Poster - #VH-45092 - Keywords: Mast Cell Activation MCAS Nutritional Biochemistry MCAS Management Protocols Acute COVID-19 Refractory MCAS Diamine Oxidase (DAO) Copper Tryptase Vitamin D EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid)

Beyond Medication: A Nutritional Blueprint for Mast Cell Activation Syndrome

Sparkle Williams, Holistic Functional Nutrition Practitioner, BSN
MCAS Nutritional Clinic

ABSTRACT:
The post-pandemic surge in the incidence of Mast Cell Activation Disorder (MCAD) brings to light gaps in our understanding of, and treatments for this hyperactive immune response. Suboptimal MCAD therapies highlight a critical need for advancements in immunopathology and more effective clinical management of this disorder. This review and case study investigates Mast Cell Activation Syndrome (MCAS) etiology, a prevalent, disproportionately female MCAD subtype. One epigenetic factor, namely nutritional deficiencies which compromise detoxification and disrupt mast cell homeostasis, will be the focus of this work. MCAS onset after COVID-19 diagnosis, and subsequent symptom exacerbation with a restrictive low histamine diet, led to an in-depth investigation of the interplay between MCAS and nutritional status. The findings of this case study demonstrate that utilizing nutritional biochemistry can enhance existing pharmacological interventions.
A refined understanding of mast cell biology and its role in pathophysiological processes, especially impact on nutritional status, is paramount. There are distinct variants of MCAD, including Systemic Mastocytosis (SM), characterized by mast cell proliferation due to inherited genetic mutations, and MCAS, distinguished by mast cell activation absent of identifiable genetic mutations. Current MCAD management includes trigger avoidance, immuno-suppressants, monoclonal antibodies (Omalizumab), kinase inhibitors, experimental therapies with nutraceuticals (arginine, glutamine, curcumin, flavonoids), and cytoreductive agents. Bringing Nutritional Biochemistry into the picture is warranted. Research shows a correlation between copper deficiency and tryptase dysregulation, which could lead to mast cell degranulation and further pro-inflammatory responses. Conversely, optimal copper concentrations modulate tryptase activity. Vitamin D's role in immunomodulation and mast cell stabilization has also been investigated, with preliminary evidence suggesting its potential to attenuate allergic responses. However, the precise mechanisms governing mast cell degranulation and subsequent allergic reactions require further elucidation. Additional research is warranted to assess these interventions’ efficacy and optimal dosing within a personalized MCAS management strategy.