It's easy to look at this article [Schott and Wills, 1975: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=491911&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/1151410)], in which Schott and Wills (1975) described a person who had had hypophosphatemia and, as a result, had become almost unable to walk from muscle weakness, and say that this type of thing couldn't occur in the present day. But this type of thing could, arguably, more easily happen in today's medical system than in 1975 (especially if someone described the symptoms in a slightly different way). It's worth noting that the authors, Schott and Wills (1975) were not the ones who had, on two occasions, dismissed the person's symptoms as having been "hysterical" in nature. Before Schott and Wills (1975) saw the person, some other doctors had seen her and had not been able to find anything objectively wrong with her. Today, a doctor might only be able to spend ten minutes with his or her patients, because of insurance issues and everything, and refer to the complaints of back pain and muscle weakness as being "somatic symptoms," etc. I don't usually do this, but here are a couple of excerpts:
"Also at that time she became aware of muscular weakness, initially causing difficulty in climbing high steps and in manoeuvring her legs when getting into a car. The weakness of both thighs subsequently progressed, and was associated with intermittent hip and low back pain. She was investigated in another hospital one year before admission here, when proximal muscle weakness and a waddling gait were noted, together with brisk tendon reflexes and bone tenderness on palpation. An electromyogram performed at that time was normal, and the only significant abnormal investigation found was a low renal threshold for glucose. The symptoms were considered to be hysterical and she was discharged. Her weakness, however, became more profound, and she had to pull herself upstairs, a task that became increasingly difficult with the development of proximal weakness in the arms, and for six months before admission she had been unable to raise her arms above her shoulders. She was admitted at that time to a second hospital for investigation, and was again thought to be psychoneurotic and no specific therapy was prescribed. She continued to deteriorate, commenced walking with a Zimmer frame, and was admitted to this hospital for further assessment. On direct questioning, she had noted that her nails had become brittle, and that she had had a tendency to vomit occasionally over the preceding 10 years. Her weight had fallen by about 13 kg over four years, although she had always eaten an adequate and normal diet. Her sister reported that the patient had 'shrunk' over the preceding two years" (Schott and Wills, 1975, p. 298).
The muscle weakness could have been partly a result of neuropathy induced by phosphate depletion [(http://scholar.google.com/scholar?hl=en&q=phosphate+hypophosphatemia+neuropathy+OR+neuropathic); (http://scholar.google.com/scholar?hl=en&q=phosphate+muscle+weakness+hypophosphatemia+neuropathy+OR+neuropathic)], given that the authors of some of those articles, in the search results, have described neurological problems resulting from phosphate depletion. The muscle weakness and exercise intolerance that can occur in phosphate depletion [(http://scholar.google.com/scholar?hl=en&q=phosphate+hypophosphatemia+exercise+intolerance); (http://scholar.google.com/scholar?hl=en&q=phosphate+muscle+weakness+hypophosphatemia)] are reminiscent of the types of symptoms that people experience in mitochondrial disorders, as discussed in past postings. Some interesting articles came up in those searches. I've only looked at the abstracts so far, but the authors of this one described a person who had had fatigue and exercise intolerance that were suggestive of some mitochondrial or bioenergetic pathology [Land et al., 1993: (http://www.ncbi.nlm.nih.gov/pubmed/8400863)]. This is another one showing the association of phosphate depletion with poor insulin sensitivity [Haap et al., 2006: (http://www.ncbi.nlm.nih.gov/pubmed/16391583)], and Haap et al. (2006) found that serum phosphorus correlated positively with a marker of insulin sensitivity. The authors mention, in the abstract, that one can't definitely say that the higher phosphate availability causes the cells to become more responsive to insulin, but it's known that ATP depletion in cells can reduce the cells' insulin sensitivities (http://scholar.google.com/scholar?hl=en&q=intracellular+ATP+insulin+sensitivity).
As far as that case report goes, however, it's also worth noting that there are many old articles describing a higher frequency of cavities ("dental caries") in the context of phosphate depletion, and there are old articles describing the "anticariogenic" effects of an adequate phosphate intake (within the normal range of dietary intakes) (http://scholar.google.com/scholar?hl=en&q=sodium+phosphate+caries+OR+anticariogenic+OR+cariogenic). On the one hand, that's not surprising. Everyone knows that hydroxyapatite contains phosphate, etc. But, in the vast majority of the research that comes out these days, there's this overriding assumption that dietary phosphate is bad for bones and is going to cause calcium to be lost from the bones, etc. Obviously, I think one should be careful with sources of phosphate and not take large amounts of any source of phosphate, from food or otherwise, at any one time, so as to allow the kidneys to filter it and to allow the phosphate to be transported into cells. But the information on the utilizable phosphate content of many vegetable/plant-based foods is probably very inaccurate, in my opinion. Phytates may provide very, very little utilizable phosphate, as discussed in past postings, but these are just my opinions.
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