LOW-DOSE HYDROCORTISONE IN CHRONIC FATIGUE SYNDROME: A RANDOMISED CROSSOVER TRIAL
Studies of the hypothalamo-pituitary adrenal (HPA) axis in chronic fatigue syndrome show a mild hypocortisolism of central origin, in contrast to the hypercortisolism of major depression. In some patients with chronic fatigue syndrome, low-dose hydrocortisone reduces fatigue levels in the short term. Treatment for a longer time and follow-up studies are needed to find out whether this effect could be clinically useful.
THE HYPOTHALAMO-PITUITARY-ADRENAL AXIS IN CHRONIC FATIGUE SYNDROME AND FIBROMYALGIA SYNDROME
The hypothalamo-pituitary-adrenal (HPA) axis plays a major role in the regulation of responses to stress. Human stress-related disorders such as chronic fatigue syndrome (CFS), fibromyalgia syndrome (FMS), chronic pelvic pain and post-traumatic stress disorder are characterized by alterations in HPA axis activity. However, the role of the HPA axis alterations in these stress-related disorders is not clear.
Most studies have shown that the HPA axis is underactive in the stress-related disorders, but contradictory results have also been reported, which may be due to the patients selected for the study, the methods used for the investigation of the HPA axis, the stage of the syndrome when the tests have been done and the interpretation of the results. There is no structural abnormality in the endocrine organs which comprise the HPA axis, thus it seems that hypocortisolemia found in the patients with stress-related disorder is functional.
It may be also an adaptive response of the body to chronic stress. In this review, tests used in the assessment of HPA axis function and the HPA axis alterations found in CFS and FMS are discussed in detail.
THE THERAPEUTIC POTENTIAL FOR TRYPTOPHAN AND MELATONIN: POSSIBLE ROLES IN DEPRESSION, SLEEP, ALZHEIMER'S DISEASE AND ABNORMAL AGING
Evidence suggests that stress and/or a dietary lack of tryptophan may make deficiencies of serotonin and melatonin common. In addition, older animals and human beings have a reduced ability to synthesize melatonin.
Disorders of melatonin levels and rhythms are suggested to be a cause of affective disease, abnormal sleep, Alzheimer's disease, and some age related disorders. If these ideas prove to be true, then preventive measures are possible.
EFFECTS OF L-TRYPTOPHAN ON SLEEPINESS AND ON SLEEP
Over the past 20 yr, 40 controlled studies have been described concerning the effects of L-tryptophan on human sleepiness and/or sleep. The weight of evidence indicates that L-tryptophan in doses of 1 g or more produces an increase in rated subjective sleepiness and a decrease in sleep latency (time to sleep).
There are less firm data suggesting that L-tryptophan may have additional effects such as decrease in total wakefulness and/or increase in sleep time. Best results (in terms of positive effects on sleep or sleepiness) have been found in subjects with mild insomnia, or in normal subjects reporting a longer-than-average sleep latency.
Mixed or negative results occur in entirely normal subjects--who are not appropriate subjects since there is no room for improvement. Mixed results are also reported in severe insomniacs and in patients with serious medical or psychiatric illness.
MELATONIN IN NONAPNEA SLEEP DISORDERS
Nonapnea sleep disorders: Nonapnea sleep disorder In humans, melatonin secretion increases soon after the onset of darkness, peaks in the middle of the night (between 2 and 4 a.m.), and gradually falls during the second half of the night
TAURINE INDUCES ANTI-ANXIETY BY ACTIVATING STRYCHNINE-SENSITIVE GLYCINE RECEPTOR IN VIVO
Taurine has a variety of actions in the body such as cardiotonic, host-defensive, radioprotective and glucose-regulatory effects. However, its action in the central nervous system remains to be characterized. In the present study, we tested to see whether taurine exerts anti-anxiety effects and to explore its mechanism of anti-anxiety activity in vivo.
The staircase test and elevated plus maze test were performed to test the anti-anxiety action of taurine. Convulsions induced by strychnine, picrotoxin, yohimbine and isoniazid were tested to explore the mechanism of anti-anxiety activity of taurine. The Rotarod test was performed to test muscle relaxant activity and the passive avoidance test was carried out to test memory activity in response to taurine. Taurine (200 mg/kg, p.o.) significantly reduced rearing numbers in the staircase test while it increased the time spent in the open arms as well as the number of entries to the open arms in the elevated plus maze test, suggesting that it has a significant anti-anxiety activity.
Taurine's action could be due to its binding to and activating of strychnine-sensitive glycine receptor in vivo as it inhibited convulsion caused by strychnine; however, it has little effect on picrotoxin-induced convulsion, suggesting its anti-anxiety activity may not be linked to GABA receptor. It did not alter memory function and muscle activity. Taken together, these results suggest that taurine could be beneficial for the control of anxiety in the clinical situations. Copyright (c) 2007 S. Karger AG, Basel.
EVALUATION OF ANTIOXIDANT SYSTEMS IN PITUITARY-ADRENAL AXIS DISEASES
Adrenal Fatigue / Hypoadrenalism - Low CoQ10 has been shown to lead to hypoadrenalism. The role of adrenal steroids in antioxidant regulation is not known. Previously, we demonstrated some Coenzyme Q(10) (CoQ(10)) alterations in pituitary diseases, which can induce complex pictures due to alterations of different endocrine axes.
Therefore we determined CoQ(10) and Total Antioxidant Capacity (TAC) in pituitary-dependent adrenal diseases: 6 subjects with ACTH-dependent adrenal hyperplasia (AH); 19 with secondary isolated hypoadrenalism (IH), 19 with associated hypothyroidism (multiple pituitary deficiencies, MPH). CoQ(10) was assayed by HPLC; TAC by the system metmyoglobin-H(2)O(2), which, interacting with the chromogenous 2,2(I)-azinobis-(3-ethylbenzothiazoline-6-sulphonate), generates a spectroscopically revealed radical compound after a latency time (Lag) proportional to the antioxidant content. CoQ(10) levels were significantly lower in IH than AH and MPH, with a similar trend when adjusted for cholesterol.
Also TAC was lower in IH than in AH and MPH, suggesting that adrenal hormones can influence antioxidants. However, since thyroid hormones modulate CoQ(10) levels and metabolism, when thyroid deficiency coexists it seems to play a prevalent influence.
REDUCTION OF SERUM UBIQUINOL-10 AND UBIQUINONE-10 LEVELS BY ATORVASTATIN IN HYPERCHOLESTEROLEMIC PATIENTS
CoenzymeQ10 is a cofactor produced by the body that aids in energy production in the Krebs cycle and mitrochondrial electron transport chain. It is converted into the antioxidant ubiquinol following ingestion: Dyslipidemia, High Cholesterol, Current statin use. CoQ10 levels decrease with age and have also been observed to be low in patients with certain disorders (e.g. cardiovascular diseases, diabetes).
CoQ10 supplementation has been shown to offset some negative side effects of statin medications. Statins + CoQ10 - HMG-CoA reductase inhibitors (lovastatin, pravastatin, rosuvastatin, and simvastatin) decrease the concentration of CoQ10 in the human body.
ASSOCIATION OF HIGH VITAMIN D STATUS WITH LOW CIRCULATING THYROID-STIMULATING HORMONE INDEPENDENT OF THYROID HORMONE LEVELS IN MIDDLE-AGED AND ELDERLY MALES
Vitamin D is recognized to be an essential element for bone metabolism and skeletal health; however, its deficiency can cause rickets in children as well as an increased propensity for osteoporosis. In addition, it may also affect extraskeletal health. Indeed, vitamin D deficiency has been identified as a risk factor for diabetes mellitus, cancers, multiple sclerosis and other autoimmune diseases, atherosclerosis, and infectious diseases. Few past studies have reported the impact of vitamin D deficiency on autoimmune thyroid disease and demonstrated inconclusive results.
Besides affecting the thyroid gland through immune-mediated processes, vitamin D has been shown to influence rat thyroid follicular cells by directly inhibiting thyrotropin-stimulated iodide uptake in a dose-dependent manner. Recently, a population-based study has reported that high vitamin D status in younger individuals is associated with low circulating thyroid-stimulating hormone (TSH). However, it remains unknown as to why no relationship between vitamin D status and serum TSH levels in middle-aged and elderly individuals was found in this study.
Therefore, in the present study, we examined the relationship between vitamin D status and circulating TSH levels in middle-aged and elderly individuals with thyroid autoimmunity, while taking thyroid function into consideration in addition to the relationship between vitamin D insufficiency and thyroid autoimmunity, the presence of thyroid nodule(s) and thyroid volume in a cross-sectional study.
ASSOCIATION OF VITAMIN D STATUS WITH SERUM ANDROGEN LEVELS IN MEN
Men with sufficient 25(OH)D levels (?30 μg/l) had significantly higher levels of testosterone and FAI and significantly lower levels of SHBG when compared to 25(OH)D insufficient (20?29·9 μg/l) and 25(OH)D-deficient (<20 μg/l) men (P < 0·05 for all). In linear regression analyses adjusted for possible confounders, we found significant associations of 25(OH)D levels with testosterone, FAI and SHBG levels (P < 0·05 for all). 25(OH)D, testosterone and FAI levels followed a similar seasonal pattern with a nadir in March (12·2 ?g/l, 15·9 nmol/l and 40·8, respectively) and peak levels in August (23·4 μg/l, 18·7 nmol/l and 49·7, respectively) (P < 0·05 for all).