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Wątek: NATURALNE sposoby optymalizacji CIAŁA i DUSZY.

  1. #781
    Sztywny Pal Azji
    May 2014
    1 978
    Study reveals biology of leptin, the hunger hormone

    In a new study, Yale researchers offer insight into leptin, a hormone that plays a key role in appetite, overeating, and obesity. Their findings advance knowledge about leptin and weight gain, and also suggest a potential strategy for developing future weight-loss treatments, they said.

    The study, led by investigators at Yale and Harvard, was published the week of June 17, 2019, in the journal PNAS.

    Leptin, which is secreted by fat cells, informs the brain when fuel stored in body fat and in the liver is becoming depleted. It has not been well understood how low leptin concentrations in plasma—the largest component of blood—increase appetite. The researchers studied the biology of leptin in rodents. They also investigated the influence of nerve cells in the brain known as AgRP neurons, which regulate eating behavior.

    The researchers discovered that the mechanisms by which reductions in plasma leptin concentrations stimulate food intake are not limited to the brain, as previously thought. In rodents, fasting first activates leptin receptors in the brain, followed by an intermediary step that involves the endocrine system. This system includes the pituitary and adrenal glands, which secrete another hormone, corticosterone, that regulates energy, stress responses, and food intake.

    The research team learned that this chain of events is required for leptin to stimulate hunger when food is restricted, or when diabetes is poorly controlled and plasma leptin concentrations drop below a critical threshold, said Gerald Shulman, M.D., the George R. Cowgill Professor of Medicine at Yale School of Medicine, and co-corresponding author of the study.

    In further experiments, the researchers also showed that plasma corticosterone activates AgRP neurons, which increases hunger when either leptin or blood-sugar levels are low, Shulman noted. In humans, leptin and blood sugar drop when people diet.

    These findings add to scientists' knowledge of leptin, which has been the focus of research on obesity and weight loss since its discovery in the 1990s. The study reveals "the basic biology of leptin, and how the endocrine system is mediating its effect to regulate food intake under conditions of starvation and poorly controlled diabetes," said Shulman.

    The research also lends support to a different strategy for developing drugs that treat obesity. "It suggests that AgRP neurons may be an attractive therapeutic target," he said.

    Afraid of food? The answer may be in the basal forebrain

    After fasting for 24 hours the typical laboratory mouse spends much time eating. Surprisingly, this is not what Jay M. Patel saw when he was studying basal forebrain circuits in mice.

    "When I joined Dr. Benjamin Arenkiel's lab, they had just discovered a unique set of circuits in the basal forebrain, a region separate from the hypothalamus, the brain area that normally regulates how much you eat depending on how much energy you spend," said Patel, a student in the neuroscience Medical Scientist Training Program (M.D./Ph.D.) at Baylor College of Medicine. "I wanted to investigate what these circuits that are linked to the feeding center of the brain were actually doing."

    Using cutting-edge technologies, including microendoscopy-imaging protocols, Patel and his colleagues first investigated what types of stimuli would activate the circuits. By recording the activity of the neurons, Patel found that food odors highly activated a subset of neurons in the basal forebrain identified by the expression of the molecule vGlut2.

    "That was very interesting because we know that the sense of smell can drive appetite. For instance, after smelling dessert, you may want to eat it even though you just had a big meal. Or conversely, after smelling a spoiled dish you won't eat it, even if you are very hungry," Patel said.

    Although researchers knew that the perception of food odors itself can affect neuronal activity in the hypothalamus, it was unclear how odor perception was relayed to the hypothalamus. They were excited at the possibility that the novel vGlut2+ basal forebrain circuits might provide an answer.

    Surprising results

    Patel and his colleagues studied the effect of specifically activating vGlut2+ neurons in the basal forebrain and observed dramatically altered feeding behavior in mice.

    "Surprisingly, four to five days after we began the experiment, the mice started to lose weight quickly," Patel said.

    The researchers determined that the animals' rapid weight loss could not be explained by metabolic dysfunction, as they found no differences between the levels of pituitary or thyroid hormones, or in the levels of glucose, insulin or leptin between the experimental and control groups. The mice lost weight rapidly because they had stopped eating.

    "They did not eat even when they were hungry, which we found remarkable because animals are compelled to eat to survive," Patel said. Interestingly, further experiments showed that naturally aversive odors had a stronger effect on vGlut2+ basal forebrain neurons than food alone, triggering a food avoidance behavior in mice.

    "It seemed that the animals were afraid of food," Patel said. "Even though they were hungry, they avoided locations where food was placed."

    "We have identified a brain circuit driven by vGlut2+ neurons in the basal forebrain that suppresses appetite when it's active and stimulates feeding behavior when it's inactive," Patel said. "We also determined that this circuit, which is formed by just a couple of thousand neurons involved in perceiving the outside world, connects with and overrides feeding behaviors regulated by the hypothalamus."

    "We think this work has potential implications that reach beyond feeding behaviors and mouse physiology," said Arenkiel, associate professor of neuroscience and molecular and human genetics and a McNair Scholar at Baylor. He is also a member of the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital. "This circuit is highly involved with how our brain perceives the outside world and brings this information to the hypothalamus, thus connecting with aspects of physiology like feeding, which relates to eating disorders that are associated with many neuropsychiatric conditions."

    Vitamin D may not help your heart

    While previous research has suggested a link between low levels of vitamin D in the blood and an increased risk of cardiovascular disease, a new Michigan State University study has found that taking vitamin D supplements did not reduce that risk.

    The large-scale study, published in the Journal of the American Medical Association Cardiology, found that vitamin D supplements did not decrease the incidence of heart attacks, strokes or other major adverse cardiovascular events.

    "We thought it would show some benefit," said Mahmoud Barbarawi, a clinical instructor in the MSU College of Human Medicine and chief resident physician at Hurley Medical Center in Flint, Michigan. "It didn't show even a small benefit. This was surprising."

    The Same Exact Foods Affect Each Person's Gut Bacteria Differently

    How does diet affect the thriving communities of microbes living in your digestive tract?

    It's personal.

    New research finds that the types of foods people eat really do impact the makeup of their gut microbiomes. However, the same food can have opposite effects in two different individuals. That means that the specifics of how diet will influence any given person's gut are still a mystery.

    Modern life is transforming the human skeleton. Humans are now developing a bone spike at the back of the head caused by regularly looking down at their smartphones, according to a recent study.

    The phenomenon is called an external occipital protuberance: a lump on the back of the head believed to be caused by the body reacting to smartphone use by growing new bone layers on the back of the skull.

    może dlatego dzieciaki nie lubią brokuł i warzyw?

    The brain consumes half of a child's energy—and that could matter for weight gain

    Weight gain occurs when an individual's energy intake exceeds their energy expenditure—in other words, when calories in exceed calories out. What is less well understood is the fact that, on average, nearly half of the body's energy is used by the brain during early childhood.

    lato idzie wiec hi-carb się zbliża

    Repeated muscle glycogen supercompensation with four days’ recovery between exhaustive exercise
    correlation doesn't imply causation

  2. #782
    Sztywny Pal Azji
    May 2014
    1 978
    Brain leptin reduces liver lipids by increasing hepatic triglyceride secretion and lowering lipogenesis

    Hepatic steatosis develops when lipid influx and production exceed the liver’s ability to utilize/export triglycerides. Obesity promotes steatosis and is characterized by leptin resistance. A role of leptin in hepatic lipid handling is highlighted by the observation that recombinant leptin reverses steatosis of hypoleptinemic patients with lipodystrophy by an unknown mechanism. Since leptin mainly functions via CNS signaling, we here examine in rats whether leptin regulates hepatic lipid flux via the brain in a series of stereotaxic infusion experiments. We demonstrate that brain leptin protects from steatosis by promoting hepatic triglyceride export and decreasing de novo lipogenesis independently of caloric intake. Leptin’s anti-steatotic effects are generated in the dorsal vagal complex, require hepatic vagal innervation, and are preserved in high-fat-diet-fed rats when the blood brain barrier is bypassed. Thus, CNS leptin protects from ectopic lipid accumulation via a brain-vagus-liver axis and may be a therapeutic strategy to ameliorate obesity-related steatosis.
    Proposed model of the role of CNS leptin in regulating hepatic lipid metabolism. Leptin secreted by white adipocytes protects the liver from ectopic lipid accumulation and lipotoxicity. Leptin reaches the brain by passing through the blood–brain barrier to increase TG secretion and reduce hepatic de novo lipogenesis via signaling in the dorsal vagal complex, where the efferent vagal motor neurons are located. These centrally mediated leptin effects require intact liver vagal innervation and are preserved under HFD-conditions when leptin is administered directly into the brain

    Nutrition: Even identical twins respond differently to food

    The largest ongoing study of its kind finds that people's responses to food vary depending on a wide variety of factors. The findings suggest that the future of nutrition lies in personalized dietary advice.

    How information is like snacks, money, and drugs—to your brain

    Can't stop checking your phone, even when you're not expecting any important messages? Blame your brain.

    A new study by researchers at UC Berkeley's Haas School of Business has found that information acts on the brain's dopamine-producing reward system in the same way as money or food.

    "To the brain, information is its own reward, above and beyond whether it's useful," said Assoc. Prof. Ming Hsu, a neuroeconomist whose research employs functional magnetic imaging (fMRI), psychological theory, economic modeling, and machine learning. "And just as our brains like empty calories from junk food, they can overvalue information that makes us feel good but may not be useful—what some may call idle curiosity."

    'Goldilocks' neurons promote REM sleep

    Every night while sleeping, we cycle between two very different states of sleep. Upon falling asleep, we enter non-rapid eye movement (non-REM) sleep where our breathing is slow and regular and movement of our limbs or eyes are minimal. Approximately 90 minutes later, how-ever, we enter rapid eye movement (REM) sleep. This is a paradoxical state where our breathing becomes fast and irregular, our limbs twitch, and our eyes move rapidly. In REM sleep, our brain is highly active, but we also become paralyzed and we lose the ability to thermoregulate or maintain our constant body temperature. "This loss of thermoregulation in REM sleep is one of the most peculiar aspects of sleep, particularly since we have finely-tuned mechanisms that control our body temperature while awake or in non-REM sleep," says Markus Schmidt of the Department for BioMedical Research (DBMR) of the University of Bern, and the Department of Neurology, Inselspital, Bern University Hospital. On the one hand, the findings confirm a hypothesis proposed earlier by Schmidt, senior author of the study, and on the other hand represent a breakthrough for sleep medicine. The paper was published in Current Biology and highlighted by the editors with a comment.


    Cold-water immersion blunts and delays increases in circulating testosterone and cytokines post-resistance exercise

    Using a randomized and counterbalanced repeated-measures design, 11 resistance-trained men completed two workouts (6 sets of 10 repetitions of back squats at 80% of maximum load) a week apart after which they took part in either 15 min of CWI (15 °C) or passive recovery. T, IL-6, and TNFα were measured in blood samples taken before (PRE) and 5 (5POST), 15 (15POST), 30 (30POST), and 60 (60POST) min post-exercise and compared between treatments and over time.

    For T, a significant interaction effect of condition over time (p = 0.030) as well as greater relative concentrations of T in CON (Δ9.2%) than CWI (Δ-0.5%, p = 0.049) at 30POST were observed. In addition, at 60POST, T dropped below PRE values in CWI (Δ-10.4%, p = 0.028) but not in CON (Δ-1.6%, p = 0.850). A suppressed cytokine response was observed after CWI in IL-6 at 30POST (CWI: Δ4.9%, CON: Δ47.5%, p = 0.041) and TNFα at 15POST (CWI: Δ5.3%, CON: Δ17.0%, p = 0.022).

    CWI blunted the T and cytokine response after a bout of resistance exercise. These results indicate that CWI results in an altered anabolic response and may help to explain the previous observation of attenuated hypertrophy when CWI is used after resistance exercise.
    BMAL1 controls glucose uptake through paired-homeodomain transcription factor 4 in differentiated Caco-2 cells.

    The transcription factor BMAL1 (aryl hydrocarbon receptor nuclear translocator-like protein 1) is an essential regulator of the circadian clock, which controls the 24-hr cycle of physiological processes such as nutrient absorption. To examine the role of BMAL1 in small intestinal glucose absorption, we used differentiated human colon adenocarcinoma cells (Caco-2 cells). Here, we show that BMAL1 regulates glucose uptake in differentiated Caco-2 cells and that this process is dependent on the glucose transporter SGLT1. Mechanistic studies show that BMAL1 regulates glucose uptake by controlling the transcription of SGLT1 involving the paired-homeodomain transcription factor 4 (PAX4), a transcriptional repressor. This is supported by the observation that CRISPR-Cas9-knock down of PAX4 increases SGLT1 and glucose uptake. ChIP and ChIP-qPCR assays show that the knock down or overexpression of BMAL1 decreases or increases the binding of PAX4 to the HNF1α binding site of the SGLT1 promoter, respectively. These findings identify BMAL1 as a critical mediator of small intestine carbohydrate absorption and SGLT1.

    High sleep variability predicts a blunted weight loss response and short sleep duration a reduced decrease in waist circumference in the PREDIMED-Plus Trial

    Whether short sleep duration or high sleep variability may predict less weight loss and reduction in measures of adiposity in response to lifestyle interventions is unknown. The aim of this study was to compare the 12-month changes in weight and adiposity measures between those participants with short or adequate sleep duration and those with low or high sleep variability (intra-subject standard deviation of the sleep duration) in PREvención con DIeta MEDiterránea (PREDIMED)-Plus, a primary prevention trial based on lifestyle intervention programs.

    Prospective analysis of 1986 community-dwelling subjects (mean age 65 years, 47% females) with overweight/obesity and metabolic syndrome from the PREDIMED-Plus trial was conducted. Accelerometry-derived sleep duration and sleep variability and changes in average weight, body mass index (BMI), and waist circumference (WC) attained after 12-month interventions were analyzed.

    The adjusted difference in 12-month changes in weight and BMI in participants in the third tertile of sleep variability was 0.5 kg (95% CI 0.1 to 0.9; p = 0.021) and 0.2 kg/m2 (0.04 to 0.4; p = 0.015), respectively, as compared with participants in the first tertile. The adjusted difference in 12-month changes from baseline in WC was −0.8 cm (−1.5 to −0.01; p = 0.048) in participants sleeping <6 h, compared with those sleeping between 7 and 9 h.

    Our findings suggest that the less variability in sleep duration or an adequate sleep duration the greater the success of the lifestyle interventions in adiposity.
    correlation doesn't imply causation

  3. #783
    Sztywny Pal Azji
    May 2014
    1 978
    tydzień z leptyną:

    Researchers find new mutation in the leptin gene

    The global obesity epidemic is so far-reaching it now has an overarching name: globesity. Texas Biomed Staff Scientist Raul Bastarrachea, M.D., is part of a team that discovered a new mutation in the gene that regulates the key hormone suppressing hunger called leptin. This new mutation could help researchers understand why people develop excess of body fat. Dr. Bastarrachea's research is aimed at helping tackle metabolic disorders like cardiovascular disease and diabetes which are fueled by obesity and impact millions of people around the world.

    "We keep learning more and more about the role of fat in normal-weight people," Bastarrachea said. "By researching what goes wrong when genes don't code correctly for the production of leptin, we are coming closer to answers that could help millions of people with metabolic disorders."

    In the field of metabolic diseases, the pinpointing of the protein Leptin in the year 2000 was a huge breakthrough. Researchers at Rockefeller University found this hormone was missing in rats that randomly became extremely fat in a laboratory setting. Humans also need adequate leptin circulating levels to inform the brain that their body fat content is enough and they do not need to keep eating more food. In other words, leptin signals mammals to stop eating.

    Leptin is a protein produced by fat cells (also known as adipose tissue). It travels through the circulation to the brain where the hormone hooks up to a leptin receptor in the hypothalamus to signal to the body that there is enough fat and no more food is needed. In other words, it is a hunger-suppressing hormone. The name leptin is derived from the Greek work "leptos" meaning thin. It is sometimes referred to as the "Fat Controller."

    A congenital leptin deficiency is a recessive genetic disorder associated with severe early-onset obesity. In an article in the journal Genes, Dr. Bastarrachea and his co-investigators examined the case of two sisters in Colombia who started off their lives as normal weight babies but who quickly suffered from childhood-onset severe obesity. Prior cases have studied people whose genetics can be traced to Pakistan, Turkey, Egypt, India and China. This is the first case studied in the Americas.

    What scientists found is that these two women—now in their 20s—have a mutation in the leptin gene on chromosome 7. The sisters' leptin levels were so low they were below the detection limit of the manufactured test kit.

    The gene mutation caused the Leptin proteins to be "misfolded," rendering them ineffective and destroying their function.

    When researching the genetics of the family, scientist noted these women were children of lineal consanguinity which means several generations before them married blood relatives. This is a common practice in about a fifth of the world population, mostly in the Middle East, West Asia and North Africa. However, health risks for children of these unions include rare diseases caused by recessive genes.

    While more work is needed to figure out how to combat leptin deficiencies on a large scale, the two Colombian women are in the queue to take Metreleptin—a synthetic analog of leptin—a very expensive injected drug. Its effects, however, can be quite dramatic and life changing.

    With obesity now a global problem, scientists around the world are searching for ways to keep the issue from becoming a healthcare burden for years to come. Texas Biomed is playing an important role.

    Time-restricted feeding restores muscle function in Drosophila models of obesity and circadian-rhythm disruption

    Pathological obesity can result from genetic predisposition, obesogenic diet, and circadian rhythm disruption. Obesity compromises function of muscle, which accounts for a majority of body mass. Behavioral intervention that can counteract obesity arising from genetic, diet or circadian disruption and can improve muscle function holds untapped potential to combat the obesity epidemic. Here we show that Drosophila melanogaster (fruit fly) subject to obesogenic challenges exhibits metabolic disease phenotypes in skeletal muscle; sarcomere disorganization, mitochondrial deformation, upregulation of Phospho-AKT level, aberrant intramuscular lipid infiltration, and insulin resistance. Imposing time-restricted feeding (TRF) paradigm in which flies were fed for 12 h during the day counteracts obesity-induced dysmetabolism and improves muscle performance by suppressing intramuscular fat deposits, Phospho-AKT level, mitochondrial aberrations, and markers of insulin resistance. Importantly, TRF was effective even in an irregular lighting schedule mimicking shiftwork. Hence, TRF is an effective dietary intervention for combating metabolic dysfunction arising from multiple causes.

    Sleep & Circadian Health are Associated with Mood & Behavior in Adolescents with Overweight/Obesity

    Objective/Background Rates of overweight/obesity and insufficient/delayed sleep are high among adolescents and are also unique risk factors for mood/behavior difficulties. This study aimed to evaluate relationships between sleep/circadian health and mood/behavior in a cohort of adolescents with overweight/obesity.

    Participants Twenty-two adolescents (16.4 ± 1.1 years) with overweight/obesity attending high school completed in the study.

    Methods Participants completed one week of home sleep monitoring (actigraphy), questionnaires assessing chronotype (diurnal preference; Morningness/Eveningness Scale for Children) and mood/behavior (Strengths & Difficulties Questionnaire), and had in-laboratory salivary melatonin sampling on a Thursday or Friday during the academic year.

    Results Linear regressions revealed later weekday bedtime and shorter weekday time in bed and sleep duration were associated with worse mood/behavior scores. Shorter duration of melatonin secretion and greater “eveningness” were also associated with worse mood/behavior scores.

    Conclusions Short and late sleep, shorter melatonin secretion, and eveningness chronotype are associated with worse mood/behavior symptoms in a cohort of adolescents with overweight/obesity. Clinicians should assess for both sleep and mood/behavior symptoms and further research is needed to evaluate the impact of improved sleep on mood/behavior in adolescents with overweight/obesity.
    ćwiczysz i bierzesz metformin ? - pozdro

    Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults.

    Metformin and exercise independently improve insulin sensitivity and decrease the risk of diabetes. Metformin was also recently proposed as a potential therapy to slow aging. However, recent evidence indicates that adding metformin to exercise antagonizes the exercise-induced improvement in insulin sensitivity and cardiorespiratory fitness. The purpose of this study was to test the hypothesis that metformin diminishes the improvement in insulin sensitivity and cardiorespiratory fitness after aerobic exercise training (AET) by inhibiting skeletal muscle mitochondrial respiration and protein synthesis in older adults (62 ± 1 years). In a double-blinded fashion, participants were randomized to placebo (n = 26) or metformin (n = 27) treatment during 12 weeks of AET. Independent of treatment, AET decreased fat mass, HbA1c, fasting plasma insulin, 24-hr ambulant mean glucose, and glycemic variability. However, metformin attenuated the increase in whole-body insulin sensitivity and VO2 max after AET. In the metformin group, there was no overall change in whole-body insulin sensitivity after AET due to positive and negative responders. Metformin also abrogated the exercise-mediated increase in skeletal muscle mitochondrial respiration. The change in whole-body insulin sensitivity was correlated to the change in mitochondrial respiration. Mitochondrial protein synthesis rates assessed during AET were not different between treatments. The influence of metformin on AET-induced improvements in physiological function was highly variable and associated with the effect of metformin on the mitochondria. These data suggest that prior to prescribing metformin to slow aging, additional studies are needed to understand the mechanisms that elicit positive and negative responses to metformin with and without exercise.
    Effects of caffeine and sex on muscle performance and delayed onset muscle soreness after exercise-induced muscle damage: a double-blind randomized tria

    The present study aims to investigate effects of caffeine ingestion and sex difference on muscle performance, delayed onset muscle soreness (DOMS) and various biomarkers under exercise-induced muscle damage (EIMD). Twenty (10 male and 10 female) healthy elite college athletes were recruited. Participants ingested either caffeine (6 mg·kg-1) or a placebo in a randomized, double-blind and counter-balanced fashion at 24 and 48 hours following EIMD. Muscle performance, DOMS and blood samples were taken an hour before and an hour after supplementation. Caffeine ingestion restored impaired maximal voluntary isometric contractions (MVIC: 10.2%; MVICpost: 7.2%) (both, p<.05) during EIMD across both sexes. Following caffeine ingestion during MVIC, whilst affected by EIMD, an interaction was found between DOMS and serum K+ (both, p<.05), with males showing greater attenuation (21.5% and 16.9%, respectively) compared to females (4.6% and 1.3%, respectively). DOMS demonstrated an inverse correlation with MVIC after caffeine ingestion both overall and among male athletes (r=−0.34 & −0.54, respectively; p<.05) but not among female athletes (r=−0.11; p>.05) under EIMD. In addition, caffeine ingestion increased post-exercise serum glucose, and lowered lactate concentrations across both sexes (both, p<.05). This is the first study to show that male athletes, compared to female athletes, experience a greater reduction in DOMS during enhanced MVIC when caffeine was consumed, suggesting males might receive greater ergogenic effects from caffeine when affected by EIMD. Furthermore, caffeine ingestion was able to restore impaired muscle power among elite collegiate athletes across both sexes.

    Heart rate abnormalities in sleep may be a new biomarker of depression: study

    Canadian researchers say they may have found an objective way to tell if someone is suffering from depression by measuring heart rate abnormalities during sleep.

    "I was surprised to see the accuracy of this," said professor Rebecca Robillard, a sleep researcher at the Royal Ottawa Institute of Mental Health Research

    Kraków czeka na wschód słońca żeby przywitać najdłuższy dzień w roku i .. lipa

    cieszmy się długimi dniami bo tak szybko odchodzą:
    correlation doesn't imply causation

  4. #784
    Sztywny Pal Azji
    May 2014
    1 978
    Performance-enhancing bacteria found in the microbiomes of elite athletes

    New research has identified a type of bacteria found in the microbiomes of elite athletes that contributes to improved capacity for exercise. These bacteria, members of the genus Veillonella, are not found in the guts of sedentary people.

    Researchers identify new hunger pathway in the brain

    A newly identified hunger pathway in the brain can quickly modify food intake in the presence of food, according to a study of mice published in JNeurosci. This pathway could be a future target for the treatment of eating disorders.

    Food intake is modified by long-term signals such as hormones and molecules released during digestion, but a newly recognized circuit in the hypothalamus can change feeding behavior on a shorter timescale.

    Using fluorescent calcium imaging and electrophysiological recording, Shane Hentges and Andrew Rau at Colorado State University identified a pathway in the hypothalamus that affects food intake and body weight through release of the neurotransmitter GABA, which can occur due to the detection, rather than consumption, of food.

    The researchers found that food-deprived mice exhibited more GABA-related neuron activity, indicating that temporary energy states can directly affect feeding behavior. The knowledge of this pathway improves our understanding of how the brain controls energy balance.

    Settling the debate on serotonin's role in sleep

    Serotonin is a multipurpose molecule found throughout the brain, playing a role in memory, cognition, and feelings of happiness and other emotions. In particular, researchers have long debated serotonin's role in sleep: Does serotonin promote sleep, or its opposite, wakefulness

    Circadian Rhythm of Vascular Function in Midlife Adults

    Adverse cardiovascular events occur more frequently in the morning than at other times of the day. Vascular endothelial function (VEF)—a robust cardiovascular risk marker—is impaired during this morning period. We recently discovered that this morning impairment in VEF is not caused by either overnight sleep or the inactivity that accompanies sleep. We determined whether the endogenous circadian system is responsible for this morning impairment in VEF. We also assessed whether the circadian system affects mechanistic biomarkers, that is, oxidative stress (malondialdehyde adducts), endothelin-1, blood pressure, and heart rate.

    Approach and Results
    Twenty-one (11 women) middle-aged healthy participants completed a 5-day laboratory protocol in dim light where all behaviors, including sleep and activity, and all physiological measurements were evenly distributed across the 24-hour period. After baseline testing, participants underwent 10 recurring 5-hour 20-minute behavioral cycles of 2-hour 40-minute sleep opportunities and 2 hours and 40 minutes of standardized waking episodes. VEF, blood pressure, and heart rate were measured, and venous blood was sampled immediately after awakening during each wake episode. Independent of behaviors, VEF was significantly attenuated during the subjective night and across the morning (P=0.04). Malondialdehyde adducts and endothelin-1 exhibited circadian rhythms with increases across the morning vulnerable period and peaks around noon (P≤0.01). Both systolic (P=0.005) and diastolic blood pressure (P=0.04) were rhythmic with peaks in the late afternoon.

    The endogenous circadian system impairs VEF and increases malondialdehyde adducts and endothelin-1 in the morning vulnerable hours and may increase the risk of morning adverse cardiovascular events in susceptible individuals.

    Effects of squat training with different depths on lower limb muscle volumes

    The relative increase in 1RM of full squat was significantly greater in FST (31.8 ± 14.9%) than in HST (11.3 ± 8.6%) (p = 0.003), whereas there was no difference in the relative increase in 1RM of half squat between FST (24.2 ± 7.1%) and HST (32.0 ± 12.1%) (p = 0.132). The volumes of knee extensor muscles significantly increased by 4.9 ± 2.6% in FST (p < 0.001) and 4.6 ± 3.1% in HST (p = 0.003), whereas that of rectus femoris and hamstring muscles did not change in either group. The volumes of adductor and gluteus maximus muscles significantly increased in FST (6.2 ± 2.6% and 6.7 ± 3.5%) and HST (2.7 ± 3.1% and 2.2 ± 2.6%). In addition, relative increases in adductor (p = 0.026) and gluteus maximus (p = 0.008) muscle volumes were significantly greater in FST than in HST.

    The results suggest that full squat training is more effective for developing the lower limb muscles excluding the rectus femoris and hamstring muscles.
    correlation doesn't imply causation

  5. #785
    Sztywny Pal Azji
    May 2014
    1 978
    Muscling in on the role of vitamin D

    A recent study conducted at The Westmead Institute for Medical Research has shed light on the role of vitamin D in muscle cells. The study looked at the role of vitamin D in muscles in mice, and showed that vitamin D signaling (how cells communicate with one another) is needed for normal muscle size and strength.
    Researchers found that mice missing the vitamin D receptor only in myocytes (muscle cells) had smaller muscles, and they were less strong. They also had significantly decreased running speed and didn't run as far as mice with normal vitamin D action.
    Lead researcher, Professor Jenny Gunton says, "For a long time, we have known that vitamin D deficiency is associated with muscle weakness and greater risk of falls and fractures. However, whether vitamin D played a direct role in muscle wasn't known.
    "We show that vitamin D receptor is present in low levels in normal muscle, and our study found that deleting muscle cell vitamin D receptors had important effects on muscle function."
    Professor Gunton says that, compared to a previous study she conducted that looked at mice missing vitamin D receptors across their whole body, this new study has highlighted some important differences.
    "We found that mice missing muscle cell vitamin D receptors had normal body size but less muscle mass and more fat mass.
    "In terms of choosing to run on a wheel in their cage, the mice had shorter running distance and slower speed. These might contribute to the lower muscle mass and increase in fat.
    In terms of muscle strength, these mice also had a significantly decreased grip strength from a very early age."

    While more research is needed, Professor Gunton says that these results suggest that maintaining normal vitamin D signaling in muscle is important for preserving muscle bulk and function.
    "These findings also have the potential to open up avenues to pursue new therapies that target muscle cell vitamin D receptors. These therapies could help to address or prevent age-related sarcopenia (degenerative loss of skeletal muscle mass) and other disorders related to muscle function."

    Increased walking activity associated with long-term health benefits

    Short term pedometer-based walking interventions can have long-term health benefits for adults and older adults, according to new research published in the open-access journal PLOS Medicine on 25 June. Tess Harris and colleagues from St George's University of London, UK and other institutions, conducted two trials of walking interventions which aimed to increase step count and physical activity. Not only did the investigators see sustained increases in physical activity at 3-4 years in the intervention group participants, they also noted fewer cardiovascular events and fractures.

    These neurons affect how much you do, or don't, want to eat

    Like a symphony, multiple brain regions work in concert to regulate the need to eat. University of Arizona researchers believe they have identified a symphony conductor—a brain region that regulates appetite suppression and activation—tucked within the amygdala, the brain's emotional hub.

    pierwszy mózg na tapecie:

    New research shows Parkinson's disease origins in the gut

    In experiments in mice, Johns Hopkins Medicine researchers say they have found additional evidence that Parkinson's disease originates among cells in the gut and travels up the body's neurons to the brain. The study, described in the June issue of the journal Neuron, offers a new, more accurate model in which to test treatments that could prevent or halt Parkinson's disease progression.

    Nutrition Recommendations for Bodybuilders in the Off-Season: A Narrative Review

    Bodybuilders in the off-season should focus on consuming a slightly hyper-energetic diet (~10–20% above maintenance calories) with the aim of gaining ~0.25–0.5% of bodyweight per week. Advanced bodybuilders are advised to be more conservative with the caloric surplus and the rate of weekly weight gain. Dietary protein intake is recommended to be 1.6–2.2 g/kg/day with a focus on sufficient protein at each meal (0.40–0.55 g/kg/meal) and an even distribution throughout the day (3–6 meals). Dietary fats should be consumed at moderate levels, neither too low nor high (0.5–1.5 g/kg/day), to prevent an unfavorable fTC ratio and to prevent reductions in testosterone levels. After calories has been devoted to protein and fat, the remaining calories should come from carbohydrates while ensuring sufficient amounts are consumed (≥3–5 g/kg/day). Minor benefits can be gained by consuming protein (0.40–0.55 g/kg/meal) in close proximity to training sessions (1–2 hours pre-exercise and within 1–2 hours post-exercise). CM (3–5 g/day), and caffeine (5–6 mg/kg) should be considered as they can yield ergogenic effects for bodybuilders. Further, BA (3–5 g/day) and CITM (8 g/day) are dietary supplements that can be considered as they may potentially be of benefit for bodybuilders, depending on individual training regimens. Bodybuilders who are unable to consume a sufficient intake of micronutrients and essential fatty acids in their diets should consider supplementing these nutrients to avoid deficiencies. The primary limitation of this review is the lack of large-scale and long-term studies on bodybuilders in the off-season. Further research is warranted in this population to optimize nutrition and dietary supplement recommendations.
    correlation doesn't imply causation

  6. #786
    Sztywny Pal Azji
    May 2014
    1 978
    Kawa może pomóc w odchudzaninu

    Naukowcy z Uniwersytetu w Nottingham donoszą, że picie kawy może stymulować brunatną tkankę tłuszczową, która uaktywnia zwiększone spalanie kalorii. Autorzy badań twierdzą, że to może być kluczem do walki z otyłością i cukrzycą.

    w PL:
    Bakterie jelitowe mogą pomóc zwiększyć wydolność fizyczną

    Sportowcy mają nie tylko mocniejsze serca i mięśnie niż przeciętny Kowalski. Mają także pewien rodzaj bakterii jelitowych, które mogą zwiększać ich wydolność fizyczną – wynika z nowych badań.

    Keeping active or becoming more active in middle and older age linked to longer life

    Keeping physically active or becoming more active during middle and older age is associated with a lower risk of death, regardless of past activity levels or existing health conditions, suggests a large UK study published by The BMJ today.

    A single episode of binge alcohol drinking causes sleep disturbance, disrupts sleep homeostasis, and down‐regulates equilibrative nucleoside transporter 1

    Binge alcohol drinking, a risky pattern of alcohol consumption, has severe consequences toward health and well‐being of an individual, his family, and society. Although, binge drinking has detrimental effects on sleep, underlying mechanisms are unknown. We used adult male C57BL/6J mice and exposed them to a single, 4‐h session of binge alcohol self‐administration, in stress‐free environment, to examine neuronal mechanisms affecting sleep. We first verified binge pattern of alcohol consumption. When allowed to self‐administer alcohol in a non‐stressful environment, mice consumed alcohol in a binge pattern. Next, effect of binge drinking on sleep–wakefulness was monitored. While sleep–wakefulness remained unchanged during drinking session, significant increase in non‐rapid eye movement (NREM) sleep was observed during 4 h of active period post‐binge, followed by increased wakefulness, reduced sleep during subsequent sleep (light) period; although the timing of sleep onset (at lights‐on) remained unaffected. Next, electrophysiological and biochemical indicators of sleep homeostasis were examined using sleep deprivation‐recovery sleep paradigm. Mice exposed to binge drinking did not show an increase in cortical theta power and basal forebrain adenosine levels during sleep deprivation; NREM sleep and NREM delta power did not increase during recovery sleep suggesting that mice exposed to binge alcohol do not develop sleep pressure. Our final experiment examined expression of genes regulating sleep homeostasis following binge drinking. While binge drinking did not affect adenosine kinase and A1 receptor, expression of equilibrative nucleoside transporter 1 (ENT1) was significantly reduced. These results suggest that binge alcohol consumption‐induced down‐regulation of ENT1 expression may disrupt sleep homeostasis and cause sleep disturbances.

    Short-term sleep deprivation with exposure to nocturnal light alters mitochondrial bioenergetics in Drosophila

    •Exposure to nocturnal light alters sleep patterns in drosophila.

    •Sleep deprivation induces mitochondrial dysfunction in drosophila.

    •Sleep deprivation induces oxidative stress in drosophila.

    •Sleep deprivation alters stress response genes in drosophila.

    Protein supplementation elicits greater gains in maximal oxygen uptake capacity and stimulates lean mass accretion during prolonged endurance training: a double-blind randomized controlled trial.

    Endurance training induces numerous cardiovascular and skeletal muscle adaptations, thereby increasing maximal oxygen uptake capacity (VO2max). Whether protein supplementation enhances these adaptations remains unclear.

    The present study was designed to determine the impact of protein supplementation on changes in VO2max during prolonged endurance training.

    We used a double-blind randomized controlled trial with repeated measures among 44 recreationally active, young males. Subjects performed 3 endurance training sessions per week for 10 wk. Supplements were provided immediately after each exercise session and daily before sleep, providing either protein (PRO group; n = 19; 21.5 ± 0.4 y) or an isocaloric amount of carbohydrate as control (CON group; n = 21; 22.5 ± 0.5 y). The VO2max, simulated 10-km time trial performance, and body composition (dual-energy X-ray absorptiometry) were measured before and after 5 and 10 wk of endurance training. Fasting skeletal muscle tissue samples were taken before and after 5 and 10 wk to measure skeletal muscle oxidative capacity, and fasting blood samples were taken every 2 wk to measure hematological factors.

    VO2max increased to a greater extent in the PRO group than in the CON group after 5 wk (from 49.9 ± 0.8 to 54.9 ± 1.1 vs 50.8 ± 0.9 to 53.0 ± 1.1 mL · kg-1 · min-1; P < 0.05) and 10 wk (from 49.9 ± 0.8 to 55.4 ± 0.9 vs 50.8 ± 0.9 to 53.9 ± 1.2 mL · kg-1 · min-1; P < 0.05). Lean body mass increased in the PRO group whereas lean body mass in the CON group remained stable during the first 5 wk (1.5 ± 0.2 vs 0.1 ± 0.3 kg; P < 0.05) and after 10 wk (1.5 ± 0.3 vs 0.4 ± 0.3 kg; P < 0.05). Throughout the intervention, fat mass reduced significantly in the PRO group and there were no changes in the CON group after 5 wk (-0.6 ± 0.2 vs -0.1 ± 0.2 kg; P > 0.05) and 10 wk (-1.2 ± 0.4 vs -0.2 ± 0.2 kg; P < 0.05).

    Protein supplementation elicited greater gains in VO2max and stimulated lean mass accretion but did not improve skeletal muscle oxidative capacity and endurance performance during 10 wk of endurance training in healthy, young males.

    Being a 'morning person' linked to lower risk of breast cancer

    Being a morning person (popularly known as larks) is associated with a lower risk of developing breast cancer than being an evening person (popularly known as owls), finds a study published by The BMJ today.

    Sleeping longer than the recommended 7-8 hours a night may also carry an increased risk, the results suggest.
    correlation doesn't imply causation

  7. #787
    Sztywny Pal Azji
    May 2014
    1 978
    Cytat Zamieszczone przez htw Zobacz posta
    Fotony docierające do płodu wpływają na rozwój siatkówki


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

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

    JUNE 27, 2019
    Too little UVB exposure in pregnancy linked with a higher risk of learning disabilities

    Too little sunlight—and specifically UVB exposure—in pregnancy has been linked with a higher risk of learning disabilities.

    In a new study looking at more than 422,500 school-age children from across Scotland, researchers found that low UVB exposure during pregnancy was associated with risk of learning disabilities.

    UVB exposure from sunlight is linked to the production of the essential nutrient vitamin D in the body.
    Publishing their results in the journal Scientific Reports, University of Glasgow researchers linked sunshine hours data from the Met Office with the month in which children were conceived. They found that there was a statistically significant relationship between lower UVB exposure over the whole of pregnancy and the risk of learning disabilities.
    The relationship was specific to UVB (not UVA) suggesting that the effect of sunlight was likely to be working via production of vitamin D.
    During the antenatal period, the foetus undergoes rapid development and growth, making it susceptible to environmental exposures, with the potential of long-term consequences. Maternal UVB exposure promotes the production of vitamin D, which is important for normal brain development of a foetus.
    The researchers also found a slightly stronger relationship with low UVB exposure in the first trimester, suggesting that early pregnancy may be the most vulnerable to the effects of insufficient UVB.
    As a result of low levels of UVB radiation from sunlight, vitamin D deficiency is common over winter months in high latitude countries such as Scotland. With Scottish residents twice as likely to be vitamin D deficient than people living in other parts of the UK.
    Professor Jill Pell, Director of the University of Glasgow's Institute of Health and Wellbeing and lead author of the study, said: "Learning disabilities can have profound life-long effects on both the affected child and their family. The importance of our study is that it suggests a possible way to prevent learning disabilities in some children. Clinical trials are now needed to confirm whether taking vitamin D supplements during pregnancy could reduce the risk of learning disabilities."
    Of the 422,512 schoolchildren included in the study, 79,616 (18.8%) had a learning disability, 49,770 (23.1%) boys and 29,846 (14.4%) girls. The percentage of children with learning disabilities varied by month of conception, ranging from 16.5% among children conceived in July, to 21.0% among those conceived in February, March and April.
    Dr. Claire Hastie, who did the analysis, said "Our study linked routinely collected health and education data with environmental data enabling us to study a very large number of children in a way that would not be possible using traditional methods."
    The study, 'Antenatal exposure to solar radiation and learning disabilities: Population cohort study of 422,512 children' is published in Scientific Reports.
    June 26, 2019
    Barefoot walking

    A groundbreaking researcher in running turns his attention to walking, with and without shoes

    Daniel E. Lieberman doesn’t hate shoes. The Edwin M. Lerner II Professor of Biological Science and chair of the Department of Human Evolutionary Biology wants to clear that up right away.

    “There has been debate about barefoot running being good or bad, or shoes being good or bad, and this is the wrong debate,” Lieberman said. “It should be about what the costs and benefits of shoes are and how we can better understand how shoes affect our feet, our health, the way we walk.”

    He should know.
    correlation doesn't imply causation

  8. #788
    Sztywny Pal Azji
    May 2014
    1 978
    What made humans 'the fat primate'?

    Blame junk food or a lack of exercise. But long before the modern obesity epidemic, evolution made us fat too.

    "We're the fat primates," said Devi Swain-Lenz, a postdoctoral associate in biology at Duke University.

    The fact that humans are chubbier than chimpanzees isn't news to scientists. But new evidence could help explain how we got that way.

    Despite having nearly identical DNA sequences, chimps and early humans underwent critical shifts in how DNA is packaged inside their fat cells, Swain-Lenz and her Duke colleagues have found. As a result, the researchers say, this decreased the human body's ability to turn "bad" calorie-storing fat into the "good" calorie-burning kind.

    The results were published June 24 in the journal Genome Biology and Evolution.

    Compared to our closest animal relatives, even people with six-pack abs and rippling arms have considerable fat reserves, researchers say. While other primates have less than 9% body fat, a healthy range for humans is anywhere from 14% to 31%.

    To understand how humans became the fat primate, a team led by Swain-Lenz and Duke biologist Greg Wray compared fat samples from humans, chimps and a more distantly-related monkey species, rhesus macaques. Using a technique called ATAC-seq, they scanned each species' genome for differences in how their fat cell DNA is packaged.

    Normally most of the DNA within a cell is condensed into coils and loops and tightly wound around proteins, such that only certain DNA regions are loosely packed enough to be accessible to the cellular machinery that turns genes on and off.

    The researchers identified roughly 780 DNA regions that were accessible in chimps and macaques, but had become more bunched up in humans. Examining these regions in detail, the team also noticed a recurring snippet of DNA that helps convert fat from one cell type to another.

    Not all fat is created equal, Swain-Lenz explained. Most fat is made up of calorie-storing white fat. It's what makes up the marbling in a steak and builds up around our waistlines. Specialized fat cells called beige and brown fat, on the other hand, can burn calories rather than store them to generate heat and keep us warm.

    One of the reasons we're so fat, the research suggests, is because the regions of the genome that help turn white fat to brown were essentially locked up -- tucked away and closed for business -- in humans but not in chimps.

    "We've lost some of the ability to shunt fat cells toward beige or brown fat, and we're stuck down the white fat pathway," Swain-Lenz said. It's still possible to activate the body's limited brown fat by doing things like exposing people to cold temperatures, she explained, "but we need to work for it."

    Humans, like chimps, need fat to cushion vital organs, insulate us from the cold, and buffer us from starvation. But early humans may have needed to plump up for another reason, the researchers say -- as an additional source of energy to fuel our growing, hungry brains.

    In the six to eight million years since humans and chimps went their separate ways, human brains have roughly tripled in size. Chimpanzee brains haven't budged.

    The human brain uses more energy, pound for pound, than any other tissue. Steering fat cells toward calorie-storing white fat rather than calorie-burning brown fat, the thinking goes, would have given our ancestors a survival advantage.

    Swain-Lenz said another question she gets a lot is: "Are you going to make me skinny?"

    "I wish," she said.

    Because of brown fat's calorie-burning abilities, numerous researchers are trying to figure out if boosting our body's ability to convert white fat to beige or brown fat could make it easier to slim down.

    Swain-Lenz says the differences they found among primates might one day be used to help patients with obesity -- but we're not there yet.

    "Maybe we could figure out a group of genes that we need to turn on or off, but we're still very far from that," Swain-Lenz said. "I don't think that it's as simple as flipping a switch. If it were, we would have figured this out a long time ago," she explained.

    27 June 2019
    The human stress response

    The human stress response has evolved to maintain homeostasis under conditions of real or perceived stress. This objective is achieved through autoregulatory neural and hormonal systems in close association with central and peripheral clocks. The hypothalamic–pituitary–adrenal axis is a key regulatory pathway in the maintenance of these homeostatic processes. The end product of this pathway — cortisol — is secreted in a pulsatile pattern, with changes in pulse amplitude creating a circadian pattern. During acute stress, cortisol levels rise and pulsatility is maintained. Although the initial rise in cortisol follows a large surge in adrenocorticotropic hormone levels, if long-term inflammatory stress occurs, adrenocorticotropic hormone levels return to near basal levels while cortisol levels remain raised as a result of increased adrenal sensitivity. In chronic stress, hypothalamic activation of the pituitary changes from corticotropin-releasing hormone-dominant to arginine vasopressin-dominant, and cortisol levels remain raised due at least in part to decreased cortisol metabolism. Acute elevations in cortisol levels are beneficial to promoting survival of the fittest as part of the fight-or-flight response. However, chronic exposure to stress results in reversal of the beneficial effects, with long-term cortisol exposure becoming maladaptive, which can lead to a broad range of problems including the metabolic syndrome, obesity, cancer, mental health disorders, cardiovascular disease and increased susceptibility to infections. Neuroimmunoendocrine modulation in disease states and glucocorticoid-based therapeutics are also discussed.

    Key points

    - The hypothalamic–pituitary–adrenal (HPA) axis is a key system that synchronizes the stress response with circadian regulatory processes.

    - Regulation of the HPA axis is very dynamic with both ultradian and circadian oscillations.

    - Short-term and longer-term stress result in different regulatory mechanisms involving hypothalamic, pituitary and adrenal activity, as well as cortisol metabolism.

    - Chronic elevation and nonphysiological patterns of cortisol result in poor cognitive, metabolic and immune function.

    Oestrogen receptor β mediates the actions of bisphenol-A on ion channel expression in mouse pancreatic beta cells

    Bisphenol-A (BPA) is a widespread endocrine-disrupting chemical that has been associated with type 2 diabetes development. Low doses of BPA modify pancreatic beta cell function and induce insulin resistance; some of these effects are mediated via activation of oestrogen receptors α (ERα) and β (ERβ). Here we investigated whether low doses of BPA regulate the expression and function of ion channel subunits involved in beta cell function.

    Microarray gene profiling of isolated islets from vehicle- and BPA-treated (100 μg/kg per day for 4 days) mice was performed using Affymetrix GeneChip Mouse Genome 430.2 Array. Expression level analysis was performed using the normalisation method based on the processing algorithm ‘robust multi-array average’. Whole islets or dispersed islets from C57BL/6J or oestrogen receptor β (ERβ) knockout (Erβ−/−) mice were treated with vehicle or BPA (1 nmol/l) for 48 h. Whole-cell patch-clamp recordings were used to measure Na+ and K+ currents. mRNA expression was evaluated by quantitative real-time PCR.

    Microarray analysis showed that BPA modulated the expression of 1440 probe sets (1192 upregulated and 248 downregulated genes). Of these, more than 50 genes, including Scn9a, Kcnb2, Kcnma1 and Kcnip1, encoded important Na+ and K+ channel subunits. These findings were confirmed by quantitative RT-PCR in islets from C57BL/6J BPA-treated mice or whole islets treated ex vivo. Electrophysiological measurements showed a decrease in both Na+ and K+ currents in BPA-treated islets. The pharmacological profile indicated that BPA reduced currents mediated by voltage-activated K+ channels (Kv2.1/2.2 channels) and large-conductance Ca2+-activated K+ channels (KCa1.1 channels), which agrees with BPA’s effects on gene expression. Beta cells from ERβ−/− mice did not present BPA-induced changes, suggesting that ERβ mediates BPA’s effects in pancreatic islets. Finally, BPA increased burst duration, reduced the amplitude of the action potential and enlarged the action potential half-width, leading to alteration in beta cell electrical activity.

    Our data suggest that BPA modulates the expression and function of Na+ and K+ channels via ERβ in mouse pancreatic islets. Furthermore, BPA alters beta cell electrical activity. Altogether, these BPA-induced changes in beta cells might play a role in the diabetogenic action of BPA described in animal models.
    correlation doesn't imply causation

  9. #789
    Sztywny Pal Azji
    May 2014
    1 978
    05 July 2019
    Dissecting the role of the gut microbiota and diet on visceral fat mass accumulation

    Both gut microbiota and diet have been shown to impact visceral fat mass (VFM), a major risk factor for cardiometabolic disease, but their relative contribution has not been well characterised. We aimed to estimate and separate the effect of gut microbiota composition from that of nutrient intake on VFM in 1760 older female twins. Through pairwise association analyses, we identified 93 operational taxonomic units (OTUs) and 10 nutrients independently linked to VFM (FDR < 5%). Conditional analyses revealed that the majority (87%) of the 93 VFM-associated OTUs remained significantly associated with VFM irrespective of nutrient intake correction. In contrast, we observed that the effect of fibre, magnesium, biotin and vitamin E on VFM was partially mediated by OTUs. Moreover, we estimated that OTUs were more accurate predictors of VFM than nutrients and accounted for a larger percentage of its variance. Our results suggest that while the role of certain nutrients on VFM appears to depend on gut microbiota composition, specific gut microbes may affect host adiposity regardless of dietary intake. The findings imply that the gut microbiota may have a greater contribution towards shaping host VFM than diet alone. Thus, microbial-based therapy should be prioritised for VFM reduction in overweight and obese subjects.

    VFM is strongly associated with gut microbiota composition and nutrient intake. (a) OTUs significantly associated with VFM using OTU as predictor of VFM and correcting for age, energy intake (kcal), and family structure. Red bars represent positive associations and green bars show negatives associations. (b) Dietary component associations with VFM and OTUs. Bubble plot represents the –log transformed p-value with negative associations (left side) and positive associations (right side) resulting from the prediction of VFM by each food component independently, correcting for age, energy intake (kcal), and family structure. The colour intensity represents the effect size, red representing positive associations and green showing negatives associations. The bar chart represents the number of significant (FDR < 5%) OTUs negatively (right) or positively (left) associated with each food component. The bars are coloured in relation to significance and direction of the association of OTUs with VFM: grey - not associated, red - positively associated, green - negatively associated. (c) Proportion of VFM-associated OTUs associated with one VFM-associated food component (dark blue), a non-VFM-associated food component (grey) or no food (light blue). (d) Potential mechanisms of action of diet and microbiota effects on host metabolism or VFM deposition. Four pathways are shown: (1) diet directly impacts the host without GM mediation (i.e. nitrogen, protein, cholesterol and tryptophan); (2) gut microbes (OTUs) directly impact VFM independent of the effect of diet; (3) microbes impact VFM and these effects can be modulated by diet; (4) dietary impacts on VFM require specific gut microbial composition.

    Diet-induced hypothalamic dysfunction and metabolic disease, and the therapeutic potential of polyphenols

    •Unhealthy diets high in fat and sugar can cause hypothalamic inflammation.

    •Hypothalamic dysfunction causes obesity, cardiovascular and neurological disorders.

    •Diets high in phytochemicals can reduce the risk of obesity and metabolic diseases.

    •Polyphenols allay harmful dietary effects by preventing hypothalamic inflammation.

    •Polyphenols protects against neuron damage and can improve overall human health.

    Chronotype in bipolar disorder: an 18-month prospective study

    Circadian dysregulation plays an important role in the etiology of mood disorders. Evening chronotype is frequent in these patients. However, prospective studies about the influence of chronotype on mood symptoms have reached unclear conclusions in patients with bipolar disorder (BD). The objective of this study was to investigate relationship between chronotype and prognostic factors for BD.

    At the baseline, 80 euthymic BD patients answered a demographic questionnaire and clinical scales to evaluate anxiety, functioning and chronotype. Circadian preference was measured using the Morningness-Eveningness Questionnaire, in which lower scores indicate eveningness. Mood episodes and hospitalizations were evaluated monthly for 18 months.

    Among the BD patients, 14 (17.5%) were definitely morning type, 35 (43.8%), moderately morning, 27 (33.7%) intermediate (neither) and 4 (5%) moderately evening. Eveningness was associated with obesity or overweight (p = 0.03), greater anxiety (p = 0.002) and better functioning (p = 0.01), as well as with mood episodes (p = 0.04), but not with psychiatric hospitalizations (p = 0.82). This group tended toward depressive episodes (p = 0.06), but not (hypo)mania (p = 0.56).

    This study indicated that evening chronotype predicts a poor prognostic for BD. It reinforces the relevance of treating rhythm disruptions even during euthymia to improve patient quality of life and prevent mood episodes.

    Cross-sectional and Prospective Associations of Actigraphy-Assessed Sleep Regularity With Metabolic Abnormalities: The Multi-Ethnic Study of Atherosclerosis

    To cross-sectionally and prospectively investigate the association between irregular sleep patterns, a potential marker for circadian disruption, and metabolic abnormalities.

    In the Multi-Ethnic Study of Atherosclerosis, participants completed 7-day actigraphy at exam 5 (2010–2013) and were prospectively followed throughout exam 6 (2016 to 2017). Sleep regularity was quantified by the 7-day SD of actigraphy-assessed sleep duration and sleep onset timing. Metabolic abnormalities were defined by 1) the National Cholesterol Education Program Adult Treatment Panel III criteria and 2) a data-driven clustering of metabolic factors.

    In the exam 5 cross-sectional analysis adjusted for sociodemographic and lifestyle factors (n = 2,003), every 1-h increase in the sleep duration SD was associated with 27% (95% CI 1.10, 1.47) higher odds of metabolic syndrome, and every 1-h increase in the sleep timing SD was associated with 23% (95% CI 1.06, 1.42) higher odds. The associations remained significant, with additional adjustment for sleep-related factors including sleep duration. In the prospective analysis (n = 970), the corresponding fully adjusted odds ratio (OR) (95% CI) was 1.27 (0.97, 1.65) for sleep duration and 1.36 (1.03, 1.80) for sleep timing. Compared with the cluster of few metabolic changes, every 1-h increase in sleep variability was associated with almost doubled odds for the cluster characterized by incidence of multiple metabolic abnormalities (OR 1.97 [95% CI 1.18, 3.30] for sleep duration and OR 2.10 [95% CI 1.25, 3.53] for sleep timing).

    Increased variability in sleep duration and timing was associated with higher prevalence and incidence of metabolic abnormalities even after considering sleep duration and other lifestyle factors.

    The role of hormonal, metabolic and inflammatory biomarkers on sleep and appetite in drug free patients with major depression: A systematic review.

    Major depressive disorder (MDD) is a complex and heterogeneous disorder in which clinical symptoms can widely differ among patients. Neurovegetative symptoms, i.e. decreased or increased appetite, changes in body weight and sleep disturbances, described as 'melancholic' or 'atypical' features of a depressive episode, are the most variable symptoms among patients with MDD. We hypothesized biomarkers differences underlying this neurovegetative variability in major depression.

    We systematically reviewed, according to the PRISMA guidelines, the role of specific metabolic, hormonal and inflammatory biomarkers in drug-free MDD patients, that could have neurobiological effects on appetite, weight regulation and circadian rhythms, influencing eating behaviour and sleep patterns. All studies regarding the co-occurrence of disturbed sleep and appetite were examined.

    Besides the well-known leptin and ghrelin, other biomarkers such as BDNF, VEGF, NPY, orexin, and the recent discovered nesfatin-1 seem to be involved in neurovegetative changes in depressive disorders playing a role in the regulation of affective states, stress reactions and sleep patterns. Interestingly, based on the existing evidence, ghrelin, orexin and nesfatin-1 could be linked both to sleep and appetite regulation in depressed patients.

    Heterogeneous studies with low sample size.

    Despite the wide heterogeneity of results, studies on biomarkers of appetite and sleep in MDD are an interesting field of research to explain the neurobiological substrates of depressive symptoms that deserve further investigation.

    Augmentation of Whole-Body Metabolic Status by Mind-Body Training: Synchronous Integration of Tissue- and Organ-Specific Mitochondrial Function

    The objective of our concise review is to elaborate an evidence-based integrative medicine model that incorporates functional linkages of key aspects of cortically-driven mind-body training procedures to biochemical and molecular processes driving enhanced cellular bioenergetics and whole-body metabolic advantage. This entails the adoption of a unified biological systems approach to selectively elucidate basic biochemical and molecular events responsible for achieving physiological relaxation of complex cellular structures. We provide accumulated evidence in support of the potential synergy of voluntary breathing exercises in combination with meditation and/or complementary cognitive tasks to promote medically beneficial enhancements in whole-body relaxation, anti-stress mechanisms, and restorative sleep. Accordingly, we propose that the widespread metabolic and physiological advantages emanating from a sustained series of complementary mind-body exercises will ultimately engender enhanced functional integration of cortical and limbic areas controlling voluntary respiratory processes with autonomic brainstem neural pattern generators. Finally, a unified mechanism is proposed that links behaviorally-mediated enhancements of whole-body metabolic advantage to optimization of synchronous regulation of mitochondrial oxygen utilization via recycling of nitrite and nitric oxide by iron-sulfur centers of coupled respiratory complexes and nitrite reductases.
    In conclusion, we provide a proposed, biological systems-based, mechanism of action linking mind-body training exercises to enhanced metabolic advantage and cellular ATP production, which is critically linked to synchronized mitochondrial function, involving physiological activation of O2-dependent recycling of NO and inorganic nitrite. This broad-based biochemical/molecular mechanism is consistent with a model that economically projects state-dependent optimization of cellular and complex tissue energy metabolism in functionally interactive CNS and peripheral regulatory centers as its unifying principle. The primordial nature of O2-dependent recycling of NO and inorganic nitrite as an existential regulatory mechanism underlying relaxation phenomena is reflected by its widespread expression in prokaryotic phyla and subsequent evolution in eukaryotic mitochondrial respiratory complexes [49]. Finally, potential points of intervention for optimization of medically beneficial effects of mind-body practices may reside in the monitored coupling of controlled nasal breathing exercises with nutraceutical agents capable of enhancing mitochondrial function via synchronized NO/nitrite recycling (Figure 3).

    Whether you're running a startup or just running to keep up, a full seven to eight hours of sleep a night is a luxury that many of us just simply don't have time for.

    A number of studies have suggested that at least seven hours of sleep is ideal for your health, but we can also dig a little deeper into that research for some potential life hacks to help those who are sleepless by choice, or not.

    A new report presented this week in Baltimore at the annual meeting of the American Society for Nutrition finds a potential link between nutrition and the amount and quality of sleep a person gets.

    In a study led and funded, it should be noted, by vitamin and supplement maker Pharmavite, scientists found that people who get less than seven hours of slumber on average also get less vitamin A, D, B1, and B3, as well as magnesium, calcium, zinc, and phosphorus.
    correlation doesn't imply causation

  10. #790
    Sztywny Pal Azji
    May 2014
    1 978
    05 July 2019
    Chronic light cycle-disruption alters central insulin and leptin signalling as well as metabolic markers in male mice

    Recent evidence suggests that the circadian timing system plays a role in energy and glucose homeostasis, and disruptions to this system are a risk factor for the development of metabolic disorders. We exposed animals to a constantly shifting lighting environment comprised of a 6-hour advance, occurring every 6 days, to chronically disrupt their circadian timing system. This treatment caused a gradual increase in body weight of 12 ± 2% after 12 phase shifts compared with a 6 ± 1% increase in mice under control lighting conditions. Additionally, following the 5th phase shift, light cycle-disrupted animals showed a reversal in their diurnal pattern of energy homeostasis and locomotor activity followed by a subsequent loss of this rhythm. To investigate potential molecular mechanisms mediating these metabolic alterations, we assessed central leptin and insulin sensitivity. We discovered that light cycle-disrupted mice had a decrease in central leptin signalling, as indicated by a reduction in the number of phosphorylated STAT3 immunoreactive cells in the arcuate nucleus of the hypothalamus. Furthermore, light cycle-disrupted animals exhibited a marked increase in fasting blood glucose (269.4 ± 21.1 mg/dl), compared with controls (108.8 ± 21.3 mg/dl). This dramatic increase in fasting glucose levels was not associated with an increase in insulin levels suggesting impairments in pancreatic insulin release. Peripheral hyperglycaemia was accompanied by central alterations in insulin signalling at the level of pAkt and IRS1, suggesting that light cycle-disruption alters central insulin signalling. These results provide mechanistic insights into the association between light cycle-disruption and metabolic disease.
    04 July 2019
    Delayed sleep-onset and biological age: late sleep-onset is associated with shorter telomere length

    We evaluated the relationship between leukocyte telomere length (LTL) and sleep duration, insomnia symptoms, and circadian rhythm, to test whether sleep and chronobiological dysregulations are associated with cellular aging.

    Data from the Netherlands Study of Depression and Anxiety (N=2,936) were used at two waves six years apart, to measure LTL. Telomeres shorten during the lifespan and are important biomarkers for cellular aging. LTL was assessed by qualitative polymerase chain reaction and converted into base pair number. Sleep parameters were: sleep duration and insomnia symptoms from the Insomnia Rating Scale. Circadian rhythm variables were: indication of Delayed Sleep Phase Syndrome (DSPS), mid-sleep corrected for sleep debt on free days (MSFsc), sleep-onset time, and self-reported chronotype, from the Munich Chronotype Questionnaire. Generalized estimating equations analysed the associations between LTL, sleep and chronobiological factors, adjusted for baseline age, sex, North European ancestry, and additionally for current smoking, depression severity, obesity and childhood trauma.

    Indicators of delayed circadian rhythm showed a strong and consistent effect on LTL, after adjustment for sociodemographic and health indicators. Late MSFsc (B=-49.9, p=.004), late sleep-onset time (B=-32.4, p=.001), indication of DSPS (B=-73.8, p=.036) and moderately late chronotype in adulthood (B=-71.6, p=.003) were associated with significantly shorter LTL across both waves; whereas sleep duration and insomnia symptoms were not. Extremely early chronotype showed significantly less LTL shortening than intermediate chronotype (B=161.40, p=.037). No predictors showed accelerated LTL attrition over 6 years.

    Individuals with delayed circadian rhythm have significantly shorter LTL, but not faster LTL attrition rates.

    Immunoregulatory role of melatonin in cancer.

    Melatonin is a ubiquitous indole amine that plays a fundamental role in the regulation of the biological rhythm. Disrupted circadian rhythm alters the expression of clock genes and deregulates oncogenes, which finally promote tumor development and progression. An evidence supporting this notion is the higher risk of developing malignancies among night shift workers. Circadian secretion of the pineal hormone also synchronizes the immune system via a reciprocal association that exists between the immune system and melatonin. Immune cells are capable of melatonin biosynthesis in addition to the expression of its receptors. Melatonin induces big changes in different immune cell proportions, enhances their viability and improves immune cell metabolism in the tumor microenvironment. These effects might be directly mediated by melatonin receptors or indirectly through alterations in hormonal and cytokine release. Moreover, melatonin induces apoptosis in tumor cells via the intrinsic and extrinsic pathways of apoptosis, while it protectsthe immune cells. In general, melatonin has a profound impact on immune cell trafficking, cytokine production and apoptosis induction in malignant cells. On such a basis, using melatonin and resynchronization of sleep cycle may have potential implications in immune function enhancement against malignancies, which will be the focus of the present paper.

    fajna fotka:

    machaniem działania melanopsynowego-spierdolenia:
    Ostatnio edytowane przez htw ; 05-07-19 o 17:06
    correlation doesn't imply causation

  11. #791
    Sztywny Pal Azji
    May 2014
    1 978
    JULY 8, 2019
    Do vitamin drips really work? The evidence says 'no', so save your money and eat real food

    Want to boost your immune system, reduce your physical signs of ageing, or cleanse your blood to get rid of toxins? Intravenous (IV) vitamin therapy, or vitamin drips, promise to help. Some claim they can even benefit serious conditions like cancer, Parkinson's disease, the eye condition macular degeneration, the pain of fibromyalgia and depression.

    Celebrities have promoted them on social media. The demand has led to alternative therapy lounges popping up around the world, including in Australia. Patients can kick back in comfy leather chairs while they're hooked up to IVs in the infusion lounge, watch Netflix and have some tea.

    But do they work? Or are you just paying for really expensive urine? Let's look at what the science says.

    Michael Phelps teaches his 2-year-old son a special ‘lion’s breath’ technique — part of the mental-health routine that Phelps says saved his life

    - The swimmer Michael Phelps, the most decorated Olympian of all time, is open about his struggles with mental health.

    - He is teaching his 2-year-old son, Boomer, some of the coping mechanisms that Phelps says helped save his life.

    - Specifically, Phelps recommends a “lion’s breath” breathing technique, which he said Boomer has already mastered.

    - Visit Business Insider’s homepage for more stories.

    - Breathe in, and breathe out.

    Early Time-Restricted Feeding Improves 24-Hour Glucose Levels and Affects Markers of the Circadian Clock, Aging, and Autophagy in Humans

    Time-restricted feeding (TRF) is a form of intermittent fasting that involves having a longer daily fasting period. Preliminary studies report that TRF improves cardiometabolic health in rodents and humans. Here, we performed the first study to determine how TRF affects gene expression, circulating hormones, and diurnal patterns in cardiometabolic risk factors in humans. Eleven overweight adults participated in a 4-day randomized crossover study where they ate between 8 am and 2 pm (early TRF (eTRF)) and between 8 am and 8 pm (control schedule). Participants underwent continuous glucose monitoring, and blood was drawn to assess cardiometabolic risk factors, hormones, and gene expression in whole blood cells. Relative to the control schedule, eTRF decreased mean 24-hour glucose levels by 4 ± 1 mg/dl (p = 0.0003) and glycemic excursions by 12 ± 3 mg/dl (p = 0.001). In the morning before breakfast, eTRF increased ketones, cholesterol, and the expression of the stress response and aging gene SIRT1 and the autophagy gene LC3A (all p < 0.04), while in the evening, it tended to increase brain-derived neurotropic factor (BNDF; p = 0.10) and also increased the expression of MTOR (p = 0.007), a major nutrient-sensing protein that regulates cell growth. eTRF also altered the diurnal patterns in cortisol and the expression of several circadian clock genes (p < 0.05). eTRF improves 24-hour glucose levels, alters lipid metabolism and circadian clock gene expression, and may also increase autophagy and have anti-aging effects in humans

    Effects of vitamin D on primary human skeletal muscle cell proliferation, differentiation, protein synthesis and bioenergetics.

    The active form of Vitamin D (1,25(OH)2D), has been suggested to have a regulatory role in skeletal muscle function and metabolism, however, the effects and mechanisms of vitamin D (VitD) action in this tissue remain to be fully established. In this study, we have used primary human skeletal muscle myoblast (HSMM) cells that display typical characteristics of human skeletal muscle function and protein levels, to investigate the effects of the active form of VitD on proliferation, differentiation, protein synthesis and bioenergetics. Myoblast cells were treated with 100 nM of VitD for 24 h, 48 h, 72 h for five days (cells were differentiated into myotubes) and then analyses were performed. We report that VitD inhibits myoblast proliferation and enhanced differentiation by altering the expression of myogenic regulatory factors. In addition, we found that protein synthesis signaling improved in myotubes after VitD treatment in the presence of insulin. We also report an increase in oxygen consumption rate after 24 h of treatment in myoblasts and after 5 days of treatment in myotubes after VitD exposure. VitD significantly impacted HSMM myogenesis, as well as protein synthesis in the presence of insulin.

    Increasing physical activity does not improve the function of brown adipose tissue

    A study conducted by researchers from the University of Granada (UGR) has found that, contrary to prevailing belief, higher levels of physical activity are not linked to a greater volume or activity of brown adipose tissue (BAT). BAT is a thermogenic organ that burns glucose and fats, releasing the energy in the form of heat.

    When BAT is activated, it consumes glucose and lipids, partially preventing them from being stored in other tissues such as white adipose tissue (or common fat), which is located, for example, around the abdomen.
    correlation doesn't imply causation

  12. #792
    Sztywny Pal Azji
    May 2014
    1 978
    JULY 9, 2019
    Blue light at night increases the consumption of sweets in rats

    A new study demonstrates that just one hour of exposure to blue light at night—the kind of light produced by the screens of many devices—raises blood sugar levels and increases sugar consumption in male rats. This study, led by Anayanci Masís-Vargas and colleagues from the University of Strasbourg and University of Amsterdam, was presented this week at the annual conference of the Society for the Study of Ingestive Behavior (SSIB) in Utrecht, Netherlands.

    Previous research has shown a strong correlation between obesity and the levels of artificial light at night. Much of the artificial light we are now exposed to comes from LED lights and LED screens, which emit high levels of blue light. Retinal cells of the eye are sensitive to this blue light and directly convey information to areas of the brain that regulate appetite

    In their study, Masís-Vargas and colleagues, exposed rats to nighttime blue light and measured their food consumption and glucose tolerance the following day. It should be noted that, in order to better model human light exposure, the rats used in this study were diurnal, meaning awake during the day and asleep at night, rather than the typical nocturnal laboratory rats which are awake during nighttime hours. The authors found that after only one hour of nocturnal blue light exposure, glucose tolerance was altered in male rats, a warning sign of pre-diabetes.

    To investigate what happens with appetite control and food choice after exposure to blue light at night, the rats were given the option to choose among a nutritionally balanced food (standard rodent food), water, lard, and sugar water. After the exposure to blue light, they observed that the male animals drank more sugar that night than during the nights with no blue light exposure.

    These studies show clearly that being exposed to light, especially blue light, at night is disruptive, and that screen use at night may increase the tendency to snack on sugary foods and disrupt the ability to process sugar, especially in males. Though the rats were tested after only one night of light exposure, over time, this could lead to weight gain and the development of diabetes.

    "Limiting the amount of time that we spend in front of screens at night is, for now, the best measure to protect ourselves from the harmful effects of blue light. In case it is necessary to be exposed to devices at night, I would recommend the use of apps and night mode features on the devices, which turn the screens more orange and less blue or the use of blue light filtering goggles that are already available in the market." Masís-Vargas says.
    Ostatnio edytowane przez htw ; 09-07-19 o 14:01
    correlation doesn't imply causation

  13. #793
    Sztywny Pal Azji
    May 2014
    1 978
    Ćwiczenia poprawiają insulinowrażliwość mózgu osób z nadmierną wagą

    Ostatnie badania wykazały, że osoby z otyłością i nadwagą są podatne na insulinooporność mózgu. Naukowcom z Uniwersytetu w Tybindze zależało więc na sprawdzeniu, czy ćwiczenia mogą poprawić insulinowrażliwość i funkcjonowanie poznawcze w tej grupie osób.

    Zespół dr Stephanie Kullman zebrał grupę 22 osób prowadzących siedzący tryb życia. Wszyscy mieli nadwagę bądź otyłość (średni wskaźnik masy ciała, BMI, wynosił 31). Ochotnicy wzięli udział w 8-tygodniowym programie treningowym, w którym uwzględniono jazdę na rowerze i marsz. Skanowanie mózgu miało miejsce przed i po interwencji. Funkcje mózgu mierzono przed i po donosowym podaniu insuliny. Naukowcy badali także nastrój, funkcje poznawcze i metabolizm obwodowy.

    Okazało się, że choć program ćwiczeń doprowadził jedynie do marginalnej utraty wagi, funkcje mózgu ważne dla metabolizmu znormalizowały się po zaledwie 8 tygodniach. Ćwiczenia zwiększyły np. miejscowy przepływ krwi w zależnych od dopaminy regionach kontroli motorycznej i procesów nagrody.

    Insulinowrażliwość wzrosła zwłaszcza w prążkowiu; reakcja mózgu osoby otyłej przypominała po 8 tygodniach odpowiedź człowieka z prawidłową masą ciała. Co ciekawe, im więcej ktoś stracił tłuszczu brzusznego, tym większa była poprawa funkcji mózgu.

    Ochotnicy wspominali też o poprawie nastroju i zdolności przełączania między zadaniami, co wskazuje na poprawę funkcji wykonawczych.,30369

    Intermittent fasting protects mice from type 2 diabetes

    Every-other-day fasting substantially reduces the likelihood of developing type 2 diabetes in mice eating a fat-rich diet, according to new research out of the German Institute of Human Nutrition Potsdam-Rehbruecke. These findings, presented this week at the annual meeting of the Society for the Study of Ingestive Behavior in Utrecht, Netherlands, suggest that periodic fasting can reduce fat accumulation in the pancreas and, in turn, prevent the onset of type 2 diabetes. "We observed that pancreatic fat cells directly affect islet insulin secretion and that this can be altered by eating patterns" said Dr. Mandy Stadion, a post-doctoral research fellow who led this study.

    Brain stimulation enhances motivation to work for food

    Electrical stimulation of the brain through the vagus nerve increases the motivations to work for food, according to recent findings of a research group at the University of Tübingen. These findings, which were presented at the annual meeting of the Society for the Study of Ingestive Behavior this week in Utrecht, Netherlands, demonstrate a novel method to alter motivation to obtain food.

    "Vigorous work is costly and has to be recuperated by energy intake. That makes it vital for us to know when it is worth the effort. The vagus nerve helps set the tone for actions by signaling, for example, if energy is readily available for that action or not," says Dr. Nils B. Kroemer, the Principal Investigator of the study and junior group leader of the University's Neuroscience of Motivation, Action, and Desire Laboratory (neuroMADLAB) . "We knew that vagus nerve stimulation changes dopamine levels in animals and that chronic stimulation improves depressive symptoms in humans, but it was not known if it could acutely improve motivation. We found that it may provide a much-needed technique to rapidly change reward-related behavior such as eating".

    Food and alcohol reduce activity in 'hunger neurons' via different brain pathways

    How does the brain process rewards? Researchers at the University of Pennsylvania are investigating how the brain responds differently to two commonly ingested rewards—food and alcohol—to understand how they alter neural activity and behavior. Their findings were presented this week in Utrecht, Netherlands at the 2019 Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), one of the leading venues for research on eating and drinking.

    z metabolicznego punktu widzenia popołudniowe ćwiczenia wykazują najlepsze wyniki.
    z punktu widzenia utraty wagi wg najnowszych danych nie koniecznie:

    09 July 2019
    The effects of exercise session timing on weight loss and components of energy balance: midwest exercise trial 2

    At month 10, weight loss was significantly greater in both Early-EX (−7.2 ± 1.2%; p < 0.001) and Sporadic-EX (− 5.5 ± 1.2%; p = 0.01) vs CON (+0.5 ± 1.0%), and Early-EX vs Late-EX (−2.1 ± 1.0%; p < 0.001). There were no between group differences for change in TDEE, EI, and non-exercise energy expenditure (P > 0.05). A significant group × time interaction (p = 0.02) was observed for NEPA (counts/min), however, after adjusting for multiple comparisons, group effects were no longer significant.

    Despite minimal differences in components of energy balance, Early-EX lost significantly more weight compared with Late-Ex. Although the mechanisms are unclear, the timing of exercise may be important for body weight regulation.

    A moderate dose of novel form of stress promotes longevity

    A newly described form of stress called chromatin architectural defect, or chromatin stress, triggers in cells a response that leads to a longer life. Researchers at Baylor College of Medicine and the Houston Methodist Research Institute report in the journal Science Advances that moderate chromatin stress levels set off a stress response in yeast, the tiny laboratory worm C. elegans, the fruit fly and mouse embryonic stem cells, and in yeast and C. elegans the response promotes longevity. The findings suggest that chromatin stress response and the longevity it mediates may be conserved in other organisms, opening the possibility of new ways to intervene in human aging and promote longevity.

    Sleep and inflammation: partners in sickness and in health

    The discovery of reciprocal connections between the central nervous system, sleep and the immune system has shown that sleep enhances immune defences and that afferent signals from immune cells promote sleep. One mechanism by which sleep is proposed to provide a survival advantage is in terms of supporting a neurally integrated immune system that might anticipate injury and infectious threats. However, in modern times, chronic social threats can drive the development of sleep disturbances in humans, which can contribute to the dysregulation of inflammatory and antiviral responses. In this Review, I describe our current understanding of the relationship between sleep dynamics and host defence mechanisms, with a focus on cytokine responses, the neuroendocrine and autonomic pathways that connect sleep with the immune system and the role of inflammatory peptides in the homeostatic regulation of sleep. Furthermore, I discuss the therapeutic potential of harnessing these reciprocal mechanisms of sleep–immune regulation to mitigate the risk of inflammatory and infectious diseases.
    correlation doesn't imply causation

  14. #794
    Sztywny Pal Azji
    May 2014
    1 978
    REM sleep silences the siren of the brain

    Upset by something unpleasant? We have all been there. Fortunately, it also passes. A new day, a new beginning. At least: if you have restful REM sleep. Researchers at the Netherlands Institute for Neuroscience discovered why you will be better able to bear tomorrow what you are distressed about today. And why that can go wrong.
    Siren of the brain
    Something frightening or unpleasant does not go unnoticed. In our brain, the so-called limbic circuit of cells and connections immediately becomes active. First and foremost, such experiences activate the amygdala. This nucleus of brain cells located deep in the brain can be regarded as the siren of the brain: attention! In order for the brain to function properly, the siren must also be switched off again. For this, a restful REM sleep, the part of the sleep with the most vivid dreams, turns out to be essential.
    Good sleepers
    The researchers placed their participants in a MRI scanner in the evening and presented a specific odor while they made them feel upset. The brain scans showed how the amygdala became active. The participants then spent the night in the sleep lab, while the activity of their sleeping brain was measured with EEG, and the specific odor was presented again on occasion. The next morning, the researchers tried to upset their volunteers again, in exactly the same way as the night before. But now they did not succeed so well in doing this. Brain circuits had adapted overnight; the siren of the brain no longer went off. The amygdala responded much less, especially in those who had had a lot of restful REM sleep and where meanwhile exposed to the specific odor.
    Restless sleepers
    However, among the participants were also people with restless REM sleep. Things went surprisingly different for them. Brain circuits had not adapted well overnight: the siren of the brain continued to sound the next morning. And while the nocturnal exposure to the odor helped people with restful REM sleep adapt, the same exposure only made things worse for people with restless REM sleep.
    Neuronal connections weaken and strengthen
    During sleep, 'memory traces' of experiences from the past day are spontaneously played back, like a movie. Among all remnants of the day, a specific memory trace can be activated by presenting the same odor as the one that was present during the experience while awake. Meanwhile, memory traces are adjusted during sleep: some connections between brain cells are strengthened, others are weakened.
    Restless REM sleep disturbs these nocturnal adjustments, which are essential for recovery and adaptation to distress.

    Transdiagnostic importance
    The findings were published on 11 July in the leading journal Current Biology. The finding can be of great importance for about two-thirds of all people with a mental disorder, as both restless REM sleep and a hyperactive amygdala are the hallmarks of post-traumatic stress disorder (PTSD), anxiety disorders, depression and insomnia. People with PTSD carry their traumatic experience to the next day: people with an anxiety disorder take their greatest fear with them, people with depression their despair, and people with chronic insomnia their tension. Authors Rick Wassing, Frans Schalkwijk and Eus van Someren predict that treatment of restless REM sleep could transdiagnostically help to process emotional memories overnight and give them a better place in the brain.

    Anxious? Cut down on caffeine

    Caffeine can boost energy, improve alertness and produce a general feeling of well-being—when used in moderation.
    Go past the sweet spot though, and that same elixir can cause insomnia, jitteriness and feelings of nervousness. Those who already struggle with anxiety may be particularly susceptible to its effects and should monitor their consumption.
    Dr. Julie Radico, a clinical psychologist with Penn State Health, said while caffeine may help with concentration and provide a boost for some individuals, including those with depressed mood, it can cause problems for those with general anxiety disorder.

    idąc za ciosem - uwaga

    Antioxidant dietary fiber isolated from spent coffee (Coffea arabica L.) grounds improves chronotype and circadian locomotor activity in young adults.

    Chrononutrition, or the circadian timing of food intake, proposes that nutrients, bioactive compounds, and foods modulate the peripheral clocks with implications on health. We evaluated the effects of biscuits supplemented with the antioxidant dietary fiber isolated from spent coffee grounds as a food ingredient (SCF-B) or a combination of spent coffee grounds and fructooligosaccharides (SC-FOS-B), and a traditional recipe (TB, without added fiber) on the modulation of circadian rhythm in young adults. The repeated intake (21 days/45 g portion) of SCF-B or SC-FOS-B decreased (p < 0.05) the evening chronotypes. SCF-B and SC-FOS-B consumption enhanced the chronodisruption associated with colonic short chain fatty acid production, thus improving the quality and length of sleep. This is the first study on the positive impact of antioxidant dietary fiber obtained from spent coffee grounds on circadian activity improvement in young adults. Further clinical trials and the role of other bioactive compounds as therapeutic candidates for health disturbances related to circadian dysfunction are necessary to confirm the results.

    No Benefit of Ingestion of a Ketone Monoester Supplement on 10-km Running Performance

    Methods On two occasions in a double-blind, randomized crossover design, eight endurance-trained runners performed 1 h of submaximal exercise at ~65% VO2max immediately followed by a 10-km self-paced TT on a motorized treadmill. An 8% carbohydrate-electrolyte solution was consumed before and during exercise, either alone (CHO+PLA), or with 573 of a ketone monoester supplement (CHO+KME). Expired air, heart rate (HR), and rating of perceived exertion (RPE) were monitored during submaximal exercise. Serial venous blood samples were assayed for plasma glucose, lactate and β-hydroxybutyrate concentrations.

    Results CHO+KME produced plasma β-hydroxybutyrate concentrations of ~1.0 to 1.3 mM during exercise (P < 0.001), but plasma glucose and lactate concentrations were similar during exercise in both trials. VO2, running economy, respiratory exchange ratio, HR and RPE were also similar between trials. Performance in the 10-km TT was not different (P = 0.483) between CHO+KME (mean = 2402 s; 95% confidence interval [CI] = 2204, 2600 s) and CHO+PLA (mean = 2422 s; 95% CI = 2217, 2628 s). Cognitive performance, measured by reaction time and a multi-tasking test, did not differ between trials.

    Conclusion Compared with carbohydrate alone, co-ingestion of KME by endurance-trained athletes elevated plasma β-hydroxybutyrate concentrations, but did not improve 10-km running TT or cognitive performance.

    Radioprotective Effect of Endogenous Melatonin Secretion Associated with the Circadian Rhythm in Irradiated Rats

    We investigated the radioprotective effect of endogenous melatonin release at different times associated with the circadian rhythm on head and neck radiotherapy.
    Materials and Methods:
    Two groups of animals were subjected daily to 8 Gy single fraction radiotherapy in the head and neck region from 5:00 to 5:30 (the morning group) or from 19:00 to 19:30 (the evening group). Corresponding untreated groups served as controls. Submandibular glands from rats sacrificed on the seventh day after irradiation were assessed biochemically and histopathologically. Melatonin, malondialdehyde and superoxide dismutase levels in blood collected immediately prior to irradiation were measured with rat-specific ELISA kits.
    In irradiated rats, melatonin, malondialdehyde and superoxide dismutase levels were significantly higher in the evening group than in the morning group. In nonirradiated rats, melatonin and superoxide dismutase levels were significantly higher in the evening group than in the morning group. The areas of seromucous acinar cells were similar between the irradiated and nonirradiated evening groups, but the area was higher in the evening irradiated group than in the morning irradiated group.
    Consideration of endogenous melatonin secretion associated with the circadian rhythm may offer new therapeutic solutions for the complications of head and neck radiotherapy.

    "Pani Garczyńska, która nie istnieje, wykonuje zawód, którego nie ma. Internet oburza się jej wypowiedzią, której nie było, na portalu który nazywa się inaczej niż sugeruje i w oryginale pisany był cyrilicą. Tak, skomplikowane, ale @Michal_Istel rozwikłał",1...em,951391.html

    Ostatnio edytowane przez htw ; 12-07-19 o 08:35
    correlation doesn't imply causation

  15. #795
    Sztywny Pal Azji
    May 2014
    1 978

    Seeing greenery linked to less intense and frequent cravings

    Being able to see green spaces from your home is associated with reduced cravings for alcohol, cigarettes and harmful foods, new research has shown.

    The study, led by the University of Plymouth, is the first to demonstrate that passive exposure to nearby greenspace is linked to both lower frequencies and strengths of craving.

    It builds on previous research suggesting exercising in nature can reduce cravings, by demonstrating the same may be true irrespective of physical activity.
    Ostatnio edytowane przez htw ; 12-07-19 o 09:14
    correlation doesn't imply causation

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