Condiciones de SaludDeficiencia de calcio se refiere a niveles inadecuados de calcio en la sangre (hipocalcemia) o ingesta/almacenamiento insuficiente de calcio en el cuerpo, que afecta la salud ósea, la función nerviosa, la contracción muscular y la salud cardiovascular. El calcio es vital para la mineralización ósea, la señalización nerviosa, la coagulación sanguínea y la función muscular. La deficiencia a largo plazo puede resultar en osteopenia, osteoporosis, espasmos musculares o ritmos cardíacos anormales.
La hipocalcemia puede surgir de una insuficiencia dietética, malabsorción o condiciones médicas subyacentes. Garantizar una ingesta adecuada de calcio, junto con cofactores como la vitamina D, es crucial para mantener la densidad ósea y la salud en general.
Tipos:
Deficiencia dietética de calcio: Ingesta inadecuada de calcio a través de los alimentos.
Hipocalcemia: Niveles bajos de calcio en la sangre debido a malabsorción, trastornos paratiroideos o enfermedad renal.
Deficiencia secundaria de calcio: Por falta de vitamina D, magnesio o exceso de fósforo que interfiere con la absorción de calcio.
Causas comunes (factores de riesgo):
Ingesta dietética inadecuada: Especialmente en veganos, personas con intolerancia a la lactosa o quienes evitan los lácteos.
Deficiencia de vitamina D: Deteriora la absorción de calcio en los intestinos.
Trastornos paratiroideos: La paratiroides hipoactiva reduce la regulación del calcio.
Enfermedad renal: Deteriora el equilibrio del calcio y la activación de la vitamina D.
Trastornos digestivos: Enfermedad celíaca, enfermedad de Crohn u otros síndromes de malabsorción.
Estado posmenopáusico: La reducción de estrógenos acelera la pérdida de calcio óseo.
Alta ingesta de fósforo: Proveniente de refrescos o alimentos procesados, interfiere con la absorción de calcio.
Ciertos medicamentos: Diuréticos, corticosteroides o anticonvulsivos.
Causas más graves (complicaciones):
Osteopenia u osteoporosis: Huesos debilitados propensos a fracturas.
Calambres o espasmos musculares: Debido a una señalización nerviosa deteriorada.
Tetania: Contracciones musculares severas por niveles bajos de calcio en sangre.
Entumecimiento u hormigueo: En los dedos de las manos, los pies o alrededor de la boca.
Arritmias cardíacas: Latido cardíaco irregular debido a una conducción eléctrica alterada.
Problemas dentales: Esmalte débil, aumento de caries.
Cuándo consultar a un médico o especialista (endocrinólogo, nutricionista):
Calambres musculares persistentes, entumecimiento u hormigueo.
Fracturas óseas o diagnóstico de osteopenia/osteoporosis.
Irregularidades en el ritmo cardíaco.
Niveles bajos de calcio detectados en análisis de sangre.
Deficiencia coexistente de vitamina D o magnesio.
Bifidobacterium infantis 35624 suppresses histamine-related allergic symptoms and demonstrates strong anti-inflammatory effects. In combination with B. longum BB536 (Lac-B), it significantly decreased histamine levels and suppressed histidine decarboxylase and H1 receptor gene expression. It belongs to Bifidobacteriaceae, which is more abundant in healthy subjects than HIT patients.
Bifidobacterium longum is identified as a histamine-degrading probiotic that does not produce histamine. Strain BB536 studied in combination with B. infantis 35624 (mixture called Lac-B) significantly suppressed allergic symptoms and decreased histamine levels, including suppression of histidine decarboxylase gene expression. It is recommended in HIT probiotic protocols.
Bovine kidney is a natural source of diamine oxidase (DAO), the primary intestinal enzyme responsible for degrading dietary histamine. Reduced DAO activity is a central mechanism in histamine intolerance (HIT). Clinical studies using kidney-derived DAO supplements have demonstrated symptom improvement in HIT patients. Evidence comes from open-label interventional and retrospective cohort studies.
Copper is a structural and catalytic component of the DAO enzyme, essential for its function. Copper deficiency directly reduces DAO activity, impairing histamine degradation and potentially causing or exacerbating histamine intolerance. Copper is identified as a required cofactor in peer-reviewed HIT literature.
Diamine oxidase (DAO) is the principal intestinal enzyme for degrading dietary histamine. Reduced DAO activity is considered the primary mechanism underlying histamine intolerance (HIT). An open-label pilot study (n=28) showed oral DAO supplementation before meals significantly reduced all HIT-related symptoms over 4 weeks, with symptom scores returning when supplementation stopped. A subsequent observational study (n=82) confirmed similar findings.
Lactobacillus plantarum has demonstrated direct histamine-degrading properties and the ability to stimulate DAO secretion from intestinal epithelial cells. A 2025 PMC study (LP115 strain) showed significant DAO secretion increase and histamine reduction in HT-29 intestinal cell models. Multiple strains of L. plantarum can degrade biogenic amines including histamine.
Luteolin is a flavonoid that stabilizes mast cells and inhibits histamine release, showing greater potency than cromolyn sodium in some assays. Animal studies confirm luteolin reduces histamine release from mast cells stimulated by histamine liberators. It is used in clinical practice for mast cell activation and histamine intolerance.
Stinging nettle (Urtica dioica) acts as a natural antihistamine through H1 receptor antagonism and mast cell tryptase inhibition, mechanisms characterized by Roschek et al. (Phytother Res, 2009). A randomized double-blind clinical trial in allergic rhinitis patients found that freeze-dried Urtica dioica reduced allergy symptoms, and a 2017 RCT confirmed significant improvement in symptom severity scores.
Quercetin is a flavonoid that inhibits mast cell degranulation and histamine release, making it relevant for histamine intolerance management. In vitro studies show quercetin equals or exceeds cromolyn sodium in blocking histamine secretion from human mast cells. It also inhibits histamine-induced calcium influx via H4 receptors and reduces pro-inflammatory cytokines IL-6, IL-8, and TNF-α.
Preclinical studies show Schizonepeta suppresses mast cell degranulation and histamine-related signaling, including in IgE-stimulated models. The 2025 systematic review confirmed histamine suppression among its documented effects. Evidence is in vitro/preclinical with no human histamine intolerance trials.
Vitamin B6 (pyridoxine/pyridoxal-5-phosphate) is an essential cofactor for DAO enzyme activity. Deficiency in B6 impairs DAO function, increasing histamine burden. Multiple reviews and mechanistic studies identify B6 repletion as a standard adjunctive strategy for improving DAO activity in histamine intolerance.
Vitamin C acts as both a cofactor for DAO enzyme function and as a direct antihistamine. Multiple studies demonstrate an inverse correlation between plasma vitamin C levels and blood histamine; supplementation with 1–2 g/day has been shown to lower blood histamine levels within days. Intravenous ascorbic acid (Hagel et al., 2013) significantly decreased serum histamine in allergic and non-allergic patients.
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