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After initial treatment,
I feel very well with supplement to counteract inflammation. For the first time, I’ve stopped my hydrocortisone without side effect.
I trained at the gym, and for two month I can do many think without problems. But in just one day my adrenal crash.
I have many symptoms of adrenal burnout : exhaustion, no energy at all, brain fog, depression, go to bed all the day, low blood pressure 10/7, muscle pain, bloated gut….
After two days with this symptoms I begin to take again HC, I feel better now.
My questions.
Why adrenal crash after two month after stopping HC ? Why I don’t have this crash the few days after stopping HC? Do the tretment for inflammation “mask” the real problems for one time ? It’s like the theory of Dr Derry “low adrenal reserve” and not adrenal fatigue.
What treatment is best for “low adrenal reserve” ?
It’s interesting to known that low adrenal reserve is a reality
Low cortisol production in chronic stress. The connection stress-somatic disease is a challenge for future research]
Rosmond R – Lakartidningen – 20-Sep-2000; 97(38): 4120-4Abstract:
There is a general assumption that distressing events or situations (stress) evoke the hypothalamic-pituitary-adrenal (HPA) system, with a resulting increase in cortisol secretion. However, our increasing understanding of the complexity of the HPA axis physiology raises questions as to the validity of this model. An increasing number of studies imply that after long-term exposure to stress, the HPA axis will eventually become dishabituated, resulting in a disruption of central regulatory systems and a net decrease of cortisol output. These findings have major implications for the interpretation of stress-induced neuroendocrine response patterns.Title: The effect of thyrotoxicosis on adrenocortical reserve.
Author: Tsatsoulis, A : Johnson, E O : Kalogera, C H : Seferiadis, K : Tsolas, O
Citation: Eur-J-Endocrinol. 2000 Mar; 142(3): 231-5
Abstract: OBJECTIVE: Variations in thyroid function are known to be associated with changes in adrenocortical activity. Previous studies in animals have suggested that long-standing hyperthyroidism may be associated with diminished adrenal functional reserve despite a continuing hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. In humans, there has been no direct assessment of adrenal secretory reserve in clinical thyrotoxicosis. This study aimed to assess adrenocortical reserve in response to low-dose ACTH, following dexamethasone suppression, in patients with severe thyrotoxicosis. DESIGN AND METHODS: Ten patients (four men and six women, 30-45 years) with severe long-standing thyrotoxicosis due to Graves’ disease (n=6) or toxic nodular goitre (n=4) were studied at diagnosis and again when in a stable euthyroid state following drug therapy for 8-12 months. All patients underwent ACTH stimulation tests at 0800h with ACTH(1-24) (Cortrosyn; 0.1microg/kg body weight, i.v.) following overnight suppression of the HPA axis with dexamethasone (1mg per os at 2300h). Serum cortisol was assayed at -15, 0, 15, 30, 60 and 90min after the administration of ACTH. RESULTS: The mean (+/-s.d.) peak and delta cortisol responses to ACTH (634.5+/-164nmol/l and 618+/- 196nmol/l respectively), as well as the net area under the response curve (36769+/-12188nmol/lx min) in the hyperthyroid patients were significantly lower compared with the values when the same patients were euthyroid (911+/-157nmol/l, 905+/-160nmol/l and 57652+/-10128nmol/lxmin respectively; Pless than 0.005). Subnormal peak cortisol responses (less than 500nmol/l) were observed in two severely toxic patients. The findings were independent of the cause of thyrotoxicosis. CONCLUSION: In patients with severe thyrotoxicosis, cortisol secretion in response to low-dose ACTH stimulation, following dexamethasone suppression, is lower in the hyperthyroid than in the euthyroid state. It appears that thyrotoxicosis is associated with subtle impairment of adrenocortical reserve.@Jean 3106 wrote:
After initial treatment,
I feel very well with supplement to counteract inflammation. For the first time, I’ve stopped my hydrocortisone without side effect.
I trained at the gym, and for two month I can do many think without problems. But in just one day my adrenal crash.
I have many symptoms of adrenal burnout : exhaustion, no energy at all, brain fog, depression, go to bed all the day, low blood pressure 10/7, muscle pain, bloated gut….
After two days with this symptoms I begin to take again HC, I feel better now.
My questions.
Why adrenal crash after two month after stopping HC ? Why I don’t have this crash the few days after stopping HC? Do the tretment for inflammation “mask” the real problems for one time ? It’s like the theory of Dr Derry “low adrenal reserve” and not adrenal fatigue.
What treatment is best for “low adrenal reserve” ?
Is it adrenal exhaustion or low adrenal reserve or is it continued inflammatory signaling from the immune system because the cause of inflammatory signaling was not yet addressed or found?
If adrenal function is suppressed – by one or more of several problems – then yes, adrenal reserve is reduced. But that doesn’t mean that the adrenal glands have something structurally wrong as in Addison’s Disease. Rather, other factors are changing signaling regulation of the adrenal glands. The treatment is to find those other problems and address them.
Gut problems, for example, may indicate that an inflammatory process is still present.
Adding hydrocortisone helps reduce inflammatory signaling. This is why some people improve on treatment with hydrocortisone. But it does not address the primary issue. It is a bandage that can help. But again, it doesn’t address the primary problem.
Did you, for example, start an irritable bowel syndrome treatment to address the gut related inflammatory process?
@DrMariano 3124 wrote:
Is it adrenal exhaustion or low adrenal reserve or is it continued inflammatory signaling from the immune system because the cause of inflammatory signaling was not yet addressed or found?
If adrenal function is suppressed – by one or more of several problems – then yes, adrenal reserve is reduced. But that doesn’t mean that the adrenal glands have something structurally wrong as in Addison’s Disease. Rather, other factors are changing signaling regulation of the adrenal glands. The treatment is to find those other problems and address them.
Gut problems, for example, may indicate that an inflammatory process is still present.
Adding hydrocortisone helps reduce inflammatory signaling. This is why some people improve on treatment with hydrocortisone. But it does not address the primary issue. It is a bandage that can help. But again, it doesn’t address the primary problem.
Did you, for example, start an irritable bowel syndrome treatment to address the gut related inflammatory process?
After stopping HC with success for two month, with plenty of energy, in one day I felt exhausted and depressed. After taking HC again everythink comeback in two day.
I thought what the problem : high intensity training, nervous stimulation from STIMULANT (coffee…) or because few days ago I’ve stopped vit D and I’ve reduced my fish oil after two month of treatment. I’ve stopped Vit D because the blood is high normal range : 99.
For the gut I’ve took some origan essentiel oil with butyric acid and PB8.
I begin now sarachomices boulardii.I don’t take antibiotics anymore because the” herxeimer’s effect” or “die off” from antibiotic use is so strong and make me so sick with big headache.
I feel well again and I’m happy for that. But my question to known is HC necessary for life because I felt very well without for two months ?
I understand that adrenal fatigue is a myth but there are a HPPAA disregulation. I’ve reading a good post that explain two differents state. I don’t known if the two states need HC ?
The upshot is that I don’t think poor stress reactivity is necessarily associated with low cortisol. For example, a few hypothetical phenotypes:
Low baseline cortisol, normal reactivity: Performance under stress (including tasks as diverse as running, working on a deadline, and engaging in high-risk activity) is initially impaired, but rapidly normalizes. Performance may even exceed that of normal individuals under a similar stressor, due to heightened MR/GR sensitivity. Recovery from stress, however, is prolonged, and characterized by depression, inflammation, and fatigue. Sleep deprivation often paradoxically improves symptoms by simulating a stress-state, whereas excessive sleep may worsen symptoms. Performance (and mood) under unstressed conditions (e.g. vacation) is characterized by fatigue and anhedonia.
Normal baseline cortisol, low reactivity: Under unstressed conditions (e.g. vacation, again, or simply relaxing at home), performance and mood are normal, with few inflammatory sequelae and at most infrequent anhedonia. Performance under stress (including tasks discussed above) is initially acceptable, but quickly fails to meet the demands of the stressor. This leads to feelings of being overwhelmed, fatigued, and non-functional during the stressor, but these symptoms at least partially abate when the stressor is removed. Symptoms are worse with sleep deprivation, but better with excessive sleep.
Low cortisol, low reactivity: You’re fucked. Combine the negative aspects of the above two.
“Adrenal fatigue” is not a myth. It is a mislabel or inappropriate term for a condition where the adrenal glands are dysregulated due to non-adrenal factors.
These other problems include mental illness, infection, autoimmune disease, nutritional problems, other endocrine problems, other nervous system problems, other metabolic problems, etc.). Rather than call the problem “adrenal fatigue”, it should be called these other problems instead. If these problems are not yet identified, then the condition should be called “adrenal dysregulation” or “hypothalamic-pituitary-adrenal axis dysregulation” or “non-adrenal illness affecting adrenal function”. This assumes, of course, that one does not have a primary adrenal disease, itself, i.e. Addison’s Disease.
What I try to point out is that it is important to try to identify and address those underlying problems. If one can do so successfully, then often the use of hydrocortisone will not be needed or at least will be temporary.
And an important reason to try to identify and address these other problems is that too often, in my experience, when these other problems are not directly addressed, hydrocortisone does not work well. For example, in severe mental illness, despite severe adrenal dysregulation, hydrocortisone may not work well at all despite having very low cortisol levels.
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That is not to say that hydrocortisone does not work well all the time. It helps many patients. Again, however, it is important to identify and address the underlying problems.
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If the underlying problems cannot be fully addressed or identified, and if hydrocortisone is effective in helping a person function, then a patient may have to use hydrocortisone indefinitely.
For example, if a person has a chronic viral infection that cannot be adequately controlled with medications, causing chronic activation of the immune system, which then causes multiple other health problems including adrenal dysregulation. Then hydrocortisone, if effective, may need to be used indefinitely or until in the future some effective control of the viral infection can be found.
Another example, if a person has attention deficit/hyperactivity disorder and has to use a high dose of a stimulant, often, the stimulant itself can cause significant stress (because it increases norepinephrine signaling, the primary signal for stress). This can lead to adrenal dysregulation. A common sign of this is an increase in irritability and aggressive behavior or insomnia. In such a person, the chronic use of hydrocortisone may be needed to help compensate for the chronic stress of stimulant treatment.
Another example, if a person has chronic, severe, and in escapable life stress (e.g. chronic poverty and unemployment with inadequate social support, having 5 or more children with inadequate social support) which leads to a chronic stress reaction with adrenal dysregulation, and if hydrocortisone is effective in improving function, then the chronic use of hydrocortisone may be necessary. Generally, in such cases, subphysiologic replacement doses are used.
In many illnesses (such as asthma, rheumatoid arthritis, etc., chronic nasal allergies) the chronic use of a corticosteroid (i.e. artificial long-half-life versions of hydrocortisone such as Fluticasone in Advair) is already done. In these conditions, the corticosteroid augmentation done since one’s adrenal output of hydrocortisone is insufficient to control the illness.
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Some patients turn out to have a primary adrenal illness. Some patients may have adrenal insufficiency of various severities. In these cases, chronic hydrocortisone use is indicated. Perhaps the hypothetical conditions you cite may be examples of this.
Thank you, I’ll keep preciously this post that summarizes well the complexity of the adrenal dysregulation
For example, if a person has a chronic viral infection that cannot be adequately controlled with medications, causing chronic activation of the immune system, which then causes multiple other health problems including adrenal dysregulation. Then hydrocortisone, if effective, may need to be used indefinitely or until in the future some effective control of the viral infection can be found.
like lyme disease, in later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to treat, in this stage antibiotics is ineffective. The illness producing effect of microbial exo- and endotoxins and put the body in inflammatory state
Most of these are neurotoxins to block the T3 receptor on the cell wall, etc. Decreased hormonal output of the gonads and adrenals is a commonly observed neurotoxin mediated problem in Lyme patients. I think that Hydrocortisone is may need to be used indefinitely.Another example, if a person has attention deficit/hyperactivity disorder and has to use a high dose of a stimulant, often, the stimulant itself can cause significant stress (because it increases norepinephrine signaling, the primary signal for stress). This can lead to adrenal dysregulation. A common sign of this is an increase in irritability and aggressive behavior or insomnia. In such a person, the chronic use of hydrocortisone may be needed to help compensate for the chronic stress of stimulant treatment.
Increases norepinephrine signaling by stimulant can be decrease by HC, but in ADD state do you think that a small dose of SSRI are another option ?
Some patients turn out to have a primary adrenal illness. Some patients may have adrenal insufficiency of various severities. In these cases, chronic hydrocortisone use is indicated. Perhaps the hypothetical conditions you cite may be examples of this.
In fact, anyway I think for “adrenal dysregulation” taking indefinitely. the subphysiologic replacement doses of HC are free for side effect.
Best regards and thank you again for this great post@Jean 3133 wrote:
Thank you, I’ll keep preciously this post that summarizes well the complexity of the adrenal dysregulation
Like lyme disease, in later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to treat, in this stage antibiotics is ineffective. The illness producing effect of microbial exo- and endotoxins and put the body in inflammatory state
Most of these are neurotoxins to block the T3 receptor on the cell wall, etc. Decreased hormonal output of the gonads and adrenals is a commonly observed neurotoxin mediated problem in Lyme patients. I think that Hydrocortisone is may need to be used indefinitely.Increases norepinephrine signaling by stimulant can be decrease by HC, but in ADD state do you think that a small dose of SSRI are another option ?
Yes, chronic Lyme disease is an example of an illness where if adrenal dysregulation occurs, hydrocortisone may need to be taken indefinitely – if it has efficacy – that is a big if.
Generally, I have to consider various options for reducing inflammatory signaling from the brain’s microglia, astrocytes and oligodendrocytes which can cause severe disruption in brain function.
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Serotonin reuptake inhibitors can be considered to help control excessive norepinephrine signaling. However, one has to be judicious about dosing.
Serotonin reuptake inhibitors both increase serotonin and decrease dopamine signaling in a dose dependent manner. Thus, too high a dose can contribute to impaired attention. If dopamine signaling is impaired due to nutritional deficiencies or a predisposition to Parkinson’s disease, then an excessive increase in serotonin signaling can lead to restless legs, anxiety, irritability, etc. This is because dopamine is also a control signal on norepinephrine. At a certain dose of a serotonin reuptake inhibitor, the balance of the signaling changes involves a low dopamine signaling state, a high norepinephrine state, and lower serotonin signaling. This can not only lead o agitation but to suicide attempts.
Thus, in attention deficit/hyperactivity disorder, if an SSRI is considered, I would first use only low doses and check for other underlying factors that can cause adverse effects as the dose increases.
Optimal serotonin signaling requires a balance – not too high, not too low.
Generally, I have to consider various options for reducing inflammatory signaling from the brain’s microglia, astrocytes and oligodendrocytes which can cause severe disruption in brain function.
“Sustained treatment with NSAIDs lowers the risk of AD by 55%, delays disease onset, attenuates symptomatic severity and slows the loss of cognitive abilities. The main cellular target for NSAIDs is thought to be microglia. This is supported by the fact that in patients taking NSAIDs the number of activated microglia is decreased by 65%.
Glucocorticosteroids are anti-inflammatory steroids that inhibit both central and peripheral cytokine synthesis and action.
Wood, Paul (2003). Neuroinflammation: Mechanisms and Management. Humana Press.I don’t known if exogenous HC at physiologic level help to control brain microglia inflammation ?
I don’t know if there are alternative from NSAIDs, but I remember reading that curcuma is far superior with time.
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