The Effect of Vitamin D Supplementation in Patients with Acute Traumatic Brain Injury
World Neurosurgery, online 20 March 2019, https://doi.org/10.1016/j.wneu.2019.02.244
This study used just a small injection of Vitamin D
Suspect they injected regular vitamin D into muscle or fat tissue
Expect faster response from injecting semiactivated or fully activated Vitamin D into the blood
100,000 IU of Vitamin D will raise the blood level a little bit
Loading doses of 400,000 and 600,000 IU of Vitamin D have been used >1 million times
By the way - I take 100,000 IU of vitamin D every 4 days (founder of VitaminDWiki May 2019)
- Mild Traumatic Brain Injury reduced by Vitamin D – May 2014
- Vitamin D aided progesterone in reducing traumatic brain injury – RCT Dec 2012
- Mild Traumatic Brain Injury prevented with Omega-3, Resveratrol, etc (in rats) – Oct 2017
- Football Brain injuries prevented by Omega-3 – RCT Jan 2016
- Magnesium may be an important way to treat brain trauma
- Vitamin D and Glutamine reduced Trauma Center deaths by half – Matthews March 2017
- Vitamin D, trauma, and blacks - Dr. Matthews interview with transcript - Jan 2019
- Vitamin D3 Attenuates Blood-Brain Barrier Disruption due to TBI (in rats) – Feb 2021
TBI appears to be prevented and/or treated by getting more vitamin D in the brain
Each of the following help, some combination should be really good
- Progesterone (VDR)
- Omega-3 (VDR)
- Resveratrol (VDR)
- Magnesium (VDR and blood)
- Vitamin D
Wonder which additonal VDR activators might also prevent/treat TBI
Vitamin D Receptor table shows what compensates for low VDR activation
Compensate for poor VDR by increasing one or more:
Increasing | Increases |
1) Vitamin D supplement Sun Ultraviolet -B | Vitamin D in the blood and thus in the cells |
2) Magnesium | Vitamin D in the blood AND in the cells |
3) Omega-3 | Vitamin D in the cells |
4) Resveratrol | Vitamin D Receptor |
5) Intense exercise | Vitamin D Receptor |
6) Get prescription for VDR activator paricalcitol, maxacalcitol? | Vitamin D Receptor |
7) Quercetin (flavonoid) | Vitamin D Receptor |
8) Zinc is in the VDR | Vitamin D Receptor |
9) Boron | Vitamin D Receptor ?, etc |
10) Essential oils e.g. ginger, curcumin | Vitamin D Receptor |
11) Progesterone | Vitamin D Receptor |
12) Infrequent high concentration Vitamin D Increases the concentration gradient | Vitamin D Receptor |
13) Sulfroaphane and perhaps sulfur | Vitamin D Receptor |
14) Butyrate especially gut | Vitamin D Receptor |
15) Berberine | Vitamin D Receptor |
Note: If you are not feeling enough benefit from Vitamin D, you might try increasing VDR activation. You might feel the benefit within days of adding one or more of the above
The risk of 40 diseases at least double with poor Vitamin D Receptor as of July 2019
Trauma and surgery category starts with the following
Trauma and Surgery category hasLarge dose Vitamin D before surgery was found to help by 35 studies
Vitamin D is needed before most surgeries – many studies and RCTs
4.8 X more likely to die within 28 days of ICU if low Vitamin D - Jan 2024
Sepsis is both prevented and treated by Vitamin D - many studies
Thyroidectomy and Vitamin D - many studies
Orthopaedic surgeries need Vitamin D – many studies
Cancer - After diagnosis chemotherapy
TBI OR "Traumatic Brain Injury - 21 in title as of Sept 2022
Superbug (Clostridium difficile) Infections strongly associated with low vitamin D - many studies
Glutamine and Omega-3 have also been proven to help several traumas/surgeries
Note: Vitamin D also prevents the need for various surgeries and Omega-3 prevents many concussions/TBI
Trauma and Surgery is associated with 22 other VitaminDWiki categories
Such as loading dose 33, Mortality 23, Infant-Child 21 Intervention 19 Cardiovascular 13, Injection 13 in Sept 2022
 Download the PDF Sci-Hub via VitaminDWiki
Objective: To investigate the acute and long-term effects of vitamin D supplementation on the recovery of patients with traumatic brain injury (TBI).
Methods
A retrospective study was conducted involving 345 patients with TBI who visited a single trauma center. Vitamin D serum levels were measured without supplementation at admission, 1 month, and 3 months post-TBI (control group) from August to December 2016. From January 2017, vitamin D supplementation was provided to patients with TBI with low vitamin D serum levels at admission (supplement group). The outcomes were investigated by assessing performance function (Extended Glasgow Outcome Scale) and cognitive function (Mini-Mental Status Examination, and Clinical Dementia Rating) at 1 week and 3 months post-TBI.
Results
The mean vitamin D serum level in patients with TBI at admission was 13.62 ± 9.01 ng/mL. The level significantly increased from 14.03 ± 8.68 ng/mL at admission to 37.42 ± 12.57 ng/mL at 3 months post TBI in the supplement group (P < 0.001). The cognitive outcomes (Mini-Mental Status Examination/Clinical Dementia Rating, P = 0.042/P = 0.044) and GOS-E score (total TBI, P = 0.003; mild-to-moderate TBI, P = 0.002) significantly improved from the first week to 3 months post TBI in the patients with vitamin D supplementation.
Conclusions
Administration of vitamin D supplements in mild-to-moderate TBI patients with significant vitamin D deficiency during the acute phase of the injury may improve long-term performance and cognitive outcomes. Therefore, the treatment strategies should be individually planned for the patients with TBI based on their baseline vitamin D level.
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