Have you already been to several doctors trying to find a real cause and an efficient treatment for your negative hormonal symptoms? Have they told you that your tests are normal and that “it’s all in your head”? Reality is that when faced with patients that suffer from disorders like chronic fatigue syndrome or adrenal dysfunction, doctors are at loss.
In a poorly informed attempt to relieve symptoms, physicians might prescribe antidepressants, muscle relaxants, pain pills or sleep medications. None of these will resolve the condition and side effects may make you feel worse.
Why doesn’t conventional medicine acknowledge and address your symptoms?
In its early stages, diagnosing adrenal insufficiency can be difficult. In conventional medical school, doctors are only taught to look for extreme adrenal malfunction (Addison’s Disease, which occurs when the glands produce far too little cortisol, and Cushing’s Syndrome, which stems from excessive cortisol production) and don’t know how to measure cumulative adrenal fatigue. This is unfortunate because millions of people suffer from adrenal insufficiency and symptoms are often overlooked.
What are the standard tests used to determine adrenal dysfunction?
Tests that measure the levels of cortisol and aldosterone are used to make a diagnosis. The ACTH stimulation test is the most commonly used test for diagnosing adrenal insufficiency. In this test, blood cortisol, urine cortisol, or both are measured before and after a synthetic form of adrenocorticotropic hormone (ACTH) is given by injection. ACTH is a hormone produced by the pituitary gland that stimulates the adrenal glands to produce cortisol.
The normal response after an ACTH injection is a rise in blood and urine cortisol levels. People with Addison’s disease or long-standing secondary adrenal insufficiency have little or no increase in cortisol levels.
When the response to the ACTH test is abnormal, a corticotropin-releasing hormone (CRH) stimulation test can help determine the cause of adrenal insufficiency. In this test, synthetic CRH is injected intravenously and blood cortisol is measured before and 30, 60, 90, and 120 minutes after the injection. People with secondary adrenal insufficiency have absent or delayed ACTH responses. CRH will not stimulate ACTH secretion if the pituitary is damaged, so an absent ACTH response points to the pituitary as the cause. A delayed ACTH response points to the hypothalamus as the cause.
The insulin-induced hypoglycemia test is used to determine how the hypothalamus, pituitary and adrenal glands respond to stress. During this test, blood is drawn to measure the blood glucose and cortisol levels, followed by an injection of fast-acting insulin. Blood glucose and cortisol levels are measured again 30, 45 and 90 minutes after the insulin injection. The normal response is for blood glucose levels to fall (this represents the stress) and cortisol levels to rise.
Are these tests accurate?
Studies that utilize central acting stimulation tests, including corticotropin-releasing hormone (CRH), insulin stress testing (IST), d-fenfluramine, ipsapirone, interleukin-6 (IL-6) and metyrapone testing, have demonstrated that HPA axis dysfunction of central origin is present in a majority of Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) patients tested.
However, ACTH stimulation tests and baseline cortisol testing lack the sensitivity to detect central hypothalamic-pituitary-adrenal (HPA) dysfunction and have resulted in controversy and confusion regarding the incidence of HPA axis dysfunction and the appropriateness of treatment.
There are a large number of studies that assess basal cortisol levels as a primary focus or as part of a subsequent stimulation test. These are of limited value as they fail to assess the function of the HPA axis during stress and lack sensitivity in detecting central HPA axis dysfunction.
Studies that utilize 24 hour urinary cortisol levels have consistently shown HPA axis dysfunction with only a few studies showing normal levels in CFS and FM patients. Ten studies were identified that assess 24 hour urine cortisol levels in CFS and FM patients with 6 demonstrating a significant decrease in 24-hour urine cortisol in FM/CFS patients and 1 demonstrating reduced levels that did not reach statistical significance.
The lack of sensitivity of the 24-hour urinary cortisol levels is demonstrated by the fact that 2 of the 4 negative studies also performed stimulation tests (ITT or IL-6) and both demonstrated HPA axis dysfunction despite having normal or non-significantly reduced 24-hour urine cortisol levels.
Current methods of testing are very poor at assessing the area of dysfunction in these complex interactions, but despite this, all studies utilizing ITT, CRH and/or metyrapone testing have shown abnormal results in cortisol levels.
Make sure your physician knows what to look for if you are experiencing symptoms associated with adrenal dysfunction.