Vitamin D deficiency is common in patients after TBI and associated with impaired cognitive function and more severe depressive symptoms. 1
Studies have shown that some patients with a traumatic brain injury have hormone deficiencies related to damage to the pituitary gland. Schnieders and her colleagues wanted to find out whether this, as well as other factors like vitamin D deficiency, might explain the fatigue commonly seen after traumatic brain injury. 2
Vitamin D minimizes inflammatory pathways in the brain, regulates oxidative damage through enhancing glutathione production, and inhibits the uptake of reactive oxygen species into nerve cells. Vitamin D also minimizes excitotoxicity, the brain state where too much glutamate triggers an over-abundance of nerve activity. Vitamin D get synthesized directly in the brain. Specific areas of the brain have large amounts of Vitamin D receptors, such as regions of the hippocampus (involved in memory and information recall). Vitamin D inhibits the production of inflammatory compounds in the body, such as pro-inflammatory cytokines and NFkB. This becomes quite important for people recovering from traumatic brain injuries. Chronic inflammatory processes in the brain following trauma, are the driving force behind many of the post-concussion symptoms people experience. In order to heal the brain, reducing inflammation is essential. Through inhibiting the pro-inflammatory cytokine and NFkB pathways, vitamin D, does exactly that. Vitamin D decreases the excitotoxicity of glutamate and blocks the uptake of reactive oxygen species into nerve cells. These are two of the distinct pathological processes that occur following traumatic brain injury, suggesting that Vitamin D can play an important role in protecting the brain after trauma. Researches also believe Vitamin D may be neuroprotective against seizures, Parkinson’s disease, and multiple sclerosis. It has been shown to have a beneficial effect on dopamine and serotonin pathways in the brain as well. Vitamin D also plays an important role in mood, energy levels, and the immune system. 3
Vitamin D ameliorates brain damage by modulating neuroinflammation, improving cell survival and down-regulating mechanisms involved in the progression of cell damage following a TBI. However, further studies are needed to evaluate the effects of vitamin D optimization in TBI outcomes. A small recent retrospective study underlined that vitamin D levels lower than 16ng/mL were prevalent in patients with a history of TBI, and showed a substantial negative association with cognitive test results, regardless of the severity or time since the injury. Those same 25OHD3 levels were inversely proportionate to the scores of the depression inventory. Overall levels were significantly lower than the general population with 80.2% testing <26ng/mL, of which 46.5% were at less than 16ng/mL. These suggest that lower levels are more prevalent among post-TBI patients (Jamall et al., 2016). As many as 20% of patients with a mild TBI will go on to experience chronic symptoms related to postconcussive syndrome (Curtis & Epstein, 2014), other estimates are as high as 30% (Vakhtin et al., 2013).
The TES taskforce established the threshold for deficiency at 20ng/mL
or 50nmol/L, aligning with the IOM parameter. However, they also defined the range between 21-29 ng/mL as insufficiency, and determined the sufficiency range to be at of 30-100 ng/mL. The insufficiency range was set just below the demonstrated ideal threshold in which parathyroid hormone levels and adequate intestinal calcium absorption are believed to be optimally balanced. Correction of serum vitamin D levels, improve calcium balance and can prevent or correct secondary hyperparathyroidism (Holick, 2006; Holick, 2007; Holick et al., 2011; Looker et al., 2002).
Low levels of 25OHD3 in patients suffering from headaches who were also diagnosed
with a sleep disorder and the discovery of high presence of VDR in regions of the hypothalamus and brainstem known to regulate sleep, led researchers to hypothesize that vitamin D could 50 possibly influence sleep patterns. Studies have found that fatigue and sleep disorders are prevalent following a TBI (Chauhan, 2014; Jamall et al., 2016; VA/DoD, 2016). A recent cohort study of TBI patients with complaints of chronic fatigue, found that vitamin D levels <20ng/mL was the number one factor shared by 65% of the cohort, when compared to poor sleep (544%), anxiety (36%), inadequate levels of growth hormone (16%) and gonads hormonal deficiencies (9%). It is worth noting that 26.6% of the remaining was considered to have insufficiency with 25OHD3 levels <30ng/mL, thus nearly 92% was bellow 30ng/mL. The incidence and severity of chronic fatigue, sleep
problems, attention and cognitive deficits after TBI are strongly and intricately related
(Schnieders, Willemsen, & de Boer, 2012) and improvements in post-TBI sleep disturbances showed significant decrease of other neuropsychological impairments related to TBI (Chauhan, 2014). 4
Vitamin D is a fat-soluble, hormone-like vitamin, which means body fat acts as a “sink” by collecting it. If you’re overweight or obese, you’re therefore likely going to need more vitamin D than a slimmer person — and the same holds true for people with higher body weights due to muscle mass. Vitamin D is a fat-soluble, hormone-like vitamin, and many therefore believe that if you’re obese you need more of it because body fat acts as a “sink” by collecting it. However, muscle and fat may well act the same when it comes to storing vitamin D for future use. New research using mathematical models has shown that a heavily muscled man and an obese man who weigh exactly the same would need the same amount of vitamin D. The key to determining how much vitamin D is appropriate for an individual appears to be body weight rather than body fat. This was not previously widely appreciated by most experts. 5
Vitamin D deficiency may be seen as symptoms such as a lack of appetite, insomnia, and vision problems. Most people living in the upper third of the US are deficient due to lack of sun exposure in the winter. Some cholesterol-lowering drugs, antacids, and steroid hormones (like cortisone) interfere with Vitamin D absorption. 6
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