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High-dose Vitamin-B6 reduces sensory over-responsivity
Rebekah O Cracknell1, Teresa Tavassoli1, David T Field1
1School of Psychology and Clinical Language Sciences, The University of Reading, Reading, Berkshire, UK.
High-dose Vitamin-B6 supplementation effectively reduced sensory over-responsivity (SOR) and postural disorder in adults. This suggests Vitamin-B6 may be a viable intervention for individuals experiencing sensory processing challenges.
Area of Science:
- Neuroscience
- Human Physiology
- Nutritional Science
Background:
- Sensory reactivity differences affect 5-15% of the population, often manifesting as sensory over-responsivity (SOR).
- SOR involves experiencing sensory stimuli intensely, impacting daily functioning.
- A potential cause of SOR is an imbalance between neural excitation and inhibition, with weakened inhibitory influences.
Purpose of the Study:
- To determine if high-dose Vitamin-B6 supplementation can reduce sensory over-responsivity (SOR) and other sensory reactivity aspects.
- To investigate the efficacy of Vitamin-B6 in modulating neural pathways involved in sensory processing.
Main Methods:
- 300 adults completed the Sensory Processing 3-Dimensions Scale (SP-3D) at baseline and after 1 month of supplementation.
- Participants were randomized to receive 100 mg Vitamin-B6, 1000 µg Vitamin-B12, or placebo.
- Analysis focused on individuals with high baseline SOR scores (above the 87th percentile).
Main Results:
- Vitamin-B6 selectively reduced SOR compared to placebo and Vitamin-B12 in individuals with baseline SOR.
- Vitamin-B6 also selectively reduced postural disorder in those with high baseline scores for this subscale.
- No significant effects were observed on the remaining four SP-3D subscales.
Conclusions:
- High-dose Vitamin-B6 shows promise in reducing sensory over-responsivity and postural disorder.
- Further clinical trials and mechanistic studies are warranted in populations with SOR, such as autism and ADHD.
- Vitamin-B6's role as a coenzyme in GABA synthesis suggests a potential neurobiological mechanism for its effects.
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