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  • Ultrad?wi?ki wspomagaj? uwalnianie nagromadzonej insuliny z komórek beta



    Naukowcy z Uniwersytetu Jerzego Waszyngtona zaprezentowali ca?kowicie nowe podej?cie do leczenia wczesnej cukrzycy typu 2. Wykazali, ?e za pomoc? terapii ultrad?wi?kowej mo?na stymulowa? u myszy wydzielanie insuliny na ??danie.

    Wystawiaj?c trzustk? na oddzia?ywanie pulsów ultrad?wi?kowych, zaobserwowano mierzalne wzrosty poziomu insuliny we krwi.

    Zespó? ma zaprezentowa? uzyskane wyniki na dorocznej konferencji Ameryka?skiego Towarzystwa Akustycznego w Louisville.

    Gdy poziom glukozy ro?nie, np. po posi?ku, komórki beta wysp trzustkowych nasilaj? produkcj? insuliny. Na pocz?tkowych etapach rozwoju cukrzycy typu 2. komórki beta staj? si? jednak przeci??one, co wi??e si? z akumulacj? insuliny. By nie dopu?ci?, aby nagromadzenie hormonu zniszczy?o komórki beta, mo?na próbowa? wspomaga? uwalnianie insuliny lekami. Tania Singh uwa?a, ?e chc?c unikn?? skutków ubocznych leków, w tym miejscu warto si?gn?? w?a?nie po ultrad?wi?ki.

    Podczas testów po sesji ultrad?wi?kowej obserwowano znacz?ce wzrosty st??enia insuliny we krwi.

    W ramach przysz?ych bada? naukowcy chc? oceni?, czy terapia pulsami ultrad?wi?kowymi nie uszkadza trzustki i/lub okolicznych narz?dów.

    Co ciekawe, cho? ekipa Singh zauwa?y?a wzrost poziomu insuliny we krwi, nie towarzyszy? temu spadek st??enia glukozy. Akademicy zamierzaj? si? wkrótce zaj?? t? kwesti?.

    Singh chce równie? rozszerzy? badania na wi?ksze zwierz?ta.
    https://kopalniawiedzy.pl/cukrzyca-t...ia-Singh,30088

    Przetworzona ?ywno?? powoduje, ?e jemy wi?cej i tyjemy


    Badania przeprowadzone w ameryka?skim Narodowym Instytucie Cukrzycy, Chorób Nerek i Uk?adu Pokarmowego (NIDDK) sugeruj?, ?e wysoko przetworzona ?ywno?? przemys?owa powoduje, ?e wi?cej jemy i przybieramy na wadze.

    Podczas pierwszych randomizowanych kontrolowanych bada? tego typu zauwa?ono, ?e osoby spo?ywaj?ce wysoko przetworzon? ?ywno?? przybiera?y na wadze bardziej, ni? osoby jedz?ce pokarmy mniej przetworzone, nawet je?li dostarczane im po?ywienie zawiera?o tyle samo kalorii i sk?adników od?ywczych.

    W eksperymencie przeprowadzonym w siedzibie NIDDK wzi??o udzia? 20 doros?ych zdrowych ochotników. Ka?demu z nich zaoferowano 6000 USD za rezygnacj? z cz??ci wolno?ci. Mieli oni przez 28 dni mieszka? na terenie NIDDK, nie mogli go opuszcza? i jedli tylko to, co otrzymywali od badaczy.

    Na potrzeby bada? skorzystano z systemu klasyfikacji ?ywno?ci NOVA, który za „ultraprzetworzone” uznaje to po?ywienie, które w przewa?aj?cej mierze zawiera sk?adniki wyst?pujace w fabrycznie wytwarzanej ?ywno?ci, takie jak t?uszcze utwardzone, syrop glukozowo-fruktozowy, wzmacniacze smaku i zapachu czy emulgatory.

    Wcze?niejsze badania obserwacyjne prowadzone na du?ych grupach ludno?ci wykaza?y istnienie korelacji pomi?dzy spo?ywaniem wysoko przetworzonej ?ywno?ci a wyst?powaniem ró?nych problemów zdrowotnych. Jednak, jako ?e osoby, od których pozyskiwano dane, nie by?y losowo przydzielana do grup spo?ywaj?cych okre?lone rodzaje po?ywienia, nie mo?na by?o jednoznacznie stwierdzi?, czy to sama wysoko przetworzona ?ywno?? powoduje problemy, czy te? ludzie, którzy j? spo?ywaj? maja problemy z innego powodu, np. dlatego, ?e nie spo?ywaj? ?wie?ych warzyw i owoców. Dlatego te? w NIDDK przeprowadzono ?ci?le kontrolowany eksperyment.

    Wzi??o w nim udzia? 10 kobiet i 10 m??czyzn, których rozlosowano do dwóch grup. Jedna grupa przez 2 tygodnia jad?a wysoko przetworzone pokarmy, druga grupa jad?a pokarmy minimalnie przetworzone. Po dwóch tygodniach diet? oby grup zamieniano. Ka?dy uczestnik badania móg? zje?? tyle ile chcia?. Posi?ek wysoko przetworzony móg? np. sk?ada? si? z bagietek z serkiem topionym i bekonem, mia?o przetworzony za? z p?atków owsianych z mlekiem, owocami i orzechami. Oba rodzaje po?ywienia mia?y tyle samo kalorii i sk?adników od?ywczych. Ponadto uczestnicy badania otrzymali lu?ne ubrania, by nie mogli obserwowa? ewentualnych zmian swojej wagi.

    Badania wykaza?y, ?e osoby jedz?ce ?ywno?? wysoko przetworzon?, spo?ywali jej wi?cej, zatem poch?aniali wi?cej kalorii i bardziej przybierali na wadze.

    Chcemy te? sprawdzi?, jak poszczególne elementy wysoko przetworzonej diety wp?ywaj? na zachowania zwi?zane z od?ywianiem si? i na przybieranie na wadze. Naszym kolejnym krokiem b?dzie zaprojektowanie podobnych eksperymentów z ró?nymi dietami wysoko przetworzonymi, by sprawdzi?, czy b?dzie to mia?o wp?yw na ilo?? spo?ywanych kalorii i wag?, mówi doktor Kevin D. Hall, g?ówny autor bada?. Nie mo?na bowiem wykluczy?, ?e ró?nice w spo?ywanych kaloriach pomi?dzy dietami wysoko i nisko przetworzonymi s? spowodowane niewielkimi ró?nicami w ilo?ci bia?ek w obu dietach.

    Z czasem ró?nice takie mog? si? akumulowa?, prowadzi? do przybierania na wadze i problemów zdrowotnych, stwierdza dyrektor NIDDK Griffin P. Rodgers. Mimo, ?e to kolejne wyniki bada? sugeruj?ce, ?e wysoko przetworzona ?ywno?? jest szkodliwa, ich autorzy przyznaj?, ?e ograniczenie tego typu ?ywno?ci mo?e by? trudne. Musimy pami?ta?, ?e przygotowanie mniej przetworzonego posi?ku wymaga wi?c pieni?dzy i czasu. Powiedzenie ludziom, by zdrowo si? od?ywiali nie przyniesie efektu, je?li nie b?d? mieli dost?pu do zdrowej ?ywno?ci, dodaje Hall.
    Stan zapalny u kobiet wywo?uje utrat? zdolno?ci odczuwania przyjemno?ci, u m??czyzn efekt nie wyst?puje

    Autorzy artyku?u z pisma Biological Psychiatry: Cognitive Neuroscience and Neuroimaging dodaj?, ?e obni?ona aktywno?? mózgowego o?rodka nagrody jest oznak? anhedonii, jednego z objawów depresji. Polega ona na utracie zdolno?ci odczuwania przyjemno?ci i rado?ci.

    U kobiet depresja jest diagnozowana 2-3-krotnie cz??ciej. Nowe ustalenia mog? w pewnym stopniu wyja?ni?, sk?d bior? si? mi?dzyp?ciowe ró?nice w tym zakresie.

    Nasze badanie jako pierwsze pokazuje, ?e w obecno?ci stanu zapalnego istniej? mi?dzyp?ciowe ró?nice w nerwowej wra?liwo?ci na nagrod? […] – podkre?la dr Naomi Eisenberger z Uniwersytetu Kalifornijskiego w Los Angeles.

    W eksperymencie wzi??o udzia? 115 osób, w tym 69 kobiet. Wylosowano je do 2 grup, którym podawano placebo lub nisk? dawk? wywo?uj?cej stan zapalny endotoksyny. Dwie godziny pó?niej ochotnicy wykonywali z?o?one zadanie (grali, by zdoby? nagrod? pieni??n?) w skanerze do fMRI.

    Naukowcy monitorowali aktywno?? brzusznego pr??kowia (ang. ventral striatum, VS), które nale?y do tzw. uk?adu nagrody. Okaza?o si?, ?e u kobiet endotoksyna prowadzi?a do obni?onej aktywno?ci VS podczas przewidywania nagrody. Zjawiska nie zaobserwowano u m??czyzn.

    U kobiet, ale nie u m??czyzn, z grupy dostaj?cej endotoksyn? spadki aktywno?ci VS podczas przewidywania nagrody wi?za?y si? ze wzrostem stanu zapalnego.

    To sugeruje, ?e przez zmniejszenie wra?liwo?ci na nagrod? kobiety z przewlek?ym stanem zapalnym mog? by? szczególnie podatne na wyst?pienie depresji. Klinicy?ci zajmuj?cy si? kobietami z zaburzeniami zapalnymi powinni [wi?c] bacznie monitorowa? pacjentki pod k?tem mo?liwych pocz?tków objawów depresyjnych – zaznacza dr Mona Moieni.
    Gniew i z?o?? pogarsza zdrowie bardziej ni? smutek

    Osoby w starszym wieku maj? zwykle wiele powodów do narzeka?. Utrata bliskich osób zwi?ksza ryzyko samotno?ci, stan zdrowia cz?sto nie pozwala ju? na kontynuowanie dotychczasowego trybu ?ycia. Okazuje si? jednak, ?e sama reakcja na rosn?ce ograniczenia mo?e istotnie wp?ywa? na samopoczucie seniorów. Wyniki bada? naukowców z Concordia University w Montrealu wskazuj? na to, ?e osoby reaguj?ce gniewem i z?o?ci? szkodz? swojemu zdrowiu bardziej ni? te, które odczuwaj? smutek. Pisze o tym w najnowszym numerze czasopismo „Psychology and Aging”.

    W miar? up?ywu lat i starzenia si? wi?kszo?? z nas musi stopniowo ogranicza? formy aktywno?ci. Utrata bliskiej osoby, k?opoty z poruszaniem si? mog? prowadzi? do z?o?ci. Nasze badania pokaza?y, ?e o ile z?o?? mo?e prowadzi? do nasilenia si? przewlek?ych chorób, sam smutek takich efektów nie przynosi – mówi pierwsza autorka pracy, Meaghan Barlow. Zdaniem autorów, z?o?? zwi?ksza ryzyko procesów zapalnych i w ten sposób przyczynia si? do dalszego pogorszenia stanu zdrowia, mi?dzy innymi zwi?kszenia ryzyka chorób serca, zapalenia stawów, czy chorób nowotworowych.

    Barlow wraz ze wspó?pracownikami bada?a wp?yw emocji, z?o?ci lub smutku, na procesy zapalne, reakcj? mechanizmu odporno?ciowego organizmu na infekcje, czy uszkodzenie tkanek. Procesy zapalne zwykle pomagaj? w obronie organizmu i gojeniu si? ran, je?li jednak przejd? w faz? przewlek?? zwi?kszaj? ryzyko przewlek?ych chorób.

    W eksperymencie uczestniczy?o 226 osób w wieku od 59 do 93 lat, podzielonych na dwie grupy wiekowe, do 79 lat i powy?ej. Przez tydzie? badani wype?niali ankiety z pytaniami mi?dzy innymi o towarzysz?ce im emocje gniewu lub smutku. Towarzyszy? temu wywiad medyczny dotycz?cy zwi?zanych z wiekiem przewlek?ych chorób i badania próbek krwi pod k?tem markerów procesów zapalnych. Wyniki eksperymentu pokaza?y, ?e uczucia z?o?ci wi?za?y si? z wy?szym poziomem markerów procesów zapalnych i wi?kszym ryzykiem przewlek?ych chorób u osób od 80 roku ?ycia wzwy?. Takiego efektu nie obserwowano u osób nieco m?odszych – dodaje wspó?autor pracy, prof. Carsten Wrosch z Faculty of Arts and Science CU.

    Naukowcy zwracaj? uwag? na to, ?e negatywne emocje, zarówno uczucie gniewu, jak i smutek, s? form? radzenia sobie z pogarszaj?cym si? stanem zdrowia, nie tylko fizycznym, ale te? psychicznym. O ile gniew ma dzia?anie mobilizuj?ce, smutek pomaga pogodzi? si? z sytuacj? i zrezygnowa? z wyznaczania sobie celów, które s? ju? nie do osi?gni?cia. Ka?da z tych emocji mo?e okaza? si? w okre?lonych okoliczno?ciach po?yteczna. Nieco m?odszym seniorom z?o?? mo?e pomóc pokonywa? wyzwania, w starszym jednak wieku, powy?ej 80 lat, zaczyna jednak przynosi? wi?cej szkody ni? po?ytku. Wtedy pewnych strat nie da si? ju? nadrobi? – dodaje Barlow.

    Zdaniem autorów pracy, konieczne jest lepsze zrozumienie mechanizmów, które kieruj? emocjami starszych osób. Edukacja i ewentualna terapia powinny pomóc obni?y? poziom stresu tam, gdzie nie przynosi po?ytku, a same straty.
    https://losyziemi.pl/gniew-i-zlosc-p...iej-niz-smutek

    Chronic caffeine exposure in adolescence promotes diurnal, biphasic mood-cycling and enhanced motivation for reward in adult mice.

    Abstract
    Adolescent's consumption of caffeine and caffeinated beverage is increasing, yet little is known about the consequences of chronic caffeine exposure during the critical development period of adolescence. In the present study, we investigated the effect of beginning chronic caffeine consumption in adolescence on locomotor, mood, sensorimotor gating, and reward seeking behaviors through adolescence and in adulthood. During the light cycle, caffeine exposed mice exhibited hypoactivity in a novel open-field box and increased anxiety-like and depressive-like behaviors, while maintaining normal home cage locomotor activity. In contrast, during the dark cycle caffeine exposed mice displayed normal locomotor activity in a novel open-field box with hyperactive home cage activity. Interestingly, we found that caffeine exposed mice also showed enhanced prepulse inhibition during the light cycle whereas they displayed a deficit of prepulse inhibition during the dark cycle. Reward seeking for sucrose was higher in caffeine exposed than control mice during the light cycle. Additionally, when granted 24?-h access to ethanol as adults, caffeine exposed mice consumed more ethanol in the absence of acute caffeine use. Altogether, mice that consumed chronic caffeine beginning in adolescence had increased reward seeking and exhibited a circadian-dependent pattern of mood fluctuations in adulthood.
    https://www.ncbi.nlm.nih.gov/pubmed/31095992?dopt=

    WHY SOME DOCTORS ARE PRESCRIBING A DAY IN THE PARK OR A WALK ON THE BEACH FOR GOOD HEALTH



    Taking a walk on a wooded path, spending an afternoon in a public park, harvesting your backyard garden and even looking at beautiful pictures of Hawaii can all make us feel good. Certainly, for many of us, it’s beneficial to have time outside in natural environments. Being cooped up inside can feel unnatural and increase our desire to get outside. The renowned biologist E.O. Wilson created a theory called the biophilia hypothesis, where he stated that people have an innate relationship to nature.

    On an intuitive level, this makes sense. Humans evolved in an open, natural environment and removing us from this environment could have a negative effect on our health. But what does the research say? Is there actually evidence that being in natural environments can promote our well-being, prevent disease and speed recovery?
    https://www.universal-sci.com/headli...or-good-health


    Effect of skipping breakfast for 6 days on energy metabolism and diurnal rhythm of blood glucose in young healthy Japanese males.

    BACKGROUND:
    Skipping breakfast has become a common trend that may lead to obesity and type 2 diabetes. Previous studies, which imposed a single incidence of breakfast skipping, did not observe any decrease in 24-h energy expenditure. Furthermore, the effects of breakfast skipping on diurnal blood glucose profiles over 24 h are contradictory.

    OBJECTIVE:
    The aim of this study was to clarify the influence of 6 consecutive days of breakfast skipping and sedentary behavior on energy metabolism and glycemic control.

    METHODS:
    Ten young men participated in 2 trials (with or without breakfast) that lasted for 6 consecutive days, and the 2 trials were conducted 1 wk apart with a repeated-measures design. During the meal intervention, each subject's blood glucose was measured using the continuous glucose monitoring system. If breakfast was skipped, subjects ate large meals at lunch and dinner such that the 24-h energy intake was identical to that of the 3-meal condition. At 2200 on the fifth day, the subjects entered a room-sized respiratory chamber, where they remained for 33 h, and were instructed to carry out sedentary behavior.

    RESULTS:
    The glucose levels were similar between the 2 meal conditions during the first 5 d of meal intervention, but the blood glucose at 2300 was higher in the breakfast-skipping condition than in the 3-meal condition. Breakfast skipping elevated postprandial glycemic response after lunch on the first day of meal intervention. On the sixth day, there were no significant differences in 24-h energy expenditure and substrate oxidation. When subjects remained in a metabolic chamber, the level of physical activity significantly decreased, glycemic stability slightly deteriorated, and mean blood glucose over 24 h was higher in the breakfast-skipping trial than in the 3-meal trial.

    CONCLUSIONS:
    Sedentary lifestyle and repeated breakfast skipping caused abnormal glucose fluctuations, whereas 24-h energy metabolism remained unaffected
    https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract


    Low-Carbohydrate Training Increases Protein Requirements of Endurance Athletes

    Introduction Training with low-carbohydrate (CHO) availability enhances markers of aerobic adaptation and has become popular to periodize throughout an endurance-training program. However, exercise-induced amino acid oxidation is increased with low muscle glycogen, which may limit substrate availability for post-exercise protein synthesis. We aimed to determine the impact of training with low-CHO availability on estimates of dietary protein requirements.

    Methods Eight endurance-trained males (27±4y, 75±10kg, 67±10ml·kg body mass-1·min-1) completed two trials matched for energy and macronutrient composition but with differing CHO periodization. In the low-CHO availability trial (LOW), participants consumed 7.8g CHO·kg-1 prior to evening high-intensity interval training (HIIT; 10 x 5 min at 10-km race pace, 1 min rest) and subsequently withheld CHO post-exercise (0.2g·kg-1). In the high-CHO availability trial (HIGH), participants consumed 3g CHO·kg-1during the day before HIIT, and consumed 5g CHO·kg-1that evening to promote muscle glycogen resynthesis. A 10km run (~80% HRmax) was performed the following morning, fasted (LOW) or 1h after consuming 1.2g CHO·kg-1 (HIGH). Whole-body phenylalanine flux (PheRa) and oxidation (PheOx) were determined over 8h of recovery via oral [13C]phenylalanine ingestion, according to standard indicator amino acid oxidation methodology, while consuming sufficient energy, 7.8g CHO·kg-1·d-1, and suboptimal protein (0.93g·kg-1·d-1).

    Results Fat oxidation (indirect calorimetry) during the 10-km run was higher in LOW compared to HIGH (0.99±0.35 vs. 0.60±0.26 g·min-1, p<0.05). PheRa during recovery was not different between trials (p>0.05) whereas PheOX (reciprocal of protein synthesis) was higher in LOW compared to HIGH (8.8±2.7 vs. 7.9±2.4 umol·kg-1·h-1, p<0.05), suggesting a greater amino acid requirement to support rates of whole-body protein synthesis.

    Conclusion Our findings suggest that performing endurance exercise with low-CHO availability increases protein requirements of endurance athletes.
    https://journals.lww.com/acsm-msse/A...ein.96605.aspx

    Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells

    Stressful life events are considered a risk factor for autoimmune disorders, though the mechanisms are unclear. Here we demonstrate that chronic social stress induces virulence-associated transcriptional patterns in the murine gut microbiota. The stress-influenced microbiota increased the presence of effector T helper cells in the mesenteric lymph nodes, including myelin-autoreactive cells. Inhibition of the bacterial quorum sensor QseC, which is also responsive to norepinephrine, diminished the presence of effector T helper cells and bacteria such as Acinetobacter in the mesenteric lymph nodes, without remarkably affecting the gut microbial composition. Together, our results delineate a model in which the immune reaction to stress-responsive microbiota may compromise tolerance to self and therefore may increase the risk for autoimmune diseases in susceptible individuals.
    https://msystems.asm.org/content/4/4/e00292-18

    correlation doesn't imply causation

    Komentarz


    • 19 May 2019
      Light and the circadian rhythm: The key to a good night's sleep?

      by:
      Russell Foster is a fellow of the Royal Society and the Academy of Medical Sciences. He is also a professor of Circadian Neuroscience and the head of the Nuffield Laboratory of Ophthalmology, which is part of the University of Oxford.
      n a review published May 17 in the journal Trends in Immunology, researchers discuss how time of day affects the severity of afflictions ranging from allergies to heart attacks.

      Researchers in Switzerland compiled studies, predominantly in mice, that looked at the connection between circadian rhythms and immune responses. For example, studies showed that adaptive immune responses—in which highly specialized, pathogen-fighting cells develop over weeks—are under circadian control. This is "striking," says senior author Christoph Scheiermann, an immunologist at the University of Geneva, "and should have relevance for clinical applications, from transplants to vaccinations."

      The body reacts to cues such as light and hormones to anticipate recurring rhythms of sleep, metabolism, and other physiological processes. In both humans and mice, the numbers of white blood cells also oscillate in a circadian manner, raising the question of whether it might be possible one day to optimize immune response through awareness and utilization of the circadian clock.

      In separate studies that compared immune cell time-of-day rhythms under normal conditions, inflammation, and disease, researchers found that:

      Heart attacks in humans are known to strike most commonly in the morning, and research suggests that morning heart attacks tend to be more severe than at night. In mice, the numbers of monocytes—a type of white blood cell that fights off bacteria, viruses, and fungi—are elevated in the blood during the day. At night, monocytes are elevated in infarcted heart tissue, resulting in decreased cardiac protection at that time of day relative to morning.

      The ability of immune cells to fight atherosclerotic plaques can depend on CCR2—a chemokine protein linked to immune function and inflammation. CCR2 exhibits a daily rhythm in mice, peaking in the morning, and based on its influence on immune cells, can be followed to understand white blood cell behaviors in mouse models of atherosclerosis.
      Parasite infections are time-of-day dependent. Mice infected with the gastrointestinal parasite Trichuris muris in the morning have been able to kill worms significantly faster than mice infected in the evening.

      A bacterial toxin tied to pneumonia initiates an inflammatory response in the lungs of mice. Recruitment of immune cells during lung inflammation displays a circadian oscillation pattern. Separately, more monocytes can be recruited into the peritoneal cavity, spleen, and liver in the afternoon, thus resulting in enhanced bacterial clearance at that time.

      Allergic symptoms follow a time-of-day dependent rhythmicity, generally worse between midnight and early morning. Hence, the molecular clock can physiologically drive innate immune cell recruitment and the outcomes of asthma in humans, or airway inflammation in mice—the review notes.

      "Investigating circadian rhythms in innate and adaptive immunity is a great tool to generally understand the physiological interplay and time-dependent succession of events in generating immune responses," Scheiermann says. "The challenge lies in how to channel our growing mechanistic understanding of circadian immunology into time-tailored therapies for human patients."
      https://medicalxpress.com/news/2019-...ing-night.html


      2019 May 16
      Association of Sunlight Exposure with Sleep Hours in Iranian Children and Adolescents: The CASPIAN-V Study.

      We aimed to assess the association of sunlight exposure with sleep duration and sleep onset time in children. Data were obtained from the fifth survey of a national school-based surveillance program in Iran. Sunlight exposure time, sleep duration, sleep onset time, physical activity time, mental health status and frequency of consuming coffee and tea were recorded. Overall, 14 274 students aged 7-18?years were recruited. Sleep duration was associated positively with sex, age, body mass index and physical activity, as well as with sunlight exposure and negatively with the consumption of coffee and tea. Higher physical activity, exposure to sunlight and mental status score in children exposed to sunlight via their face, hands, arms and feet, reduced the likelihood of sleep onset time after midnight (odds ratio (OR) = 0.909, 0.741 and 0.554 respectively). Daily exposure to sunlight may increase sleep duration and advance the sleep onset time in children and adolescents.
      https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract

      Sleep duration tied to adverse measures of glycemia

      Self-reported short and long sleep are both associated with adverse measures of glycemia among adults with prediabetes, according to a study published online May 10 in Diabetes Care.

      Babak Mokhlesi, M.D., from the University of Chicago, and colleagues assessed the effect of sleep disturbances and circadian misalignment on adults with prediabetes. The analysis included 962 overweight/obese adults (55 percent male; mean age, 52.2 years) with prediabetes or recently diagnosed, untreated type 2 diabetes who completed a two-hour oral glucose tolerance test and validated sleep questionnaires.

      The researchers found that mean sleep duration was 6.6 hours. More than half of participants reported poor sleep quality (54 percent) and high risk for obstructive sleep apnea (64 percent). Among those reporting less than five hours or more than eight hours of sleep per night, hemoglobin A1c was significantly higher. There was also an association between sleep duration of more than eight hours and higher fasting glucose and between sleep duration of less than six hours and higher body mass index.

      "Further research using objective measures of sleep is needed to better
      delineate the relationship between sleep and glycemia in adults with prediabetes or type 2 diabetes," the authors write.
      Exercising with low muscle glycogen content increases fat oxidation and decreases endogenous, but not exogenous carbohydrate oxidation.

      BACKGROUND:
      Initiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear.

      PURPOSE:
      Determine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism.

      METHODS:
      Using a randomized, crossover design, 12 men (mean?±?SD, age: 21?±?4 y; body mass: 83?±?11?kg; VO2peak: 44?±?3?mL/kg/min) completed 2?cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5?g/kg carbohydrate, 3.0?g/kg fat) or adequate (AD; 6.0?g/kg carbohydrate, 1.0?g/kg fat) glycogen stores. Participants then performed 80-min of steady-state cycle ergometry (64?±?3% VO2peak) while consuming a carbohydrate drink (95?g glucose +51?g fructose; 1.8?g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and 13C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase activity, and gene expression were assessed in muscle.

      RESULTS:
      Initiating steady-state exercise with LOW (217?±?103) or AD (396?±?70; P?<?0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84?±?0.14, AD: 0.87?±?0.16; P?>?0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75?±?0.29 and 0.55?±?0.10) than AD (1.17?±?0.29 and 0.38?±?0.13; all P?<?0.05). Before and after exercise PDH activity was lower (P?<?0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P?<?0.05) in LOW than AD.

      CONCLUSION:
      Initiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.
      https://www.ncbi.nlm.nih.gov/pubmed/31095946

      nauka przez rozdupcanie:

      correlation doesn't imply causation

      Komentarz


      • spacerkiem do szko?y:

        Children who walk to school less likely to be overweight or obese, study suggests

        Children who regularly walk or cycle to school are less likely to be overweight or obese than those who travel by car or public transport, a new study suggests.

        Based on results from more than 2000 primary-age schoolchildren from across London, the researchers found that walking or cycling to school is a strong predictor of obesity levels, a result which was consistent across neighbourhoods, ethnicities and socioeconomic backgrounds. The results are reported in the journal BMC Public Health.

        The study, led by researchers from the University of Cambridge, is the first to assess the impact of physical activity on childhood overweight and obesity levels for primary schoolchildren by simultaneously relating two of the main types of extracurricular physical activity: daily commuting to school and frequency of participation in sport.

        Instead of using Body-mass index (BMI) as a measure of obesity, the researchers measured body fat and muscle mass and assessed how these were correlated with physical activity levels. BMI is the most commonly-used metric to measure obesity levels due to its simplicity, however, it is limited as BMI looks at total weight, including 'healthy' muscle mass, rather than fat mass alone.

        "Both BMI itself and the points at which high BMI is associated with poor health vary with age, sex and ethnicity," said Lander Bosch, a Ph.D. candidate in Cambridge's Department of Geography, and the study's first author. "While adjustments have been made in recent years to account for these variations, BMI remains a flawed way to measure the health risks associated with obesity."

        The current research is based on data from the Size and Lung Function in Children (SLIC) study, carried out at University College London between 2010 and 2013. More than 2000 London primary schoolchildren, from a range of ethnic and socioeconomic backgrounds, were included in the study, which looked at their physical activity levels, body composition and socioeconomic status.

        Close to half of children in the study took part in sport every day, and a similar proportion actively commuted to school, travelling on foot, by bicycle or scooter. The researchers found that children who actively commuted to school had lower body fat, and therefore were less likely to be overweight or obese.

        Paradoxically, using conventional BMI percentiles, children who took part in sport every day appeared more likely to be overweight or obese than those who engaged in sport less than once a week. However, when looking at fat mass and muscle mass separately, children who engaged in sport every day had significantly more muscle development, while their fat mass did not significantly differ.

        "The link between frequent participation in sport and obesity levels has generated inconsistent findings in previous research, but many of these studies were looking at BMI only," said Bosch. "However, when looking at body fat instead, we showed there was a trend whereby children who were not active were more likely to be overweight or obese. It's likely that when looking at BMI, some inactive children aren't classified as obese due to reduced muscle mass."

        The researchers say that it is vital to understand the relationship between obesity levels and different types of physical activity in order to develop informed policy measures that could contribute to the reversal of the childhood obesity epidemic.

        "Our findings suggest that interventions promoting regular participation in sports, and particularly active commuting to school could be promising for combating childhood obesity—it's something so easy to implement, and it makes such a big difference," said Bosch
        https://medicalxpress.com/news/2019-...ght-obese.html

        Sleep problems in teenagers reversed in just one week by limiting screen use

        Sleep in teenagers can be improved by just one week of limiting their evening exposure to light-emitting screens on phones, tablets and computers, according to findings to be presented in Lyon, at the European Society of Endocrinology annual meeting, ECE 2019. The study indicates that by simply limiting their exposure to blue-light emitting devices in the evening, adolescents can improve their sleep quality and reduce symptoms of fatigue, lack of concentration and bad mood, after just one week.

        Recent studies have indicated that exposure to too much evening light, particularly the blue light emitted from screens on smartphones, tablets and computers can affect the brain's clock and the production of the sleep hormone melatonin, resulting in disrupted sleep time and quality. The lack of sleep doesn't just cause immediate symptoms of tiredness and poor concentration but can also increase the risk of more serious long-term health issues such as obesity, diabetes and heart disease. Other studies have suggested that sleep deprivation related to screen time may affect children and adolescents more than adults, but no studies have fully investigated how real-life exposure is affecting sleep in adolescents at home and whether it can be reversed.

        In this collaborative study between the Netherlands Institute of Neuroscience, the Amsterdam UMC and the Dutch National Institute for Public Health and the Environment, researchers investigated the effects of blue light exposure on adolescents at home. Those who had more than 4 hours per day of screen time had on average 30 minutes later sleep onset and wake up times than those who recorded less than 1 hour per day of screen time, as well as more symptoms of sleep loss. The team conducted a randomised controlled trial to assess the effects of blocking blue light with glasses and no screen time during the evening on the sleep pattern of 25 frequent users. Both blocking blue light with glasses and screen abstinence resulted in sleep onset and wake up times occurring 20 minutes earlier, and a reduction in reported symptoms of sleep loss in participants, after just one week.

        Dr. Dirk Jan Stenvers from the department of Endocrinology and Metabolism of the Amsterdam UMC says, "Adolescents increasingly spend more time on devices with screens and sleep complaints are frequent in this age group. Here we show very simply that these sleep complaints can be easily reversed by minimising evening screen use or exposure to blue light. Based on our data, it is likely that adolescent sleep complaints and delayed sleep onset are at least partly mediated by blue light from screens"

        Dr. Stenvers and his colleagues are now interested in whether the relationship between reduced screen time and improved sleep has longer lasting effects, and whether the same effects can be detected in adults.

        Dr. Stenvers comments, "Sleep disturbances start with minor symptoms of tiredness and poor concentration but in the long-term we know that sleep loss is associated with increased risk of obesity, diabetes and heart disease. If we can introduce simple measures now to tackle this issue, we can avoid greater health problems in years to come."
        https://medicalxpress.com/news/2019-...-limiting.html

        Walking and strength training may decrease the risk of dying from liver disease

        Physical activity, including walking and muscle-strengthening activities, were associated with significantly reduced risk of cirrhosis-related death, according to new research. Chronic liver disease is increasing, partly due to the obesity epidemic, and currently there are no guidelines for the optimal type of exercise for the prevention of cirrhosis-related mortality.
        https://www.sciencedaily.com/release...0519162350.htm

        Metals influence C-peptide hormone related to insulin

        Metals such as zinc, copper and chromium bind to and influence a peptide involved in insulin production, according to new work from chemists at the University of California, Davis. The research is part of a new field of "metalloendocrinology" that takes a detailed look at the role of metals in biological processes in the body.
        https://www.sciencedaily.com/release...0517133514.htm


        Circadian Disruption Changes Gut Microbiome Taxa and Functional Gene Composition

        Disrupted circadian rhythms and alterations of the gut microbiome composition were proposed to affect host health. Therefore, the aim of this research was to identify whether these events are connected and if circadian rhythm disruption by abnormal light–dark (LD) cycles affects microbial community gene expression and host vulnerability to intestinal dysfunction. Mice were subjected to either a 4-week period of constant 24-h light or of normal 12-h LD cycles. Stool samples were collected at the beginning and after the circadian rhythm disruption. A metatranscriptomic analysis revealed an increase in Ruminococcus torques, a bacterial species known to decrease gut barrier integrity, and a decrease in Lactobacillus johnsonii, a bacterium that helps maintain the intestinal epithelial cell layer, after circadian rhythm disruption. In addition, genes involved in pathways promoting host beneficial immune responses were downregulated, while genes involved in the synthesis and transportation of the endotoxin lipopolysaccharide were upregulated in mice with disrupted circadian cycles. Importantly, these mice were also more prone to dysfunction of the intestinal barrier. These results further elucidate the impact of light-cycle disruption on the gut microbiome and its connection with increased incidence of disease in response to circadian rhythm disturbances.
        http://snip.ly/i2du8v#https://www.nc...s_Wg5DQgeR6Tw4

        Human sebum requires de novo lipogenesis, which is increased in acne vulgaris and suppressed by acetyl-CoA carboxylase inhibition

        Sebum plays important physiological roles in human skin. Excess sebum production contributes to the pathogenesis of acne vulgaris, and suppression of sebum production reduces acne incidence and severity. We demonstrate that sebum production in humans depends on local flux through the de novo lipogenesis (DNL) pathway within the sebocyte. About 80 to 85% of sebum palmitate (16:0) and sapienate (16:1n10) were derived from DNL, based on stable isotope labeling, much higher than the contribution of DNL to triglyceride palmitate in circulation (~20%), indicating a minor contribution by nonskin sources to sebum lipids. This dependence on local sebocyte DNL was not recapitulated in two widely used animal models of sebum production, Syrian hamsters and Göttingen minipigs. Confirming the importance of DNL for human sebum production, an acetyl-CoA carboxylase inhibitor, ACCi-1, dose-dependently suppressed DNL and blocked synthesis of fatty acids, triglycerides, and wax esters but not free sterols in human sebocytes in vitro. ACCi-1 dose-dependently suppressed facial sebum excretion by ~50% (placebo adjusted) in human individuals dosed orally for 2 weeks. Sebum triglycerides, wax esters, and free fatty acids were suppressed by ~66%, whereas non–DNL-dependent lipid species, cholesterol, and squalene were not reduced, confirming selective modulation of DNL-dependent lipids. Last, individuals with acne vulgaris exhibited increased sebum production rates relative to individuals with normal skin, with >80% of palmitate and sapienate derived from DNL. These findings highlight the importance of local sebocyte DNL for human skin sebaceous gland biology and illuminate a potentially exploitable therapeutic target for the treatment of acne vulgaris.
        https://stm.sciencemag.org/content/11/492/eaau8465

        Researchers document impact of coffee on bowels

        Coffee drinkers know that coffee helps keep the bowels moving, but researchers in Texas are trying to find out exactly why this is true, and it doesn't seem to be about the caffeine, according to a study presented at Digestive Disease Week (DDW) 2019. Researchers, feeding rats coffee and also mixing it with gut bacteria in petri dishes, found that coffee suppressed bacteria and increased muscle motility, regardless of caffeine content.
        https://medicalxpress.com/news/2019-...ee-bowels.html
        Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
        correlation doesn't imply causation

        Komentarz


        • Meal Timing, Aging, and Metabolic Health

          A growing body of evidence suggests that meal timing is an important factor for metabolic regulation and that the circadian clock tightly interacts with metabolic functions. The proper functioning of the circadian clock is critical for maintaining metabolic health. Therefore, chrononutrition, a novel discipline which investigates the relation between circadian rhythms, nutrition, and metabolism, has attracted increasing attention in recent years. Circadian rhythms are strongly affected by obesity, type 2 diabetes, and other dietary-induced metabolic diseases. With increasing age, the circadian system also undergoes significant changes which contribute to the dysregulation of metabolic rhythms. Metabolic diseases are a major health concern, particularly in light of a growing aging population, and effective approaches for their prevention and treatment are urgently needed. Recently, animal studies have impressively shown beneficial effects of several dietary patterns (e.g., caloric restriction or time-restricted feeding) on circadian rhythms and metabolic outcomes upon nutritional challenges. Whether these dietary patterns show the same beneficial effects in humans is, however, less well studied. As indicated by recent studies, dietary approaches might represent a promising, attractive, and easy-to-adapt strategy for the prevention and therapy of circadian and metabolic disturbances in humans of different age.

          https://www.mdpi.com/1422-0067/20/8/1911

          Anxiety might be alleviated by regulating gut bacteria

          People who experience anxiety symptoms might be helped by taking steps to regulate the microorganisms in their gut using probiotic and non-probiotic food and supplements, suggests a review of studies published today in the journal General Psychiatry.
          https://medicalxpress.com/news/2019-...-bacteria.html

          Do your gut microbes affect your brain dopamine?

          Increasing evidence shows changes in gut microbiota composition in association with psychiatric disorders, including anxiety and depression. Moreover, it has been reported that perturbations in gut microbe diversity and richness influence serotonergic, GABAergic, noradrenergic, and dopaminergic neurotransmission. Among these, dopamine is regarded as a main regulator of cognitive functions such as decision making, attention, memory, motivation, and reward. In this work, we will highlight findings that link alterations in intestinal microbiota and dopaminergic neurotransmission, with a particular emphasis on the mesocorticolimbic circuit, which is involved in reward to natural reinforcers, as well as abuse substances. For this, we reviewed evidence from studies carried out on germ-free animals, or in rodents subjected to intestinal dysbiosis using antibiotics, and also through the use of probiotics. All this evidence strongly supports that the microbiota-gut-brain axis is key to the physiopathology of several neuropsychiatric disorders involving those where dopaminergic neurotransmission is compromised. In addition, the gut microbiota appears as a key player when it comes to proposing novel strategies to the treatment of these psychiatric conditions.
          https://link.springer.com/article/10...13-019-05265-5

          Stress from work, home can harm women's hearts

          Even with supportive spouses, many women still find themselves helping the kids with homework and cleaning up household messes, often while scrambling to make dinner after a 10-hour workday filled with deadlines and challenging colleagues.

          All that stress could put women at higher risk than men for having a stroke or developing diabetes, heart disease and other chronic conditions, according to a growing number of studies.
          https://medicalxpress.com/news/2019-...en-hearts.html

          Heavy teen boys may face higher heart disease risk as adults

          (HealthDay)—Just a few extra pounds during adolescence may translate into higher odds for heart disease in adulthood, a new study of young men suggests.

          It included about 1.7 million Swedish men who began military service at ages 18 or 19 between 1969 and 2005. They were followed for up to 46 years.

          During the follow-up, nearly 4,500 were diagnosed with cardiomyopathy, an uncommon heart muscle condition that can lead to heart failure. Average age at diagnosis was 45.5 years.
          https://medicalxpress.com/news/2019-...her-heart.html

          Obesity risk may be increased by exposure to common environmental chemicals

          Exposure to common every day chemicals, called phthalates, may increase the risk of metabolic disorders including obesity and diabetes, according to findings to be presented in Lyon, at the European Society of Endocrinology annual meeting, ECE 2019
          https://medicalxpress.com/news/2019-...chemicals.html


          jajka jednak zdrowe

          Dietary cholesterol and egg consumption do not increase the risk of stroke

          A new study from the University of Eastern Finland shows that a moderately high intake of dietary cholesterol or consumption of up to one egg per day is not associated with an elevated risk of stroke. Furthermore, no association was found in carriers of the APOE4 phenotype, which affects cholesterol metabolism and is remarkably common among the Finnish population. The findings were published in the American Journal of Clinical Nutrition.
          https://medicalxpress.com/news/2019-...nsumption.html


          The Temperature Dependence of Sleep.

          Mammals have evolved a range of behavioural and neurological mechanisms that coordinate cycles of thermoregulation and sleep. Whether diurnal or nocturnal, sleep onset and a reduction in core temperature occur together. Non-rapid eye movement (NREM) sleep episodes are also accompanied by core and brain cooling. Thermoregulatory behaviours, like nest building and curling up, accompany this circadian temperature decline in preparation for sleeping. This could be a matter of simply comfort as animals seek warmth to compensate for lower temperatures. However, in both humans and other mammals, direct skin warming can shorten sleep-latency and promote NREM sleep. We discuss the evidence that body cooling and sleep are more fundamentally connected and that thermoregulatory behaviours, prior to sleep, form warm microclimates that accelerate NREM directly through neuronal circuits. Paradoxically, this warmth might also induce vasodilation and body cooling. In this way, warmth seeking and nesting behaviour might enhance the circadian cycle by activating specific circuits that link NREM initiation to body cooling. We suggest that these circuits explain why NREM onset is most likely when core temperature is at its steepest rate of decline and why transitions to NREM are accompanied by a decrease in brain temperature. This connection may have implications for energy homeostasis and the function of sleep.
          https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
          correlation doesn't imply causation

          Komentarz


          • Czytam pedalski, to z entuzjazmem zajrza?em a tu dupa, ci?gle to samo.

            Komentarz


            • I jeszcze po zagramanicznemu..

              Komentarz


              • Zamieszczone przez paavo Zobacz posta
                Czytam pedalski, to z entuzjazmem zajrza?em a tu dupa, ci?gle to samo.
                wybacz przyjacielu, ?e ci?gle o tej t?czy pierdole .. w zasadzie to mi si? powoli nudzi wi?c temat w najbli?szym czasie pójdzie pewnie do zamkni?cia.

                wi?c ?eby zasia? ziarno niepewno?ci powiem tak:

                Circadian mechanism may not be driver behind compound linked to obesity and diabetes

                SR9009 is a compound that can lead to a wide range of health benefits in animals, including reduced risk of obesity and type 2 diabetes. Until now, researchers—and companies that sell the compound for human use in the form of a nutraceutical—have attributed the effects to SR9009's role in altering the body's circadian clock, specifically its work through proteins called REV-ERBS that link metabolism and circadian rhythm. However, in a first-of-its-kind study from Penn Medicine, published today in PNAS, researchers found that SR9009 can effect cell growth and metabolic function without the involvement of REV-ERBs.
                https://medicalxpress.com/news/2019-...nd-linked.html

                pisa?em, ?e insulina jest hormonem solarnym, ale wi?cej ?miechu by?o ni? powagi, wi?c teraz z przytupem, a jednocze?nie ?eby uspokoi?

                "a s?owo cia?em si? sta?o"
                Insulin under the influence of light



                The disruption of internal clocks seems to play a significant role in the explosion of metabolic diseases observed in recent decades, particularly diabetes. Scientists have improved understanding of the importance of day-night alternation on the effect of insulin and the body's glycemic management, but what about the mechanisms involved? How does the organism synchronize its clocks?

                By understanding how the brain links the effects of insulin to light, researchers at the University of Geneva (UNIGE) are deciphering how insulin sensitivity fluctuates according to circadian cycles, but also according to the organs involved. At the heart of their discovery are neurons of the ventromedial hypothalamic nucleus, a part of the brain that masters this delicate balance. These results, to be reported in the journal Cell Reports, should also encourage diabetic patients and their doctors to consider the best time to take insulin to properly control its effect and limit the risk of hypoglycemia.

                The balance between the secretion and action of hormones is essential for the body to function properly. Thus, the secretion of several hormones, including insulin, varies over a 24-hour period and any change in this rhythm seems to predispose to metabolic diseases. To synchronize itself, the body takes into account two essential elements: the alternation of light and darkness as well as that of feeding and fasting. Indeed, the light perceived by retinal neurons is transmitted to the brain, which in turn regulates the peripheral clocks located throughout the body.

                "Our hypothesis was that insulin sensitivity varies according to the daily 24-hour cycle, but also according to the tissues. Since we already knew that some neurons in the ventromedial hypothalamic nucleus (VMH)—a region of the hypothalamus—controls the sympathetic nervous system output to skeletal muscle in mice, we looked at these neurons—called VMH SF1 neurons—in regulating insulin action in this tissue," explains Roberto Coppari, professor at the Diabetes Centre of UNIGE Faculty of Medicine, who led this work.

                From the brain to the organs: different mechanisms depending on the tissue

                First, the scientists performed a complete evaluation of insulin action in different tissues in mice (gastrocnemius and soleus muscles, both located in the leg, adipose tissue, and liver) and observed significant variation in all tissues involved. By keeping mice in a cycle of 12 hours of light and 12 hours of darkness, insulin sensitivity was logically the lowest during the rest period.

                They repeated the same measurements on animals in which the SIRT1 gene (a gene linked to the regulation of core clock molecular components) was deleted only in the few thousands of VMH SF1 neurons. "Indeed, we already knew that mice with an alteration of this gene in VMH SF1 neurons had propensity to insulin resistance. But by which mechanism?" says Giorgio Ramadori, a researcher at the Diabetes Centre and the first author of this study.

                By modulating the time of exposure to light, the researchers demonstrated that the SIRT1 gene of the VMH SF1 neurons plays a key role in the action of insulin in the gastrocnemius muscle, but not in other tissues, Roberto Coppari says. "This teaches us two things: On the one hand, different neurons have the task of conveying light/darkness cycle inputs to diverse organs, but on the other hand, the disruption of only one of these regulatory pathways is enough to increase the individual's risk of developing diabetes."

                To better assess the effect of light on tissue sensitivity to insulin, researchers measured insulin-induced glucose absorption. It turns out that a small disturbance in photic inputs (e.g. an hour of light exposure in the middle of the dark cycle, or light removal for two days) is enough to cause a negative effect. Indeed, increased or decreased light exposure can profoundly influence the sensitivity of tissues to insulin and the alteration, however minimal, of this mechanism is sufficient to significantly disrupt metabolic homeostasis. This would explain why people exposed to light at the wrong time—workers in shift patterns, for example—are more likely to develop metabolic diseases (e.g. diabetes).

                Taking into account the time of day

                Today, more than 450 million people worldwide have diabetes and many of them need daily insulin injections. When endogenous insulin is not produced in sufficient amounts, such as in people with type 1 diabetes insulin, therapy is the only treatment available, but this approach is not without risk—including potentially severe hypoglycemia that can lead to coma and even death.

                "In practice, the amount of insulin administered to patients is calculated on the basis of carbohydrate intake," says Roberto Coppari. If, as our results indicate, insulin sensitivity varies with time of day and individuals' circadian rhythm, this parameter should be taken into account for patients to better manage their treatment and limit its risks. "Beyond insulin, the influence of time of day on the effectiveness of drug treatments should be studied much more broadly."
                a jakby komu? za pedalsko si? zrobi?o

                ???? ????

                Dawn-to-sunset fasting suggests potential new treatment for obesity-related conditions

                Fasting from dawn to sunset for 30 days increased levels of proteins that play a crucial role in improving insulin resistance and protecting against the risks from a high-fat, high-sugar diet, according to research presented at Digestive Disease Week (DDW) 2019. The study, which was based on the fasting practices of Ramadan, a spiritual practice for Muslims, offers a potential new treatment approach for obesity-related conditions, including diabetes, metabolic syndrome and non-alcoholic fatty liver disease (NAFLD).

                "According to World Health Organization data, obesity affects over 650 million people worldwide, placing them at risk for any number of health conditions," said Ayse Leyla Mindikoglu, MD, MPH, lead author of the study and associate professor of medicine and surgery at Baylor College of Medicine, Texas. "Feeding and fasting can significantly impact how the body makes and uses proteins that are critical to decreasing insulin resistance and maintaining a healthy body weight. Therefore, the timing of and duration between meals could be important factors to consider for people struggling with obesity-related conditions."

                The pilot study included 14 healthy individuals who fasted (no food or drink) approximately 15 hours a day from dawn to sunset for 30 days during Ramadan. Researchers collected blood samples from the individuals before beginning the religious fast, again at the fourth week of fasting, and then one-week post-fasting. Resulting blood samples showed increased levels of tropomyosin (TPM) 1, 3 and 4, proteins that have a role in maintaining healthy cells and cell repairs important to the body's response to insulin.

                TPM3 plays a key role in increasing insulin sensitivity, which allows the cells of the body to use blood glucose more effectively, reducing blood sugar. Findings from the study showed a significant increase in TPM3 gene protein products between the initiation of the fast and the test one week afterwards. Similar results over that period were found for TPM1 and TPM4 gene protein products.

                "We are in the process of expanding our research to include individuals with metabolic syndrome and NAFLD to determine whether results are consistent with those of the healthy individuals," said Dr. Mindikoglu. "Based on our initial research, we believe that dawn-to-sunset fasting may provide a cost-effective intervention for those struggling with obesity-related conditions."
                https://medicalxpress.com/news/2019-...y-related.html

                katolickie ?winie ....

                The Circadian Syndrome: is the metabolic syndrome and much more!



                The Metabolic Syndrome is a cluster of cardio?metabolic risk factors and comorbidities conveying high risk of both cardiovascular disease and type 2 diabetes. It is responsible for huge socio?economic costs with its resulting morbidity and mortality in most countries. The underlying aetiology of this clustering has been the subject of much debate. More recently, significant interest has focussed on the involvement of the circadian system, a major regulator of almost every aspect of human health and metabolism. The circadian syndrome has now been implicated in several chronic diseases including type 2 diabetes and cardiovascular disease. There is now increasing evidence connecting disturbances in circadian rhythm with not only the key components of the Metabolic Syndrome but also its main co?morbidities including sleep disturbances, depression, steatohepatitis and cognitive dysfunction. Based on this, we now propose that circadian disruption may be an important underlying aetiological factor for the Metabolic Syndrome and we suggest that it be renamed the “Circadian Syndrome”. With the increased recognition of the “Circadian Syndrome”, circadian medicine, through the timing of exercise, light exposure, food consumption, dispensing of medications and sleep, is likely to play a much greater role in the maintenance of both individual and population health in the future.
                https://onlinelibrary.wiley.com/doi/...111/joim.12924

                A FOOD PYRAMID FOR KIDS' MEDIA CONSUMPTION
                https://www.wired.com/story/kids-screen-time-pyramid/

                no dobra wracamy do nudy:

                Exercise: Psych patients' new primary prescription

                When it comes to inpatient treatment of a range of mental health and mood disorders—from anxiety and depression to schizophrenia, suicidality and acute psychotic episodes—a new study advocates for exercise, rather than psychotropic medications, as the primary prescription and method of intervention. Findings from the study reveal that physical exercise is so effective at alleviating patient symptoms that it could reduce patients' time admitted to acute facilities and reliance on psychotropic medications.
                https://medicalxpress.com/news/2019-...scription.html

                Why lack of sleep is bad for your heart

                In recent years, numerous studies have shown that people who don't get enough sleep are at greater risk of stroke and heart attack.
                A new University of Colorado Boulder study, published in the journal Experimental Physiology, helps explain why.
                It found that people who sleep fewer than 7 hours per night have lower blood levels of three physiological regulators, or microRNAs, which influence gene expression and play a key role in maintaining vascular health.
                https://medicalxpress.com/news/2019-...bad-heart.html

                Earlier bedtimes help kids fight obesity

                (HealthDay)—With childhood obesity rates high, many studies have investigated lifestyle factors that can make a difference—which ones increase the risk and which ones reduce it.
                Beyond diet, a lack of sleep has been linked to weight gain both in adults and children, so it's important that kids get enough shuteye, even with their—and your—busy schedules.
                Since a child's wake-up time is usually determined by when school or day care starts and can't be easily altered, an earlier bedtime is needed to ensure kids get the sleep they need, according to research published in The Journal of Pediatrics.
                https://medicalxpress.com/news/2019-...s-obesity.html

                Exercise may help teens sleep longer, more efficiently

                Getting more exercise than normal—or being more sedentary than usual—for one day may be enough to affect sleep later that night, according to a new study led by Penn State.

                In a one-week micro-longitudinal study, the researchers found that when teenagers got more physical activity than they usually did, they got to sleep earlier, slept longer and slept better that night.
                https://medicalxpress.com/news/2019-...ficiently.html

                a na koniec - pavo co? ze specjalna dedykacj? !

                Phytonutrients: Paint your plate with the colors of the rainbow



                Did you know that adding color to your meals will help you live a longer, healthier life? Colorful fruits and vegetables can paint a beautiful picture of health because they contain phytonutrients, compounds that give plants their rich colors as well as their distinctive tastes and aromas. Phytonutrients also strengthen a plant’s immune system. They protect the plant from threats in their natural environment such as disease and excessive sun.
                https://www.health.harvard.edu/blog/...ampaign=buffer

                Zamieszczone przez semozo Zobacz posta
                I jeszcze po zagramanicznemu..
                od bidy:
                https://translate.google.pl/

                wrzucam przecie? w PL jak wyjdzie co? ciekawego, ale wi?kszo?? niusów omija nasz wspania?y j?zyk
                Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
                correlation doesn't imply causation

                Komentarz


                • Ja tak tylko. Co? tam paniumaju.

                  Komentarz






                  • Vitamin D deficiency tied to gestational diabetes risk

                    (HealthDay)—Maternal vitamin D deficiency, as early as the first trimester of pregnancy, is associated with an increased risk for gestational diabetes mellitus (GDM), according to a study recently published in Diabetes, Obesity and Metabolism.

                    Jin Xia, from the Richard M. Fairbanks School of Public Health at Indiana University in Indianapolis, and colleagues used data from the Fetal Growth Studies-Singleton Cohort to prospectively investigate the relationship between vitamin D status during early to midpregnancy and GDM risk. Plasma levels of 25-hydroxyvitamin D2 and D3 and vitamin D binding protein were measured at gestational weeks 10 to 14, 15 to 26, 23 to 31, and 33 to 39 in 107 women with GDM and 214 controls.
                    https://medicalxpress.com/news/2019-...stational.html

                    tak przy okazji warto wiedzie?:

                    Fotony docieraj?ce do p?odu wp?ywaj? na rozwój siatkówki

                    ?wiat?o podczas ?ycia p?odowego jest niezb?dne do prawid?owego rozwoju oka, a konkretnie siatkówki.

                    Odkryli?my ?wiat?owra?liwy szlak, który kontroluje liczb? neuronów siatkówki i rozwój unaczynienia oka, a nale?y pami?ta?, ?e wiele powa?nych chorób oka to w?a?nie choroby naczyniowe - podkre?la dr Richard Lang z Centrum Medycznego Cincinnati Children's Hospital.

                    Kilka etapów rozwoju mysich oczu zachodzi po urodzeniu, dlatego zawsze zak?adali?my, ?e je?li ?wiat?o odgrywa jak?? rol? w kszta?towaniu oka tych gryzoni, dzieje si? to ju? po opuszczeniu przez m?ode ?ona matki - ujawnia dr David Copenhagen z Uniwersytetu Kalifornijskiego w San Francisco. W ramach nowego studium Amerykanie zauwa?yli jednak, ?e aby powsta?o zdrowe oko, do aktywacji ?wiat?owra?liwego szlaku powinno doj?? jeszcze w czasie ci??y. Do ok. 16. jej dnia barier? matczynego cia?a musi pokona? wystarczaj?ca liczba fotonów.

                    Zespó? zauwa?y?, ?e fotony aktywuj? u p?odów melanopsyn?, pomagaj?c w ten sposób zainicjowa? normalny rozwój unaczynienia i neuronów siatkówkowych.

                    Jedn? z funkcji ?wiat?owra?liwego szlaku jest kontrola liczby naczy? krwiono?nych. W tym samym czasie musi doj?? do regresji p?odowej waskulatury (oczyszczenia szlaku wzrokowego) i uformowania unaczynienia siatkówkowego (neurony siatkówki maj? du?e potrzeby metaboliczne). O tym, jak wa?na jest precyzyjna kontrola tego procesu, ?wiadczy retinopatia wcze?niaków, czyli uszkodzenie siatkówki wywo?ane rozplemem naczy?.

                    Zespó? Langa i Copenhagena przeprowadzi? na myszach szereg eksperymentów. Gryzonie wychowywano w kompletnych ciemno?ciach lub w warunkach normalnego nast?powania po sobie dnia i nocy. Oba scenariusze wdro?ono pod koniec ci??y. W ten sposób mo?na by?o sprawdzi?, jak rozwijaj? si? naczynia. Funkcj? ?wiat?owra?liwego szlaku weryfikowano, wywo?uj?c mutacj? genu Opn4, który odpowiada za produkcj? melanopsyny.

                    Zarówno u myszy rosn?cych w ciemno?ci, jak i u osobników ze zmutowanym Opn4 wyst?powa? nap?dzany czynnikiem wzrostu ?ródb?onka naczyniowego (ang. vascular endothelial growth factor, VEGF) rozplem naczy?. Ósmego dnia po urodzeniu utrzymywa?a si? jeszcze waskulatura p?odowa. W zwyk?ych warunkach ?wiat?owra?liwy szlak "przyci??by" liczb? neuronów siatkówki i ograniczy?by niedotlenienie, wp?ywaj?c w konsekwencji na miejscow? ekspresj? VEGF.
                    +

                    Modelowa siatkówka z in vitro

                    Biolodzy z Uniwersytetu Johnsa Hopkinsa w Baltimore stworzyli od zera ludzk? siatkówk?, aby okre?li?, w jaki sposób powstaj? komórki pozwalaj?ce widzie? ?wiat w wielu barwach.

                    Wyniki prac, opublikowane w czasopi?mie „Science", stanowi? podstaw? do opracowania terapii chorób oczu, takich jak daltonizm i zwyrodnienie plamki ?ó?tej.

                    ORGAN Z PROBÓWKI
                    Fascynuj?cy jest fakt, ?e polem badania rozwoju cz?owieka na poziomie komórkowym by?y stworzone przez laboratorium organoidy. S? one zminiaturyzowan? i uproszczon?, ale trójwymiarow? wersj? ludzkiego narz?du. Produkowane in vitro, pochodz? z jednej lub kilku komórek danej tkanki, zarodkowych lub indukowanych pluripotencjalnych (przewa?nie pobranych z cia?a osoby doros?ej) komórek macierzystych. S? zdolne do odtworzenia specyficznych funkcji narz?du, takich jak skurcz, aktywno?? nerwowa, wydzielanie hormonalne, filtracja i wydalanie.

                    Komórki organoidów s? pogrupowane i rozmieszczone przestrzennie, podobnie jak w naturalnym organie. Powsta?y jako narz?dzie do badania podstawowych procesów biologicznych, takich jak komunikacja w obr?bie organów, ich interakcje z otoczeniem.

                    Kultura in vitro czyni ten system ?atwym do manipulowania i u?atwia jego monitorowanie. Pe?ne narz?dy by?yby trudne do wyhodowania, poniewa? ich wielko?? ogranicza przenikanie do wewn?trz sk?adników od?ywczych. Niewielki rozmiar organoidów eliminuje ten problem. Z drugiej strony nie wykazuj? one wszystkich cech narz?dowych, a przecie? interakcje z innymi organami nie s? mo?liwe do odtworzenia in vitro.

                    Organoidy w znacznym stopniu przyczyni?y si? do poszerzenia naszego zrozumienia tworzenia si? tkanek i biologii rozwojowej, na przyk?ad o?rodkowego uk?adu nerwowego, do zrozumienia si? fizycznych, które le?? u podstaw powstawania siatkówki. S? równie? wykorzystywane do badania przep?ywu substancji – pobierania sk?adników od?ywczych, transportu leków i wydzielania hormonów metabolicznych. Ma to wielkie znaczenie w kontek?cie chorób zwi?zanych ze z?ym wch?anianiem i schorze? takich jak oty?o??, insulinooporno?? i cukrzyca.

                    – To, co badamy, wygl?da jak normalnie rozwijaj?ce si? oko, rosn?ce w naczyniu – mówi prof. Robert Johnston, biolog rozwojowy w Johns Hopkins. – Mamy model, którym mo?emy manipulowa? bez bezpo?redniej ingerencji w ludzki organizm.

                    Laboratorium Johnstona bada, w jaki sposób tworzy si? tkanka, co dzieje si? w ?onie matki, gdy rozwijaj?ca si? komórka przekszta?ca si? w specyficzny organ. To aspekt ludzkiej biologii, który jest w du?ej mierze nieznany.

                    ?WIAT W TRZECH BARWACH
                    Johnston i jego zespó? skupili si? na komórkach, które pozwalaj? ludziom zobaczy? kolor niebieski, czerwony i zielony – s? to trzy fotoreceptory w kszta?cie sto?ka znajduj?ce si? w ludzkim oku.

                    Wi?kszo?? bada? nad wzrokiem wykonuje si? na myszach i rybach, ale ?aden z tych gatunków nie ma umiej?tno?ci widzenia w kolorze tak, jak cz?owiek. St?d tak wa?ne by?o zastosowanie ludzkich komórek macierzystych.

                    Gdy ros?y one w laboratorium i sta?y si? pe?nowymiarowymi siatkówkami, zespó? odkry?, ?e komórki wykrywaj?ce barw? niebiesk? zmaterializowa?y si? jako pierwsze, dopiero pó?niej przyszed? czas na rozpoznaj?ce kolor czerwony i zielony. W obu przypadkach okaza?o si?, ?e kluczem do zmiany molekularnej by? hormon tarczycy. Co wa?ne, jego poziom by? kontrolowany w ca?o?ci przez samo oko, a nie przez tarczyc?, której oczywi?cie nie by?o w naczyniu.

                    Dzi?ki zrozumieniu, w jaki sposób pewna ilo?? hormonu tarczycy wp?ywa na ten rodzaj komórek, zespó? by? w stanie manipulowa? wynikiem, tworz?c siatkówki, które gdyby by?y cz??ci? kompletnego ludzkiego oka, zobaczy?yby tylko kolor niebieski, i takie, które mog?yby ujrze? wy??cznie zielon? i czerwon? barw?.

                    Odkrycie roli hormonu tarczycy w procesie rozwoju siatkówki daje wgl?d w to, dlaczego u wcze?niaków cz??ciej wyst?puj? zaburzenia widzenia, poniewa? po od??czeniu si? od matczynych zapasów spada u nich poziom hormonów tarczycy. – Je?li potrafimy odpowiedzie? na pytanie, co prowadzi komórk? do jej formy docelowej, jeste?my bli?ej mo?liwo?ci przywrócenia widzenia kolorów osobom, których receptory zosta?y uszkodzone – powiedzia?a autorka badania Kiara Eldred.

                    Naukowcy chc? w przysz?o?ci u?ywa? organoidów do szerszych bada? na temat postrzegania kolorów, a tak?e ?ó?tej plamki, której zwyrodnienie jest jedn? z g?ównych przyczyn ?lepoty u ludzi.
                    a jakby kogo? zaintrygowa?o to zapraszam:

                    The circadian clock gene Bmal1 controls thyroid hormone-mediated spectral identity and cone photoreceptor function


                    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647869/

                    Exposure to solar ultraviolet radiation limits diet-induced weight gain, increases liver triglycerides and prevents the early signs of cardiovascular disease in mice.

                    BACKGROUND AND AIMS: Sunlight exposure is associated with a number of health benefits including protecting us from autoimmunity, cardiovascular disease, obesity and diabetes. Animal studies have confirmed that ultraviolet (UV)-B radiation, independently of vitamin D, can limit diet-induced obesity, metabolic syndrome and atherosclerosis. The aim of this study is to investigate whether exposure to the UV radiation contained in sunlight impacts on these disease parameters.

                    METHODS AND RESULTS: We have trialled an intervention with solar UV in obese and atherosclerosis-prone mice. We have discovered that solar-simulated UV can significantly limit diet-induced obesity and reduce atheroma development in mice fed a diet high in sugar and fat. The optimal regime for this benefit was exposure once a week to solar UV equivalent to approximately 30 min of summer sun. Exposure to this optimal dose of solar UV also led to a significant increase in liver triglycerides which may protect the liver from damage.

                    CONCLUSION: Our results show that the UV contained in sunlight has the potential to prevent and treat chronic disease at sites distant from irradiated skin. A major health challenge going forward will be to harness the power of the sun safely, without risking an increase in skin cancers.
                    https://www.ncbi.nlm.nih.gov/m/pubmed/30956026/

                    MAY 22, 2019
                    Contact with nature during childhood could lead to better mental health in adulthood



                    Adults who had close contact with natural spaces during their childhood could have a better mental health than those who had less contact, according to a new study by the Barcelona Institute for Global Health (ISGlobal) involving four European cities.
                    Exposure to natural outdoor environments has been associated with several health benefits, including a better cognitive development and better mental and physical health. However, few studies have explored the impact of childhood exposure to natural environments on mental health and vitality in adulthood. Furthermore, studies have more frequently considered green spaces (gardens, forests, urban parks) than blue spaces (canals, ponds, creeks, rivers, lakes, beaches, etc.).
                    This study, published in the International Journal of Environment Research and Public Health, was performed within the framework of the PHENOTYPE project with data from almost 3,600 adults from Barcelona (Spain), Doetinchem (Netherlands), Kaunas (Lithuania) and Stoke-on-Trent (United Kingdom).
                    https://www.ncbi.nlm.nih.gov/m/pubmed/30956026/

                    wczesne igranie z neuronami dopaminergicznymi ko?czy si?
                    predisposes brain to addiction later
                    Early life exposure to nicotine alters neurons, predisposes brain to addiction later

                    Neonatal exposure to nicotine alters the reward circuity in the brains of newborn mice, increasing their preference for the drug in later adulthood, report researchers at University of California San Diego School of Medicine in a study published "in press" April 24, 2019 in Biological Psychiatry.
                    a co z telefonami ?

                    WFT !

                    Hypertension found in children exposed to flower pesticides

                    Neonatal exposure to nicotine alters the reward circuity in the brains of newborn mice, increasing their preference for the drug in later adulthood, report researchers at University of California San Diego School of Medicine in a study published "in press" April 24, 2019 in Biological Psychiatry.
                    https://medicalxpress.com/news/2019-...esticides.html

                    Leaving school earlier could increase the risk of heart disease

                    Although it has been known for a long time, that education, and socioeconomic position affect health, particularly in later life, there was limited knowledge as to why. New research has found that increased levels of BMI, blood pressure and smoking partly explain why people who left school at an earlier age could be at an increased risk of heart disease.

                    The study led by the University of Bristol and Imperial College London, and published in the BMJ today, investigated the role of body mass index (BMI), systolic blood pressure (SBP) and smoking in European populations to explain the effect of education on the risk of cardiovascular disease, which affects the heart or blood vessels and includes heart disease, heart attack and stroke.
                    https://medicalxpress.com/news/2019-...t-disease.html


                    Researchers identify genetic switch that controls conversion of bad to good fat



                    Fat cells. They are the bane of a dieter's existence, but fat is important. Previous studies showed the subcutaneous white fat cells can transform to brown and beige varieties when exposed to cold stress. These dusky forms of fat, burn energy more effectively to keep an organism warm. Researchers at University of Utah Health have figured out a way to make more of these energy-burning fat cells. They have identified TLE3, a genetic switch that stops the conversion of white fat into these thermogenic varieties. The results are available online in the May 23 issue of the journal Genes and Development.

                    "Our story highlights that there are different types of fat cells, and TLE3 is one way to address how fat cells are programmed," said Claudio Villanueva, Ph.D., assistant professor in biochemistry at U of U Health and senior author on the paper. "If we could find therapeutic ways to inhibit TLE3, we may be able to develop interventions for type II diabetes. Therapies that help lower blood glucose levels are gravely needed."

                    Fat cells come in three varieties. White fat, the most common variety, is stored fat associated with metabolic disorders, like diabetes and obesity. Brown and beige fat contain more mitochondria, the energy centers of the cell, allowing these varieties to burn fuel more efficiently. Brown fat is activated in cold conditions and burned to create heat. Beige fat is found in bundles nestled within white fat, but little is known about it.

                    Previous research found that white fat tissue that overexpresses early B-cell factor 2 (EFB2) recruits more beige fat cells, but this protein-coding gene is triggered by many factors. Villanueva and his team focused on transducing-like enhancer 3 (TLE3), a protein situated in the same region as EFB2. They found that TLE3 acts like a switch, stopping EFB2 from converting white to beige fat and preventing energy expenditure and glucose use.

                    The team deleted TLE3 in mice and placed the animals in cold conditions for several days. According to Villanueva, they tried to recreate a situation where an animal would be trying to develop beige fat cells to understand impact of the loss of TLE3. In the absence of this gene, the knock-out mice recruited more beige fat cells. The team examined the impact of the abundance of beige fat on animal metabolism.

                    "The knock-out mice experienced enhanced energy expenditure under normal conditions and weight loss during cold conditions," said Stephanie Pearson, Ph.D., a researcher working in Villanueva's lab and first author on the paper. "Even without cold stimulation, the knock-out mice did not gain as much weight."

                    Villanueva believes these results could be used to create interventions for metabolic disorders.

                    "Long-term we want to identify or develop drugs that will target TLE3 that can be used as an intervention for patients with type 2 diabetes and obesity," he said.

                    Therapeutic Potential of Exogenous Ketone Supplement Induced Ketosis in the Treatment of Psychiatric Disorders: Review of Current Literature

                    Globally, psychiatric disorders, such as anxiety disorder, bipolar disorder, schizophrenia, depression, autism spectrum disorder, and attention-deficit/hyperactivity disorder (ADHD) are becoming more prevalent. Although the exact pathological alterations are not yet clear, recent studies have demonstrated that widespread changes of very complex metabolic pathways may partially underlie the pathophysiology of many psychiatric diseases. Thus, more attention should be directed to metabolic-based therapeutic interventions in the treatment of psychiatric disorders. Emerging evidence from numerous studies suggests that administration of exogenous ketone supplements, such as ketone salts or ketone esters, generates rapid and sustained nutritional ketosis and metabolic changes, which may evoke potential therapeutic effects in cases of central nervous system (CNS) disorders, including psychiatric diseases. Therefore, the aim of this review is to summarize the current information on ketone supplementation as a potential therapeutic tool for psychiatric disorders. Ketone supplementation elevates blood levels of the ketone bodies: D-?-hydroxybutyrate (?HB), acetoacetate (AcAc), and acetone. These compounds, either directly or indirectly, beneficially affect the mitochondria, glycolysis, neurotransmitter levels, activity of free fatty acid receptor 3 (FFAR3), hydroxycarboxylic acid receptor 2 (HCAR2), and histone deacetylase, as well as functioning of NOD-like receptor pyrin domain 3 (NLRP3) inflammasome and mitochondrial uncoupling protein (UCP) expression. The result of downstream cellular and molecular changes is a reduction in the pathophysiology associated with various psychiatric disorders. We conclude that supplement-induced nutritional ketosis leads to metabolic changes and improvements, for example, in mitochondrial function and inflammatory processes, and suggest that development of specific adjunctive ketogenic protocols for psychiatric diseases should be actively pursued.

                    https://www.frontiersin.org/articles...019.00363/full

                    i na koniec ciekawostka:

                    Ethnic Differences in Nighttime Melatonin and Nighttime Blood Pressure: A Study in European Americans and African Americans.

                    BACKGROUND:
                    Ethnic differences in nighttime blood pressure (BP) have long been documented with African Americans (AAs) having higher BP than European Americans (EAs). Recently, lower nighttime melatonin, a key regulator of circadian rhythms, has been associated with higher nighttime BP levels in EAs. This study sought to test the hypothesis that AAs have lower nighttime melatonin secretion compared with EAs. We also determined if this ethnic difference in melatonin could partially explain the ethnic difference in nighttime BP.

                    METHODS:
                    A total of 150 young adults (71 AA; 46% females; mean age: 27.7 years old) enrolled in the Georgia Stress and Heart study provided an overnight urine sample for the measurement of 6-sulfatoxymelatonin, a major metabolite of melatonin. Urine melatonin excretion (UME) was calculated as the ratio between 6-sulfatoxymelatonin concentration and creatinine concentration. Twenty-four-hour ambulatory BP was assessed and nighttime systolic BP (SBP) was used as a major index of BP regulation.

                    RESULTS:
                    After adjustment of age, sex, body mass index, and smoking, AAs had significantly lower UME (P=0.002) and higher nighttime SBP than EAs (P=0.036). Lower UME was significantly associated with higher nighttime SBP and this relationship did not depend on ethnicity. The ethnicity difference in nighttime SBP was significantly attenuated after adding UME into the model (P =0.163).

                    CONCLUSION:
                    The present study is the first to document the ethnic difference in nighttime melatonin excretion, demonstrating that AAs have lower melatonin secretion compared with EAs. Furthermore, the ethnic difference in nighttime melatonin can partially account for the established ethnic difference in nighttime SBP.
                    Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
                    correlation doesn't imply causation

                    Komentarz




                    • Czyli jednak i tabletkowa D3 dzia?a? Nie trzeba chodzi? pod promiennik dla kurczaków?

                      Fotony docieraj?ce do p?odu wp?ywaj? na rozwój siatkówki
                      "fotony" te z wifi albo 4g mog? by?? Czy te z rentgena lepiej?

                      Komentarz


                      • Zamieszczone przez fazzeerr Zobacz posta


                        Czyli jednak i tabletkowa D3 dzia?a? Nie trzeba chodzi? pod promiennik dla kurczaków?
                        no nawet taka, takie badania to pisz? a co dopiero:



                        strach si? ba? normalnie.

                        "fotony" te z wifi albo 4g mog? by?? Czy te z rentgena lepiej?
                        pytasz si? o bezpiecze?stwo p?odu pod wp?ywem fal niejonizuj?cych co nie wypierdalaj? elektronu?

                        taka ciekawosta na temat rengena:

                        Zdj?cia rentgenowskie wymy?li? Wilhelm Röntgen. Powsta?y one na pocz?tku XX wieku i jest to odrobin? krwawa historia.
                        - Na pocz?tku wieku Röntgen, badaj?c wy?adowania jarzeniowe w gazach, zauwa?y?, ?e wytworzy? równie? promienie, które rozchodz? si? prostoliniowo i przenikaj? praktycznie przez ca?? materi?, ale w ró?nym stopniu - mówi profesor Aleksy Bartnik z Wydzia?u Fizyki Uniwersytetu Warszawskiego. - Promienie te ?atwo przenikaj? przez lekkie pierwiastki, jak wodór, tlen czy w?giel, natomiast trudniej przez ci??kie, jak z?oto czy wapie?.
                        Pierwszym zdj?ciem rentgenowskim by?o prze?wietlenie r?ki ?ony Röntgen, na którym wida? ko?ci, kawa?ek cia?a i obr?czk?.

                        Odkrycie Wilhelma Röntgena zmieni?o wszystko. Teraz wszyscy chcieli by? lekarzami tzw. nowego typu, czyli u?ywaj?cymi prze?wietle?, a nie stetoskopów.
                        Nawet sklepy z obuwiem dla dzieci wyposa?one by?y w aparaty do prze?wietle?. Rodzic, wk?adaj?c nó?k? dziecka do bucika, móg? zrobi? zdj?cie rentgenowskie i wiedzia? czy dana para butów nie jest za ma?a lub za du?a.
                        Niestety bardzo szybko si? okaza?o, ?e promienie rentgena niszcz? DNA w komórkach, czego efektem mog? by? nowotwory lub choroba popromienna. Na szcz??cie dzi? wszystko wygl?da troch? inaczej i zdjecie rentgenowskie, które robimy nie cz??ciej ni? raz w roku, w ogóle nie zagra?a naszemu zdrowiu.
                        https://www.polskieradio.pl/10/484/A...n-bez-tajemnic
                        Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
                        correlation doesn't imply causation

                        Komentarz


                        • pytasz si? o bezpiecze?stwo p?odu pod wp?ywem fal niejonizuj?cych co nie wypierdalaj? elektronu?
                          Pytam bo napisanie czego? w stylu "musz? dotrze? fotony do siatkówki p?odu" nie mówi mi nic o tym jakich energii/d?ugo?ci fali maj? by? te fotony. To maj? by? fotony z zakresu fal d?ugich? Czy mo?e fal gamma? Nie wiadomo.

                          Komentarz


                          • Zamieszczone przez fazzeerr Zobacz posta
                            nie mówi mi nic o tym jakich energii/d?ugo?ci fali maj? by? te fotony. To maj? by? fotony z zakresu fal d?ugich? Czy mo?e fal gamma? Nie wiadomo.
                            Zespó? zauwa?y?, ?e fotony aktywuj? u p?odów melanopsyn?, pomagaj?c w ten sposób zainicjowa? normalny rozwój unaczynienia i neuronów siatkówkowych.
                            chodzi o melanopsyn?, wi?c 470nm.

                            https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746810/
                            correlation doesn't imply causation

                            Komentarz


                            • Metabolit bakterii kwasu mlekowego wp?ywa na komórki odporno?ciowe




                              Pewien metabolit bakterii kwasu mlekowego wi??e si? z receptorami cz?owiekowatych, w tym ludzi, i wywo?uje migracj? monocytów. To w ten sposób fermentowane pokarmy "porozumiewaj? si?" z naszym uk?adem odporno?ciowym.
                              Claudia Stäubert z Uniwersytetu w Lipsku podkre?la, ?e spo?ywanie bakterii kwasu mlekowego, które np. przekszta?caj? mleko w jogurt, a kapust? w kapust? kiszon?, zapewnia wiele korzy?ci zdrowotnych, ale naukowcy nadal nie rozumiej?, jak na poziomie molekularnym bakterie te oddzia?uj? na nasz uk?ad odporno?ciowy. Ostatnio jednak Niemcy odkryli jedn? z takich ?cie?ek.
                              Zespó? bada? receptory dla kwasów hydroksykarboksylowych (HCA). Wi?kszo?? zwierz?t dysponuje dwoma typami takich receptorów, jednak cz?owiekowate maj? ich a? trzy. Okazuje si? przy tym, ?e metabolit bakterii kwasu mlekowego, kwas D-fenylomlekowy (D-PLA) ,wi??e si? silnie z 3. typem tego receptora - HCA3 - sygnalizuj?c uk?adowi odporno?ciowemu ich obecno??.
                              Autorzy artyku?u z pisma PLoS Genetics sugeruj?, ?e HCA3 pojawi? si? u wspólnego przodka cz?owiekowatych, umo?liwiaj?c im spo?ywanie pokarmów, które zacz??y si? ju? psu?, np. podniesionych z ziemi owoców.
                              Jeste?my przekonani, ?e ten receptor po?redniczy w niektórych korzystnych, np. przeciwzapalnych, oddzia?ywaniach bakterii kwasu mlekowego na ludzi. Dlatego uwa?amy, ?e mo?e by? potencjalnym celem dla leków do terapii chorób zapalnych.
                              Przysz?e badania maj? pokaza?, czy kwas D-fenylomlekowy oddzia?uje na komórki t?uszczowe, na powierzchni których równie? znajduje si? HCA3.
                              https://kopalniawiedzy.pl/bakterie-k...Staubert,30132

                              nie nie to nie tak jak my?lisz, chodzi jak zawsze o zegar

                              Low-carb breakfasts reduce sugar spikes in those with Type 2 diabetes

                              Keto, low-carb, low glycemic index, Mediterranean, DASH diet, low-fat: there are a dizzying array of diets claiming to optimize health. Some are based on sound science and some are not.

                              For anyone living with type 2 diabetes, a disease that affects about one in 12 people globally, figuring out what to eat can be even more confusing because their bodies have difficulty processing sugars.

                              When they eat carbohydrates—the sugars and starches found in many foods—they get large spikes in blood sugar. Poor control of blood sugar by the body can damage organs, particularly blood vessels, eyes and kidneys.

                              The goal of my research lab at the University of British Columbia's Okanagan campus is to research diet and exercise interventions for the treatment and prevention of type 2 diabetes. We conduct human studies testing how different lifestyle strategies impact blood glucose control and other health markers important for the management of this disease.

                              What does our science say about some of these fad diets? What are some simple strategies that those living with type 2 diabetes can use to cut through the hype and improve their health?

                              The first is probably the simplest and easiest to implement: restrict carbohydrate-containing foods, like oatmeal and toast, at breakfast.

                              A reversed circadian rhythm

                              I have been using continuous glucose monitoring for 10 years to study how diet and exercise influence blood sugar control. From studying hundreds of individuals with type 2 diabetes, I can point to one consistency: breakfast leads to the biggest glucose spike of the day.

                              I always assumed this was due to the fact that typical Western breakfast foods, like cereal, toast, oatmeal and fruit, are high in carbohydrates.

                              However, it could also be that circadian rhythm—the internal clock that sets our 24-hour metabolism—is "reversed" in type 2 diabetes.

                              Instead of waking up and being most glucose tolerant and insulin sensitive early in the day, circadian rhythm is disrupted in those with type 2 diabetes—so that their bodies are even worse at handling carbohydrates in the morning. If they eat a typical breakfast they get a very pronounced glucose spike.

                              This led us to conduct our recent study, published in The American Journal of Clinical Nutrition, which asked the simple question: "What would happen to overall glucose control if people with type 2 diabetes avoided carbohydrates at breakfast?"

                              Desire for sweet foods lower

                              As predicted, we completely eliminated the large breakfast glucose spike by providing a low-carbohydrate breakfast consisting of an egg, cheese and spinach omelet.

                              Not only that, blood sugar spikes after lunch and dinner were the exact same regardless of the breakfast. So overall exposure to damaging glucose spikes was improved and markers of glucose volatility were better with the simple switch to a very low-carbohydrate breakfast.

                              We also discovered that both pre-meal hunger and desire to eat sweet foods were lower at dinner on the low-carbohydrate breakfast day.

                              This suggests that eating a low-carbohydrate breakfast could reduce energy intake and help curb cravings for treats later in the day. A simple and powerful strategy not just for those with type 2 diabetes, but for anyone looking to improve their diet.

                              It should be noted that encouraging findings are preliminary and we don't know if all low-carbohydrate breakfast foods would lead to the same effects.

                              You might also be asking yourself, if breakfast glucose spikes are such a problem, then why didn't you ask participants just to skip breakfast? We know from previous research that skipping breakfast is probably not the greatest idea for someone with type 2 diabetes because it leads to exaggerated glucose spikes at lunch and dinner, and may lead to metabolic compensation —so that people eat more, or expend less energy, later in the day.

                              Diabetes 'remission' with keto diet

                              The second strategy for those with type 2 diabetes in particular, is to follow a low-carbohydrate or ketogenic diet.

                              Evidence for the benefits of a keto diet for type 2 diabetes are accumulating, with studies showing that with the proper support and medical guidance, over 50 percent of patients might be able to get their condition into "remission."

                              That means their blood glucose control is back to normal and they do not have to take glucose-lowering medications anymore. It's an astounding and life-changing result for the many people who have become dependent on daily medications like insulin or metformin.

                              In the real-world though, adherence to any restrictive dietary patterns is generally poor. Some people can stick to it, but usually at least half of participants fall off the wagon within six to 12 months of starting any new diet, whether low-carb or not.

                              One or two low-carb meals

                              There may also be some risks to a hardened ketogenic diet approach. One recent study from my lab also warns that the occasional "cheat day" when on a strict ketogenic diet might cause damage to blood vessels.

                              Switching just one or two meals per day to low-carb could be an attainable goal that maximizes the benefits while also minimizing the potential risks for many individuals with type 2 diabetes.

                              In an age when pharmaceuticals are the norm for managing most diseases, I'm encouraged to be discovering some simple alternatives that can be tested in scientific research studies. It's not every day that we in the health fields see diseases seemingly reverse in our patients.

                              Because normal circadian rhythm dictates that humans are most tolerant to glucose in the morning, this strategy might not optimal for someone without diabetes. However, the lower feelings of hunger later in the day, when a low-carbohydrate breakfast is consumed, might be attractive for lots of people who are trying to control their weight.

                              We hope to test out some of these ideas in the coming years as we continue our research on optimizing lifestyle approaches for type 2 diabetes.
                              https://medicalxpress.com/news/2019-...-diabetes.html

                              nie nie NIE ! to znowu nie, chodzi o ?arcie

                              Researchers investigate hormonal links between diet and obesity

                              Obesity is a growing public health crisis, bringing with it many serious risk factors, including cardiovascular disease and type 2 diabetes. As the number of people who are either overweight or obese now outnumbers those with a healthy body weight by a ratio of two to one, researchers face an urgent need to better understand how the body burns fuel.

                              In a recent paper published in The Journal of Biological Chemistry, Saint Louis University researchers collaborating with scientists at the University of California, Davis School of Veterinary Medicine reported that low levels of a circulating hormone called adropin predict increased weight gain and metabolic dysregulation during consumption of a high-sugar diet in a nonhuman primate model.

                              The researchers hope these findings will help set the stage to develop new therapies for managing metabolic diseases.

                              Several years ago, Andrew Butler, Ph.D., professor of pharmacology and physiology at SLU, and his lab discovered the peptide hormone adropin. Research by Butler's lab suggests that adropin regulates whether the body burns glucose or fat. In previous studies performed in mice, researchers found that low levels of the hormone observed in obese mice may contribute to diabetes and the associated reduced ability of the body to use glucose.

                              They also found that young men with high adropin levels had lower body mass index (BMI) levels. Moreover, some studies indicated low adropin is associated with biomarkers of insulin resistance.

                              In the current study, Butler and his UC, Davis colleagues have conducted studies at California National Primate Research Center located on UC, Davis campus in order to explore adropin's role in metabolic health.

                              They examined the plasma of 59 adult male rhesus macaques fed a high sugar diet.

                              Overall, consumption of the fructose diet produced a 10% gain in body weight and increases of fasting levels of insulin, indicating insulin resistance, which reduces glucose use and elevated fasting triglycerides which in humans increases the risk of cardiovascular disease.

                              Animals with low plasma adropin concentrations developed a more severe metabolic syndrome. Interestingly, development of type 2 diabetes was only observed in animals with low plasma adropin concentrations. These animals also showed more pronounced dysregulation of glucose and lipid metabolism.

                              Fasting hyperglycemia was also limited to animals with low circulating adropin, indicating glucose intolerance.

                              "Monkeys with low adropin may therefore not be oxidizing glucose as well, explaining their higher fat content as the glucose is converted to lipids instead of being used as a metabolic fuel," Butler said.

                              The team also examined a baboon transcriptome (genetic) data set to explore expression of the adropin gene in a nonhuman primate. Adropin is encoded by the Energy Homeostasis Associated (ENHO) gene.

                              "Last year we reported that adropin appeared to be an output of the biological clock using mouse models and cultured human cells," Butler said. "What we show in this paper is that expression of the ENHO gene is higher in daytime and lower at night in most primate tissues."

                              This is consistent with the idea that adropin expression is controlled via "clock-related" mechanisms.

                              Every cell in the body maintains its own internal clock to control daily rhythms in metabolism. There is a growing awareness of the importance of the biological clocks that control the "circadian rhythm" in health and disease. The current finding suggests that adropin may link the biological clock to rhythms in the way the body uses sugar and fats as metabolic fuel.

                              "To further get at what this might mean, data suggests that enhanced use of glucose as fuel happens at certain times of day," Butler said. "At night time, the body relies on energy reserves stored as lipids in fat cells and in the daytime relies more on the carbohydrates coming in from the diet."

                              In this way, stimulation of adropin expression by our internal clocks may contribute to increasing the use of glucose as a metabolic fuel during the daytime.

                              Other findings show that adropin expression is co-regulated with clusters of genes involved in glucose and fat metabolism in the liver.
                              https://medicalxpress.com/news/2019-...t-obesity.html

                              brak poszanowania dla zachodu = depresja?

                              Pineal gland abnormality in major depressive disorder.

                              Abstract
                              Patients with major depressive disorder (MDD) often have circadian rhythm alteration and sleep disturbance. The pineal gland regulates the circadian rhythm and sleep by the secretion of melatonin neurohormone. However, the relationship between pineal abnormality and MDD remains elusive. 50 patients with MDD and 35 gender- and age-matched healthy controls underwent high-resolution structural MRI. Pineal parenchymal volume (PPV) was measured manually. Inter-group differences in prevalence of pineal cyst and PPV were examined. In addition, we investigated the correlations between PPV and symptom severity as well as sleep variables in the patient group. Compared to healthy controls, patients with MDD had a higher prevalence of pineal cyst. Moreover, patients had significantly decreased PPV relative to controls. However, no significant correlations were observed between PPV and symptom severity as well as sleep variables. Our findings suggest that pineal abnormality may play a critical role in depression.
                              https://www.sciencedirect.com/scienc...408?via%3Dihub

                              The role of short-chain fatty acids in microbiota–gut–brain communication



                              Key points
                              Short-chain fatty acids (SCFAs) are speculated to have a mediational role in the microbiota–gut–brain axis crosstalk.

                              SCFAs might influence psychological functioning via interactions with G protein-coupled receptors or histone deacetylases and exert their effects on the brain via direct humoral effects, indirect hormonal and immune pathways and neural routes.

                              Dietary intervention studies indirectly implicate a mediational role for SCFAs in cognition and emotion.

                              Animal studies provide direct evidence of the effects of SCFAs on neuropsychiatric disorders and psychological functioning, whereas human studies are sparse, suffer from methodological limitations and offer inconsistent conclusions.

                              SCFAs should be quantified in the systemic circulation in dietary intervention studies, in which the effects on psychological functioning and psychopathology are an outcome of interest.

                              SCFAs could ultimately be used as interventional substances to target microbiota–gut–brain interactions in humans.
                              https://www.nature.com/articles/s41575-019-0157-3

                              i ciekawostka - jak komóreczki komunikuj? si? miedzy sob?:

                              Scientists discover signalling circuit boards inside body's cells

                              The first ever images of the cell-wide web have been captured by scientists at the University of Edinburgh thanks to computing techniques similar to those used for the first picture of a black hole. The findings reveal cells in the body are wired like computer chips to direct signals that instruct how they function. Unlike a fixed circuit board, however, cells can rapidly rewire their communication networks to change their behavior. Credit: The University of Edinburgh


                              Cells in the body are wired like computer chips to direct signals that instruct how they function, research suggests.
                              Unlike a fixed circuit board, however, cells can rapidly rewire their communication networks to change their behaviour.
                              The discovery of this cell-wide web turns our understanding of how instructions spread around a cell on its head.
                              It was thought that the various organs and structures inside a cell float around in an open sea called the cytoplasm.
                              Signals that tell the cell what to do were thought to be transmitted in waves and the frequency of the waves was the crucial part of the message.
                              Researchers at the University of Edinburgh found information is carried across a web of guide wires that transmit signals across tiny, nanoscale distances.

                              It is the movement of charged molecules across these tiny distances that transmit information, just as in a computer microprocessor, the researchers say.
                              These localised signals are responsible for orchestrating the cell's activities, such as instructing muscle cells to relax or contract.
                              When these signals reach the genetic material at the heart of the cell, called the nucleus, they instruct minute changes in structure that release specific genes so that they can be expressed.
                              These changes in gene expression further alter the behaviour of the cell. When, for instance, the cell moves from a steady state into a growth phase, the web is completely reconfigured to transmit signals that switch on the genes needed for growth.
                              Researchers say understanding the code that controls this wiring system could help understand diseases such as pulmonary hypertension and cancer, and could one day open up new treatment opportunities.
                              The team made their discovery by studying the movement of charged calcium molecules inside cells, which are the key messages that carry instructions inside cells.
                              Using high-powered microscopes, they were able to observe the wiring network with the help of computing techniques similar to those that enabled the first ever image of a black hole to be obtained.
                              Scientists say their findings are an example of quantum biology—an emerging field that uses quantum mechanics and theoretical chemistry to solve biological problems.
                              The study, published in Nature Communications, was funded by the British Heart Foundation.
                              Professor Mark Evans, of the University of Edinburgh's Centre for Discovery Brain Sciences, said: "We found that cell function is coordinated by a network of nanotubes, similar to the carbon nanotubes you find in a computer microprocessor.
                              "The most striking thing is that this circuit is highly flexible, as this cell-wide web can rapidly reconfigure to deliver different outputs in a manner determined by the information received by and relayed from the nucleus. This is something no man-made microprocessors or circuit boards are yet capable of achieving."
                              https://phys.org/news/2019-05-scient...ody-cells.html

                              Bioluminescencyjne glony morskie:

                              Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
                              correlation doesn't imply causation

                              Komentarz


                              • The role of short-chain fatty acids in microbiota–gut–brain communication




                                https://www.nature.com/articles/s41575-019-0157-3

                                sorki bo zapomnia?em:

                                The circadian clock regulates the diurnal levels of microbial short?chain fatty acids and their rhythmic effects on colon contractility in mice

                                Results
                                Diurnal fluctuations in faecal SCFA concentrations (peak 4 hours after lights on) were observed that were in phase with the rhythm of Ffar2/3 expression in the colonic muscle layer. Olfr78 expression was not diurnal and Hcar2 was not detectable. The inhibitory effect of a SCFA mix on neural contractions in colonic smooth muscle strips showed a diurnal rhythm and oscillated in phase with faecal SCFA concentrations and Ffar2/3 expression. In contrast, neither excitatory neural responses nor acetylcholine?induced smooth muscle contractions showed a diurnal rhythm. In Bmal1?/? mice, no fluctuations in faecal SCFA levels, Ffar3 expression and neural responses to SCFAs were observed.

                                Conclusion
                                Diurnal microbial SCFA levels regulate the rhythm of Ffar3 expression in the colonic myenteric plexus, which causes rhythmicity in SCFA?induced colonic motility. Deletion of Bmal1 abolishes rhythmicity of SCFA levels and their downstream effects.
                                https://onlinelibrary.wiley.com/doi/...111/apha.13193
                                Ostatnio edytowany przez htw; [ARG:4 UNDEFINED].
                                correlation doesn't imply causation

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