RESUMEN
BACKGROUND: Sensory reactivity differences are experienced by between 5% and 15% of the population, often taking the form of sensory over-responsivity (SOR), in which sensory stimuli are experienced as unusually intense and everyday function is affected. A potential mechanism underlying over-responsivity is an imbalance between neural excitation and inhibition in which inhibitory influences are relatively weakened. Therefore, interventions that boost neural inhibition or reduce neural excitation may reduce SOR; Vitamin-B6 is the coenzyme for the conversion of excitatory glutamate to inhibitory gamma-aminobutyric acid (GABA), and in animal models, it both increases the concentration of GABA and reduces glutamate. AIMS: To discover whether taking a high dose of Vitamin-B6 reduces SOR and other aspects of sensory reactivity. METHODS: We recruited 300 adults (249 females) from the general population who completed the Sensory Processing 3-Dimensions Scale (SP-3D) first at baseline, and again following randomisation to either 1 month's supplementation with 100 mg Vitamin-B6, or one of two control conditions (1000 µg Vitamin-B12 or placebo). To focus on individuals who experience SOR, we analysed the effects of supplementation only on individuals with high baseline SOR scores (above the 87th percentile). RESULTS: In individuals with SOR at baseline, Vitamin-B6 selectively reduced SOR compared to both placebo and Vitamin-B12. We also found that Vitamin-B6 selectively reduced postural disorder in individuals with high scores on this subscale at baseline, but there were no effects on the four remaining SP-3D subscales. CONCLUSIONS: Clinical trials and mechanistic studies should now be conducted in autism, attention deficit hyperactivity disorder and other groups with SOR.
RESUMEN
OBJECTIVE: Vitamins B6 and B12 are involved in metabolic processes that decrease neural excitation and increase inhibition. This double-blind study investigated the effects of supplementation for 1 month with a high-dose of B6 or B12, compared to placebo, on a range of behavioural outcome measures connected to the balance between neural inhibition and excitation. METHODS: 478 young adults were recruited over five linked phases. Self-reported anxiety (N = 265) and depression (N = 146) were assessed at baseline and after supplementation. Several sensory measures acted as assays of inhibitory function and were assessed post-supplementation only; these were surround suppression of visual contrast detection (N = 307), binocular rivalry reversal rate (N = 172), and a battery of tactile sensitivity tests (N = 180). RESULTS: Vitamin B6 supplementation reduced self-reported anxiety and induced a trend towards reduced depression, as well as increased surround suppression of visual contrast detection, but did not reliably influence the other outcome measures. Vitamin B12 supplementation produced trends towards changes in anxiety and visual processing. CONCLUSIONS: Our results suggest that high-dose Vitamin B6 supplementation increases inhibitory GABAergic neural influences, which is consistent with its known role in the synthesis of GABA.