Forskningsstudier om binyrefunksjon
Her er en oversikt over forskning på binyrenes funksjon og forskjellige problemer.
Backhaus, J., Junghanns, K., Hohagen, F. (2004). Sleep disturbances are correlated with decreased morning awakening salivary cortisol
Psychoneuroendocrinology; Volume 29, Issue 9, Pages 1184–1191.
Results: Cortisol after awakening was significantly decreased in primary insomnia. Salivary cortisol at the time of awakening correlated negatively with the subjective estimation of sleep quality, i.e. a low salivary cortisol level directly after awakening correlated with a higher frequency of nightly awakenings, a diminished sleep quality and a decreased feeling of recovery after awakening.
Cleare, A.J., Miell, J., Heap, E. Sookdeo, S., Young, L., Malhi, G.S., O’Keane, V. (2001). Hypothalamo-Pituitary-Adrenal Axis Dysfunction in Chronic Fatigue Syndrome, and the Effects of Low-Dose Hydrocortisone Therapy. The Journal of Clinical Endocrinology & Metabolism; vol. 86 no. 8 3545-3554.
Results: In this group, there was a significant increase in the cortisol response to human CRH, which reversed the previously observed blunted responses seen in these patients. We conclude that the improvement in fatigue seen in some patients with chronic fatigue syndrome during hydrocortisone treatment is accompanied by a reversal of the blunted cortisol responses to human CRH.
Di Giorgio, A., Hudson, M., Jerjes, W., Cleare, A. (2005). 24-Hour Pituitary and Adrenal Hormone Profiles in Chronic Fatigue Syndrome.
Psychosomatic Medicine; vol. 67 no. 3 433-440
Conclusions: Patients with CFS demonstrated subtle alterations in HPA axis activity characterized by reduced ACTH over a full circadian cycle and reduced levels during the usual morning physiological peak ACTH secretion. This provides further evidence of subtle dysregulation of the HPA axis in CFS. Whether this dysregulation is a primary feature of the illness or instead represents a biologic effect secondary to having the illness itself remains unclear.
Head, K.A., Kelly, G.S. (2009) Nutrients and Botanicals for Treatment of Stress: Adrenal Fatigue, Neurotransmitter Imbalance, Anxiety, and Restless Sleep. Alternative Medicine Review; Jun;14(2):114-40.
Abstract: Research shows a dramatic increase in use of the medical system during times of stress, such as job insecurity. Stress is a factor in many illnesses – from headaches to heart disease, and immune deficiencies to digestive problems. A substantial contributor to stress-induced decline in health appears to be an increased production of stress hormones and subsequent decreased immune function. Non-pharmaceutical approaches have much to offer such patients. This article focuses on the use of nutrients and botanicals to support the adrenals, balance neurotransmitters, treat acute anxiety, and support restful sleep.
|Hills, S.R., Reiss, R.S., Orsham, P.H., George, W.T. (1950) The effect of adrenocorticotropin and cortisone on thyroid function: thyroidadrenocortical interrelationships. The Journal of Clinical Endocrinology & MetabolismExcerpt: A depression of thyroid function in animals and in man has been reported following stress, the administration of cortisone acetate (11-dehydro-17-hydroxycorticosterone acetate), ACTH (adrenocorticotropic hormone) and epinephrine (25–29). In patients with Addison’s disease, the thyroid depression induced by cortisone was preceded by an initial stimulation. The availability of ACTH, TSH and cortisone for clinical use and the improvement in the techniques of measuring thyroid and adrenal cortical function have stimulated further work on the thyroid-adrenal relationship.|
Holtorf, K. (2007). Diagnosis and treatment of hypothalamic-pituitary-adrenal (HPA) axis dysfunction in patients with chronic fatigue syndrome (CFS) and fibromyalgia (FM). Journal of Chronic Fatigue Syndrome, 14(3), 59-88.
Abstract: Because treatment with low physiologic doses of cortisol (<15 mg) has been shown to be safe and effective and routine dynamic ACTH testing does not have adequate diagnostic sensitivity, it is reasonable to give a therapeutic trial of physiologic doses of cortisol to the majority of patients with CFS and FM, especially to those who have symptoms that are consistent with adrenal dysfunction, have low blood pressure or have baseline cortisol levels in the low or low-normal range.
Kamilaris, C.T., Debold, C.R., Pavlous, S.N., Island, D.P., Hoursanidis, A. Orth, D.N. (1987) Effect of Altered Thyroid Hormone Levels on Hypothalamic-Pituitary-Adrenal Function. The Journal of Clinical Endocrinology & Metabolism; vol. 65 no. 5 994-999. Conclusions: These results indicate that thyroid hormone deficiency of short duration 1) increases corticotroph sensitivity to oCRH, 2) may diminish the plasma ACTH response to metyrapone-induced hypocortisolemia, and 3) has no apparent effect on the acute adrenal response to ACTH. These data together with those of previous studies that have shown reduced responses of the hypothalamic-pituitary-adrenal axis to metyrapone and hypoglycemia in hypothyroid patients suggest that the release of hypothalamic CRH and/or other ACTH secretagogues may be decreased in hypothyroidism.
Musselman, D.L., Nemeroff, C.B. (1996). Depression and endocrine disorders: focus on the thyroid and adrenal system. The British Journal of Psychiatry. 1996(30):123-128. Abstract: Concerning the HPT axis, depressed patients have been reported to have: (a) alterations in thyroid-stimulating hormone response to thyrotropin-releasing hormone (TRH); (b) an abnormally high rate of antithyroid antibodies; and (c) elevated cerebrospinal fluid (CSF) TRH concentrations. Moreover, tri-iodothyronine has been shown conclusively to augment the efficacy of various antidepressants. Concerning the HPA axis, depressed patients have been reported to exhibit: (a) adrenocorticoid hypersecretion; (b) enlarged pituitary and adrenal gland size; and (c) elevated CSF corticotropin-releasing factor concentrations.
Peterson, R.E. (1958) The Influence of the Thyroid on Adrenal Cortical Function. The Journal of Clinical Investigation; vol 37(5).
Conclusions: It is suggested from these data that there is a homeostatic mechanism mediated through the liver-pituitary-adrenals which results in a decreased synthesis of cortisol in patients with myxedema in whom the rate of removal of cortisol by the liver is impaired, and an increased synthesis of cortisol in patients of thyrotoxicosis in whom the rate of removal of cortisol by the liver is accelerated.
Rodríguez-Gutiérrez, R., González-Velázquez, C., González-Saldívar, G., Villarreal-Pérez, J. Z., & González-González, J. G. (2014).
Glucocorticoid Functional Reserve in Full-Spectrum Intensity of Primary Hypothyroidism.International Journal of Endocrinology, 2014.
Conclusion: Patients with different degrees of intensity of primary hypothyroidism had improved cortisol response after reaching euthyroidism. The incidence of adrenal insufficiency was 6.7–18.3% and more than 50% of the cases had a normal cortisol response after L-T4 therapy. This finding could have important clinical implications especially in the setting of acute stress situations occurring during the period while a euthyroid state is still not achieved.
Scott, L.V., Salahuddin, F., Cooney, J., Svec, F., Dinan, T. (1999). Differences in adrenal steroid profile in chronic fatigue syndrome, in depression and in health. Journal of Affective Disorders; vol 5: issues 1-2: 129-137.
Results: DHEA and DHEA-S levels were significantly lower in the CFS compared to the healthy group; DHEA-S levels, but not DHEA, were lower in the depressives; cortisol and 17-alphahydroxyprogesterone did not differ between the three groups. Conclusions: A potential role for DHEA, both therapeutically and as a diagnostic tool, in CFS, is suggested.
Van Den Eede F., Moorkens G., Van Houdenhove B., Cosyns P, Claes S. (2007) Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome. Neuropsychobiology; Vol. 55, No. 2, 2007.
Abstract: There is evidence for a hypofunction of the hypothalamic-pituitary-adrenal (HPA) axis in a proportion of the patients with chronic fatigue syndrome (CFS), despite the negative studies and methodological difficulties. In this review, we focus on challenge studies and on the role of the HPA axis in the pathogenesis of CFS. Mild hypocortisolism, blunted adrenocorticotropin response to stressors and enhanced negative feedback sensitivity to glucocorticoids are the main findings. Several underlying mechanisms have been proposed. Currently, it is a matter of debate whether these disturbances have a primary role in the pathogenesis of CFS. However, even if the HPA axis dysfunctions are secondary to other factors, they are probably a relevant factor in symptom propagation in CFS.