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Wątek: NATURALNE sposoby optymalizacji CIAŁA i DUSZY.

  1. #931
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    produkcja melatoniny rozpoczęta, a kolacja przed Tobą?

    Late-Night Eating-Induced Physiological Dysregulation and Circadian Misalignment Are Accompanied by Microbial Dysbiosis.

    SCOPE:
    Irregular eating habits, such as late-night eating, will cause increased risk of obesity and other metabolic diseases. The aim of this study is to elucidate the impacts of late-night eating on physiological function and gut microbiota.

    METHODS AND RESULTS:
    Male Wistar rats under 16 h/8 h-light/dark cycle are divided into four groups with specific dietary habits, which mimicked breakfast, lunch, dinner, and late-night eating. Late-night eating, including skipping dinner for a night eating (BLN) and skipping breakfast and having a night eating (LDN), causes an increase of body weight, which is associated with decreased physical activity. Additionally, late-night eating results in hepatic lipid accumulation and systemic inflammation in peripheral tissues, compared to those of free feeding (FF) or breakfast, lunch, and dinner (BLD) groups. The phases of key clock genes are similar in FF, BLD, and BLN groups, while LDN feeding causes an overall 4 h phase delay in peripheral tissues. Moreover, late-night eating, especially LDN feeding, results in a significant alternation in the compositions and functions of gut microbiota, which further contributes to the development of metabolic disorder.

    CONCLUSION:
    Late-night eating causes physiological dysregulation and misalignment of circadian rhythm, together with microbial dysbiosis
    https://www.ncbi.nlm.nih.gov/pubmed/31628714
    correlation doesn't imply causation

  2. #932
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    śmiechu było sporo - teraz na poważnie.

    NOVEMBER 13, 2019
    Stress with disrupted body clock increases risk of metabolic disease

    Everyday stress coupled with disruptions to the body's internal clock may increase the risks of developing metabolic disorders including obesity and type 2 diabetes, according to a study presented at the Society for Endocrinology annual conference in Brighton. These mouse data indicate that environmental stress coupled with alterations in normal body clock function can affect food intake, promote weight gain and have long-lasting effects on stress responses. This may help explain why shift-work, jet lag and chronic stress in people can lead to metabolic disorders, as well as highlight therapeutic targets to investigate for future treatment.


    In modern society the prevalence of everyday stress has been linked to the development of metabolic diseases, including diabetes and obesity. These diseases are also more common in people suffering from disruption to their normal body clock, such as shift workers. The internal body clock, or circadian rhythm, is a natural 24 hour cycle that regulates processes related to hormones, sleep and feeding that are essential for good health and can be affected by external factors. External stress induces release of the stress hormone, cortisol, to adapt energy metabolism to a perceived fight-or-flight situation. Levels of cortisol throughout the day are also regulated by our body clock. The connection between the circadian system and the stress response is very well characterised in rodents but the interaction between stress, our body clock and metabolism is not yet fully understood.

    In order to investigate this interaction, Professor Henrik Oster and colleagues at the University of Lübeck in Germany performed experiments using mice with genetic alterations in different parts of their body clock machinery. Mice exposed to social stress, in which male animals were repeatedly exposed to an unknown, dominant male, had increased stress responses that were dependent on the time of day of the stress exposure. Further experiments indicated that these stress responses were dependent on the body clock system, and that food intake and body weight were more likely to be negatively affected when stress occurs during their inactive phase (daytime for a mouse, night-time in humans). Repeated exposure to stress also led to long-lasting adaptations to responsiveness of the stress system that negatively affect metabolism.

    Professor Oster states, "We have shown that stress responses depend on the time of day, are affected by the internal body clock and can interact to negatively affect food intake and body weight to predispose to metabolic disorders. These data suggest that body clock rhythm may be an underestimated factor in assessing the impact of chronic stress on general health and well-being."

    Prof Oster now plans to further analyse the molecular targets of the body clock-stress interaction with the aim of identifying the mechanisms that affect metabolism and how these adverse health effects may be counteracted. Whilst rodent studies provide a useful and effective model for investigating this system, clinical studies would be required to confirm these effects in people.
    Professor Oster comments, "Although in rodents, these data provide some mechanistic explanations for the negative effects of shift work and chronic stress on people, suggesting that both the timing and levels of stress are important factors for development of metabolic disease."
    Prof Oster continues, "Further investigation of this system could lead to recommendations for better timing of working hours, stressful meetings and rest that may increase productivity and enhance quality of life, reducing the financial burden of care for work-related stress."
    https://medicalxpress.com/news/2019-...metabolic.html
    correlation doesn't imply causation

  3. #933
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    Melatonin in type 2 diabetes mellitus and obesity



    Despite considerable advances in the past few years, obesity and type 2 diabetes mellitus (T2DM) remain two major challenges for public health systems globally. In the past 9 years, genome-wide association studies (GWAS) have established a major role for genetic variation within the MTNR1B locus in regulating fasting plasma levels of glucose and in affecting the risk of T2DM. This discovery generated a major interest in the melatonergic system, in particular the melatonin MT2 receptor (which is encoded by MTNR1B). In this Review, we discuss the effect of melatonin and its receptors on glucose homeostasis, obesity and T2DM. Preclinical and clinical post-GWAS evidence of frequent and rare variants of the MTNR1B locus confirmed its importance in regulating glucose homeostasis and T2DM risk with minor effects on obesity. However, these studies did not solve the question of whether melatonin is beneficial or detrimental, an issue that will be discussed in the context of the peculiarities of the melatonergic system. Melatonin receptors might have therapeutic potential as they belong to the highly druggable G protein-coupled receptor superfamily. Clarifying the precise role of melatonin and its receptors on glucose homeostasis is urgent, as melatonin is widely used for other indications, either as a prescribed medication or as a supplement without medical prescription, in many countries in Europe and in the USA.
    https://www.nature.com/articles/s41574-018-0130-1

    Effects of an energy‐restricted low‐carbohydrate, high unsaturated fat/low saturated fat diet versus a high‐carbohydrate, low‐fat diet in type 2 diabetes: A 2‐year randomized clinical trial
    https://onlinelibrary.wiley.com/doi/...1111/dom.13164

    A randomized cross-over trial to determine the effect of a protein vs. carbohydrate preload on energy balance in ad libitum settings
    https://nutritionj.biomedcentral.com...0497-4/metrics

    Ludzie, którzy piją czerwone wino, mają bardziej zróżnicowany skład mikroflory jelitowej. Dodatkowo wyniki zgromadzone przez zespół z King’s College London pokazują, że spożycie czerwonego wina wiąże się z niższymi poziomami złego cholesterolu i otyłości.

    Wpływ piwa, cydru, czerwonego i białego wina oraz mocniejszych alkoholi na mikrobiom jelitowy i stan zdrowia badano m.in. w grupie 916 brytyjskich bliźniaczek. Okazało się, że flora jelitowa kobiet spożywających czerwone wino była bardziej zróżnicowana, w porównaniu do ochotniczek niepijących czerwonego wina. Podobnych zależności nie stwierdzono w przypadku białego wina, piwa i mocniejszych alkoholi.
    https://losyziemi.pl/mikroflora-jeli...ki-polifenolom
    correlation doesn't imply causation

  4. #934
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    nie możesz się oprzeć słodkością ?

    po raz kolejny - dopaminowe spierdolenie.

    NOVEMBER 15, 2019
    Your brain on sugar: What the science actually says

    We love sweet treats. But too much sugar in our diets can lead to weight gain and obesity, Type 2 diabetes and dental decay. We know we shouldn't be eating candy, ice cream, cookies, cakes and drinking sugary sodas, but sometimes they are so hard to resist.

    It's as if our brain is hardwired to want these foods.

    As a neuroscientist my research centers on how modern day "obesogenic," or obesity-promoting, diets change the brain. I want to understand how what we eat alters our behavior and whether brain changes can be mitigated by other lifestyle factors.

    Your body runs on sugar—glucose to be precise. Glucose comes from the Greek word glukos which means sweet. Glucose fuels the cells that make up our body—including brain cells (neurons).

    Dopamine "hits" from eating sugar

    On an evolutionary basis, our primitive ancestors were scavengers. Sugary foods are excellent sources of energy, so we have evolved to find sweet foods particularly pleasurable. Foods with unpleasant, bitter and sour tastes can be unripe, poisonous or rotting—causing sickness.

    So to maximize our survival as a species, we have an innate brain system that makes us like sweet foods since they're a great source of energy to fuel our bodies.

    When we eat sweet foods the brain's reward system—called the mesolimbic dopamine system—gets activated. Dopamine is a brain chemical released by neurons and can signal that an event was positive. When the reward system fires, it reinforces behaviors—making it more likely for us to carry out these actions again.

    Dopamine "hits" from eating sugar promote rapid learning to preferentially find more of these foods.

    Our environment today is abundant with sweet, energy rich foods. We no longer have to forage for these special sugary foods—they are available everywhere. Unfortunately, our brain is still functionally very similar to our ancestors, and it really likes sugar. So what happens in the brain when we excessively consume sugar?
    oponka oznaką starości, wyjątkowym źródłem stanu zapalnego oraz początkiem chorób metabolicznych.

    NOVEMBER 15, 2019
    New finding offers possibility for preventing age-related metabolic disease

    A study by researchers at Yale has uncovered why belly fat surrounding organs increases as people age, a finding that could offer new treatment possibilities for improving metabolic health, thereby reducing the likelihood for diseases like diabetes and atherosclerosis that stem from inflammation.


    Led by Dr. Vishwa Deep Dixit, the Waldemar Von Zedtwitz Professor of Comparative Medicine and of Immunobiology, the study was published Nov. 14 in Cell Metabolism.

    Previous work found that as people age, their body's ability to generate energy by burning belly fat is reduced. Consequently, fat that surrounds the internal organs increases in the elderly. Dixit's lab had found that the immune cells necessary to the fat-burning process, called macrophages, were still active but their overall numbers declined as belly fat increased with aging.

    This latest study found that something else is happening as well. Adipose B cells in belly fat unexpectedly proliferated as animals aged, contributing to increased inflammation and metabolic decline. "These adipose B cells are a unique source of inflammation," Dixit said, "normally the B cells produce antibodies, and defend against infection. But with aging, the increased adipose B cells become dysfunctional, contributing to metabolic disease."
    https://medicalxpress.com/news/2019-...c-disease.html
    Ostatnio edytowane przez htw ; 15-11-19 o 16:40
    correlation doesn't imply causation

  5. #935
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    Za oknem lipa, procesy fotosyntezy wstrzymane, bananów za oknem brak, malin i jabłek również.

    o, taki ładny obrazek, jak robimy cukier



    chlorofil nie zassa odpowiedniego spektrum, cukru nie będzie:



    tutaj cała historia:
    https://i.ibb.co/DpXY4Y5/EHK010-OWk-AAXvni.jpg

    Dieta zimowa czyli nastawiona na beta-oksydację okazuje się, że spory potencjał w aktywacji układu odpornościowego np zwalczaniu wirusa grypy .. ciekawe co taka oczywista oczywistość, ale warto zauważyć.

    Ketogenic diet helps tame flu virus



    A high-fat, low-carbohydrate diet like the Keto regimen has its fans, but influenza apparently isn't one of them.
    Mice fed a ketogenic diet were better able to combat the flu virus than mice fed food high in carbohydrates, according to a new Yale University study published Nov. 15 in the journal Science Immunology.

    The ketogenic diet—which for people includes meat, fish, poultry, and non-starchy vegetables—activates a subset of T cells in the lungs not previously associated with the immune system's response to influenza, enhancing mucus production from airway cells that can effectively trap the virus, the researchers report.

    "This was a totally unexpected finding," said co-senior author Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and Molecular, Cellular and Developmental Biology, and an investigator of the Howard Hughes Medical Institute.
    The research project was the brainchild of two trainees—one working in Iwasaki's lab and the other with co-senior author Visha Deep Dixit, the Waldemar Von Zedtwitz Professor of Comparative Medicine and of Immunobiology. Ryan Molony worked in Iwasaki's lab, which had found that immune system activators called inflammasomes can cause harmful immune system responses in their host. Emily Goldberg worked in Dixit's lab, which had shown that the ketogenic diet blocked formation of inflammasomes.
    The two wondered if diet could affect immune system response to pathogens such as the flu virus.
    They showed that mice fed a ketogenic diet and infected with the influenza virus had a higher survival rate than mice on a high-carb normal diet. Specifically, the researchers found that the ketogenic diet triggered the release of gamma delta T cells, immune system cells that produce mucus in the cell linings of the lung—while the high-carbohydrate diet did not.
    When mice were bred without the gene that codes for gamma delta T cells, the ketogenic diet provided no protection against the influenza virus.
    "This study shows that the way the body burns fat to produce ketone bodies from the food we eat can fuel the immune system to fight flu infection," Dixit said.
    https://medicalxpress.com/news/2019-...flu-virus.html
    Ostatnio edytowane przez htw ; 16-11-19 o 07:14
    correlation doesn't imply causation

  6. #936
    htw, czy to się nada na DIY lampę antydepresyjną?
    https://allegro.pl/oferta/zarowka-sw...e27-5692231964

    btw2, czy czytacie przy infraredowych zarowkach?


    btw3 xD czy ktos probowal temat ponizej?
    https://biohaker.pl/2019/03/27/okula...eskie-swiatlo/

  7. #937
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    Cytat Zamieszczone przez LubięFazę Zobacz posta
    muszę pomyśleć, ile tam luksów emituje? jak min 10 000 to może, ale lepiej coś dedykowanego.

    btw2, czy czytacie przy infraredowych zarowkach?
    ofkors.

    btw3 xD czy ktos probowal temat ponizej?
    tak próbował, mam takie i szklane również żebym ludzi nie staszył
    okulary to podstawa, chyba że jesteś pustelnikiem z Bieszczad
    Ostatnio edytowane przez htw ; 16-11-19 o 20:34
    correlation doesn't imply causation

  8. #938
    htw,
    czy zamiast lampy antydepresyjnej można stosować Okulary LUMINETTE? efekt będzie ten sam ? niby jest mniej luksów 1500 w porównaniu do 10 000 lampy,ale bliżej oka. Co o nich myślisz ?

  9. #939
    Lampa antydepresyjna

  10. #940
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    Cytat Zamieszczone przez BMX Zobacz posta
    htw,
    czy zamiast lampy antydepresyjnej można stosować Okulary LUMINETTE? efekt będzie ten sam ? niby jest mniej luksów 1500 w porównaniu do 10 000 lampy,ale bliżej oka. Co o nich myślisz ?
    nie wiem, jakiś potencjał jest, ale trudno mi się wypowiedzieć.

    Fala elektromagnetyczna to naprawdę skomplikowane zagadnienie, zobacz:


    jakby się ktoś chciał wklikać bez utraty jakości:
    https://i.redd.it/gos68u2sml7y.png

    przed kombinacjami lepiej mi tu powiedz:

    1) fala niebieska jest blokowana na wieczór?
    2) możesz się wyspać do swojej naturalnej godziny, podejrzewam że będzie do godz 6-7. Jak się interesujesz to jesteś bardziej sową niż skowronkiem
    pytam czy dajesz szanse kortyzolowi się podnieść i wykonać planowaną pobudkę czy tępym urządzeniem gwałcisz swój zaspany mózg?
    3) ile raz w tygodniu i na ile Twoje oczy lądują przed pracą poza budynkiem?
    correlation doesn't imply causation

  11. #941
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    Intermittent fasting increases longevity in cardiac catheterization patients



    While Intermittent fasting may sound like another dieting craze, the practice of routinely not eating and drinking for short periods of time has shown again to lead to potentially better health outcomes.

    In a new study by researchers at the Intermountain Healthcare Heart Institute in Salt Lake City, researchers have found that cardiac catheterization patients who practiced regular intermittent fasting lived longer than patients who don't. In addition, the study found that patients who practice intermittent fasting are less likely to be diagnosed with heart failure.
    https://medicalxpress.com/news/2019-...erization.html

    z rzeczy nie oczywistych, bezlitosna fala:

    GSM 900 MHz Microwave Radiation-Induced Alterations of Insulin Level and Histopathological Changes of Liver and Pancreas in Rat.

    BACKGROUND:
    The rapidly increasing use of mobile phones has led to public concerns about possible health effects of these popular communication devices. This study is an attempt to investigate the effects of radiofrequency (RF) radiation produced by GSM mobile phones on the insulin release in rats.

    METHODS:
    Forty two female adult Sprague Dawley rats were randomly divided into 4 groups. Group1 were exposed to RF radiation 6 hours per day for 7 days. Group 2 received sham exposure (6 hours per day for 7 days). Groups 3 and 4 received RF radiation 3 hours per day for 7 days and sham exposure (3 hours per day), respectively. The specific absorption rate (SAR) of RF was 2.0 W/kg.

    RESULTS:
    Our results showed that RF radiations emitted from mobile phone could not alter insulin release in rats. However, mild to severe inflammatory changes in the portal spaces of the liver of rats as well as damage in the cells of islet of Langerhans were observed. These changes were linked with the duration of the exposures.

    CONCLUSION:
    RF exposure can induce inflammatory changes in the liver as well causing damage in the cells of islet of Langerhans.
    https://www.ncbi.nlm.nih.gov/pubmed/...gar&utm_medium

    +

    Effects of exposure to electromagnetic field radiation (EMFR) generated by activated mobile phones on fasting blood glucose.

    OBJECTIVE:
    Extensive use of mobile phones has been accompanied by a common public debate about possible adverse effects on human health. No study has been published so far to establish any association between the fastest growing innovation of mobile phone and fasting blood glucose. The aim was to determine the effects of exposure to electromagnetic field radiation generated by mobile phones on fasting blood glucose in Wistar Albino rats.

    MATERIALS AND METHODS:
    40 Male Albino rats (Wistar Strain) were divided into 5 equally numerous groups. Group A served as the control one, group B received mobile phone radiation for less than 15 min/day, group C: 15-30 min/day, group D: 31-45 min/day, and group E: 46-60 min/day for a total period of 3 months. Fasting blood glucose was determined by using Spectrophotometer and serum insulin by Enzyme-linked Immunosorbent Assay (ELISA). The Homeostatic Model (HOMA-B) was applied for the assessment of β-cell function and (HOMA-IR) for resistance to insulin.

    RESULTS:
    Wister Albino rats exposed to mobile phone radiation for longer than 15 min a day for a total period of 3 months had significantly higher fasting blood glucose (p < 0.015) and serum insulin (p < 0.01) compared to the control group. HOMA-IR for insulin resistance was significantly increased (p < 0.003) in the groups that were exposed for 15-30 and 46-60 min/day compared to the control rats.

    CONCLUSION:
    The results of the present study show an association between long-term exposure to activated mobile phones and increase in fasting blood glucose and serum insulin in Albino rats.
    https://www.ncbi.nlm.nih.gov/pubmed/...ar&utm_medium=

    dodawanie fruktozy do tłuszczu zmienia wielkość i funkcję mitochondriów, utlenianie tłuszczu zostaje upośledzone.

    Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins

    Dietary sugars, fructose and glucose, promote hepatic de novo lipogenesis and modify the effects of a high-fat diet (HFD) on the development of insulin resistance. Here, we show that fructose and glucose supplementation of an HFD exert divergent effects on hepatic mitochondrial function and fatty acid oxidation. This is mediated via three different nodes of regulation, including differential effects on malonyl-CoA levels, effects on mitochondrial size/protein abundance, and acetylation of mitochondrial proteins. HFD- and HFD plus fructose-fed mice have decreased CTP1a activity, the rate-limiting enzyme of fatty acid oxidation, whereas knockdown of fructose metabolism increases CPT1a and its acylcarnitine products. Furthermore, fructose-supplemented HFD leads to increased acetylation of ACADL and CPT1a, which is associated with decreased fat metabolism. In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.


    https://www.sciencedirect.com/scienc...50413119305042
    Ostatnio edytowane przez htw ; Dzisiaj o 12:24
    correlation doesn't imply causation

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