Cortisol Suppression and Hearing Thresholds in Tinnitus After Low-Dose Dexamethasone Challenge

http://www.biomedcentral.com/1472-6815/12/4

Abstract

Background
Tinnitus is a frequent, debilitating hearing disorder associated with severe emotional and psychological suffering. Although a link between stress and tinnitus has been widely recognized, the empirical evidence is scant. Our aims were to test for dysregulation of the stress-related hypothalamus-pituitary adrenal (HPA) axis in tinnitus and to examine ear sensitivity variations with cortisol manipulation.

Methods
Twenty-one tinnitus participants and 21 controls comparable in age, education, and overall health status but without tinnitus underwent basal cortisol assessments on three non-consecutive days and took 0.5 mg of dexamethasone (DEX) at 23:00 on the first day. Cortisol levels were measured hourly the next morning. Detection and discomfort hearing thresholds were measured before and after dexamethasone suppression test.

Results
Both groups displayed similar basal cortisol levels, but tinnitus participants showed stronger and longer-lasting cortisol suppression after DEX administration. Suppression was unrelated to hearing loss. Discomfort threshold was lower after cortisol suppression in tinnitus ears.

Conclusions
Our findings suggest heightened glucocorticoid sensitivity in tinnitus in terms of an abnormally strong glucocorticoid receptor (GR)-mediated HPA-axis feedback (despite a normal mineralocorticoid receptor (MR)-mediated tone) and lower tolerance for sound loudness with suppressed cortisol levels. Long-term stress exposure and its deleterious effects therefore constitute an important predisposing factor for, or a significant pathological consequence of, this debilitating hearing disorder.

...

Discussion
We report three novel findings that establish differences between tinnitus participants and controls in terms of cortisol hypersuppression, longer-lasting effects of the DEX test on basal cortisol levels, and hearing discomfort threshold. The first novel finding is that tinnitus participants had more strongly suppressed cortisol levels than controls after pharmacological challenge, despite similar basal cortisol levels. This is consistent with the normal diurnal and blunted response to psychosocial stress in tinnitus participants described in a previous study [23], and supports the hypothesis that tinnitus participants have greater sensitivity to HPA axis negative feedback. Hypersuppression in the presence of normal or near-normal basal cortisol levels has also been found in other clinical populations, such as patients with chronic fatigue syndrome [45-47] and burnout [48]. All these findings are consistent with the notion that basal cortisol and post-DEX cortisol suppression are mediated by two separate receptor feedback systems. More importantly, the suppression effect was independent of hearing loss. This is a key finding, because these factors are difficult to disentangle in tinnitus studies [19,23], and it argues for a true effect of tinnitus in addition to, but unrelated to, hearing loss. Our findings therefore directly link tinnitus to a stress-related disorder, and not just to a hearing-related disorder, as some recent population studies suggest [12,49].

...

In any case, considering tinnitus as a stress-related disorder by demonstrating HPA axis disturbance can open up new research avenues. For instance, studies of similar disorders show the same anomalies. There is a great need for new pharmacological targets in tinnitus [57], and a deeper understanding of HPA disturbance could lead to the development of pharmacotherapy targeting the HPA axis [58] as well as monitoring tools to assess the efficacy of tinnitus treatments and therapies.

Read more at the link....

 

Dexamethasone

Dexamethasone is a potent synthetic member of the glucocorticoid class of steroid drugs. It acts as an anti-inflammatory and immunosuppressant. When taken orally, it is 26.6 times more potent than the naturally occurring hormone cortisol and 6.6 times more potent than prednisone.[citation needed]

Therapeutic use

Anti-inflammatory
Dexamethasone is used to treat many inflammatory and autoimmune conditions, such as rheumatoid arthritis and bronchospasm.[1] Idiopathic thrombocytopenic purpura, decreased numbers of platelets due to an immune problem, responds to 40 mg daily for four days; it may be administered in 14-day cycles. It is unclear whether dexamethasone in this condition is significantly better than other glucocorticoids.[2]
It is also given in small amounts[3] (usually five or six tablets) before and/or after some forms of dental surgery, such as the extraction of the wisdom teeth, an operation which often leaves the patient with puffy, swollen cheeks.
It is injected into the heel when treating plantar fasciitis, sometimes in conjunction with triamcinolone acetonide.
It is useful to counteract allergic anaphylactic shock, if given in high doses.
It is present in certain eye drops – particularly after eye surgery– and as a nasal spray (trade name Dexacort), and certain ear drops (Sofradex, when combined with an antibiotic and an antifungal).
Dexamethasone is used in transvenous screw-in cardiac pacing leads to minimize the inflammatory response of the myocardium. The steroid is released into the myocardium as soon as the screw is extended and can play a significant role in minimizing the acute pacing threshold due to the reduction of inflammatory response. The typical quantity present in a lead tip is less than 1.0 mg.
Dexamethasone is often administered before antibiotics in cases of bacterial meningitis. It then acts to reduce the inflammatory response of the body to the bacteria killed by the antibiotics (bacterial death releases proinflammatory mediators that can cause a response which is harmful to the patient), thus improving prognosis and outcome.[4]



Oncologic uses
Cancer patients undergoing chemotherapy are given dexamethasone to counteract certain side effects of their antitumor treatment. Dexamethasone can augment the antiemetic effect of 5-HT3 receptor antagonists, such as ondansetron.
In brain tumors (primary or metastatic), dexamethasone is used to counteract the development of edema, which could eventually compress other brain structures. It is also given in cord compression, where a tumor is compressing the spinal cord.
Dexamethasone is also used as a direct chemotherapeutic agent in certain hematological malignancies, especially in the treatment of multiple myeloma, in which dexamethasone is given alone or in combination with other chemotherapeutic drugs, including most commonly with thalidomide (thal-dex), lenalidomide, bortezomib (Velcade; Vel-dex),[5] or a combination of Adriamycin (doxorubicin) and vincristine (VAD) or VRD- Velcade, Revlamid and Dexamethasone.

Endocrine
Dexamethasone is the treatment for the very rare disorder of glucocorticoid resistance.[6][7]
In adrenal insufficiency and Addison's disease, dexamethasone is prescribed when the patient does not respond well to prednisone or methylprednisolone.

Obstetrics
Dexamethasone may be given to women at risk of delivering prematurely to promote maturation of the fetus' lungs. This has been associated with low birth weight, although not with increased rates of neonatal death.[8]

High altitude illnesses
Dexamethasone is used in the treatment of high altitude cerebral edema, as well as pulmonary edema. It is commonly carried on mountain climbing expeditions to help climbers deal with altitude sickness.[9][10]

Off-label use

Congenital adrenal hyperplasia
Dexamethasone has been used as an off-label prenatal treatment for the symptoms of congenital adrenal hyperplasia (CAH) in female fetuses. CAH causes a variety of physical abnormalities, notably ambiguous genitalia in girls. Early prenatal CAH treatment has been shown to reduce some CAH symptoms, but it does not treat the underlying congenital disorder.
A small clinical trial found long-term effects on verbal working memory among the small group of children treated prenatally, but the small number of test subjects means the study cannot be considered definitive.[11][12] Administration of prenatal dexamethasone has been the subject of controversy over issues of informed consent and because treatment must predate a clinical diagnosis of CAH in the female fetus.
A study utilizing Freedom of Information Act findings to "detail an extremely troubling off-label medical intervention employed in the U.S. on pregnant women to intentionally engineer the development of their fetuses for sex normalization purposes." [13] Glucocorticoids may alter “fetal programming,” potentially resulting in serious metabolic problems that will not become apparent until adulthood.[11][14][13] Prenatal treatment of female fetuses could prevent those fetuses from becoming lesbians after birth, may make them more likely to engage in "traditionally" female-identified behaviour and careers, and more interested in bearing and raising children.[15] Referring to a prospective father who attempted to mitigate the effects of the fraternal birth order effect on increasing the chances of homosexuality in male children by using a surrogate mother, the essay suggests prenatal "dex" treatments constitute the first known attempt to use an in utero method to attempt to reduce the incidence of homosexuality in humans.[16] A medical consensus in 2010 by the Endocrine Society and affiliated organizations indicated prenatal dexamethasone for CAH should be regarded as experimental and should only be used in Institutional Review Board-approved controlled clinical trials at centers large enough to collect meaningful data.[17]

Abuses
Dexamethasone has also been used in the hope of enhancing sports performance.[18]
Long term use of dexamethasone under the brand name Oradexon is widespread among prostitutes in Bangladesh in spite of the dangers, because it helps them develop fat easily.[19][20]
Since dexamethasone is a CYP2D6 enzyme inducer, it can increase the effects of many prodrugs and protoxins which are metabolized via CYP2D6 (ex. tramadol, codeine) by directly increasing the amount of the active metabolite produced.

Diagnostic use
Dexamethasone is also used in a diagnostic context, namely in its property to suppress the natural pituitary-adrenal axis.
Patients presenting with clinical signs of glucocorticoid excess (Cushing's syndrome) are generally diagnosed by a 24-hour urine collection for cortisol or by a dexamethasone suppression test. During the latter, the response of the body to a high dose of glucocorticoids is monitored. Various forms are performed. In the most common form, a patient takes a nighttime dose of either 1 or 4 mg of dexamethasone, and the serum cortisol levels are measured in the morning. If the levels are relatively high (over 5 µg/dL or 150 nmol/L), then the test is positive and the patient has an autonomous source of either cortisol or ACTH, indicating Cushing's syndrome where the tumor does not have a feedback mechanism. If ACTH levels are lowered by at least 50%, this would indicate Cushing's disease, since the pituitary adenoma has a feedback mechanism that has been reset to a higher level of cortisol. Longer versions rely on urine collections on oral dexamethasone over various days.

Veterinary use
Combined with marbofloxacin and clotrimazole, dexamethasone is available under the name Aurizon, CAS number 115550-35-1, and used to treat difficult ear infections, especially in dogs. It can also be combined with trichlormethiazide to treat horses with swelling of distal limbs and general bruising.[21]

Contraindications
Some of these contraindications are relative:

• Existing gastrointestinal ulceration
• Cushing's syndrome
• Severe forms of heart insufficiency
• Severe hypertension
• Uncontrolled diabetes mellitus
• Systemic tuberculosis
• Severe systemic viral, bacterial, and fungal infections
• Pre-existing wide angle glaucoma
• Osteoporosis

Side effects
If dexamethasone is given orally or by injection (parenteral) over a period of more than a few days, side effects common to systemic glucocorticoids may occur. These may include:

• Stomach upset, increased sensitivity to stomach acid to the point of ulceration of esophagus, stomach, and duodenum
• Increased appetite leading to significant weight gain
• A latent diabetes mellitus often becomes manifest, glucose intolerance is worsened in patients with pre-existing diabetes
• Immunosuppressant action, particularly if given with other immunosuppressants, such as cyclosporine, may allow bacterial, viral, and fungal disease to progress more easily and can become life-threatening; fever as a warning symptom is often suppressed.
• Psychiatric disturbances, including personality changes, irritability, euphoria, or mania and mood swings.
• Osteoporosis under long term treatment, pathologic fractures (e.g., hip)
• Muscle atrophy, negative protein balance (catabolism)
• Elevated liver enzymes, fatty liver degeneration (usually reversible)
• Cushingoid (syndrome resembling hyperactive adrenal cortex with increase in adiposity, hypertension, bone demineralization, etc.)
• Depression of the adrenal gland is usually seen, if more than 1.5 mg daily are given for more than three weeks to a month.
• Hypertension, fluid and sodium retention, edema, worsening of heart insufficiency (due to mineral corticoid activity)
• Dependence with withdrawal syndrome is frequently seen.
• Increased intraocular pressure, certain types of glaucoma, cataract (serious clouding of eye lenses)
• Dermatologic: Acne, allergic dermatitis, dry scaly skin, ecchymoses and petechiae, erythema, impaired wound-healing, increased sweating, rash, striae, suppression of reactions to skin tests, thin fragile skin, thinning scalp hair, urticaria.
• Pronounced night sweats.
• Allergic reactions (though infrequently): Anaphylactoid reaction, anaphylaxis, angioedema.

Other side effects have been noted, and should cause concern if they are more than mild.
The short-time treatment for allergic reaction, shock, and diagnostic purposes usually does not cause serious side effects.
Novelist Michael Cox believed his first book, The Meaning of Night was a side effect of prescription dexamethasone, giving him both "formidable energy" while quelling his creative doubts.[22]

Interactions

• NSAIDs and alcohol: increased risk of gastrointestinal ulceration
• Mineralocorticoids: increased risk of hypertension, edema and heart problems
• Oral antidiabetic drugs and insulin: antidiabetic therapy may have to be adjusted
• Tramadol: increased conversion to O-desmethyltramadol
• Codeine: increased conversion to morphine

Other interactions (with certain antibiotics, estrogens, ephedrine, digoxin) are known.

https://en.wikipedia.org/wiki/Dexamethasone

 

Hypothalamic–pituitary–adrenal axis




Basic hypothalamic–pituitary–adrenal axis summary (corticotropin-releasing hormone=CRH, adrenocorticotropic hormone=ACTH).
The hypothalamic-pituitary-adrenal axis (HPA or HTPA axis), also known as the limbic-hypothalamic-pituitary-adrenal axis (LHPA axis) and, occasionally, as the hypothalamic-pituitary-adrenal-gonadotropic axis, is a complex set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal (also called "suprarenal") glands (small, conical organs on top of the kidneys).
The interactions among these organs constitute the HPA axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes, including digestion, the immune system, mood and emotions, sexuality and energy storage and expenditure. It is the common mechanism for interactions among glands, hormones, and parts of the midbrain that mediate the general adaptation syndrome (GAS).[1] While steroids are produced only by vertebrates, the physiological role of the HPA axis and corticosteroids in stress response is so fundamental that analogous systems can be found in invertebrates and monocellular organisms as well.

Anatomy
The key elements of the HPA axis are:

• The paraventricular nucleus of the hypothalamus, which contains neuroendocrine neurons that synthesize and secrete vasopressin and corticotropin-releasing hormone (CRH). These two peptidesregulate:
  • The anterior lobe of the pituitary gland. In particular, CRH and vasopressin stimulate the secretion of adrenocorticotropic hormone (ACTH), once known as corticotropin. ACTH in turn acts on:
  • the adrenal cortex, which produces glucocorticoid hormones (mainly cortisol in humans) in response to stimulation by ACTH. Glucocorticoids in turn act back on the hypothalamus and pituitary (to suppress CRH and ACTH production) in a negative feedback cycle.

CRH and vasopressin are released from neurosecretory nerve terminals at the median eminence. CRH is transported to the anterior pituitary through the portal blood vessel system of the hypophyseal stalk and vasopressin is transported by axonal transport to the posterior pituitary. There, CRH and vasopressin act synergistically to stimulate the secretion of stored ACTH from corticotrope cells. ACTH is transported by the blood to the adrenal cortex of the adrenal gland, where it rapidly stimulates biosynthesis of corticosteroids such as cortisol from cholesterol. Cortisol is a major stress hormone and has effects on many tissues in the body, including the brain. In the brain, cortisol acts on two types of receptor - mineralocorticoid receptors and glucocorticoid receptors, and these are expressed by many different types of neurons. One important target of glucocorticoids is the hypothalamus, which is a major controlling centre of the HPA axis.
Vasopressin can be thought of as "water conservation hormone" and is also known as "antidiuretic hormone." It is released when the body is dehydrated and has potent water-conserving effects on the kidney. It is also a potent vasoconstrictor.
Important to the function of the HPA axis are some of the feedback loops:

• Cortisol produced in the adrenal cortex will negatively feedback to inhibit both the hypothalamus and the pituitary gland. This reduces the secretion of CRH and vasopressin, and also directly reduces the cleavage of proopiomelanocortin (POMC) into ACTH and β-endorphins.
• Epinephrine and norepinephrine are produced by the adrenal medulla through sympathetic stimulation and the local effects of cortisol (upregulation enzymes to make E/NE). E/NE will positively feedback to the pituitary and increase the breakdown of POMCs into ACTH and β-endorphins.

Function
Release of CRH from the hypothalamus is influenced by stress, physical activity, illness, by blood levels of cortisol and by the sleep/wake cycle (circadian rhythm). In healthy individuals, cortisol rises rapidly after wakening, reaching a peak within 30–45 minutes. It then gradually falls over the day, rising again in late afternoon. Cortisol levels then fall in late evening, reaching a trough during the middle of the night. An abnormally flattened circadian cortisol cycle has been linked with chronic fatigue syndrome,[2] insomnia[3] and burnout.[4]
Anatomical connections between brain areas such as the amygdala, hippocampus, and hypothalamus facilitate activation of the HPA axis. Sensory information arriving at the lateral aspect of the amygdala is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear. At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis.

Increased production of cortisol mediates alarm reactions to stress, facilitating an adaptive phase of a general adaptation syndrome in which alarm reactions including the immune response are suppressed, allowing the body to attempt countermeasures.

Glucocorticoids have many important functions, including modulation of stress reactions, but in excess they can be damaging. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of glucocorticoids. Deficiencies of the hippocampus may reduce the memory resources available to help a body formulate appropriate reactions to stress.

Stress and disease
The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, posttraumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism.[5] Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function.[6]
Experimental studies have investigated many different types of stress, and their effects on the HPA axis in many different circumstances.[7] Stressors can be of many different types—in experimental studies in rats, a distinction is often made between "social stress" and "physical stress", but both types activate the HPA axis, though via different pathways.[8] Several monoamine neurotransmitters are important in regulating the HPA axis, especially dopamine, serotonin and norepinephrine (noradrenaline). There is evidence that an increase in oxytocin, resulting for instance from positive social interactions, acts to suppress the HPA axis and thereby counteracts stress, promoting positive health effects such as wound healing.[9]

The HPA axis is a feature of mammals and other vertebrates. For example, biologists studying stress in fish showed that social subordination leads to chronic stress, related to reduced aggressive interactions, to lack of control, and to the constant threat imposed by dominant fish. Serotonin (5HT) appeared to be the active neurotransmitter involved in mediating stress responses, and increases in serotonin are related to increased plasma α-MSH levels, which causes skin darkening (a social signal in salmonoid fish), activation of the HPA axis, and inhibition of aggression. Inclusion of the amino acid L-tryptophan, a precursor of 5HT, in the feed of rainbow trout made the trout less aggressive and less responsive to stress.[10] However, the study mentions that plasma cortisol was not affected by dietary L-tryptophan.

Studies on people show that the HPA axis is activated in different ways during chronic stress depending on the type of stressor, the person's response to the stressor and other factors. Stressors that are uncontrollable, threaten physical integrity, or involve trauma tend to have a high, flat diurnal profile of cortisol release (with lower-than-normal levels of cortisol in the morning and higher-than-normal levels in the evening) resulting in a high overall level of daily cortisol release. On the other hand, controllable stressors tend to produce higher-than-normal morning cortisol. Stress hormone release tends to decline gradually after a stressor occurs. In post-traumatic stress disorder there appears to be lower-than-normal cortisol release, and it is thought that a blunted hormonal response to stress may predispose a person to develop PTSD.[11]

https://en.wikipedia.org/wiki/Hypothalamic–pituitary–adrenal_axis

 

http://eoa.umontreal.ca/documents/pdf/publicationsHebertS_soundStressCortisol.pdf
Neuroscience Letters 411 (2007) 138–142

The sound of stress: Blunted cortisol reactivity to psychosocial stress in tinnitus sufferers

Abstract
Clinical observations suggest that tinnitus is modulated by stress. However, there is little empirical data to support the link between stress and tinnitus. In this study, we measured the stress hormone cortisol to examine the reactivity of the hypothalamic-pituitary-adrenal (HPA) axis in tinnitus participants as well as in healthy controls without tinnitus. Eighteen participants with tinnitus and 18 controls without tinnitus were exposed to the Trier Social Stress Task and cortisol sampling and subjective ratings were obtained at regular intervals. Tinnitus participants displayed a blunted
cortisol response to psychosocial stress, in comparison with healthy controls who had a typical cortisol release about 30 min after the beginning of the experiment. The blunted cortisol response displayed by the tinnitus participants suggests that they have an anomaly along the HPA axis. Their cortisol response is similar to that found in other bodily stress-related diseases and thus suggests that tinnitus is related to stress. However, tinnitus intensity might not be modulated by stress in a concurrent manner.

 

HELP... Is there a Greek interpreter or molecular biologist in the house? Whew, will need a second read on this one!

There was an article recently published from Swedish researchers indicating that stressed women were more sensitive to loud noise. Their research helps to support the information you have posted. The original article can be found at the following link:

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052945

Extracted from it is the following, which indicates what your information supports. That a low cortisol response can make especially women more sensitive to noise after a stressful event:

Hormonal Changes after Acute Stress
The stress hormone cortisol (logarithmized) was assessed before and after the acute stress test. There was a significant time effect (two-way ANCOVA: All F = 28.093df = 1, p<0.0001; Men F = 22.040df = 1, p<0.0001; Women F = 10.586df = 1, p = 0.001), i.e. change over time in cortisol levels, for both women and men when adjusting for baseline cortisol levels, age and time of blood sampling. There was no significant time × group effect for the EE (Emotional Exhaustion - added for clarity, not in the original section of article) -groups when taking blood sampling time into account. This demonstrates that the different EE-groups did not change statistically differently over time. The cortisol levels decreased for all women. Additional statistical analyses were undertaken to understand the decrease in cortisol levels found for women. The findings showed that a variety of factors (age, estradiol levels, phase of the menstrual cycle, birth control pills and estrogen intake) confounds the cortisol response to stress in women. In response to acute stress, the cortisol changes in men increased. However, there were tendencies, albeit not statistically significant, showing that those with low and medium EE levels increased in cortisol concentration while those with high EE decreased.

Also included is the following:

Results
The results demonstrate that women with high EE-levels display hyperacusis after an acute stress task. The odds of having hyperacusis were 2.5 (2 kHz, right ear; left ns) and 2.2 (4 kHz, right ear; left ns) times higher among those with high EE compared to those with low levels. All these results are adjusted for age, hearing loss and ear wax.

Conclusion
Women with high levels of emotional exhaustion become more sensitive to sound after an acute stress task. This novel finding highlights the importance of including emotional exhaustion in the diagnosis and treatment of hearing problems.

/End article


My T came on after a series of stressful events. The hammering, which occurred while preparing for my sons birthday party, which is a stressful event for me. I was up late, doing more work than usual, etc. Also, had just finished my final paper to earn my degree after two stressful years of late nights, and long days.

So, I wonder if my doctor can easily measure my level of cortisol? It says this data was gathered through blood samples. Will it be lower now or would it only be lower after the stressful event? Has anyone ever tried the dexamethasone? Is this something I should ask my doctor to prescribe, and see what happens?

Great post as usual, Calin! I think the dedicated, intelligent people on this site will do great things for T! Keep going!

 

I found the following on WedMD related to cortisol at the following link:

http://www.webmd.com/a-to-z-guides/cortisol-14668

The following is an interesting excerpt, which follows many T suffers description of their T patterns of loudness:

"Normally, cortisol levels rise during the early morning hours and are highest about 7 a.m. They drop very low in the evening and during the early phase of sleep."

This follows my pattern of T, quietest in the morning, loudest at the end of the day. Typically loud as I go to sleep and goes quiet during the night. It usually stays quiet until I get up. It starts to get louder as the day progresses. The few times I am awakened at night by my T is usually due to indigestion (stressful), or hot flashes (STRESSFUL). My T ramps up for either of those. This is interesting...

 

Yes it is since my generally follows the same pattern

 

Thanks! Very kind of you!

I am getting more convinced that those of us with little to no hearing loss has had a prolonged stressful life and or had a traumatic experience before the onset of tinnitus.

Like you, my Tinnitus came after high stress: life stresses, changing BP meds a couple of times, and then getting a big scare when suddenly my right eye had brown web floaters clouding my vision. I thought I was loosing my retina. I was in the ER for hours and then went straight to an Ophthalmologist for testing. No retina detachment... just a bad case of floaters. My BP went to 100+ over 90+. Not good! A couple of days later I noticed the tinnitus sounds.

Of the people I know that have tinnitus (didn't know about them until I got tinnitus) are hypertensive or under high stresses constantly, except for one after surgery and another after surgery due to tumor.

Let us know if you talk to your doctor about the dexamethasone.

I had another post up yesterday but was deleted. A summary: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371598/

Based on the information collected here, following hypothetical models could possibly explain the causative connection of stress and tinnitus:

• First, stress may potentially activate the local HPA axis in the inner ear. The consequences of local overdrive in the HPA system in cochlea are so far unknown.
• Second, stress-activated HPA corticosterone release may affect mineralcorticoid receptor function in cochlea and possibly influence the concentration of potassium secreted by stria vascularis, resulting in tinnitus.
• Third, stress-induced activation of HPA axis and corticosteroid release could provoke pre- or post-synaptic neuronal plasticity of the auditory system (Figure ​(Figure55).

 

Interesting stuff! Just a warning about the Dexamethasone though, I have bottles of it laying around but have not touched it - it was used for my fathers cancer (used with his chemo to reduce inflammation, etc) and remember multiple specialists mentioning that prolonged use is not an option to due liver toxicity or something along those lines. So unless there are proven long term benefits to using it, I would probably stay away from it.

 

Yes yonkapin. Thank you for bringing that to our attention. I have the wiki information above on this drug. I also saw while researching the web that it is used for chemo side effects.

The above study was done with low dose (.5 mg) dexamethasone.

And on the link the forum poster indicates that her doctor was hesitant about giving her more to take. She had good results with both drugs.

 

This is very fascinating. Thanks for posting this research article!

 

Thanks for the additional information. I will research and see what I can find out. I wonder if anyone of the forums has ever taken any of these for their T? I wonder why a one physician would recommend the drugs, but none of the others seem to know anything about them? Ah, the medical world...

 

I just visited my sister (terminal lung cancer) and the nurse came in and gave her dexamethasone. Weird! The nurse couldn't pronounce it or even say what she was giving it to her for. I told her! They are giving her 1.0 DEX for mucus in her lungs... breaks it up. I joked and said that - " and if you have tinnitus, it can reduce it!" She knows I have it. She laughed.

 

Glad you found it interesting.

Your pattern seems to be a match. I notice when I eat corn syrup or See's Candy (the best!) my tinnitus increases in volume. It may increase at times during the afternoon, but doesn't decrease noticeably until after I take a shower. My shower head has that germanium in it. It creates negative ions. Weird, huh?!

 

Hi Karen.

My sister has had it with chemo. She also had radiation before that. Being only 90 pounds, she looks frail and IS frail of course.

I have gotten her turned around to actually want to live, so now I have to give her more hope. She was despondent before the diagnosis due to the economy (unemployment ran out) and of course she is in a nursing home with no hope of job if she lives, no money, no means of income other than SS, no husband...etc.

I have thrown every little trick in the book that I can find to keep her comfortable (too much pain), healthy, and living longer. With pain and vomiting (chemo) her outlook on wanting to live is an uphill battle for me. She has 4 girls (adults).

My next "hope" is a new alternative treatment. I have researched all alternatives!!!! You know how I am! I had to rule out things that would lower her already low blood pressure, medication contraindications, tolerance, neurotoxicities, etc. I am quite excited about it. It isn't so cheap, but that's what my credit cards are for! haha

Salvestrol. http://www.salvestrol.ca

Alimentation naturelle : Hippocrate avait raison

I am ordering the "supplements" tomorrow. I have given her e-cigs to get her off cigarettes as the carbon monoxide in cigarette smoke inhibits the enzyme in cancer cells that is needed to be active so the salvestrol can destroy the enzyme CYP1B1 in the cancer cell. If her cancer was anywhere other than in her lungs then she could continue to smoke and the salvestrol would do it's thing. I got this straight from Prof. Potter. So, lets say she continues to sneak a cig or two, the salvestrol would hunt down cancer cells that could have spread, but she would still have tumors in her lungs. Switching to e-cigs eliminates the carbon monoxide, but gives her the nicotine fix she needs.

I have read the case studies, and they are good. She has a 90% chance of recovery based on the founder/professor Gerry Potter's own words. Since her lung cancer is inoperable, this is her last chance. The recovery from I have read takes months to a year or two, but that is longer than what she had with the diagnosis. And if she doesn't get the benefit of the new treatment, then I would feel that I have done everything I could to help her.

I just may start using this supplement myself as a preventative.

 

You are so kind Karen. Thanks!

 

haha... no. I will call the company that makes the supplement http://www.salvestrol.ca/index.asp on Monday and have a chat though.

I got the information from a cancer forum where I found him addressing questions about salvestrol. Really impressive.
http://www.cancercompass.com/message-board/message/all,50825,0.htm and then I just went to his replies under his name. http://www.cancercompass.com/profile/gerrypotter (click messages on the left under his picture.)

I don't want to digress much here under this thread - could get in a heap of trouble! I will start a thread under the Chat section here if anyone wants more information. We can chat more there if you are interested.

 

Hi Karen!

I can now say that I did talk directly to the Professor. He returned an email. Nice man in my view!

 

2014winner here. My otolaryngologist has been giving me intratympanic injections of Dexamethasone every three or four months; for over 1 year. It may be effective somewhat in that the tinnitus could probably be even worse, guys.
Since the Dexamethasone is administered directly into the tympanic membrae, there should not be macro systemic latent side effects. Like, 20 years from now opthamaological problems. So we will see how it goes.
I would be intereseted in hearing from anyone else who has tried this for tinnitus. Thank you. !!

 

Hi. Sounds pretty drastic. I have not had any such treatment and am seeking feedback too. So how's it been for you. I hope your t has dininished. Have there been any hearing changes over the course of the treatment? .....and was this recommended by your ent. I can't seem to find any one to lend an ear to my T let alone suggest treatment.

Best of luck though. And welldone to have tried

Cheers

 

Hi Dhaval. Perhaps if I did not have the intratympanic injection the t would be greater than it is now.... Ha.
Yes, my ent did suggest it and therein I guess, recommended it. His name is Dr. Stephen Parnes (United States) : you can look him up on the net. You asked about hearing changes: sometimes my hearing is fairly okay, and there are times when the t blocks some of my hearing. Best of luck to you, too.

 

Hi. After how much time of onset did you start your treatment and how did you get your t. Mine seems to be a combination of several things drugs. Stress. Noise. So I m not quite sure what's going to help. So am just trying out different things in a hope that something works.

Any side effects, pain, etc. Also was any hearing loss detected and after Tht have you Doberman an audiogram again?

Best of luck.

 

Hey thanks for all the great info in here. I didn't know there were so many natural ways to control your cortisol, I've actually been taking this supplement a lot of athletes at my gym take and it's worked really well for me so far. I feel like my stress levels and overall health has increased since taking it. Here is a link if anybody wants to check it out. http://www.amazon.com/Neon-Sport-Intercept-Aromatase-Inhibitor/dp/B00VAPRET4