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Dear Bruno:
I have long ago stopped using the term “adrenal fatigue” because it is an inaccurate term. It is also an emotionally inflammatory term that can cause the physician risk to their medical license because it clashes with the existing definition of “adrenal insufficiency” and endocrinologists.
I have better names to use for the condition that do not clash with endocrinologists.
One problem is that though the term “adrenal fatigue” does describe the organ and symptom involved, it implies there is something structurally wrong with the organ. Unfortunately, this is inaccurate. There is nothing structurally wrong with the adrenal glands. And if there is something structurally wrong with the adrenal gland, the more accurate term is “adrenal insufficiency”. I say “unfortunately” because “adrenal insufficiency” has criteria determined by endocrinologists. And the criteria for diagnosis are such, that almost all people with “adrenal fatigue” do not meet the criteria for “adrenal insufficiency”.
Jefferies, in his book “The Safe Use of Cortisol”, uses the term “MILD ADRENAL INSUFFICIENCY” to describe conditions that can fall under the term “adrenal fatigue”. Thus his book is cited as supporting literature for the term “adrenal fatigue”. Again, however, the endocrinologist criteria for adrenal insufficiency do not cover most of the people that Jefferies would say have “mild adrenal insufficiency”. Thus, his use of the term can be criticized for also being inaccurate by endocrinologists. And, I have never heard of Jefferies (who died about 3 years ago) ever risking his reputation by using the term “adrenal fatigue”. Since the term “mild adrenal insufficiency” can be much more easily supported – particularly since some of the criteria are arbitrary – one would be in better grounds using such a term to defend one’s use of the treatments. However, one would also be forced to refer such a patient to an endocrinologist, who would then shoot down that diagnosis using his/her criteria. This would leave the patient in a grey area of practice where the diagnosis is not clear since two physicians disagree on the condition.
The second problem with the term “adrenal fatigue” is that it does not describe the actually cause of the condition. Since it does not describe the cause or pathophysiology, then one possible alternative and valid term to use is “ADRENAL FATIGUE SYNDROME”. The addition of “syndrome” would be a more acceptable term since it implies no cause. Then it would be up to the physician to determine the list of symptoms and signs appropriate to the syndrome. And, of course, one criteria would be low output of cortisol – with “low” set at a level that is looser than defined by endocrinologists. This would be similar to the use of the term “SUBCLINICAL” when describing some conditions. Examples of “subclinical” include “subclinical hypothyroidism” as used in psychiatry to describe one contributing cause to bipolar disorder or major depressive disorder.
From my point of view, as a psychiatrist, the term “HYPOTHALAMIC-PITUITARY-ADRENAL AXIS DYSREGULATION” (HPAAD) is the most accurate and supported term in the literature that can be used instead of “adrenal fatigue”.
In various mental illnesses (such as depression, bipolar disorder, anxiety disorders), the psychiatric literature is full of articles describing problems with cortisol production in mental illnesses. These conditions do not fit the criteria for adrenal insufficiency determined by endocrinologists. But clearly something is wrong with the hypothalamic-pituitary-adrenal system. And this problem is one of the central causes of mental illness.
In these conditions, the adrenal glands do change in size – enlargements or shrinkage. The adrenal glands do change in output – excessive or underproducing cortisol output. But there is nothing structurally wrong with the adrenal glands. It is in the regulation of adrenal function that something is wrong. And it is not due to a problem with ACTH production, primarily.
Some psychiatrists would argue that one problem with CRH production. CRH is both a hormone and a neurotransmitter produced by the brain and spinal cord. As a neurotransmitter, psychiatrists, in general, are more comfortable with the idea of using CRH problems as a cause, than if CRH was considered a hormone. However, from my point of view, there are other signals (neurotransmitters, hormones, cytokines, etc.) and metabolic problems that also contribute to HPAD. It is a complex condition.
This brings to mind, however, that the term “adrenal fatigue” is also more accurately described by the term “NON-ADRENAL ILLNESS AFFECTING ADRENAL FUNCTION” (NAIAAF) For example, in posttraumatic stress disorder, I frequently encounter cortisol levels under 5 ug/dL. These patients do not meet the criteria for adrenal insufficiency. But chronically, these patients do not have adequate output of cortisol in response to stress. The low output of cortisol in posttraumatic stress disorder is a repeated and valid finding in the medical literature. Clearly, it is dysregulation of the adrenal glands due to non-adrenal causes. Psychiatrists would point to problems with the sympathetic nervous system and CRH production as contributing factors. There is a psychiatric literature supporting the use of cortisol treatment for NAIAAF in such illnesses as major depressive disorder and posttraumatic stress disorder.
Endocrinologists would be much more comfortable with the term NAIAAF since this condition does not contradict their definition of adrenal insufficiency. Endocrinologists, for example, are comfortable with the term “NON-THYROID ILLNESS AFFECTING THYROID FUNCTION”. These describe patients who have physical signs of hypothyroidism but do not have structural problems with the thyroid gland, where TSH is in the normal range. Again, often, these patients have mental illnesses. For example, in anorexia nervosa, patients often have problems with thyroid function due to metabolic problems. Yet they don’t often meet the criteria for hypothyroidism as defined by endocrinologists.
Note that there is NO ICD-code for Adrenal Fatigue or Hypothalamic-Pituitary-Adrenal Dysregulation or Non-Adrenal Illlness Affecting Adrenal Function or Adrenal Fatigue Syndrome. THE ACTUAL DIAGNOSIS IS THE NON-ADRENAL ILLNESS INVOLVED. One cannot use an ICD code for adrenal illness since the definition of these illnesses are already used and defined by endocrinologists and would risk your reputation and medical license to use unless your patient actually can meet the endocrinologist criteria.
Since Adrenal Fatigue often describes a syndrome involving “fatigue”, alternative medicine doctors often use the diagnosis, 780.79 Lethargy or Asthenia NOS or 780.71 Chronic Fatigue Syndrome. These are appropriate when the specific causes of the illness are unknown.
Adrenal Fatigue often describes a syndrome involving “stress” as a contributing factor to adrenal dysregulation. “Stress” is a mental health term and concept, since there is no stress if there is no brain. In this case, the appropriate psychiatric diagnosis can be used. For example, I may use 296.90 Mood Disorder NOS, 311 Depressive Disorder NOS, 300.00 Anxiety Disorder NOS, or any of the other appropriate psychiatric diagnoses. 300.5 Neurasthenia can also be used. Neurasthenia is a very common condition in response to stress, contributing to general fatigue.
In these conditions, the condition known as “Adrenal Fatigue” is considered a component of the actual illness involved.
In closing and summary, the term “adrenal fatigue” is a syndrome involving inadequate cortisol production in response to stress that does not meet the criteria for adrenal insufficiency. It involves dysregulation of the hypothalamic-pituitary-adrenal axis. From my point of view, contributing factors to dysregulation of the HPA Axis may include psychological/physical/environmental stress, nervous system problems, other endocrine problems, immune system problems, and metabolic-nutritional problems. The appropriate diagnosis is not “adrenal fatigue” but THE IDENTIFIED NON-ADRENAL ILLNESS INVOLVED. “Adrenal fatigue” is a subset of the symptoms and signs of this non-adrenal illness. A more appropriate term for “adrenal fatigue” is HYPOTHALAMIC-PITUITARY-ADRENAL AXIS DYSREGULATION or NON-ADRENAL ILLNESS AFFECTING ADRENAL FUNCTION. The treatment may include supportive treatment – such as treatment with Cortisol, etc. – at the physician’s discretion and/or treatments aimed at the pathophysiology of the non-adrenal illness involved.
Best,
Dr. Mariano.
On Apr 27, 2010, at 2:03 AM, LACROIX BRUNO wrote:
Dear Dr Mariano,
Dr Scally criticizes the term “adrenal fatigue” and all the work of Jefferies in this blog and brings even more confusion.
http://forum.mesomorphosis.com/mens-health-forum/adrenal-fatigue-glucocorticoid-use-134286967.html
This radio show of Dr.John Crisler ausssi will appear in the same directionhttp://superhumanradio.com/super-human-radio-show/460-pregnenolone-the-progenitor-hormone.html
What do you think about this ? More confusion. Thank you.
friendships
BrunoThis is from the thread: http://www.definitivemind.com/forums/showthread.php?t=49
@Shaolin 312 wrote:
What happens if you treat the adrenals with low dose of testosterone monotherapy or try some low dose tamoxifen/clomiphene citrate instead of directly treating with cortisol and other adrenal steroids??
Since you have many times stated that testosterone is a strong norepinephrine signal reducer couldnt low doses of T over a long long period of time restore the HPA axis and adrenal responsiveness??
Do you feel that not only adrenal output is impaired but also the sensitivity of tissues to cortisol effects plays some role too??
When i was at my lowest levels i felt i had way decreased spatial orientation and understanding of 3d environment plus low levels of taste and smell, but never really understood if it was due to cortisol on its own or other hormones played a role in that as well. I supplemented with HC at that time but didnt see any serious improvement, apart from sleep issues which got slightly better.
To summarize some issues a lot (since the actual mechanisms can be mind-bogglingly complex):
Chronic or traumatic stress may lead to hypothalamic-pituitary-adrenal axis dysregulation (the term which I believe is more accurate to use than the term “adrenal fatigue”), HPA dysregulation for short.
HPA dysregulation leads to lower production of adrenal cortex signals/hormones. This includes lower cortisol and/or DHEA, progesterone, pregnenolone, testosterone, estradiol, or aldosterone.
The primary signal for stress is norepinephrine. Norepinephrine is in a positive feedback loop with corticotropin releasing hormone. This positive feedback loop is interrupted by cortisol signaling. To increase norepinephrine, the brain has to also reduce production of some or all of the control signals that suppress norepinephrine signaling. These include reductions in serotonin, dopamine, GABA, etc.
Stress (particularly if it is a perceived threat), may lead to an increase in pro-inflammatory cytokine signaling from the brain and from the immune system (which is directly innervated by neurons of the sympathetic nervous system – the primary norepinephrine-releasing neurons of the nervous system). Stress may also lead to an increase in histamine signaling from brain mast cells. These changes lead to an activation of the immune system. These changes in large excesses may lead to an increase in inflammatory processes. The loss of anti-inflammatory signaling – which includes cortisol, DHEA, progesterone and testosterone – exacerbates these pro-inflammatory changes.
Excessive pro-inflammatory cytokine signaling may trigger automatic defensive programs in the brain. Defensive programs may induce behavioral changes including depressed mood, loss of interest or motivation in activities, loss of enjoyment from activities, social isolation, changes in sleep including the desire to sleep excessively.
There may be a loss of energy from excessive pro-inflammatory cytokine signaling. The actual mechanisms of the loss of energy are not clear. I currently speculate that perhaps there may be impaired brain astrocyte conversion of thyroxine (T4) to triiodothyronine (T3) – which leads to a hypothyroid central nervous system with a euthyroid body (as in Alzheimer’s disease). Perhaps the increase in pro-inflammatory cytokines is one of the signaling problems leading to HPA dysregulation, aside from excessive norepinephrine signaling. However, other regulatory systems may also be involved – such as the opiate signaling systems (which also involve dopamine signaling).
HPA dysregulation, from whatever cause, leads to a loss of energy. The loss of energy production, however, under some circumstances. These circumstances include bipolar disorder and attention deficit/hyperactivity disorder with hyperactivity. In these cases, norepinephrine production is an effective signal for energy.
Nutrition plays a large role in the development of HPA dysregulation. Omega 3 vs. Omega 6 balance helps determine the balance between inflammation and anti-inflammation. Various nutrients (such as the B-vitamins, fat soluble vitamins, magnesium, etc) are cofactors for many of the processes involving signal production. Vitamin A and D are generally anti-inflammatory signals. Vitamin D reduces insulin resistance (which helps the body tolerate low blood sugar from impaired cortisol signaling), increases serotonin and dopamine production. Vitamin A helps regulate the sensitivity to various hormones/signals such as thyroid hormone.
The other endocrine signaling systems such as the reproductive system are in play. Testosterone helps reduce norepinephrine, increases dopamine production. It also suppresses adrenocorticotropin releasing hormone and directly inhibits adrenal cortex activity – this may be significant depending on the sum of signaling interactions and problems a person has. Estrogen acts similarly to a monoamine oxidase inhibitor – thus increasing serotonin, norepinephrine and dopamine (but serotonin primarily). Estrogen in relative excess may be pro-inflammatory, reduces free thyroid hormone. Thyroid hormone signaling loss is compensated by an increase in norepinephrine production with simultaneous activation of adrenal cortex signals. Over time, however, this compensation may fail as HPA dysregulation occurs. Insulin, glucagon, the incretins, etc. also have a role. Insulin, itself, is pro-inflammatory. Growth hormone has a calming effect and is anti-inflammatory. Etc. etc. etc. etc.
The entry point of all these processes is stress. This is represented primarily by norepinephrine signaling. However histamine (from brain mast cells) and pro-inflammatory cytokines (from brain microglia) are also involved in the process. Stress induces responses that are ostensibly designed to improve survival. The problem is that in the modern world, these responses may be dysfunctional instead.
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Given the complexity of the interactions involved, a single intervention may or may not work. Which direction an intervention goes depends on the sum of the changes that occur as a result of that intervention. In psychiatry, the usual answer to a question is “It depends.”
Stress is the entry point. Environmental and behavioral interventions would clearly help with few downsides.
Low dose testosterone may help, particularly in women, by helping to reduce norepinephrine and increasing dopamine signaling, and helping to reduce pro-inflammatory signaling. Low dose testosterone would not help in men since it may do nothing or it would suppress endogenous production of testosterone, leading to lower overall testosterone levels. Men would need replacement doses of testosterone. Testosterone, however, may also worsen adrenal cortex function depending on a person’s susceptibility to this. In men, exogenous testosterone treatment also suppresses testicular thyroid releasing hormone production, leading to a loss of thyroid hormone production, which then leads to an increase in norepinephrine production. This is why in certain men, even if hypogonadal, testosterone treatment is intolerable. The rest of the system has to be optimized before testosterone treatment can be done.
Tamoxifen (I would prefer this to Clomiphene due to the visual changes that can occur with Clomiphene) is a weak estrogen. This blocks the stronger estrogens from being sensed by the brain. This then causes the brain to release more Luteinizing Hormone to stimulate testosterone production, leading to estrogen production. The increase in testosterone would have the effects listed previously. The problem is that Tamoxifen also blocks estrogen. This leads to lower estrogen signaling activity. Estrogen helps control norepinephrine by increasing serotonin and dopamine production. Estrogen is also needed to improve sensitivity to testosterone by increasing testosterone receptor production. Estrogen is also important in generating energy, motivation, drive, competitiveness, sex drive (libido). Estrogen (particularly in women) is important for neuron growth and memory. The loss of estrogen signaling, depending on the balance with testosterone, may lead to negative effects. If testosterone production is driven high enough, then perhaps this would improve things overall. This is particularly true in men. However, in women, this may not occur and destabilization of the system and dysfunction may occur instead. This is why many women do not like treatment with Tamoxifen or Arimidex for breast cancer.
Cortisol treatment alone may or may not work. Cortisol treatment in sub-replacement doses helps because it helps break the norepinephrine-CRH positive feedback loop. Cortisol also acts in the brain to improve concentration/focus by allowing the brain to ignore emotionally distracting memories or information. Cortisol also is the most important anti-inflammatory signal that reduces immune system activity. Cortisol triggers gluconeogenesis – helping improve blood sugar production. etc. etc. Thus it can be a useful component of treatment. However, Cortisol treatment alone also suppresses adrenal cortex activity. Thus, there is also a loss of pregnenolone, progesterone, DHEA, testosterone, estradiol, aldosterone, etc. If this loss is large enough, then the person may be worse off than without treatment. Since the majority of these other signals are calming, help control norepinephrine, are anti-inflammatory signals, a significant loss may cause the opposite intended effect of cortisol treatment. This is where some people become more tired, get “brain fog”, become more anxious, etc. on cortisol monotherapy.
A systematic treatment has to be considered to address the multiple issues that invariably occur, contributing to HPA dysregulation. Single modality treatments may help – particularly in those people who don’t have large problems in the rest of their system. But often, in more severe cases, they don’t. A systemic approach would then be needed. I would count the person who responds to monotherapy as very fortunate.
To eat or not to eat?
Well, possibly enemas should work better?
Suitable donor may be important issue.
Comments please.
Boracay eats and it helps him.
http://musclechatroom.com/forum/showthread.php?t=13652&highlight=boracay&page=10===========================================
http://perfecthealthdiet.com/?p=269
Bacterial Replacement Therapies Work
So if IBS patients are missing 25% of the thousand or so species that should populate the gut, or 250 species, and if common probiotics provide only 8 or so species and not the ones that are missing, how are the missing species to be restored?The answer is simple but icky. Recall that half the dry weight of stool consists of bacteria. A healthy person daily provides a sample of billions of bacteria from every one of the thousand species in his gut. They are in his stool.
So a “fecal transplant” of a healthy person’s stool into the gut of another person will replenish the missing species.
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