I’ve got a weird little tidbit for you today, a journal article called “Early manifestation of hypophosphatemic rickets in goslings: a potential role of insufficient muscular adenosine triphosphate in motility impairment of early P-deficient geese.”

It popped up in my email from a Google alert I have for anything new relating to “hypophosphatemic.” I almost deleted it, because, really, hypophosphatemia in geese? Sure, that could be a problem for farmers, but what could it tell us in the XLH community? It’s not even studying genetically altered geese who have XLH (like hyp mice have been bred to essentially have XLH).

But I was avoiding some work, so I decided I’d rather read about waddling geese than do my work. And I’m glad I did! Because there’s an important lesson for clinicians here.

I’m not sure the authors fully absorbed the lesson, since they defined the geese’s condition as “rickets” instead of “phosphate deficiency.” They were looking for answers to how soon the phosphate deficiency would affect the geese, so that’s what they focused on, and it’s not really relevant to us.

What is relevant is the data showing that “Dietary P[hosphorus] levels significantly affect motion ability, skeletal size, hardness and morphology, and muscular ATP production.” (emphasis added) They also found that the low ATP production had a significant correlation with poor mobility in the phosphate-deficient geese. Which, of course, makes sense, since ATP is the fuel for muscles, so if geese (and humans) have low ATP production, our muscles can’t work properly.

I’m not aware of any other research connecting hypophosphatemia with low ATP production and mobility challenges, so this study is a good start. It’s a reminder that chronic hypophosphatemia is really much more than “rickets,” and is a whole-body, whole-life disorder.

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Please note that the author is a well-read patient, not a doctor, and is not offering medical or legal advice.

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