Vitamin D rich foods to prevent seizures

Foods that provide vitamin D include:
  • Fatty fish, like tunamackerel, and salmon
  • Foods fortified with vitamin D, like some dairy productsorange juicesoy milk, and cereals
  • Beef liver
  • Cheese
  • Egg yolks

Our client has epilepsy and goes on seizure many times a month. She has poor appetite but loves walking especially during sunny days. She loves cheese. She is on many medications.

card mother

Some anti-seizure medications interfere with how vitamin D is processed in the body. Supplemental vitamin D may be necessary for people who have these risk factors to maintain normal blood levels. A study published in 2012 showed that correcting vitamin D deficiency reduced seizures in people with epilepsy.

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Epilepsy

Natural and Complementary Therapies

Many natural compounds also affect the brain and may be able to influence epilepsy; natural compounds will likely be most beneficial as adjuvants to conventional therapies.

Vitamins and Minerals

Epilepsy patients should also be aware that long-term use of anti-epileptic drugs (AEDs) can negatively affect their vitamin and mineral status. For instance, patients taking anti-epileptic drugs (AEDs) have significantly lower levels of vitamin D in their blood (Menon and Harinarayan 2010, Shellhaas and Joshi 2010, Pack 2004, Valsamis et al. 2006, Mintzer S et al 2006). This is because many AEDs increase the activity of a liver enzyme known as cytochrome P450, which also breaks down vitamin D. Vitamin D is essential for the absorption of calcium; consequently, patients taking AEDS absorb less calcium in their diet, which increases their risk of developing osteoporosis. Patients who are taking AEDs may need to take vitamin D and calcium supplements (Fong et al. 2011).

Anti-epileptic drugs have also been shown to reduce levels of several B vitamins, including folate and vitamins B6 and B12 (Sener et al. 2006Linnebank et al. 2011) These vitamins are critical for controlling metabolism in the body; low levels of these vitamins can also lead to low red blood cell levels, causing fatigue and pallor. One of the most serious consequences of the low folate levels caused by AEDs is high levels of the compound homocysteine, a risk factor for heart disease (Sener et al. 2006; Kurul et al 2007, Apeland et al 2001). Elevated levels of homocysteine have been implicated in the increased risk of heart disease seen in epileptics. Moreover, some studies have indicated that elevated homocysteine may contribute to AED resistance or increase seizures in epileptics (Diaz-Arrastia 2000). Based on these findings, some researchers call for routine supplementation with the B vitamins, especially the metabolically active form of folic acid, L-methylfolate, to reduce homocysteine levels (Morrell MJ 2002). Folate deficiencies can also lead to seizures, particularly in infants. Impaired folate transport in the body can be a cause of seizures that do not respond well to typical treatments (Djukic A 2007). In addition, epileptics often have reduced folic acid levels, possibly due to the use of AEDs (Asadi-Pooya 2005). Doctors of epileptics should routinely monitor folic acid, vitamin B12 and homocysteine levels in patients to help prevent an increased risk of cardiovascular disease that could otherwise be treated.

Some forms of epilepsy are directly linked to vitamin B6 deficiencies; these convulsions, known as pyridoxine-dependent seizures, can only be treated with high doses of vitamin B6 (Asadi-Pooya 2008). Low vitamin B6 levels are also associated with general epilepsy. Even in patients without pyridoxine-dependent seizures, low levels of pyridoxine might increase seizure sensitivity, although more research needs to be done to determine if pyridoxine can treat seizures (Gaby 2007). Some types of seizures cannot be treated with pyridoxine, but they can be effectively managed with pyridoxal-5-phosphate, the biologically active form of vitamin B6 (Tamura et al. 2000, Jiao et al. 1997, Wang et al. 2005).

Antioxidants, such as vitamin Evitamin C and selenium are able to mitigate mitochondrial oxidative stress in the brain and other tissues, lowering seizure frequency in various types of epilepsy (Tamai et al. 1988, Zaidi et al. 2004, Savaskan et al. 2003, Yamamoto et al. 2002, Ogunmekan et al. 1979, 1989 and 1985). Animal models have shown that alpha-tocopherol alone is able to prevent several types of seizures (Levy et al 1990; Levy et al 1992). Epileptics are also more likely to have low vitamin E levels, though this may be a result of taking anti-epileptic drugs (Higashi et al. 1980).

Magnesium helps maintain connections between neurons. It has been shown to suppress EEG activity and limit seizure severity in animal models, and magnesium deficiency is associated with seizures in humans (Oladipo 2007; Nuytten et al 1991, Borges et al. 1978). Within the body, ionic magnesium acts as a natural calcium channel blocker, offsetting the excitatory influence of ionic calcium in a manner similar to the calcium channel blocker class of conventional AEDs (Touyz 1991). Moreover, magnesium levels decline sharply following seizures in patients with idiopathic epilepsy (Gupta 1994). In fact, intravenous or intramuscular magnesium is often administered to women to safely prevent eclampsia, a pregnancy-associated disorder characterized by seizures (Bhattacharjee 2011).

A recently developed form of magnesium, known as magnesium-L-threonate, may be particularly effective in epilepsy and other neurological disorders. This form of magnesium appears to be better at penetrating the blood-brain barrier and thus is more efficiently delivered to brain cells (Slutsky et al. 2010, Abumaria et al. 2011). In fact, in an animal model, magnesium-L-threonate boosted magnesium levels in spinal fluid by an impressive 15% compared to virtually no increase with conventional magnesium. Moreover, oral magnesium-L-threonate was able to modulate learning and memory, indicating that it does indeed impact the central nervous system (Abumaria 2011).

Thiamine, manganese and biotin are often low in epileptics as well (Gaby 2007).

Melatonin plays an important role in the brain, particularly in regulating the brain’s sleep-wake cycle. It also exerts a calming effect at the neuronal level by reducing glutaminergic (excitatory) signaling and augmenting GABAergic (inhibitory) signaling (Banach et al. 2011). Melatonin is widely used as a sleep aid and to treat jet lag; the side effects of taking melatonin are mild and it is one of the most commonly used supplements in the United States. Animal models have shown that melatonin can be effective in reducing epileptic seizures (Lima et al. 2011, Costa-Latufo et al. 2002). Melatonin has also been beneficial in humans with epilepsy and is particularly effective in the treatment of cases of juvenile epilepsy that do not respond well to anti-epileptic drugs (AED’s) (Banach et al. 2011). Due to its widespread use and minimal side effects, melatonin has potential to improve control of epilepsy (Fauteck et al. 1999).

Polyunsaturated Fatty Acids (PUFAs), such as omega-3 fatty acids, are a type of essential fat that play an important role in maintaining central nervous system health. Animal studies have suggested that PUFAs, including omega-3 and some omega-6 fatty acids, may be able to modulate neuronal excitability (Blondeau et al. 2002, Taha et al. 2010). This is further supported by the fact that children on the ketogenic diet often have higher levels of PUFAs in their cerebrospinal fluid, which suggests that increased PUFA levels is one of the ways that the ketogenic diet prevents seizures (Xu et al. 2008, Auvin 2011). Clinical trials in adults have yielded mixed results. In one such study, 57 epileptic patients were given 1 g EPA and 0.7 g DHA daily. Seizure activity was reduced over the first six weeks, although the effect was temporary. The researchers called for more in-depth studies, with larger doses and larger observational groups (Yuen AW et al 2005). However, a randomized controlled trial did not find that fish oil reduced seizure frequency; although, the study did find, that PUFAs reduced seizures when administered in an open-label format, meaning when subjects knew that they were not receiving a placebo (Bromfeld et al. 2008). An ongoing National Institutes of Health-sponsored trial is examining the effects of fish oil on cardiac health in epileptics (ClinicalTrials.gov).

Life Extension suggests that the omega-6 to omega-3 ratio should be kept below 4 to 1 for optimal health. More information on testing and optimizing your omega-6 to omega-3 ratio can be found in the Life Extension Magazine article entitled “Optimize Your Omega-3 Status“.

Resveratrol, derived from red grapes and Japanese knotweed (Polygonum cuspidatum), and the plant Bacopa monnieri both appear to be promising in the management of seizure-related neurotoxicity. Resveratrol and bacopa-derived compounds have been extensively studied in experimental settings and consistently shown to guard against neuronal damage (Jyoti 2007; Hosamani 2009; Kanthasamy 2011; Chung 2011). In the context of epilepsy, numerous mechanisms by which resveratrol might prevent seizures have been proposed (Shetty 2011), and, indeed, in an animal model resveratrol prevented chemical-induced seizures (Wu 2009); though studies on epileptic humans have yet to be performed. Likewise, bacopa has been the subject of several animal model experiments, many of which have revealed a clear benefit relating to seizure frequency and post-seizure brain cell damage (Pandey 2010; Mathew 2010; Krishnakumar 2009). Nonetheless, bacopa also has yet to be studied in a controlled manner in a population of epileptic humans.

Phytocannabinoids (pCBs), which are compounds found in marijuana that closely resemble chemicals the body produces naturally called endocannabinoids, have shown great potential in the treatment of epilepsy. Phytocannabinoids can affect both the central and peripheral nervous system because neurons have receptors that respond directly to binding by cannabinoids. One of the major effects of pCBs is to reduce neuronal excitability by modulating electrical activity around synapses; as a result, these chemicals are sometimes referred to as potential “circuit breakers” for neurological disorders, including epilepsy (Wallace et al. 2003, Katona and Freund 2008). Therefore, researchers have been studying the effects of tetrahydrocannabinol (THC) and other phytocannabinoids on the brain to try to develop new mechanisms for treating epilepsy (Hoffman and Frazier 2011, Hill et al 2012). One small clinical trial found that the phytocannabinoid, cannabidiol, did reduce seizures in epileptics who were already taking AEDs (Cunha et al 1980). Another study that was largely based on epidemiology found an association between marijuana use and decreased risk of seizure (Ng et al 1990). Moreover, it has been reported that patients treated for epilepsy subjectively feel that marijuana use helps eases their epilepsy (Gross et al 2004). More research is needed to determine the efficacy and safety of natural and synthetic cannabinoids for the treatment of seizures. A comprehensive review of studies examining the effects of cannabinoids on seizure frequency in humans is currently being carried out by the Cochrane Epilepsy Group (Gloss and Vickrey 2011). Marijuana is illegal except as a prescribed treatment for medical problems in certain states; Life Extension does not recommend consuming illegal drugs as a treatment for epilepsy. However, the benefits of these phytocannabinoids do suggest that marijuana-derived compounds may soon become an accepted form of therapy for epilepsy and other neurological disorders.

Lifestyle Modifications

Seizure Interruptions. Although auras do not occur in all individuals with seizure disorders, some people are aware of a change in their sensory perception (whether auditory, olfactory, sensory, visual, or gustatory, sometimes involving malaise, vertigo, or the sense of deja vu) that signals the onset of a seizure. Anecdotal reports indicate that some people have learned to interrupt their seizure process by replacing the aura-induced perception with another. In these individuals, the aura is a known signal of seizure onset. For example, if the aura is a smell or unpleasant odor, these individuals can often interrupt the seizure by immediately smelling something else (in general, something with a more pleasing smell than the aura).

Some people are able to take the interruption technique a step further. By simply relying on mental imagery (e.g., remembering a pleasant, positive smell), they can arrest a seizure. Some find that anger can effectively interrupt a seizure; they are able to arrest their seizures by yelling at them. Other individuals who have seizures with an observable onset pattern enlist a support person to shout at them or give them a quick shake when the pattern commences. The techniques that successfully “interrupt” an aura vary from patient to patient and must be performed at a specific time to stop the seizure (Wolf 1994). However, the use of aura interruption may be able to help reduce or eliminate seizures (Elsas et al. 2011).

Stress Reduction Getting a good night’s sleep on a regular basis is a very important component of seizure prevention. Some scientists hypothesize that one major function of REM sleep is to reduce the brain’s susceptibility to epileptogenic influences (Jaseja H 2004). Stress reduction and relaxation techniques such as meditation may also aid in reducing seizures (Swinehart 2008).

Physical exercise can also be an important way to relieve stress that may be particularly beneficial for epileptics. Not only can exercise reduce stress, improve social integration and improve quality of life, regular physical exercise may directly help reduce seizure frequency (Arida et al. 2010). Physical exercise may “desensitize” neurons to emotional stress, helping avert seizures brought on by other triggers (Arida et al. 2009).

Biofeedback, another relaxation technique, can also be helpful. When the autonomic nervous system (or the involuntary nervous system) is in a state of overarousal, the likelihood of seizure activity can increase. Biofeedback is a technique that uses displays of some form of biological monitoring, such as an EEG, to help patients identify how their body responds to certain situations. By observing changes in EEG readings, patients are able to learn how to partially control the electrical activity in their brains and can develop the ability to reduce their risk of having seizures. Although most clinical trials involving biofeedback have been small (Tozzo CA et al 1988; Andrews DJ et al 1992; Ramaratnam S et al 2001), a comprehensive review of many studies found that biofeedback can provide significant relief for epileptics, particularly those that have not had success with anti-epileptic drugs (AEDs) (Tan et al. 2009). On average, almost 75 percent of people who try EEG biofeedback for epilepsy will experience fewer seizures. Biofeedback using other biologic responses, such as slow cortical potential feedback and galvanic skin response has also been promising (Nagai 2011).

Other behavioral interventions may reduce seizure frequency as well. Yoga can improve quality of life and result in fewer seizures (Lundgren et al. 2008, Khan et al. 2010) Acupuncture may also be helpful in seizure prevention. A thorough review of published trials found that acupuncture may be beneficial, but that more and better designed studies need to be done (Cheuk 2008). Studies of the benefits of other relaxation techniques and cognitive behavioral therapy have also found a possible benefit (Ramaratnam 2004).


Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the treatments discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. The publisher has not performed independent verification of the data contained herein, and expressly disclaim responsibility for any error in literature.

VITAMINS suggested by our Neurologist… | Epilepsy Foundation

 

 

I have now been using vitamin B6 to control my seizures for over 38 years. My seizure medication now consists of B vitamins only. In over 38 years I have never …

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https://www.drweil.com › Health & Wellness › Balanced Living › Healthy Living

 

I have been told that vitamin B6 has been used to help patients with seizures. Is this true, and if so what dose do you recommend? – September 22, 2009.

 

 

Alzheimer clues

Vagus Nerve Stimulation Boosts Post-Stroke Motor Skill Recovery

Vagus Nerve Stimulation Boosts Post-Stroke Motor Skill Recovery

Summary: Vagus nerve stimulation coupled with physical therapy following a stroke can significantly help to boost motor skill recovery, researchers report.

Source: University of Texas at Dallas.

Researchers at The University of Texas at Dallas have demonstrated a method to accelerate motor skill recovery after a stroke by helping the brain reorganize itself more quickly.

In a preclinical study, the scientists paired vagus nerve stimulation (VNS) with a physical therapy task aimed at improving the function of an upper limb in rodents. The results showed a doubled long-term recovery rate relative to current therapy methods, not only in the targeted task but also in similar muscle movements that were not specifically rehabbed. Their work was recently published in the journal Stroke.

A clinical trial to test the technique in humans is underway in Dallas and 15 other sites across the country.

Dr. Michael Kilgard, associate director of the Texas Biomedical Device Center (TxBDC) and Margaret Forde Jonsson Professor of Neuroscience in the School of Behavioral and Brain Sciences, led the research team with Dr. Seth Hays, the TxBDC director of preclinical research and assistant professor of bioengineering in the Erik Jonsson School of Engineering and Computer Science, and postdoctoral researcher Eric Meyers PhD’17.

“Our experiment was designed to ask this new question: After a stroke, do you have to rehabilitate every single action?” Kilgard said. “If VNS helps you, is it only helping with the exact motion or function you paired with stimulation? What we found was that it also improves similar motor skills as well, and that those results were sustained months beyond the completion of VNS-paired therapy.”

Kilgard said the results provide an important step toward creating guidelines for standardized usage of VNS for post-stroke therapy.

“This study tells us that if we use this approach on complicated motor skills, those improvements can filter down to improve simpler movements,” he said.

Building Stronger Cell Connections

When a stroke occurs, nerve cells in the brain can die due to lack of blood flow. An arm’s or a leg’s motor skills fail because, though the nerve cells in the limb are fine, there’s no longer a connection between them and the brain. Established rehab methods bypass the brain’s damaged area and enlist other brain cells to handle the lost functions. However, there aren’t many neurons to spare, so the patient has a long-lasting movement deficit.

The vagus nerve controls the parasympathetic nervous system, which oversees elements of many unconscious body functions, including digestion and circulation. Electrical stimulation of the nerve is achieved via an implanted device in the neck. Already used in humans to treat depression and epilepsy, VNS is a well-documented technique for fine-tuning brain function.

The UT Dallas study’s application of VNS strengthens the communication path to the neurons that are taking over for those damaged by stroke. The experiments showed a threefold-to-fivefold increase in engaged neurons when adding VNS to rehab.

“We have long hypothesized that VNS is making new connections in the brain, but nothing was known for sure,” Hays said. “This is the first evidence that we are driving changes in the brain in animals after brain injury. It’s a big step forward in understanding how the therapy works — this reorganization that we predicted would underlie the benefits of VNS.”

In anticipation of the technique’s eventual use in humans, the team is working on an at-home rehab system targeting the upper limbs.

“We’ve designed a tablet app outlining hand and arm tasks for patients to interact with, delivering VNS as needed,” Meyers said. “We can very precisely assess their performance and monitor recovery remotely. This is all doable at home.”

Expanding the Possibilities for Therapy

The researchers are motivated in part by an understanding of the practical limitations of current therapeutic options for patients.

“If you have a stroke, you may have a limited time with a therapist,” Hays said. “So when we create guidelines for a therapist, we now know to advise doing one complex activity as many times as possible, as opposed to a variety of activities. That was an important finding — it was exciting that not only do we improve the task that we trained on, but also relatively similar tasks. You are getting generalization to related things, and you’re getting sustained improvement months down the line.”

vns

For stroke patients, the opportunity to benefit from this technology may not be far off.

“A clinical trial that started here at UTD is now running nationwide, including at UT Southwestern,” Kilgard said. “They are recruiting patients. People in Dallas can enroll now — which is only fitting, because this work developed here, down to publishing this in a journal of the American Heart Association, which is based here in Dallas. This is a homegrown effort.

“The ongoing clinical trial is the last step in getting approved as an established therapy,” Kilgard said. “We’re hopefully within a year of having this be standard practice for chronic stroke.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: his research was funded by the National Institutes of Health. Other UT Dallas researchers involved include Dr. Robert Rennaker, director of the TxBDC, Texas Instruments Distinguished Chair in Bioengineering and chairman of the Department of Bioengineering; research assistant and Green Fellow Elaine S. Lai, research assistant Bleyda R. Solorzano BS’14 and neuroscience senior Justin James.

Source: Stephen Fontenot – University of Texas at Dallas
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Manu5. Licensed CC BY SA 4.0.
Original Research: Abstract for “Vagus Nerve Stimulation Enhances Stable Plasticity and Generalization of Stroke Recovery” by Eric C. Meyers, Bleyda R. Solorzano, Justin James, Patrick D. Ganzer, Elaine S. Lai, Robert L. Rennaker, Michael P. Kilgard, Sand eth A. Hays in Stroke. Published online January 25 2018.
doi:10.1161/STROKEAHA.117.019202

 

University of Texas at Dallas “Vagus Nerve Stimulation Boosts Post-Stroke Motor Skill Recovery.” NeuroscienceNews. NeuroscienceNews, 28 March 2018.
<http://neurosciencenews.com/stroke-motor-skill-vn-8703/&gt;.

Abstract

Vagus Nerve Stimulation Enhances Stable Plasticity and Generalization of Stroke Recovery

Background and Purpose—Chronic impairment of the arm and hand is a common consequence of stroke. Animal and human studies indicate that brief bursts of vagus nerve stimulation (VNS) in conjunction with rehabilitative training improve recovery of motor function after stroke. In this study, we tested whether VNS could promote generalization, long-lasting recovery, and structural plasticity in motor networks.

Methods—Rats were trained on a fully automated, quantitative task that measures forelimb supination. On task proficiency, unilateral cortical and subcortical ischemic lesions were administered. One week after ischemic lesion, rats were randomly assigned to receive 6 weeks of rehabilitative training on the supination task with or without VNS. Rats then underwent 4 weeks of testing on a task assessing forelimb strength to test generalization of recovery. Finally, the durability of VNS benefits was tested on the supination task 2 months after the cessation of VNS. After the conclusion of behavioral testing, viral tracing was performed to assess synaptic connectivity in motor networks.

Results—VNS enhances plasticity in corticospinal motor networks to increase synaptic connectivity to musculature of the rehabilitated forelimb. Adding VNS more than doubled the benefit of rehabilitative training, and the improvements lasted months after the end of VNS. Pairing VNS with supination training also significantly improved performance on a similar, but untrained task that emphasized volitional forelimb strength, suggesting generalization of forelimb recovery.

Conclusions—This study provides the first evidence that VNS paired with rehabilitative training after stroke (1) doubles long-lasting recovery on a complex task involving forelimb supination, (2) doubles recovery on a simple motor task that was not paired with VNS, and (3) enhances structural plasticity in motor networks.


Connie’s comments at http://www.clubalthea.com

Observations with one of our clients (65 yr old female hispanic) where we sent caregivers for her to help with daily living after a stroke:

We massage (softer in the neck) her head, neck, legs and arms with rosemary and coconut oil. We serve soup daily. We ensured that when she walked , we are at her side. We taught her to move her legs in sitting position. Calming music and soft lights are used.

We ensured that family members give her a hug and kiss and avoid fights and verbal abuse.

She is thriving slowly.

If she was my mom, I would buy whole foods rich in folate and Vitamin B complex, probiotic, CQ10 and omega 3 supplements , sunshine exposure early morn and late afternoon, clean water, and a routine with less clutter, obstruction, confusion and calming environment.

And to remind her deep breathing exercises and bed exercises similar to Pilates.

Email motherhealth@gmail.com as your health coach ($500 per year, family plan) and to order essential supplements for your heart delivered at your door monthly from Life Extension. Paypal conniedbuono@gmail.com or mail check at 1708 Hallmark Lane San Jose CA 95124. Chase Bank is still processing our merchant service account.

Autism Like Behaviors in Children Linked to Low Vitamin D Levels in Mothers

Autism Like Behaviors in Children Linked to Low Vitamin D Levels in Mothers

Summary: Researchers have identified a link between low vitamin D levels in pregnant and breastfeeding mothers, and autism like behaviors in their offspring. The study reveals low levels vitamin D in mothers may be associated with altered brain development that can lead to social behavioral deficits in their children.

Source: Society for Endocrinology.

Low levels of vitamin D during pregnancy and breast feeding may be related to an unusual pattern of brain development that can lead to differences in social behaviour of children in later life, according to a study published in the Journal of Endocrinology. Rats with vitamin D deficiency during pregnancy and lactation produced offspring that displayed altered social behaviours in adulthood. Differences in social behaviours are a hallmark of numerous human conditions, including autism spectrum disorder (ASD), and these findings provide further evidence of the importance of maternal vitamin D levels during pregnancy for brain development of offspring.

ASD is a lifelong condition that ranges in severity and impacts on how individuals interact and communicate with the world. Human studies have found that lower levels of maternal Vitamin D during pregnancy are associated with an increased risk of ASD in children. However, the biological mechanisms underpinning this relationship remain unclear.

To examine how maternal vitamin D levels may influence brain development, Dr Caitlin Wyrwoll and colleagues at the University of Western Australia, assessed alterations in markers of brain function and social behaviours of adult rats, born to mothers that were vitamin D deficient during pregnancy and lactation. They found that rats with vitamin D-deficient mothers displayed abnormal social behaviours, altered brain chemistry and impaired learning and memory.

Dr Caitlin Wyrwoll states, “Our work reinforces that vitamin D levels in early life influence brain development and can impact on how the brain functions in later life.”

pregnant belly

Dr Wyrwoll comments, “We know that early life environment can be a powerful determinant of health outcomes in offspring and, although this is a rat study, these data indicate that vitamin D levels during pregnancy are important for brain development, and may point to a contributing factor in the development of neurodevelopmental conditions, such as ASD. However, further work is needed to establish whether these associations also apply to humans.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Society for Endocrinology
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Vitamin D is crucial for maternal care and offspring social behaviour in rats” by Nathanael J Yates, Dijana Tesic, Kirk W Feindel, Jeremy T Smith, Michael W Clarke, Celeste Wale, Rachael C Crew, Michaela D Wharfe, Andrew J O Whitehouse and Caitlin S Wyrwoll in Journal of Endocrinology. Published online March 2018.
doi:10.1530/JOE-18-0008

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Society for Endocrinology “Autism Like Behaviors in Children Linked to Low Vitamin D Levels in Mothers.” NeuroscienceNews. NeuroscienceNews, 26 March 2018.
<http://neurosciencenews.com/vitamin-d-autism-8686/&gt;.

Vitamin D is crucial for maternal care and offspring social behaviour in rats

Early life vitamin D plays a prominent role in neurodevelopment and subsequent brain function, including schizophrenic-like outcomes and increasing evidence for an association with autism spectrum disorder (ASD). Here, we investigate how early life vitamin D deficiency during rat pregnancy and lactation alters maternal care and influences neurodevelopment and affective, cognitive and social behaviours in male adult offspring. Sprague–Dawley rats were placed on either a vitamin D control (2195 IU/kg) or deficient diet (0 IU/kg) for five weeks before timed mating, and diet exposure was maintained until weaning of offspring on postnatal day (PND) 23. MRI scans were conducted to assess brain morphology, and plasma corticosterone levels and neural expression of genes associated with language, dopamine and glucocorticoid exposure were characterised at PND1, PND12 and 4 months of age. Compared to controls, vitamin D-deficient dams exhibited decreased licking and grooming of their pups but no differences in pup retrieval. Offspring neurodevelopmental markers were unaltered, but vitamin D-deficient pup ultrasonic vocalisations were atypical. As adults, males that had been exposed to vitamin D deficiency in early life exhibited decreased social behaviour, impaired learning and memory outcomes and increased grooming behaviour, but unaltered affective behaviours. Accompanying these behavioural changes was an increase in lateral ventricle volume, decreased cortical FOXP2 (a protein implicated in language and communication) and altered neural expression of genes involved in dopamine and glucocorticoid-related pathways. These data highlight that early life levels of vitamin D are an important consideration for maternal behavioural adaptations as well as offspring neuropsychiatry.

Connection between light sensitive nerve cells in eyes and brain that regulate mood

Less melanin in white people leads to less folate for blood production

Less melanin in white leads to less folate and more melanin in dark colored skin people affects Vitamin D and Calcium absorption

White people must get sunshine to help in folate absorption (folic acid – important nutrient for the blood ) while dark-colored skin people must eat whole foods rich in Vitamin D3 , calcium , omega 3 , Vitamin K2 and magnesium to protect them from diseases related to the heart and circulation/vascular system.

As a result, depression is prevalent among whites while circulatory health issues are common among dark colored skin.

See your doctor for more preventive measures.

Connie Dello Buono

The color of skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred into the keratinocytes via a cellular organelle called a melanosome (Figure 5.7).

This figure consists of two diagrams side by side. The right diagram shows development of light colored skin; the left shows development of dark-colored skin. In both, a brown melanocyte sits at the border between the dermis and epidermis. The melanocyte has a large nucleus and six finger-like extensions. These reach between cells of the stratum basalis. Sections of the extensions detach and travel through the skins. These are melanosomes. In the left diagram, both the melanocyte and melanosomes contain melanin particles, shown as dark dots. Melanosomes travel upwards to outer skin layers, releasing melanin. As a result, keratinocytes in the left diagram contain several melanin particles that darken skin color. In light colored skin, the melanocyte contains no melanin. It still releases melanosomes into upper layers of the skin; however, these melanosomes contain no melanin. Therefore, the skin does not darken and remains light.
Figure 5.7. Skin Pigmentation
The relative coloration of the skin depends of the amount of melanin produced by melanocytes in the stratum basale and taken up by keratinocytes.

Melanin occurs in two primary forms. Eumelanin exists as black and brown, whereas pheomelanin provides a red color. Dark-skinned individuals produce more melanin than those with pale skin. Exposure to the UV rays of the sun or a tanning salon causes melanin to be manufactured and built up in keratinocytes, as sun exposure stimulates keratinocytes to secrete chemicals that stimulate melanocytes.

The accumulation of melanin in keratinocytes results in the darkening of the skin, or a tan. This increased melanin accumulation protects the DNA of epidermal cells from UV ray damage and the breakdown of folic acid, a nutrient necessary for our health and well-being.

In contrast, too much melanin can interfere with the production of vitamin D, an important nutrient involved in calcium absorption.

Thus, the amount of melanin present in our skin is dependent on a balance between available sunlight and folic acid destruction, and protection from UV radiation and vitamin D production.

It requires about 10 days after initial sun exposure for melanin synthesis to peak, which is why pale-skinned individuals tend to suffer sunburns of the epidermis initially. Dark-skinned individuals can also get sunburns, but are more protected than are pale-skinned individuals. Melanosomes are temporary structures that are eventually destroyed by fusion with lysosomes; this fact, along with melanin-filled keratinocytes in the stratum corneum sloughing off, makes tanning impermanent.

Too much sun exposure can eventually lead to wrinkling due to the destruction of the cellular structure of the skin, and in severe cases, can cause sufficient DNA damage to result in skin cancer.

When there is an irregular accumulation of melanocytes in the skin, freckles appear. Moles are larger masses of melanocytes, and although most are benign, they should be monitored for changes that might indicate the presence of cancer (Figure 5.8).

Five photos of moles. The three upper photos show moles that are small, flat, and dark brown. The bottom left photo shows a dark black mole that is raised above the skin. The bottom right photo shows a large, raised, reddish mole with protruding hairs.
Figure 5.8. Moles
Moles range from benign accumulations of melanocytes to melanomas. These structures populate the landscape of our skin. (credit: the National Cancer Institute)
 
 

SKIN DISCOLORATION

The first thing a clinician sees is the skin, and so the examination of the skin should be part of any thorough physical examination. Most skin disorders are relatively benign, but a few, including melanomas, can be fatal if untreated. A couple of the more noticeable disorders, albinism and vitiligo, affect the appearance of the skin and its accessory organs. Although neither is fatal, it would be hard to claim that they are benign, at least to the individuals so afflicted.

Albinism is a genetic disorder that affects (completely or partially) the coloring of skin, hair, and eyes. The defect is primarily due to the inability of melanocytes to produce melanin. Individuals with albinism tend to appear white or very pale due to the lack of melanin in their skin and hair. Recall that melanin helps protect the skin from the harmful effects of UV radiation. Individuals with albinism tend to need more protection from UV radiation, as they are more prone to sunburns and skin cancer. They also tend to be more sensitive to light and have vision problems due to the lack of pigmentation on the retinal wall. Treatment of this disorder usually involves addressing the symptoms, such as limiting UV light exposure to the skin and eyes.

In vitiligo, the melanocytes in certain areas lose their ability to produce melanin, possibly due to an autoimmune reaction. This leads to a loss of color in patches (Figure 5.9). Neither albinism nor vitiligo directly affects the lifespan of an individual.

This photo shows the back of a man’s neck. There is a large, discolored patch of skin at the base of his hairline. The discolored area extends over the ears onto the cheeks, toward the front of the face. The man’s head and facial hair are mostly gray, but white patches of hair are seen above the discolored skin.
Figure 5.9. Vitiligo
Individuals with vitiligo experience depigmentation that results in lighter colored patches of skin. The condition is especially noticeable on darker skin. (credit: Klaus D. Peter)
 

Other changes in the appearance of skin coloration can be indicative of diseases associated with other body systems. Liver disease or liver cancer can cause the accumulation of bile and the yellow pigment bilirubin, leading to the skin appearing yellow or jaundiced (jaune is the French word for “yellow”). Tumors of the pituitary gland can result in the secretion of large amounts of melanocyte-stimulating hormone (MSH), which results in a darkening of the skin. Similarly, Addison’s disease can stimulate the release of excess amounts of adrenocorticotropic hormone (ACTH), which can give the skin a deep bronze color.

A sudden drop in oxygenation can affect skin color, causing the skin to initially turn pale (white), a condition called pallor. With a prolonged reduction in oxygen levels, dark red deoxyhemoglobin becomes dominant in the blood, making the skin appear blue, a condition referred to as cyanosis (kyanos is the Greek word for “blue”).

This happens when the oxygen supply is restricted, as when someone is experiencing difficulty in breathing because of asthma or a heart attack. However, in these cases the effect on skin color has nothing do with the skin’s pigmentation.

INTERACTIVE LINK

This ABC video follows the story of a pair of fraternal African-American twins, one of whom is albino. Watch this video to learn about the challenges these children and their family face. Which ethnicities do you think are exempt from the possibility of albinism?

Calcium and magnesium balance 60:40 ratio

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