Posts Tagged vitamin D

[NEWS] Vitamin D Deficiency Linked to Loss in Brain Plasticity

Feb 21, 2019 | Original Press Release from the University of Queensland

Vitamin D Deficiency Linked to Loss in Brain Plasticity

Perineuronal nets (bright green) surround particular neurons (blue). Fluorescence labelling reveals just how detailed these structures are. Credit: Phoebe Mayne, UQ

University of Queensland research may explain why vitamin D is vital for brain health, and how deficiency leads to disorders including depression and schizophrenia.

 

via Vitamin D Deficiency Linked to Loss in Brain Plasticity | Technology Networks

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[WEB SITE] Beginner’s Guide to Light Therapy for Brain Injury

February 5, 2018

Beginner’s Guide to Light Therapy for Brain Injury

In its most general sense light therapy refers to the use of light, typically red or near-infrared light, to stimulate and heal injured tissue. One of the major mechanisms by which light therapy is thought to work is by improving the mitochondrial function of compromised cells. The improved mitochondrial function leads to an increase in ATP production, providing the energy needed for the cells to heal [1]. Research supporting the use of light therapy for a number of disorders, including those of the brain, has been overwhelmingly good.

Related: 5 Ways Light Therapy Heals the Brain

Sources of Light Therapy

Sunlight

Sunlight was used long before the invention of antibiotics to speed healing of wounds, treat skin diseases, and even fight infections. Physicians in ancient Greece would often prescribe sunbathing to promote good health and vitality. Today, we have shifted our focus from the benefits of sun exposure to the hazards. How could this outlook be affecting our brains?

Sunlight is the main source of vitamin D for most people. Due to a lack of adequate exposure to the sun, vitamin D deficiency is now recognized as a worldwide pandemic [2]. Over 1,000 different genes in the body are regulated by vitamin D [3]. A study investigating vitamin D and brain development found that it stimulates the production of neurotransmitters and improves synaptic density [4].

Other studies have linked lower levels of sunlight to cognitive impairment [5].

Finally, sunlight influences our circadian rhythm by impacting melatonin and serotonin levels in the blood. Exposure to sunlight in the morning boosts melatonin production at night translating to faster sleep onset. High serotonin levels from adequate sun exposure result in a more positive mood and a calm, focused metal state [3].

Light Emitting Diode (LED)

LED therapy is noninvasive, painless, and non-thermal. It has been cleared by the United States FDA as an insignificant risk device [1]. Compared to lasers, LEDs are inexpensive, easy to obtain for at home use, and vary widely in size making it easier to treat larger areas of the body. Though there isn’t a lot of research available for LEDs as a treatment for the brain, the existing research has been encouraging.

In one case study two subjects with traumatic brain injury applied an LED array to their foreheads. After eight weeks of LED treatments, subject 1’s ability to concentrate on a task increased from 20 minutes to 3 hours. She also reported better memory when reading, improved math skills, and decreased sensitivity of her scalp. When the study began, subject 1 was seven years post injury.  Subject 2 had been on medical disability for 5 months prior to treatment, but after 4 months of LED treatments she was able to return to work. Additionally, neuropsychological testing showed a significant improvement in her memory and executive functioning [6].

A similar study was performed on eleven subjects to determine if LED therapy could improve cognition in patients with mild traumatic brain injury. The subjects ranged from 10 months to 8 years post-TBI. The subjects’ cognitive performance levels were tested periodically and a significant positive trend was observed for cognitive performance and LED treatment over time. Additionally subjects reported improved sleep, fewer PTSD symptoms, and enhanced ability to perform social functions [1].

Cold Lasers

Cold laser therapy is also known as low-level laser therapy (LLLT) or photobiomodulation. Lasers differ from LEDs in that lasers are a coherent source of light. Coherent light means that all the light waves travel perfectly together in a single beam. LED light, like sunlight, is incoherent meaning each light wave can travel in a different direction than the other light waves. As a result, lasers are much more concentrated and powerful than LEDs. Here’s what the research says:

A case study involving a subject who suffered a brainstem stroke two years before beginning LLLT showed dramatic improvements after eight weeks of light therapy. Her mood and memory improved. Her double vision was eliminated. Her muscle spasticity decreased, she gained increased function in her left and right hands, and her arm and leg strength increased [7].

In animal models with spinal cord injury, LLLT has been shown to increase total axon number and average length of axonal regrowth [8][9].

A patient with a moderate TBI showed favorable results after receiving laser treatments for two months. After receiving the treatments he showed decreased depression, insomnia, anxiety, and headaches, while cognition and quality of life improved [10].

Additionally LLLT has shown promising results as a treatment for chronic pain [11].

What are the Risks?

Light therapy is generally safe, but there have been some minor side effects reported. The most common side effects include eyestrain, headaches, and nausea. Side effects are usually relieved by decreasing the amount of time exposed to the light.

Because coherent light is so powerful, there is potential that it could damage your retina if you look directly into the laser beam. To protect your eyes, you should always wear protective goggles when working with a cold laser. Eye damage is not a concern when working with LEDs, since they are a non-coherent light source.

I would recommend consulting your chiropractor or physician before starting a light therapy routine. They will be able to help you determine the best locations and length of exposure for optimum results.

Purchasing a Light Therapy Device

LED arrays are easy to obtain and fairly cheap. I would recommend buying an array that has both red (600-700nm) and near infrared light (760-940nm) to get a wider range of benefits. The one my family uses is the DPL FlexPad*.  There are many to choose from so you may want to do some research and choose the one that works best for you.

Getting a cold laser is a little more complicated and the restrictions on who can own one vary from state to state. Because they are so expensive (expect to pay $5,000+) I would suggest not buying one and getting treatments from your chiropractor instead. In my experience cold laser treatments are more reasonably priced, ranging from $30 -$60 per session.

Where can I find more Information?

I would highly recommend reading Norman Doidge’s book The Brain’s Way of Healing*, even if you aren’t interested in light therapy. For light therapy, I would suggest you start with chapter seven (the chapters can be read independently so you can go back and read the earlier ones later).

Michael Hamblin is another great resource. You can search him on YouTube and find several interviews where he discusses light therapy. In addition, here is a fairly comprehensive literature review he wrote addressing light therapy and the brain.

See my other post on this topic: 5 Ways Light Therapy Heals the Brain.

You may also be interested in reading: 

PoNS Device – The Key to Neuroplastic Healing 

Restoring Sleep-Wake Cycle after Brain Injury

 

via Beginner’s Guide to Light Therapy for Brain Injury – How To Brain

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[WEB SITE] The effects of vitamin D on epilepsy

Student NT editor Rebecca Hammond says we should be mindful of the importance of vitamin D.
rebecca hammond close up 1
“Where has the sun gone?” and “Will we have a good summer?” are questions I and others living in Scotland have often asked ourselves.

 

Growing up, I always remembered vitamin D as being the ’sunshine vitamin’. However, since starting my nursing training, I have been interested in researching the importance and health benefits of vitamin D.

In the UK, we are encouraged to eat a healthy, balanced diet. This provides all needed nutrients excluding vitamin D. Oily fish has been identified as a significant source, whereas meat, egg yolks and other fortified foods, including margarine and some breakfast cereals, provide smaller amounts.

The prevalence of vitamin D deficiency in the UK is significant: during the winter, 30-40% of people in the general population and belonging to all age groups are vitamin D deficient. Near the end of the summer months, 13% of adolescents and 8% of adults are vitamin D deficient.

The intake of vitamin D and its status are imperative for overall health and wellbeing, as well as for bone and calcium-phosphate metabolism.

Without adequate vitamin D, bones may become brittle, thin or misshapenLiterature suggests that sufficient vitamin D status is protective against autoimmune diseases, cardiovascular disease, musculoskeletal disorders, neurocognitive dysfunction and respiratory infections.

Compared to the general population, individuals with learning disabilities have an increased risk of developing low bone mineral density, osteopenia, osteoporosis and fractures. This is mainly attributed to the higher prevalence of obesity or undernutrition, inactive lifestyles and polypharmacy.

Epilepsy is the most common neurological condition within the learning disability population. One in four people with a learning disability experience epilepsy, compared to one in five in the general population.

”The identified prevalence of vitamin D deficiencies among epilepsy patients is high”

Approximately, 30% of individuals with learning disabilities are prescribed anti-epileptic drugs (AEDs), an identified risk factor for fractures and low bone-mass density. Reasons for this have not been definitively known, but it could potentially be due to AEDs breaking down the body’s vitamin D stores at a higher degree than normal.

Consequently, this could result in AEDs causing a vitamin D deficiency, which could potentially lead to osteoporosis and osteomalaica and an increased risk of fractures.

The identified prevalence of vitamin D deficiencies among epilepsy patients is high, however, the number of research studies assessing the effect of vitamin D on seizure control is limited.

One of these research studies, conducted in 2012, measured vitamin D levels and through the administration of vitamin D3, normalised levels in 13 patients with pharmacoresistant epilepsy.

To identify whether vitamin D3 was impactful on seizure frequency, the study compared numbers of seizures during a 90-day period, prior and following treatment commencement. The study found the median seizure reduction to be 40% and concluded that normalisation of vitamin D levels can have an anticonvulsant effect.

Due to very little evidence on the effect of vitamin D on epilepsy, it is acknowledged that this area needs researched further. However, as nurses this is something we could be mindful of.

 

via The effects of vitamin D on epilepsy | Opinion | Nursing Times

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[ARTICLE] Vitamin D for the Treatment of Epilepsy: Basic Mechanisms, Animal Models and Clinical Trials – Full Text

There is increasing evidence supporting dietary and alternative therapies for epilepsy, including the ketogenic diet, modified Atkins diet, and omega-3 fatty acids. Vitamin D is actively under investigation as a potential intervention for epilepsy. Vitamin D is fat soluble steroid which shows promise in animal models of epilepsy. Basic research has shed light on the possible mechanisms by which Vitamin D may reduce seizures, and animal data support the efficacy of Vitamin D in rat and mouse models of epilepsy. Very little clinical data exists to support the treatment of human epilepsy with Vitamin D, but positive findings from preliminary clinical trials warrant larger Phase I and II clinical trials in order to more rigorously determine the potential therapeutic value of Vitamin D as a treatment for human epilepsy.

Introduction

Epilepsy affects approximately two million Americans and 65 million people worldwide (1). Among those with epilepsy, 22–30% have drug-resistant epilepsy (DRE) (1, 2). DRE causes cognitive and mood impairment, injuries, and increased risk of death including sudden death in epilepsy (SUDEP) (13). Antiepileptic drugs (AEDs) are the primary medical treatment for epilepsy. However, even for those whose seizures are well controlled by AEDs, allergies, neurological and systemic toxicity, depression, memory loss, and osteoporosis are common problems (4, 5). Because of the limitations and potential toxicity of existing AEDs, there is significant clinical interest in finding alternative therapies for epilepsy.

In the search for alternative epilepsy treatments, Vitamin D3 is an intriguing candidate (6). As early as 1974, Christiansen postulated that supplementation of Vitamin D might improve calcium and magnesium levels and may decrease hyperexcitability in patients with epilepsy. In the four decades since, progress has been made in understanding the biochemical and cellular mechanisms of Vitamin D3’s anticonvulsant properties. Animal data have supported the anticonvulsant effects of Vitamin D3 in mice and rats (711). Existing evidence for the use of Vitamin D3 in treating human epilepsy is very limited (6, 12). There is a critical need for larger clinical trials to establish the safety and efficacy of vitamin D3 in epilepsy. In this review, we will critically analyze the animal and human evidence to date supporting the use of Vitamin D3 as a treatment for epilepsy.

Vitamin D3 Overview: Biochemistry and Role in Human Health

The most biologically active form of Vitamin D in humans is Vitamin D3 (cholecalciferol), which is a fat-soluble steroid hormone (13). Dietary sources of Vitamin D3 include dairy, meat, fish, and mushrooms (14). The primary source of Vitamin D3 is exposure of the skin to ultraviolet sunlight (14). The metabolic pathway of Vitamin D3 is summarized in Figure 1. 7-dehydrocholesterol is converted to Vitamin D3 in the skin after exposure to sunlight. Vitamin D3 is converted to 25-hydroxy-cholecalciferol (25-OH Vitamin D3) in the liver. 25-OH Vitamin D3 is the major circulating form of Vitamin D, but it itself is biologically inactive and must be converted to the active form 1,25-dihydroxy-Vitamin D3 (1,25 Vitamin D3) in the kidneys (1315). Vitamin D3 is important for calcium metabolism, bone health, cardiac function, and blood pressure maintenance, among other health benefits (14, 16, 17). Vitamin D3 deficiency is a marker of poor health and overall mortality (16). However, 40–50% of Americans have insufficient Vitamin D3 levels, and insufficiency is even more prevalent in underserved populations, including Hispanics (69%) and African Americans (82%) (18).

Figure 1. Vitamin D metabolism.

Continue —> Frontiers | Vitamin D for the Treatment of Epilepsy: Basic Mechanisms, Animal Models and Clinical Trials | Epilepsy

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[WEB SITE] Vitamin D deficiency associated with chronic fatigue in brain injured patients.  

New evidence presented at the European Congress of Endocrinology has shown that vitamin D deficiency is closely associated with the chronic fatigue that often follows post traumatic brain injury (TBI).

TBI is a major cause of death and disability worldwide. In the European Union the annual incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000 people. This means that on average a large European state such as the UK, France or Germany, will have around 140,000 new traumatic brain injuries every year (national figures vary). Around two-thirds of post TBI patients go on to suffer chronic fatigue. Now a group of researchers in the Netherlands have linked vitamin D deficiency to chronic fatigue in post-TBI sufferers.

The group, led by Dr Jessica Schnieders from Rijnstate Hospital in Arnham, The Netherlands, looked at vitamin D and hormone levels in 90 fatigued and non-fatigued subjects. They also systematically evaluated pituitary hormones and factors such as sleep, attention, emotional well-being, quality of life, coping style, and daily activity. They found that 51% of TBI patients were severely fatigued 10 years after the trauma. Vitamin D deficiency was present in 65% of post TBI patients and significantly related with fatigue (P<0.05), with patients who suffered from fatigue more likely to be vitamin D deficient. The group also found a higher incidence of growth hormone and sex hormone deficiency in the fatigued group, but they found no evidence that these deficiencies contributed to the fatigue.

This work opens the possibility that correcting the vitamin D deficiency might help to reduce some of the chronic fatigue in TBI patients. However, as vitamin D levels in the body are affected by diet and time spent in the sunshine, further studies are now needed to confirm whether low vitamin D levels are a cause of the fatigue or whether they are a consequence of altered lifestyle led due to suffering from fatigue.

Lead researcher, Dr Jessica Schnieders said: “In the Netherlands we have 30,000 people every year who suffer a traumatic brain injury and many of these go on to suffer from chronic fatigue. This is early work, so we need to confirm that vitamin D is the cause of this fatigue, and if so to see if taking vitamin D, perhaps coupled with improved sleep patterns, can alleviate some of the symptoms.

“We looked at patients around 10 years after their trauma. Fatigued post traumatic brain injury patients are less active, and generally experience a reduced quality of life. They have difficulties in maintaining relationships and keeping jobs, and are less independent than people who have not had to cope with such trauma.”


Story Source:

The above post is reprinted from materials provided by European Society of Endocrinology. Note: Materials may be edited for content and length.

Source: Vitamin D deficiency associated with chronic fatigue in brain injured patients — ScienceDaily

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[WEB SITE] Omega-3 Fatty Acids and Vitamin D May Control Brain Serotonin, Affecting Behavior and Psychiatric Disorders

Although essential marine omega-3 fatty acids and vitamin D have been shown to improve cognitive function and behavior in the context of certain brain disorders, the underlying mechanism has been unclear.

In a new paper published in FASEB Journal* by Rhonda Patrick, PhD and Bruce Ames, PhD of Children’s Hospital Oakland Research Institute (CHORI), serotonin is explained as the possible missing link tying together why vitamin D and marine omega-3 fatty acids might ameliorate the symptoms associated with a broad array of brain disorders.

In a previous paper published last year, authors Patrick and Ames discussed the implications of their finding that vitamin D regulates the conversion of the essential amino acid tryptophan into serotonin, and how this may influence the development of autism, particularly in developing children with poor vitamin D status.

Here they discuss the relevance of these micronutrients for neuropsychiatric illness. Serotonin affects a wide-range of cognitive functions and behaviors including mood, decision-making, social behavior, impulsive behavior, and even plays a role in social decision-making by keeping in check aggressive social responses or impulsive behavior.

Many clinical disorders, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, and depression share as a unifying attribute low brain serotonin. “In this paper we explain how serotonin is a critical modulator of executive function, impulse control, sensory gating, and pro-social behavior,” says Dr. Patrick. “We link serotonin production and function to vitamin D and omega-3 fatty acids, suggesting one way these important micronutrients help the brain function and affect the way we behave.”

Eicosapentaenoic acid (EPA) increases serotonin release from presynaptic neurons by reducing inflammatory signaling molecules in the brain known as E2 series prostaglandins, which inhibit serotonin release and suggests how inflammation may negatively impact serotonin in the brain. EPA, however, is not the only omega-3 that plays a role in the serotonin pathway. Docosahexaenoic acid (DHA) also influences the action of various serotonin receptors by making them more accessible to serotonin by increasing cell membrane fluidity in postsynaptic neurons.

Their paper illuminates the mechanistic links that explain why low vitamin D, which is mostly produced by the skin when exposed to sun, and marine omega-3 deficiencies interacts with genetic pathways, such as the serotonin pathway, that are important for brain development, social cognition, and decision-making, and how these gene-micronutrient interactions may influence neuropsychiatric outcomes. “Vitamin D, which is converted to a steroid hormone that controls about 1,000 genes, many in the brain, is a major deficiency in the US and omega-3 fatty acid deficiencies are very common because people don’t eat enough fish,” said Dr. Ames.

This publication suggests that optimizing intakes of vitamin D, EPA, and DHA would optimize brain serotonin concentrations and function, possibly preventing and ameliorating some of the symptoms associated with these disorders without side effects

via Health News – Omega-3 Fatty Acids and Vitamin D May Control Brain Serotonin, Affecting Behavior and Psychiatric Disorders.

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[REVIEW] Medical Complications Post Stroke | EBRSR – Evidence-Based Review of Stroke Rehabilitation – Full Text PDF

Abstract

Medical issues post stroke are those which are within the domain of the doctor and the nurses, but are unrelated to secondary stroke prevention. Not only do these complications occur relatively frequently, but they have also been shown to contribute to poor outcome. As such, an understanding of these disorders is critically important to stroke care and management. Although the number of potential medical complications is extensive, this review will focus on five of the most common and clinically relevant: urinary incontinence, venous thromboembolism, seizures, osteoporosis and central pain states. Both short-term and long-term complications will be evaluated.

Get Full Text PDF

via Medical Complications Post Stroke | EBRSR – Evidence-Based Review of Stroke Rehabilitation.

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