مگر چندبار به دنيا مي آييم؟ آيا وقت آن نرسيده كه بيشتر مراقب سلامتي مان باشيم؟! سلامتي شامل تامین رفاه کامل جسمی و روانی و اجتماعی انسان است. وزن مناسب از مهمترين اركان سلامتي است. تا زماني كه به سلامتي نرسيده ايم از پا نخواهيم نشست. متاسفانه برخي از افراد با تقليد و دست به دست كردن رژيم دكتر تغذيه،‌ فرصت هاي طلايي كاهش وزن را هدر مي دهند و در اين بين افراد معدودي هستند كه دست به تقليد طراحي رژيم متخصصان ديگر مي زنند بي آنكه از فلسفه و دليل گنجاندن برخي مواد غذايي در رژيم مطلع باشند. خلق را تقليدشان بر باد داد..............اي دوصد لعنت بر اين تقليد باد 

معرفی به دوستان اشتراک گذاری

در اين مقاله دكتر راست منش استدلال علمي مي آورد كه مصرف ملاتونين چه به صورت خوراكي و چه دارويي مي تواند به درمان دژنراسيون ماكولار چشم كمك كند... براي مطالعه اصل مقاله مي توانيد به كتابخانه كنگره ملي آمريكا به آدرس زير مراجعه نماييد https://www.ncbi.nlm.nih.gov/pubmed/20884126 در كتاب دانشگاهي Advances in Retinal Degeneration Research and Treatment: 2012 Edition به اين فرضيه دكتر راست منش استناد شده است.

فرضيه دكتر راست منش در خصوص درمان بيماري دژنراسيون ماكولار سالمندي با كمك ملاتونين

Med Hypotheses. 2011 Jan;76(1):79-85
Potential of melatonin to treat or prevent age-related macular degeneration through stimulation of telomerase activity
Rastmanesh R

Abstract

Melatonin may play a causal role in the occurrence of age-related macular degeneration (AMD). Replicative capacity and response to injury in the retinal pigment epithelium (RPE) is compromised during aging. Prevention of telomere shortening by antioxidants may be a useful approach for reducing the cumulative effects of oxidative stress in RPE cells. Melatonin, a well known antioxidant, which acts advantageously as an amphiphilic agent, may benefit AMD patients more than commonly used lipophilic or hydrophilic antioxidants. It also may act through mechanisms other than antioxidant mechanisms because melatonin has receptors localized in the RPE, which act locally as a neurohormone and/or neuromodulator. Results of a clinical trial showed that 3mg melatonin given orally each night at bedtime for 3 months to AMD patients reduced pathologic macular changes. I hypothesize that melatonin exerts additional benefit through down-regulating hTERT (catalytic subunit if telomerase) expression and stimulated telomerase activity in RPE, which subsequently helps to prevent or treat AMD. I suggest that melatonin therapy as pharmacologic agents and/or melatonin-rich foods, especially in AMD patients with measured low serum melatonin levels or high risk patients would be possibly an alternative approach to prevent and/or treat AMD. I suggest that melatonin has potential to prevent telomere shortening in RPE, while not precluding other mechanisms, namely antioxidative properties and/or restoration of inner blood-retina barrier (iBRB) integrity, reduced vascular endothelial growth factor (VEGF) and nitric oxide (NO) levels as well as leakage of horseradish peroxidase (HRP), inhibiting hypoxia-inducible factor-1 alpha (HIF-1 alpha) stabilization under hypoxia.


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