Institut National de la Santé et de le Recherche Medicale, Hôpital Fernand Widal, Paris, France
Declaration of interest The project was partly funded by a grant from the Merck, Sharp and Dohme-Chibret Company and EISAI (France).
Correspondence: Dr Sabrina Paterniti, INSERM U360, Hôpital La Salpêtrière, 75651 Paris Cedex 13, France. Tel: 0083 1 42162554; Fax: 0033 1 42162541
![]() |
ABSTRACT |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Aims To examine the temporal relation between low blood pressure and depression in a two-year follow-up.
Method The study group consisted of 1389 subjects aged 59-71 years; 1272 (92%) were examined after two years. Subjects completed the Center for Epidemiological StudiesDepression (CESD) and the Spielberger inventory scales to assess depressive and anxiety symptoms respectively. Data were collected on socio-demographic characteristics, smoking and drinking habits, medical history, drug use and blood pressure measures.
Results Among 1112 subjects who were considered as non-depressed at baseline, logistic regression models showed that low diastolic blood pressure (DBP) and decrease of blood pressure were predictors of high depressive symptomatology at follow-up. Baseline high CESD scores did not predict low blood pressure two years after.
Conclusions In our study, low blood pressure was a risk factor for, but not a consequence of, high depressive symptomatology.
![]() |
INTRODUCTION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
METHOD |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Procedure and instruments
Interviews and examinations were conducted at the study centre. Data on
demographic background, occupation, medical history, drug use and smoking and
drinking habits were obtained using a standardised questionnaire during a
face-to-face interview. Depressive symptoms were assessed by the Center for
Epidemiological StudiesDepression Scale (CESD)
(Radloff, 1977). The
CESD consists of 20 self-report items concerning symptoms and feeling
experienced during the preceding week. Each item is scored from 0-3 according
the frequency of the symptom. Validation of the CESD in a French
population has shown that men and women scoring more than 16 and 22,
respectively, were considered at high risk for clinical depression; the
sensitivity and specificity of the CESD were, respectively, 0.76 and
0.71 (Fuhrer & Rouillon,
1989). The CESD scale has been widely used in
epidemiological studies, including studies in elderly populations
(Radloff & Teri, 1986;
Beekman et al, 1995).
Trait anxiety was evaluated by means of the French translation of the 20-item
Spielberger Inventory Trait questionnaire (Form X-2)
(Spielberger et al,
1970). The Spielberger Inventory Trait questionnaire (Form X-2) is
a self-report questionnaire, which has been used extensively in research and
practice; its factorial validity has been shown in elderly
(Nesselroade et al,
1984). Each item of this scale is rated from 1-4 in terms of
frequency categories (almost never, sometimes,
often, almost always).
Two independent measurements of systolic and diastolic blood-pressure (SBP and DPB, respectively) using a digital electronic tensiometer (SP9; Spengler, Paris) were made after a 10-minute rest. The mean value was used for the analysis. Weight and height were measured and body mass index (BMI) was computed as weight (kg) divided by height squared (m2).
The current use of drugs was investigated as follows. The interviewer asked the participant for all medical prescriptions corresponding to the drugs (psychotropics and other drugs) regularly used in the last month and recorded the name of the drug directly from the medical prescription. The drugs were subsequently coded according to the classification proposed by the French national prescription formulary (Guide National de Prescription des Médicaments, 1990). Psychotropic drugs included anxiolytics, hypnotics, sedatives, neuroleptics, antidepressants and normothimics.
Statistical analysis
Since there is no well established definition of low blood pressure, men
with SBP or DBP in the first quartile of the SBP/DBP distribution were
classified as having low SBP/DBP. Women were classified in the same way.
Changes in blood pressure were defined as difference between baseline value
from the two-year follow-up value. The quartiles of the gender-specific
distribution of blood pressure changes were defined such as individuals with
the greatest decrease were included in the first quartile.
Associations between blood pressure and the covariates were assessed using variance analysis and Pearson's correlation coefficient.
Relationship between baseline low blood pressure and depression at two-year follow-up was tested with four logistic regression models, using as independent variables low SBP and low DBP and high decrease of SBP and DBP and as dependent variable a high depressive symptomatology at follow-up (CESD score above the gender-specific cut-off). Individuals with high depressive symptomatology or taking antidepressant at baseline were excluded from the analysis.
Conversely, relationship between baseline high depressive symptomatology, low SBP or DBP at follow-up and a high SBP or DBP decrease was tested with four logistical regressions, using blood pressure variables as dependent variables and high depressive symptomatology as independent variable. Individuals with low blood pressure at baseline were excluded from the analysis.
All analyses were adjusted for gender, age, BMI, use of antihypertensive drugs and Spielberger and CESD scores at baseline. For logistic regressions examining the relationship between blood pressure changes and depression, baseline blood pressure and BMI change were added to the adjustment variables.
All analyses were carried out using the SAS Institute (1989) statistical package.
![]() |
RESULTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
|
Of the 1272 individuals who participated in the follow-up, 60 had not completed either baseline or follow-up CESD. One hundred and ninety-eight on 1212 remaining individuals (13.6%) had high depressive symptomatology at baseline. These 198 subjects were excluded from the logistic regression testing the relationship between blood pressure and follow-up high depressive symptomatology.
Covariates
Age, gender, BMI, use of antihypertensive drugs and anxiety scores were
considered as covariates in logistic regression models, because of the strong
relationship between these variables and blood pressure
(Table 2).
|
In our sample, the other plausible co-variates of depression and low blood pressure (alcohol and tobacco use, number of chronic diseases, antidepressant and neuroleptic drugs) were not associated with low blood pressure or depressive symptoms (data not shown).
Low baseline blood pressure and depression at follow-up
The logistic regressions which were performed in the 422 men and 592 women
who were considered as non-depressed at baseline showed that low DBP at
baseline was a significant risk factor for depression at two-year follow-up
(adjusted odds ratios=1.9; 95% CI 1.0-3.6)
(Table 3). The association
between low SBP and depression was not statistically significant (adjusted
odds ratio=1.3; 95% CI 0.7-2.6). Moreover, it appeared that depression at
follow-up was associated with decrease of SBP or DBP (adjusted odds ratios for
low SBP=2.6, 95% CI 1.2-5.7; adjusted odds ratios for low DBP=1.8, 95% CI
0.9-3.6). Further adjustment on psychotropic use did not change the findings
(data not shown).
|
Antihypertensive drugs are associated with higher blood pressure at baseline and they are known to produce depressive symptoms; therefore they could mask the association between low blood pressure and the incidence of depression. On the other hand, they may decrease blood pressure, so an association between blood pressure decrease and depression incidence could be due to the antihypertensive drug effects. When we excluded subjects taking antihypertensive drugs (n=330), results were similar (low SBP, odds ratio=1.7, 95% CI 0.8-3.5, low DBP, odds ratio=1.2, 95% CI 0.6-2.5; SBP decrease, odds ratio=2.2, 95% CI 0.9-5.2, DBP decrease, odds ratio=4.0, 95% CI 1.5-10.8).
Baseline depressive symptomatology and low blood pressure at
follow-up
Individuals who were classified as having low blood pressure at baseline
(see Method) were not included in this part of the analysis. We did not find
any association between high baseline depressive symptomatology and subsequent
low blood pressure (adjusted odds ratios for low SBP=0.6 (95% CI 0.3-1.1), low
DBP=0.8 (95% CI 0.4-1.5)). Similar results were obtained when the analysis was
performed including individuals with low blood pressure at baseline (adjusted
odds ratios for low SBP=0.9 (95% CI 0.6-1.4), low DBP=0.6 (95% CI 0.4-1.0)).
The results remained unchanged when CESD scores at follow-up were
included in the multivariate logistic regression model.
![]() |
DISCUSSION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Cross-sectional relations between depression and low blood pressure have been described in a large population study by Barrett-Connor & Palinkas (1994), who found an association of low blood pressure with higher depressive symptoms scores measured with the Beck Depression Inventory, which was independent of age or weight loss. However, in the absence of a longitudinal study, chronology of the relationship could not be examined.
Mechanisms of association
One simple explanation for the cross-sectional relationship between
depression and low blood pressure is that decreasing blood pressure is due to
loss of weight and decrease of activities that are associated with depression.
The present study does not support this explanation. Indeed, our data
suggested that low blood pressure is succeeded by depression.
There are pathophysiological mechanisms that would explain that hypotension produces somatic symptoms and fatigue (Simpson, 1990). These chronic symptoms could lead to psychological discomfort and subsequent depressive symptoms. An alternative explanation is that a common factor gives rise to both depression and low blood pressure. For instance, a disorder of central monoamine activity could produce both psychological (depression) and physiological (low blood pressure) symptoms. Finally, the effect of chronic low blood pressure on brain functioning is debated. Studies in elderly populations have suggested that low blood pressure was associated with cognitive decline (Elias et al, 1993) and accelerated worsening of dementia (Guo et al, 1996). Other studies did not confirm these findings. On another hand, high blood pressure is a well-established risk factor for dementia and cognitive deterioration (Strandgaard & Paulson, 1994). The fact that high blood pressure has deleterious effects on brain functioning does not allow us to exclude the possibility that low blood pressure also might have some negative consequences.
Finally, some drugs prescribed in the elderly may lower blood pressure and
also predispose to depression. Many of these drugs were included in the class
antihypertensive drugs (reserpine, ß-adrenergic, blocking
agents, -methyldopa, clonidine, calcium channel blockers and
angiotensin-converting enzyme-inhibitors), which were considered as covariate.
Some of these drugs were also prescribed with indications different from
hypertension in a small group of subjects (n=29); levodopa, which may
lower blood pressure and predispose to depression was prescribed only for four
subjects. So, it is not likely that the association between low blood pressure
and depressive symptoms is explained, in our study, by drug use.
Depression is not predictive of low blood pressure
In our study, baseline high depressive symptomatology was not a risk factor
for low blood pressure irrespective of the CESD score at follow-up.
Recovery from depression may be associated with blood pressure increase.
Alternatively, sustained depression may result in increased blood pressure.
Indeed chronic depression is commonly associated with a higher risk of
hypertension (Chrousos & Gold,
1992).
Limitations of the study
While conducted on a large population, the methodology of the present study
carries some limitations. The symptoms or depressive episodes during the
two-year interval were not assessed. Subjects with high depressive
symptomatology at follow-up could have suffered from depression throughout the
two years or only the week preceding the interview. Also, data could be biased
because the individuals who were not followed up differed from those followed
up for psychopathological and blood pressure measure. However, 91.6% of
subjects were followed up, which is a high response rate. Furthermore, the
absence of a clinical diagnosis of the patients may actually have led to
inclusion of patients with chronic fatigue syndrome or atypical depression.
Finally, we did not consider exercise as a confounding factor, as we had not
standardised measures for this variable.
![]() |
Clinical Implications and Limitations |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
LIMITATIONS
![]() |
REFERENCES |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Beekman, A. T. F., Deeg, D. J. H., Tilburg, T.V., et al (1995) Major and minor depression in later life: a study of prevalence and risk factors. Journal of Affective Disorder, 36, 65-75.[CrossRef][Medline]
Chrousos, G. P. & Gold, P.W. (1992) The concept of stress and stress system disorders. Overview of physical and behavioral homeostasis. Journal of the American Medical Association, 267, 1244-1252.[Abstract]
Elias, M. F., Wolf, P.A., D'Agostino, R. B., et al (1993) Untreated blood pressure is inversely related to cognitive functioning: the Framingham study. American Journal of Epidemiology, 138, 353-361.[Abstract]
Fuhrer, R. & Rouillon, F. (1989) La version française de l'échelle CESD (Center for Epidemiologic StudiesDepression scale). Description et traduction de l'échelle d'autovaluation. Psychiatrie & Psychobiologie, 4, 163-166.
Golberg, E. L., Comstock, G. W. & Graves, C. G. (1980) Psychosocial factors and blood pressure. Psychological Medicine, 10, 243-255.[Medline]
Guide National de Prescription des Médicaments (1990) Guide National de Prescription des Médicaments, 1991. Paris: Editions du Vidal.
Guo, Z., Viitanen, M., Fratiglioni, L., et al
(1996) Low blood pressure and dementia in elderly people: the
Kungsholmen project. British Medical Journal,
312,
805-808.
Henderson, A. S., Korten, A. E., Jacomb, P. A., et al (1997) The course of depression in elderly: a longitudinal community-based study in Australia. Psychological Medicine, 27, 119-129.[CrossRef][Medline]
Jonas, B. S., Franks, P. & Ingram D. D. (1997) Are symptoms of anxiety and depression risk factors for hypertension? Archives of Family Medicine, 6, 43-49.[Abstract]
Nesselroade, J. R., Mitteness, L. S. & Thompson, L. K. (1984) Older adulthood: short-term changes in anxiety, fatigue, and other psychological states. Research on Aging, 6, 3-23.[Medline]
Pemberton, J. (1989) Does constitutional hypotension exist? British Medical Journal, 298, 660-662.[Medline]
Pilgrim, J. A., Stansfeld, S. & Marmot, M. G. (1992) Low blood pressure, low mood? British Medical Journal, 304, 75-78.[Medline]
Radloff, L. S. (1977) The CESD scale: a self-report depression scale for research in the general population. Applied Psychological Measurement, 1, 385-401.
Radloff, L. S. & Teri, L. (1986) Use of the CESD with older adults. Clinical Gerontologist, 5, 119-136.
Rosengren, A., Tibblin, G. & Wilhelmsen, L. (1993) Low systolic blood pressure and self-perceived wellbeing in middle-aged men. British Medical Journal, 306, 243-246.[Medline]
SAS Institute (1989) SAS/STAT User's Guide, Version 6 (4th edn). Cary, NC: SAS Institute Inc.
Simpson, L. O. (1990) Symptoms of low blood pressure. British Medical Journal, 301, 815-816.
Spielberger, C. D., Gorsuch, R. L. & Lushene, R. E. (1970) STAI manual for the StateTrait Anxiety Inventory. Palo Alto, CA: Consulting Psychologists' Press.
Strandgaard, S. & Paulson, O. B. (1994) Cerebrovascular consequences of hypertension. Lancet, 344, 519-521.[CrossRef][Medline]
Wessely, S., Nickson, J. & Cox, B. (1990) Symptoms of low blood pressure: a population study. British Medical Journal, 301, 18-25.
Received for publication July 20, 1999. Revision received November 9, 1999. Accepted for publication November 10, 1999.