The Demography of Hypertension in Indonesia:

the Past and Future Implications of Changing Weight

Dynamics and Population Aging
Nikkil Sudharsanan∗

Population Studies Center

University of Pennsylvania

Extended Abstract

Hypertension is the leading risk factor for premature mortality in many developing countries.
Although studies have shown that hypertension is rising, the reasons for this growth are unclear.
Two dynamics in particular may be driving the rise of hypertension in developing countries: (1)
unhealthy weight is increasing and (2) populations are aging. Using four waves of data from
Indonesia, I combine a mathematical model of hypertension change with panel-data estimates of
the relationship between BMI and hypertension. I then model the growth in hypertension between
1997 and 2014 as a function of rising BMI and changing age structure. The reasons for the sharp
increase in hypertension varied between urban and rural areas: in rural areas, the dramatic growth
in BMI explained a large fraction of rising hypertension; surprisingly, population aging was the
sole driver of rising hypertension in urban areas. My planned analyses will project the effects of
changing BMI and population aging on the future prevalence of hypertension. My results suggest
that rising BMI is an important cause of increasing hypertension in rural Indonesia. The prevalence
of hypertension is likely to keep rising as unhealthy weight continues to increase and the population
ages.

∗
I am grateful to Michel Guillot, Irma Elo, Hans-Peter Kohler, Jere Berhman, and Sam Preston for their input.
All errors are my own

1
1 Introduction

The prevalence of non-communicable diseases (NCDs) is rising in developing countries, prompting

concern and calls for action from health and policy experts globally (Lozano et al., 2013; Murray
et al., 2013; Lloyd-Sherlock et al., 2014). This growth has been especially pronounced in Asia:
the burden of stroke, diabetes, heart disease, and hypertension have all increased over the past
20 years (Dans et al., 2011; Ghaffar et al., 2004). Rising hypertension in particular may have
substantial health consequences, since hypertension is the leading risk factor for adult mortality
in many developing countries (Lim et al., 2013). For example, hypertension is the primary risk
factor for the top two causes of death in Indonesia: stroke (21% of all deaths) and ischemic heart
disease (9% of all deaths) (World Health Organization, 2010). The populations of many developing
countries are also aging, placing greater fractions of the population at the ages where the risk of
hypertension is high (World Bank Group, 2012). The combined effects of population aging and
the epidemiological transition have created an urgent need to understand and reduce the burden
of hypertension in developing countries.

Although many studies have shown that hypertension is rising in developing countries, the reasons
for this growth are ambiguous. While population aging, urbanization, changing diets, and changing
physical activity patterns have all been implicated, the empirical evidence linking these changes to
rising hypertension is limited. At the population level, two changes in particular may be driving
the rise of hypertension. First, obesity and unhealthy weight are rising in developing countries.
Rising weight is especially important since it is one of the primary risk factors for high blood
pressure (Staessen et al., 1989). Second, populations in many developing countries are aging.
Since hypertension displays a near linear rise in prevalence over age in almost every context (He
and Whelton, 1997), a greater share of the population at the older ages would result in a higher
population prevalence of hypertension, since more people are living at the ages with higher age-
specific risks of disease. Both these sources of population change are occurring simultaneously and
the unique contribution of each to the rise in the prevalence of hypertension is unknown.

The goal of this study is to fill in this gap in the literature. Using data from Indonesia – the
third largest developing country and one of the only developing countries with multiple waves
of longitudinal, nationally representative measured biomarker data – I quantify the contribution
of population level epidemiological and demographic changes to the growth in hypertension over
a 17-year period. Specifically, I use panel data to estimate the relationship between BMI and
hypertension in Indonesia. I then combine a mathematical model of hypertension change with the
panel-data estimates to model the growth in hypertension between 1997 and 2014 as a function of
rising BMI and changing age structure. This approach provides an estimate of the contribution
of changing BMI to the growth in hypertension over the period. Finally, I project the effects of
changing weight dynamics and population aging on future levels of hypertension in Indonesia. By
measuring the underlying epidemiological and demographic reasons for growing hypertension, the

2
results of this study can inform policy by identifying which ages should be targeted to best reduce
the burden of hypertension. In addition, knowing how hypertension might unfold in the future can
prepare health systems to prevent, diagnose, and manage future levels of disease.

2 Data

Data are from the 1997, 2000, 2007, and 2014 waves of the Indonesian Family Life Survey (IFLS)
(Frankenberg et al., 1995; Strauss et al., 2004, 2009). The IFLS is a longitudinal survey of over
30,000 individuals from 13 of Indonesia’s 27 provinces – making the IFLS representative of 83% of
the Indonesian population. The IFLS is also one of the few longitudinal ,surveys from developing
countries with multiple waves of measured biomarker and anthropometric health data, provid-
ing a rare source of directly measured information on changes in non-communicable diseases over
time.

To select households, the IFLS first randomly sampled 321 enumeration areas based on Indonesia’s
SUSENAS survey. Within each selected EA, between 200-300 households were randomly selected.
For each identified household, information on household characteristics, household members, and
household expenditure and consumption were provided by the household member most knowledge-
able about household affairs. Individuals above the age of 30 were asked to provide information on
self-reported health conditions; in addition, trained assessors collected measured blood pressure,
height, and weight for each of these individuals.

2.1 Main variables

The main outcome is measured hypertension. Consistent with the World Health Organization
cutoffs, individuals were classified as hypertensive if they had a measured systolic blood pressure
≥ 140 mmHg or a measured diastolic blood pressure ≥ 90 mmHg (World Health Organization,
2003)1 . In many developed countries, individuals are classified as hypertensive based on measured
cutoffs and whether they are taking medication for high blood pressure. Unfortunately, only the
most recent wave of IFLS data has information on medication; however, even in 2014, less than 5%
of individuals reported taking medication for high blood pressure (based on author’s calculations),
so this source of measurement error is unlikely to greatly affect my rates.

Unhealthy weight is one of the main risk factors for hypertension (Staessen et al., 1989). To assess
role of changing weight dynamics on hypertension, I calculate each individual’s body mass index
(BMI) based on assessor measured height and weight (unfortunately information on the other main
risk factors for hypertension, such as dietary sodium intake and physical activity, was not collected
in the IFLS).
1
For the 2007 and 2014 waves, two separate measurement of blood pressure were collected. For these waves, I
averaged the two measurements before classifying individuals.

3
Finally, I classify individuals into age-sex-urban/rural groups based on self reported age, sex, and
census classifications of urban/rural.

3 Methods

To decompose the growth in hypertension and obesity into the portion explained by population ag-
ing and the portion explained by changing age-specific prevalences rates, I utilize the “line-integral”
method of decomposition developed by Horiuchi, Wilmoth, and Pletcher (2008). Although demog-
raphers have a long tradition of employing decomposition methods to understand the change in
rates (Kitagawa, 1955; Gupta, 1993), this method is unique because it provides a clear mathemat-
ical motivation and justification for decomposition that can be applied to any rate with a defined
derivative.

To conduct the decomposition, first note that the while the prevalence is usually calculated as the
number of cases at all ages divided by the total population, it can equivalently be represented by
equation 1.
X
P (t) = cx (t) ∗ mx (t) (1)
age groups

where P (t) is the prevalence rate at time t, cx is the proportion of the population in the xth age
group at time t, and mx (t) is the age-specific prevalence rate in the xth age group at time t. This
formulation is insightful because it provides a mathematical basis for how changes in population age
structure affect the prevalence: population aging is mathematically a growth in the cx (t)’s in the
older ages, placing greater weight on the mx (t)’s at the those age. Since the mx (t)’s are higher in
the older ages, a greater weight placed on those age-specific rates will cause P (t) to increase.

Using the line integral method, the change in the prevalence between time points t1 and t2 can be
expressed equivalently by equation 2.

X Z ci (t2 )
max
∂P (t) Xmax Z mi (t2 )
∂P (t)
P (t2 ) − P (t1 ) = dci (t) + dmi (t) (2)
ci (t1 ) ∂ci (t) mi (t1 ) ∂mi (t)
i=1 i=1

The first term represents the contribution of changes in the proportion of the population in each age
group i while the second term is contribution of changes in the age-specific rates for age group i. For
a more detailed exposition of the method please see Horiuchi, Wilmoth, and Pletcher (2008).

While this decomposition estimates the contribution of changes in the age-specific rates of hyper-
tension to the overall prevalence, an important question is how much of the change in hypertension
is plausibly related to the changing age-specific levels of BMI? Answering this question requires
two important pieces of information: (1) a measure of the “effect” of BMI on hypertension, and (2)
a mathematical formulation of the relationship between age-specific levels of BMI and the overall
prevalence of hypertension.

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The relationship between BMI and hypertension could be estimated using a logistic regression of
hypertension on BMI (adjusting for age) for each sex and urban-rural group:

θi X max
ln( ) = α + β ∗ BMIi + γi ∗ age groupj i (3)
1 − θi
j=1

However, if unobserved characteristics, such as diet, were related to both BMI and hypertension,
the estimated β̂ would be biased. Assuming that these unobserved sources of bias do not vary
over time, the longitudinal structure of the data can be used to difference out these sources of
confounding by estimating the following fixed-effects logistic regression:

θi X max X max
ln( ) = α + β ∗ BMIi + γi ∗ age groupj i + γi (4)
1 − θi
j=1 i=2

where γi is the individual level fixed effect for individual i. While the β̂ from this regression
may still be biased by time variant confounders, the fixed effects approach still provides an im-
provement over the standard approach by controlling for observed and unobserved time-invariant
confounders.

Once β̂ is known, an equation relating BMI to the crude prevalence of hypertension is needed to
assess the contribution of BMI to changes in hypertension over time. Taking equation (2), I replace
the mx (t)’s with:
eα̂+β̂∗E(BMI)(t)+γx ∗age groupx +E(γi )
m̂x (t) = (5)
1 + eα̂+β̂∗E(BMI)(t)+γx ∗age groupx +E(γi )
where m̂x (t) are the predicted prevalence rates at age x calculated using the estimated regression
coefficients and E(BM I)(t), the average BMI for age group x at time t. This substitution into
equation (2) results in the following equation (replacing E(BM I) with φ):

X Z ci (t2 )
max
∂P (t)
max Z φi (t2 )
X ∂P (t)
max Z ǫi (t2 )
X ∂P (t)
P (t2 ) − P (t1 ) = dci (t) + dφi (t) + dǫi (t) (6)
ci (t1 ) ∂ci (t) φi (t1 ) ∂φi (t) ǫi (t1 ) ∂ǫi (t)
i=1 i=1 i=1

Here ǫ is the portion of m that is not explained by BMI. I can now apply the line-integral decom-
position procedure to equation (6) to measure the contribution of changing age-specific mean levels
of BMI to the growth in hypertension over time.

3.1 Approach

I first describe the overall trend in hypertension between 1997 and 2014 by presenting the crude
prevalence of hypertension for each survey year separately by sex. To highlight the underlying
population dynamics driving this change in hypertension, I then show how the proportionate size
and mean BMI for each age group changed over the period.

5
To measure how much of the change over time is due to changing age structure and how much
to change age-specific rates of hypertension, I apply the line-integral decomposition to the overall
prevalence of hypertension, separately by sex and urban-rural residence.

My next goal is to understand how much of the change in prevalence over time was due to changing
age-specific levels of weight. To answer this question, I first estimate regressions of the form (3)
and (4) separately by sex and urban/rural residence to determine the relationship between BMI
and hypertension. Next, I combine the age-specific levels of BMI for each time period with the
estimated regression coefficients to form equation (6), and apply the decomposition procedure to
this equation. This approach splits the overall change in hypertension into the portion explained by
aging, the portion by changes in the age-specific levels of BMI, and the portion explained by changes
in the age-specific prevalence rates of hypertension that are unrelated to changing BMI.

My future analyses will combine information on changing weight dynamics and population aging to
project the prevalence of hypertension into the future under different scenarios of weight dynamics.
This approach would build on the projection method developed by Preston, Person, and other
Person.

4 Preliminary Results

Figure 1 graphs the crude prevalence of hypertension for the years 1997, 2000, 2007, and 2014 by
sex. The first main conclusion is that for both men and women, the overall levels of hypertension
are very high (between 32% and 42%). The prevalence of hypertension also grew substantially over
this period: between 1997 and 2014 hypertension grew from around 32% to 36% for men and from
35% to 42% for women.

Figure 2 shows the age dynamics of the proportionate size and mean BMI for each age group over
the period. There are two main conclusions. First, the population is aging for both men and
women. For example, for both sexes, the 30-40 age group was the largest fraction of the population
in 1997. By 2014, the 40-50 and 50-60 age groups became the largest. The second main conclusions
is that the age-specific levels of BMI have increased sharply, especially between ages 30-60. One
important note is that although mean BMI increased substantially, the levels are still within the
normal weight range, indicating that obesity is not widely prevalent.

Table 1 quantifies the contribution of population aging and changes in the age-specific rates over
time to the growth in hypertension. With the exception of urban men, the prevalence of hyper-
tension grew between 6-8 percentage points over the period. The majority of this growth was due
to population aging: for rural men 63% was due to population, 77% for rural women, and more
than 100% for women (contributions greater than 100% occur when the aging effect was counter-
balanced by decreasing rates). However, while population aging was responsible for the majority
of the growth in hypertension, for rural men and women, a large fraction was also due to rising

6
age-specific rates of hypertension (Table 1, 2.4 percentage points or 37% for rural men and 1.7
percentage points or 23% for rural women).

In Figure 3, the portion of the overall change in prevalence due to increasing rates is further
decomposed to identify which ages contributed the most to the overall rate contribution. The graph
reveals that for rural men and women, rising hypertension above age 40 was primarily responsible
for the change in hypertension due to increasing rates. Visually, the largest single contribution is
from the 35-40 age group for men and the 40-45 age group for women. The next series of results
explore the role of rising weight for these changes across age.

Table 2 presents logistic regression estimates for the relationship between BMI and hypertension
by sex and urban-rural group. The table shows 4 different specifications: pooled regressions with
a linear BMI effect, fixed effects regressions with a linear BMI effect, pooled regressions with a
quadratic BMI effect, and fixed effect regressions with a quadratic BMI effect. For almost every sex-
urbanicty-specification group, BMI displays a strong association with hypertension. Interestingly,
the magnitude of this association increases between he pooled and fixed effects regressions. There
is also strong evidence that relationship between BMI and hypertension is non-linear. For most
of the quadratic specifications, the squared term is negative, indicating a declining relationship
between BMI and hypertension as higher levels of BMI.

Table 3 presents preliminary results of the contribution of changing BMI to the growth in hyperten-
sion between 1997 and 2014 (as of now, only one set of regression estimates were used; future results
will include the results from all specifications). For both rural men and women, the results reveal
that almost all the growth in hypertension attributable rising age-specific rates can be explained
by increasing BMI. For example, 92% of the 2.4 percentage point contribution of changing rates
was due to rising BMI for rural men while 71% of the 1.7 percentage point contribution was due
to rising BMI for rural women.

5 Preliminary Discussion and Next Steps

Hypertension is the leading risk factor for adult mortality in developing countries and is related to
both stroke and heart disease. I find that the prevalence of hypertension in Indonesia is very high
and increased substantially between 1997 and 2014 for men and women. Over this same period
there were important population dynamics underlying the growth in hypertension: demographically
the population of Indonesia aged while epidemiologically the levels of BMI grew substantially in
the younger middle ages.

Population aging was primarily responsible for the growth in hypertension for men and women in
both rural and urban areas. This finding has strong implications for the future levels of hyperten-
sion: since the population of Indonesia is projected to continue aging, these results suggest that
even if the age-specific rates of hypertension do not change over time, the prevalence of hypertension

7
and consequently the number of hypertensive individuals will continue to rise.

There were important urban-rural differences in the contribution of aging: in urban areas, all of
the growth in hypertension was due to populations getting older, not to rising age-specific rates of
hypertension. In contrast, the growth in hypertension in rural areas was split between aging and
rising rates, with between 20-40% of the growth due to rising levels of hypertension in the older
middle ages. These patterns suggest that changing behavioral or risk factor patterns, such as rising
unhealthy weight, may be driving changes in hypertension in rural areas.

Although the average BMI in Indonesia is in the normal weight range, there was a steady increase
in weight between 1997 and 2014. Even at the very low levels of unhealthy weight in Indonesia, I
still find strong evidence that changes in BMI are associated with an increased risk hypertension.
This finding suggests that changing age-specific levels of weight are plausibly explain the rise in
age-specific rates of hypertension in rural areas. Indeed, based on my preliminary findings, I find
that nearly all of the rise in hypertension attributable to rising age-specific rates in rural areas can
be explained by growing levels of weight. This suggests that the prevalence of hypertension in the
future may continue to rise as unhealthy weight grows.

Based on my preliminary findings, both changing weight and population aging contributed to the
growth in hypertension in Indonesia. Planned future analyses will examine the robustness of these
findings and project the implications of continued aging and weight change for the future prevalence
of hypertension.

5.1 Next Steps

The final paper will incorporate a few additional steps:

1. Build on the projection methods developed by Preston et al (2014) to project the effect of
changes in BMI and population aging on the future prevalence of hypertension in Indonesia.

• This will be done for different patterns of aging, BMI, and hypertension to document
several potential scenarios

2. Test the sensitivity of my results to the estimated relationship between BMI and hypertension
by estimating the contribution of BMI based on various model specifications (fill in Table 3
below)

3. Test the sensitivity of my results to alternate measures of unhealthy weight, including a

dichotomous indicator for obese and measured waist circumference.

8
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sion among older adults in low-and middle-income countries: prevalence, awareness and control.
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Staessen, J., Fagard, R., Lijnen, P., and Amery, A. (1989). Body weight, sodium intake and blood
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Tables and Figures

Figure 1: Crude prevalence of hypertension between 1997 and 2014 by sex, Indonesian Family Life
Survey
.42
.4
Prevalence
.36 .38
.34
.32

1995 2000 2005 2010 2015

Year

Men Women

11
Figure 2: Age dynamics of proportionate population size and mean BMI by 10 year groups, 1997-
2014, Indonesian Family Life Survey

Men − Age structure Men − BMI

40−50
.4

23
50−60
Percent of population

30−40
.3

21 22
50−60 60−70
40−50
30−40
Mean
.2

60−70 70−80
20
.1

70−80 80+
19

80+
0

1997 2000 2003 2006 2009 2012 2015 1997 2000 2003 2006 2009 2012 2015
Year Year

Women − Age structure Women − BMI

26
.4

40−50
Percent of population

30−40
50−60
24
.3

40−50 60−70
50−60
Mean

30−40
22
.2

70−80
60−70
80+
20
.1

70−80
80+
18
0

1997 2000 2003 2006 2009 2012 2015 1997 2000 2003 2006 2009 2012 2015
Year Year

12
Table 1: Decomposition of the change in hypertension between 1997 and 2014, Indonesian Family
Life Survey
Prevalence Rate contribution Aging contribution
1997 2014 Change Abs % of tot Abs % of tot
Rural Men 0.300 0.365 0.065 0.024 0.37 0.041 0.63
Urban Men 0.365 0.379 0.014 -0.022 -1.59 0.036 2.59
Rural Women 0.350 0.425 0.075 0.017 0.23 0.058 0.77
Urban Women 0.352 0.428 0.076 -0.004 -0.05 0.080 1.05
Notes: Contributions for hypertension for urban men are very irregular since the change in hyper-
tension over that period was small.

Figure 3: Age-specific contributions to the growth in hypertension between 1997 and 2014, Indone-
sian Family Life Survey

Rural Men Rural Women

0.10

0.10
% contribution

% contribution
0.00

0.00
−0.10

−0.10

30 40 50 60 70 80 30 40 50 60 70 80

Age group Age group

13
 Table 2: Estimated relationship between BMI and hypertension, Indonesian Family Life Survey
Rural Men Rural Men Urban Men Urban Men Rural Women Rural Women Urban Women Urban Women
VARIABLES Pooled Fixed Effects Pooled Fixed Effects Pooled Fixed Effects Pooled Fixed Effects

bmi 0.153*** 0.199*** 0.149*** 0.178*** 0.106*** 0.162*** 0.0982*** 0.137***

(0.00773) (0.0263) (0.00625) (0.0243) (0.00565) (0.0199) (0.00508) (0.0179)
14

bmi 0.333*** 0.469*** 0.349*** 0.678*** 0.161*** 0.127 0.167*** 0.262**

(0.0419) (0.0827) (0.0411) (0.117) (0.0373) (0.110) (0.0374) (0.0964)
bmi squared -0.00379*** -0.00556*** -0.00408*** -0.00997*** -0.00113 0.000701 -0.00131+ -0.00238
(0.000844) (0.00148) (0.000812) (0.00221) (0.000735) (0.00221) (0.000712) (0.00180)

Observations 14,210 4,381 15,178 4,210 15,572 5,279 17,309 5,108

*** p<0.001, ** p<0.01, * p<0.05, + p<0.1.
Robust standard errors in parentheses. Models include dummy variables for each age group and time period.
Table 3: Contribution of changing BMI to the growth in hypertension between 1997 and 2014,

Indonesian Family Life Survey

Contribution of BMI

Linear - Pooled Linear - FE Quad - Pooled Quad - FE

Rate cont. Abs % of tot Abs % of tot Abs % of tot Abs % of tot

Rural Men 0.024 0.022 0.92 * * * * * *

Rural Women 0.017 0.012 0.71 * * * * * *

Notes: Results for urban men and women were not shown since changing rates did not contribute

to the growth in hypertension for these groups. Cells with stars correspond to planned future anal-

yses. Estimated contributions correspond to four different model specifications of the relationship

between BMI and hypertension (linear BMI effect with pooled regression, linear BMI effect with

a fixed effects regression, quadratic BMI effect with pooled regression, and quadratic BMI effect

with fixed effects regression). Contributions were estimated from equation (6).

15