HHS Public Access

Author manuscript
Cardiol Clin. Author manuscript; available in PMC 2016 May 01.
Author Manuscript

Published in final edited form as:

Cardiol Clin. 2015 May ; 33(2): 325–333. doi:10.1016/j.ccl.2015.01.005.

Dyslipidemia in Special Ethnic Populations

Jia Pu, PhDa, Robert Romanelli, PhDa, Beinan Zhao, MSa, Kristen M.J. Azar, RN, MSN/
MPHa, Katherine G. Hastings, BAb, Vani Nimbal, MPHa, Stephen P. Fortmann, MDc, and
Latha P. Palaniappan, MD, MSb
aPalo Alto Medical Foundation Research Institute, Palo Alto, CA
bStanford University School of Medicine, Stanford, CA
Author Manuscript

cKaiser Permanente Center for Health Research, Portland, OR

Synopsis
This manuscript reviewed racial/ethnic differences in dyslipidemia, including prevalence of
dyslipidemia, its relation to CHD and stroke mortality rates, response to lipid-lowering agents, and
lifestyle modification. In particular, among all racial/ethnic groups, Asian Indians, Filipinos and
Hispanics are at higher risk for dyslipidemia, which is consistent with the higher coronary heart
disease (CHD) mortality rates in these groups. In addition, compared to other racial/ethnic groups,
statins may have a higher efficacy for Asians. Studies suggest lower starting dosage in Asians, but
the data are mixed. Genetic differences in statin metabolism can in part explain this racial/ethnic
difference in statin sensitivity and adverse effects. Furthermore, lifestyle modification is
recommended as part of dyslipidemia control and management. Both African Americans and
Author Manuscript

Hispanics have more sedentary behavior and less favorable diet profile. Hispanic subgroups (i.e.
Mexican, Puerto Rican, etc.) and Asian (i.e. Chinese, South Asian, etc.) subgroups should be
disaggregated for lifestyle interventions due to cultural differences among the subgroups. Further
studies are needed to better understand racial/ethnic-specific risk factors contributing to the

© 2015 Published by Elsevier Inc.

Correspondence to: Jia Pu.
Jia Pu, Palo Alto Medical Foundation Research Institute, Ames Building, 795 El Camino Real, Palo Alto, CA 94301, Phone:
650-326-8120, Fax: 650-329-9114, puj@pamfri.org
Robert Romanelli: Palo Alto Medical Foundation Research Institute, Ames Building, 795 El Camino Real, Palo Alto, CA 94301,
Phone: 650-330-5865, Fax: 650-329-9114, romanellir@pamfri.org
Beinan Zhao: Palo Alto Medical Foundation Research Institute, Ames Building, 795 El Camino Real, Palo Alto, CA 94301, Phone:
650-326-8120, Fax: 650-329-9114, zhaob@pamfri.org
Author Manuscript

Kristen M.J. Azar: Palo Alto Medical Foundation Research Institute, Ames Building, 795 El Camino Real, Palo Alto, CA 94301,
Phone: 650-326-8120, Fax: 650-329-9114, JadelrabK@pamfri.org
Katherine G. Hastings: Stanford University School of Medicine, 1265 Welch Road, Stanford, 94305, Phone: 650-725-5339, Fax:
650-329-9114, katiegh@stanford.edu
Vani Nimbal: Palo Alto Medical Foundation Research Institute, Ames Building, 795 El Camino Real, Palo Alto, CA 94301, Phone:
650-326-8120, Fax: 650-329-9114, nimbalv@pamfri.org
Stephen P. Fortmann: Kaiser Permanente Center for Health Research, 3800 North Interstate Avenue, Portland, Oregon 97227, Phone:
503-335-2459, Fax: 503-335-2428, Stephen.P.Fortmann@kpchr.org
Latha P. Palaniappan: Stanford University School of Medicine, 1265 Welch Road, Stanford, 94305, Phone: 650-853-3359, Fax: 650-
329-9114, lathap@stanford.edu
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our
customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of
the resulting proof before it is published in its final citable form. Please note that during the production process errors may be
discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Conflicts of Interest: All authors declare they have no conflicts of interest.
 Pu et al. Page 2

observed differences in dyslipidemia, CHD, and stroke. Culturally-tailored prevention and

Author Manuscript

intervention should be provided to the minority populations with elevated risk for dyslipidemia
and considerably more research is needed to determine the best approaches to helping specific
subgroups.

Keywords
Dyslipidemia; Racial/ethnic differences; Prevalence; Mortality; Treatment; Lifestyle modification

Introduction
Dyslipidemia, including high levels of low density lipoprotein cholesterol (LDL-C) (≥130
mg/dL), total cholesterol (≥200 mg/dL), and triglycerides (TG) (≥150 mg/dL), or low levels
Author Manuscript

of high density lipoprotein cholesterol (HDL-C) (<40 [men] and <50 [women] mg/dL), is
one of the leading risk factors for coronary heart disease (CHD) and stroke.1 A report of the
National Health and Examination Survey (NHANES) from 2003–2006 estimated that 53%
(105.3M) of U.S. adults have at least one lipid abnormality: 27% (53.5M) have high LDL-C,
23% (46.4M) have low HDL-C, and 30% (58.9M) have high triglycerides (TG). In addition,
21% (42.0M) of U.S. adults have mixed dyslipidemia, defined as the presence of high LDL-
C combined with at least one other lipid abnormality.2

Significant heterogeneity in patterns of dyslipidemia prevalence, its relation to CHD and

stroke mortality rates, and response to lipid-lowering agents has been observed across racial/
ethnic groups.3 These differences in dyslipidemia provide important information that may in
part explain the variation in CVD burden observed across racial/ethnic subgroups. Better
understanding of dyslipidemia in special racial/ethnic populations is needed to guide
Author Manuscript

prevention, screening, and treatment efforts.

Prevalence of dyslipidemia subtypes among special racial/ethnic groups

The National Health and Nutrition Examination Survey (NHANES) is the primary data
source for national prevalence rates of dyslipidemia in the U.S, sampling mainly non-
Hispanic whites (whites), non-Hispanic blacks (blacks) and Mexican Americans. The
NHANES has very limited samples from the Asian subgroups.4 Other data sources, such as
primary care settings and observational studies contribute to a comprehensive picture of
racial/ethnic differences in dyslipidemia by providing important information about races and
ethnicities that are less represented in the NHANES. One should be aware that the
prevalence of dyslipidemia varies by data source. The observed differences in the prevalence
Author Manuscript

rates of dyslipidemia between studies can be attributable to factors such as study design,
sampling methods, time period, geographic variation, and participants’ characteristics.

Low Density Lipoprotein Cholesterol

NHANES data in 2013 showed the prevalence rate of high LDL-C was highest among
Mexican men (40%) and women (30%), followed by non-Hispanic black men (33%) and

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 3

women (31%). Non-Hispanic white men (30%) and women (29%) had the lowest
Author Manuscript

prevalence of high LDL-C among the three racial/ethnic groups.5

Similarly, data from a clinic based cohort in northern California from 2008–2011 showed
63% of black men and 57% of black women had high LDL-C, which were slightly higher
than the prevalence rates among non-Hispanic white men (62%) and women (53%).3
Further, Mexican American men (66%) and women (57%) also had higher prevalence of
high LDL-C compared to non-Hispanic whites.3 Filipino men (73%) and women (63%) had
the highest prevalence rates of high LDL-C among Asian subgroups, non-Hispanic whites,
non-Hispanic blacks, and Hispanics.3

Several other studies provide further estimates for variation in prevalence among race/ethnic
minority subgroups. Data from the Hispanic Community Health Study (HCHS)/Study of
Latinos (SOL), an observational study in San Diego, Chicago, New York City, and Miami,
Author Manuscript

showed variations among Hispanic subgroups with particularly high prevalence of

dyslipidemia among Central American men (55%) and Puerto Rican women (41%).6 The
Study of Health Assessment and Health Risk in Ethnic groups (SHARE) investigated
prevalence of CHD risk factors for a multi-ethnic cohort from three Canadian cities. They
found that South Asians, mainly Asian Indians, had an increased prevalence of higher total
and LDL cholesterol compared to Europeans and Chinese.7

High Density Lipoprotein Cholesterol

NHANES data in 2013 showed 20% of black men and 10% of black women had low HDL-
C, defined as less than 40mg/dL in both men and women, which were lower than the
prevalence rates among non-Hispanic white men (33%) and women (12%).5 NHANES data
also showed Mexican American men (34%) and women (15%) had higher prevalence of low
Author Manuscript

HDL-C compared to non-Hispanic whites.5 According to NHANES data from 2011–2012,

25% of Asian American men and 5% of Asian American women had low HDL-C.8

Although NHANES data showed Asian Americans had the lowest prevalence of low HDL-
C as an aggregated group, data from a clinic based cohort with disaggregated Asian ethnic
groups in northern California between 2008–2011 found that Asian Indian men (53%) and
women (55%) had the highest prevalence of low HDL-C among Asian American subgroups;
their prevalence was also higher than Mexican American men (48%) and women (51%),
non-Hispanic black men (34%) and women (40%), and non-Hispanic white men (36%) and
women (31%).3 Similarly, data from the SHARE study showed South Asians including
Asian Indians had an increased prevalence of low HDL-C compared to Europeans and
Chinese.7
Author Manuscript

Triglycerides
NHANES data from 1999–2008 showed 35% of Mexican Americans had high TG, followed
by 33% among non-Hispanic whites, and 16% among non-Hispanic blacks.9

Data from a clinic based cohort in northern California from 2008–2011 found Filipino men
(60%) and Mexican women (45%) had the highest prevalence of high TG, compared to

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 4

Mexican men (56%) and Filipino women (42%), Asian Indian men (55%) and women
Author Manuscript

(37%), non-Hispanic white men (43%) and women (28%), and non-Hispanic black men
(30%) and women (18%).3

Data from the SHARE study showed South Asians had the highest prevalence of high TG
among South Asians, Chinese, and Europeans.7

Potential explanations for racial/ethnic differences in dyslipidemia prevalence have been

explored by several studies. In the Multi-Ethnic Study of Atherosclerosis (MESA),
researchers found that ethnic disparities were attenuated substantially by adjusting for access
to healthcare.10 The racial/ethnic differences could also be related to lifestyle, genetic, and
cultural differences associated with total and LDL cholesterol concentrations.11 For
example, the predilection of South Asians to have lower HDL-C levels has been attributed to
the higher prevalence of insulin resistance and related metabolic abnormalities, which may
Author Manuscript

be the consequence of a combination of genetic predisposition, physical inactivity, and a

high-carbohydrate diet.12,13,14

Dyslipidemia-related mortality in special racial/ethnic groups

Dyslipidemia often results in an increased risk of premature atherosclerosis, a major risk
factor for coronary heart disease (CHD).15 CHD is the leading cause of mortality for both
men and women in the U.S. and worldwide with increasing evidence of gender and racial/
ethnic minority disparities in CHD morbidity and mortality.16–19 Despite declines in CHD
death rates over the past decades, CHD contributes to over one-third of all deaths for those
over the age of 35 years.20

CHD mortality rate differences have been found across races/ethnicities. In the U.S. CHD
Author Manuscript

mortality rates are highest in blacks, intermediate in whites and Hispanics, and lowest in
some Asian subgroups.15,21,22 These CHD rates are paralleled with observed racial/ethnic
disparities in dyslipidemia prevalence, with higher CHD rates seen in Hispanics and blacks
potentially due to limited healthcare access and other less favorable behavioral factors seen
in these groups.10

Meanwhile, although traditionally known as the “model minority”, disproportionate

mortality burden due to CHD and stroke has been shown among certain Asian subgroups
such as Asian Indians, Filipinos, and Japanese.23,24 Of note, the landmark Ni-Hon-San study
showed increased CHD mortality rates and decreased stroke rates among Japanese-
American men compared to rates in Japan, suggesting a differential disease impact of
acculturation to Westernized lifestyles.25 A recent study found higher proportional mortality
Author Manuscript

due to CHD among Asian Indians, especially in younger age groups, compared to all other
racial/ethnic groups.17 Increased burden from CHD mortality has been well documented in
both native and immigrant Asian Indian populations.7,26,27 This observation is consistent
with the higher prevalence rates of dyslipidemia (especially low HDL-C) in Asian Indians
compared to other Asian subgroups and non-Hispanic whites in the U.S.3,7,28

Environmental and social factors (e.g. acculturation, socio-economic status, diet) have been
known to increase CHD mortality risk.29,30 Cultural diets high in fat, increasing the risk for

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 5

dyslipidemia, are also of concern.31 Differences in susceptibility to CHD may also have a
Author Manuscript

genetic basis, although this has not yet been adequately determined. Thus it is critical for
clinicians to modify lipid management appropriately among these rapidly growing
populations.

Treatment of Dyslipidemia
1. Overview
There are several U.S. Food and Drug Administration (FDA)-approved HMG-CoA
reductase inhibitors (statins) and a variety of non-statin therapies available for the treatment
of dyslipidemia, including bile acids sequestrants, cholesterol absorption inhibitors, fibrates,
niacin, and omega-3 fatty acids. Statins are the most widely prescribed treatment for
dyslipidemia, and one of the most commonly prescribed drugs in the U.S.32 In the most
recent national cholesterol treatment guidelines, published in November 2013 by the
Author Manuscript

American College of Cardiology (ACC)/American Heart Association (AHA),1 the Expert

Panel determined from robust clinical trial data that statins have the most acceptable CVD-
risk reduction benefit and side-effect profile, and that the addition of non-statin therapy does
not appear to provide further benefit in reducing CVD. Clinical trials on which cholesterol
treatment guidelines are based have often underrepresented racial/ethnic minority groups.
Accordingly, our knowledge of optimal statin treatment regimens, and the effectiveness,
tolerability, and safety of these regimens in clinical practice, is limited across diverse racial/
ethnic populations.

2. Racial/ethnic differences in risk stratification

The most recent ACC/AHA guidelines expand the criteria for patients who would benefit
from statin treatment, and more than 80% of newly eligible patients are expected to have no
Author Manuscript

prior CVD.33 Therefore, they would be assessed for optimal statin treatment based on the
new Atherosclerotic CVD (ASCVD) Risk Estimator.33 This estimator is intended to
improve upon previous CVD-risk estimators, including the Framingham34 and Adult
Treatment Panel III35 risk algorithms. It was derived from several longitudinal
epidemiologic cohort studies of non-Hispanic whites and blacks, and was externally
validated in two cohort studies with similar populations (MESA and REGARDS),36 as well
as in contemporary samples of the derivation cohorts. However, studies among other race/
ethnic minority groups are lacking. The ACC/AHA Work Group, which developed the
algorithm for the ASCVD Risk Estimator, acknowledges that it should be used only in men
and women of non-Hispanic white or non-Hispanic black decent, and that it may not
accurately predict risk in other racial/ethnic groups.37 Specifically, there is concern of
overestimate of risk in Mexican Americans and East Asians and underestimate risk in other
Author Manuscript

groups, such as Puerto Ricans and South Asians.37,38 Other countries with diverse racial/
ethnic minority populations, such as the United Kingdom, have validated algorithms
predicting risk for over 9 specific racial/ethnic sub-populations (http://qrisk.org/).39

3. Race/Ethnic Differences in Statin Response

3.1 Statin metabolism and drug sensitivity—Much of the data on race/ethnic
differences in statin metabolism have shown that some Asian subgroups are slower to

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 6

metabolize statins compared to non-Hispanic whites, which leads to higher systemic drug
Author Manuscript

concentrations. Pharmacokinetic studies indicate rosuvastatin plasma concentrations are

two-fold higher in Japanese relative to non-Hispanic white individuals. Rosuvastatin plasma
concentrations have been shown to be similarly elevated in other Asian subgroups; these
included Chinese, Malay, and Asian Indians, whose rosuvastatin concentrations were
approximately 2 times higher relative to non-Hispanic whites/Hispanic whites.40

There are several genetic variants that are associated with altered statin metabolism. Such
variants include, but are not limited to, single nucleotide polymorphisms (SNPs) in the genes
that encode the organic anion-transporting polypeptide (OATP)1B1 (521T>C), which
regulates hepatic uptake of statins, and the adenosine triphosphate-binding cassette G2
(ABCG2) transporter (421C>A), which regulates hepatic efflux.41,42 Variants of both genes
are associated with increased statin plasma concentrations within multiple race/ethnic
groups.41–44 421C>A has been found to be a SNP candidate to explain the observed racial
Author Manuscript

differences in statin metabolism: the allelic frequency of 421C>A in ABCG2 is higher in

Chinese (~35%) relative to Caucasians (9–14%).43,45

Higher plasma levels of statins in Asians compared to non-Hispanic whites has led to
concern about increased risk for statin-induced side effects in this population. Such concerns
have led to a revised package insert recommending lower starting doses of rosuvastatin in
this population (5mg, vs. 10mg for non-Hispanic whites).46 Notably, in Japan, starting doses
for most statins are half of what is recommended in the U.S.47

There is less information on statin metabolism in other racial/ethnic minority groups. We are
aware of one study that evaluated the pharmacokinetics of single-dose pravastatin in non-
Hispanic blacks versus European Americans.44 In this study, the OATP1B1 521T>C
Author Manuscript

polymorphism was significantly associated with higher statin plasma concentrations in

subjects of European vs. African ancestry.44 This may be explained by the low allelic
frequency of OATP1B1 521T>C in non-Hispanic blacks (~1%)44 relative to non-Hispanic
whites. To our knowledge no studies have been published on the pharmacokinetics of statins
in Hispanics.

Myalgia (i.e., muscle pain) is one of the most commonly observed side effect associated
with statins, but has been reported to occur at varying frequencies (5%–20%) in randomized
controlled trials (RCT) and observational studies.48–50 More severe, but rare muscle side
effects have also been reported, including myopathy (0.01%–0.3%) and rhabdomyolysis
(0.003%–0.01%).51 To date, high-dose simavastatin (80mg) is the only statin to receive a
U.S. FDA warning for increased risk of muscle damage.52 The use of statins in combination
with other drugs has also been shown to increase the risk of adverse events.53,54 In HPS2-
Author Manuscript

THRIVE, which included 25,673 adults from Europe and China on simvastatin 40mg/daily,
a higher risk of adverse events, including myopathy, were reported in patients randomized to
niacin-laropiprant relative to placebo.55 Furthermore, the relative risk of musculoskeletal
events (mostly myopathy) in the niacin-laropiprant versus placebo group was markedly
higher among Chinese participants than European participants.55 To our knowledge no
safety concerns have been raised for statins alone or in combination with agents in non-
Hispanic blacks or Hispanics.

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 7

3.2 Statin efficacy in Asian populations—Studies conducted in Asian countries have

Author Manuscript

documented that lower statin doses can achieve similar therapeutic effects in Asian
populations.

• In an open-label study of Japanese patients receiving simvastatin (initial dose 5 mg/

daily), LDL-C decreased by 26% over six months; an effect that corresponds to
simvastatin 20mg/daily in Western studies56

• In a multicenter double-blind randomized controlled trial in six Asian countries,

patients randomized to receive 10mg simvastatin or atorvastatin daily over eight
weeks had an average LDL-c reduction of 35% and 43%, respectively, with more
than 80% of patients achieving a National Cholesterol Education Program LDL-C
target.57 To see similar effects in non-Hispanic whites would generally require at
least double this dose of simvastatin.
Author Manuscript

• In a prospective RCT of the primary prevention of CVD in Japan, pravastatin 10–

20mg/daily reduced LDL-C by only 18% but reduced coronary heart disease by
33% relative to diet alone;58 this level of risk reduction in CVD is similar to trials
of predominantly non-Hispanic white populations taking higher daily doses of
pravastatin (40mg)59 or a higher potency statin (atorvastatin 10mg/daily)60

It is tempting to speculate that the apparently increased effect of statins in Asians relative to
non-Hispanic whites is due to genetic differences in statin metabolism; however, because
comparisons in these studies were indirect and were conducted on ethnic populations outside
of the U.S. or Europe, underlying cultural differences in diet and lifestyle cannot be ruled
out as a causal factor.

In addition, other studies have failed to demonstrate differences in response to statins in

Author Manuscript

Asian and non-Hispanic white populations.

• In combined analysis of two small multicenter open-label studies, GOALLS

(included non-Asian and Asian participants) and STATT (included Asians only),
the authors compared cholesterol outcomes among patients with coronary heart
disease treated with simvastatin for 14 weeks.61 There were no differences in
changes in LDL-C among Asians in the STATT study (N=133; −45.4 mg/dL)
relative to Asians (N=15) or non-Asians (N=183) in the GOALLS study (−41.1
mg/dL and −41.2 mg/dL, respectively)61

• In an observational, prospective study in Canada, no difference in the magnitude of

LDL-C lowering was observed among non-Hispanic whites and South Asians
(−41% vs. −43%, respectively; P=0.40), taking atorvastatin or simvastatin (20 mg
Author Manuscript

median dose for each) for more than three years in the secondary prevention of
CVD62

• Using data from an RCT evaluating atorvastatin versus placebo in a multi-ethnic

population in the U.K., Chapman and colleagues matched White (N=198) and
South Asian (N =76) cohorts receiving atorvastatin to evaluate the effects of statins
across race/ethnic groups.63 The authors again found no difference in the percent
reduction in LDL-C among whites and South Asians (−40% vs. −39%; P=0.92)63

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 8

To our best knowledge, no existing studies have shown differences in statin efficacy in non-
Author Manuscript

Hispanic blacks, Hispanics, and non-Hispanic whites.63,64,65

4. Lifestyle modification in special racial/ethnic groups

Lifestyle modification has been recommended to treat dyslipidemia and to reduce ASCVD
risk, both prior to and in addition to the use of lipid-lowering agents.1 These lifestyle risk
factors include unhealthy diet, overweight and obesity, and physical inactivity. The
American Heart Association has the following specific recommendations for individuals
with dyslipidemia:66

• Diet: Increase the intake of vegetables, fruits, and whole grains and limit intake of
sweets; reduce the intake of saturated fat and trans fat

• Physical activity: engage in aerobic physical activity; 3–4 40-minute sessions per
Author Manuscript

week; moderate-to-vigorous intensity physical activity

Racial/ethnic disparities also exist in these lifestyle risk factors. According to data from the
Behavioral Risk Factor Surveillance System (BRFSS) in 2002, non-Hispanic whites had
more fruits and vegetables in their diet compared to Hispanics and non-Hispanic blacks.6,67
According to the National Health Interview Survey (NHIS) 2008–2010, 71% of Hispanics
were overweight or obese, followed by non-Hispanic blacks (70%), non-Hispanic whites
(62%), and Asian Americans (42%). In addition, NHIS 2008–2010 also found that compared
to non-Hispanic whites (20%), non-Hispanic black (17%), Asian American (16%), and
Hispanic (13%) adults were less likely to meet the 2008 guidelines for aerobic and muscle
strengthening through leisure time activity.68 All these data indicate both non-Hispanic
blacks and Hispanics are at higher risk for having both diet and lifestyle risk factors, and
Asian Americans are more likely to be physically inactive.
Author Manuscript

A recent systematic review included nutrition and physical activity intervention studies in
adult African Americans, from 2000 to 2011.69 This study found both diet and physical
activity interventions for weight loss improved cholesterol clinical outcomes among African
Americans.69 In particular, it provided evidence to support interventions in community-
based settings among African Americans. A 2011 systematic review included intervention
studies that promote physical activity in Hispanic adults published between 1988–2011.70
This study concluded that physical activity interventions in Hispanics should include
community-based settings, social support strategy, culturally sensitive intervention design,
and staff from the same ethnic group. A systemic review of RCTs of lifestyle interventions
for Asian Americans published between 1995 and 2013 concluded that lifestyle
interventions improved physical activity, healthy diet, and weight control in Asian
Americans.71 However, the studies included in this review were limited in cultural
Author Manuscript

appropriateness. In particular, Asian subgroups were aggregated together although they have
different cultures and health behavior patterns. Other recommendations include individual
tailoring, education and modeling of lifestyle behaviors, and providing support during a
maintenance phase.

Immigration and acculturation have a profound impact on lifestyle in both Hispanics and
Asians in the U.S. For example, traditional Hispanic diets contain high levels of fiber.

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 9

However, studies found US-born Hispanics had a hard time retaining traditional diets and
Author Manuscript

consumed more fat and sugar compared to their counterparts in their home countries.72,73
They have less access to high nutritional quality foods and are at risk for overweight/
obesity.72,74 Similarly, traditional East Asian diets contain less total and saturated fat but
more sodium intake compared to western diets and Asian Indian diets.75,76 However,
Chinese immigrants who have lived in the U.S for more than ten years had more unhealthy
diet and less physical activity compared to recent immigrants.30 In contrast, higher
acculturation levels were associated with more physical activity among Korean
Americans.77 Future studies should consider providing culturally-tailored, ethnic-specific
interventions to these diverse immigrant populations.

Conclusions
There are significant racial/ethnic differences in dyslipidemia prevalence, dyslipidemia
Author Manuscript

related mortality rates, and response to lipid-lowering agents. Among all racial/ethnic
groups, Asian Indians, Filipinos and Hispanics are at most elevated risk for dyslipidemia,
which is consistent with the higher CHD mortality rates in these groups. More attention
should be paid to these at-risk groups for screening and treatment purposes. Compared to
other racial/ethnic groups, statins may have a higher efficacy for Asians, which may
potentially be explained by genetic differences in statin metabolism, but overall the data are
mixed. At present it may be wise to start with a lower statin dose in an individual with Asian
ancestry until the treatment and adverse effects can be determined. In addition, racial/ethnic
differences in health behavior patterns should be taken into consideration when promoting
lifestyle modification among individuals with dyslipidemia. In particular, Hispanic
subgroups (i.e. Mexican, Puerto Rican, etc.) and Asian (i.e. Chinese, South Asian, etc.)
subgroups should be disaggregated in lifestyle interventions. Further studies are needed to
Author Manuscript

better understand racial/ethnic-specific risk factors contributing to the observed differences

in dyslipidemia, CHD, and stroke. Culturally-tailored prevention and intervention should be
provided to the minority populations with elevated risk for dyslipidemia and considerably
more research is needed to determine the best approaches to helping specific subgroups.

References
1. Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA Guideline on the Treatment of Blood
Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation.
2013
2. Toth PP, Potter D, Ming EE. Prevalence of lipid abnormalities in the United States: the National
Health and Nutrition Examination Survey 2003–2006. Journal of clinical lipidology. 2012; 6(4):
325–330. [PubMed: 22836069]
Author Manuscript

3. Frank AT, Zhao B, Jose PO, Azar KM, Fortmann SP, Palaniappan LP. Racial/ethnic differences in
dyslipidemia patterns. Circulation. 2014; 129(5):570–579. [PubMed: 24192801]
4. Holland AT, Palaniappan LP. Problems with the collection and interpretation of Asian-American
health data: omission, aggregation, and extrapolation. Ann Epidemiol. 2012; 22(6):397–405.
[PubMed: 22625997]
5. Statistical fact sheet 2013 update: high blood cholesterol & other lipids. 2013 http://
www.heart.org/idc/groups/heartpublic/@wcm/@sop/@smd/documents/downloadable/
ucm_319586.pdf.

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 10

6. Rodriguez, Cj; Fau - Allison, M.; Allison, M.; Fau - Daviglus, ML.; Daviglus, Ml; Fau - Isasi, CR.,
et al. Status of cardiovascular disease and stroke in Hispanics/Latinos in the United States: a science
Author Manuscript

advisory from the American Heart Association. (1524-4539 (Electronic)).

7. Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atherosclerosis and cardiovascular
disease between ethnic groups in Canada: the study of health assessment and risk in ethnic groups
(SHARE). Indian Heart J. 2000; 52 Suppl(7):S35–S43. [PubMed: 11339439]
8. Aoki Y, Yoon SS, Chong Y, Carroll MD. Hypertension, abnormal cholesterol, and high body mass
index among non-Hispanic Asian adults: United States, 2011–2012. NCHS Data Brief. 2014; (140):
1–8. [PubMed: 24429341]
9. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific
statement from the American Heart Association. Circulation. 2011; 123(20):2292–2333. [PubMed:
21502576]
10. Goff DC Jr, Bertoni AG, Kramer H, et al. Dyslipidemia prevalence, treatment, and control in the
Multi-Ethnic Study of Atherosclerosis (MESA): gender, ethnicity, and coronary artery calcium.
Circulation. 2006; 113(5):647–656. [PubMed: 16461837]
11. Huang MH, Schocken M, Block G, et al. Variation in nutrient intakes by ethnicity: results from the
Author Manuscript

Study of Women's Health Across the Nation (SWAN). Menopause. 2002; 9(5):309–319.
[PubMed: 12218719]
12. McKeigue PM, Miller GJ, Marmot MG. Coronary heart disease in south Asians overseas: a review.
J Clin Epidemiol. 1989; 42(7):597–609. [PubMed: 2668448]
13. Chambers JC, Kooner JS. Diabetes, insulin resistance and vascular disease among Indian Asians
and Europeans. Seminars in vascular medicine. 2002; 2(2):199–214. [PubMed: 16222611]
14. Radhika G, Ganesan A, Sathya RM, Sudha V, Mohan V. Dietary carbohydrates, glycemic load and
serum high-density lipoprotein cholesterol concentrations among South Indian adults. European
journal of clinical nutrition. 2009; 63(3):413–420. [PubMed: 17987051]
15. Enas, EA. [Accessed date: Nov 15, 2014] Clinical Implications: Dyslipidemia in the Asian Indian
Population. 2002. https://southasianheartcenter.org/docs/AAPImonograph.pdf.
16. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart Disease and Stroke Statistics—2011 Update: A
Report From the American Heart Association. Circulation. 2011; 123(4):e18–e209. [PubMed:
21160056]
Author Manuscript

17. Jose POFA, Kapphahn KI, Goldstein BA, Eggleston K, Hastings KG, Cullen MR, Palaniappan LP.
Cardiovascular Disease Mortality in Asian Americans (2003 to 2010). Journal of the American
College of Cardiology. 2014 In press.
18. Palaniappan L, Wang Y, Fortmann SP. Coronary heart disease mortality for six ethnic groups in
California, 1990–2000. Ann Epidemiol. 2004; 14(7):499–506. [PubMed: 15310526]
19. Keppel KG, Pearcy JN, Heron MP. Is there progress toward eliminating racial/ethnic disparities in
the leading causes of death? Public Health Rep. 2010; 125(5):689–697. [PubMed: 20873285]
20. Farnier M, Chen E, Johnson-Levonas AO, McCrary Sisk C, Mitchel YB. Effects of extended-
release niacin/laropiprant, simvastatin, and the combination on correlations between
apolipoprotein B, LDL cholesterol, and non-HDL cholesterol in patients with dyslipidemia. Vasc
Health Risk Manag. 2014; 10:279–290. [PubMed: 24855368]
21. Enas E, Yusuf S, Mehta J. Meeting of International Working Group on coronary artery disease in
South Asians. Indian Heart J. 1996; (48):727–732. [PubMed: 9062031]
22. Hoyert DL. 75 years of mortality in the United States, 1935–2010. NCHS Data Brief. 2012; (88):
1–8. [PubMed: 22617094]
Author Manuscript

23. Ye J, Rust G, Baltrus P, Daniels E. Cardiovascular risk factors among Asian Americans: results
from a National Health Survey. Ann Epidemiol. 2009; 19(10):718–723. [PubMed: 19560369]
24. Klatsky AL, Tekawa IS, Armstrong MA. Cardiovascular risk factors among Asian Americans.
Public Health Rep. 1996; 111(Suppl 2):62–64. [PubMed: 8898779]
25. Marmot MG, Syme SL, Kagan A, Kato H, Cohen JB, Belsky J. Epidemiologic studies of coronary
heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of
coronary and hypertensive heart disease and associated risk factors. Am J Epidemiol. 1975;
102(6):514–525. [PubMed: 1202953]

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 11

26. Balarajan R. Ethnic differences in mortality from ischaemic heart disease and cerebrovascular
disease in England and Wales. Bmj. 1991; 302(6776):560–564. [PubMed: 2021718]
Author Manuscript

27. Enas EA, Garg A, Davidson MA, Nair VM, Huet BA, Yusuf S. Coronary heart disease and its risk
factors in first-generation immigrant Asian Indians to the United States of America. Indian Heart J.
1996; 48(4):343–353. [PubMed: 8908818]
28. Karthikeyan G, Teo KK, Islam S, et al. Lipid profile, plasma apolipoproteins, and risk of a first
myocardial infarction among Asians: an analysis from the INTERHEART Study. J Am Coll
Cardiol. 2009; 53(3):244–253. [PubMed: 19147041]
29. Marmot MG, Syme SL. Acculturation and coronary heart disease in Japanese-Americans.
American journal of epidemiology. 1976; 104(3):225–247. [PubMed: 961690]
30. Taylor VM, Yasui Y, Tu SP, et al. Heart disease prevention among Chinese immigrants. J
Community Health. 2007; 32(5):299–310. [PubMed: 17922202]
31. Gupta M, Brister S. Is South Asian ethnicity an independent cardiovascular risk factor? The
Canadian journal of cardiology. 2006; 22(3):193–197. [PubMed: 16520847]
32. Bartholow M. Rx Focus: Top 200 Drugs of 2012. Pharmacy Times. 2012
33. Pencina MJ, Navar-Boggan AM, D'Agostino RB Sr, et al. Application of new cholesterol
Author Manuscript

guidelines to a population-based sample. N Engl J Med. 2014; 370(15):1422–1431. [PubMed:

24645848]
34. D'Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in
primary care: the Framingham Heart Study. Circulation. 2008; 117(6):743–753. [PubMed:
18212285]
35. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final
report. Circulation. 2002; 106(25):3143–3421. [PubMed: 12485966]
36. Goff DC Jr, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of
cardiovascular risk: a report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(25 Pt B):2935–2959. [PubMed:
24239921]
37. Goff DC Jr, Lloyd-Jones DM. 2013 Report on the Assessment of Cardiovascular Risk: Full Work
Group Report Supplement. 2013 http://jaccjacc.cardiosource.com/acc_documents/
Author Manuscript

2013_FPR_S5_Risk_Assesment.pdf.
38. Stone NJ, Robinson JG, Lichtenstein AH. 2013 Report on the Treatment of Blood Cholesterol to
Reduce Atherosclerotic Cardiovascular Disease in Adults: Full Panel Report Supplement. 2013
http://www.kcumb.edu/uploadedFiles/Content/Academics/_Assets/CME_Presentations/
Moriarty12_5_full.pdf.
39. Hippisley-Cox J, Coupland C, Vinogradova Y, et al. Predicting cardiovascular risk in England and
Wales: prospective derivation and validation of QRISK2. BMJ. 2008; 336(7659):1475–1482.
[PubMed: 18573856]
40. Lee E, Ryan S, Birmingham B, et al. Rosuvastatin pharmacokinetics and pharmacogenetics in
white and Asian subjects residing in the same environment. Clin Pharmacol Ther. 2005; 78(4):
330–341. [PubMed: 16198652]
41. Nishizato Y, Ieiri I, Suzuki H, et al. Polymorphisms of OATP-C (SLC21A6) and OAT3
(SLC22A8) genes: consequences for pravastatin pharmacokinetics. Clin Pharmacol Ther. 2003;
73(6):554–565. [PubMed: 12811365]
42. Niemi M. Transporter pharmacogenetics and statin toxicity. Clin Pharmacol Ther. 2010; 87(1):
Author Manuscript

130–133. [PubMed: 19890253]

43. Zhang W, Yu BN, He YJ, et al. Role of BCRP 421C>A polymorphism on rosuvastatin
pharmacokinetics in healthy Chinese males. Clin Chim Acta. 2006; 373(1–2):99–103. [PubMed:
16784736]
44. Ho RH, Choi L, Lee W, et al. Effect of drug transporter genotypes on pravastatin disposition in
European- and African-American participants. Pharmacogenet Genomics. 2007; 17(8):647–656.
[PubMed: 17622941]

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 12

45. Keskitalo JE, Zolk O, Fromm MF, Kurkinen KJ, Neuvonen PJ, Niemi M. ABCG2 polymorphism
markedly affects the pharmacokinetics of atorvastatin and rosuvastatin. Clin Pharmacol Ther.
Author Manuscript

2009; 86(2):197–203. [PubMed: 19474787]

46. AstraZeneca. CRESTOR (rosuvastatin) Prescribing Information. 2014 http://
www1.astrazenecaus.com/pi/crestor.pdf.
47. Liao JK. Safety and efficacy of statins in Asians. Am J Cardiol. 2007; 99(3):410–414. [PubMed:
17261409]
48. Bruckert E, Hayem G, Dejager S, Yau C, Begaud B. Mild to moderate muscular symptoms with
high-dosage statin therapy in hyperlipidemic patients--the PRIMO study. Cardiovasc Drugs Ther.
2005; 19(6):403–414. [PubMed: 16453090]
49. Stewart A. SLCO1B1 Polymorphisms and Statin-Induced Myopathy. PLoS Curr. 2013; 5
50. Fung EC, Crook MA. Statin myopathy: a lipid clinic experience on the tolerability of statin
rechallenge. Cardiovasc Ther. 2012; 30(5):e212–e218. [PubMed: 21884002]
51. Law M, Rudnicka AR. Statin safety: a systematic review. Am J Cardiol. 2006; 97(8A):52C–60C.
52. [Accessed Nov. 15, 2014] FDA Drug Safety Communication: new restrictions, contraindications,
and dose limitations for Zocor (simvastatin) to reduce the risk of muscle injury. 2011. http://
Author Manuscript

www.fda.gov/Drugs/DrugSafety/ucm256581.htm.
53. Thompson PD, Clarkson P, Karas RH. Statin-associated myopathy. JAMA. 2003; 289(13):1681–
1690. [PubMed: 12672737]
54. Pasternak RC, Smith SC Jr, Bairey-Merz CN, et al. ACC/AHA/NHLBI clinical advisory on the use
and safety of statins. J Am Coll Cardiol. 2002; 40(3):567–572. [PubMed: 12142128]
55. Group HTC, Landray MJ, Haynes R, et al. Effects of extended-release niacin with laropiprant in
high-risk patients. The New England journal of medicine. 2014; 371(3):203–212. [PubMed:
25014686]
56. Matsuzawa Y, Kita T, Mabuchi H, et al. Sustained reduction of serum cholesterol in low-dose 6-
year simvastatin treatment with minimum side effects in 51,321 Japanese hypercholesterolemic
patients. Circ J. 2003; 67(4):287–294. [PubMed: 12655157]
57. Wu CC, Sy R, Tanphaichitr V, Hin AT, Suyono S, Lee YT. Comparing the efficacy and safety of
atorvastatin and simvastatin in Asians with elevated low-density lipoprotein-cholesterol--a
multinational, multicenter, double-blind study. J Formos Med Assoc. 2002; 101(7):478–487.
Author Manuscript

[PubMed: 12353340]
58. Nakamura H, Arakawa K, Itakura H, et al. Primary prevention of cardiovascular disease with
pravastatin in Japan (MEGA Study): a prospective randomised controlled trial. Lancet. 2006;
368(9542):1155–1163. [PubMed: 17011942]
59. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men
with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. The New
England journal of medicine. 1995; 333(20):1301–1307. [PubMed: 7566020]
60. Colhoun HM, Betteridge DJ, Durrington PN, et al. Primary prevention of cardiovascular disease
with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS):
multicentre randomised placebo-controlled trial. Lancet. 2004; 364(9435):685–696. [PubMed:
15325833]
61. Morales D, Chung N, Zhu JR, et al. Efficacy and safety of simvastatin in Asian and non-Asian
coronary heart disease patients: a comparison of the GOALLS and STATT studies. Curr Med Res
Opin. 2004; 20(8):1235–1243. [PubMed: 15324526]
62. Gupta M, Braga MF, Teoh H, Tsigoulis M, Verma S. Statin effects on LDL and HDL cholesterol
Author Manuscript

in South Asian and white populations. J Clin Pharmacol. 2009; 49(7):831–837. [PubMed:
19398601]
63. Chapman N, Chang CL, Caulfield M, et al. Ethnic variations in lipid-lowering in response to a
statin (EVIREST): a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT). Ethn
Dis. 2011; 21(2):150–157. [PubMed: 21749017]
64. Albert MA, Glynn RJ, Fonseca FA, et al. Race, ethnicity, and the efficacy of rosuvastatin in
primary prevention: the Justification for the Use of Statins in Prevention: an Intervention Trial
Evaluating Rosuvastatin (JUPITER) trial. Am Heart J. 2011; 162(1):106–114. e102. [PubMed:
21742096]

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 13

65. Lipworth L, Fazio S, Kabagambe EK, et al. A prospective study of statin use and mortality among
67,385 blacks and whites in the Southeastern United States. Clin Epidemiol. 2014; 6:15–25.
Author Manuscript

[PubMed: 24379700]
66. Eckel, Rh; Fau - Jakicic, JM.; Jakicic, Jm; Fau - Ard, JD.; Ard, Jd; Fau - de Jesus, JM., et al. 2013
AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
(1524-4539 (Electronic)).
67. Behavioral Risk Factor Surveillance System: BRFSS 2002 survey data and documentation. http://
www.cdc.gov/brfss/annual_data/annual_2002.htm.
68. Schoenborn CA, Adams PF, Peregoy JA. Health behaviors of adults: United States, 2008–2010.
Vital Health Stat 10. 2013; (257):1–184. [PubMed: 25116426]
69. Lemacks J, Wells BA, Ilich JZ, Ralston PA. Interventions for improving nutrition and physical
activity behaviors in adult African American populations: a systematic review, January 2000
through December 2011. Prev Chronic Dis. 2013; 10:E99. [PubMed: 23786910]
70. Ickes MJ, Sharma M. A systematic review of physical activity interventions in Hispanic adults. J
Environ Public Health. 2012; 2012:156435. [PubMed: 22496702]
Author Manuscript

71. Bender MS, Choi J, Won GY, Fukuoka Y. Randomized controlled trial lifestyle interventions for
Asian Americans: a systematic review. Prev Med. 2014; 67:171–181. [PubMed: 25086326]
72. Dhokarh R, Himmelgreen Da, Fau - Peng Y-K, Peng Yk, Fau - Segura-Perez S, Segura-Perez S,
Fau - Hromi-Fiedler A, Hromi-Fiedler A, Fau - Perez-Escamilla R, Perez-Escamilla R. Food
insecurity is associated with acculturation and social networks in Puerto Rican households.
(1878-2620 (Electronic)).
73. Mainous AG 3rd, Diaz Va Fau - Geesey ME, Geesey ME. Acculturation and healthy lifestyle
among Latinos with diabetes. (1544-1717 (Electronic)).
74. Lin H, Bermudez Oi, Fau - Tucker KL, Tucker KL. Dietary patterns of Hispanic elders are
associated with acculturation and obesity. (0022-3166 (Print)).
75. Palaniappan LP, Araneta MR, Assimes TL, et al. Call to action: cardiovascular disease in Asian
Americans: a science advisory from the American Heart Association. Circulation. 2010; 122(12):
1242–1252. [PubMed: 20733105]
76. Zhou BF, Stamler J, Fau - Dennis B, Dennis B, Fau - Moag-Stahlberg A, et al. Nutrient intakes of
Author Manuscript

middle-aged men and women in China, Japan, United Kingdom, and United States in the late
1990s: the INTERMAP study. (0950-9240 (Print)).
77. Song YJ, Hofstetter Cr, Fau - Hovell MF, Hovell Mf, Fau - Paik HY, et al. Acculturation and
health risk behaviors among Californians of Korean descent. (0091-7435 (Print)).
Author Manuscript

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.

 Pu et al. Page 14

Key Points
Author Manuscript

• Among all racial/ethnic groups, Asian Indians, Filipinos and Hispanics are at
higher risk for dyslipidemia, which is consistent with the higher coronary heart
disease (CHD) mortality rates in these groups

• Compared to other racial/ethnic groups, statins may have a higher efficacy for
Asians. Studies suggest lower starting dosage in Asians, but the data are mixed.

• Genetic differences in statin metabolism can in part explain this racial/ethnic

difference in statin sensitivity and adverse effects

• Lifestyle modification is recommended as part of dyslipidemia control and

management and both African Americans and Hispanics have more sedentary
behavior and less favorable diet profile.
Author Manuscript
Author Manuscript
Author Manuscript

Cardiol Clin. Author manuscript; available in PMC 2016 May 01.