there's also iodized sea salt available. ages ago i read an estimate somewhere saying that 75% of average joe's sodium intake comes from processed food.
i would be extremely surprised if there is anyone out there counting on salt to deliver their various mineral requirements.
as for sodium, that reminds me of some of the oldest reading i did on ms.. the first book and maybe only book on the subject that someone handed to me in person. by a local woman who did a lot of research with the crew at mcmaster, looking at the whole thing in terms of axon damage and sodium channels etc.
Sodium Channels and Multiple Sclerosis: Roles in Symptom Production, Damage and Therapyhttp://www.ncbi.nlm.nih.gov/pubmed/17388954
Our understanding of the potential role of sodium channels in multiple sclerosis (MS) has grown substantially in recent years. The channels have long had a recognized role in the symptomatology of the disease, but now also have suspected roles in causing permanent axonal destruction, and a potential role in modulating the intensity of immune activity. Sodium channels might also provide an avenue to achieve axonal and neuronal protection in MS, thereby impeding the otherwise relentless advance of permanent neurological deficit. The symptoms of MS are largely determined by the conduction properties of axons and these, in turn, are largely determined by sodium channels. The number, subtype and distribution of the sodium channels are all important, together with the way that channel function is modified by local factors, such as those resulting from inflammation (eg, nitric oxide). Suspicion is growing that sodium channels may also contribute to the axonal degeneration primarily responsible for permanent neurological deficits. The proposed mechanism involves intra-axonal sodium accumulation which promotes reverse action of the sodium/calcium exchanger and thereby a lethal rise in intra-axonal calcium. Partial blockade of sodium channels protects axons from degeneration in experimental models of MS, and therapy based on this approach is currently under investigation in clinical trials. Some recent findings suggest that such systemic inhibition of sodium channels may also promote axonal protection by suppressing inflammation within the brain.
nutrient connections re one particular type of sodium channel:
Intracellular thiol-mediated modulation of epithelial sodium channel activityhttp://www.ncbi.nlm.nih.gov/pubmed/15623528
The epithelial sodium channel ENaC is physiologically important in the kidney for the regulation of the extracellular fluid volume, and in the lungs for the maintenance of the appropriate airway surface liquid volume that lines the pulmonary epithelium. Besides the regulation of ENaC by hormones, intracellular factors such as Na(+) ions, pH, or Ca(2+) are responsible for fast adaptive responses of ENaC activity to changes in the intracellular milieu. In this study, we show that ENaC is rapidly and reversibly inhibited by
internal sulfhydryl-reactive molecules such as methanethiosulfonate derivatives of different sizes, the metal cations Cd(2+) and Zn(2+)
, or copper(II) phenanthroline, a mild oxidizing agent that promotes the formation of disulfide bonds. At the single channel level, these agents applied intracellularly induce the appearance of long channel closures, suggesting an effect on ENaC gating. The intracellular reducing agent dithiothreitol fully reverses the rundown of ENaC activity in inside-out patches. Our observations suggest that changes in intracellular redox potential modulate ENaC activity and may regulate ENaC-mediated Na(+) transport in epithelia. Finally, substitution experiments reveal that multiple cysteine residues in the amino and carboxyl termini of ENaC subunits are responsible for this thiol-mediated inhibition of ENaC.
(nb cadmium bad.. body mistakes it for zinc so cd can tie up zinc receptors)
VERY recent research... (feb 2013)
just throwing this in to make the ENaC/MS connection:
Inhibition of Neuronal Degenerin/Epithelial Na+ Channels by the Multiple Sclerosis Drug 4-Aminopyridine http://www.jbc.org/content/early/2013/0 ... 3.full.pdf
Background: 4-AP treats the symptoms of MS because it inhibits Kv channels. Deg/ENaC channels contribute to the progression of MS. Results: 4-AP also inhibits Deg/ENaC channels. Conclusions: Effects on both Kv and Deg/ENaC
(are 'capsules' a new thing, or have i just not been reading the journals that use them??)