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Considering the intestine is where most of dietary sodium is absorbed, it is plausible to hypothesise that blocking intestinal CLDN2 and CLDN15 may lead to lower sodium uptake and, thus, BP
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BPC-157 Supports Vascular and Neurological Repair One underappreciated hallmark of long COVID is endothelial dysfunction damage to the lining of blood vessels that impairs circulation, oxygenation, and tissue delivery.7 BPC-157 has demonstrated angiogenic (new blood vessel formation) effects in research models, upregulating VEGFR2 and promoting collateral circulation in ischemic tissue.8 This matters for two reasons: Cardiovascular symptoms (breathlessness, reduced exercise tolerance, tachycardia) may partly reflect impaired tissue oxygenation from vascular damage Neurological symptoms (brain fog, cognitive impairment) may similarly reflect reduced cerebral blood flow BPC-157's neuroprotective effects shown across models of traumatic brain injury, dopamine dysregulation, and serotonin syndrome also suggest value in supporting the neurotransmitter disruption many long COVID patients experience.9 BPC-157 Modulates Inflammation Without Immune Suppression This is critical
These complementary profiles have motivated research interest in combined study designs, though direct head-to-head comparison data in identical models remain limited
