Sodium Problems

[postman]

Salt gives me edema (facial swelling), worsened brainfog, agitated mood and horrible mood swings. What is the cause of this? It doesn't matter if it's table salt or sea salt or iodized salt or Mortons canning/pickling salt, or even sodium bicarbonate, it's all the same to me. I seem to have problems with calcium too. Both of these are supposed to be extracellular minerals but my body doesn't seem to be able to regulate this, they flood into the cells and cause havoc. I feel the best on a very low sodium and low calcium diet, contrary to everything that Ray says. Just increasing intake does absolutely nothing to fix it, there is either some other underlying mechanism that is dysfunctional in my body that needs to be fixed, or Ray is wrong.

 

[Terma]

What I suspect for my cardiovascular issue and reactions to Cl/NaCl is that angiotensin leads to NADPH oxidase (Angiotensin II, NADPH Oxidase, and Redox Signaling in the Vasculature) and H+/Na exchanger activity. Some authors believe the superoxide stays in the cell, but I think it may be circumstantial or affected by experimental procedures; this author (The function of the NADPH oxidase of phagocytes and its relationship to other NOXs in plants, invertebrates, and mammals) suggested that vasoconstriction - and I imagine some forms of bloating - are worsened or due to superoxide leaving endothelial cells along with H+, which leads to import of Cl and Na, followed by osmosis of H2O into the cell - which does seem elegant:

It is generally believed that blood pressure is regulated by contraction of the muscular wall of the resistance vessels. Another possibility is that blood pressure is regulated, at least in part, by the osmotic swelling and shrinkage of cells in response to fluxes of ions driven by NOX-induced charge compensation and associated NHE activity. According to Hagen–Poiseuille's law, the resistance to fluid flow through a vessel is related to the fourth power of the radius, as a consequence of which minor alterations in the size of the cells, either in the smooth muscle or endothelium, can cause significant alterations in resistance and consequently in blood pressure.

This process could be driven and regulated by NOXs and could occur in any of the cells in the vessel walls in which these electron transport chains are expressed. On the basis of the model system described above, the efflux of electrons would be balanced by the influx of Cl− and the exchange of intracellular H+s for extracellular Na+ through sodium proton exchangers, followed by the osmotic movement of water. The inhibition of the influx of Na+ through NHEs, which are inhibited by thiazide diuretics, could explain the antihypertensive effect of these drugs, which appear to exert their action through vasodilatation rather than saluresis or loss of free water (Conway & Lauwers, 1960; van, Man in ’t Veld, & Schalekamp, 1980).