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    Are you hydrated when you exercise? A new study says probably not.

    70%. Of all the fluids Americans drink every day, that’s how much isn’t water, according to the most recent U.S. National Health Nutrition Examination Survey. Although the study reveals that most men reach their target for total fluid intake, only 30% of that is made up of water. Which isn’t doing their health any favors, particularly if they’re exercising regularly.

    Why? A humble glass of H2O may not be the most popular pre-workout tipple for Americans, but it's certainly the most essential. A study published in the journal Sports Medicine found dehydration "consistently attenuates strength (by 2%), power (by 3%) and high-intensity endurance (by 10%)."

    As a rule of thumb, drink a 250ml glass of water 30 minutes before you hit the gym to ensure your muscles are firing on all cylinders. Then follow that up with 500ml within 30 minutes of finishing. Deciding how much to sip mid-session is more subjective. "Around 500ml of water during the course of a one-hour workout is sensible," says nutritional therapist Jo Scott-Dalgeish.

    After 90 minutes moderate exercise, water is no longer enough. At this point, your glycogen stores are mere fumes and it's time to start sipping electrolyte-rich sports drinks. For endurance athletes, managing minerals is exceptionally important and, although the concept of drinking too much water may seem strange, it can be dangerous.

    Downing liters of water without replacing electrolytes can cause a condition called hyponatremia, which may lead to seizures, organ failure and even death. If you're tackling long distance runs, ensure you have a tried-and-tested hydration strategy in place.

    By: Edward Lane 

    Low levels of two components of vitamin D can help predict risk of heart attack

    Summary:Low levels of total vitamin D and bioavailable vitamin D can help predict a person's risk of major adverse cardiovascular events such as a heart attack, stroke, heart failure or death.


    Low levels of total vitamin D and bioavailable vitamin D can help predict a person's risk of major adverse cardiovascular events such as a heart attack, stroke, heart failure or death, according to a first-of-its-kind study from the Intermountain Medical Center Heart Institute in Salt Lake City.

    "Our study found that low levels of both total vitamin D and bioavailable vitamin D appear to be associated with poor cardiovascular outcomes," said lead author Heidi May, PhD, MSPH, a cardiovascular epidemiologist with the Intermountain Medical Center Heart Institute.

    The study evaluated 4,200 participants between the ages of 52 and 76. A quarter of the study participants were diabetic and 70 percent had coronary artery disease.

    Clinicians tested participants' vitamin D metabolite levels, which included components of vitamin D that are formed during metabolism, to determine the metabolites' association with future major adverse cardiovascular events. Bioavailable vitamin D results from vitamin D being absorbed into the blood stream without binding to surrounding proteins.

    During metabolism, only 10-15 percent of total vitamin D is available in the body to act on target cells, as most are bound to vitamin D binding proteins. Therefore, evaluating whether the proportion of vitamin D that can be used may be important, as only unbound vitamin D, such as bioavailable vitamin D, is available to act on target cells.

    The study tested many different types of vitamin D, but found that measuring total vitamin D and bioavailable vitamin D were the most accurate in predicting harmful cardiovascular events.

    "This study is the first research that evaluates the association of vitamin D metabolites with cardiovascular events," said Dr. May. "And evaluating usable vitamin D could mean the difference on the amount of vitamin D prescribed, if it's prescribed at all."

    The study expands on the results of several observational studies, including some performed at Intermountain Healthcare, but researchers recommend conducting more studies on non-Caucasian populations because past research shows vitamin D metabolites affect Caucasian and non-Caucasian races differently.

    Story Source:

    The above post is reprinted from materials provided by Intermountain Medical Center. Note: Materials may be edited for content and length.

     

    Is artificial lighting making us sick?

    Summary:Along with eating right and exercising, people should consider adding another healthy habit to their list: turning out the lights. That's according to a new study showing many negative health consequences for mice kept under conditions of constant light for a period of months.

    New findings suggest that more care should be taken in considering the amount of light exposure people get.
    Credit: © meepoohyaphoto / Fotolia
    .

    Along with eating right and exercising, people should consider adding another healthy habit to their list: turning out the lights. That's according to a new study reported in the Cell Press journal Current Biology on July 14 showing many negative health consequences for mice kept under conditions of constant light for a period of months.

    "Our study shows that the environmental light-dark cycle is important for health," says Johanna Meijer of Leiden University Medical Center in the Netherlands. "We showed that the absence of environmental rhythms leads to severe disruption of a wide variety of health parameters."

    Those parameters included pro-inflammatory activation of the immune system, muscle loss, and early signs of osteoporosis. The researchers say that the observed physiological changes were all indicative of "frailty" as is typically seen in people or animals as they age. But there was some more encouraging news, too.

    "The good news is that we subsequently showed that these negative effects on health are reversible when the environmental light-dark cycle is restored," Meijer says.

    To investigate the relationship between a loss of the light-dark cycle and disease, Meijer and colleagues, including Eliane Lucassen, exposed mice to light around the clock for 24 weeks and measured several major health parameters. Studies of the animals' brain activity showed that the constant light exposure reduced the normal rhythmic patterns in the brain's central circadian pacemaker of the suprachiasmatic nuclei (SCN) by 70 percent.

    Strikingly, the disruption to normal light and dark patterns and the circadian rhythm led to a reduction in the animals' skeletal muscle function as measured in standard tests of strength. Their bones showed signs of deterioration, and the animals entered a pro-inflammatory state normally observed only in the presence of pathogens or other harmful stimuli. After the mice were returned to a standard light-dark cycle for 2 weeks, the SCN neurons rapidly recovered their normal rhythm, and the animals' health problems were reversed.

    The findings suggest that more care should be taken in considering the amount of light exposure people get, particularly those who are aging or otherwise vulnerable. That's important given that 75 percent of the world's population is exposed to light during the night. Constant light exposure is very common in nursing homes and intensive care units, and many people also work into the night.

    "We used to think of light and darkness as harmless or neutral stimuli with respect to health," Meijer says. "We now realize this is not the case based on accumulating studies from laboratories all over the world, all pointing in the same direction. Possibly this is not surprising as life evolved under the constant pressure of the light-dark cycle. We seem to be optimized to live under these cycles, and the other side of the coin is that we are now affected by a lack of such cycles."

    The bottom line, according to the researchers is "light exposure matters."

    They say they now plan to perform more in-depth analysis of the influence of distorted light-dark cycles on the immune system. They'd also like to investigate possible health benefits to patients exposed to more normal conditions of light and dark.

    Story Source:

    The above post is reprinted from materials provided by Cell Press. Note: Materials may be edited for content and length.


    Journal Reference:

    1. Lucassen et al. Environmental 24-hr Cycles Are Essential for Health.Current Biology, 2016 DOI: 10.1016/j.cub.2016.05.038

    How anxiety can kill your social status

    Summary: Neuroscientists have identified a brain region that links anxious temperament to low social status. The researchers were able to tweak social hierarchy in animals using a regular vitamin.
    .

    A magnified transmission electron microscopy view of the rat nucleus accumbens neurons containing mitochondria in different cellular compartments.

    Credit: Graham Knott (EPFL)

    Neuroscientists at EPFL identify a brain region that links anxious temperament to low social status. The researchers were able to tweak social hierarchy in animals using a regular vitamin.

    There are important differences in how individuals approach life. While some people are relaxed and calm, others often see situations as threatening, making them worried and tense. This kind of 'trait' anxiety has significant consequences on a person's social life, undermining their confidence to compete for social standing. In our competitive world, high-anxious individuals have a disadvantage and can feel overlooked and rejected; as a result this can lead to what psychologists call 'social subordination'. Publishing in PNAS, neuroscientists at EPFL have pinpointed an area of the brain related to motivation and depression that could link trait anxiety to social subordination.

    Trait anxiety and low social status: chicken and egg

    Both animals and humans establish social ranks through competition, which in turn determines the hierarchy of a social group. The ability to compete depends on different features including size, age, and previous social experience. Some research shows that social competition is also influenced by personality traits, but this has not been explored in depth.

    There is a growing suspicion among social scientists and psychologists that when individuals present high anxiety as a personality characteristic, it might actually predispose a person to perform poorly in social competition, trapping them in a vicious cycle of trait anxiety and low social status. However, we know very little about the neuroscience behind this cycle, which could be the key to breaking it.

    Rat revelations

    The lab of Carmen Sandi at EPFL now brings biological evidence to bear upon the field. The researchers performed a series of experiments to identify the brain areas involved in trait anxiety and social competition. The experiments involved categorizing rats on a spectrum of trait anxiety, from low-anxious to high-anxious rats, which model trait anxiety.

    The animals underwent several behavioral tests that required high-anxious rats to compete socially with their low-anxious counterparts, and their performance was quantified and analyzed statistically. In addition, the researchers examined the brains of the rats to identify changes in biological function.

    The experiments highlighted an area of the brain known as the 'nucleus accumbens', which has been long-associated with motivation, reward and depression -- in humans too. When competing socially, most of the high-anxious rats took on a lower social status -- technically described as becoming 'socially subordinate'.

    The nucleus accumbens of these particular rats showed a reduced energy metabolism. This involves the mitochondria, which are the cell's organelles that are in charge of breathing and energy production. The researchers found that the high-anxious rats showed lower mitochondrial function than more relaxed ones.

    Reversing social status with drugs?

    The scientists confirmed their findings with pharmacological manipulation: they gave the nucleus accumbens of rats compounds that either block or enhance mitochondria; these included vitamin B3. When rats received blocking agents, their social competitiveness dropped, taking their social status with it.

    On the other hand, when high-anxious rats were given enhancers, rats performed significantly better socially, thereby achieving higher social status. But the effects were not permanent: when the drugs wore off, the rats generally returned to their original rung of the social ladder.

    The study confirms that trait anxiety can actually predispose an individual to a lower social status. This could mean that pharmacological manipulation of mitochondria in the nucleus accumbens could potentially influence the social rank of a person. The study is also the first to show that the brain's energy metabolism influences the establishment of social hierarchies.

    Carmen Sandi remains cautious, since the study involved rats rather than humans; after all, brain function is just one of the many elements that influence social dynamics. "Social interactions are immensely complex," says Sandi. "They involve so many factors that it is difficult to examine the impact of each in isolation. However, this is an exciting finding; it shows a brain mechanism whereby anxious personality affects social competitiveness of individuals, and it points to very promising directions in this field."

    The above post is reprinted from materials provided by  Ecole Polytechnique Federale de Lausanne. Note: Materials may be edited for content and length.

     

     

    Depression is more than a mental disorder: it affects the whole organism

    Summary:   Scientists have shown for the first time, that depression is more than a mental disorder: it causes important alterations of the oxidative stress, so it should be considered a systemic disease, since it affects the whole organism. The results of this work could explain the significant association that depression has with cardiovascular diseases and cancer, and why people suffering from depression die younger. At the same time, this research may help finding new therapeutic targets for the prevention and treatment of depression. 

    An international team of researchers lead by the University of Granada (UGR) has demonstrated, for the first time, that depression is more than a mental disorder: it causes important alterations of the oxidative stress, so it should be considered a systemic disease, since it affects the whole organism.

    The results of this work could explain the significant association that depression has with cardiovascular diseases and cancer, and why people suffering from depression die younger. At the same time, this research may help finding new therapeutic targets for the prevention and treatment of depression.

    The lead author of this work is Sara Jiménez Fernández, PhD student at the UGR and psychiatrist at the Child and Adolescent Mental Health Unit at Jaén Medical Center (Jaén, Spain). The co-authors are the UGR Psychiatry professors Manuel Gurpegui Fernández de Legaria and Francisco Díaz Atienza, in collaboration, among others, with Christoph Correll from the Zucker Hillside Hospital (New York, USA).

    A study with 3961 people

    This research is a meta analysis of 29 previous studies which comprise 3961 people, and it's the first detailed work of its kind about what happens in the organism of people suffering from depression. It studies the imbalance between the individual increase of various oxidative stress parameters (especially malondialdehyde, a biomarker to measure the oxidative deterioration of the cell membrane) and the decrease in antioxidant substances (such as uric acid, zinc, and the superoxide dismutase enzyme).

    The researchers have demonstrated that, after receiving the usual treatment against depression, the patients' malondialdehyde levels are significantly reduced, to the point that they are indistinguishable from healthy individuals. At the same time, zinc and uric acid levels increase until reaching normal levels (something that does not occur in the case of the superoxide dismutase enzyme).

    Story Source:

    The above post is reprinted from materials provided by University of Granada . Note: Materials may be edited for content and length.  

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