Vitamin D deficiency changes the intestinal microbiome reducing B vitamin production in the gut. The resulting lack of pantothenic acid adversely affects the immune system, producing a "pro-inflammatory" state associated with atherosclerosis and autoimmunity.

STUDY OBJECTIVES: Vitamin D blood levels of 60-80ng/ml promote normal sleep. The present study was undertaken to explore why this beneficial effect waned after 2years as arthritic pain increased. Pantothenic acid becomes coenzyme A, a cofactor necessary for cortisol and acetylcholine production. 1950s experiments suggested a connection between pantothenic acid deficiency, autoimmune arthritis and insomnia. The B vitamins have been shown to have an intestinal bacterial source and a food source, suggesting that the normal intestinal microbiome may have always been the primary source of B vitamins. Review of the scientific literature shows that pantothenic acid does not have a natural food source, it is supplied by the normal intestinal bacteria. In order to test the hypothesis that vitamin D replacement slowly induced a secondary pantothenic acid deficiency, B100 (100mg of all B vitamins except 100mcg of B12 and biotin and 400mcg of folate) was added to vitamin D supplementation. METHODS: Vitamin D and B100 were recommended to over 1000 neurology patients. Sleep characteristics, pain levels, neurologic symptoms, and bowel complaints were recorded by the author at routine appointments. RESULTS: Three months of vitamin D plus B100 resulted in improved sleep, reduced pain and unexpected resolution of bowel symptoms. These results suggest that the combination of vitamin D plus B100 creates an intestinal environment that favors the return of the four specific species, Actinobacteria, Bacteroidetes, Firmicutes and Proteobacteria that make up the normal human microbiome. HYPOTHESES: 1) Seasonal fluctuations in vitamin D levels have normally produced changes in the intestinal microbiome that promoted weight gain in winter. Years of vitamin D deficiency, however, results in a permanently altered intestinal environment that no longer favors the "healthy foursome". 2) Humans have always had a commensal relationship with their intestinal microbiome. We supplied them vitamin D, they supplied us B vitamins. 3) The four species that make up the normal microbiome are also commensal, each excretes at least one B vitamin that the other three need but cannot make. 4) Improved sleep and more cellular repairs eventually depletes body stores of pantothenic acid, causing reduced cortisol production, increased arthritic pain and widespread "pro-inflammatory" effects on the immune system. 5) Pantothenic acid deficiency also decreases available acetylcholine, the neurotransmitter used by the parasympathetic nervous system. Unopposed, increased sympathetic tone then produces hypertension, tachycardia, atrial arrhythmias and a "hyper-adrenergic" state known to predispose to heart disease and stroke.

The world epidemic of sleep disorders is linked to vitamin D deficiency.

An observation of sleep improvement with vitamin D supplementation led to a 2 year uncontrolled trial of vitamin D supplementation in 1500 patients with neurologic complaints who also had evidence of abnormal sleep. Most patients had improvement in neurologic symptoms and sleep but only through maintaining a narrow range of 25(OH) vitamin D3 blood levels of 60-80 ng/ml. Comparisons of brain regions associated with sleep-wake regulation and vitamin D target neurons in the diencephalon and several brainstem nuclei suggest direct central effects of vitamin D on sleep. We propose the hypothesis that sleep disorders have become epidemic because of widespread vitamin D deficiency. The therapeutic effects together with the anatomic-functional correspondence warrant further investigation and consideration of vitamin D in the etiology and therapy of sleep disorders.

Bilateral aortoostial coronary artery disease: moyamoya of the heart?

Moyamoya is a vascular occlusive disease typically limited to the cerebral arterial system. We report a case of severe stenosis of the left main and right coronary arteries occurring in association with moyamoya disease, supporting the concept that moyamoya may be an intracranial manifestation of a systemic arterial disorder.

Sciatic schwannoma of the thigh causing foot pain mimicking plantar neuropathy.

Two patients with plantar foot pain, one mistakenly thought to have tarsal tunnel syndrome, had complete resolution of pain after resection of a sciatic nerve schwannoma of the midthigh. The entire extent of the sciatic nerve should be evaluated in patients presenting with unilateral, neuropathic foot pain.

Motor nerve inexcitability in Guillain-Barré syndrome. The spectrum of distal conduction block and axonal degeneration.

We studied 34 patients with the Guillain-Barré syndrome (GBS) to clarify the clinical significance of inexcitable motor nerves and of low amplitude compound muscle action potentials (CMAPs). The patients were subdivided into two groups. Group 1 included eight patients who had electrically inexcitable motor nerves within 2 wks of the first symptom. (Two patients without extensive conduction studies had only one inexcitable motor nerve.) The outcome in this group at 1 yr varied from complete recovery (five patients) to severe motor sequelae (three patients). Group 2 included 26 patients who had two electrophysiological assessments, and in whom the serial changes in CMAP amplitudes were analysed and correlated to outcome. Fourteen of these 26 sets of serial studies were performed within 1 mth. Twelve of 26 patients in Group 2 showed decrease in the amplitude of CMAPs between serial studies; only six of these had a good outcome at 1 yr. Nine of 26 patients showed increase in CMAP amplitude between serial studies, of these eight had a good clinical outcome. Low-amplitude CMAPs or inexcitable motor nerves in the initial stages of GBS are due to distal pathology of the motor axons, either distal conduction block or axonal degeneration. The nature of these changes cannot be predicted by the results of the initial electrophysiological evaluation, including the presence or absence of active denervation. However, improvement of CMAP amplitude on sequential studies suggests a good outcome at 1 yr. We believe that, in the absence of a biological marker for GBS, individualization of an 'axonal variant' of the syndrome is not warranted at the present time.