Hypothalamic-pituitary-adrenal axis activity

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Presentation transcript:

Hypothalamic-pituitary-adrenal axis activity in major depressive disorder Carmilla Licht & Nicole Vogelzangs

Cardiovascular disease Depression Biological black box Metabolic changes, atherosclerosis Cardiovascular disease

Cardiovascular disease Depression inflammation autonomic HPA-axis nervous system Metabolic changes, atherosclerosis Cardiovascular disease

Cardiovascular disease Depression inflammation autonomic HPA-axis nervous system Metabolic changes, atherosclerosis Cardiovascular disease

Hypothalamic-pituitary-adrenal axis

Function HPA axis Acute versus Chronic Hersenen: oa geheugen

Function cortisol Primary defense mechanism in reaction to stress, to regain homeostatis, including lowering cortisol Essential for optimal emotional and cognitive functioning  removing stressor Hersenen: oa geheugen

Role of HPA axis in depression?

Some indications Stress and depression Cushing’s disease and depression Somatic consequences of depression Symptoms of depression

What is the evidence?

Depression and Cortisol Increased HPA-as activity Caroll (1976), Holsboer (1984), Nemeroff (1984), Gold (1986), Young (1994), Bhagwagar (2005) Decreased HPA-as activity Chrousos en Gold (1992), Asnis (1995), McGinn (1996), Levitan (2002), Stetler en Miller (2005) No association Schlechte (1986), Strickland (1998), Anisman (1999), Posener (2000), Young (2002)

Why investigate HPA-axis? Knowledge pathophysiology depression Identifying risk groups Medication?

How investigate HPA-axis? CRH, ACTH, cortisol Liquor, blood, urine, saliva 95% bound, 5% free Stress versus basal

Diurnal rhythm => multiple time points CAR, basal Cortisol nmol/l Awakening Sleep Awakening

Major depressive disorder and Hypothalamic-pituitary-adrenal axis activity Sophie Vreeburg WJG Hoogendijk, J van Pelt, RH de Rijk, JCM Verhagen, R van Dyck, JH Smit, FG Zitman, BWJH Penninx Supported by the Geestkracht program of ZonMW and matching funds of participating organisations

Research question Do cortisol levels (Cortisol Awakening Response, evining level and DST) differ between depressive persons and controls in a large sample? Do remitted and current cases differ? What is the role of comorbid anxiety?

Assessment of cortisol in saliva Saliva collected at home 73% of samples returned to lab LUMC 7 samples: Cortisol awakening response (CAR): T1: at awakening T2: +30 minuten T3: +45 minuten T4: +60 minuten Evening: T5: 22:00u T6: 23:00u DST: 0.5 mg dexamethason at 23:05 T7: at awaking Most previous studies are rather small, no extensive psychiatric studies => NESDA

Cortisol measures CAR Evening level DST

area under the curve (AUC) AUC to increase Cortisol nmol/l AUC to ground Minutes after awakening

Cortisol measures CAR Evening level: T5 at 22.00u and T6 at 23.00u DST Mean of 2 measures

Cortisol measures CAR Avond waarde DST: 0.5 mg dexamethason Cortisol suppression Ratio T1/T7

Covariates Sociodemografic factors Sex, age, SES Health factors Smoking, physical activity Sampling factors Work status, weekday, season, time at awakening, sleep duration

Current vs remitted MDD

Cortisol Awakening Response MDD+anxiety (n=830) MDD (n=450) Anxiety (n=255) Controls (n=308) Cortisol (nmol/l) direct groepseffect tijd*groep effect MDD+anxiety vs controles p<.001 p=.03 MDD lifetime vs controles p=.01 p=.04 Anxiety lifetime vs controles p=.03 p=.67

Evening cortisol REF Cortisol (nmol/l) p=.90 p=.50 p=.05 Cortisol (nmol/l) REF controles anxiety MDD MDD+anxiety

Cortisol, after dexamethason (T7) p=.90 p=.48 p=.21 p=0.10 p=0.81 Cortisol (nmol/l) REF controles anxiety MDD MDD+anxiety

Conclusions Persons with depression or anxiety show a modest but significant higher cortisol awakening response Persons with comorbid anxiety+MDD also have higher evening cortisol levels No difference between current and remitted MDD