Postural orthostatic tachycardia syndrome is a type of dysautonomia (dysfunction in the autonomic nervous system) where a rapid increase in heart rate is seen upon standing. Orthostatic intolerance (an excessively low blood volume returning to the heart upon standing) is the main pillar of POTS, but symptoms such as chest pain, headache, severe fatigue, insomnia, brain fog, constipation, early satiety, palpitations, shortness of breath, cold extremities, and joint or muscle pain can all be part of the patient’s symptom constellation [1].
In hyperadrenergic POTS, norepinephrine is elevated upon standing (which contributes to tachycardia), whereas in neuropathic POTS, pooling of blood in the legs is associated with a kind of nerve damage or neuropathy that causes blood vessel constriction in the lower limbs [2]. Thirdly, many POTS patients exhibit abnormal profiles of renin, angiotensin, and aldosterone, which may account for the common disturbances in blood pressure regulation [3]. Renin is an enzyme produced in the kidneys which converts angiotensinogen (made by the liver) into angiotensin I. Angiotensin I is largely inert and is converted into angiotensin II by angiotensin-converting enzyme, which is located mostly in the lungs (many antihypertensive drugs block this enzyme). Angiotensin II chiefly constricts blood vessels, but it also stimulates the adrenal glands’ release of aldosterone, which increases sodium and water reabsorption (as well as potassium excretion), and this raises blood volume and thus blood pressure. POTS is often diagnosed via a tilt table test, but heart rate and blood pressure measurements in the supine and standing positions can also be taken and compared at 2-, 5-, and 10-minute intervals. Other assessments like the quantitative sudomotor axon reflex test (QSART) or the thermoregulatory sweat test may also be employed. It’s important that about 50% of POTS patients have reported an acute or subacute onset of the condition, often following a viral infection [4]. Accordingly, ganglionic autoantibodies have been looked at as possible drivers (meaning POTS may have an autoimmune component) [5]. Some patients develop POTS after contracting mononucleosis (Epstein-Barr virus usually being the contagion) or after suffering a concussion or some form of brain trauma. Curiously, an association has been found between POTS and joint hypermobility (often in the form of Ehlers-Danlos syndrome) [6]. Other associations have been identified between POTS and mitochondrial disorders, mast cell activation syndrome (hyperresponsive production of leukotrienes and histamine by mast cells), heavy metal toxification, Lyme disease, anemia (too few red blood cells or too little hemoglobin), low iron or vitamin D, vitamin B1 or B12 deficiency, prediabetes, and the Gardasil (HPV) vaccine, among others [7] [8] [9] [10] [11] [12] [13]. I’d like to place special emphasis on the Gardasil vaccine, for thousands of adverse drug reactions (ADRs) have been reported after its administration (thousands in England alone) – some of these reactions include paralysis and death [14] [15] [16] [17]. Many have reported the onset of POTS almost immediately after having received the Gardasil vaccine, and let’s note that POTS is far more common in women than men [18]. POTS is similar to long QT syndrome (LQTS), a condition involving abnormal repolarization of the heart where the interval between the Q and T waves as measured by an ECG is abnormally lengthy, which can trigger arrhythmias, especially during exercise or stress [19]. LQTS can be responsible for inducing fainting or syncope, but some folks with LQTS exhibit no obvious signs or symptoms. Inherited mutations in one of several genes can give rise to LQTS, but the condition can also be acquired as a result of kidney or liver impairment, electrolyte imbalance, or the use of certain pharmaceuticals (more than 50 drugs have demonstrated the capacity to induce LQTS, some of which are of the antibiotic, antihistamine, diuretic, antidepressant, and anticholesterolemia classes) [20]. Unexplained syncope can also be seen with short QT syndrome, a related condition also said to be inherited in which a mutation in one of three genes associated with potassium ion channels may be seen [21]. So how do we treat POTS naturally? Because POTS can present itself in a variety of forms, certainly the treatment plan would need to be customized for the needs of the patient. But there are definitely some general recommendations that we can cover, and despite the conventional stance that there is no cure for POTS, POTS can and has been corrected [22]. Firstly, I support the prescribing of a balanced intake of calcium, magnesium, vitamin D, and vitamin K2 for the treatment of POTS. Increasing the patient’s consumption of water, vitamin B1, vitamin B12, and Himalayan pink salt or Celtic sea salt may also be appropriate. Next, proper exercise has been shown to be quite effective in the treatment of POTS (especially when deconditioning is one of the major contributors), and therefore should be considered [23]. Because antibodies against adrenergic receptors have been found in POTS patients, correction of some degree of autoimmunity may be necessary (healing a leaky gut would likely be the primary goal here) [24]. The reactivation or proliferation of microbes and/or viruses should also be considered, especially in those who have received the Gardasil vaccine. Accordingly, an antiviral and/or antibacterial regimen may need to be administered (Mycoplasma pneumoniae and one or more of the herpesviruses are likely to be the main targets). Improving the health of the body’s mitochondria and the microbiota of the gut are probably going to be indicated. Lastly, a heavy metal detoxification program of some degree could be required as well. Hopefully this was of some use. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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