Sugar Cravings Explained by Gut to Brain Circuit

New research has shown that while the sensation of sweetness begins on the tongue, sugar molecules also trip sensors found in the gut which directly send signals to the brain. A little bit of sugar can make a person desire just about anything, but its sweetness doesn’t totally explain our desire. The new study shows that this molecule has a indirect channel to the brain.

The team at Howard Hughes Medical Institute shows while sugar triggers specialized taste buds found on the tongue, it also turns on a completely separate neurological pathway that beings in the gut. Signals in the intestines heralding the arrival of sugar travel to the brain. Here they nurture a desire for more, the researcher’s experiments with mice have shown. This particular gut to brain pathway appears to be selective responding primarily to sugar molecules and not artificial sweeteners.

Scientists have already known that sugar exerted unique control over the brain. In a 2008 study, mice that do not have the ability to taste sweetness could still desire sugar. The recent study’s discovery of the sugar sensing pathway can help explain why sugar is different and directs ways a person might quell their insatiable appetite for it. By separating the concepts of sweet and sugar, the team says sweet is linking and sugar is wanting.

The term sugar is a group which encompasses a variety of substances our bodies use as fuel. Consuming sugar activates the brain’s system of reward making mice and humans alike feel good. But, in our world where sugar that has been refined is plentiful, this deeply ingrained appetite could run out of control.

The normal American’s yearly sugar intake has skyrocketed from less than 10 lbs. in the late 1800s increasing to more than 100 lbs. currently with that increase coming at a cost. Studies have tied together excess consumption of sugar to a variety of health problems including type 2 diabetes and obesity.

Earlier research has shown that sugar and artificial sweeteners turn on the same taste sensing system. In the mouth, these molecules start up the sweet taste receptors found on taste buds which activates signals that travel to the part of the brain that processes the sweetness.

However, sugar affects behavior in a way that artificial sweeteners do not. The team ran a test pitting sugar against the artificial sweetener Acesulfame K which is typically found in diet sodas, sweetening packets and other food and beverage products. When offered water with the sugar or sweetener, mice initially drank both. However, within two days they switched almost exclusively to the water that contained sugar. The team reasoned that this unquenchable motivation the mice have for eating sugar instead of sweetness, might have a neural basis.

Through brain activity visualization when the mice consumed sugar vs. artificial sweetener or water, the team identified for the first time the region of the brain that responds only to sugar – the caudal nucleus of the solitary tract (cNST). The cNST which is found in the brain stem separate from where mice process taste, is a hub for information about the state of the body.

The team determined that the path to the cNST begins in the lining of the intestine. Here, sensor molecules initiates a signal that travels by the vagus nerve providing a direct relay of information from the intestines and on to the brain.

This gut to brain circuit has a preference for one form of sugar – glucose and similar molecules. It ignores artificial sweeteners which might explain why these additives can’t seem to fully replicate the appeal of sugar. It also overlooks other types of sugar, mostly fructose which is found in fruit. Glucose is an energy source for all living things. This could explain why the system’s specificity for the molecule has evolved.

Earlier scientists speculated that sugar’s amount of energy or calories might explain its appeal since many artificial sweeteners are lacking in calories. However, the recent study has shown this is not the case since calorie free, glucose like molecules can also activate the gut to brain sugar sensing pathway.

The group is now studying the links between this gut brain circuit and other systems of the brain such as feeding, reward, and emotions to better understand how the brain’s strong preference for sugar develops. And although the study has been on mice, the team believes that essentially the same glucose sensing pathway exists in people.

Through discovering this circuit that explains how sugar directly impacts our brain to drive consumption, it also exposes new potential opportunities and targets for strategies to help curtail the insatiable appetite for sugar many of us have.

To view the original scientific study click below

The gut–brain axis mediates sugar preference.

A New Biomarker May Help Stem Cells Heal Brain Injuries

Researchers at Sanford Burnham Prebys Medical Discovery Institute and Loma Linda University Health have shown the possibility of applying MRI to predict the efficacy of employing human neural stem cells to treat brain injuries. This is the first ever biomarker for regenerative medicine that may help personalize treatments with stem cells for neurological disorders and also improve efficacy.

The team hope to test their findings in a clinical trial evaluating stem cell therapy in newborns who are experiencing brain injury during birth which is known as perinatal hypoxic-ischemic brain injury (HII).

The team is hopeful that MRI which is currently being used during the course of and care for newborns with perinatal hypoxic ischemic brain injury, will help ensure that those infants with the injury get the best and most appropriate treatment possible.

Sometime in the future, MRI could possibly help guide the use of stem cells to treat additional brain disorders such as spinal cord injury and stroke.

Scientists now understand that in many cases, human neural stem cells are therapeutic because they are able to protect living cells. This is in contrast to replacing or re-animating nerve cells that are already dead. Thus, understanding the health of brain tissue before a stem cell implant is crucial to the treatment’s possible success.

Tools that can help predict the efficacy of neural stem therapy might increase the success of clinical trials such as those ongoing in people with Parkinson’s Disease, injury to the spinal cord, and other neurological conditions. This could also spare people who do not respond to treatment from an invasive procedure that offers false hope.

Stem cell therapies offer extraordinary promise. The current study suggests that a readily available technique, MRI which is already being used in many injuries of the brain to determine the extent of neurological damage, could be a useful tool in determining who will and will not benefit from the stem cell treatment.

Evan Snyder, M.D., Ph.D., has envisioned using human neural stem cells in an effort to protect newborns with acute perinatal HII from damage to the brain. He and his team made the discovery that MRI can be used as a quantifiable, objective and easily available basis for exclusion and inclusion criteria for the stem cell treatments while engaged in preclinical trials required prior to beginning human clinical trials for newborns with HII.

This particular brain injury affects two to four newborns out of every 1,000 babies that are born in the U.S. and is attributable to a variety of complications including disrupted maternal blood pressure, maternal infection, and umbilical cord compression.

The hope is that human neural stem calls could help rescue enough vulnerable and injured, though not dead, neural cells. This could potentially help prevent the most severely affected infants from developing epilepsy, cerebral palsy, intellectual disability, and other neurological disorders that will often appear after HII if left untreated.

In the current study, the team used MRI to measure two different areas surrounding the regions of HII brain injury in rats – the penumbra which is a region which consists of mildly injured and stunned neurons, and the core which is an area which consists of neurons that are dead. They discovered that rats with a larger penumbra and smaller core which had received human neural stem cells, had better neurological outcomes which included improved memory which was demonstrated by their ability to swim to a hidden platform and a greater willingness to venture to a brightly lit area.

In the rats, the penumbra to which the neural stem cells honed avidly, became normal tissue while the core did not improve and attracted fewer cells (based on MRI and histological standards). Penumbra which did not receive cells become part of the core which was populated by dead neurons, indicating the benefit of the treatment with the stem cells.

The approach to brain lesion classification is a very strong patient stratification tool that allowed the team to identify newborns who might benefit from the stem cell therapy and can also protect others from having unnecessary treatments done. Based on their findings, only those newborns with a large penumbra volume in relation to core volume, should consider having a transplant of human neural stem cells. And just as important, newborns so severely injured that only the core is present, or babies with a mild case of HII that not even a penumbra is present, should not receive the stem cells as the treatment would unlikely be impactful.

To view the original scientific study click below

A Biomarker for Predicting Responsiveness to Stem Cell Therapy Based on Mechanism-of-Action: Evidence from Cerebral Injury.

Covid-19 and Sleep Changes

During the last 3 months of the COVID-19 pandemic, changes in sleep are just one of the many daily activities that have been impacted by this virus. A report from late March 2020 by Fitbit has shown that their sleep tracker app was showing major changes in sleep patterns for millions of Americans.

Getting a good might’s sleep is a highly important daily routine that many people don’t do. And whether it is due to child care, work, a noisy environment or other reasons, few Americans actually make sleep a priority. About 68% or 164 million Americans struggle with sleep at least once during a week. Millions of people suffered from insomnia before the pandemic, and unfortunately the pandemic has created a host of new challenges even for those people who previously had no sleep problems.

With social distancing in place along with quarantines, school closures, and working from home, profound changes to normal daily routines for people of all ages and walks of life have occurred.

Fitbit report shows that people are going to bed later but are getting more sleep in addition to a better quality of sleep. For those people whose quality of sleep has shown improvement, they have been spending more time in REM or deep sleep. Our bodies recharge while we sleep both repairing and building muscle and tissue. Levels of cortisol, our stress hormone, fall during the evening. Getting the recommended seven to nine hours of sleep per night will help boost the immunity – something that is especially important now.

Sleep is critical to both physical health and effective functioning of the immune system. It is also a key promoter of mental health and emotional wellness. It helps to beat back depressions, stress and anxiety.

From a report by the Smithsonian in late April 2020, researchers started to study other more ominous changes in sleep patterns. Sleep study centers from around the world reported increasingly vivid and strange dreams from those who had entered their second month of stay at home orders.

It was reported that a growing group are experiencing insomnia which is an inability to fall asleep which seems to be symptoms of stress due in part to the shared anxiety surrounding the COVID-19 virus. In the same report, researchers in France at The Lyon Neuroscience Research Center discovered a 35% increase in dream recall and a 15% increase in negative dreams.

For people who are not on the front lines of emergency and healthcare response, fears of the virus are projected onto threats such as bug, zombies, and shadowy figures which represent the pandemic metaphorically.

Dreams typically occur during the REM phase of sleep. Low activity and anxiety during the day can make it more difficult to get a good night’s sleep. Additionally, waking up frequently throughout the night can increase the likelihood that dreams will be remembered the next day.

REM sleep which is associated with dreaming, is believed to help us handle intense emotions and particularly negative emotions. And obviously the COVID-19 pandemic is producing a lot of anxiety and stress.

It is imperative that we let our bodies and brains rest and relax. This not only allows us to enter REM sleep and cope with stress, but a good night’s sleep also increases the production of vital neurotransmitters and hormones that our brain needs replenished every day.

The Sleep Foundation has ways we can cope with the profound changes of activity and stress that may be affecting sleep during the pandemic. Set a schedule and routine and avoid variations in daily sleep time. This includes waking up the same time every day, winding down time to relax to get ready for sleep, showering and dressing even when not leaving the house, eating meals at the same time each day, blocking of specific times for exercise and work, and avoiding naps.

We should also avoid bringing a computer to bed to do work or watch a movie in bed. It is also beneficial to frequently change bed sheets, fluff pillows and making the bed each day so it feels fresh when going to bed.

Exposure to light also plays a critical role in helping our bodies regulate sleep. Light based cues have a positive effect on circadian rhythm. If possible, spend some time outside in natural light during the day. As much as possible, open blinds and windows to let light in during the day.

And very importantly, avoid too much blue light which is produced by electronic devices. Blue light interferes with the body’s natural sleep promoting process. Excess screen time especially later in the day can have detrimental impact on sleep. It not only stimulates the brain in ways that make it difficult to wind down, but blue light from screens can suppress the natural production of melatonin which is a hormone they body makes to help us sleep.

And lastly, stay active. Continuing or starting regular daily activities has a variety of important benefits including for sleep.

To view the original scientific study click below

Covid-19 and Changing Sleep Patterns.

Mouthwash May Help Reduce the Spread of Covid-19

Recent research has speculated that mouthwash may inhibit the spread of SARS-CoV-2 which is the virus responsible for COVID-19. The scientific review has suggested that publicly available mouthwashes may in theory, inhibit this virus.

If clinical trials do prove effective, the findings may provide another method for people to help reduce the spread of the virus while scientists continue to work on producing an effective and publicly available vaccine.

In the meantime, scientists are focused on ways to reduce the rate of infection to more controllable levels which will not overwhelm hospital intensive care units. One area of research has involved disrupting the way in which the virus can take over a cell of a host as it replicates itself.

SARS-CoV-2 like other types of coronaviruses, is an enveloped virus which means it creates an outer membrane through drawing on the cells of a host organism. This membrane will allow the virus to effectively replicate. If scientists can find a way to disrupt this envelope, then it may be possible to slow down the spread of the virus within an organism.

Using a disinfectant or soap and water can disrupt a viral envelope and therefore kill the virus. Research has shown that disinfectants can kill the SARS-CoV-2 virus. This is why the health community has encouraged people to wash their hands and surfaces with alcohol based products or soap on a regular basis.

The current review has proposed that some widely available mouthwashes may also be able to help fulfill the role of killing the virus.

It has been shown that the virus significantly replicates in the throat. This means that a patient with the virus is likely to have the highest concentration of the virus within this area. And with these high levels of the virus in the throat, it is easy for someone to transmit the virus through coughing, sneezing, and breathing.

Previous research into alcohol’s ability to disrupt the virus envelope has mainly focused on products with a high alcohol content of between 60% and 70%. This is due to manufacturers who typically design alcohol based products to be effective in a variety of circumstances including bacteria, viruses and fungi.

However, there is isn’t very much high quality research exploring how lower strength alcohol based products may also affect the viral envelope. The current studies team sought out to see if alcohol based mouthwashes which come into contact with a person’s throat, could in theory inhibit the transmission of the virus or at least reduce its severity.

If a significant spread of the virus originates in the throat, then it would make sense to trial the efficacy of products which may have the potential to kill the virus at this location. However, due to the speed of how the virus emerged, there is still much to learn about how it functions.

Scientists do not currently known how the virus moves from a person’s nose or throat to their lungs. It is possible this could occur through breathing in dead viral cell debris, viral shedding or neighboring cells becoming infected.

However, with the current urgency of the public health crisis, it is necessary to propose speculative theories which scientists can test in laboratories and then in clinical trials. And although there is little scientific literature which explores the effect of low alcohol concentrations on viral envelopes, the team drew on research that looked at the effects on mammalian cells.

The virus will develop its envelope from these cells. Therefore, it may be possible to compare the effects on these cells to the potential effects on the viral envelope.

The researchers discovered after studying the literature, there was good reason to suppose that some low alcohol based products may in theory be able to disrupt the viral envelope of SARS-CoV-2. They have made it clear though, their research is speculative. More research is needed, nonetheless this current work shows that in s principle this is a valuable area to study.

To view the original scientific study click below

Potential role of oral rinses targeting the viral lipid envelope in SARS-CoV-2 infection.

Can Eating Fish Reduce Risk of Cardiovascular Disease?

According to a recent most exhaustive study carried out to date, researchers have found that consuming a diet rich in fish or Omega 3 modulates the concentration of lipids which are passed on to cells through lipoproteins and can reduce the risk of cardiovascular disease. The research was carried out by Universitat Rovira I Virgili along with researchers from Harvard Medical School.

Through analysis of lipoprotein samples from 26,034 women, the association between the consumption of Omega 3 and the reduction in the risk of suffering cardiovascular disease has been demonstrated by the research teams. It is the largest and most detailed study ever carried out. This study is particularly noteworthy because cardiovascular disease is the most common cause of death with 1 in 3 people dying from a cardiovascular event.

Until recently, it has been shown that a high consumption of Omega 3 fatty acids was associated with lower levels of triglycerides in the blood. However, it has also been linked to an increase in LDL cholesterol which is low density cholesterol transported by lipoproteins and also known as bad cholesterol. LDL cholesterol increases the risk of a person developing cardiovascular diseases as it can accelerate the formation of atherosclerosis which is the process where the arteries harden and lose their elasticity.

However, the recent study has discovered that increased consumption of LDL cholesterol from fish is associated mainly with the cholesterol transported by the largest LDL particles which are less atherogenic, and not an increase in the total number of LDL particles. The decrease in the number of triglycerides transported by any type of lipoprotein will help protect a person from heart disease.

The three different types of Omega 3 fatty acids studied in the research, namely a-linoleic acid (ALA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) are all present in fish and other foods and are known to be essential to human physiology. The study has discovered that they differ in their association with the risk of cardiovascular diseases.

It was found that there was no increase in the smallest LDL lipoproteins which transport cholesterol. Instead the increase was among the largest LDL lipoproteins which are not associated with the risk of heart disease. There was a decrease in all of the triglyceride transporting particles, and the average size of the HDL and LDL particles increased which is a phenomenon that is linked with increased protection from cardiovascular illness.

The conclusions were obtained through mathematical modeling of the consumption of fish and Omega 3 (both as a whole and of the different types of ALA, DHA and EPA) and the profile of lipoproteins. The study results were obtained by Nuclear Magnetic Resonance which can go much further than simply analyzing triglyceride and cholesterol content and can quantify the size and number of the different subtypes of plasmatic lipoprotein. Among the LDL particles that transport cholesterol, it is the smallest that are linked with a future cardiovascular event.

An additional and important element of the study is that the mathematical models that were used to evaluate the link between consumption of fish and the reduction in cardiovascular risk have isolated other nutritional factors that affect the result – such as the concentration of Omega 3 according to the origin of the fish (farmed or wild), the consumption of other foods, and traditional risk factors such as age, sedentary lifestyle, smoking and body mass index.

The study analyzed a cohort from the Women’s Health Study by the Brigham and Women’s Hospital and affiliate of Harvard Medical School. It involved the use of Nuclear Magnetic Resonance to characterize the plasma of 26,034 women who had an average age of 53 (most participants were between 48 and 59 years of age).

After confirming the risk factor linked with cholesterol concentration, lipids, triglycerides and the different subtypes of particles is modulated by the consumption of Omega 3 fatty acids, the team now wants to find out if the consumption of fish is linked with lower mortality from both cardiovascular diseases and other causes. And although the risk is lower in relation to lipids, they want to look at other pro-inflammatory factors and questions such as exposure to heavy metals.

To view the original scientific study click below

The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients.

Vitamin D and Covid-19 Mortality Rates

Patients who exhibit a severe deficiency of Vitamin D are twice as likely to experience significant complications from COVID-19. Led by Northwestern University, the team conducting the research studied global data from the current COVID-19 pandemic and have discovered a strong correlation between a severe Vitamin D deficiency and mortality rates in patients with the virus.

The researchers analyzed data from 10 countries and found a correlation between low levels of Vitamin D and hyperactive immune systems. Vitamin D strengthens innate immunity and also prevents overactive immune responses. These findings may explain several mysteries including why children are unlikely to die from the virus.

The statistical analyses was from data at clinics and hospitals in France, Germany, China, Iran, Italy, Spain, South Korea, the United Kingdom, Switzerland and the United States. The team observed that patients from the countries with high COVID-19 mortality rates, such as Spain, Italy and the UK, had lower levels of Vitamin D when compared to patients in the countries that were not as severely affected.

The data obtained from the study may also illuminate the mechanism of mortality and if proven, may lead to new therapeutic targets.

The team was inspired to study the vitamin after noticing unexplained differences in COVID-19 mortality rates from country to country. Some hypothesized that differences in age distributions in populations, differences in healthcare quality, testing rates, or different strains of the virus might be responsible. However, the team remained skeptical.

It appeared none of these factors seemed to play a significant role. In Italy, the healthcare system is one of the best in the world. And differences in mortality exist even when one looks across the identical age group. And while the restrictions on testing do vary, the disparities in mortality still exist when populations or countries for which similar testing rates apply. Instead, the team saw a significant correlation with a Vitamin D deficiency.

Through analyzing publicly available data from around the world, the team discovered a strong correlation between levels of Vitamin D and cytokine storm which is a hyperinflammatory condition caused by an overactive immune system, and also a correlation between the vitamin and mortality.

Cytokine storm can severely damage the lungs and can lead to acute respiratory distress syndrome and even death in patients. This is what appears to kill the majority of COVID-19 patients and not the destruction of the lungs by the virus itself, but the complications that arise from the misdirected fire from the immune system.

This is where the team believes Vitamin D plays a significant role. Not only does the vitamin enhance our innate immune system, it will also prevent our immune systems from becoming dangerously overactive. This indicates that having healthy levels of Vitamin D may protect patients against developing severe complications including death from the virus.

The analysis has shown that it might be as high as cutting the mortality rate by 50%. It will not protect people from getting the virus, but it might reduce the development of complications and prevent death in those who have been infected with COVID-19.

The team explains that the correlation may help explain the many mysteries that surround the virus such as why children are less likely to die from the virus. Children do not have a fully developed acquired immune system which is the immune system’s second line of defense and is more likely to overreact. Children mainly rely on their innate immune system which may explain why their mortality rate is lower.

It is not known what dose is most beneficial and it will vary from person to person, however it is clear that a deficiency in the vitamin is harmful and it can easily be addressed with appropriate supplementation. This could be another key to helping protect the vulnerable populations such as elderly patients and African-Americans who typically have a prevalence of Vitamin D deficiency.

To view the original scientific study click below

The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients.

Loss of Taste and Smell Linked to Higher Chance of Covid-19

Both the loss of taste and smell have been anecdotally linked to a higher chance of developing the COVID-19 virus. The recent study has shown people are more than 10 times more likely to develop the virus infection than any other causes of infection.

Researchers at UC San Diego Health have reported that the first empirical findings strongly associate sensory loss with COVID-19. The team surveyed 1,480 patients who had flu-like symptoms and concerns regarding the potential of infection. Contained in that total, 102 patients tested positive for the virus and 1,378 tested negative. The study included responses from 203 COVID-19 negative patients and 59 positive patients.

68% of the positive participants reported loss of smell and 71% reported loss of taste as compared with 16% and 17% of negative patients respectively. None of the participants in the study required hospitalization or invasive breathing support. However, if social distancing was not in place, these individuals could possibly spread the infection to others within their community despite not experiencing severe symptoms.

The study has demonstrated the unique presentation and high prevalence of certain sensory impairments in patients who were positive with the virus. Of those patients who reported loss of taste and smell the loss typically profound and not mild. However, encouragingly the rate of recovery of taste and smell was high and typically occurred within two to four weeks after infection.

The study not only showed that the high occurrence of taste and smell loss is specific to the COVID-19 virus, but also fortunately has shown that the majority of people experienced sensory recovery fairly rapidly. Within the COVID-19 patients with loss of smell, more than 70% reported improvement in smell at the time of the survey. Most of those who hadn’t reported improvement had only been diagnosed recently.

The return of taste and smell typically matched the timing of recovery from the disease. Interestingly, the researchers found that people who reported experiencing a sore throat more often tested negative for the virus.

To help decrease the risk of virus transmission, UC San Diego Health now includes loss of taste and smell as a screening requirement for staff and visitors. The screening is also a marker for testing patients who might be positive for the virus.

Other symptoms of COVID-19 include fatigue, fever, difficulty breathing, and cough. Respondents in the study were most often people with milder forms of COVID-19 infection who did not require hospitalization or intubation. The team’s findings stress the importance of identifying subtle and early symptoms of the virus in people who might be at risk of transmitting the disease as they recuperate within their community.

The CDC has officially listed loss of taste and smell as symptoms of the virus which is a validation of the ruminating concerns about these symptoms around the world. It is the hope that the team’s findings inspire other institutions to follow suit and not only list taste and smell loss as a symptom of the virus, but also use it as a screening measure for the virus around the world.

To view the original scientific study click below

Association of chemosensory dysfunction and Covid-19 in patients presenting with influenza-like symptoms.

Does Sleep Loss Cause Obesity?

New research has found that quite the opposite is true. Previously a growing body of research has suggested that a poor quality of sleep is linked to an increased risk of obesity through deregulating appetite which results in higher caloric consumption. However, the latest study actually shows a flip side to that suggesting obesity leads to poor sleep. It isn’t the loss of sleep that leads to obesity, but instead it is excess weight that can lead to poor sleep.

It is thought that sleep is a function of the body trying to conserve energy where energetic levels are going down. The recent studies findings suggest that if a person were to fast for a day, they would get sleepy because their energetic stores would be depleted.

In humans, acute disruption of sleep can result in an increase in appetite and also insulin resistance. People who chronically get less than 6 hours of sleep per night are more likely to be diabetic and obese. However, starvation in rats, worms, fruit flies and humans has been shown to affect sleep which indicates that it is regulated at least in part by the availability of nutrients. However, the ways in which eating and sleeping work in tandem has been unclear.

The study team wanted to know what is sleep actually doing? Short periods of sleep and other chronic conditions such as diabetes, are linked but it is just an association. It isn’t clear if short sleep is causing the propensity for obesity or instead that the obesity itself causes the propensity of short sleep.

To research the association between sleep and metabolism, the team genetically altered C elegan worms to turn off a neuron that controls sleep. These worms could still breathe, eat and reproduce, but lost their ability to sleep. With the neuron disabled, the team saw a severe drop in adenosine triphosphate (ATP) levels which is the body’s energy currency.

In earlier research, a gene in C elegans called KIN-29 was studied. This particular gene is homologous to the Salt Inducible Kinase (SIK-3) gene found in humans. This gene had already known to promote sleep pressure. When the researchers knocked out the KIN-29 gene to promote sleepless worms, the mutant C elegans amassed more fat which resembles the human condition of obesity, although their ATP levels were decreased.

The team hypothesized that releasing fat stores is a control by which sleep is encouraged and the reasons KIN-29 mutants could not sleep was because they were not able to release the fat. By testing this, the team again manipulated the KIN-29 mutant worms by releasing an enzyme that discharged their fat. Because of this manipulation, once again the worms were able to sleep.

The team said this could explain a reason why people who are obese may experience sleep problems. There may be a signaling problem between the brain cells that control sleep and fat stores.

There is still much to unravel about sleep, however the new research provides a step closer to understanding sleep’s core functions and how to treat common sleep disorders. There appears to be a common overarching sentiment within the sleep field that sleep is all about the brain or the nerve cells. The new work suggests that may not be true. There are complex interactions between the brain and the rest of the human body that connects to regulation of sleep.

To view the original scientific study click below

A salt-induced kinase is required for the metabolic regulation of sleep.

Vitamin D Supplementation may Reduce Risk of Both the Flu and Covid-19

With the world in the middle of the COVID-19 pandemic, public health policies that could decrease the danger of infection and even death along with less quarantines are greatly needed. Vitamin D supplementation shows promise in reducing those risks in both the COVID-19 virus and influenza.

Through a variety of mechanisms, Vitamin D could decrease the chance of infections. These mechanisms such as inducing defensins and cathelicidins which are both cysteine rich cationic proteins that play a critical role in mammalian innate immune defense against invasive bacterial infections. These proteins may decrease viral replication rates and reduce concentration levels of pro-inflammatory cytokines that cause inflammation that damages the lung linings and may lead to pneumonia and increasing concentration levels of anti-inflammatory cytokines also.

Vitamin D is a modulator of adaptive immunity. It suppresses responses mediated by the T help cell type by primarily repressing production of inflammatory cytokines. Serum concentrations tend to decrease with age which may be critical to COVID-19 because case fatality rates increase with age.

Several clinical trials and observational studies have reported that taking Vitamin D decreased the risk of influenza, and others could not. Supporting evidence of the role Vitamin D may play in reducing the risk of COVID-19 includes that the outbreak resulted in the winter which is a time when
25-hydroxyvitamin D (25(OH)D) concentrations are at their lowest. The amount of cases in the Southern Hemisphere at summers end are low. Additionally it has been found that Vitamin D deficiency may promote acute respiratory distress syndrome and that fatality rates can increase as a person ages and with extreme disease comorbidity, which both are associated with decreased (25(OH)D) concentration.

To minimize the promotion of infection, it has been recommended that if you are at risk of influenza and/or COVID-19 would maybe take 10,000 IU/d of Vitamin D3 for a couple of weeks to rapidly increase 25(OH)D) levels followed by 5,000 IU/d. The goal is to increase 25(OH)D) levels of concentrations above 40-60 ng/mL. For the treating people that have already become infected with COVID-19, higher levels of Vitamin D3 doses could be useful.

Magnesium supplementation is recommended when taking Vitamin D supplements as it helps activate Vitamin D which in turn promotes regulation of calcium and phosphate homeostasis to affect maintenance and growth of bones. All enzymes which will metabolize Vitamin D appear to need Magnesium, acting as a cofactor in the enzymatic reactions of the kidneys and liver. The dose of Magnesium should be in the range of 250-500 mg/d along with twice the dose of calcium.

Although some contradictory data exists, the evidence available shows that supplementation with several micronutrients with immune supporting roles can vary immune function and help decrease the risk of infection. Micronutrients that haveh the strongest indications for immune support are Vitamins D and C along with Zinc.

To view the original scientific study click below

Evidence that Vitamin D Supplementation Could Reduce Risk of Influenza and COVID-19 Infections and Deaths.

Stem Cell Technology Rejuvenates Old Human Cells

According to a new study by researchers at Stanford University of Medicine, old human cells will return to a more vigorous and youthful state following being induced to briefly express a protein panel involved in embryonic development. They team also discovered that elderly mice regained their youthful strength after their existing muscle stem cells were subjected to the protein treatment rejuvenation and then transplanted back into their bodies.

The proteins which are known as Yamanaka factors are typically used to transform adults cells into induced pluripotent stem cells or iPS cells. These iPS cells can become nearly any type of cell within the body regardless of the cell from which they originated. They have become important in regenerative medicine and drug discoveries.

The current study found that inducing old human cells in a lab dish for a brief period to express these proteins rewinds many of the molecular hallmarks of aging. They render the treated cells nearly indistinguishable from their younger counterparts.

When adult cells make iPS cells they become pluripotent and youthful. The team wondered if it might be possible to just rewind the aging clock without inducing pluripotency. They found that by tightly controlling the duration of the exposure to these protein factors, they were able to promote rejuvenation in multiple types of human cells.

The researchers make iPS cells from adult cells such as those that compose skin through repeatedly exposing them over a two week period to a panel of proteins which are vital to early embryonic development. They do so by introducing daily short lived RNA messages into the adult cells. The RNA messages then encode the instructions for making the Yamanaka proteins. These proteins over time rewind the fate of the cell by pushing them backward along the timeline of development until they resemble young, embryonic like pluripotent cells from which they originated.

During the process the cells shed any memories of their previous identities and they revert to a younger state. They accomplish this by wiping their DNA clean of the molecular tags that not only differentiate for example a skin cell from a heart muscle cell, but of other tags that accumulate as cell age.

The team wondered if old human cells would respond similarly and whether the response would be limited to a few cell types or generalizable for many tissues. They created a way to use genetic material called messenger RNA to temporarily express six reprogramming factors which were the four Yamanaka factors plus two additional proteins found in blood vessel cells and human skin. Messenger RNA will rapidly degrade in cells which allowed the researchers to tightly control the duration of the signal.

The team then compared the gene expression pattern of the treated cells and control cells which were both obtained from older adults, with those of untreated cells from younger people. They discovered that cells from the older adults exhibited signs of aging reversal following four days of exposure to the reprogramming factors. However the untreated older cells expressed higher levels of genes associated with known aging pathways. Treated older cells more closely resembled younger cells in their patterns of gene expression.

When they studied the patterns of aging associated chemical tags which are known as methyl groups which serve as indicators of a cell’s chronological age, they discovered that the treated cells appeared to be approximately 1-1/2 to 3-1/2 younger on average than the untreated cells from the older people. They showed peaks of 3-1/2 years (in skin cells) and 7-1/2 years in cells that line blood vessels.

The researchers then compared several hallmarks of aging including how cells metabolize compounds to create energy and dispose of cellular trash and how cells sense nutrients, among cells from young people, treated cells from older adults and untreated cells fro older adults.

They saw a dramatic rejuvenation across all the hallmarks but one in all the types of cells that were tested. The last and most experiment was done stem cells found in the muscles. Although these cell types are naturally endowed with the ability to self renew, this ability wanes with aging. The team wondered if they could also rejuvenate these stem cells and have a long term effect?

When they transplanted elderly mouse muscle stem cells that had been treated back into elderly mice, the mice regained the muscle strength similar to younger mice.

The team then isolated cells from the cartilage of people without and with osteoarthritis. They discovered that the temporary exposure of the osteoarthritic cells to the reprogramming factors reduced the secretion of inflammatory molecules and also improved the ability of the cells to divide and function.

The team is now optimizing the panel of reprogramming proteins needed to rejuvenate human cells. They are also looking at the possibility of treating tissues or cells without removing them from the body.

To view the original scientific study click below

Transient non-integrative expression of nuclear reprogramming factors promotes multifaceted amelioration of aging in human cells.

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