Blue Light Filtering Glasses Improve Workday Productivity and Sleep

New research has shown that by wearing blue-light glasses right before sleeping a person can get a better night’s sleep and also contribute to better workday productivity. This is especially important since people are learning and working from home as well as binge watching TV more than ever before due to the pandemic.

The team discovered that if a person wears blue-light filtering glasses, it can be an effective way to not only improve sleep but also task performance, work engagement and organizational citizenship behaviors. It also reduced work behavior that was counterproductive. These glasses create a form of physiologic darkness which leads to improved sleep quality and quantity.

Most of the technology people use such as smartphones, computer screens, and tablets all emit blue light. Past research has shown that these devices through the blue light they emit can disrupt sleep. As we currently navigate school and work, people have become more dependent on these devices.

The new research has helped extend the understanding of the circadian rhythm which is a natural, internal process that regulates our sleep/wake cycle and repeats approximately every 24 hours. Before modern times people were not exposed to blue light after the sunset. Wearing blue light filtering glasses produces a similar effect. To get the best results the glasses should be worn starting about two hours before going to bed and until the lights in the bedroom are turned off. Some people put them on right after it gets dark.

Generally speaking, the effects of wearing blue-light filtering glasses are stronger for night owls as opposed to morning larks. Night owls tend to sleep during later times in the day while larks tend to sleep earlier in the day.

Although most anyone can benefit from reducing their exposure to blue light, night owl employees benefit more as they have greater changes between their internal clock and their work time which is externally controlled. The team’s research shows just how and when a person wears the blue-light filtering glasses can help employees to work and live better.

The team’s research discovered that daily engagement of task performance may be related to underlying processes such as the circadian process. The research pushes the chronotype literature to think about the relationship between employees’ performance and the timing of circadian processes. A good night’s sleep will not only benefit workers, it will also help their employer’s bottom lines.

Through two studies, the team collected data from 63 company managers and 67 call center reps at Brazil based offices for a United States multinational financial firm and measured task performance from clients. The participants were randomly chosen to test blue-light filtered glasses or those that were placebo glasses.

Employees can often be asked to work early in the morning which can lead to a change between the externally controlled work time and their internal clock. The team found that their analyses showed a general pattern that blue-light filtration can have a cumulative effects on key performance variables at least in the short term.

They note that blue-light exposure should be a concern to organizations. The ubiquity of this phenomenon suggests that blue-light exposure control might be a viable first step to protect the circadian cycles of their employees from disruption.

To view the original scientific study click below

The effects of blue-light filtration on sleep and work outcomes.

Why Average Body Temperature has Dropped in Healthy Adults

Almost two centuries ago the current “normal” body temperature in humans was established at 98.6 degrees Fahrenheit and has been used as the measure for assessing fevers. However, over time lowering of body temperature has been widely substantiated in healthy adults.

A study conducted in 2017 among 35,000 adults in the U. K. found average body temperatures to be lower at 97.9F and a study in 2019 in the U. S. found normal body temperatures at about 97.5F.

Interestingly, recent studies in both the U. S. and the U. K. have found a decrease similar in the Tsimane which is an indigenous population of forager horticulturists located in the Bolivian Amazon. A team that has been observing this population have observed a rapid decline in body temperature of 0.09 degrees Fahrenheit such that today this population’s body temperatures are about 97.7F.

In less than twenty years researchers are seeing the same levels of decline as that which has been observed in the U. S. over about two centuries. The analysis is based on a large sample of 18,000 observations of about 5,500 adults with adjustments for factors that can affect body temperature such as body mass and ambient temperature.

It is clear that something about human physiology has changed. The researchers leading hypothesis is that we have recorded fewer infections due to clean water, improved hygiene, medical treatment and vaccinations. In the recent study, they were able to test these ideas directly. They have information on clinical diagnosis and also biomarkers of inflammation and infection at the time each participant had been seen.

Although some infections were associated with high body temperatures, adjusting for those did not account for the steep decline in temperatures over time. The same kind of thermometer was used for most of the study so the changes were not due to changes in instruments.

No matter how they did the analysis, the declines were still there. Even when they restricted analysis to under 10% of adults who were diagnosed as completely healthy, they still observed the same decline in body temperatures over time.

A key question became then is why are body temperatures declining in both Americans and the Tsimane population. Data available from the team’s long-term research in Bolivia addressed some of the possibilities. Declines could be due to an increase of modern health care and less incidence of lingering mild infections compared to the past. However, while health has improved over the past two decades, infections are still widespread in rural areas of Bolivia. This then suggests that reduced infection alone isn’t why the decline in body temperatures.

It may be that people are in general in better condition which means their bodies could be working less to fight infection. Greater access to antibiotics and other medical treatments means that the duration of infections is shorter now than was in the past. The team did find that respiratory infection in the early period of the study led to having a high body temperature than having the same infection more recently.

Another possible explanation is that a person’s body doesn’t have to work as hard to maintain the internal temperature due to air conditioning in the warmer temperatures and heating in the colder temperatures. Although Tsimane body temperatures will change with time of year and patterns of the weather, these people do not use any advanced technology for helping to regulate their body temperature. They do however, have more access to blankets and clothes.

The research team was initially surprised to find no single magic bullet that would explain the decline in body temperature. They believe it is likely due to a combination of factors which all point to improved conditions.

Temperature as a vital sign is an indicator of what is occurring physiologically inside the body. One thing that has been known for a while is that there is not universal body temperature for everyone at all times. Despite the fixation on 98.6F, most clinicians know that normal temperatures have a range and throughout the day, temperatures can vary by as much as 1 degree Fahrenheit from lowest in the morning to its highest in the afternoon. It will also vary following physical activity, across the menstrual cycle, and tends to decrease with age.

Through linking improvements in the broader epidemiological and socioeconomic landscape to body temperature changes, the study does suggest that information in regards to body temperature may provide clues to a population’s overall health along with other normal expectations such as life expectancy. Since body temperature is easy to measure, it can easily be added to routine large-scale surveys that monitor the health of populations.

To view the original scientific study click below

Rapidly declining body temperature in a tropical human population.

Positive Outlook and Less Memory Decline

A new study has shown that people who are cheerful and feel enthusiastic or what is known as the “positive effect”, are not likely to experience decline in memory with aging. This study adds to a increasing body of research that shows the role a positive outlook has on aging.

Many of wish some of our memories could last a lifetime. However, emotional and physical factors can impact negatively our ability to remember information throughout a person’s life.

The research team analyzed data from 991 older and middle aged adults in the United States who had participated in a study that was conducted nationally at three different time periods – 1995 and 1996, 2004 and 2006, and 2013 and 2014.

With each assessment the study participants identified a range of positive emotions they experienced during the previous 30 days. In the last two assessments, they also completed tests of memory performance. These tests involved participants recalling words immediately following their presentation and again 15 minutes later.

The team then examined the association between positive effect and memory decline. They accounted for gender, age, education, negative effect, depression and extroversion.

The findings indicated that memory did decline with age. However, participants with higher levels of positive effect declined less with their memory over the period of almost a decade.

Future research will look at addressing the pathways that could connect memory and positive effect such as social relationships and physical health.

To view the original scientific study click below

Positive Affect Is Associated With Less Memory Decline: Evidence From a 9-Year Longitudinal Study

Hair Loss and Regulating Stem Cell Metabolism

New research has identified a mechanism that appears to be able to prevent hair loss. A group of researchers in Helsinki and Cologne Germany have demonstrated that a protein known as Rictor holds a important role in the process.

Hair follicle stem cells promote hair growth and can also retain their life by changing their metabolic state. Environmental factors such as ultraviolet radiation damage skin and different tissues daily. The body continues to remove and renew the damaged tissues. Human sheds about 500,000,000 cells daily and an amount of hair weighing an amount of 1.5 grams.

Material that is dead is replaced through specialized stem cells that further growth of tissue. The function of tissues is reliant on the health and activity of these stem cells. Impaired activity will result in the aging of the tissues.

The part of stem cells and aging that is critical has been established, however not very much information is available about mechanisms that administer maintenance on a long term basis of these vital cells. The follicle of the hair which is well understood and has known identifiable stem cells is the prefect model system for researchers to study this question.

At the final stages of a hair follicle’s regenerative cycle and when a new hair is established, stem cells go back to their ideal location and maintain a quiescent state. The most important finding in the research team’s study is that the return to the stem cell state must have a change in the cell’s metabolic state. The cells switch from cellular respiration and glutamine based metabolism to glycolysis. This is a shift brought on by a signal that is induced by the Rictor protein in return to the concentration of low oxygen in the tissue. The study demonstrates that the absence of this protein influenced the stem cells reversal ability. This initiated a limited stem cell exhaustion and loss of hair due to aging.

The team’s creation of a genetic mouse model for the purpose of studying the Rictor protein. They observed that regeneration and cycle of the hair follicle were delayed quite significantly in mice who lacked the protein. Older mice suffering from a deficiency of this protein showed a limited decrease in their stem cell which resulted in hair loss.

Additional research will be conducted to investigate how the pre-clinical findings might be utilized in human stem cell biology and also lead to therapies with drugs that may protect the aging of hair follicles. The mechanisms found in the recent study might possibly be utilized in preventing loss of hair.

The team was most excited about their realization that the intent of a glutaminase inhibitor was able to bring back the function of the stem cells in the Rictor deficient mice. This proved the principle that by changing metabolic pathways, an important way to increase the regenerative amount of our tissues occurred.

To view the original scientific study click below

Glutamine Metabolism Controls Stem Cell Fate Reversibility and Long-Term Maintenance in the Hair Follicle

Brain Circuit Damage Due to Childhood Social Isolation

A research team at the Icahn School of Medicine at Mt. Sinai have identified certain sub-populations of brain cells located in the prefrontal cortex that are needed for normal sociability in adults and are also profoundly vulnerable to social isolation in juvenile mice. The prefrontal cortex in the brain is a key part of the brain that regulates social behavior. The study conducted on mice shows long lasting effects and also directs the way to potential treatments.

Loneliness and isolation are both recognized as serious threats to mental health. Young people are feeling an increasing sense of isolation even as the world becomes quite a bit more connected through digital platforms. The COVID-19 pandemic which has forced many countries around the world to implement school closures and social distancing, increases the need for better understanding of the mental health consequences of loneliness and social isolation.

Research has shown that being socially isolated during childhood is damaging to adult brain function and behaviors across mammalian species. However, the core neural circuit mechanisms are poorly understood.

The research team’s discovery sheds light on a previously unrecognized role of the sub-populations of brain cells in the prefrontal cortex. These cells are known as medial prefrontal cortex neurons projecting to the paraventricular thalamus which is the area of the brain that sends signals to specific components of the brain’s reward circuitry. If the team’s findings can be produced in humans, this could advance to treatments for psychiatric disorders that are associated with isolation.

The team also demonstrated that the vulnerable circuit they identified is a promising target for treatments for deficits in social behaviors. By stimulating the specific prefrontal circuit projecting to the thalamic area in adulthood, they were able to rescue sociability deficits caused by social isolation during the childhood.

The team discovered that in male mice 2 weeks of being socially isolated as soon as they are weaned could lead to a failure to create medial prefrontal cortex neurons eminated to the paraventricular thalamus for periods of social exposure in adults. They discovered that childhood isolation led to not only reduced excitability of the prefrontal neurons projecting to the paraventricular thalamus, but also increased inhibitory input from other related neurons. This suggests that a circuit mechanism underlies sociability deficits caused by childhood isolation.

In order to determine if acute restoration of the activity of the prefrontal projections to the paraventricular thalamus is sufficient to ameliorate sociability deficits in adult mice that had been put under juvenile social isolation, the researchers used a technique known as optogenetics to primarily stimulate the projections to the thalamus.

In addition, they used chemogenetics in the study which enabled them to stimulate particular neurons in freely moving animals through pulses of light. Chemogenetics allows non-invasive chemical control over populations of cells.

By employing both techniques, the team was able to substantially increase social interaction in the mice once light pulses or drugs were given to them. The team checked the presence of social behavior deficits just before stimulation and when they checked the behavior while the stimulation was going on, they found that the social behavior deficits were reversed.

Since social behavior shortfalls are commonly a characteristic of a lot of neurodevelopmental and psychiatric disorders like schizophrenia and autism, identification of these certain prefrontal neurons will lead towards therapeutic targets for improving the social behavior shortfalls that are shared across a spectrum of psychiatric disorders. The circuits found in this study could possibly be modulated through techniques such as transcranial magnetic stimulation and/or transcranial direct current stimulation.

To view the original scientific study click below

A prefrontal–paraventricular thalamus circuit requires juvenile social experience to regulate adult sociability in mice. Nature Neuroscience, Aug. 31, 2020; DOI: 10.1038/s41593-020-0695-6

Nano-Particles and Effects on Health

Nano-particles can be useful and even valuable in a variety of products, however according to a recent study they can also damage our cells. Researchers are now concerned about the effects of lifelong exposures to this human organism.

Nano-particles are used in a wide variety of manufacturing processes and products. This is due to the fact that the properties of a material can dramatically change when that material comes down in nano form.

These particles are used to transport medicine around the body and to purify wastewater. They are also added to pillows, socks, phone covers, mattresses and refrigerators which supplies these items with an antibacterial surface.

A large amount of research has been conducted on how nano-particles affect the environment and humans. Some studies have shown that nano-particles can damage or disrupt human cells. This has been recently confirmed by the new study that also studied how cells react when they have been exposed to more than one type of nano-particle at the same time.

We are exposed to many different kinds of nano-particles throughout our lifetime. The research team involved with the new study set out to investigate how the combination of different nano-particles can affect us and in addition whether an accumulation throughout a life can harm us.

In the new study, the team looked at nano-platinum and nano-silver. They not only looked at the individual effect but also whether exposure to both types result in a synergy effect in two types of cells in the brain.

Nano-silver was chosen because it is already known to be able to damage cells and nano-platinum because it is considered to be a bio-inert which means it has a minimal interaction with human tissue.

Both nano-particles were tested on two types of cells found in the brain – astrocytes and endothelial cells. Astrocytes are supporter cells found in the central nervous system which helps in supplying the nervous system with nutrients and repair brain damage. Endothelial cells reside on the inside of the blood vessels and transport substances from the bloodstream to the brain.

When the team exposed endothelial cells to nano-platinum nothing happened. When they were exposed to nano-silver their ability to divide resulted in deterioration. When the cells were exposed to both nano-platinum and nano-silver, the resulting effect amplified and large numbers of the cells died. Additionally, their defense mechanisms decreased and they also had difficulty communicating with each other.

Even though nano-platinum by itself did no harm, something drastic happened when they were combined with a different kind of nano-particle. The astrocytes were hardy and only reacted with impaired ability to divide when they were exposed to both nano-platinum and nano-silver.

An earlier study has shown a dramatic synergy effect of nano-silver and cadmium ions which are naturally found all around us on earth. This study showed that 72% of cells in the intestine died when they were exposed to both nano-silver and cadmium ions. When these cells were exposed to just
nano-silver 25% died. When exposed to cadmium ions alone, 12% died.

Unfortunately, little is known about how large concentrations of nano-particles are used in industrial products. It is also not known what size particles are used. Size has also shown an effect on whether they can enter a cell. What we do know is that many people are involuntarily exposed to nano-particles and there can easily be lifelong exposure.

Currently there are no restrictions on adding nano-particles to products. However, in the EU manufacturers must have approval if they want to use nano-particles in products that have antibacterial properties and in Denmark, they must also declare nano-contact on product labels containing them.

To view the original scientific study click below

The Cytotoxicity of Metal Nanoparticles Depends on Their Synergistic Interactions

Regenerating Neurons in the Brain and Eye

The death of neurons whether in the eye or in the brain can result in a variety of human neurodegenerative diseases that range from blindness to Parkinson’s disease. Treatments currently available for these type of disorders only slow the progression of the illness. This is because once a neuron dies it cannot be replaced.

A study conducted by researchers from the University of Notre Dame, Johns Hopkins University, Ohio State University and the University of Florida have identified networks of genes that regulate the process which is responsible for determining if neurons will regenerate in certain animals such as zebrafish.

The study is proof of principle indicating that it is possible to regenerate neurons in the retina. The team also believes the process for regenerating neurons located in the brain will be similar.

For the research, the team mapped genes of animals that have the ability to regenerate neurons in the retina. One example is found in zebrafish. When their retina is damaged, cells known as Muller glia go through a reprogramming process. During this process, the Muller glia cells change their gene expression and become like progenitor cells or cells that are used during early organism development. These now progenitor cells can become any cell that is necessary to fix the retina that has become damaged.

People also have Muller glia cells. However, when a human retina is damaged, the Muller glia cells respond with gliosis which is a process that will not allow them to reprogram.

After the team determined the different animal processes for retina damage recovery, they had to decipher if the process for gliosis and reprogramming were similar. They wondered if the Muller glia follow the identical path in non-regenerating and regenerating animals or would the paths be totally different. This knowledge would be important so they would be able to use Muller glia cells to regenerate neurons in the retina in humans. Understanding whether it would be a matter of redirecting the current Muller glia path or if an entirely different process would be required.

They found that the regeneration process only needed the organism to turn back on its early processes of development. They were also able to illustrate that during zebrafish regeneration Muller glia also go through gliosis. This means that organisms that have the ability to regenerate retinal neurons do follow a similar path to animals that cannot.

The network of genes in zebrafish are able to move Muller glia cells from gliosis into the reprogrammed state, however the network of genes in mice models blocked the Muller glia from reprogramming. From here, the team was able to modify zebrafish Muller glia cells into a similar state that blocked the reprogramming while also having mice models regenerate some neurons in the retina.

The next step for the researchers is to try and identify the number of gene regulatory networks that are responsible for neuronal regeneration and exactly which genes within the network are the ones responsible for regulating regeneration.

To view the original scientific study click below

Gene regulatory networks controlling vertebrate retinal regeneration

Coffee After Breakfast for Metabolic Control

Research from the Centre for Nutrition, Exercise and Metabolism at the University of Bath (UK) looked at the combined effects of caffeine and disrupted sleep on our metabolism and found surprising results. They found that a strong, black cup of coffee to wake you up following a bad night’s sleep might impair control of blood sugar levels.

The team showed that while one night of poor sleep has limited impact on a person’s metabolism, drinking coffee to perk up from a slumber can have a negative effect on blood sugar control. Due to the importance of keeping our blood sugar levels in a safe range to reduce the risk of conditions such as heart disease and diabetes, the team’s results could have far reaching implications on health. This is especially important considering the worldwide popularity of coffee.

For the study the physiologists at the University of Bath had 29 healthy women and men undergo three different overnight experiments which were in a random order. In one, these participants had a normal night’s sleep and were then asked to consume a sugary beverage on waking in the morning.

In another experiment, the participants experienced a disrupted night’s sleep (the researchers woke them up every hour for a five minute period), and then on waking were given the identical sugary beverage as the first group.

For the third experiment, the participants experienced the same disrupted sleep as the second group but in this group they were given a strong, black cup of coffee 30 minutes prior to drinking the sugary beverage.

Blood samples were taken from all participants in each of the tests. They were taken after consuming the sugary beverage which in energy calories mirrored what might typically be consumed for breakfast.

The team’s findings highlight that one night of disrupted sleep did not result in any worsening of the participant’s blood glucose/insulin responses at breakfast when compared to a normal night’s sleep. Earlier research has suggested that losing many hours of sleep over one night and/or multiple nights might have negative effects on metabolism. Based on the new research, a single night of fragmented sleep which could be due to noise disturbance, insomnia or other disruptions, does not have the same effect.

However, a cup of strong, black coffee before breakfast substantially increased the blood glucose response to breakfast by about 50%. Population based surveys have indicated that coffee may be associated with good health although past research has demonstrated that caffeine has the ability to cause insulin resistance.

The new study reveals that the remedy of consuming coffee following a bad night’s sleep may solve the problem of feeling sleepy, however could lead to limiting the body’s ability to tolerate sugar consumed with breakfast.

The team notes that nearly half of us will wake up in the morning and prior to doing anything else will reach for a cup of coffee. Intuitively, the more tired we are the stronger the coffee we will consume. This new study is important and shows far reaching health implications as until now we have had limited knowledge in regards to what this may be doing to our bodies and in particular to our blood sugar and metabolic control.

The study shows that consuming coffee first thing in the morning and particularly after a bad night’s sleep, impairs our blood sugar control. We may be able to improve this by eating breakfast first and consuming coffee later if we feel we need it.

The results have indicated that one night of disrupted sleep did not worsen the participant’s blood glucose/insulin response to the sugary beverage compared to a normal night’s sleep which can be reassuring to many of us. However, beginning the day following a poor night’s sleep with a strong cup of coffee did have a negative effect of about 50% on glucose metabolism.

People should try to balance the potentially stimulating benefits of caffeinated coffee in the morning with the potentially higher blood glucose levels. It may be better to drink coffee after breakfast rather than before.

There is still a lot more to be learned about the effects of sleep on our metabolism. Questions remain as to how much sleep disruption is required to impair our metabolism and what longer term implications of this might be. Also, can exercise for instance help to counter some of this.

To view the original scientific study click below

Glucose control upon waking is unaffected by hourly sleep fragmentation during the night, but is impaired by morning caffeinated coffee

Fructose and Inflammatory Bowel Disease

A new study conducted on mice has suggested that a diet that is high in the sugar fructose exacerbates inflammatory bowel disease (IBD). It appears that changes in gut bacteria mediate the effect.

IBD is an overall term for a variety of conditions that feature chronic inflammation of the digestive system. The two most common types are Crohn’s Disease and ulcerative colitis. Symptoms of IBD include stomach pain, persistent diarrhea, bloody stools or rectal bleeding, fatigue and unexplained weight loss.

The CDC reports that the number of adults who receive an IBD diagnosis every year in the U. S. has increased from 2 million in the year 1999 to 3 million in 2015.

Earlier research in animals found that a diet which is high in fructose can damage the colon and also lead to inflammation. This suggests that a higher intake of fructose may be a reason for the increased incidence of IBD in recent years.

Population studies have not always indicated a link between refined sugar intake and IBD. One large study did not find an association between any specific dietary pattern and IBD although the results did show that a diet which is high in soft drinks and sugar did increase the risk of a person developing ulcerative colitis in cases where intake of vegetables was low.

High fructose corn syrup is added to candy, baked goods, sodas and other processed foods by manufacturers of these products. Consumption of fructose has increased by nearly one-third in the U.S. over the last 30 years according to estimates. The increase in IBD parallels the higher levels of the consumption of fructose not only in the U. S. but other countries as well.

The team involved in the recent study set out to investigate whether fructose exacerbates inflammation in mouse models with IBD. They additionally tested the idea that changes in the microbiota in the gut mediate the inflammatory effects of consuming fructose.

The team’s findings have provided evidence of a direct association between IBD and dietary fructose which support the idea that the high consumption of fructose could exacerbate the disease in people who have IBD. This is especially relevant because the potential exists in providing people with IBD guidance on diet choices.

The team performed a variety of experiments with the goal of investigating which effects a diet high in fructose could have on three different mouse models with IBD.

The first model which used a chemical known as dextran sodium sulfate which provokes the type of inflammatory response which will occur in IBD, showed that the a high fructose diet did increase the severity of this inflammation. However in contrast, a high glucose diet did not increase this inflammation.

The team also noted that giving antibiotics to the mice reduced the damaging effects of a diet high in fructose on the colon. This suggests that bacteria found in the gut were mediating the harmful effects.

In contract, transplants of fecal material obtained from mice that had been fed the high fructose diet increased inflammation in the mice who had received them. This shows additional evidence of the role gut bacteria play in IBD.

When the team looked more closely at the mucus layer which protects the cells that line the colon, they discovered that the diet high in fructose reduced the thickness by almost one-fifth. Bacteria infiltrated the mucus and became in direct contact with the cells.

They also found that the diet changed the prevalence of a variety of species of bacteria that live in the gut. It boosted the population of a species known as Akkermansia muciniphila. In earlier studies, researchers have shown that this particular species has the ability to degrade mucus and that it is associated with inflammation in the colon.

The second model of IBD used in the experiments involved infecting the mice with a bacterium known as Citrobacter rodentium which also provokes the inflammation found in IBD. These mice were fed high amounts of fructose which worsened the inflammation and also promoted the growth of the bacteria.

The team confirmed the association between IBD and fructose in a genetic model of this disease. This particular model recreates a type of immune response that has the ability to make some people with IBD more likely to develop inflammation in the colon. Once again, consumption of high amounts of fructose increased the inflammation of the colon in these mice.

Researchers say the next step is to conduct more studies on whether people with IBD are at an increased risk of developing colon cancer due to a lifetime of chronic inflammation of the gut. They also plan on developing interventions to help prevent the pro-inflammatory effects dietary fructose.

To view the original scientific study click below

Dietary Fructose Alters the Composition, Localization and Metabolism of Gut Microbiota in Association with Worsening Colitis

Cognitive Decline Offset by Lifestyle Changes

According to the CDC at least 5 million people living in the U.S. live with Alzheimer’s Disease and related dementias. As the population ages, experts believe this number will increase quite significantly. A new study of older adults has shown that how increasing physical activity and changing diet can reduce the risk of dementia related diseases even if the person already has a cognitive decline diagnosis.

Dementia is a group of disorders that are characterized by difficulties in remembering, thinking and reasoning. Alzheimer’s is the most common type of cognitive decline. Even though scientists do not know the exact biological cause of Alzheimer’s, they do know that a variety of lifestyle factors does increase a person’s risk of developing dementia.

Lifestyle changes that affect this risk include alcohol consumption, smoking, physical activity and diet. One study has estimated that close to half of all cases of Alzheimer’s disease worldwide could have links to certain lifestyle factors.

A recent study led by The Australian National University in Canberra, conducted trials of a series of lifestyle interventions in people who were already experiencing cognitive decline. The goal was to see whether these changes might improve a person’s cognitive state and potentially reduce the risk of developing dementia.

The research team discovered that people who actively changed certain aspects of their lifestyle choices, were able to experience significant improvements in their cognition. This suggests that by making certain lifestyle changes, the course of cognitive decline could be altered and could also reduce a person’s risk of developing Alzheimer’s.

The study involved 119 participants aged 65 or older who had either subjective cognitive decline (SCD) which is the self reported experience of memory loss of confusion, or had mild cognitive impairment (MCI) which is a clinically diagnosed form of cognitive decline. Medical professionals consider both forms of cognitive decline as early onset symptoms of dementia, although not everyone with MCI or SCD will develop dementia.

The study which is a part of the Body, Brain, Life for Cognitive Decline trial, set out to determine whether activity levels and diet can reduce the risk of dementia in people diagnosed with cognitive decline.

The participants were split roughly into two groups. Over an eight week period, the active control group completed online modules on the risk of dementia including information on dementia, lifestyle factors, physical diet, Mediterranean diet, and cognitive relations. These participants were given the instructions to blend this information into their own lifestyles.

The intervention group of participants received the identical online information in addition to active components to help with implementing their information into their lifestyles. These included an exercise physiologist session, dietitian sessions, and online brain training.

At the end of the study, the intervention group’s cognition levels were significantly higher than the other group. Over the six months of follow-up, researchers noted that these participants were able to improve their lifestyle choices and had higher cognition scores. They measured this using a variety of tools including the Alzheimer’s Disease Assessment Scale Cognitive Subscale.

The team also assessed exposure to lifestyle risk factors for developing Alzheimer’s and showed that the intervention group was also significantly lower at the 3 month follow-up. However, at the six month follow-up this was not the case. This suggests that people need to maintain their diet and activity improvements to see continued benefits.

The study shows that people who are already experiencing cognitive declines, can reduce their risk for developing dementia later in life. With the right interventions, they may retain sufficient neuroplasticity of their brain to bounce back from decline. The fact that people can achieve this by adapting cost effective and relatively simple lifestyle changes, is very promising.

The research team notes that a follow-up trial with more participants than the original 119 and over a longer period will be important to confirm their findings and additionally demonstrate sustained cognitive improvements. They also note that participants who did not maintain a reduced risk of Alzheimer’s by the end of the study, suggests that some people may require “booster” sessions to ensure continuation of benefits.

To view the original scientific study click below

Lifestyle Risk Factors and Cognitive Outcomes from the Multidomain Dementia Risk Reduction Randomized Controlled Trial, Body Brain Life for Cognitive Decline (BBL?CD)

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