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Phototherapy improves quality of life, says new study

Posted on: August 19, 2013   by  John Cannell, MD


After atmospheric and ozone filtering, only about 3% of the total energy of sunlight at solar noon is ultraviolet, although that depends on latitude, season, altitude, and atmospheric conditions. The ultraviolet portion of outdoor sunlight is approximately 95% UVA and 5% UVB, although atmospheric, seasonal, and geographic variables change that ratio each time you step outside.

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3 Responses to Phototherapy improves quality of life, says new study

  1. Rita and Misty

    Dear readers,

    I’ve posted this before, but the info is interesting (at least to me 🙂 ), that I thought to share it again:

    Benefits of Sunlinght: A Bright Spot for Human Health

    I’ve also posted the below information previously:

    Sun-dependent pathways:

    1. Melatonin
    2. Serontonin
    3. Direct immune suppression

    Melatonin and Alzheimer’s disease:

    “Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients. Half of severely ill AD patients develop chronobiological day-night rhythm disturbances like an agitated behavior during the evening hours (so-called “sundowning”). Melatonin replacement has been shown effective to treat sundowning and other sleep wake disorders in AD patients. The antioxidant, mitochondrial and antiamyloidogenic effects of melatonin indicate its potentiality to interfere with the onset of the disease. This is of particularly importance in mild cognitive impairment (MCI), an etiologically heterogeneous syndrome that precedes dementia. The aim of this manuscript was to assess published evidence of the efficacy of melatonin to treat AD and MCI patients. PubMed was searched using Entrez for articles including clinical trials and published up to 15 January 2010. Search terms were “Alzheimer” and “melatonin”. Full publications were obtained and references were checked for additional material where appropriate. Only clinical studies with empirical treatment data were reviewed. The analysis of published evidence made it possible to postulate melatonin as a useful ad-on therapeutic tool in MCI. In the case of AD, larger randomized controlled trials are necessary to yield evidence of effectiveness (i.e. clinical and subjective relevance) before melatonin´s use can be advocated.”

    Serotonin and Alzheimer’s disease:

    “Mounting evidence accumulated over the past few years indicates that the neurotransmitter serotonin plays a significant role in cognition. As a drug target, serotonin receptors have received notable attention due in particular to the role of several serotonin-receptor subclasses in cognition and memory. The intimate anatomical and neurochemical association of the serotonergic system with brain areas that regulate memory and learning has directed current drug discovery programmes to focus on this system as a major therapeutic drug target. Thus far, none of these programmes has yielded unambiguous data that suggest that any of the new drug entities possesses disease-modifying properties, and significantly more research in this promising area of investigation is required. Compounds are currently being investigated for activity against serotonin 5-HT(1), 5-HT(4) and 5-HT(6) receptors. This review concludes that most work done in the development of selective serotonin receptor ligands is in the pre-clinical or early clinical phase. Also, while many of these compounds will likely find application as adjuvant therapy in the symptomatic treatment of Alzheimer’s disease, there are currently only a few drug entities with activity against serotonin receptors that may offer the potential to alter the progression of the disease.”

    Pro-inflammatory cytokines and neuronal death:

    “Increasing concurrent evidence suggests that inflammation significantly contributes to the pathogenesis of AD. The generation and secretion of proinflammatory mediators may interact at multiple levels with neurodegeneration. Thus, proinflammatory cytokines may not only contribute to neuronal death, but they might also influence classical neurodegenerative pathways such as APP processing and τ phosphorylation.The concomitant release of anti-inflammatory mediators may partly antagonize this action ultimately leading to chronic disease. Future studies need to determine whether the course of AD can be influenced by anti-inflammatory treatment strategies, and clinically novel approaches to analyze early neuroinflammation in the human brain are needed to improve how to monitor and control treatment strategies that are targeting inflammatory mechanisms.”

    Vitamin D as anti-inflammatory agent

    “This newly identified DNA-binding site for the vitamin-D receptor, and the specific pathways inhibited by higher levels of vitamin D provide a plausible mechanism for many of the benefits that have been associated with vitamin D,” said Dr. Goleva. ‘The fact that we showed a dose-dependent and varying response to levels commonly found in humans also adds weight to the argument for vitamin D’s role in immune and inflammatory conditions.”

  2. JBG

    The Feldmeyer et al DLQI results suggest placebo effects to me. Too bad they didn’t have a placebo group since, if the effects are real, it would be nice to be able to have confidence in them.

  3. Rita and Misty

    I have not seen the DLQI instrument…yet I do think questionnaires in general provide shaky data at best…the questionnaire is a very subjective instrument in my opinion….

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