Deficiencies of a number of B vitamins have been reported to result in leg abnormalities.
In particular, pyridoxine (Vitamin B6) deficiency has been associated with stunted longitudinal
bone growth, and supplementation has been shown to reduce the incidence (Masse et
al., 1996). Pyridoxine may exert its beneficial effect via involvement with zinc homeostasis.
The metabolic process is further complicated through the interaction of dietary protein, as a
high level of dietary protein presumably increases the metabolic requirement for pyridoxine
through processes as transamination and/or deamination (Daghir, 1976).