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Impact of Waist Circumference on the Relationship Between

Blood Pressure and Insulin


The Quebec Health Survey
Paul Poirier, Isabelle Lemieux, Pascale Maurie`ge, Eric Dewailly, Carole Blanchet,
Jean Bergeron, Jean-Pierre Despres
AbstractHyperinsulinemia has been suggested to be involved in the etiology of obesity-associated hypertension. The
objective of the present study was to quantify, in a population-based study, the respective contributions of excess
adiposity (body mass index [BMI]), waist circumference (WC), fasting insulin levels, and insulin sensitivity to the
variation of resting blood pressure. The Quebec Health Survey was used to obtain fasting plasma insulin and glucose
levels and resting blood pressure as well as anthropometric measurements in a representative sample of 907 men and
937 women. When the sample was divided into tertiles of BMI and further stratified on the basis of the 50th percentile
of WC (88 cm in men), nonobese men in the first BMI tertile (23.2 kg/m2) but with abdominal obesity were
characterized by an increased systolic blood pressure (SBP) compared with nonobese men with low WC (13018 versus
12011 mm Hg; meanSD; P0.075). The SBP was comparable to SBP values measured among men in the top BMI
tertile (12914 mm Hg for BMI 26.6 kg/m2). When subjects were classified into tertiles of fasting insulin and WC,
no association between insulin levels and blood pressure was noted, once the variation in WC was considered. Insulin
sensitivity (estimated with homeostasis model assessment [HOMA]) did not explain variation in blood pressure in men,
whereas the contribution of HOMA in women was of marginal clinical significance (R2 of 1.3%; P0.0001). These
results suggest that the documented association between obesity, fasting insulin, insulin sensitivity, and blood pressure
is largely explained by concomitant variation in WC. (Hypertension. 2005;45:363-367.)
Key Words: insulin blood pressure obesity

t is well known that there is a greater prevalence of


hypertension in obese patients than among normal-weight
subjects.1,2 However, not every obese patient is hypertensive,
another indication that obesity is a heterogeneous condition.3
Although excess fatness may contribute to hypertension in
some obese patients, the mechanisms responsible for the
weight-related increase in blood pressure are still unclear.
One possible link between weight gain and hypertension is
the insulin-resistant and compensatory hyperinsulinemic state
frequently observed in obese individuals.4,5 Insulin resistance,
hyperinsulinemia, and blood pressure have been correlated
not only in obese but also in lean hypertensive patients.6 8
However, the association between fasting plasma insulin and
hypertension has been inconsistent among studies.8 10
Nevertheless, insulin has been shown in multiple studies to
have acute actions on the sympathetic nervous system, renal
function, and the cardiovascular system that could lead to
hypertension if these effects are sustained.4,11 Despite the fact
that abdominal obesity is often accompanied by features of
the metabolic syndrome, including (but not always) hyper-

tension, the respective contributions of abdominal obesity


versus hyperinsulinemia to high blood pressure are poorly
defined. Recently, Hayashi et al12 reported that visceral
obesity was associated with an increased odds of hypertension in Japanese Americans independently of fasting plasma
insulin. Of note, 40% of the cohort was diagnosed with
hypertension.12 Thus, the aim of the present study was to
quantify, in a population-based sample (the Quebec Health
Survey), the respective contributions of excess adiposity (as
crudely estimated by the body mass index [BMI]), abdominal
fat accumulation (estimated by waist circumference [WC]),
fasting insulin levels, and insulin sensitivity (assessed with
the homeostasis model assessment [HOMA]) to the variation
of resting blood pressure.

Methods
As part of the federalprovincial Canadian Heart Health Initiative,
Sante Quebec (an organization of the Quebec Statistics Institute)
conducted the Heart Health and Nutrition Survey among Quebecers.
The primary objective of the survey was to determine the prevalence
of cardiovascular risk factors and participants knowledge and

Received October 7, 2004; first decision October 25, 2004; revision accepted November 10, 2004.
From the Quebec Heart and Lungs Institute (P.P., I.L., J.-P.D.), Laval Hospital Research Center, Canada; and Lipid Research Center (P.M., J.B.) and
Public Health Research Center (E.D., C.B.), Centre Hospitalier de lUniversite Laval Research Center, Quebec, Canada.
Correspondence to Paul Poirier MD, PhD, FRCPC, FACC, Institut Universitaire de Cardiologie et de Pneumologie/Laval Hospital, 2725 Chemin
Sainte-Foy, Sainte-Foy, Quebec, Canada G1V 4G5. E-mail Paul.Poirier@crhl.ulaval.ca
2005 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org

DOI: 10.1161/01.HYP.0000155463.90018.dc

363
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Hypertension

March 2005

awareness of the causes and the consequences of these factors.13


Individuals excluding the aboriginal populations represented the
sample of the Quebec Health Survey. The global sample included
5 000 371 individuals taken from the 6 700 000 citizens of the
Quebec province, which covered most of the entire adult population.
The study population consists of 1944 noninstitutionalized subjects
(907 men and 937 women; aged 18 to 74 years). Participants
constituted a stratified probability sample of the population and were
selected according to a statistical sampling design. The sampling
design, developed by the Quebec Bureau of Statistics, has been
described previously.13 In brief, the territory was divided in primary
units of sampling (PUS; n95); each unit counted 40 participants
from a target sample of 3800 individuals. Thereafter, the PUS were
stratified and subjects were divided into 6 groups according to age
and sex (18 to 34, 35 to 64, and 65 to 74 years of age for men and
women). Individuals were selected from health insurance files, and
2056 subjects completed the evaluation, which consisted of interviews, validated questionnaires for medical history, physical examination, and blood sampling. Complete data sets were available from
1944 patients. Participants were asked to fast overnight before giving
blood samples. Lipid profile and plasma insulin levels were analyzed
as described previously.14 17 Insulin sensitivity was estimated from
the HOMA (fasting insulinfasting glucose/22.5).18 Written informed consent was obtained from all subjects.
Height was measured in standing position, with shoulders and
buttocks against the wall, the subject looking straight ahead, with
joined feet, and arms hanging on both sides. Body weight was
measured with a calibrated beam scale. WC was obtained using a
graduated tape when subjects were in standing position. WC was
measured as the narrowest circumference of the trunk. However,
when the position of the narrowest circumference could not be
identified, the measurement was taken at the level of the last rib.16,17
BMI was calculated as weight/height (kg/m2). Resting blood pressure
was taken in a sitting position after a 5-minute rest using a mercury
sphygmomanometer according to standard procedures.16 Subjects
were asked to refrain from eating or smoking for 30 minutes before
the procedure. Per protocol design, trained nurses visited participants
at their homes. Also, participants came to the clinic after an
overnight fast and met a physician who performed a medical history
and physical examination. Blood pressure values are means of 4
different measurements: 2 taken at home and 2 taken at the clinic.

Statistical Analysis
Results presented in this article were derived from weighed data, to
re-establish the equiprobability of an individual being selected from
the sample and to take into account nonresponse by age, sex, and
geographic stratum. To achieve this objective, each respondent was
given a value (weight) corresponding to the number of persons he or
she represented in the Quebec population.16 Thus, all the data used in
the present analyses were weighed and are representative of the
entire Quebec adult population. Pearson correlation coefficients were
calculated to quantify the univariate associations among variables.
Comparisons among subgroups were performed by an ANOVA with
the General Linear Model, and the Duncan post hoc test was used
when a significant group effect was observed. Covariance analysis
was also conducted to adjust variables for age-related differences
among subgroups. Furthermore, multiple regression analyses were
performed to quantify the independent contribution of BMI, WC,
fasting insulin levels, and insulin sensitivity (HOMA) to the variance
of systolic blood pressure (SBP) or diastolic blood pressure. Subjects
on hypertensive medications were included. All analyses were
performed with the SAS statistical package (SAS Institute).

Results
The characteristics of the 907 men and 937 women included
in this study are shown in Table 1. The average BMI was 25
kg/m2 in both genders, whereas average WC values corresponded to 89.711.1 cm in men and 77.312.1 cm in
women. The range of BMI was 16.7 to 46.9 kg/m2 in men and

TABLE 1. Characteristics of Men and Women of the Quebec


Health Survey
Parameter

Men
(n907)

Women
(n937)

4115

4215

P Value

Physical characteristics
Age, years

0.5738

Weight, kg

76.212.6

62.212.1

0.0001

BMI, kg/m2

25.43.9

24.44.9

0.0001

WC, cm

89.711.1

77.312.1

0.0001

Cholesterol, mmol/L

5.281.07

5.211.05

0.4683

LDL cholesterol, mmol/L

3.280.93

3.170.92

0.0400

HDL cholesterol, mmol/L

1.190.30

1.410.34

0.0001

Triglycerides, mmol/L

1.851.51

1.390.78

0.0001

Cholesterol/HDL, cholesterol

4.701.58

3.901.25

0.0001

6849

6436

17.317.8

15.011.5

0.0001

Fasting glucose, mmol/L

5.51.7

5.11.1

0.0001

SBP, mm Hg

12514

11917

0.0001

789

749

0.0001

Metabolic profile

Fasting insulin, pmol/L


HOMA

Diastolic blood pressure, mm Hg

0.4398

Values are meansSD.

15.0 to 48.5 kg/m2 in women. There were 44 men (4.8%) and


75 women (8%) with hypertension (140/90 mm Hg) or
using antihypertensive medications. Correlations between
BMI, WC, and fasting insulin levels and either resting
diastolic blood pressure or SBP are presented in Table 2.
There were significant associations between BMI, WC, and
fasting insulin concentrations and diastolic blood pressure or
SBP in women, whereas no association was found between
fasting insulin levels and diastolic blood pressure in men.
Therefore, although most correlations were statistically significant, the highest correlations with either SBP or diastolic
blood pressure were obtained in both genders with WC.
Multivariate analyses revealed that WC was the best variable,
explaining a significant proportion of variance of either
diastolic blood pressure or SBP (Table 3). Insulin sensitivity
estimated from the HOMA18 did not add statistically significant information in men, whereas the information provided
with HOMA in women may be considered clinically
nonsignificant.
Figure 1 presents diastolic blood pressure and SBP values
according to the 50th percentile of WC and tertiles of BMI
among men and women, respectively, after adjustment for
age by covariance analysis (Figure 1A and 1B).
TABLE 2. Correlations Between BMI, WC, and Fasting Insulin
Levels and Either Diastolic Blood Pressure (DBP) or SBP
Parameter

DBP (mm Hg)

SBP (mm Hg)

Men

Women

Men

Women

BMI, kg/m

r0.31*

r0.40*

r0.29*

r0.43*

WC, cm

r0.35*

r0.44*

r0.38*

r0.47*

Fasting insulin, pmol/L

r0.05

r0.20*

r0.09

r0.24*

HOMA

r0.06

r0.23*

r0.11

r0.30*

*P0.0001; P0.05.

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Poirier et al

Waist Circumference, Blood Pressure, and Insulin

365

Figure 1. Diastolic blood pressure and


SBP according to WC and BMI among
men (A) and women (B) of the Quebec
Health Survey. 1, 2, 3, 4, and 5 indicate
significantly different from the corresponding subgroup. Men (A), All
P0.0001; age-adjusted all P0.03);
women (B), all P0.0001; age-adjusted
all P0.05.

Nonobese men with abdominal obesity (88 cm) were


characterized by an elevation in SBP, which was comparable
to SBP values measured among men in the top BMI tertile
(26.6 kg/m2). Regarding diastolic blood pressure, WC
seemed to have a greater influence than BMI in the determination of elevated diastolic blood pressure (Figure 1A).
Among women, the highest SBP was observed for
subjects who were in the upper tertile of BMI (24.8
kg/m2) and characterized by an elevated WC (74 cm).
Finally, the highest diastolic blood pressure was observed
among women in the upper tertile of BMI and with an
elevated WC (Figure 1B).
When men (Figure 2A) and women (Figure 2B) were
classified on the basis of tertiles of fasting insulin (49.6,
TABLE 3. Multivariate Regression Analyses Showing the
Independent Contribution of WC to the Variance of Diastolic
Blood Pressure (DBP) or SBP
Dependent
Variables

Independent
Variables

Partial
(R 2100)

Total
(R 2100)

P Value

WC

12.4%

12.4%

0.0001

Men
DBP

SBP

Fasting insulin

0.37%

12.8%

0.03

BMI

0.21%

13.0%

0.1464

WC
BMI

14.4%
0.24%

14.4%

0.0001

14.6%

0.1170

18.8%

0.0001

Women
DBP

WC
BMI

SBP

WC

18.8%
0.23%
22.1%

19.0%

0.1047

22.1%

0.0001

Fasting insulin

0.94%

23.1%

0.0008

HOMA

0.36%

23.4%

0.0001

Variables included in the model were BMI, WC, fasting insulin concentrations, and HOMA (fasting insulinfasting glucose/22.5).

49.6 to 66.5, and 66.5 pmol/L in men and 48.3, 48.3 to


64.9, and 64.9 pmol/L in women) and WC (84, 84 to 93,
and 93 cm in men and 69, 69 to 79, and 79 cm in
women), no association was found between variation in
insulin and blood pressure once the variation in WC was
taken into account. Data were adjusted for age. For instance,
diastolic blood pressure and SBP values were elevated in the
upper tertiles of WC, irrespective of the presence/absence of
hyperinsulinemia (Figure 2A and 2B).

Discussion
Results of the present study suggest that the well-documented
association between obesity, fasting insulin, insulin sensitivity, and blood pressure may largely, if not entirely, be
explained by phenomena related to the concomitant variation
in the amount of abdominal fat, as estimated by a simple
clinical parameter: WC.
In whites, there have been many reports supporting an
association between insulin resistance and hypertension.6,19
On the other hand, in some studies, 50% of hypertensive
subjects were above their recommended weight.20 Concordance rates of 15% for dizygotic and 31% for monozygotic
twins have been reported in those with obesity and hypertension.21 Obesity and insulin resistance are closely interrelated
with at-risk obesity (ie, the metabolic syndrome), suggesting also a common underlying pathogenesis for obesity and
hypertension. Indeed, it has been reported that WC was the
strongest independent predictor (age, gender, BMI, and insulin resistance included) of SBP and diastolic blood pressure in
413 normoglycemic Chinese that included 56% individuals
with hypertension.22 In this previous study, WC was found to
be the major determinant of blood pressure, accounting for
20% of its variance.22 A similar association has been
reported recently between the prevalence of hypertension and
intra-abdominal fat accumulation but not with WC in a cohort

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366

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March 2005

Figure 2. Diastolic blood pressure and


SBP according to WC and fasting insulin
tertiles among men (A) and women (B) of
the Quebec Health Survey. 1, 2, 3, 4, 5,
6, 7, and 8 indicate significantly different
from the corresponding subgroup. Men
(A), All P0.0001; age-adjusted all
P0.04; women (B), all P0.0001; ageadjusted all P0.05.

of 563 Japanese Americans.12 However, this cohort included


nearly 40% of individuals with hypertension.12 On the other
hand, the Baltimore Longitudinal Study of Aging reported, in
a white population of 649 patients, that the simple correlation
between fasting insulin and blood pressure was secondary to
the confounding effects of age and obesity.23 Again, a
significant number of patients had hypertension (25%) in that
study.23 Nevertheless, the correlations of blood pressure
measurements were considerably stronger in both sexes with
BMI, percent body fat, and waist-to-hip ratio than with
insulin levels.23 In contrast to these 3 studies, our cohort only
included 6.5% of subjects with hypertension because it was
a population-based study. This is important because it is well
known that some antihypertensive medications may negatively or positively influence insulin sensitivity and the
metabolic risk profile over time. Therefore, our sample had
the advantage of being representative of the whole population
of adult Quebecers aged 18 to 74 years.
Several mechanisms may contribute to the increase in
blood pressure resulting from increasing levels of abdominal
adiposity in a manner independent of insulin resistance.
Sympathetic activation associated with obesity24 and molecules released by hypertrophied fat cells are 2 factors that
may promote the formation of angiotensin II (Ang II) and
aldosterone, which have direct vasopressor and antinatriuretic
effects.25 A local renin-angiotensinogen system (RAS) has
been found to be present in human adipose tissue and may act
as a distinct system from the plasma RAS.26,27 Indeed, all
components of the RAS system (angiotensinogen [AGT],
Ang II type 1 [AT1] receptor, and angiotensin-converting
enzyme but not renin and AT2 receptor) are found in adipose
tissue.28
Fasting insulin may be related to hypertension by being a
crude marker of the metabolic abnormalities associated with
insulin resistance. However, results of the present study
suggest WC may be a better marker of a cluster of blood

pressureraising abnormalities than fasting insulin. Mechanistic studies will be required to validate the above possibilities for a direct role of the expanded abdominal adipose
tissue mass on blood pressure modulation.

Limitations
The population of people studied was young, with a lower
average BMI and WC than in the US population.29,30 The
prevalence of the metabolic alterations16 and the hypertriglyceridemic waist in that cohort17 has been the subject of
previous reports. However, because there is a well-defined
linear relationship between blood pressure and mortality from
ischemic heart disease such that a lower blood pressure
confers lower risk of mortality,31 our findings may be of
clinical importance because even a relatively small rise in
blood pressure has been known to increase the risk of
cardiovascular death.32 Our population was predominantly
white, with a relatively low prevalence of hypertension. This
may limit the generalizability of our findings to other populations such as blacks, Hispanics, etc.

Perspectives
Our results may reconcile some apparently inconsistent results
linking insulin resistance with hypertension.610,23,33 Although there
is a high correlation between indices of obesity and indexes of
insulin sensitivity, the multivariate statistical analysis determined
that the documented association between obesity, fasting insulin,
insulin sensitivity, and blood pressure was largely explained by
variation in WC. Therefore, central obesity assessed by WC may
appear to have a predominant role compared with insulin levels in
explaining individual differences in blood pressure, at least in a
white population. It is plausible that cross-talks exist between
visceral adipose tissue, Ang II, and insulin in the overweight/obesity
state in human, and this process may contribute to conditions such
as development of cardiovascular and dysmetabolic complications.
Further studies are needed to document such an association in
different ethnic groups.

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Poirier et al

Waist Circumference, Blood Pressure, and Insulin

Acknowledgments
Some of the investigators were supported by a grant from the
Canadian Institute of Health Research. P.P. and J.B. are clinical
research scholars from the Fonds de la Recherche en Sante du
Quebec (FRSQ). J.-P.D. is chair professor of human nutrition,
lipidology, and prevention of cardiovascular diseases, which is
supported in part by Pfizer, Provigo, and by the Foundation of
Corporation of the Quebec Heart Institute.

References
1. Stamler R, Stamler J, Riedlinger WF, Algera G, Roberts RH. Weight and
blood pressure. Findings in hypertension screening of 1 million
Americans. J Am Med Assoc. 1978;240:16071610.
2. Chiang BN, Perlman LV, Epstein FH. Overweight and hypertension. A
review. Circulation. 1969;39:403 421.
3. Poirier P, Despres JP. Waist circumference, visceral obesity, and cardiovascular risk. J Cardiopulm Rehabil. 2003;23:161169.
4. DeFronzo RA. The effect of insulin on renal sodium metabolism. A
review with clinical implications. Diabetologia. 1981;21:165171.
5. Berglund G, Ljungman S, Hartford M, Wilhelmsen L, Bjorntorp P. Type
of obesity and blood pressure. Hypertension. 1982;4:692 696.
6. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M,
Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S. Insulin resistance in
essential hypertension. N Engl J Med. 1987;317:350 357.
7. Reaven GM, Hoffman BB. A role for insulin in the aetiology and course
of hypertension? Lancet. 1987;2:435 437.
8. Haffner SM, Valdez R, Morales PA, Mitchell BD, Hazuda HP, Stern MP.
Greater effect of glycemia on incidence of hypertension in women than in
men. Diabetes Care. 1992;15:12771284.
9. Haffner SM, Miettinen H, Gaskill SP, Stern MP. Metabolic precursors of
hypertension. The San Antonio Heart Study. Arch Intern Med. 1996;156:
1994 2001.
10. Johnson D, Prudhomme D, Despres JP, Nadeau A, Tremblay A,
Bouchard C. Relation of abdominal obesity to hyperinsulinemia and high
blood pressure in men. Int J Obes Relat Metab Disord. 1992;16:881 890.
11. Landsberg L. Obesity, metabolism, and hypertension. Yale J Biol Med.
1989;62:511519.
12. Hayashi T, Boyko EJ, Leonetti DL, McNeely MJ, Newell-Morris L, Kahn
SE, Fujimoto WY. Visceral adiposity and the prevalence of hypertension
in Japanese Americans. Circulation. 2003;108:1718 1723.
13. MacLean DR, Petrasovits A, Nargundkar M, Connelly PW, MacLeod E,
Edwards A, Hessel P. Canadian heart health surveys: a profile of cardiovascular risk. Survey methods and data analysis. Canadian Heart Health
Surveys Research Group. CMAJ. 1992;146:1969 1974.
14. Dewailly EE, Blanchet C, Gingras S, Lemieux S, Sauve L, Bergeron J,
Holub BJ. Relations between n-3 fatty acid status and cardiovascular
disease risk factors among Quebecers. Am J Clin Nutr. 2001;74:603 611.
15. Despres JP, Lamarche B, Maurie`ge P, Cantin B, Dagenais GR, Moorjani
S, Lupien PJ. Hyperinsulinemia as an independent risk factor for ischemic
heart disease. N Engl J Med. 1996;334:952957.
16. Scarsella C, Almeras N, Maurie`ge P, Blanchet C, Sauve L, Dewailly E,
Bergeron J, Despres JP. Prevalence of metabolic alterations predictive of
cardiovascular disease risk in the Quebec population. Can J Cardiol.
2003;19:5157.
17. Lemieux I, Almeras N, Maurie`ge P, Blanchet C, Dewailly E, Bergeron J,
Despres JP. Prevalence of hypertriglyceridemic waist in men who

18.

19.

20.

21.

22.

23.

24.

25.
26.

27.

28.

29.

30.

31.

32.

33.

367

participated in the Quebec Health Survey: association with atherogenic


and diabetogenic metabolic risk factors. Can J Cardiol. 2002;18:
725732.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner
RC. Homeostasis model assessment: insulin resistance and beta-cell
function from fasting plasma glucose and insulin concentrations in man.
Diabetologia. 1985;28:412 419.
Mykkanen L, Haffner SM, Ronnemaa T, Watanabe RM, Laakso M.
Relationship of plasma insulin concentration and insulin sensitivity to
blood pressure. Is it modified by obesity? J Hypertens. 1996;14:399 405.
MacMahon SW, Blacket RB, Macdonald GJ, Hall W. Obesity, alcohol
consumption and blood pressure in Australian men and women. The
National Heart Foundation of Australia Risk Factor Prevalence Study.
J Hypertens. 1984;2:8591.
Carmelli D, Cardon LR, Fabsitz R. Clustering of hypertension, diabetes,
and obesity in adult male twins: same genes or same environments? Am J
Hum Genet. 1994;55:566 573.
Thomas GN, Critchley JA, Tomlinson B, Anderson PJ, Lee ZS, Chan JC.
Obesity, independent of insulin resistance, is a major determinant of
blood pressure in normoglycemic Hong Kong Chinese. Metabolism.
2000;49:15231528.
Muller DC, Elahi D, Pratley RE, Tobin JD, Andres R. An epidemiological
test of the hyperinsulinemia-hypertension hypothesis. J Clin Endocrinol
Metab. 1993;76:544 548.
Poirier P, Hernandez TL, Weil KM, Shepard TJ, Eckel RH. Impact of
diet-induced weight loss on the cardiac autonomic nervous system in
severe obesity. Obes Res. 2003;11:1040 1047.
Poirier P, Eckel RH. Obesity and cardiovascular disease. Curr Atheroscler Rep. 2002;4:448 453.
Karlsson C, Lindell K, Ottosson M, Sjostrom L, Carlsson B, Carlsson
LM. Human adipose tissue expresses angiotensinogen and enzymes
required for its conversion to angiotensin II. J Clin Endocrinol Metab.
1998;83:39253929.
Paul M, Wagner J, Dzau VJ. Gene expression of the renin-angiotensin
system in human tissues. Quantitative analysis by the polymerase chain
reaction. J Clin Invest. 1993;91:2058 2064.
Giacchetti G, Faloia E, Mariniello B, Sardu C, Gatti C, Camilloni MA,
Guerrieri M, Mantero F. Overexpression of the renin-angiotensin system
in human visceral adipose tissue in normal and overweight subjects. Am J
Hypertens. 2002;15:381388.
Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome
among US adults: findings from the third National Health and Nutrition
Examination Survey. J Am Med Assoc. 2002;287:356 359.
Ardern CI, Katzmarzyk PT, Janssen I, Ross R. Discrimination of health
risk by combined body mass index and waist circumference. Obes Res.
2003;11:135142.
Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific
relevance of usual blood pressure to vascular mortality: a meta-analysis of
individual data for one million adults in 61 prospective studies. Lancet.
2002;360:19031913.
Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL
Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ. Seventh
report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42:
1206 1252.
Garcia-Estevez DA, Araujo-Vilar D, Fiestras-Janeiro G, SaavedraGonzalez A, Cabezas-Cerrato J. Insulin resistance in essential hypertension: a conflictive point of view. Diabet Med. 2003;20:1035.

Downloaded from http://hyper.ahajournals.org/ by guest on October 28, 2015

Impact of Waist Circumference on the Relationship Between Blood Pressure and Insulin:
The Quebec Health Survey
Paul Poirier, Isabelle Lemieux, Pascale Maurige, Eric Dewailly, Carole Blanchet, Jean
Bergeron and Jean-Pierre Desprs
Hypertension. 2005;45:363-367; originally published online January 24, 2005;
doi: 10.1161/01.HYP.0000155463.90018.dc
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 2005 American Heart Association, Inc. All rights reserved.
Print ISSN: 0194-911X. Online ISSN: 1524-4563

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