial stress. We hope to provide an evi-dence base that can inform further examination of the role of racism in the development and course of HTN.
We specifically investigate the effects of racism on black Americans, because the majority of published research on the relation of racism to HTN has focused on black Americans. It is important to note, though, there are also significant dispari-ties for other ethnic groups.3,6,19,20
ConstruCts and definitionsMost broadly, racism has been defined as “the beliefs, attitudes, institutional arrangements, and acts that tend to denigrate indi-viduals or groups because of phenotypic characteristics or ethnic group affiliation.”16 Racism or ethnic discrimination can be
Racism and Hypertension: A Review of the Empirical Evidence and Implications for Clinical PracticeElizabeth Brondolo1, Erica E. Love2, Melissa Pencille1, Antoinette Schoenthaler3 and Gbenga Ogedegbe3
1Department of Psychology, St Johns University, Jamaica, New York, USA; 2Department of Clinical Trials, NYU School of Medicine, New York, New York, USA; 3Center for Healthful Behavior Change, Division of General Internal Medicine, Department of Medicine, NYU School of Medicine, New York, New York, USA. Correspondence: E. Brondolo ([email protected])
Received 14 June 2010; first decision 16 July 2010; accepted 25 December 2010
© 2011 American Journal of Hypertension, Ltd.
BaCkgroundDespite improved hypertension (HTN) awareness and treatment, racial disparities in HTN prevalence persist. An understanding of the biopsychosocial determinants of HTN is necessary to address racial disparities in the prevalence of HTN. This review examines the evidence directly and indirectly linking multiple levels of racism to HTN.
MethodsPublished empirical research in EBSCO databases investigating the relationships of three levels of racism (individual/interpersonal, internalized, and institutional racism) to HTN was reviewed.
resultsDirect evidence linking individual/interpersonal racism to HTN diagnosis is weak. However, the relationship of individual/interpersonal racism to ambulatory blood pressure (ABP) is more consistent, with all published studies reporting a positive relationship of interpersonal racism to ABP. There is no direct evidence linking
internalized racism to BP. Population-based studies provide some evidence linking institutional racism, in the forms of residential racial segregation (RRS) and incarceration, to HTN incidence. Racism shows associations to stress exposure and reactivity as well as associations to established HTN-related risk factors including obesity, low levels of physical activity and alcohol use. The effects vary by level of racism.
ConClusionsOverall the findings suggest that racism may increase risk for HTN; these effects emerge more clearly for institutional racism than for individual level racism. All levels of racism may influence the prevalence of HTN via stress exposure and reactivity and by fostering conditions that undermine health behaviors, raising the barriers to lifestyle change.
Keywords: ambulatory blood pressure; blood pressure; hypertension; racial discrimination; racism
American Journal of Hypertension, advance online publication 17 February 2011; doi:10.1038/ajh.2011.9
Race, Racism, and HypertensionSTATE OF THE ART
2 AMERICAN JOURNAL OF HYPERTENSION
tab
le 1
| in
terp
erso
nal
, in
tern
aliz
ed, a
nd
inst
itu
tion
al ra
cism
an
d b
lood
pre
ssu
re
Aut
hor
Sam
ple
Rac
ism
mea
sure
Blo
od p
ress
ure
mea
sure
Pote
ntia
l cov
aria
tes
Fin
din
gs
Inte
rper
sona
l rac
ism
Ba
rksd
ale
et a
l.5021
1 Bl
ack
men
and
w
omen
, con
veni
ence
sa
mpl
e
PRS27
Mea
n SB
PN
one
used
in th
e an
alys
isN
o re
latio
n
Br
oman
5631
2 A
fric
an A
mer
ican
ad
ults
rand
omly
se
lect
ed
Que
stio
nnai
re a
sses
sing
“exp
erie
nces
of
disc
rimin
atio
n or
bei
ng p
reve
nted
from
doi
ng
som
ethi
ng, h
ave
been
has
sled
or m
ade
to fe
el
infe
rior b
ecau
se y
ou a
re B
lack
” in
any
of fi
ve
situ
atio
ns. A
ny p
ositi
ve re
spon
se in
dica
ted
disc
rimin
atio
n
Self-
repo
rted
hy
pert
ensi
onAg
e, se
x, e
duca
tion,
fa
mily
inco
me,
em
ploy
men
t sta
tus
No
rela
tion
Co
zier
et a
l.5859
,000
Bla
ck w
omen
, ta
rget
ed sa
mpl
ing,
sn
owba
ll re
crui
t
Que
stio
nnai
re a
sses
sing
self-
repo
rted
exp
osur
e to
ty
pes o
f per
sona
lly m
edia
ted
raci
sm (i
.e., r
ecei
ved
poor
er se
rvic
e, tr
eate
d as
not
inte
llige
nt, p
eopl
e ac
t af
raid
, tre
ated
as d
isho
nest
, peo
ple
act a
s if t
hey
are
bett
er th
an) a
nd “i
nstit
utio
nal r
acis
m” (
i.e., u
nfai
r tr
eatm
ent o
n th
e jo
b, in
hou
sing
, and
by
polic
e)
Self-
repo
rted
an
tihyp
erte
nsiv
e us
e or
hy
pert
ensi
ve st
atus
with
us
e of
a d
iure
tic
Age,
BM
I, bi
rthp
lace
, ty
pe o
f nei
ghbo
rhoo
d,
educ
atio
n
Posi
tive
rela
tion
for
wom
en b
orn
outs
ide
the
Uni
ted
Stat
es a
nd
born
in p
redo
min
atel
y w
hite
nei
ghbo
rhoo
ds
only
D
in-D
ziet
ham
et a
l.5735
6 Bl
ack
adul
ts,
popu
latio
n-ba
sed
sam
ple
Auth
or d
evel
oped
mea
sure
. Que
stio
ns in
clud
e “w
heth
er th
e pa
rtic
ipan
ts h
ad p
erso
nally
ex
perie
nced
any
raci
st o
r dis
crim
inat
ory
enco
unte
rs
in g
ener
al, w
ork
and
med
ical
sett
ings
Nur
se m
easu
red
SBP
and
DBP
and
self-
repo
rted
ph
ysic
ian-
diag
nose
d hi
gh
bloo
d pr
essu
re a
t tw
o or
m
ore
visi
ts
Age;
mar
ital s
tatu
s SES
; BM
I; co
ping
, abi
litie
sN
o re
latio
n
D
ress
ler52
186
Blac
k, ra
ndom
se
lect
ion,
4
com
mun
ities
Four
item
s ass
essi
ng th
e de
gree
to w
hich
pa
rtic
ipan
ts p
erce
ived
that
pay
rais
es a
nd o
ther
w
ork-
rela
ted
issu
es w
ere
base
d on
race
BP m
easu
rem
ents
take
n at
hom
e w
ith a
nero
id
sphy
gmom
anom
eter
BMI,
age,
sex,
skin
col
orN
o re
latio
n
Ja
mes
et a
l.5513
2 Bl
ack
men
, pr
obab
ility
sam
ple,
1
com
mun
ity
Thre
e qu
estio
ns a
bout
race
as a
hin
dran
ce o
r hel
p to
job
Two
mea
sure
s of r
estin
g BP
take
n du
ring
inte
rvie
wAg
e, e
duca
tion,
que
tlet
inde
x, #
cig
aret
tes,
time
of d
ay
No
dire
ct re
latio
nshi
p
Ja
mes
et a
l.4989
Min
ority
adu
lts
(18.
1% B
lack
) co
nven
ienc
e sa
mpl
e of
em
ploy
ees
Org
aniz
atio
nal P
reju
dice
-Dis
crim
inat
ion
Scal
e49M
ean
SBP
and
DBP
Self-
este
em; c
olle
ctiv
e es
teem
; val
ue d
iffer
ence
s w
ith p
eers
& su
perv
isor
s;
expr
essi
vene
ss
Posi
tive
rela
tion
Kr
iege
r5910
1 Bl
ack
and
whi
te
wom
en, r
ando
m
sam
ple
Inte
rvie
w q
uest
ions
: Hav
e yo
u ev
er e
xper
ienc
ed
disc
rimin
atio
n, b
een
kept
from
doi
ng so
met
hing
, or
been
has
sled
or m
ade
to fe
el in
ferio
r (at
scho
ol, a
t w
ork,
get
ting
a jo
b, a
t hom
e, g
ettin
g m
edic
al c
are)
be
caus
e of
you
r rac
e?
Mea
n SB
P an
d D
BPAg
eN
egat
ive
rela
tion,
no
t sig
nific
ant w
hen
adju
sted
for a
ge
Kr
iege
r and
Sid
ney48
4,08
6 Bl
ack
and
whi
te,
targ
eted
recr
uitm
ent
Self-
adm
inis
tere
d qu
estio
nnai
re: f
ive
sets
of
ques
tions
whi
ch a
ddre
ssed
whe
ther
they
had
eve
r ex
perie
nced
dis
crim
inat
ion,
bee
n pr
even
ted
from
do
ing
som
ethi
ng o
r bee
n ha
ssle
d or
mad
e to
feel
in
ferio
r in
seve
ral s
ituat
ions
bas
ed o
n ra
ce o
r col
or
(at s
choo
l, ge
ttin
g a
job,
at w
ork,
get
ting
hous
ing,
ge
ttin
g m
edic
al c
are,
on
the
stre
et o
r in
a pu
blic
se
ttin
g an
d fr
om th
e po
lice
or in
the
cour
ts)
Mea
n SB
P an
d D
BPAg
e; so
cial
cla
ss; a
nnua
l fa
mily
inco
me,
edu
catio
n,
mar
ital s
tatu
s
U-s
hape
d re
latio
n,
effe
cts v
ary
by g
ende
r an
d so
cial
cla
ss
tab
le 1
| Con
tin
ued
on
nex
t pag
e
Race, Racism, and Hypertension STATE OF THE ART
AMERICAN JOURNAL OF HYPERTENSION 3
tab
le 1
| Con
tin
ued
Aut
hor
Sam
ple
Inte
rper
son
al ra
cism
mea
sure
Blo
od p
ress
ure
mea
sure
Pote
ntia
l cov
aria
tes
Fin
din
gs
Pe
ters
5416
2 Bl
ack
adul
ts,
conv
enie
nce
sam
ple
RaLE
S;26
,125
KRD
Q59
Mea
n SB
P an
d D
BPAg
e, tr
ait a
nger
, tra
it an
xiet
y, a
nger
exp
ress
ion
No
rela
tion
Po
ston
et a
l.4722
1 Bl
ack
med
ical
pr
ofes
sion
als,
born
in
Uni
ted
Stat
es o
r Afr
ica
PRS27
Mea
n SB
PBi
rthp
lace
, BM
I, ag
eN
o re
latio
n
Ry
an e
t al.51
666
Blac
k or
Lat
ino(
a)
adul
ts (1
90 B
lack
), sn
owba
ll sa
mpl
ing
BRFS
S re
actio
ns to
race
mod
ule—
thre
e qu
estio
ns
“How
oft
en d
o yo
u fe
el d
isco
mfo
rt, o
r ang
er b
y th
e w
ays o
ther
s tre
at y
ou in
you
r eve
ryda
y lif
e be
caus
e of
you
r rac
e? d
o yo
u fe
el th
at “r
acia
l dis
crim
inat
ion
dim
inis
hes y
our a
bilit
y to
ach
ieve
you
r goa
ls fu
lly?”
“Y
ou h
ave
been
rece
ivin
g le
ss th
an th
e be
st h
ealth
ca
re b
ecau
se o
f you
r rac
e?”
Mea
n BP
Ethn
icity
, age
, gen
der,
toba
cco
use,
exe
rcis
e,
BP m
eds,
BMI,
inco
me,
ed
ucat
ion,
em
ploy
men
t, in
sura
nce
U-s
hape
d re
latio
n—bo
th th
e lo
wes
t and
hi
ghes
t lev
els o
f ex
posu
re h
ad h
ighe
r BP
than
indi
vidu
als
with
mod
erat
e ex
posu
re
Br
ondo
lo e
t al.62
357
Blac
k an
d La
tino
adul
ts, 2
45 w
ith
nigh
ttim
e re
adin
gs,
conv
enie
nce
sam
ple
Perc
eive
d Et
hnic
Dis
crim
inat
ion
Que
stio
nnai
re-
Com
mun
ity V
ersi
on24
ABP
-day
and
nig
htAg
e, ra
ce, g
ende
r, BM
I, cy
nici
sm/h
ostil
ity,
indi
vidu
al-le
vel m
easu
res
of S
ES, a
lso
obse
rvat
ion
leve
l mea
sure
s of c
affe
ine
and
alco
hol,
post
ure,
sm
okin
g
PR p
ositi
vely
as
soci
ated
with
ni
ghtt
ime
SBP
and
DBP
, inv
erse
ly re
late
d to
BP
dipp
ing
H
ill e
t al.66
40 B
lack
stud
ents
, co
nven
ienc
e sa
mpl
ePR
S,27
raci
sm in
aca
dem
ic se
ttin
gs, p
ublic
sett
ing,
ra
cist
stat
emen
tsA
BP-d
ay a
nd n
ight
Gen
der,
BMI
PR in
aca
dem
ic se
ttin
g po
sitiv
ely
asso
ciat
ed
with
day
time
DBP
and
ni
ghtt
ime
DBP
. No
effe
cts f
or S
BP
Sm
art R
ichm
an
et a
l.6561
Bla
ck a
nd w
hite
adu
lts,
conv
enie
nce
sam
ple
Ever
yday
unf
air t
reat
men
t (di
scrim
inat
ion)
(n
o qu
estio
ns o
n at
trib
utio
n to
race
)A
BP-d
ay a
nd n
ight
Sex,
age
, rac
e, S
ES, B
MI,
host
ility
, neu
rotic
ism
, an
d ob
serv
atio
nal l
evel
va
riatio
ns in
pos
ture
UT/
D p
ositi
ve re
latio
n to
ove
rall
DBP
. Tim
e tr
end:
for h
igh
UT/
D
(vs.
low
) inc
reas
e ov
er th
e da
y, sh
allo
w
decr
easi
ng sl
ope
durin
g ni
ght
Si
ngle
ton
et a
l.6352
Bla
ck a
dults
, co
nven
ienc
e sa
mpl
ePR
S,27
ove
rall,
exp
osur
e in
pub
lic p
lace
s, ra
cist
st
atem
ents
ABP
-day
and
nig
htN
o in
form
atio
nRa
cism
in p
ublic
se
ttin
gs p
ositi
vely
re
late
d to
nig
httim
e SB
P an
d D
BP. N
o ef
fect
s for
day
time
BP
To
mfo
hr e
t al.64
91 B
lack
and
whi
te a
dults
, co
nven
ienc
e sa
mpl
eEv
eryd
ay u
nfai
r tre
atm
ent (
disc
rimin
atio
n), n
o qu
estio
ns o
n at
trib
utio
n to
race
68A
BP-t
wo
days
and
two
nigh
tsAg
e, g
ende
r, ra
ce,
BMI,
defe
nsiv
enes
s/so
cial
des
irabi
lity
SES,
an
d av
erag
e BP
, hos
tility
, m
arita
l sta
tus,
wee
kly
cons
umpt
ion
of a
lcoh
olic
be
vera
ges,
and
smok
ing.
UT/
D is
ass
ocia
ted
with
less
nig
httim
e di
ppin
g of
SBP
and
D
BP. N
o in
tera
ctio
ns
with
race
. UT/
D
med
iate
s rac
e di
ffere
nces
in d
ippi
ng.
tab
le 1
| Con
tin
ued
on
nex
t pag
e
Race, Racism, and HypertensionSTATE OF THE ART
4 AMERICAN JOURNAL OF HYPERTENSION
tab
le 1
| Con
tin
ued
Aut
hor
Sam
ple
Rac
ism
mea
sure
HTN
mea
sure
Pote
ntia
l cov
aria
tes
Fin
din
gs
Inte
rnal
ized
raci
sm
Tu
ll et
al.89
Age
and
body
mas
s m
atch
ed sa
mpl
es o
f A
fric
an-C
arib
bean
, no
ndia
betic
wom
en a
ged
25–6
0. Tw
enty
-sev
en
with
hig
h in
tern
aliz
ed
raci
sm a
nd tw
enty
-six
w
ith lo
w in
tern
aliz
ed
raci
sm
Nad
anol
itiza
tion
scal
e31M
ean
SBP
and
DBP
or
pres
ence
of
hype
rten
sion
Perc
eive
d st
ress
sc
ore,
def
eate
d co
ping
st
yle
No
rela
tion
Aut
hor
Sam
ple
Rac
ism
mea
sure
HTN
mea
sure
Pote
ntia
l cov
aria
tes
Fin
din
gs
Inst
itutio
nal r
acis
m
Fa
ng e
t al.96
All
resi
dent
s of N
YC
draw
n fr
om c
ensu
s 199
0 an
d de
ath
regi
stra
tions
fr
om 1
988
to 1
994
Cont
rast
bet
wee
n la
rgel
y bl
ack
and
larg
ely
whi
te
area
s (la
rgel
y bl
ack
≤75%
bla
ck, l
arge
ly w
hite
≤75
%
whi
te),
plus
Har
lem
Dea
th re
gist
ratio
n in
form
atio
n fr
om N
YC
DO
H, c
ause
of d
eath
is
repo
rted
by
a ph
ysic
ian
(ICD
- 9.
401–
404)
Age,
edu
catio
n,
unem
ploy
men
t, bi
rth
in
Sout
h of
US
No
rela
tion
G
rady
and
Ram
irez92
91,7
48 R
ecor
ds o
f bla
ck
and
whi
te m
othe
rs d
raw
n fr
om N
YC D
epar
tmen
t of
Hea
lth V
ital
reco
rds
Loca
l spa
tial s
egre
gatio
n in
dex
Pres
ence
of c
hron
ic H
TN
or p
regn
ancy
-rel
ated
HTN
Age,
mar
ital s
tatu
s, pl
ace
of b
irth,
edu
catio
n,
Med
icai
d us
e, p
over
ty
Posi
tive
rela
tions
hip:
hi
gher
segr
egat
ion,
gr
eate
r ris
k of
ch
roni
c an
d pr
egna
ncy
HTN
M
oble
y et
al.10
9Sa
mpl
e of
200
1–20
02
data
of 2
,692
wom
en
enro
lled
in th
e W
ISEW
OM
AN
pro
gram
of
the
Cent
ers o
f Dis
ease
Co
ntro
l and
Pre
vent
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Race, Racism, and Hypertension STATE OF THE ART
AMERICAN JOURNAL OF HYPERTENSION 5
considered as a form of social ostracism. Phenotypic or cultural characteristics are used to render individuals outcasts, making them targets of social exclusion, unfair treatment, and harass-ment; and consequently, either directly or indirectly, depriving them of social and economic opportunities and threatening per-sonal safety.21 Detailed reviews concerning the conceptualiza-tion and measurement of racism are available elsewhere.16,18,22
Racism can occur on multiple levels: individual/inter-personal, internalized, and institutional.22,23 Individual-level racism includes episodes of race-based maltreatment that are perpetrated by individuals and targeted at other individuals.17,22 In the context of an interpersonal exchange, these exchanges are considered interpersonal racism, which has been defined as “directly perceived discriminatory inter-actions between individuals whether in their institutional roles or as public and private individuals.”22 Individual-level racism is typically assessed with self-report surveys inquiring about exposure to acts perceived as discriminatory, unfair, or disrespectful (i.e., refs. 24–27). Self-report surveys assess the subset of experiences of ethnicity-related maltreatment that are directly perceived by the target and are generally labeled perceived racism or ethnic discrimination.
Internalized racism is defined as “the acceptance, by mar-ginalized racial populations, of the negative societal beliefs and stereotypes about themselves.”28 The internalization of negative stereotypes about ones’ own group may develop in response to repeated exposure to ethnicity-based maltreat-ment, as a function of cultural communications of attitudes toward stigmatized groups, and from familial or other sociali-zation processes, as well as other mechanisms.29,30 In studies of BP among black individuals, internalized racism has been assessed with a self-report scale (i.e., Nadanolitization scale)31 that measure the degree of agreement with typical stereotypes about the black individuals.
Institutional racism refers to specific policies and/or pro-cedures of institutions (i.e., government, business, schools, churches, etc.) which consistently result in unequal treatment or outcomes for particular groups, even though other non-race-related factors may also be associated with the disparate outcomes.32,33 Policies resulting in unequal treatment can be considered as a form of racism, despite the absence of evidence of deliberate racial prejudice on the part of the policy-makers. This is the case when majority-group policy-makers are less aware of or responsive to the consequences of these policies for minority stakeholders.34 In general, research on the rela-tionship of institutional racism to HTN has focused on the relationship of BP to the tangible outcomes of these policies, including access to education or health care, residential seg-regation, incarceration, among other outcomes.35,36 Two out-comes that have been specifically studied in relation to HTN include residential racial segregation (RRS) and incarceration.ta
ble
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Race, Racism, and HypertensionSTATE OF THE ART
6 AMERICAN JOURNAL OF HYPERTENSION
Residential segregation refers to “the degree to which groups of people categorized on a variety of scales (race, eth-nicity, income) occupy different space within urban areas.”37 We focus on race-based residential segregation (RRS), which is likely to be a function of a number of both historical and current actions on the part of institutions (i.e., real estate developers, lending organizations, employers) as well as the actions of individuals within neighborhoods.37 RRS also serves as a proxy for the extent to which black individuals are ostra-cized by other groups.38 Across all income groups, blacks tend to live in more racially segregated areas than do whites, but RRS is most pronounced among individuals with low levels of income and education.35 Strategies for conceptualizing and quantifying RRS have been well reviewed elsewhere.37,39,40 Examples of measures include the index of dissimilarity and the proportion of black residents in a given area, a measure used in most studies of HTN despite some limitations to its interpretability.37,41
Rates of incarceration in the criminal justice system can also be regarded as an index of institutional racism.42,43 In compar-ison to whites, most evidence suggests that black Americans are more likely to be incarcerated, even when controlling for a wide range of case and jurisdiction-related variable.42 These differences have developed in part, because of stereotypes about the propensity of black Americans to be violent, as well as legal and policing policies and practices.42,43
This review extends our prior work and examines studies of adults linking each level of racism to HTN diagnosis or to BP levels (with BP levels serving as a proxy for a documented diag-nosis of HTN).14,44 To obtain all relevant studies, we searched all EBSCO-host-related databases, including MEDLINE and Psych Info using the terms: racism, racial discrimination, eth-nic discrimination, institutional racism, internalized racism, self-stereotyping, residential segregation, racial segregation, racial residential segregation, and incarceration combined with BP, cardiovascular response, reactivity, HTN, and health. All papers were searched for any additional relevant refer-ences. Papers available through August 2010 were included. Table 1 includes the details of all reviewed studies for each level of racism.
To further understand the mechanisms through which rac-ism may affect HTN, we also investigate the relationship of racism to obesity, low levels of fitness, and excess alcohol con-sumption. Each has been documented to be associated with increased HTN prevalence.20,45 Reductions in these risk fac-tors have been associated with improvements in BP, and they are frequent targets of physician recommendations.45
We include data on psychosocial stress as a risk factor, although the relationship is not as well documented or accepted as lifestyle-related risk factors. Events and conditions are perceived as stressful when they are appraised as salient and
threatening, and present demands for coping that are perceived to exceed the individual’s resources.46 Both systematic and conceptual reviews suggest that chronic, but not acute stres-sors are more likely to be associated with increased risk for HTN.47,48
All levels of racism can result in acute stress exposure, but racism is widely regarded as a chronic stressor.16,21,49 Interpersonal racism takes the form of discrete events, includ-ing both overt and covert episodes of race-related maltreat-ment. These acute events can become chronic stressors if they occur frequently and/or if the experience has persistent negative effects. For example, the acute effects of race-related maltreatment may be maintained if the targeted individual experiences constraints on his or her ability to resolve the situation or cope with its aftermath.21,46 Institutional racism is associated with conditions (e.g., residential segregation, incarceration) that present additional obstacles or sustained demands that can act as chronic stressors.
raCisM and htn: exaMining the assoCiations of interpersonal, internalized, and institution‑alized raCisM to htn diagnosis or Bp levels and htn‑related risk faCtorsindividual/interpersonal racismThe bulk of the research on racism and HTN has investigated the effects of individual-level or interpersonal racism.15,17 Most studies employed within-group designs to investigate the degree to which the intensity of exposure to racism affects risk for HTN within black individuals. In our prior review,14 we indicated limited direct relationships of racism to HTN diag-nosis. The subsequent publications support this conclusion.
To date there have been 12 observational studies (described in 13 papers) which included black adults and which examined the relationship between self-reported exposure to interpersonal racism and resting BP level (e.g., a mean of two or three read-ings taken under standardized conditions)47–55 or self-reported or physician-diagnosed hypertensive status.48,56–58 Seven stud-ies did not find a direct relationship between perceived rac-ism and BP when the investigators examined the sample as a whole.47,50,52–54,56,57 Two studies have found a negative relation-ship either among older participants54 or among the participant group as a whole.59 There are two studies that report a U-shaped relationship of racism to HTN, in which, depending on partici-pants’ race, gender, and social class, there were elevated BP lev-els in those experiencing high levels of racism or no racism vs. moderate levels of racism.48,51 There are only two studies that reported a positive relationship between self-reported racism and either BP level or self-reported diagnosis of HTN either in the group overall49 or in one subgroup (i.e., non-US born women).58 However, one of these studies included a small sam-ple (n = 89), only 18% of whom were black.49
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In contrast, the data from ambulatory BP (ABP) monitoring studies are more consistent. ABP, and in particular nocturnal ABP, is regarded as a more reliable predictor of target organ damage than are clinic measures.60 Ambulatory monitoring also captures BP reactivity to daily events. The six studies of adults all reported positive relationships between perceived racism/discrimination and either daytime ABP,61 nighttime ABP or BP dipping,62–65 or both.66
There are substantial variations in the quality of these stud-ies of HTN diagnosis, clinic BP or ABP. Only four of the studies employed population-based or randomly selected samples.55–57,59 As shown in Table 1, some studies employed measures with a small number of items inquiring about dis-crimination in general or experiences of discrimination in spe-cific venues (i.e., such as work or medical care),48,52,55,56,59 and very little psychometric information was provided about these measures. Others studies included measures that have been subjected to extensive psychometric testing (e.g., Perceived Racism Scale, Everyday Discrimination, or the Perceived Ethnic Discrimination Questionnaire-Community Version).47,49,50,54 The studies of ABP (vs. those of BP level or HTN diagnosis) were more likely to include measures with known and good psychometric properties. However, it is important to note that neither the more limited scales, nor those with good psycho-metric properties yielded positive effects in studies of clinic BP or HTN status. In contrast, the same scales (i.e., the Perceived Racism Scale, Everyday Discrimination/Unfair treatment) were associated with ABP, even in studies with much smaller samples.61–66
As is the case with all self-report measures, scores on meas-ures of perceived racism may contain some error. The scales measuring perceived racism cannot distinguish between the target’s perceptions of racial bias in cases in which these per-ceptions are accurate (i.e., the perpetrators’ actions were moti-vated by racial bias) vs. those in which the target’s perceptions are a function of misperceptions or misattributions to discrimi-nation. To attempt to control for intrapersonal factors such as hostility or neuroticism that might influence the percep-tions of racism (and potentially HTN), but may develop from nonracism- related factors (e.g., temperament, family function-ing, etc.), some investigators have included measures of per-sonality characteristics as covariates.62,65 Three ABP studies in which measures of negative-affect related traits (e.g., hostility or neuroticism) were included as covariates find that the effects of perceived racism on ABP remain robust and significant.62,64,65
Measures of perceived racism which inquire about dis-crimination in a variety of venues could elicit answers reflect-ing perceptions of institutional racism (i.e., perceptions of being mistreated as a function of institutional policies) rather than experiences of interpersonal maltreatment. Racism may also affect an individual’s access to economic and social
resources, and in turn affect HTN risk through deprivation. Consequently, most investigators included measures of indi-vidual level or neighborhood socioeconomic status (SES) as a partial control for the effects of these environmental or insti-tutional variables. In studies in which the effects of SES were explicitly evaluated,67 the inclusion of SES as a control variable did not eliminate the effects of perceived racism/discrimina-tion on ABP.62 However, some studies suggest that SES mod-erates the effects of racism on BP, although the direction of effects is not consistent and additional work is needed.48,55,57
Individual-level racism may also have health effects in cir-cumstances in which the targeted individual is unaware of the exposure.68,69 Some investigators have advocated the use of measures of unfair treatment or discriminatory behavior (e.g., the Everyday Unfair Treatment Scale68,69) which assess exposure to interpersonal experiences that are likely to be a function of racial discrimination, without requiring participants to attribute the maltreatment to racial bias. These scales can be considered as a measure of the construct “ everyday unfair treat-ment” rather than racial discrimination per se, because individ-uals can perceive themselves as targeted for unfair treatment for many reasons (i.e., including their social class or gender). Some investigators have included additional questions about the attri-butions for the maltreatment; however, none of the studies of HTN or ABP in adults included these items.
All studies of HTN and clinic BP employed measures directly referring to race. All ABP studies included measures assessing experiences of unfair or discriminatory treatment in everyday life (i.e., Everyday Unfair Treatment, Perceived Racism Scale, and Perceived Ethnic Discrimination Questionnaire-Community Version). Four of these studies included meas-ures which explicitly refer to race as a cause for the unfair treatment (i.e., Perceived Racism Scale and Perceived Ethnic Discrimination Questionnaire-Community Version),61–63,66 whereas two other studies included measures of unfair treat-ment that did not explicitly refer to race.64,65 Associations of unfair treatment/discrimination to ABP among blacks were found using either type of measure of unfair treatment.
Interpersonal racism and risk factors for HTN. Although two recent studies reported no concurrent relationship of racism to body mass index,70,71 another prospective investigation reported that increases in interpersonal racism were positively associated with weight gain over a period of 8 years.72 To our knowledge there have been no studies of the relationship of indi-vidual-level racism and the intake of specific nutrients such as sodium or potassium. Perceived racism has been associated with greater risk for any level of alcohol use (but not binge or heavy drinking) among black Americans.73 Prospective studies also indicate a relationship of perceived discrimination to increases in alcohol use, partially mediated by discrimination-related
Race, Racism, and HypertensionSTATE OF THE ART
8 AMERICAN JOURNAL OF HYPERTENSION
changes in psychological distress.74 The one study specifically examining physical activity in a large population-based sample, did not find a relationship with racism.75
In contrast, there is substantial, clear and consistent evidence that individual-level racism is associated with indices of psycho-logical distress (e.g., negative affect, anger, depression, and anx-iety), as well as personality characteristics (e.g., hostility, trait negative mood) that increase the experience of distress.15,17,76,77 Racism may also influence cardiovascular responses to stress exposure. BP reactivity to stress has been identified as an inde-pendent predictor of the development of HTN.78,79 Several studies report that perceived individual-level racism predicts the magnitude of BP reactivity to laboratory-induced stres-sors.80–85 However, others studies found no direct relation-ship of individual-level racism to BP reactivity or recovery, and report that the effects of racism emerged only when moderated by other characteristics (e.g., support or hostility).80,82,86
Interpersonal racism is more consistently related to perceived stress and negative emotions than to lifestyle-related factors, including physical activity or obesity. It is worth noting that some,50,57 although not all,54 studies of racism and HTN found that stress reactions to racism were associated with HTN diag-nosis or BP level, even when exposure to race-based maltreat-ment was not. However, there are still very limited data.
internalized racismTo our knowledge, there is only one study directly assessing the effects of internalized racism, assessed with a modified ver-sion of the Nadanolitization scale on BP in Afro-Caribbean women. The authors did not find a direct relationship of inter-nalized racism to resting BP.87
The measure of internalized racism (i.e., the Nadanolitization scale) assesses the belief that members of one’s group have characteristics that correspond to common stereotypes about the group. This may or may not be related to self- stereotyping (i.e., the degree to which the individual has incorporated these stereotypes into his or her self-concept). New research is employing methods from cognitive psychology, including variations on the Implicit Association Test, to assess noncon-scious self-stereotyping.88
Internalized racism and HTN risk factors. Internalized racism does not show a relationship with body mass index,87 but is more closely associated with abdominal obesity, with three of four studies reporting a significant positive relationship.89–91 One study suggests that internalized racism is associated with perceived stress among black women.87
institutional racismThe data linking racial residential segregation to HTN is mixed. RRS has been associated with greater risk for HTN
among both black and white mothers, such that mothers living in more racially segregated areas (e.g., areas in which there were high percentages of black individuals and in which residents were less likely to interact with others who were not black) were more likely to report having chronic HTN and to be at risk for pregnancy-related HTN, controlling for neigh-borhood poverty and other factors.92 Another study reported that the percentage of black individuals living in an area was correlated with the percentage of individuals with HTN, but did not control for other facets of the neighborhood in which black individuals predominate, including higher density and lower cost of housing, variables independently associated with HTN.93
In contrast, two population-based studies of black adults did not find any relationship of the proportion of blacks living in the neighborhood to prevalence of HTN among black adults94 controlling for other neighborhood risks.95 Fang et al. reports that for black adults, there was no effect of residential area on HTN-related mortality.96 Finally, a large population-based study of black women from communities varying in size, seg-regation, and other factors found that racial segregation, as assessed by an index evaluating the likelihood that individu-als would interact with others of another ethnicity or race, was negatively associated with a measure of 10-year risk for coronary heart disease in which HTN was one factor used to comprise the measure.64
To our knowledge, there is only one study specifically exam-ining the link between incarceration and HTN.97 The inves-tigators report that a history of incarceration was associated with HTN prevalence and new incidences of HTN because incarceration across both black and white adults drawn from a national sample of young adults drawn from the Coronary Artery Risk Development in Young Adults (CARDIA) study. The effects were strongest for black men, the group most likely to have been incarcerated, but interactions of race and incar-ceration were not significant.
There is substantial evidence that black Americans live in more disadvantaged communities than other groups.34 The limited available evidence suggests that neighborhood disad-vantage may mediate the relationship of RRS to HTN.40 Low levels of neighborhood economic resources, including hous-ing quality and affluence have been associated with increased prevalence of HTN,98,99 as have perceptions of social stress in the community, including crime, perceptions of safety, marital instability, and crowding.100–103 There may also be additional environmental factors influencing racial disparities in HTN, given the wide geographic disparities in rates of HTN among both blacks Americans.104 Efforts to intervene to reduce HTN will require an understanding of the specific circumstances or deprivations that are most closely associated with HTN and which mediate the effects of RRS on HTN.40
Race, Racism, and Hypertension STATE OF THE ART
AMERICAN JOURNAL OF HYPERTENSION 9
Institutional racism and HTN risk factors. Data from most,105–
108 but not all109 studies suggest that living in neighborhoods with higher levels of RRS is associated with a higher prevalence of obesity. The data on the association of neighborhood afflu-ence to obesity is clear: rates of obesity are higher in neighbor-hoods with low vs. high SES.37,110
To our knowledge, there is no direct evidence that RRS is independently linked to higher rates of alcohol abuse or dependence. However, there is evidence that economically disadvantaged neighborhoods and those with higher levels of neighborhood stress are associated with a higher rate of alco-holism.111–113 The available data on RRS suggest that indi-viduals living in more segregated communities are less likely to be physically active.114 RRS has been associated with both objective indices of stress (e.g., crime),115 subjective reports of neighborhood stress,116 and fewer community resources for stress reduction (e.g., parks, recreational facilities, etc.).117
A portion of these neighborhood effects on HTN risk fac-tors may be a function of the barriers to obtaining healthy foods and accessing recreational facilities, combined with greater access to liquor stores.110,118–121 In one experimental study in which very low income individuals from low income neighborhoods were randomly assigned to live in new, higher income neighborhoods revealed decreases in obesity (but not HTN) over a 5-year period.122 Similarly, in the Yonkers project, low income minority families who were randomly assigned to be able to move to middle class neighborhoods reported less alcohol abuse than did families unable to move.123
suMMaryBlack individuals remain at higher risk for the development of HTN than do white individuals, despite improvements in awareness and treatment. There is evidence that racism appears to affect risk for HTN, but the effects are complex. Among black Americans, interpersonal racism is associated with ABP,61–
63,66,124 and in particular nocturnal BP, although it does not appear to be reliably associated with resting measures of BP or HTN diagnosis.47,50,52–54,56,57,59 There is mixed evidence link-ing RRS, an index of institutional racism, to HTN prevalence and BP levels,92,93 and emerging evidence that prison incarcer-ation is associated with HTN prevalence.97 It is not clear if the effects of RRS are attributable to the degree of racial isolation or the degree of deprivation associated with the neighborhood, as neighborhood SES is inversely associated with HTN inci-dence.98,99 There is no evidence directly linking internalized racism to BP, but there have been very few studies.
Racism may influence the incidence of HTN by increasing the incidence of HTN-related risk factors. There is limited evidence that interpersonal racism is associated with the development of obesity.72 RRS is associated with higher levels of obesity93 and lower levels of fitness.114 Both interpersonal
racism and neighborhood deprivation and stress have been linked to alcohol use, but more data are needed on the effects of internalized racism and RRS. All levels of racism are associ-ated with perceived stress, and individual-level racism, in par-ticular, is associated with distress21 and stress reactivity.125
ConClusionsTaken together, the evidence suggests that institutional and interpersonal racism are likely to contribute to the develop-ment of HTN, although multiple mechanisms and trajectories may be involved. Individual-level racism, and potentially inter-nalized racism, may act in part by increasing the frequency, magnitude, duration, and psychophysiological effects of stress exposure. The harsh or impoverished environments that are a function of institutional racism may add additional stress and raise barriers to achieving a healthy lifestyle.
The relationship of perceived racism to BP emerges more clearly, when the measures inquire about episodes of interper-sonal maltreatment vs. global judgments of exposure to dis-crimination. This may reflect problems with the reliability of global discrimination measures or the strategies for measur-ing BP. However, it is also possible that the findings reflect the aspects of individual-level racism (i.e., stressful interpersonal maltreatment) that are most closely associated with BP.
Exposure to race-related maltreatment has been shown to be positively related to increased rates of negative interpersonal interactions in general.73,77 If the effects of perceived racism on BP are mediated through exposure to daily interpersonal maltreatment, the effects of racism on BP may not be apparent during brief conditions involving rest (or neutral or positive interactions with medical personnel). Instead, the effects of racism may be more likely to emerge when BP is assessed dur-ing everyday events, including episodes of interpersonal con-flict. This is consistent with the finding that perceived racism/discrimination is more closely related to ABP than to resting clinic BP. The importance of ongoing interpersonal conflict to BP is underscored by our recent report that the level of daily interpersonal harassment predicted masked HTN (i.e., clinic normotension plus elevated ABP) in a sample of black and Latino(a) adults.126 Further study of the effects of racism on psychobiological responses to interpersonal relationships is needed, as is research on coping strategies that might moder-ate or buffer these effects.
Institutional racism is associated with conditions includ-ing neighborhood poverty, segregation, and incarceration that provide limited access to health promoting resources and constraints on the development and/or deployment of health promoting coping strategies.110 This suggests that resources and coping may mediate the relationship of institu-tional racism to HTN. Yet, experimental data suggest that the ways in which these variables act as mediators is complex. For
Race, Racism, and HypertensionSTATE OF THE ART
10 AMERICAN JOURNAL OF HYPERTENSION
example, moving to a less impoverished area was associated with decreases in obesity and alcohol abuse, but was not asso-ciated with changes in hypertensive status.122,123
Research is needed to understand the specific community-level variables that affect HTN incidence. It is possible that multiple environmental factors (e.g., high levels of stress expo-sure plus limited access to healthy foods) must be present to trigger the onset of HTN. Alternatively, environmental vari-ables may exert an effect on risk for HTN only in the presence of genetic vulnerability. Different levels of racism may inter-act to compound risk by impairing coping. For example, the negative mood states that are a persistent effect of exposure to interpersonal racism may undermine the motivation needed to overcome the effects of institutional racism, including environ-ments with few resources for healthy living.62 Risk factors may operate differently over the course of development. The early life effects of racism, including the well-documented effects of racism on birth weight,127,128 may set the stage for increased vulnerability to the additional challenges presented by chronic interpersonal maltreatment or neighborhood poverty.
Despite progress, research on racism and HTN is still in its early stages. To more fully understand the relationship of rac-ism to HTN, it will be important to identify the ways each level of racism acts as a stressor or as a barrier to health promotion. These continued efforts will be necessary to identify targets for prevention and intervention.
Acknowledgments: This publication was made possible by prior support to E.B. from grant R01HL68590 and ongoing support to G.O. from the following grants: P60MD003421; R01HL087301; and R01HL078566. The contents of this work are solely the responsibility of the authors and do not represent the official views of NIH.
Disclosure: The authors declared no conflict of interest.
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