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(Hypertension. 1999;33:1364-1368.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Cortisol Effects on Body Mass, Blood Pressure, and Cholesterol in the General Population
From the MRC Blood Pressure Group, Western Infirmary (R.F., M.C.I., N.H.A., E.D., J.M.C.C.)and MONICA Project (C.M.), Royal Infirmary, Glasgow, Scotland, UK.
Correspondence to Dr Robert Fraser, MRC Blood Pressure Group, Western Infirmary, Glasgow G11 6NT, Scotland, UK.
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Abstract |
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Abstract—The effects of excess cortisol secretion on blood pressure and fat deposition are well documented, but the importance of this glucocorticoid in controlling these processes in normal individuals is less clear. We studied the relationship between cortisol excretion rate (tetrahydrocortisol [THF]+allo-THF+tetrahydrocortisone [THE]) and a range of important cardiovascular risk factors in 439 normal subjects (238 male) sampled from the North of Glasgow (Scotland) population. There were marked gender differences: female subjects were lighter and had lower blood pressures and cortisol levels, whereas HDL cholesterol was higher. The pattern of cortisol metabolism was also different; the index of 11ß-hydroxysteroid dehydrogenase activity (THF+allo-THF/THE) was lower and that of 5
-reductase (allo-THF/THF) was higher. There was a
strong correlation of blood pressure (positive),
cholesterol (positive), and HDL cholesterol
(negative in women, positive in men) with age. Cortisol excretion rate
did not correlate with blood pressure but correlated strongly with
parameters of body habitus (body mass index and waist and
hip measurements [positive]) and HDL cholesterol
(negative). With multiple regression analysis, there remained a
significant association of cortisol excretion rate with HDL
cholesterol in men and women and with body mass index in
men. These results suggest that glucocorticoids regulate key components
of cardiovascular risk.
Key Words: glucocorticoids • blood pressure • body mass index • cholesterol
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Introduction |
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Clinical1 and experimental2 cortisol excesses are associated with increases in blood pressure and profound alteration of intermediary metabolism, resulting in characteristic obesity, insulin resistance, and changes in lipid metabolism. In groups of subjects with essential hypertension, plasma3 or urinary4 cortisol levels may be mildly but significantly higher than those of matched normal subjects, and the efficiency of cortisol metabolism by 11ß-hydroxysteroid dehydrogenase (11ß-HSD) or 5
-reductase may be abnormal.5 6
Moreover, similar alterations in cortisol metabolism may
contribute to obesity and to increased abdominal fat deposition in
polycystic ovary disease.7 However, in the general
population, the contribution of cortisol to blood pressure and to
relative obesity is less well established despite the fact that these
are important predisposing factors to cardiovascular
disease. A recent study of a small group of subjects concluded that
differences in the level of cortisol and its metabolic
disposal may be a contributory cause of obesity.8 In the
present study, we examined the association between cortisol and
cardiovascular risk factors in a large sample of the
middle-aged population of an area with a high prevalence of
cardiovascular disease. |
Methods |
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Population
A random sample of the North Glasgow, Scotland, population was selected as a stratified random sample of the patient lists of 30 general practitioners, randomly selected from all those practicing in North Glasgow. The subjects were those participating in the fourth Glasgow MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) coronary risk examination, which included the recording of the mean of 2 seated blood pressure measurements made by random-zero sphygmomanometer after a 10-minute rest. Approval was obtained from the appropriate ethics committees. Of the original sample of 597 subjects in whom full urinary corticosteroid data were available, 158 were excluded from the study on the grounds that they were receiving medication likely to alter cardiovascular risk parameters (eg, cardioactive drugs or hormone replacement therapy) or adrenal function (eg, inhaled or topical steroids). There remained 238 male and 201 female subjects; their demographic details are summarized in Table 1.
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Biochemical Analyses
Blood samples were drawn from the antecubital vein for
measurement of cholesterol and HDL cholesterol
by standard laboratory methods. The subjects were not fasting. A
24-hour urine sample was collected with thymol used as preservative,
and aliquots were stored frozen until analysis. Excretion rates
of the cortisol metabolites tetrahydrocortisol (THF), allo-THF, and
tetrahydrocortisone (THE) were measured by the method of
Shackleton9 with minor modifications. The total (ie,
THF+allo-THF+THE) was used as an index of cortisol excretion rate, the
ratio THF+allo-THF/THE as an index of 11ß-HSD activity, and the ratio
THF/allo-THF as an index of 5-reductase activity.
Data Analyses
Data have been expressed as medians with interquartile ranges.
They were tested for normality of distribution (Anderson-Darling
test10 ) and, where necessary, they were logarithmically
transformed before statistical evaluation. Comparison of data from male
and female subjects was performed by ANOVA and simple regression
analysis by calculation of Pearson correlation coefficients,
and multivariate models were fitted by a combination of
stepwise and best subsets regression methods.
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Results |
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There were marked gender differences both in demographic variables (Table 1) and in cortisol metabolite excretion rates (Table 2). Although not significantly different in age or body mass index (BMI), female subjects had lower blood pressures and weighed less. Total cholesterol concentration was similar in the 2 groups, but female subjects had higher HDL cholesterol levels. Male subjects had higher cortisol excretion rates than female subjects, and there were gender differences in the pattern of metabolism. Thus, the index of 11ß-HSD activity was higher in male subjects; the reverse was true of the index of 5
-reductase activity. Blood
pressure and cholesterol correlated positively with age in
both men and women; HDL cholesterol and age correlated
positively in men but not in women (Table 3).
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BMI as well as waist and hip measurements correlated significantly with systolic and diastolic blood pressures (Table 4). However, there was no relationship between corticosteroid variables and blood pressure. Plasma total cholesterol concentration correlated with systolic and diastolic blood pressures (except in female subjects), but HDL cholesterol levels did not correlate with blood pressure.
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Cortisol excretion rate was positively correlated with BMI in both gender groups, as was waist measurement. There was a significant correlation with hip measurement only in male subjects (Table 5). In both groups, HDL cholesterol concentration was negatively correlated with cortisol excretion, but there was no relationship with total cholesterol concentration.
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Table 6 summarizes the multiple regression analysis of these data. From the equations, the cortisol-related variables, particularly cortisol excretion rate, contributed significantly with body habitus to the determination of HDL cholesterol levels. Age was also a factor in men. Cortisol levels also appear to contribute to BMI in men but not in women. Cortisol-related variables did not appear to make an important contribution to blood pressure in this population. The relationship between cortisol excretion, HDL cholesterol levels, and BMI for the 2 gender groups is illustrated in the Figure.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Gender and Age Differences
The finding of higher cortisol excretion rates in men than in women is in general agreement with previous studies (eg, References 8, 11, and 128 11 12 ), although Weaver et al13 found no gender differences. Because plasma cortisol concentration is not influenced by gender, this suggests a difference in metabolism or tissue binding (see Reference 1414 ). Apparent 11ß-HSD activity was higher in men, but 5
-reductase activity, in agreement with Andrew et
al,8 was higher in women. The higher HDL
cholesterol level in women may reflect the negative
correlation with cortisol excretion rate and is likely to be influenced
by estrogens.
Cortisol and Blood Pressure
Several studies have reported clear differences in the level of
plasma or urinary cortisol and the pattern of its
metabolism between normal subjects and groups of frankly
hypertensive but otherwise matched subjects. For example, Filipovsky et
al15 found morning plasma cortisol concentration to be
higher in hypertensive than in normotensive subjects, particularly in
lean hypertensive subjects. Similarly, Litchfield et al4
reported higher urinary free cortisol excretion rates in hypertensive
patients; rates were higher in men than women and higher with high salt
intake. Young adults with a predisposition to hypertension have mildly
but significantly higher plasma cortisol concentrations3
or secretion rates16 than those without this trait. The
study by Walker et al16 also noted differences in cortisol
metabolism between these groups. Differences in cortisol
metabolite excretion rates between hypertensive and normotensive
subjects, indicative of differences in 11ß-HSD or 5-reductase
activity, have also been described.6
No relationship between cortisol excretion and blood pressure was
discernible, nor did the cortisol metabolite ratio indexes of 11ß-HSD
or 5-reductase correlate with blood pressure. However, it should be
emphasized that our study group was normotensive and had a narrow blood
pressure range. Although these observations suggest that cortisol
secretion rate is not a direct determinant of blood pressure in
normotensive adults, it may act through differences in glucocorticoid
receptor kinetics16 17 18 or by in utero fetal
programming.19
Body Habitus and Blood Pressure
The significant relationship between blood pressure and aspects of
body habitus agrees with previous studies. According to Wing et
al,20 obese subjects have higher blood pressures and lower
HDL levels; as in our subjects, HDL cholesterol was not
related to body parameters. Fat distribution seemed to be
the key determinant, because the significance of the correlation of
blood pressure with waist/hip ratio (WHR), also seen in the present
study, survived correction for BMI. This may reflect an underlying
relationship between sensitivity to insulin and blood
pressure.21
Cortisol and Obesity
The tendency to obesity with characteristic fat distribution
in Cushing's syndrome is well established. Moreover, chronically
stressed primates show a similar distribution of fat,22
and psychosocial influences have also been identified in human
subjects.20 Glucocorticoid secretion in obese human
subjects and genetically obese rats may be more sensitive to ACTH or
"stress," and in rats, some of the effects are prevented by
adrenalectomy.23 24 Cortisol secretion is said not to be
resistant to dexamethasone suppression in
obesity,25 but a more recent study found that levels in
obese men were not as well suppressed as those of normal
men.26
The majority of studies have found that cortisol excretion rate but not plasma concentration may correlate with parameters of body habitus. Urinary cortisol excretion rate has been reported to correlate with abdominal diameter and WHR,25 in agreement with the present study. However, BMI and cortisol were unrelated in the previous study. Previous investigations27 also claim that when corrected for creatinine excretion, cortisol excretion rates did not correlate with weight, nor were there gender differences. Conversely, Andrew et al8 reported clear gender differences, also seen in the present study, but also found cortisol excretion to be unrelated to hip or waist circumference. This latter population was only mildly obese and thus more comparable with our own.
In our larger study, univariate analysis revealed a clear positive correlation between cortisol excretion rate and BMI or WHR. Such an association does not necessarily imply causality. However, it is possible that a small but chronic excess of cortisol does eventually result in a central fat deposition qualitatively similar to that in Cushing's syndrome (see Reference 2828 ). Alternatively, changes in metabolism, perhaps as a consequence of excess central fat tissue expression of 11ß-HSD, may alter secretion rate, although there was no correlation between 11ß-HSD activity and either BMI or WHR. If increased exposure to cortisol favors the development of central obesity, the relationship should persist in multiple regression analysis. This was the case in men but not in women, again emphasizing gender differences. The clear relationship in men suggests a role for cortisol within the normal range in modulating the amount and distribution of body fat. Central girth is a powerful index of cardiovascular risk,29 and these data provide a possible explanation of this relationship in the general population.
The clear pathological effects of cortisol hypersecretion on body fat
levels and the difficulty in identifying a similar relationship in
normal or even clinically obese subjects may mean that differences in
the potency of cortisol at the target tissue are important. Fat
deposition may be affected by the affinity or concentration of
glucocorticoid receptors. Also, the clearance rate of the hormone from
the tissue might be altered with a higher proportion of 5-reductase
than 5ß-reductase metabolism.8 In the
present study, the ratio of cortisol to cortisone metabolites did
not correlate with body parameters, but the ratio of
5-reductase to 5ß-reductase metabolites was a contributory
factor in determining HDL cholesterol levels (negative
influence) and BMI (positive influence) in men.
Rosmond et al30 weighted cortisol secretion measurements by a factor based on amplitude of individual diurnal variation of plasma cortisol concentration to control for variable stress. These values correlated positively with BMI, WHR, and total or HDL cholesterol in obese subjects. Cortisol correlated with HDL cholesterol but not total cholesterol in the present study. The inverse relationship between cortisol and HDL cholesterol was significant in both men and women and survived stepwise multiple regression analysis. Thus, cortisol may affect peripheral cholesterol metabolism to alter HDL cholesterol formation. Because lower HDL levels are strongly associated with cardiovascular risk,31 a small long-term excess of cortisol may explain in part the risk associated with obesity. For both genders, the lowest HDL cholesterol levels are seen in subjects with the highest cortisol excretion rates and BMI (Figure).
Excess secretion of cortisol increases the risk of cardiovascular disease. Within a relatively normal population, the present study has identified a 3-way association between this steroid, BMI, and HDL cholesterol that may explain this risk.
Received November 12, 1998; first decision December 30, 1998; accepted January 29, 1999.
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J. Westerbacka, H. Yki-Jarvinen, S. Vehkavaara, A.-M. Hakkinen, R. Andrew, D. J. Wake, J. R. Seckl, and B. R. Walker Body Fat Distribution and Cortisol Metabolism in Healthy Men: Enhanced 5{beta}-Reductase and Lower Cortisol/Cortisone Metabolite Ratios in Men with Fatty Liver J. Clin. Endocrinol. Metab., October 1, 2003; 88(10): 4924 - 4931. [Abstract] [Full Text] [PDF]
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D. J. Wake, E. Rask, D. E. W. Livingstone, S. Soderberg, T. Olsson, and B. R. Walker Local and Systemic Impact of Transcriptional Up-Regulation of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue in Human Obesity J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3983 - 3988. [Abstract] [Full Text] [PDF]
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R. S. Lindsay, D. J. Wake, S. Nair, J. Bunt, D. E. W. Livingstone, P. A. Permana, P. A. Tataranni, and B. R. Walker Subcutaneous Adipose 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity and Messenger Ribonucleic Acid Levels Are Associated with Adiposity and Insulinemia in Pima Indians and Caucasians J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2738 - 2744. [Abstract] [Full Text] [PDF]
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B. R. Walker and R. Andrew Cortisol Metabolism in Type 2 Diabetes J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2951 - 2952. [Full Text] [PDF]
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 E. D. Bruder, D. L. Ball, T. L. Goodfriend, and H. Raff An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2003; 284(6): R1631 - R1635. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, N. Crabtree, P. M. S. Clark, G. Holder, A. A. Toogood, C. H. L. Shackleton, and P. M. Stewart Low-Dose Growth Hormone Inhibits 11{beta}-Hydroxysteroid Dehydrogenase Type 1 but Has No Effect upon Fat Mass in Patients with Simple Obesity J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 2113 - 2118. [Abstract] [Full Text] [PDF]
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 T. Dimitriou, C. Maser-Gluth, and T. Remer Adrenocortical activity in healthy children is associated with fat mass Am. J. Clinical Nutrition, March 1, 2003; 77(3): 731 - 736. [Abstract] [Full Text] [PDF]
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D. Tiosano, I. Eisentein, D. Militianu, G. P. Chrousos, and Z.'e. Hochberg 11{beta}-Hydroxysteroid Dehydrogenase Activity in Hypothalamic Obesity J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 379 - 384. [Abstract] [Full Text] [PDF]
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R. C. Andrews, O. Herlihy, D. E. W. Livingstone, R. Andrew, and B. R. Walker Abnormal Cortisol Metabolism and Tissue Sensitivity to Cortisol in Patients with Glucose Intolerance J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5587 - 5593. [Abstract] [Full Text] [PDF]
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J. W. Tomlinson, B. Sinha, I. Bujalska, M. Hewison, and P. M. Stewart Expression of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 in Adipose Tissue Is Not Increased in Human Obesity J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5630 - 5635. [Abstract] [Full Text] [PDF]
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N. Draper, S. M. Echwald, G. G. Lavery, E. A. Walker, R. Fraser, E. Davies, T. I. A. Sorensen, A. Astrup, J. Adamski, M. Hewison, et al. Association Studies between Microsatellite Markers within the Gene Encoding Human 11{beta}-Hydroxysteroid Dehydrogenase Type 1 and Body Mass Index, Waist to Hip Ratio, and Glucocorticoid Metabolism J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 4984 - 4990. [Abstract] [Full Text] [PDF]
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E. Rask, B. R. Walker, S. Soderberg, D. E. W. Livingstone, M. Eliasson, O. Johnson, R. Andrew, and T. Olsson Tissue-Specific Changes in Peripheral Cortisol Metabolism in Obese Women: Increased Adipose 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Activity J. Clin. Endocrinol. Metab., July 1, 2002; 87(7): 3330 - 3336. [Abstract] [Full Text] [PDF]
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A. Johansson, R. Andrew, H. Forsberg, K. Cederquist, B. R. Walker, and T. Olsson Glucocorticoid Metabolism and Adrenocortical Reactivity to ACTH in Myotonic Dystrophy J. Clin. Endocrinol. Metab., September 1, 2001; 86(9): 4276 - 4283. [Abstract] [Full Text] [PDF]
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 J. A. Gusenoff, S. M. Harman, J. D. Veldhuis, J. J. Jayme, C. St. Clair, T. Munzer, C. Christmas, K. G. O'Connor, T. E. Stevens, M. F. Bellantoni, et al. Cortisol and GH secretory dynamics, and their interrelationships, in healthy aged women and men Am J Physiol Endocrinol Metab, April 1, 2001; 280(4): E616 - E625. [Abstract] [Full Text] [PDF]
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G. A. Laughlin and E. Barrett-Connor Sexual Dimorphism in the Influence of Advanced Aging on Adrenal Hormone Levels: The Rancho Bernardo Study J. Clin. Endocrinol. Metab., October 1, 2000; 85(10): 3561 - 3568. [Abstract] [Full Text]
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D. E. W. Livingstone, G. C. Jones, K. Smith, P. M. Jamieson, R. Andrew, C. J. Kenyon, and B. R. Walker Understanding the Role of Glucocorticoids in Obesity: Tissue-Specific Alterations of Corticosterone Metabolism in Obese Zucker Rats Endocrinology, February 1, 2000; 141(2): 560 - 563. [Abstract] [Full Text] [PDF]
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G. C. Inglis, M. C. Ingram, C. D. Holloway, L. Swan, D. Birnie, W. S. Hillis, E. Davies, R. Fraser, and J. M. C. Connell Familial Pattern of Corticosteroids and Their Metabolism in Adult Human Subjects - the Scottish Adult Twin Study J. Clin. Endocrinol. Metab., November 1, 1999; 84(11): 4132 - 4137. [Abstract] [Full Text]
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