Sympathoadrenal system

The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism's physiological response to outside stimuli.^[1] When the body receives sensory information, the sympathetic nervous system sends a signal to preganglionic nerve fibers, which activate the adrenal medulla through acetylcholine. Once activated, norepinephrine and epinephrine are released directly into the blood by adrenomedullary cells where they act as the bodily mechanism for "fight-or-flight" responses. Because of this, the sympathoadrenal system plays a large role in maintaining glucose levels, sodium levels, blood pressure, and various other metabolic pathways that couple with bodily responses to the environment.^[1] During numerous diseased states, such as hypoglycemia or even stress, the body's metabolic processes are skewed. The sympathoadrenal system works to return the body to homeostasis through the activation or inactivation of the adrenal gland. However, more severe disorders of the sympathoadrenal system such as pheochromocytoma (a tumor on the adrenal medulla) can affect the body's ability to maintain a homeostatic state. In these cases, curative agents such as adrenergic agonists and antagonists are used to modify epinephrine and norepinephrine levels released by the adrenal medulla.^[2]

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This is Dr. Lam. Adrenal Fatigue has four stages of development and stage 3 is called adrenal exhaustion. Today we’re going to spend our time to discuss this very, very important stage because this is the stage where most of the symptoms become very perplexed and very difficult to resolve from a conventional medicine perspective. This full article, “Adrenal Exhaustion,” is available free at my public educational website called www.DrLam.com. You can read that at your leisure, you can follow along. I’ll try to point out some of the key points here for you to understand and help you to study as you go. Let us review first the four stages of Adrenal Fatigue relatively quick. Stage 1 is called, “Alarm Reaction,” and this is where you have the fight or flight response. People who are under stress can have an alarm reaction and not even know it. There are no physical signs to speak of, sometimes you may be tired and then you get better and don’t even know it after a nap. Usually recover is relatively fast. If that fails, the body goes into stage 2, which is, “Resistance Response.” In this case, the body starts to have some anxiety, the person becomes irritable, insomnia may be common and infections become more recurrent and PMS and menstrual irregularity starts to come in. They don’t come in all at the same time and sometimes you can have one symptom more than the other, so it’s kind of irregular, but they do show up if you pay attention. Now if the body stress are not being dealt with and this Adrenal Fatigue get worse, then you go into stage 3, which is what we call, “Exhaustion.” Within exhaustion, this is the time that the adrenals are no longer able to keep up with the increasing demands of the hormones and it basically starts to fall apart. What is different from this stage, as compared to the previous stage is that the symptoms become so severe that oftentimes it’s almost impossible to function regularly and a tremendous amount of rest is necessary. If this fails and Adrenal Fatigue progresses to stage 4, that is when failure occurs and that could be a medical emergency because the body has basically given up and is really in a survival mode. Unfortunately, most conventional doctors are not well trained in Adrenal Fatigue to begin with. The most common complaints to a doctor’s office is fatigue, sluggishness, insomnia, and they were brushed aside. When Adrenal Fatigue is not attended to well, patients are often sent home to self-navigate and they try their best, but to no avail and self-navigation programs normally fail and the adrenals get worse and worse with time. Now, adrenal exhaustion, as we talked about, is stage 3 of Adrenal Fatigue and this is where we’re going to concentrate on in this paper. Within this stage of Adrenal Fatigue, there are actually four phases that you can divide into: Single system dysfunction, then it moves on, if it’s a little bit more serious to multiple endocrine axis imbalances or dysfunction, and the class example of that OAT axis imbalance, which is ovarian adrenal thyroid axis imbalance, and on my paper we’ll address that in much more detail. This is oftentimes what brings a lot of the patients to their knees because they just simply cannot figure out what is going on and the bodies keep getting worse. If that is allowed to continue, and then the body gets into a little more serious state, where it really enters a critical point of what we call disequilibrium, which is phase 3. This is the time when the hormones are really so deranged that the emergency system of the body kicks in and you have a lot of paradoxical reactions with mood swings, blood sugar level that is irregular, hypoglycemia, low blood pressure, posterior hypertension, night sweats, severe anxiety, for example. People normally at this stage have limited ability to even do their daily chores, it’s limited to 12 hours or less. If this phase is surprised and phase 3 comes into place, phase 3 is when you really have a more severe situation where the adrenal glands are in near failure stage. That is when the bodies hormones are so low that it really has a difficult time to even maintain normal function. My paper will then go through with you each of the phases in great detail and what to expect out of each phase, the symptoms, the clinical presentations, and what usually happens in each one of these phases, I will not go through it here in great detail because it involves a lot of multiple organ systems that is dysfunctioning at the same time as you proceed forward. I do want to spend a little bit of time to discuss the phase 3C, which is when you have a disequilibrium state, because this is a state that is so confusing and the symptoms are so convoluted, that most people have a hard time understanding. Now we talked about adrenal exhaustion being stage 3 of Adrenal Fatigue and stage 3C is the disequilibrium phase and this is where the body’s thermostat, so to say, internally is broken. The body’s ability to regulate itself is compromised. The body doesn’t like that and in a situation like this, the body activates the autonomic nervous system as an emergency backup plan to try to regulate the body temperature, to regulate the blood sugar, to regulate the salt craving, to regulate the insulin level, for example. But unfortunately the back-up system, or the emergency system, is very crude. Because of its crudeness, it is not very fine-tuned and as a result the ride that the body has to go through is quite bumpy. Adrenalin is being released in great amount. This is what we call the activation of the sympathoadrenal system. Now, the consequences of this is that the body then becomes flooded in a sea of adrenaline. What happens is that adrenaline will cause a set of reactions that is tremendously difficult to resolve. It is called the reactive sympathoadrenal response. The result of this response includes things like fragile blood pressure, spacy-ness, tachycardia, irregular heart rate, an inability to stand for a long time, temperature intolerance, body and fluid imbalances, dizziness, a feeling of impending doom, for example. So these are very, very significant events that can bring many to the emergency room only to be told after extensive tests that they are fine. They were set home and then it repeats itself. So the clinical picture just keeps getting worse and worse. Now if this is not resolved and it goes to the phase D, where the Adrenal Fatigue comes to the point where it’s near failure and that oftentimes requires strong medication, as well as admission to the hospital. Overall, I want you to understand that adrenal exhaustion, as a state of Adrenal Fatigue, can be helped. The biggest problem is that most people don’t understand how the various symptoms are tied in together. The tendency is to treat symptom by symptom and forgetting that there is an underlying root cause that is still existing. When you try to only patch up the symptoms, then invariably when one symptom is resolved, you’re going to trigger another symptom. There’s no end to this. The more symptoms are being addressed instead of the root cause, the more the body becomes weak. This is almost a self-inflicted wound over a period of time, as the body slowly continues to get decompensated and worse and worse. The key to identification, as well as from recovery from adrenal exhaustion is not any laboratory test, because unfortunately most laboratory tests at this point is simply not sensitive enough to pick them up. What you really need to do is number one, to understand this yourself, and my article will help you to do that. Number two, is to educate your provider if he or she is not attune yet to this state of Adrenal Fatigue or Adrenal Fatigue in itself. Until your provider understands what is going on, it’s highly unlikely that he or she will be able to have a program of recovery that’s fitting for you. On the other hand, if your provider really understands this, they can usually spot this right off very quickly. Most people do recover from adrenal exhaustion, if you are given the right program. At the same time, most self-navigation programs fail and only get worse. So my advice to most people is try not to self-navigate if you are at this point of Adrenal Fatigue. Find somebody that really knows what they’re doing and that is the number one step to your recovery. My article will address all these issues. We’ll give you the knowledge, we’ll give you the tools for you to help yourself if you so want to. At the same time, we’ll give you the tools to help your provider so that they can better help you. If you have any questions after you read the article, feel free to write to me, you can do that on my website. The article that I mentioned is on my website, www.DrLam.com. If you have a personal attention necessary, as far as a personalized program for you to overcome this, you can call my office.

Function

The normal function of the sympathoadrenal system is to help the body regulate responses to environmental stimuli. These stimuli travel through the sympathetic nervous system by means of preganglionic nerve fibers that emerge from the thoracic spinal cord.^[3] Electrical impulses carried by the sympathetic nervous system are converted to a chemical response in the adrenal gland. Chromaffin cells contained in the adrenal medulla act as postganglionic nerve fibers that release this chemical response into the blood as a circulating messenger. The sympathoadrenal system can activate and discharge chemical messengers as a single unit to activate an organism's “fight or flight” response. This “sympathoadrenal discharge” causes an increase in heart rate, cardiac output, blood pressure, triglyceride and glucose levels. These sympathoadrenal functions show the combined responses of the central nervous system on a multitude of external stimuli.^{[citation needed]}

Chemical messengers

The two main chemical messengers of the sympathoadrenal system are norepinephrine and epinephrine (also called noradrenaline and adrenaline respectively). These chemicals are created by the adrenal glands after receiving neuronal signals from the sympathetic nervous system. The different physiological effects of these chemicals depend on the particular tissue that it innervates. As part of the sympathoadrenal system, these chemicals act rapidly and dispel quickly as opposed to the longer-lasting effect of hormones.^{[citation needed]}

Stress

In the brain, reception of a signal for a stressor by the hypothalamus leads to an increase in activity of the sympathoadrenal system, essentially within the nerves that send signals to the adrenal glands. This is done through the activation by the corticotropin-releasing factor (CRF), also known as the corticotropin-releasing hormone (CRH).^[4] Increased activity of the adrenal nerves is done through the receptors for the corticotropin-releasing factor within the ganglia within the sympathetic nervous system.^[4] Corticotropin-releasing factors travel to the pituitary gland, where they activate the release of adrenocorticotropic hormone (ACTH). The release of the adrenocorticotropic hormone is determined by the release of the corticotropin-releasing factor as the interruption of the corticotropin-releasing factor causes a weakening of the adrenocorticotropic hormone response.^[4]

Adrenocorticotropic hormones bind to ACTH receptors on the cells within the adrenal medulla and adrenal cortex, causing a signal cascade within the adrenomedullary cell, ultimately releasing catecholamines like epinephrine and norepinephrine.^[5] Concomitantly, adrenocortical cells secrete corticosteroids. These hormones (i.e., catecholamines and corticosteroids) affect a variety of organs like skeletal muscles along with the muscles surrounding certain bodily systems such as the cardiovascular system and respiratory system, causing an increase in force production by the skeletal muscles along with accelerated heart rate and breathing rate. Glucocorticoids also are in effect during times of stress for the sympathoadrenal system, but provide an inhibitory function for the protection of the body from its own immune system. The glucocorticoids work to inhibit reactions produced from the immune system during times of stress that could cause damage within the body.^[4] Glucocorticoids work to inhibit the uptake of catecholamines, like norepinephrine and epinephrine, by the nerves.^[4] The increase in activity of synthesis of norepinephrine and epinephrine within the medulla is done from glucocorticoids through the increase in reaction rate of certain enzymes, such as: tyrosine hydroxylase, aromatic L-amino acid decarboxylase, dopamine-β-hydroxylase, and phenylethanolamine N-methyltransferase.^[4]

Hypertension and obesity

The release of adrenocorticotropic hormone is usually regulated within the sympathoadrenal system as it is tasked with maintenance of homeostasis; however, there are certain cases in which the levels of adrenocorticotropic hormones may be in excess, causing hypertension, or even Cushing's syndrome. Hypertension, or high blood pressure, has a multitude of possible causes, one of which being the elevated levels of ACTH.^[6] Hypertension also causes an increase in catecholamine release during experiments of stress-induced situations.^[7] While hypertension and Cushing's syndrome are not correlational, roughly 80% of individuals diagnosed with Cushing's syndrome also have hypertension.^[6] Both Cushing's syndrome, termed Cushing's disease in this case, and hypertension involve the excess production and release of adrenocorticotropic hormone.^[6] Hypertension can also be caused by the overproduction of molecules released from the sympathoadrenal system besides ACTH, such as mineralocorticoids and glucocorticoids.^[8] Overproduction of these molecules causes an increase in the production and release of the catecholamines, leading the cardiovascular system to become elevated in the systolic blood pressure and the diastolic blood pressure, along with the increase in the heart rate of the individual.^[8]

Weight gain can be accomplished through the ingestion of and storage of carbohydrates and fat. Under normal conditions, adrenal hormone receptors, type I and type II, mediate the storage of carbohydrates and fats during eating.^[9] In some cases, obesity in individuals is due to the overproduction of corticoids leads to the over-activation of receptor type I and type II, causing the deposition of fat and the storage of carbohydrates, respectively; furthermore, activation of either receptor causes the individual to sustain eating.^[9]

Exercise and Metabolism

During exercise, the body undergoes a stress response in which more oxygen and energy is needed for physical activity. The stress induced during exercise results in an increase in the hormones, epinephrine and norepinephrine, which are known for the body's "fight or flight" response. As a result, the body's heart rate increases allowing for more blood to pump through the body system and carry oxygen needed for breathing to enhance cardiorespiratory function. In exercise trained individuals, levels of epinephrine and norepinephrine are lower compared to those who do not actively train as much. This is due to untrained individuals undergoing greater amounts of stress on their body and the greater need for oxygen and energy to perform rigorous activities. Trained individuals become accustomed to utilizing less oxygen such as when performing anaerobic exercises so that their body will eventually feel the stress on their body over a longer period of time. Along with an increase in epinephrine and norepinephrine, increased sympathoadrenal activity results in an increase in glycogen hydrolysis which ultimately increases glucose release needed for energy.^[10]

Metabolism, or the processes within living cells or organisms to maintain life, is affected by the sympathoadrenal system, especially glucose and fat metabolism. Glucose, a necessary source of energy for cells, can undergo an increase in production due to elevated secretion of epinephrine in the body. The mechanism lies in epinephrine being secreted by the adrenal medulla and activating glycogenolysis (the breakdown of glycogen into glucose, or promoting gluconeogenesis (glucose formation). While epinephrine has a greater effect in glucose production, norepinephrine can also increase glucose levels but at high concentrations. It has even been found that norepinephrine may play a role in enhancing the uptake of glucose in skeletal muscle and adipose tissues. As for fat metabolism, the catecholamines (epinephrine and norepinephrine) help stimulate lipolysis (the breakdown of fat) resulting in an increase in energy and a decrease in fat.^[11] This explains the need for exercise to help increase the body's metabolism.^{[citation needed]}

Diseases

Hypoglycemia

Hypoglycemia, or low blood glucose, causes cardiovascular physiological effects as a result of the sympathoadrenal system. These physiological changes include an increased heart rate, increased heart contractility, and decreased peripheral arterial resistance. Together, the effects increase peripheral blood pressure, but decrease central blood pressure. This can have larger effects on those with diabetes. Hypoglycemia may cause greater arterial wall stiffness and less elasticity, which in turn decreases blood pressure and increases the heart's workload.^[12] Symptoms of hypoglycemia related to the symapthoadrenal system include anxiety, tremors, irregular heartbeat, sweating, hunger, and paresthesia. Hypothermia and neurological deficits can also occur. Permanent brain damage is uncommon but have been seen in some who suffer from hypoglycemia. The activation of the system is assisted by norepinephrine, acetylcholine, and epinephrine. Hypoglycemia unawareness can occur because the symapthoadrenal system response is reduced, in turn, the symptoms are reduced. Since the symptoms go unnoticed, this may lead to a dangerous cycle of hypoglycemia and an increased risk of severe hypoglycemia, which can have serious consequences.^[13]

Insulin is essential in triggering the sympathoadrenal system (the release of norepinephrine and epinephrine) to respond to hypoglycemia, which then raises glucagon levels. The insulin present in the brain acts on the central nervous system by crossing the blood-brain barrier and affecting the sympathetic nervous system. Thereby, helping to initiate a response to hypoglycemia through the sympathoadrenal system.^[14] Individuals with hypoglycemia should self-monitor their blood glucose level and can take glucose in the forms of tablets or foods high in glucose. Parenteral therapy may be necessary for severe hypoglycemia.^[13] Hypoglycemia-associated autonomic failure (HAAF) can occur if left untreated. The sympathoadrenal system activity is significantly reduced because the changed glycemic threshold allows for lower glucose concentrations. Glucose cannot effectively regulate itself, decreasing epinephrine responses.^[15]

Pheochromocytoma

Pheochromocytoma are rare tumors that secrete catecholamines and affect the sympathoadrenal system. They are typically found inside the adrenal medulla, but can also be present right outside the adrenal medulla in tissue. Symptoms include headaches, sweating, palpitations, hypertension, hypoglycemia, anxiety, weight loss, fever, nausea, and cardiovascular complications. Pheochromocytoma can be treated through blocking the effects of the secreted catecholamines. Ideally, removal of the tumor is the preferred treatment and should be done in a timely manner for the best prognosis. On average, there is a delay of three years between initial symptoms and diagnosis because the tumors are hard to find. Diagnosis is also difficult because the symptoms are highly variable and very common in other diseases. If pheochromocytoma remains untreated, it may lead to fatal consequences especially to the cardiovascular system.^[16]

References

^ ^a ^b Christensen, N.J. (1991-06-01). "The biochemical assessment of sympathoadrenal activity in man". Clinical Autonomic Research. 1 (2): 167–72. doi:10.1007/bf01826215. PMID 1822765. S2CID 41312221.
^ Goldstein, David S. (2010-11-01). "Adrenal responses to stress". Cellular and Molecular Neurobiology. 30 (8): 1433–1440. doi:10.1007/s10571-010-9606-9. ISSN 1573-6830. PMC 3056281. PMID 21061156.
^ Sapru, Hreday N. (2007). Essential Neuroscience. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-9121-2.
^ ^a ^b ^c ^d ^e ^f Chrousos, George (1995). Stress: Basic Mechanisms and Clinical Implications. New York, NY: New York Academy of Sciences. pp. Vol. 771. 130–135.
^ Hinson, Joy; Raven, Peter; Chew, Shern (2010-01-01), Hinson, Joy; Raven, Peter; Chew, Shern (eds.), "The Adrenal Glands Part I", The Endocrine System (Second Edition), Churchill Livingstone, pp. 53–60, doi:10.1016/b978-0-7020-3372-8.00005-7, ISBN 978-0-7020-3372-8, retrieved 2024-02-14
^ ^a ^b ^c Kaplan, Norman M (2002). Kaplan's Clinical Hypertension. Philadelphia: Lippincott Williams & Wilkins. p. 480.
^ Garafova, A (15 August 2014). "Cardiovascular and Sympathetic Responses to a Mental Stress Task in Young Patients With Hypertension and/or Obesity" (PDF). Physiological Research: S459–S467. doi:10.33549/physiolres.932931. PMID 25669677. Retrieved 29 March 2016.
^ ^a ^b Schrier, Robert W (1999). Atlas of Diseases of the Kidney. Philadelphia, PA: Blackwell Science. pp. Volume 3.
^ ^a ^b Bray, George A (2004). Handbook of Obesity: Etiology and Pathophysiology. New York, New York: Marcel Dekker.
^ Ball, Derek (2015-02-01). "Metabolic and endocrine response to exercise: sympathoadrenal integration with skeletal muscle". The Journal of Endocrinology. 224 (2): R79–95. doi:10.1530/JOE-14-0408. ISSN 1479-6805. PMID 25431226.
^ Nonogaki, K. (2000-05-01). "New insights into sympathetic regulation of glucose and fat metabolism". Diabetologia. 43 (5): 533–549. doi:10.1007/s001250051341. ISSN 0012-186X. PMID 10855527.
^ Yang, S; Park, K; Zhou, Y (2015). "The Impact of Hypoglycemia on the Cardiovascular System: Physiology and Pathophysiology". Angiology. 67 (9): 802–809. doi:10.1177/0003319715623400. PMID 26685181. S2CID 9348873.
^ ^a ^b Cryer, P.E.; Davis, S.N; Shamoon, H (2003). "Hypoglycemia in Diabetes". Diabetes Care. 26 (6): 1902–1912. doi:10.2337/diacare.26.6.1902. PMID 12766131.
^ Fisher, S.J.; Brüning, J.C.; Lannon, S.; Kahn, C.R. (2005). "Insulin Signaling in the Central Nervous System Is Critical for the Normal Sympathoadrenal Response to Hypoglycemia". Diabetes. 54 (5): 1447–1451. doi:10.2337/diabetes.54.5.1447. PMID 15855332.
^ Cryer, P.E. (2006). "Mechanisms of sympathoadrenal failure and hypoglycemia in diabetes". Journal of Clinical Investigation. 116 (6): 1470–1473. doi:10.1172/JCI28735. PMC 1464914. PMID 16741570.
^ Lender, Lender J.; Eisenhofer, G.; Mannelli, M.; Pacak, K. (2005). "Phaeochromocytoma". The Lancet. 366 (9486): 665–675. doi:10.1016/S0140-6736(05)67139-5. PMID 16112304. S2CID 208788653.

This page was last edited on 9 March 2024, at 13:39

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