“…The result regarding the significant association between hair cortisol levels and CD4 count was in line with part of previous studies that also reported a negative association between CD4 count and cortisol levels in plasma and saliva [ 5 – 9 ] but differed from the results from some published studies in which a nonsignificant association was reported by using serum cortisol levels [ 15 , 18 – 20 ], urinary cortisol levels [ 12 , 13 , 16 , 17 ], or hair cortisol levels [ 21 ]. Interestingly, we found stronger associations between hair cortisone levels and CD4 count than hair cortisol levels did, which was in line with some previous studies that also reported stronger associations between hair cortisone levels and variables studied than hair cortisol levels did, including Parkinson’s disease [ 39 ], Cushing’s syndrome [ 40 ], cardiometabolic variables [ 41 , 42 ], and stress-related variables [ 39 , 43 ]. In addition, we found hair cortisone levels and hair cortisol levels were positively correlated, which is similar to the findings in previous studies [ 39 , 41 , 42 , 44 – 46 ].…”
Section: Discussionsupporting
confidence: 92%
“…Interestingly, we found stronger associations between hair cortisone levels and CD4 count than hair cortisol levels did, which was in line with some previous studies that also reported stronger associations between hair cortisone levels and variables studied than hair cortisol levels did, including Parkinson’s disease [ 39 ], Cushing’s syndrome [ 40 ], cardiometabolic variables [ 41 , 42 ], and stress-related variables [ 39 , 43 ]. In addition, we found hair cortisone levels and hair cortisol levels were positively correlated, which is similar to the findings in previous studies [ 39 , 41 , 42 , 44 – 46 ]. Previous studies indicated that salivary cortisone levels were more closely associated with unbound, biologically active cortisol levels than total cortisol levels [ 26 ], and hair cortisone levels were significantly associated with salivary cortisone levels [ 45 , 47 ].…”
Background
Existing literature mostly investigated the relationship of acute or short-term glucocorticoid exposure to HIV disease progression using cortisol levels in serum, saliva, or urine. Data are limited on the relationship of long-term glucocorticoid exposure to HIV disease progression. This study examined whether hair glucocorticoid levels, novel retrospective indicators of long-term glucocorticoid exposure, are associated with two common indicators of HIV disease progression (CD4 count and HIV viral load) among a large cohort of combination antiretroviral therapy treated Chinese people living with HIV (PLHIV).
Methods
A total of 1198 treated PLHIV provided hair samples for glucocorticoid (cortisol and cortisone) assay and completed a survey assessing sociodemographic, lifestyle, and HIV-related characteristics. Meanwhile, CD4 count and HIV viral load were retrieved from their medical records. Spearman correlation was used to examine the associations of hair cortisol and cortisone levels to continuous CD4 count and HIV viral load. Multivariate logistic regression was used to predict CD4 count < 500 cells/mm3.
Results
Both hair cortisol and cortisone levels were negatively associated with CD4 count but not with HIV viral load. The odds ratio for CD4 count < 500 cells/mm3 was 1.41 [95% CI 0.99–2.00] and 2.15 [95% CI 1.51–3.05] for those with hair cortisol and cortisone levels in the highest quartile compared to the lowest when controlling for sociodemographic, lifestyle, HIV-related covariates, and HIV viral load.
Conclusion
Hair glucocorticoid levels were associated with CD4 count but not viral load in treated Chinese PLHIV. Our data furtherly supported the hypothesis that elevated glucocorticoid levels are associated with the lower CD4 count.
“…The result regarding the significant association between hair cortisol levels and CD4 count was in line with part of previous studies that also reported a negative association between CD4 count and cortisol levels in plasma and saliva [ 5 – 9 ] but differed from the results from some published studies in which a nonsignificant association was reported by using serum cortisol levels [ 15 , 18 – 20 ], urinary cortisol levels [ 12 , 13 , 16 , 17 ], or hair cortisol levels [ 21 ]. Interestingly, we found stronger associations between hair cortisone levels and CD4 count than hair cortisol levels did, which was in line with some previous studies that also reported stronger associations between hair cortisone levels and variables studied than hair cortisol levels did, including Parkinson’s disease [ 39 ], Cushing’s syndrome [ 40 ], cardiometabolic variables [ 41 , 42 ], and stress-related variables [ 39 , 43 ]. In addition, we found hair cortisone levels and hair cortisol levels were positively correlated, which is similar to the findings in previous studies [ 39 , 41 , 42 , 44 – 46 ].…”
Section: Discussionsupporting
confidence: 92%
“…Interestingly, we found stronger associations between hair cortisone levels and CD4 count than hair cortisol levels did, which was in line with some previous studies that also reported stronger associations between hair cortisone levels and variables studied than hair cortisol levels did, including Parkinson’s disease [ 39 ], Cushing’s syndrome [ 40 ], cardiometabolic variables [ 41 , 42 ], and stress-related variables [ 39 , 43 ]. In addition, we found hair cortisone levels and hair cortisol levels were positively correlated, which is similar to the findings in previous studies [ 39 , 41 , 42 , 44 – 46 ]. Previous studies indicated that salivary cortisone levels were more closely associated with unbound, biologically active cortisol levels than total cortisol levels [ 26 ], and hair cortisone levels were significantly associated with salivary cortisone levels [ 45 , 47 ].…”
Background
Existing literature mostly investigated the relationship of acute or short-term glucocorticoid exposure to HIV disease progression using cortisol levels in serum, saliva, or urine. Data are limited on the relationship of long-term glucocorticoid exposure to HIV disease progression. This study examined whether hair glucocorticoid levels, novel retrospective indicators of long-term glucocorticoid exposure, are associated with two common indicators of HIV disease progression (CD4 count and HIV viral load) among a large cohort of combination antiretroviral therapy treated Chinese people living with HIV (PLHIV).
Methods
A total of 1198 treated PLHIV provided hair samples for glucocorticoid (cortisol and cortisone) assay and completed a survey assessing sociodemographic, lifestyle, and HIV-related characteristics. Meanwhile, CD4 count and HIV viral load were retrieved from their medical records. Spearman correlation was used to examine the associations of hair cortisol and cortisone levels to continuous CD4 count and HIV viral load. Multivariate logistic regression was used to predict CD4 count < 500 cells/mm3.
Results
Both hair cortisol and cortisone levels were negatively associated with CD4 count but not with HIV viral load. The odds ratio for CD4 count < 500 cells/mm3 was 1.41 [95% CI 0.99–2.00] and 2.15 [95% CI 1.51–3.05] for those with hair cortisol and cortisone levels in the highest quartile compared to the lowest when controlling for sociodemographic, lifestyle, HIV-related covariates, and HIV viral load.
Conclusion
Hair glucocorticoid levels were associated with CD4 count but not viral load in treated Chinese PLHIV. Our data furtherly supported the hypothesis that elevated glucocorticoid levels are associated with the lower CD4 count.
“…However, chronic stress leads to dysregulation of this feedback mechanism, resulting in elevated glucocorticoid levels, and this has indeed been observed in PD cohorts. 10 To reduce the detrimental effects of chronic stress in PD, adequate self-management strategies are essential. In recent years, evidence for the effect of nonpharmacological treatments for PD, such as exercise, has accumulated, 11 but the evidence for stress-alleviating interventions is much less clear.…”
“…Individuals with PD have elevated cortisol secretion in blood and saliva, especially in the morning [ 58 , 65 , 66 ]. More recently, glucocorticoid concentrations measured in the hair of PD patients showed an excess of cortisone, the main cortisol metabolite, but not cortisol itself [ 67 ].…”
Section: Cortisol and Klotho In Neurodegenerative Diseasementioning
confidence: 99%
“…MDD patients also show neurochemical changes in CRH in the PVN, a structure now known to contain inclusions of α-synuclein, hallmark of PD pathology [ 186 ]. In individuals with PD, cortisol has been shown to correlate with the severity of depression [ 187 ] and with prevalence of anxiety and anhedonia [ 67 ]. In PD patients with impulse control disorders, increased cortisol is associated with more risk-taking behavior [ 188 ].…”
Section: Cortisol and Klotho Associations With Pd Symptomatologymentioning
The pathogenesis of Parkinson’s disease (PD) is complex, multilayered, and not fully understood, resulting in a lack of effective disease-modifying treatments for this prevalent neurodegenerative condition. Symptoms of PD are heterogenous, including motor impairment as well as non-motor symptoms such as depression, cognitive impairment, and circadian disruption. Aging and stress are important risk factors for PD, leading us to explore pathways that may either accelerate or protect against cellular aging and the detrimental effects of stress. Cortisol is a much-studied hormone that can disrupt mitochondrial function and increase oxidative stress and neuroinflammation, which are recognized as key underlying disease mechanisms in PD. The more recently discovered klotho protein, considered a general aging-suppressor, has a similarly wide range of actions but in the opposite direction to cortisol: promoting mitochondrial function while reducing oxidative stress and inflammation. Both hormones also converge on pathways of vitamin D metabolism and insulin resistance, also implicated to play a role in PD. Interestingly, aging, stress and PD associate with an increase in cortisol and decrease in klotho, while physical exercise and certain genetic variations lead to a decrease in cortisol response and increased klotho. Here, we review the interrelated opposite actions of cortisol and klotho in the pathogenesis of PD. Together they impact powerful and divergent mechanisms that may go on to influence PD-related symptoms. Better understanding of these hormones in PD would facilitate the design of effective interventions that can simultaneously impact the multiple systems involved in the pathogenesis of PD.
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