- Where you live. The further away from the Equator you live, the less vitamin D–producing UVB light reaches the earth's surface during the winter. Residents of Boston, for example, make little if any of the vitamin from November through February. Short days and clothing that covers legs and arms also limit UVB exposure.
- Air quality. Carbon particles in the air from the burning of fossil fuels, wood, and other materials scatter and absorb UVB rays, diminishing vitamin D production. In contrast, ozone absorbs UVB radiation, so pollution-caused holes in the ozone layer could end up enhancing vitamin D levels.
- Use of sunscreen. Sunscreen prevents sunburn by blocking UVB light. Theoretically, that means sunscreen use lowers vitamin D levels. But as a practical matter, very few people put on enough sunscreen to block all UVB light, or they use sunscreen irregularly, so sunscreen's effects on vitamin D might not be that important. An Australian study that's often cited showed no difference in vitamin D between adults randomly assigned to use sunscreen one summer and those assigned a placebo cream.
- Skin color. Melanin is the substance in skin that makes it dark. It "competes" for UVB with the substance in the skin that kick-starts the body's vitamin D production. As a result, dark-skinned people tend to require more UVB exposure than light-skinned people to generate the same amount of vitamin D.
- Weight. Body fat sops up vitamin D, so it's been proposed that it might provide a vitamin D rainy-day fund: a source of the vitamin when intake is low or production is reduced. But studies have also shown that being obese is correlated with low vitamin D levels and that being overweight may affect the bioavailability of vitamin D.
- Age. Compared with younger people, older people have lower levels of the substance in the skin that UVB light converts into the vitamin D precursor. There's also experimental evidence that older people are less efficient vitamin D producers than younger people.http://www.health.harvard.edu/staying-healthy/6-things-you-should-know-about-vitamin-d
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Saturday, September 24, 2016
6 things you should know about vitamin D
FoxFeed Blog - Bionic Dystonic: How I Advocate for Dystonia Awareness
Fake Towns Could Help People With Alzheimer’s Live Happier Lives
“We have so many family caregivers who cannot take their loved ones to the movie theater or to a restaurant because they don't know what those interactions are going to be like,” Scott Tarde, CEO of the Glenner Center, tells Linda Poon for CityLab. “So we wanted to be able to provide these experiences in a safe environment.”
A model of Glenner Town Square's city hall, based on San Diego's 1950s-era real-life city hall. (San Diego Opera)
Caring for people with Alzheimer’s-related dementia can be stressful for both the patient and their family. Traditional round-the-clock care in homes can be very expensive, but caring for a parent or family member with dementia can be a struggle for people without specialized training. At the same time, living with the disease can be frustrating for the patients, who can become disoriented and lash out. While traditional therapy for Alzheimer’s patients tends to rely on nursing homes and drugs, in recent years centers like Glenner Town Square have begun popping up in communities across the world as a means to care for people with dementia while exposing them to things aimed at triggering happy memories, Poon reports.
“Structure is very important for individuals [with dementia],” Tarde tells Poon. “If you do not engage them, behaviors can start to escalate in the evening because there wasn't a lot of mental stimulation during the day.”
While Glenner Town Square is meant to provide day care for elderly dementia patients, others do provide round-the-clock care and community. One of the first examples of a center structured around this technique (known as “reminiscence therapy”) is Hogewey, a small, enclosed village built outside of Amsterdam that provides dormitories, shops and community spaces for residents with dementia to safely live more independent lives, Ben Tinker reported for CNN.
"We have Dutch design, Dutch cultures, Dutch lifestyles, but the concept is to value the person, the individual... to support them to live their life as usual, and you can do that anywhere," Yvonne van Amerongen, one of Hogewey’s founders, told Tinker.
Glenner Town Square is being designed and built by scenic carpenters and designers with the San Diego Opera, with plans to begin operations in 2018. By building an experience for people with dementia, the center could help provides some sense of structure and normalcy for those who have become unmoored from their memories.
A room inside city hall, complete with working typewriter and books that visitors with dementia can read and write with (George G. Glenner Alzheimer's Family Centers, Inc.)
http://www.smithsonianmag.com/smart-news/fake-towns-could-help-people-alzheimers-live-happier-lives-180960518/ |
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Friday, September 23, 2016
Research on Stress Hormone Effects on the Brain Reveals Unexpected Findings
Summary: New findings suggest common concepts cited in textbooks may need to be adjusted.
The researchers also discovered that MRs and GRs don’t always act separately but can actually bind together at the same site within hippocampal genes after stress, possibly resulting in a boost in the expression of such genes. NeuroscienceNews.com image is credited to the researchers.
Stress is a common problem often resulting in poor health and mental disorders. New research has revealed that current concepts on how stress hormones act on the brain may need to be reassessed.
It is thought that disturbances in the action of stress hormones play a key role in causing mental disorders, like major depression and post-traumatic stress disorder (PTSD).
Learning to cope with stressful events is known to require changes in the expression of genes in the hippocampus, a limbic brain region involved in learning and memory. Such changes in gene expression are brought about by stress-induced glucocorticoid hormones acting via receptors that can directly bind to genes and alter their expression.
A BBSRC-funded study, published in the international journal Proceedings of the National Academy of Sciences (PNAS), has found that the action of mineralocorticoid receptors (MRs) at the neuronal genome cannot be predicted based solely on receptor occupancy by glucocorticoid hormone. As a result the concept on tonic and feedback action, which over the past few decades has been cited in textbooks, may require some adjustment.
Professor Hans Reul together with Dr Karen Mifsud, of the University’s School of Clinical Sciences, investigated the actual binding of MRs and glucocorticoid receptors (GRs) to genes in the hippocampus after stress.
To their surprise they found the binding of MRs to genes was not constantly high but actually low under non-stress conditions and increased substantially after stress. GRs, however, followed the expectation that binding to target genes would be minimal under baseline conditions and increase dramatically after stress following the GR binding profile to glucocorticoids.
Hans Reul, Professor of Neuroscience, said: “These novel findings are a significant step forward in our understanding of how glucocorticoid hormones act on the brain after stressful events. They allow for the first time identification of genes within the hippocampus of the brain that are directly affected by GR/MR binding after stress. Given that stress-related psychiatric diseases such as major depression, anxiety and PTSD are an ever-increasing burden in our society, these new insights are important to find novel treatments and therapies in the future.”
The researchers also discovered that MRs and GRs don’t always act separately but can actually bind together at the same site within hippocampal genes after stress, possibly resulting in a boost in the expression of such genes. Their work provides the first strong evidence in vivo that MR and GR are heterodimerising and that MRs may require the presence of GRs in order to bind to specific target genes.
Thirty years ago, Professor Reul, who was working at Utrecht University in The Netherlands, observed that glucocorticoids exert their effects on the brain via two different types of receptors, the MRs and the GRs.
Professor Reul discovered that due to their extraordinarily high affinity for glucocorticoids, MRs are always fully occupied by these hormones whereas GRs, as a result of their lower binding affinity, only became occupied after a stressful event. Based on these results, the concept was launched that MRs have a constant (‘tonic’) action on brain function whereas GRs mediated negative feedback and enhance learning and memory after stress. Due to Dr Mifsud and Professor Reul’s new research at the University of Bristol, this concept may require reassessment.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Professor Reul and Dr Mifsud will pursue this ground-breaking work after recently receiving grants over £1 million from BBSRC to continue with this successful stress research programme.
Source: University of Bristol
Image Source: This NeuroscienceNews.com image is adapted from the University of Bristol press release.
Original Research: Abstract for “Acute stress enhances heterodimerization and binding of corticosteroid receptors at glucocorticoid target genes in the hippocampus” by Karen R. Mifsud and Johannes M. H. M. Reul in PNAS. Published online September 21 2016 doi:10.1073/pnas.1605246113
Abstract
Acute stress enhances heterodimerization and binding of corticosteroid receptors at glucocorticoid target genes in the hippocampus
A stressful event results in secretion of glucocorticoid hormones, which bind to mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) in the hippocampus to regulate cognitive and affective responses to the challenge. MRs are already highly occupied by low glucocorticoid levels under baseline conditions, whereas GRs only become substantially occupied by stress- or circadian-driven glucocorticoid levels. Currently, however, the binding of MRs and GRs to glucocorticoid-responsive elements (GREs) within hippocampal glucocorticoid target genes under such physiological conditions in vivo is unknown.
We found that forced swim (FS) stress evoked increased hippocampal RNA expression levels of the glucocorticoid-responsive genes FK506-binding protein 5 (Fkbp5), Period 1 (Per1), and serum- and glucocorticoid-inducible kinase 1 (Sgk1). Chromatin immunoprecipitation (ChIP) analysis showed that this stressor caused substantial gene-dependent increases in GR binding and surprisingly, also MR binding to GREs within these genes. Different acute challenges, including novelty, restraint, and FS stress, produced distinct glucocorticoid responses but resulted in largely similar MR and GR binding to GREs. Sequential and tandem ChIP analyses showed that, after FS stress, MRs and GRs bind concomitantly to the same GRE sites within Fkbp5 and Per1 but not Sgk1.
Thus, after stress, MRs and GRs seem to bind to GREs as homo- and/or heterodimers in a gene-dependent manner. MR binding to GREs at baseline seems to be restricted, whereas after stress, GR binding may facilitate cobinding of MR. This study reveals that the interaction of MRs and GRs with GREs within the genome constitutes an additional level of complexity in hippocampal glucocorticoid action beyond expectancies based on ligand–receptor interactions.
“Acute stress enhances heterodimerization and binding of corticosteroid receptors at glucocorticoid target genes in the hippocampus” by Karen R. Mifsud and Johannes M. H. M. Reul in PNAS. Published online September 21 2016 doi:10.1073/pnas.1605246113
http://neurosciencenews.com/ptsd-cortisol-neuroscience-5115/
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Parkinson’s Researchers Shed Light on Brain Area Controlling Eye Movements
Using Unified Parkinson’s Disease Rating Scale for the Evaluation
Whole Body Vibration, Exercise May Improve Motor Performance In Parkinson's
September 23, 2016
Pharmacologic intervention is the current standard of care for Parkinson’s disease, yet medications frequently fail to control some symptoms, including tremor and postural instability. |
- UPDRS score at baseline: 29.53±7.60
- UPDRS score 1 day following treatment: 18.00±7.09
- UPDRS score 4 days following treatment: 17.53±5.78
- From baseline to 1 day post-intervention (10.13, 95% confidence interval [CI]: 4.86-15.41; P<.001)
- From baseline to 4 days post-intervention (10.73, 95% CI: 6.22-15.25; P <.001)
Can brain 'pacemaker' improve lives of head trauma patients?
September 23, 2016 by Don Rauf, Healthy Reporter
Forest Payne builds golf course; helps him battle Parkinson's disease
September 22, 2016
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