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Dysautonomia, Postural Orthostatic Tachycardia Syndrome, and Mast Cell Activation Syndrome – Potential Role of Therapeutic Carbohydrate Reduction
Dysautonomia, Postural Orthostatic Tachycardia Syndrome, and Mast Cell Activation Syndrome – Potential Role of Therapeutic Carbohydrate Reduction
Author: Sarah M. Rice
Author: Sarah M. Rice
*Please correctly attibute this work if you were directed through Google scholar*
*Please correctly attibute this work if you were directed through Google scholar*
Dysautonomia refers to conditions of autonomic nervous system dysregulation which include postural orthostatic tachycardia syndrome (POTS), the most common phenotype (1). The association of dysautonomia with covid-19 suggests the incidence of this condition is increasing (1–3). Clinical experience using an exclusion protocol ketogenic diet approach (similar to the ‘gut and physiology syndrome’ (GAPS) diet (4)) to treat dysautonomia has shown benefits (5). From the pathophysiology, there are lines of evidence that support the potential benefit of therapeutic carbohydrate reduction (TCR) or a ketogenic approach in conditions occurring as a feature of dysautonomia.
Postural orthostatic tachycardia syndrome
POTS is an autonomic dysregulation that includes features of 'volume depletion, inflammatory disorders and autoimmune diseases' (6) and may occur following various triggers, including viraemia (20-50%), trauma, or surgery (7). TCR is known to improve multiple pathways involved in inflammation and autoimmune disease (8–10). Looking at the list of symptoms (and associated conditions) (2, 7), they include those that have been reported to improve with TCR (10) – notably impaired cognitive function or brain fog (11, 12), migraine (13), gut disturbances (14), and fibromyalgia (15).
Subtypes and aetiologies fall into the following categories: neuropathic (neuropathy/sympathetic denervation); hyperadrenergic (increased sympathetic tone); hypovolemic (decreased blood volumes – low renin/aldosterone – impaired RAAS system); autoimmune (may include abnormal mast cell activation); and deconditioning and muscle wasting (cause/effect unclear) (7, 16). In addition, gastrointestinal dysfunction is common (7).
The following evidence streams, derived from the POTS pathophysiology and observed associations, can be considered:
• TCR can promote neuroprotection, especially in the ketogenic state (17) and could modulate heart rate and sympathetic activity positively (18).
• Hyperglycaemia is associated with reduced plasma sodium concentrations which may affect the RAAS system and associated haemodynamics (19–21), and increased sodium intake is recommended in POTS management (1). TCR promotes normoglycaemia (22) and has been shown to influence the RAAS system, increasing aldosterone, which is reduced in POTS (7, 23).
• Migraine (40%) and IBS (30%) are significantly comorbid with POTS (7) and can respond to TCR approaches (13, 14).
• TCR modulates the gut microbiome (24) and may help with autoimmune disorders (25), especially if an exclusion protocol is applied (26, 27). The ketogenic diet has been mentioned as an intervention in conjunction with long covid, specifically in connection with immune function, sarcopenia, and the microbiome (28).
• TCR has been shown to improve immune system function (29–31) and has been explored in the context of covid-19, showing promise in the preclinical (32) and clinical (30, 33) settings.
• Carbohydrate restriction in the form of a gluten-free diet has been shown to benefit features of POTS, notably for orthostatic intolerance, vasomotor, and gastrointestinal symptoms (34, 35).
• Deconditioning, muscle wasting (inactivity), and skeletal muscle damage may be associated with POTS (6, 7, 28). TCR, particularly in the ketogenic range, has demonstrated preservation of muscle mass and improved strength during weight loss (36, 37). Nutritional ketosis may be supported by the addition of exogenous ketones, potentially increasing the protective effect on muscle mass (38–41).
Mast cell activation syndrome
Mast cell activation syndrome (MCAS) may be a feature of POTS (7, 42) and is an immune-mediated condition causing the release of histamine, prostaglandins, and other inflammatory markers. Intestinal symptoms, which may be a feature of MCAS, can be interpreted as IBS, possibly leading to underdiagnosis (43).
Mast cell-driven inflammation, autoimmune, and hypersensitivity conditions have been shown to respond to ketones and fasting (44, 45). Dysbiosis of the microbiome and changes in gut permeability can trigger the innate immune system, leading to systemic immune responses (46), which may play a role in MCAS or other features of POTS (47).
Small intestinal bacterial overgrowth (SIBO) has been observed in association with MCAS and POTS – in one study, 41% of MCAS participants had an abnormal lactulose breath test (43). Suggested diets for SIBO include several on the carbohydrate-reduced spectrum, including a low-FODMAP, specific carbohydrate diet, and low-carbohydrate paleo diet (48, 49). SIBO has also been seen to respond to a zero-carbohydrate diet as an exclusion and reintroduction protocol (50). TCR in this context may also support recovery of the SIBO-MCAS subset (with or without POTS).
The NLRP3 inflammasome is implicated in the development of allergic disease, and NLRP3 inflammasome inhibitors are being investigated as a therapeutic target in this setting (51, 52). A ketogenic diet has been shown to suppress inflammasome activity in macrophages (53), and ketone bodies have demonstrated the same effect in preclinical studies (54), lending support to the potential benefit of a TCR approach in MCAS.
Non-pharmacological interventions and considerations
An increased intake of salt and fluid is recommended to offset the hypovolemia and raised plasma norepinephrine seen in POTS (55). A minimum of 2–3 litres of water per day (avoiding caffeine and alcohol) and one or two additional teaspoons of salt per day are recommended (a range of 3-10g sodium can be considered) (1, 7). Of interest is the role of salt in both POTS and migraine management (56, 57) and the comorbidity of migraine found in POTS. Other recommendations are compression garments and a graded exercise programme (7).
A note on bone broth
Bone broth is a popular recommendation when embarking on TCR or a ketogenic diet – it can be used as a vehicle for additional salt in the diet. Community commentary posits bone broth can have elevated glutamate, glutamine, and histamine profiles when extended cooking times are utilised (home cooked), which may be triggering for sensitive individuals (4, 58, 59). How significant this is in accounting for the quantity of amino acids in terms of mg/g compared to animal products in general and other biological effects (e.g., presence of histamine) may be difficult to predict on an individual level (60, 61). Glutamine can have healing effects on the gut (62, 63), but glutamate in the context of sensitive individuals can be detrimental – possibly driven by gut dysbiosis (64, 65). Glutamate sensitivity is associated with migraine (66), Gulf War syndrome (67), psychiatric disorders (68), and epilepsy (69) – therefore, it may be prudent to consider this in patients with POTS who may have increased sensitivity. Of note, emerging research points to modulation of the gut microbiome as a feature of therapeutic response in conditions thought to be sensitive to glutamate. These same conditions have also been shown to respond to a ketogenic diet, with modulation of the microbiome occurring as a feature of therapeutic effect (70, 71).
A prudent approach would be to consider less than 3 hours cooking time of the broth (sometimes referred to as meat stock) to reduce the risk of any hypersensitivity, as recommended on community forums (4, 59). Store-bought bone broth should be checked for added monosodium glutamate and other additives that may be potentially triggering. Progression to longer-cooked bone broths can be considered as tolerance improves.
Conclusion
Various evidence streams reflect the potential benefit of a TCR approach in POTS and associated conditions, as observed in clinical practice (5).
© 2023 Sarah M. Rice. All rights reserved.
Update
Update
A recent case study demonstrates a successful implementation of a ketogenic intervention for dysautonomia and associated conditions.
Colgan, D.D. et al. (2025) ‘Clinically Meaningful Improvements in Long COVID Symptoms Following Ketogenic Metabolic Therapy Combined with Lifestyle Interventions—A Clinical Case Report and Review of the Literature’, Case Reports in Clinical Medicine, 14(8), pp. 391–410. Available at: https://doi.org/10.4236/crcm.2025.148052.
Key points:
The patient was diagnosed with post-viral dysautonomia, specifically POTS and ME/CFS , with severe physical and cognitive fatigue and PEM and a neuroimmune disorder
In February 2024, the patient enrolled in a community-based 12-week educational program designed for dysautonomia, termed Enable Your Healing (this is the same programme developed by Ruddick, as referenced in article above [5]), which combined ketogenic metabolic therapy with lifestyle components.
Within the first two weeks of the intervention, her chronic hypotension resolved, and she discontinued IV saline therapy. She reported a notable increase in energy, which coincided with the onset of ketosis.
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