Adrenal Fatigue & Glucocorticoid Use

Discussion in 'Men's Health Forum' started by Michael Scally MD, Feb 28, 2010.

  1. 2yung4this

    2yung4this Member

    Its not BS if you are on long term GC use that your adrenals atrophy....I should know.

    GC, are exactly like any external hormone...its shuts down production. My docs tried to get me off Gc's three times, and i failed all times. So even thought my docs thinks I no longer needs the GC for my transplant, I cant come off and am on 5mg of pred, probably for life.

    PS, MRI of adrenals showed almost nonexistent and atrophied....
     
  2. CubbieBlue

    CubbieBlue Member

    Who the fuck is the Dr. House that published this study? 99% of the doctors I've seen in my life would go: Hey, these ears look weird on this read out. Weird, huh?

    PLUS, why did they check his ears during a physical examination? I don't think I've ever even had a doctor check my ears.

    Seriously - this guy is lucky he had the doc he did.
     
  3. vantage108

    vantage108 Member

    I always laugh when I hear folks running around whining that they have "adrenal insufficiency".

    You don't run around if you have real adrenal insufficiency. You lie flat on your back in an ER wondering why blinking your eyes takes so much damn energy while the nurse puts 4 or 5 liters of saline in your arm and all the residents stand around going "wow, an Addisonian crisis."

    I've had real full-blown primary adrenal insufficiency -- aka Addison's -- since the late 1980s. It is not pretty, it is not fun, all of the existing treatments for it suck, and it leaves you really vulnerable -- a minor car accident or a bout of flu can put you into shock. You guys messing around with GCs and Florinef because you feel kinda run down are asking for a lot more trouble than you may realize. Try eating better for a couple of weeks instead.
     
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  4. 2yung4this

    2yung4this Member

    Word :)
     
  5. Michael Scally MD

    Michael Scally MD Doctor of Medicine

  6. CubbieBlue

    CubbieBlue Member

  7. imrj

    imrj Junior Member

    well it is BS for me thats for sure, it certainly doesnt explain my case since if it were as you put it then my adrenals would have dissapeared long ago......

    and interesting that you mention an MRI, I just had one done and my adrenals are quite healthy, even after 2 years of GC treatment.....and thats on 10mg pred day, even higher on stress dose days....

    GCs get a bad rap all over the place, yet many people cant live w/o them and, oh, i am pretty sure its the only hormone you cannot live w/o, how ironic that is.
     
  8. Structure

    Structure Member

    C'mon, dude. You know as well as everyone else does that we're not talking about cases like addison's disease. Were talking about "adrenal fatigue".

    The criteria for prescribing any medication is always the same: the benefits need to outweigh the risks. This cannot be said for adrenal fatigue. Obviously, you do not have adrenal fatigue, you have a form of addison's (secondary hypocortisolism), and your case justifies the use. Do you remember goatboy from the last thread where we talked about this? And remember that his doctor gave him shitloads of GC, without any justification? This is the quackery that this thread is meant to address, not legitimate medical applications like your situation.
     
  9. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Davidson ZE, Walker KZ, Truby H. Do Glucocorticosteroids Alter Vitamin D Status? A Systematic Review with Meta-Analyses of Observational Studies. Journal of Clinical Endocrinology & Metabolism. Do Glucocorticosteroids Alter Vitamin D Status? A Systematic Review with Meta-Analyses of Observational Studies

    Context: Vitamin D supplementation is an important adjunct therapy for the prevention and management of glucocorticoid-induced osteoporosis. There has been little exploration of the relationship between glucocorticosteroid (GCS) use and serum 25-hydroxyvitamin D [25(OH)D].

    Objective: The aim of this study was to systematically explore how serum 25(OH)D is altered in adult patients receiving GCS.

    Data Sources: We reviewed Medline and Cinahl databases between January 1970 and August 2011.

    Study Selection: Experimental studies were included where 25(OH)D was measured in patients more than 18 yr of age receiving GCS therapy. Studies were excluded if patients received at least 400 IU/d (10 ?g/d) vitamin D, if GCS treatment was less than 2-wk duration, if more than 50% of the study population received GCS for renal or hepatic disease or after transplant, or if the study population included patients with Cushing's syndrome. A consensus method was used to classify studies. Of identified studies, 3% met the selection criteria.

    Data Extraction: Data were extracted by a single author. Study quality was assessed using criteria developed by the American Dietetic Association.

    Data Synthesis: The weighted mean 25(OH)D (by sample size or SD) was 22.4 [95% confidence interval (CI), 19.4, 25.3] ng/ml and 21.0 (95% CI, 13.5, 28.5) ng/ml, respectively. Random effects meta-analysis was used to compare serum 25(OH)D in patients treated with GCS compared to steroid-naive controls (either healthy or with active disease) and in patients before and after GCS administration. Serum 25(OH)D in GCS users was on average ?0.5 (95% CI, ?1.0, ?0.1) ng/ml lower than in healthy controls (P = 0.03; I2 = 56.4%). Serum 25(OH)D did not differ between GCS users and disease controls [standardized mean difference = 0.0 (95% CI, ?0.2, 0.3) ng/ml; P = 0.793; I2 = 16.2%].

    Conclusion: The suboptimal concentrations of serum 25(OH)D found in adults receiving GCS are inadequate for prevention and management of glucocorticoid-induced osteoporosis. Recommendations for vitamin D supplementation should be adjusted accordingly.
     
  10. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Osteoporosis Management after New Initiations of Long Term Systemic Glucocorticoids

    Long-term systemic glucocorticoid therapy is the most common cause of secondary osteoporosis, and up to 1% of adults are treated with glucocorticoids each year. Glucocorticoid-induced osteoporosis (GIOP) occurs rapidly (6–12% loss of bone mass within the first year), and the risk of fracture increases within 3 months of starting therapy. The first presentation of GIOP may be a fracture, and as many as 30–50% of patients exposed to glucocorticoids will eventually sustain a fracture. Furthermore, although sustained daily doses of 7.5–10 mg prednisone (or equivalent) commonly lead to bone loss and fractures, doses as low as 2.5 mg prednisolone daily have been reported to increase risk of vertebral and hip fractures. Although GIOP is not entirely preventable, it is certainly ameliorable, and there are several relatively consistent guidelines with evidence-based recommendations that suggest bone mineral density (BMD) testing and prophylactic osteoporosis treatment in most if not all patients starting a course of daily 5–10 mg prednisone for 3 months or longer.

    Previous studies that have examined the quality of guideline-concordant GIOP preventive care among patients starting a new course of long-term systemic glucocorticoids have reported a large care-gap with rates of BMD testing or osteoporosis treatment far lower than would be expected for such a common iatrogenic condition. Even randomized trials of interventions to improve GIOP care among repeat glucocorticoid prescribers have achieved testing or treatment rates of only 40– 50%. Previous studies of the GIOP care gap have had limitations that include small sample sizes, inclusion of both incident and prevalent glucocorticoid users simultaneously, biased or nonrepresentative populations, older data (to our knowledge, the most recent published audit was in 2003), and/or an inability to examine longer-term temporal trends.

    Therefore, researchers conducted a decade-long population based cohort study in the province of Manitoba, Canada, in all adults newly initiating long-term systemic glucocorticoid therapy. Their objectives were to 1) describe temporal trends in the quality of GIOP preventive care from 1998–2008 and 2) determine the rates and correlates of high-quality GIOP preventive care defined as the composite of either a BMD test or new osteoporosis treatment within 6 months of a new long-term systemic glucocorticoid initiation.

    In a large population-based cohort, they found that the quality of GIOP preventive care improved 51% over the decade from 1998–2008, although their study also suggests that these improvements have reached a plateau. In absolute terms, GIOP prevention remains suboptimal because only 25% of those starting long-term glucocorticoids received a BMD test or were treated for osteoporosis within 6 months. Several sociodemographic and clinical characteristics were independently associated with lower rates of BMD testing or osteoporosis treatment, most notably, younger age, male sex, and initiation by general practitioners.


    Majumdar SR, Lix LM, Yogendran M, Morin SN, Metge CJ, Leslie WD. Population-Based Trends in Osteoporosis Management after New Initiations of Long-Term Systemic Glucocorticoids (1998-2008). Journal of Clinical Endocrinology & Metabolism. Population-Based Trends in Osteoporosis Management after New Initiations of Long-Term Systemic Glucocorticoids (1998–2008)

    Objectives: Our objective was to describe changes in glucocorticoid-induced osteoporosis (GIOP) preventive care from 1998–2008 including rates and correlates of bone mineral density (BMD) testing and osteoporosis treatment in new long-term glucocorticoid initiations.

    Methods: A population-based study of adults aged 20 yr or older in Manitoba, Canada, was conducted using linked healthcare databases. Subjects with new long-term (?90 d) systemic glucocorticoid initiations were identified within each fiscal year. High-quality GIOP preventive care was defined by the composite of BMD testing or osteoporosis treatment within 6 months of starting glucocorticoids. For each initiation, we identified sociodemographic and clinical characteristics, prednisone dose equivalents, and prescriber specialty. Multivariable Poisson regression models were used to calculate adjusted incidence rate ratios (aIRR).

    Results: We studied 17,736 new long-term glucocorticoid initiations; one third were at least 10 mg prednisone daily, and most (64%) were prescribed by general practitioners. Overall, 6-month rates of BMD testing were 6%, osteoporosis treatment 22%, and the composite of testing or treatment 25%. From 1998–2008, there were modest increases in BMD testing (from 4 to 6%), osteoporosis treatment (from 15 to 24%), and testing or treatment [from 17 to 27%; aIRR = 1.51; 95% confidence interval (CI) = 1.40–1.63]. High-quality GIOP preventive care varied significantly by age (16% for those <50 yr vs. 27% for those ?70 yr; aIRR = 0.57; 95% CI = 0.52–0.63), sex (13% for men vs. 34% for women; aIRR = 0.40; 95% CI = 0.37–0.43), and prescriber (23% general practice vs. 44% rheumatology; aIRR = 0.56; 95% CI = 0.52–0.60).

    Conclusions: Quality of GIOP preventive care has improved but remains suboptimal with only one quarter of those starting long-term glucocorticoids receiving BMD testing or osteoporosis treatment. Interventions to improve GIOP prevention, especially targeting younger patients, men, and nonspecialists, are needed.
     
    Last edited: May 8, 2012
  11. foreveryoung

    foreveryoung Member

    great post, and should be required reading for all that are wanting to "take a pill" or "inject something" to "fix" their problems, meanwhile ignoring all the obvious causes of poor health, poor nutrition and eating habits, poor sleep habits, poor exercise habits, other unhealthy habits
     
  12. thrombus

    thrombus Member

    Long thread. Unfortunately, there seems little agreement on how low cortisol should be treated.
     
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  13. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Transgenerational Effects of Prenatal Synthetic Glucocorticoids on Hypothalamic-Pituitary-Adrenal Function

    Iqbal M, Moisiadis VG, Kostaki A, Matthews SG. Transgenerational Effects of Prenatal Synthetic Glucocorticoids on Hypothalamic-Pituitary-Adrenal Function. Endocrinology. Transgenerational Effects of Prenatal Synthetic Glucocorticoids on Hypothalamic-Pituitary-Adrenal Function

    Approximately 10% of pregnant women are at risk of preterm delivery and receive synthetic glucocorticoids (sGC) to promote fetal lung development. Studies have indicated that prenatal sGC therapy modifies hypothalamic-pituitary-adrenal (HPA) function in first-generation (F1) offspring. The objective of this study was to determine whether differences in HPA function and behavior are evident in the subsequent (F2) generation. Pregnant guinea pigs (F0) received betamethasone (BETA; 1 mg/kg) or saline on gestational d 40/41, 50/51, and 60/61. F1 females were mated with control males to create F2 offspring. HPA function was assessed in juvenile and adult F2 offspring. Locomotor activity was assessed in juvenile offspring. Analysis of HPA-related gene expression was undertaken in adult hippocampi, hypothalami, and pituitaries. Locomotor activity was reduced in F2 BETA males (P < 0.05). F2 BETA offspring displayed blunted cortisol response to swim stress (P < 0.05). After dexamethasone challenge, F2 BETA males and females displayed increased and decreased negative feedback, respectively. F2 BETA females had reduced pituitary levels of proopiomelanocortin (and adrenocorticotropic hormone), and corticotropin-releasing hormone receptor mRNA and protein (P < 0.05). F2 BETA males displayed increased hippocampal glucocorticoid receptor (P < 0.001), whereas in BETA females, hippocampal glucocorticoid receptor and mineralocorticoid receptor mRNA were decreased (P < 0.05).

    In conclusion, prenatal BETA treatment affects HPA function and behavior in F2 offspring. In F2 BETA females, pituitary function appears to be primarily affected, whereas hippocampal glucocorticoid feedback systems appear altered in both F2 BETA males and females. These data have clinical implication given the widespread use of repeat course glucocorticoid therapy in the management of preterm labour.
     
  14. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Inder WJ, Dimeski G, Russell A. Measurement of salivary cortisol in 2012 – laboratory techniques and clinical indications. Clinical Endocrinology. Measurement of salivary cortisol in 2012 &ndash; laboratory techniques and clinical indications - Inder - Clinical Endocrinology - Wiley Online Library

    The utility of measuring salivary cortisol has become increasingly appreciated since the early 1980s. Salivary cortisol is a measure of active free cortisol and follows the diurnal rhythm of serum or plasma cortisol. The saliva sample may be collected by drooling or through the use of absorbent swabs which are placed into the mouth until saturated. Salivary cortisol is therefore convenient for patients and research participants to collect non-invasively on an outpatient basis. Several assay techniques have been used to measure salivary cortisol including radioimmunoassay and more recently liquid chromatography-tandem mass spectrometry. The analytical sensitivity varies between these assay methods, as does the potential for cross reactivity with other steroids. The interpretation of salivary cortisol levels relies on rigorous standardization of sampling equipment, sampling protocols and assay technology with establishment of a local reference range. Clinically, the commonest use for salivary cortisol is measuring late night salivary cortisol as a screening test for Cushing's syndrome. Several studies have shown diagnostic sensitivities and specificities of over 90%, which compares very favourably with other screening tests for Cushing's syndrome such as the 24 hour urinary free cortisol and the 1mg overnight dexamethasone suppression test. There are emerging roles for the use of salivary cortisol in diagnosing adrenal insufficiency, particularly in conditions associated with low cortisol binding globulin levels, and in the monitoring of glucocorticoid replacement. Finally, salivary cortisol has been used extensively as a biomarker of stress in a research setting, especially in studies examining psychological stress with repeated measurements.
     
  15. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Overman RA, Yeh J-Y, Deal CL. Prevalence of oral glucocorticoid usage in the United States: A general population perspective. Arthritis Care & Research. Prevalence of oral glucocorticoid usage in the United States: A general population perspective - Overman - Arthritis Care & Research - Wiley Online Library

    Objective. There is little information on oral glucocorticoid use in the general United States (US) population. Previously, there have been published estimates of glucocorticoid use in countries outside of the US. This study aimed to estimate the prevalence of glucocorticoid use, duration of use, and concomitant use of anti-osteoporosis pharmaceuticals in the US population ?20 years of age.

    Method. Data from five cycles (1999-2008) of the National Health and Nutrition Examination Survey (NHANES) were used to provide nationally representative, weighted estimates. Oral glucocorticoids and concomitant use of anti-osteoporosis pharmaceuticals (bisphosphonates, calcitonin, calcium, hormone replacement therapies, teriparatide, and vitamin D) were analyzed.

    Result. There were 356 NHANES respondents ?20 years of age who reported use of an oral glucocorticoid in the combined cycles between 1999 and 2008. The weighted prevalence of oral glucocorticoid use was 1.2% (95% CI, 1.1-1.4) from 1999-2008, corresponding to 2,513,259 persons in the US. The mean duration of oral glucocorticoid use was 1605.7 days (95% CI, 1261.2-1950.1) and 28.8% (95% CI, 22.2-35.4) of oral glucocorticoid users reported use for ?5 years. Concomitant use of a bisphosphonate was reported by 8.6% (95% CI, 5.1-11.7) of oral glucocorticoid users and 37.9% (95% CI, 31.7-44.0) reported usage of any anti-osteoporosis pharmaceutical.

    Conclusion. Based on 1999-2008 NHANES data, it is estimated the prevalence of glucocorticoid use in the US is 1.2% with a long duration of use and infrequent use of anti-osteoporotic medications compared to other estimates.
     
  16. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Benson S, Neumann P, Unger N, et al. Effects of standard glucocorticoid replacement therapies on subjective well-being: A randomized, double-blind cross-over study in patients with secondary adrenal insufficiency. European Journal of Endocrinology. Effects of standard glucocorticoid replacement therapies on subjective well-being: A randomized, double-blind cross-over study in patients with secondary adrenal insufficiency

    Objective: For secondary adrenal insufficiency, established biochemical parameters for dosage control are lacking and no optimal substitution dosage and daily distribution have been determined yet. Therefore, in clinical practice the individual total dose is often adjusted based on patients´ subjective well-being.

    Design: Effects of three standard glucocorticoid replacement regimens on psychological variables were assessed in patients with secondary insufficiency (SAI) based on a randomized double-blind study design.

    Methods: N=18 SAI patients were treated with three different established glucocorticoid replacement regimens in a randomized, double-blind, cross-over study (treatment A: hydrocortisone 10-placebo-5-placebo; treatment B: hydrocortisone 10-5-placebo-5; treatment C: prednisone 5-placebo-placebo-placebo). Following each 4-week replacement regimen, quality-of-life (SF-36) and emotional distress (BSI) were assessed along with diurnal changes in current well-being (Bf-S) and alertness (SSS) using validated questionnaires, and additionally compared to patient (patients with pituitary disease and adrenal sufficiency) and healthy control groups.

    Results: SAI patients showed improvements in physical quality-of-life (i.e. SF-36 physical function, p<0.05; physical role function, p<0.05) and current well-being (at 18:00 p<0.05) under treatment A (hydrocortisone 10-0-5-0 mg) compared to the other replacement regimens. Quality-of-life and current well-being were significantly impaired compared to healthy controls, but did not differ from patient controls.

    Conclusions: Although the observed improvements in psychological parameters were comparatively small, our results indicate beneficial effects of a 10-0-5-0 mg hydrocortisone replacement regimen. Nevertheless, treatment effects were insufficient to restore subjective health as compared to healthy controls, indicating the need for improved replacement regimens and supportive psychosocial interventions in SAI patients.
     
  17. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Manenschijn L, Schaap L, van Schoor NM, et al. High Long-Term Cortisol Levels, Measured in Scalp Hair, Are Associated With a History of Cardiovascular Disease. Journal of Clinical Endocrinology & Metabolism. High Long-Term Cortisol Levels, Measured in Scalp Hair, Are Associated With a History of Cardiovascular Disease

    Background: Stress is associated with an increased incidence of cardiovascular disease. The impact of chronic stress on cardiovascular risk has been studied by measuring cortisol in serum and saliva, which are measurements of only 1 time point. These studies yielded inconclusive results. The measurement of cortisol in scalp hair is a novel method that provides the opportunity to measure long-term cortisol exposure. Our aim was to study whether long-term cortisol levels, measured in scalp hair, are associated with cardiovascular diseases.

    Methods: A group of 283 community-dwelling elderly participants were randomly selected from a large population-based cohort study (median age, 75 y; range, 65-85 y). Cortisol was measured in 3-cm hair segments, corresponding roughly with a period of 3 months. Self-reported data concerning coronary heart disease, stroke, peripheral arterial disease, diabetes mellitus, and other chronic noncardiovascular diseases were collected.

    Results: Hair cortisol levels were significantly lower in women than in men (21.0 vs 26.3 pg/mg hair; P < .001). High hair cortisol levels were associated with an increased cardiovascular risk (odds ratio, 2.7; P = .01) and an increased risk of type 2 diabetes mellitus (odds ratio, 3.2; P = .04). There were no associations between hair cortisol levels and noncardiovascular diseases.

    Conclusions: Elevated long-term cortisol levels are associated with a history of cardiovascular disease. The increased cardiovascular risk we found is equivalent to the effect of traditional cardiovascular risk factors, suggesting that long-term elevated cortisol may be an important cardiovascular risk factor.
     
  18. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Ceccato F, Barbot M, Zilio M, et al. Diagnostic performance of salivary cortisol in the diagnosis of Cushing's syndrome, adrenal incidentaloma and adrenal insufficiency. European Journal of Endocrinology. Diagnostic performance of salivary cortisol in the diagnosis of Cushing's syndrome, adrenal incidentaloma and adrenal insufficiency

    Objective: Salivary cortisol has been recently suggested for studies on the hypothalamic-pituitary-adrenal (HPA) axis: lack of circadian rhythm is a marker of Cushing's syndrome (CS), and some authors report that low salivary cortisol levels may be a marker of adrenal insufficiency. The aim of our study was to define the role of salivary cortisol in specific diagnostic setting of HPA axis disease.

    Subjects and Methods: We analyzed morning salivary cortisol (MSC) and late night salivary cortisol (LNSC) in 406 subjects: 52 Cushing's disease (CD), 13 ectopic-CS, 17 adrenal-CS, 27 CD in remission (mean follow-up of 66 ± 39 months), 45 adrenal incidentalomas, 73 patients assessed of CS and then ruled out for endogenous hypercortisolism, 75 patients with adrenal insufficiency and 104 healthy subjects.

    Results: A LNSC value above 5.24 ng/mL differentiated CS from controls with high sensitivity (96.3%) and specificity (97.1%), we found higher LNSC in ectopic-CS than in CD. We found no difference in MSC and LNSC levels between CD in remission and healthy subjects. Both MSC and LNSC were higher in adrenal incidentaloma than in healthy controls. MSC below 2.65 ng/mL distinguished patients with adrenal insufficiency from controls with high sensitivity (97.1%) and specificity (93.3%).

    Conclusions: salivary cortisol is a useful tool to assess endogenous cortisol excess or adrenal insufficiency and to evaluate stable CD in remission.
     
  19. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Sacre K, Dehoux M, Chauveheid MP, et al. Pituitary-adrenal function after prolonged glucocorticoid therapy for systemic inflammatory disorders: an observational study. Journal of Clinical Endocrinology & Metabolism. Pituitary-adrenal function after prolonged glucocorticoid therapy for systemic inflammatory disorders: an observational study

    Context Glucocorticoid therapy is being used in a wide variety of systemic disorders. Reference papers, published more than 20 years ago, showed no correlation between adrenal insufficiency risk and dose or duration of glucocorticoid therapy.

    Objective To evaluate the extent to which long-term glucocorticoid therapy damages the pituitary-adrenal axis in patients with systemic inflammatory disorders.

    Design Retrospective observational study from January 2011 to August 2012
    Setting Monocentric study, Department of Internal Medicine, Bichat Hospital, Paris-Diderot University, Paris, France.

    Participants Sixty consecutive patients who were receiving long-term prednisone therapy for systemic inflammatory disorders and in whom discontinuation of glucocorticoid treatment was planned.

    Intervention A short synacthen test (SST) was performed. A bolus of 0.25mg of 1–24-ACTH was injected in the morning, 24 hours after the most recent dose of prednisone. Cortisol was measured at baseline and 60 minutes after synacthen injection.

    Main outcome measures Frequency and risk estimate of pituitary-adrenal dysfunction.

    Results Twenty-nine patients (48.3%) had adrenal insufficiency defined by a plasmatic cortisol <100 nmol/l (n=13) at baseline (T0) or <550 nmol/l (n=16) 60 minutes (T60) after synacthen injection. Cumulative dose (area under the ROC curve, AUC 0.77 [95% CI: 0.62–0.91], p=0.007) and exposure (AUC 0.80 [95% CI: 0.67–0.93], p=0.002) to prednisone were predictive for adrenal insufficiency based on a T0 <100 nmol/l. Prednisone was stopped in 29/31 (93.5 %) patients showing a normal response to SST; none of these patients required hydrocortisone replacement with a mean follow-up of 10 (± 6) months.

    Conclusion Adrenal insufficiency is frequent in patients treated with long-term glucocorticoids for systemic inflammatory disorders and is related to duration and cumulative dose of steroids.
     
  20. PeterSam

    PeterSam Junior Member

    Hi, first time posting on this forum. This post is clearly a controversial and necessary topic of discussion in today's medical setting. I am someone who had low testosterone and low cortisol levels and all the symptoms associated with each. My PCP and Endo's refused to do anything for me once my ACTH stimulation test came back normal and they basically just said its all in your head. I went to see a holistic medicine doc who looked me over and reviewed a comprehensive collection of test results and logs I had been keeping on my overall health and immediately prescribed me 5mg HC (1/2 in the morning and 1/2 in the early afternoon) allowing me to ramp up to 5/5. He also said I was a poor T4 to t3 converter and prescribed T3 5mcg but asked me to hold off taking it until my adrenals recovered a bit.

    Due to some planned surgeries, Varicocele and Hernia I was reluctant to start on these meds so instead I took a holistic approach using Licorice Extract, B5,B6, Vit C, Adrenal Glandular, Panax Ginseng and a few other herbs. Over the period of a couple months I was able to get my am cortisol from 5.0 to 11.9 and my testosterone levels correspondingly went from 154 total/46 free to 329total/74 free.

    Other test results
    SHBG -17.7
    DHEAs - 179
    LH - 2.1
    FSH - 2.4
    prolactin - 4

    I then had the Unilateral Grade III Varicocele surgery so I backed off of everything but the B5,B6 and Vit. C. Over the next 3 months, my Cortisol levels dropped back down to 8.8 but my testosterone levels remained unchanged.

    I just started TCyp through my Urologist and while I am still working with him on a final dosage at this point he is only willing to dose 100mg TCyp biweekly. I know this is probably not gonna cut it, but I am hopeful hat by supporting both by adrenals and testosterone levels I can finally feel like my young self again.

    For what it is worth one of the main reasons I avoided the HC was because of all of the concern about becoming dependent on it and shutting down normal production although I understood at the levels prescribed it wouldn't probably do that. I felt I should the above solutions first and it did seem to help me. I do wonder however if my low T couldn't be improved more if I would have gotten my adrenal glands functioning to a point where my am cortisol was consistently in the teens. In the end it's basically impossible to get a conventional MD to think through the complexities of this and the integrative docs often just throw a standard solution at you when they see a familiar pattern.

    If anyone has any thoughts or advice on my situation I am all ears.