Source: Controlling Memory By Triggering Specific Brain Waves During Sleep
Controlling Memory By Triggering Specific Brain Waves During Sleep
Summary: Using optogenetics, researchers manipulated pulses of neural activity during non REM sleep that made mice either remember of forget things they had learned. This novel study demonstrated that altering sleep spindle oscillations during sleep has an impact on memory formation and retention.
IBS researchers find that manipulating the pulses of electrical activity in the thalamus during non-REM deep sleep make mice remember or forget.
Have you ever tried to recall something just before going to sleep and then wake up with the memory fresh in your mind? While we absorb so much information during the day consciously or unconsciously, it is during shut eye that a lot of facts are dispatched to be filed away or fall into oblivion. A good quality sleep is the best way to feel mentally refreshed and memorize new information, but how is the brain working while we sleep? Could we improve such process to remember more, or maybe even use it to forget unwanted memories?
Scientists at the Center for Cognition and Sociality, within the Institute for Basic Science (IBS), enhanced or reduced mouse memorization skills by modulating specific synchronized brain waves during deep sleep. This is the first study to show that manipulating sleep spindle oscillations at the right timing affects memory. The full description of the mouse experiments, conducted in collaboration with the University of Tüebingen, is published in the journal Neuron.
The research team concentrated on a non-REM deep sleep phase that generally happens throughout the night, in alternation with the REM phase. It is called slow-wave sleep and it seems to be involved with memory formation, rather than dreaming.
During slow-wave sleep, groups of neurons firing at the same time generate brain waves with triple rhythms: slow oscillations, spindles, and ripples. Slow oscillations originate from neurons in the cerebral cortex. Spindles come from a structure of the brain called thalamic reticular nucleus and spike around 7-15 per second. Finally, ripples are sharp and quick bursts of electrical energy, produced within the hippocampus, a brain component with an important role in spatial memory.
“Often during the night a regular pattern is manifested, where a slow oscillation from the cortex is immediately followed by a thalamic spindle and while this happens, a hippocampal ripple appears in parallel. We believe that the correct timing of these three rhythms acts like a communication channel between different parts of the brains that facilitates memory consolidation,” explains Charles-Francois V. Latchoumane, first co-author of the study.
The researchers focused on spindles because it was shown that the number of spindles is connected with memorization. It has been shown that the number of spindles increases following a day stuffed with learning and declines in the elderly, and in patients with schizophrenia. This is the first study to show that artificial thalamic spindles affect memory, if administered in sync with slow oscillations.
In the experiment, mice were put in a special cage and given a mild electric shock after hearing a tonal noise. The day after, their memory was tested, by checking their fear reaction in response to either the same noise or the same cage. Latchoumane explains that this could be simplified and compared to the experience of hearing a fire alarm in a certain location, like a cafe. The incident would be followed by either another visit to the same cafe or the sound of the fire alarm in another cafe on the following day.
At nighttime between the two days, scientists introduced artificial thalamic spindles in some of the mice using a light-based technique called optogenetics. The mice were divided into three groups. The first group received the light input just after the slow oscillations, so their spindle could form a triple rhythm (in phase): slow oscillation-spindle-ripples. In the second group the light stimulations were applied later “out of sync”. The third group was used as a control and did not receive any light stimulation.
The day after, mice were placed in the same location and their movement was recorded. The mice of the first group were frozen in fear 40% of the time, even in absence of the noise. On the contrary, mice in the second and third groups only froze up to 20%. Instead, when the mice heard the same tone in a different location, remembered the tone and froze in fear up to 40% of the time, independently from the group they belonged to. The hippocampus is involved in spatial memories which might explain the difference.
The opposite was also true: it was possible to make mice forget. By reducing the number of overnight spindles, the researchers could reduce the memory recall.
The research team thinks that the thalamus is the coordinator of long-term memory consolidation, the process where recently acquired information is transferred from the hippocampus to the cortex to be filed away as long-term memory. The hippocampus is like a hub, where a lot of information comes in and has to be redirected to the correct destination within the brain, especially to the cortex. This study shows that the thalamus seems to mediate the information exchange between hippocampus and cortex. “We think that memorization during deep sleep has to do with time coordination. If the hippocampus tries to exchange information when the cortex neurons are not ready to receive it, the information could be wasted,” describes Latchoumane. “Slow oscillations might be the signal used by the cortex to flag that it is ready to accept information. Then, the thalamus would alert the hippocampus via the spindles.”
It is possible to foresee that patients with memory deficiencies could benefit from translation of this research into humans. However, several points need to be clarified: can we manipulate single memories independently? Is the REM phase influencing the outcome? How is stored memory retrieved? While waiting for the next research outcomes on the science of sleep, sweet dreams… and sweet memories too.
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Source: Jung Gyu Kim – Institute For Basic Science
Image Source: NeuroscienceNews.com image is credited to IBS.
Original Research: Abstract for “Thalamic Spindles Promote Memory Formation during Sleep through Triple Phase-Locking of Cortical, Thalamic, and Hippocampal Rhythms” by Charles-Francois V. Latchoumane, Hong-Viet V. Ngo, Jan Born, and Hee-Sup Shin in Neuron. Published online July 6 2017 doi:10.1016/j.neuron.2017.06.025
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Institute For Basic Science “Controlling Memory By Triggering Specific Brain Waves During Sleep.” NeuroscienceNews. NeuroscienceNews, 6 July 2017.
<http://neurosciencenews.com/memory-sleep-brain-waves-7040/>.
<http://neurosciencenews.com/memory-sleep-brain-waves-7040/>.
Abstract
Thalamic Spindles Promote Memory Formation during Sleep through Triple Phase-Locking of Cortical, Thalamic, and Hippocampal Rhythms
Highlights
•Spindles in-phase with slow oscillation up-states boost hippocampus-dependent memory
•Phase coupling of slow oscillations, spindles, and ripples underlies memory formation
•Thalamic spindle stimulation drives cross-regional co-occurrence of spindles
•Thalamic inhibition phase-locked to slow oscillation up-states impairs memory
Summary
While the interaction of the cardinal rhythms of non-rapid-eye-movement (NREM) sleep—the thalamo-cortical spindles, hippocampal ripples, and the cortical slow oscillations—is thought to be critical for memory consolidation during sleep, the role spindles play in this interaction is elusive. Combining optogenetics with a closed-loop stimulation approach in mice, we show here that only thalamic spindles induced in-phase with cortical slow oscillation up-states, but not out-of-phase-induced spindles, improve consolidation of hippocampus-dependent memory during sleep. Whereas optogenetically stimulated spindles were as efficient as spontaneous spindles in nesting hippocampal ripples within their excitable troughs, stimulation in-phase with the slow oscillation up-state increased spindle co-occurrence and frontal spindle-ripple co-occurrence, eventually resulting in increased triple coupling of slow oscillation-spindle-ripple events. In-phase optogenetic suppression of thalamic spindles impaired hippocampus-dependent memory. Our results suggest a causal role for thalamic sleep spindles in hippocampus-dependent memory consolidation, conveyed through triple coupling of slow oscillations, spindles, and ripples.
“Thalamic Spindles Promote Memory Formation during Sleep through Triple Phase-Locking of Cortical, Thalamic, and Hippocampal Rhythms” by Charles-Francois V. Latchoumane, Hong-Viet V. Ngo, Jan Born, and Hee-Sup Shin in Neuron. Published online July 6 2017 doi:10.1016/j.neuron.2017.06.025
What’s the Difference Between Alzheimer’s Disease and Dementia?
Not all dementia is Alzheimer’s—but it can be just as devastating when it affects loved ones.
While often used interchangeably, dementia and Alzheimer’s disease are not the same. Dementia is a general term for a decline in mental ability severe enough to interfere with daily life. Alzheimer’s disease is a specific type of dementia that causes memory loss and impairment of other important mental functions. An expert from the Texas A&M School of Public Health describes how these conditions can impact the lives of both patients and those around them, and provides insights into ways of minimizing risks.
Dementia (and Alzheimer’s)
“Dementia is an umbrella term for a serious decline in mental ability that impacts one’s overall health and functioning,” said Marcia Ory, PhD, MPH, head of the Center for Population Health and Aging and Regents and Distinguished Professor at the Texas A&M School of Public Health. “There are different types of dementia, and the most common type of dementia is Alzheimer’s.”
Alzheimer’s disease makes up between 60 to 80 percent of dementia cases. It is a progressive disease, which means that the symptoms gradually worsen over a number of years. Alzheimer’s is also the sixth-leading cause of death in the United States, and those with Alzheimer’s live an average of eight years after their symptoms became noticeable to others.
Other specific types of dementia include vascular dementia and mixed dementia. Vascular dementia is considered the second-most common form of dementia after Alzheimer’s disease and is usually the result from injuries to the vessels supplying blood to the brain—often after a stroke or series of strokes.
Other less-common types of dementia come from frontotemporal disorders and Lewy body dementia. Frontotemporal disorders are a form of dementia caused by a family of brain diseases known as frontotemporal lobar degeneration (FTLD), and Lewy body dementia is caused by abnormal deposits of a protein—called alpha-synuclein—in the brain.
Mixed dementia is a term that describes having multiple types of dementia, such as both Alzheimer’s disease and vascular dementia. In a person with mixed dementia, it may not be clear which symptoms are attributed to one type of dementia over the other. Researchers are still working to understand how the disease processes influence one another in mixed dementia patients.
In some cases, it’s not known what type of dementia someone has or if it’s not a specific, named type at all. The causes of dementia are not always known, and some older people may develop age-associated memory impairment—which is different than dementia and Alzheimer’s disease.
Risk factors for dementia
Two of the most common risk factors for Alzheimer’s and dementia are age and genetics. Most individuals with Alzheimer’s are 65 or older, and those who have a parent or sibling with Alzheimer’s are more likely to develop the disease. However, there is evidence to suggest that there are other factors that people can influence.
According to research from the University of Cambridge, one-third of Alzheimer’s disease cases were attributed to preventable risk factors. The seven main risk factors for Alzheimer’s disease are diabetes, hypertension, obesity, physical inactivity, depression, smoking and low educational attainment.
“Minimizing the risk of these factors can potentially minimize the onset of dementia, but to an unknown degree,” Ory said. “We know that physical activity, a healthy diet and healthy lifestyle can help reduce the symptomology of many major diseases, and similarly these can affect the onset and progression of dementia symptomatology.”
If you’re looking for a start to reducing the risk for dementia or Alzheimer’s, a healthy diet and getting enough exercise is a good start. Exercise has been shown to increase blood flow and help connections between neurons, which is important with cognitive functioning.
“Systematic review of all the studies of physical activity conclude that it’s a modifiable risk factor,” Ory said. “We don’t know what type, how much or how often we should exercise. Further, the newest frontier is to go beyond a single risk factor approach and identify all the good behaviors—such as diet, exercise and cognitive exercises—and examine how the combination can lower the risk or symptomology of dementia.”
Overall, because there are multiple risk factors, the solutions should be multi-pronged intervention programs. “Similar to how there are a lot of risk factors for falls, there are a lot of risk factors that increase likelihood of dementia,” Ory said. “It’s complicated to minimize the risk, but you’ll do best with multi-dimensional approach.”
Talking with your health care provider
Aging is a difficult process for many people, and talking to your health care provider about your concerns can be very beneficial. They can provide you with information and resources to help ease your concerns or improve your quality of life if you have any of these conditions.
“There are simple screening tests that health care professionals can perform during routine medical visits,” Ory said. “Knowing the signs and symptomatology of dementia is important as there are medications that can reduce your symptomatology, and, along with being more active and engaging in other healthy lifestyles, can improve your quality of life.”
Although there are no medications or treatment that can cure dementia or Alzheimer’s, medications and a healthy lifestyle will help you process your condition as well as possible. Ask your physician about safety and limitations. There is nothing shameful about having dementia.
“Before people talked about dementia in medical terms, they’d say that the patient was ‘crazy’ or ‘senile,’” Ory said. “People don’t use those terms now because they recognize it’s a medical condition and not about personality or willpower. Alzheimer’s and dementia are far too common and are not something we can ignore.”
Ory also recommended that caregivers of someone with dementia look into programs or support groups. “Don’t ignore your own care when you are caring for someone with dementia,” she said. “It takes a group effort sometimes, and joining a program or being able to discuss the difficulties with others or experts, can help immensely.”
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Source: Holly Shive – Texas A&M
Image Source: NeuroscienceNews.com image is adapted from the Texas A&M news release.
Hidden Herpes Virus May Play Role in Multiple Sclerosis and Other Brain Disorders
Hidden Herpes Virus May Play Role in Multiple Sclerosis and Other Brain Disorders
Summary: A new study in Scientific Reports concludes human herpesvirus 6 may impair the brain’s ability to repair itself in demylination diseases, such as multiple sclerosis. HHV-6 is the most common human herpes virus, with an estimated 80% of people being exposed to infection during childhood. Researchers found the virus produces a protein that can impair the ability of brain cells to repair damaged myelin.
Source: University of Rochester Medical Center.
The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain’s ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.
“While latent HHV-6 — which can be found in cells throughout the brain — has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases,” said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. “These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin.”
It is estimated that more than 80 percent of people have been exposed to HHV6 at some point during their early childhood. HHV-6 is the most common human herpesvirus and infections that occur during childhood often go unnoticed but the virus can cause roseola, which is characterized by a fever and rash in infants. A much smaller number — one percent of people -have congenital HHV6 where a single copy of the virus is acquired through either the father’s sperm or mother’s egg and is passed on to the developing child.
While the immune system fights off the most active forms of the infection, the virus never truly leaves our bodies and can reactivate later in life. The herpesvirus 6 accomplishes this form of latency by integrating itself into our genetic code and thus hiding in cells and evading the immune system.
One of the first studies to show an association between latent HHV-6 infection and demyelinating disorders was conducted in 2003 by URMC researchers David Mock, M.D., who is a co-author of the current study, Andrew Goodman, M.D. and others. They noted that HHV6 genetic code could be found in the brain cells of individuals with severe forms of multiple sclerosis.
Viruses have long been suspected to contribute to multiple sclerosis, a disorder in which the body’s own immune system attacks and destroys myelin — the fatty tissue that insulates the connections between nerve cells. However, while the 2003 study indicated that the herpes virus played some role in multiple sclerosis, it has subsequently become clear that the virus is unlikely to trigger the disease.
The Rochester researchers in the current paper took a new approach and asked instead whether the virus could have an impact on a critical support cell found in the brain called oligodendrocyte progenitor cells (OPCs). These cells play an important role in maintaining the brain’s supply of myelin. When myelin is lost to disease, age, or injury, OPCs are activated, migrate to where they are needed, and mature into myelin-producing cells which repair the damage.
The researchers examined the impact of the latent HHV-6 on the activity of human OPCs, which was possible through the work of Chris Proschel, a co-author of the manuscript with expertise in the generation of human OPCs. One of the ways the virus stays hidden in cells is by expressing a protein called U94 that helps it keep its place in the human DNA and remain undetected from the immune system. By studying human cells and transplanting human OPCs into animal models, the team discovered that when U94 was expressed in OPCs, the cells stopped migrating to where they were needed.
What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?
“More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases,” said Mayer-Proschel. “But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases.”
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Additional authors of the study include Andrew Campbell, Jessica Hogestyn and Brittany Lopez with URMC and Christopher Folts with Harvard Medical School.
Funding: The study was supported with funding from National Multiple Sclerosis Society, the New York State Department of Health, and the Link Foundation.
Source: Mark Michaud – University of Rochester Medical Center
Image Source: NeuroscienceNews.com image is credited to the National Cancer Institute.
Original Research: Full open access research for “Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration” by Andrew Campbell, Jessica M. Hogestyn, Christopher J. Folts, Brittany Lopez, Christoph Pröschel, David Mock & Margot Mayer-Pröschel in Scientific Reports. Published online June 21 2017 doi:10.1038/s41598-017-04432-y
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University of Rochester Medical Center “Hidden Herpes Virus May Play Role in Multiple Sclerosis and Other Brain Disorders.” NeuroscienceNews. NeuroscienceNews, 10 July 2017.
<http://neurosciencenews.com/hhv6-herpes-ms-7050/>.
<http://neurosciencenews.com/hhv6-herpes-ms-7050/>.
Abstract
Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration
Progression of demyelinating diseases is caused by an imbalance of two opposing processes: persistent destruction of myelin and myelin repair by differentiating oligodendrocyte progenitor cells (OPCs). Repair that cannot keep pace with destruction results in progressive loss of myelin. Viral infections have long been suspected to be involved in these processes but their specific role remains elusive. Here we describe a novel mechanism by which HHV-6A, a member of the human herpesvirus family, may contribute to inadequate myelin repair after injury.
“Expression of the Human Herpesvirus 6A Latency-Associated Transcript U94A Disrupts Human Oligodendrocyte Progenitor Migration” by Andrew Campbell, Jessica M. Hogestyn, Christopher J. Folts, Brittany Lopez, Christoph Pröschel, David Mock & Margot Mayer-Pröschel in Scientific Reports. Published online June 21 2017 doi:10.1038/s41598-017-04432-y
The New Yorker: Donald Trump Is Dragging Down America
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Health Care from Bernie Sanders
This is what Sen. Mitch McConnell woke up to this morning:
I want to thank all of you who supported our trip this weekend to West Virginia and Kentucky, two states at the center of the fight over the disastrous Republican health care legislation which could come up for a vote this week or next. We wanted to go right into deeply Republican states and tell the working people there what it means to throw 22 million Americans off of health insurance, cut Medicaid by almost $800 billion, raise premiums for older workers and defund Planned Parenthood – all to provide $500 billion in tax breaks to the top 2 percent, insurance companies and the pharmaceutical industry.
Our goal was to put this horrible legislation in human terms. At each of our events ordinary Americans stood up and told their stories of what the disastrous Republican health care bill would do to them and their loved ones. It takes a lot of courage to get up in front of a large crowd, along with the hundreds of thousands who watched the events online, and talk about very personal issues. But they did it, and I want to thank them all for speaking up for millions of Americans who face similar problems.
We heard from a man in West Virginia with hemophilia, in need of a liver transplant, whose life was saved by the Affordable Care Act. We listened to a young woman from Fairmont, West Virginia, who requires $70,000 a year in medicine to stay alive. A young man from West Virginia who survived cancer, wondering whether he would live or die, told us about his struggles to get coverage as he watched his disease spread.
In Covington, Kentucky, we heard from a woman who relies on Medicaid to care for her father, a World War II veteran. We listened to a young mother whose son needed a kidney transplant at 18 months old, but is now a happy five year old. He will require medication for the rest of his life and will always have a preexisting condition. They and other worried out loud what happens if, once again, people with pre-existing conditions are unable to get affordable medical care. How will they stay alive?
We also heard from a mother in Kentucky, a mental health provider in West Virginia, and the Mayor of Covington, Joe Mayer, about the impact the opioid crisis has had on his city and the region.
You can watch these and other incredible stories from our tour this weekend here.
Let us never forget: a great nation is not judged by the number of billionaires it has, or by the tax breaks they receive. It is judged by how we treat the most vulnerable amongst us: the children, the sick, the elderly, the disabled and the poor.
That is why our first job is to defeat the moral outrage that is the Trump-Ryan-McConnell health plan. Get involved and make sure you make your voice heard this week.
But defeating this terrible bill is not enough. Our next job is to organize nationally to demand that the United States joins every other major country on earth in guaranteeing health care for all as a right through a Medicare-for-all, single-payer program.
Thank you for all you are doing.
In solidarity,
Bernie Sanders
Association of Coffee Consumption With Total and Cause-Specific Mortality Among Nonwhite Populations
Chewing and brain growth: Reduced Mastication Impairs Memory and Learning Function
Chewing and brain growth: Reduced Mastication Impairs Memory and Learning Function
According to researchers, the frequency of mastication has dramatically decreased along with changes in dietary habits. Masticatory stimulation has influence on the development of the central nervous system as well as the growth of maxillofacial tissue in children. Deterioration of masticatory function due to aging and the consequent reduction of brain function has become major problems. Although the relationship between mastication and brain function is potentially important, the mechanism underlying is not fully understood.
In order to prevent brain function disorders, including those relating to memory and learning, it is an urgent task to elucidate the linkage between masticatory function and brain function.
Researchers found that growth of the maxillofacial bone and muscle were suppressed in mice with reduced masticatory stimuli by feeding with powder food. In addition, behavioral experiments revealed that reduced mastication impaired memory and learning functions. In the hippocampus, a major component responsible for memory, neural activity, synapse formation and expression of brain-derived neurotrophic factor (BDNF) were reduced in these mice .
Thus, the authors demonstrated that the changes in masticatory stimuli can modulate neurogenesis and neuronal activity in the hippocampus, functionally contributing to cognitive function.
This research suggests that maintaining or strengthening of masticatory function would be effective in preventing dementia and memory/learning dysfunction. It is also suggested that further elucidation of the mechanism linking mastication and brain function can lead to novel treatments and preventive measures for memory/learning dysfunction in the future.
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Funding: Japan Agency for Medical Research and Development, Japan Science and Technology Agency, Ministry of Education, Culture, Sports, Science and Technology funded this study.
Source: Takashi Ono – Tokyo Medical and Dental University
Image Source: NeuroscienceNews.com image is credited to Department of Cell Signaling,Department of Orthodontic Science (TMDU).
Original Reserch: Abstract for “Reduced Mastication Impairs Memory Function” by Y. Fukushima-Nakayama, Takehito Ono, M. Hayashi, M. Inoue, H. Wake, Takashi Ono, and T. Nakashima in Journal of Dental Research. Published online June 16 doi:10.1177/0022034517708771
Tokyo Medical and Dental University “Chew On This: Reduced Mastication Impairs Memory and Learning Function.” NeuroscienceNews. NeuroscienceNews, 10 July 2017.
<http://neurosciencenews.com/mastication-memory-learning-7052/>.
<http://neurosciencenews.com/mastication-memory-learning-7052/>.
Abstract
Reduced Mastication Impairs Memory Function
Mastication is an indispensable oral function related to physical, mental, and social health throughout life. The elderly tend to have a masticatory dysfunction due to tooth loss and fragility in the masticatory muscles with aging, potentially resulting in impaired cognitive function. Masticatory stimulation has influence on the development of the central nervous system (CNS) as well as the growth of maxillofacial tissue in children. Although the relationship between mastication and cognitive function is potentially important in the growth period, the cellular and molecular mechanisms have not been sufficiently elucidated.
Here, we show that the reduced mastication resulted in impaired spatial memory and learning function owing to the morphological change and decreased activity in the hippocampus.
We used an in vivo model for reduced masticatory stimuli, in which juvenile mice were fed with powder diet and found that masticatory stimulation during the growth period positively regulated long-term spatial memory to promote cognitive function.
The functional linkage between mastication and brain was validated by the decrease in neurons, neurogenesis, neuronal activity, and brain-derived neurotrophic factor (BDNF) expression in the hippocampus.
These findings taken together provide in vivo evidence for a functional linkage between mastication and cognitive function in the growth period, suggesting a need for novel therapeutic strategies in masticatory function–related cognitive dysfunction.
“Reduced Mastication Impairs Memory Function” by Y. Fukushima-Nakayama, Takehito Ono, M. Hayashi, M. Inoue, H. Wake, Takashi Ono, and T. Nakashima in Journal of Dental Research. Published online June 16 doi:10.1177/0022034517708771
Association of Coffee Consumption With Total and Cause-Specific Mortality Among Nonwhite Populations
Higher consumption of coffee was associated with lower risk for death in African Americans, Japanese Americans, Latinos, and whites.
Coffee is one of the most widely consumed beverages in the world and in the U.S. population (1). Therefore, even a small health-promoting effect of coffee could have a substantial impact on public health. Previous studies have indicated that coffee consumption is inversely associated with several types of cancer (2), diabetes (3, 4), liver disease (5), Parkinson disease (6, 7), and other chronic diseases (8). Cohort studies have shown that coffee consumption is associated with lower risk for total and cause-specific death (8–10). However, these studies included mainly white participants, and their results may not be generalizable to other populations with different lifestyles, confounding factors, and disease susceptibilities. Data in U.S. minority populations are scarce, and research is needed in nonwhite populations (10).
This study examined the association between coffee drinking and risk for total and cause-specific death among more than 185 000 African Americans, Japanese Americans, Native Hawaiians, Latinos, and whites in the MEC (Multiethnic Cohort) study.
The MEC is a prospective cohort of more than 215 000 adults aged 45 to 75 years who were enrolled between 1993 and 1996. The MEC study design and baseline characteristics have been described in detail previously (11). Potential participants were identified by means of Department of Motor Vehicles driver’s license records, voter registration lists, and Health Care Financing Administration data files. The response rates were highest in Japanese Americans (51%), whites (47%), and Native Hawaiians (42%) and lowest in African Americans (26%) and Latinos (21%). A baseline questionnaire assessed diet; lifestyle; anthropometrics; family and personal medical history; and, for women, menstrual and reproductive history and hormone use. For this analysis, we excluded participants who were not in the 5 main ethnic groups (n = 13 986), had implausible dietary energy and macronutrient intakes (n = 8258), or were missing smoking information (n = 7521). The resulting cohort included 185 855 participants for the final analysis. The Institutional Review Boards of the University of Southern California and the University of Hawai’i approved this study.
Assessment of Coffee Consumption and Covariates
Dietary information, including coffee consumption, was obtained using a quantitative food-frequency questionnaire (QFFQ) designed for use in this multiethnic population (11). A calibration study of the QFFQ was conducted using three 24-hour recalls from a random subsample of participants selected within groups based on sex and race/ethnicity (12); this study revealed a high correlation between the QFFQ and 24-hour recalls for energy-adjusted nutrients. The median correlation coefficient for coffee intake was 0.72, as assessed by the QFFQ and 24-hour recalls (13). On the baseline QFFQ, participants were asked to indicate their average consumption of caffeinated and decaffeinated coffee in the previous year using 9 predefined categories from “never or hardly ever” to “4 or more cups daily.” Data on potential confounders, such as education level, body size, diabetes, smoking history, and alcohol intake, were obtained from the baseline questionnaire. Body mass index (BMI) was calculated by dividing weight (in kilograms) by the square of height (in meters).
Assessment of Death
We ascertained deaths by means of annual linkage to files of state death certificates in California and Hawaii and periodic linkage to the National Death Index. Death ascertainment ended on 31 December 2012. The primary outcome was total mortality. Secondary outcomes were mortality from the 10 leading causes of death in the United States that accounted for 74% of deaths in 2014 (14). We used codes from the International Classification of Diseases, Ninth Revision (ICD-9) and 10th Revision (ICD-10), to classify the primary cause of death specified on each certificate. Causes were defined as follows: heart disease (ICD-9 codes 390 to 398, 402, 404, and 410 to 429; ICD-10 codes I00 to I09, I11, I13, and I20 to I51), cancer (ICD-9 codes 140 to 239; ICD-10 codes C00 to C97 and D00 to D48), chronic lower respiratory disease (ICD-9 codes 490 to 494 and 496; ICD-10 codes J40 to J47), stroke (ICD-9 codes 430 to 434 and 436 to 438; ICD-10 codes I60 to I69), accident (ICD-9 codes E800 to E869 and E880 to E929; ICD-10 codes V01 to X59 and Y85 to Y86), Alzheimer disease (ICD-9 code 331.0; ICD-10 code G30), diabetes mellitus (ICD-9 code 250; ICD-10 codes E10 to E14), influenza and pneumonia (ICD-9 codes 480 to 487; ICD-10 codes J10 to J18), kidney disease (ICD-9 codes 580 to 589; ICD-10 codes N00 to N07, N17 to N19, and N25 to N27), and intentional self-harm (ICD-9 codes E950 to E959; ICD-10 codes X60 to X84 and Y87.0).
Statistical Analysis
We categorized coffee consumption as never, 1 to 3 cups per month, 1 to 6 cups per week, 1 cup per day, 2 to 3 cups per day, and 4 or more cups per day. Similar categories were used for caffeinated and decaffeinated coffee, with those who never drink coffee as the reference group. In the analysis of coffee type, we examined consumption of exclusively caffeinated and exclusively decaffeinated coffee. We used multiple imputation, based on 5 replications and the Markov-chain Monte Carlo method in the SAS MI procedure, to account for missing data on education, BMI, and physical activity. This resulted in the exclusion of 30 participants for whom imputation was not possible. We also performed sensitivity analyses using a complete-case analysis (n = 174 579).
Follow-up time for each participant was calculated from the date of cohort entry to the date of death or the end of follow-up (31 December 2012). Hazard ratios (HRs) and 95% CIs were calculated for mortality associated with coffee intake, using Cox proportional hazards models with age as the underlying time metric. Cox models were first adjusted for the strata variables of age at cohort entry (<50, 50 to 54, 55 to 59, 60 to 64, 65 to 69, 70 to 74, or ≥75 years), sex, and race/ethnicity. They were further adjusted for smoking using a detailed model to account for smoking cessation over time, which was common but varied by race/ethnicity (15). Smoking variables included ethnicity, smoking status, average number of cigarettes, squared average number of cigarettes, number of years smoking (time-dependent), number of years since quitting (time-dependent), and interactions between ethnicity and smoking status. The Cox models were then further adjusted for the following covariables in the log-linear component: BMI (<18.5, 18.5 to 22.9, 23.0 to 24.9, 25.0 to 29.9, 30.0 to 34.9, or ≥35.0 kg/m2), education (high school or less, vocational school or some college, or college graduate), vigorous physical activity (for men, <0.1, 0.1 to <0.25, 0.25 to <0.80, or ≥0.80 hour per day; for women, <0.1, 0.1 to <0.25, 0.25 to <0.5, or ≥0.5 hour per day), alcohol (ethanol) consumption (for men, 0, 1 to <5.2, 5.2 to <23, or ≥23 g/d; for women, 0, 1 to <2.5, 2.5 to <10, or ≥10 g/d), total energy intake (<1317, 1317 to 1717, 1718 to 2159, 2160 to 2835, or ≥2836 kcal/d), energy from fat (<23.7%, 23.7% to 28.0%, 28.1% to 31.8%, 31.9% to 35.9%, or ≥36.0%), and preexisting chronic disease at baseline (self-reported heart attack or angina, stroke, diabetes, or high blood pressure, and cancer that was self-reported or ascertained from tumor registries).
We performed tests for linear trend by entering the median value of each category of coffee consumption as a continuous variable in the models. A competing risk analysis was done to compare the association with coffee intake among causes of death, where each cause was simultaneously modeled as a different event (16). We used a Wald test to compare the parameter estimates between causes of death. The proportional hazards assumption over all ages was tested by modeling the interaction of age with coffee consumption, and no violation was found. Direct adjusted mortality curves by category of coffee consumption were computed over the age range from the Cox model as the average of the model-based curves at observed profiles for the following covariates (17, 18): age at cohort entry; sex; ethnicity; smoking status; average number of cigarettes; squared average number of cigarettes; number of years smoking; number of years since quitting; interactions between ethnicity and smoking status, average number of cigarettes, squared average number of cigarettes, and number of years smoking; BMI; education; physical activity; alcohol consumption; total energy intake; energy from fat; and preexisting illness.
We did subgroup analyses by race/ethnicity, sex, age at cohort entry, and smoking status. Heterogeneity across subgroups was tested using the Wald statistics for cross-product terms of trend variables and subgroup membership. To assess potential reverse causality, we performed sensitivity analysis by excluding deaths that occurred within the first 5 years of follow-up. We also did a formal sensitivity analysis, as described by Lin and colleagues (19), to assess the potential effect of unmeasured confounding on our results. For all analyses, we used SAS, version 9.4 (SAS Institute). All P values were 2-sided.
Role of the Funding Source
The MEC was supported by the National Cancer Institute, which had no role in the study design; recruitment; data collection and analysis; or preparation, approval, or publication of the manuscript.
Results
Baseline Characteristics of Study Participants, by Coffee Consumption
About 16% of participants did not drink coffee, 7% drank 1 to 3 cups per month, 13% drank 1 to 6 cups per week, 31% drank 1 cup per day, 25% drank 2 to 3 cups per day, and 7% drank 4 or more cups per day (Table 1). Participants who drank more coffee were more likely to be younger, male, and white and to drink more alcohol. There was a strong correlation between higher coffee consumption and smoking status; among non–coffee drinkers, 58% were never-smokers, but among those who drank 4 or more cups per day, 26% were never-smokers. The proportion of preexisting illness at baseline was lower among participants who drank coffee more frequently.
Table 1. Baseline Characteristics of Participants in the Multiethnic Cohort, by Coffee Consumption*
Association of Coffee Consumption With Total Mortality
During an average of 16.2 years of follow-up (3 195 484 person-years), we identified 58 397 deaths in the cohort. In the age-, sex-, and ethnicity-adjusted analysis, consuming 4 or more cups of total (caffeinated and decaffeinated) coffee per day was associated with a higher risk for all-cause death (Table 2). However, after adjustment for smoking and other covariates, we saw significant inverse associations between increasing coffee consumption and all-cause mortality. The HR for death (vs. no coffee) was 1.00 (95% CI, 0.95 to 1.05) for 1 to 3 cups of coffee per month, 0.97 (CI, 0.93 to 1.01) for 1 to 6 cups per week, 0.88 (CI, 0.85 to 0.91) for 1 cup per day, 0.82 (CI, 0.79 to 0.86) for 2 to 3 cups per day, and 0.82 (CI, 0.78 to 0.87) for 4 or more cups per day. Exclusive consumption of either caffeinated coffee (P for trend < 0.001) or decaffeinated coffee (P for trend = 0.008) was inversely associated with total mortality. Associations were similar in men and women (Appendix Table 1).
Table 2. Coffee Consumption and Total Mortality in the Multiethnic Cohort, 1993–2012
Appendix Table 1. Coffee Consumption and Total Mortality in the Multiethnic Cohort, by Sex, 1993–2012
The adjusted mortality rates by different levels of coffee consumption are presented in the Figure. The inverse association applies to consumption of at least 1 to 6 cups of caffeinated coffee per week and seems to be monotonic with increased consumption.
FIGURE.
Adjusted mortality in the Multiethnic Cohort, by age by category of coffee consumption, 1993–2012.
Direct adjusted curves were generated using the Cox model as the average of the model-based curves at observed profiles for the following covariates: age at cohort entry, sex, ethnicity, smoking variables (smoking status; average number of cigarettes; squared average number of cigarettes; number of years smoking [time-dependent]; number of years since quitting [time-dependent]; and interactions between ethnicity and smoking status, average number of cigarettes, squared average number of cigarettes, and number of years smoking), body mass index, education, physical activity, alcohol consumption, total energy intake, energy from fat, and preexisting illness. For categorical covariates, dummy variables were used. The “None” and “1-3 cups/mo” lines overlap.
The results of the sensitivity analysis indicated that the associations between coffee consumption and mortality were robust to unmeasured confounders, except in the case of a strong unmeasured confounder, on the order of smoking or diabetes, that was substantially associated with coffee drinking (Appendix Table 2).
Appendix Table 2. HRs for Consumption of ≥4 Cups per Day Compared With Nondrinkers, Corrected for Different Levels of Confounding by an Unmeasured Dichotomous Confounder Using Sensitivity Analysis*
Association of Coffee Consumption With Total Mortality, by Race/Ethnicity
We examined the association of coffee consumption and total mortality across the 5 racial/ethnic groups in the MEC (Table 3). We found no indication that the associations varied by race/ethnicity (P for heterogeneity = 0.166). Coffee consumption was significantly associated with lower risk for death in African Americans (P for trend = 0.001), Japanese Americans (P for trend < 0.001), Latinos (P for trend = 0.002), and whites (P for trend = 0.003). Although similar patterns were seen for Native Hawaiians, these associations did not reach statistical significance (P for trend = 0.141).
Table 3. Coffee Consumption and Total Mortality in the Multiethnic Cohort, by Race/Ethnicity, 1993–2012*
Association of Coffee Consumption With Cause-Specific Mortality
The 10 leading causes of death in the United States accounted for 81% of deaths in the MEC, with cardiovascular disease (36%) and cancer (31%) accounting for the largest proportions. We investigated the associations between coffee consumption and each of the 10 leading causes of death (Table 4). Coffee consumption was inversely associated with risk for death due to heart disease (P for trend < 0.001), cancer (P for trend = 0.023), chronic lower respiratory disease (P for trend = 0.015), stroke (P for trend < 0.001), diabetes (P for trend = 0.009), and kidney disease (P for trend < 0.001). There was no significant association between coffee consumption and deaths from influenza and pneumonia, Alzheimer disease, accidents, and intentional self-harm. In a competing risk analysis, the association of mortality with coffee consumption did not statistically differ among causes of death (P = 0.92).
Table 4. Coffee Consumption and Cause-Specific Mortality in the Multiethnic Cohort, 1993–2012*
Subgroup Analyses
Smoking is a known strong confounder of the coffee–mortality association. We therefore examined the associations between coffee consumption and mortality stratified by smoking status (Table 5). In never-smokers, former smokers, and current smokers, coffee consumption was inversely associated with total mortality (P for heterogeneity = 0.120).
Table 5. Coffee Consumption and Total Mortality in the Multiethnic Cohort, by Smoking Status at Baseline, 1993–2012
We conducted a stratified analysis by baseline health status (Appendix Table 3). We found significant inverse associations of coffee consumption with total mortality among participants with self-reported heart disease and cancer at baseline. Among participants without self-reported heart disease and cancer at baseline who were never-smokers, we saw similar inverse associations between coffee consumption and total mortality. We conducted stratified analysis by age at cohort entry (<55, 55 to 70, and >70 years) and education level (high school or less, vocational school or some college, and college graduate) (Appendix Table 4). Inverse associations were found in all subgroups (P for trend ≤ 0.014 for each), with a stronger association in younger participants (P for heterogeneity = 0.019). In sensitivity analyses excluding deaths within the first 5 years of follow-up, the inverse associations between total coffee consumption and total mortality remained statistically significant.
Appendix Table 3. Coffee Consumption and Total Mortality in the Multiethnic Cohort, by Baseline Health Status, 1993–2012
Appendix Table 4. Coffee Consumption and Total Mortality, by Age Group and Education Level, in the Multiethnic Cohort, 1993–2012*
Discussion
In this large multiethnic population, we found an inverse association between coffee consumption and total mortality after adjustment for smoking and other potential confounders. Similar trends were observed for caffeinated and decaffeinated coffee. Among the 10 leading causes of death in the United States, mortality was inversely related to coffee consumption for heart disease, cancer, respiratory disease, stroke, diabetes, and kidney disease. Inverse associations were seen in never-smokers, former smokers, and current smokers; 4 of 5 racial/ethnic groups; those with and without preexisting heart disease and cancer; those with different education levels; and all age groups.
Overall, our finding of decreased risk for all-cause death with coffee consumption is consistent with meta-analyses (8, 20–22) and subsequent cohort studies done in the United States (9, 10), Europe (23, 24), and Japan (25). Risk reduction for all-cause death in our study was 18% (CI, 14% to 21%) for 2 to 3 cups versus 0 cups of coffee per day, which was similar to previous reports from other large U.S. cohorts. The Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (10) saw a risk reduction of 18% (CI, 12% to 23%), and the National Institutes of Health–AARP Diet and Health Study (26) found risk reductions of 10% (CI, 7% to 14%) in men and 13% (CI, 8% to 17%) in women. In a pooled analysis of the Nurses’ Health Study, Nurses’ Health Study II, and Health Professionals Follow-up Study, drinking more than 1 to 3 cups of coffee per day was associated with 9% (CI, 5% to 12%) lower risk for all-cause death than drinking no coffee (9).
However, until now, few data have been available on the association between coffee consumption and mortality in nonwhites in the United States and elsewhere. Such investigations are important because lifestyle patterns and disease risks can vary substantially across racial/ethnic backgrounds, and findings in one group may not necessarily apply to others. On the other hand, findings that persist across different racial/ethnic groups have greater biological plausibility. Because of the unique opportunity that the MEC provides, we were able to investigate the coffee–mortality associations in participants from 5 racial/ethnic backgrounds using the same method and as part of the same cohort. We saw similar inverse associations between coffee drinking and mortality in 4 of the 5 racial/ethnic groups; the association in Native Hawaiians did not reach statistical significance, likely owing to fewer participants in that group.
Our findings for specific causes of death were generally similar to those of previous cohorts (9, 10, 26). One difference was for cancer mortality. Several recent cohort studies (9, 10, 23, 25) and 2 meta-analyses (20, 21) of prospective studies reported no significant association between total cancer mortality and coffee consumption, although other studies have reported inverse associations (24). We saw a modest reduction in risk for cancer death (8% lower risk with 2 to 3 cups vs. 0 cups per day). One advantage of our study was our ability to comprehensively adjust for cigarette smoking, a strong cancer risk factor, which may have allowed us to observe an inverse association with cancer mortality. We note that our findings persisted across several strategies for controlling for smoking, including analyses by smoking subgroup and models that adjusted for smoking information collected only at baseline (smoking status, years smoking, and number of cigarettes).
We also examined whether associations varied by age at enrollment. Two previous studies have reported inconsistent associations between coffee drinking and mortality in younger people. One cohort reported increased risk for all-cause death among persons younger than 55 years who drank more than 4 cups per day (27), whereas a second study found no association among women younger than 50 years (23). We found inverse associations across categories of age at enrollment in our cohort, although the association seemed stronger in younger participants than in older ones. Hazard ratios among younger participants (<55 years) in the cohort were 0.85 (CI, 0.77 to 0.95) for 1 cup, 0.73 (CI, 0.66 to 0.82) for 2 to 3 cups, and 0.74 (CI, 0.64 to 0.85) for 4 or more cups per day. Therefore, our findings do not suggest a harmful effect of coffee consumption among younger adults.
Coffee contains many biologically active chemicals, including caffeine and phenolic compounds, that may impact health by means of various mechanisms, such as antioxidant and antimutagenic capacity, insulin sensitivity, liver function, and chronic inflammation (28–31). We observed similar associations for both caffeinated and decaffeinated coffee, as seen in most other studies, suggesting that these associations may be related not to caffeine but to the many other compounds found in coffee. However, future mechanistic work is needed to characterize the many compounds in coffee and elucidate possible physiologic effects.
Our study has several key strengths, including its prospective design, large sample size (>185 000 participants with >58 000 deaths), relatively long follow-up (an average of 16 years), and inclusion of substantial numbers of participants from various racial/ethnic backgrounds. To reduce the effect of reverse causality, we excluded deaths within the first 5 years of follow-up in sensitivity analyses and also restricted the analyses to participants who did not report preexisting disease. We had extensive information on potential confounders (for example, smoking, alcohol use, physical activity, and preexisting illness) because of our comprehensive baseline questionnaire.
Our study also has limitations. As with any observational study, we cannot exclude the possibility of residual or unmeasured confounding. However, we are reassured by similar findings within different racial/ethnic populations in our cohort and in previous studies in the United States, Europe, and Japan. Also, a formal sensitivity analysis showed that the coffee–mortality association was robust to all but very strong levels of unmeasured confounding, which seems unlikely. On the other hand, self-reported coffee consumption at baseline is subject to measurement error, and consumption might have changed throughout follow-up. Among the participants who responded to the repeated QFFQ in 2003 to 2007 (n = 84 170) (average 11.0 years between measurements), the intraclass correlation coefficient between the 2 QFFQs was 0.60, which reflects potential changes over time or misclassification of coffee consumption. In the subset of participants with follow-up data on coffee consumption, the analysis using a time-dependent model yielded similar results. Because the highest level of coffee consumption in the QFFQ was 4 or more cups per day, we were not able to examine associations with higher levels. A recent meta-analysis of 15 prospective studies found similar associations for 4 cups per day and 5 or more cups per day (21), although the numbers of participants drinking more than 5 cups per day in epidemiologic studies have typically been small. Future studies are needed to examine associations in the heaviest coffee drinkers to address potential toxicity at high doses. In addition, we lacked information on preparation, which may affect the composition and bioavailability of coffee compounds (32).
In summary, higher coffee consumption was associated with lower risk for all-cause death and death from heart disease, cancer, respiratory disease, stroke, diabetes, and kidney disease. Inverse associations were found in African Americans, Japanese Americans, Latinos, and whites; never-smokers, former smokers, and current smokers; those with preexisting heart disease or cancer; and healthy participants. Our findings support the recent dietary guidelines from the U.S. Department of Agriculture (33), which indicate that moderate coffee consumption can be integrated into a healthy diet and lifestyle, by confirming an inverse association with mortality and suggesting that association’s generalizability to different racial/ethnic groups.
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U.S. Department of Health and Human Services and U.S. Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th ed. HHS publication no. HHS-ODPHP-2015-2020-01-DGA-A. Washington, DC: U.S. Department of Health and Human Services; 2015. Accessed at http://health.gov/dietaryguidelines/2015/guidelines on 20 March 2017.
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Purpose in Life by Day Linked to Better Sleep at Night
Purpose in Life by Day Linked to Better Sleep at Night
Source: Northwestern University
Older adults whose lives have meaning enjoy better sleep quality and less sleep apnea and restless leg syndrome.
Having a good reason to get out of bed in the morning means you are more likely to sleep better at night with less sleep apnea and restless leg syndrome, reports a new Northwestern Medicine and Rush University Medical Center study based on older adults.
This is the first study to show having a purpose in life specifically results in fewer sleep disturbances and improved sleep quality and over a long period of time. Previous research showed having a purpose in life generally improves overall sleep when measured at a single point in time.
Although the participants in the study were older, researchers said the findings are likely applicable to the broader public.
“Helping people cultivate a purpose in life could be an effective drug-free strategy to improve sleep quality, particularly for a population that is facing more insomnia,” said senior author Jason Ong, an associate professor of neurology at Northwestern University Feinberg School of Medicine. “Purpose in life is something that can be cultivated and enhanced through mindfulness therapies.”
The paper will be published Sunday, July 9, in the journal Sleep Science and Practice.
Individuals have more sleep disturbances and insomnia as they get older. Clinicians prefer to use non-drug interventions to improve patients’ sleep, a practice now recommended by the American College of Physicians as a first line treatment for insomnia, Ong said.
The next step in the research should be to study the use of mindfulness-based therapies to target purpose in life and resulting sleep quality, said Arlener Turner, the study’s first author and a former postdoctoral fellow in neurology at Feinberg.
The 823 participants — non-demented individuals 60 to 100 years old with an average age of 79 — were from two cohorts at Rush University Medical Center. More than half were African American and 77 percent were female.
People who felt their lives had meaning were 63 percent less likely to have sleep apnea and 52 percent less likely to have restless leg syndrome. They also had moderately better sleep quality, a global measure of sleep disturbance.
For the study, participants answered a 10-question survey on purpose in life and a 32-question survey on sleep. For the purpose in life survey, they were asked to rate their response to such statements as, “I feel good when I think of what I’ve done in the past and what I hope to do in the future.”
The next step in the research should be to study the use of mindfulness-based therapies to target purpose in life and resulting sleep quality, Turner said.
Poor sleep quality is related to having trouble falling asleep, staying asleep and feeling sleepy during the day. Sleep apnea is a common disorder that increases with age in which a person has shallow breathing or pauses in breathing during sleep several times per hour. This disruption often makes a person feel unrefreshed upon waking up and excessively sleepy during the day.
Restless leg syndrome causes uncomfortable sensations in the legs and an irresistible urge to move them. Symptoms commonly occur in the late afternoon or evening hours and are often most severe at night when a person is resting, such as sitting or lying in bed.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: This research was supported by grants R01AG22018, P30G10161, R01AG17917, P20MD6886 from National Institute on Aging of the National Institutes of Health and the Illinois department of public health. The cohorts were from the Minority Aging Research Study and the Rush Memory and Aging Project.
Source: Marla Paul – Northwestern University
Image Source: NeuroscienceNews.com image is in the public domain.
Original Reserch: Abstract for “Is purpose in life associated with less sleep disturbance in older adults?” by Arlener D. Turner, Christine E. Smith and Jason C. Ong in Sleep Science and Practice. Published online July 10 doi:10.1186/s41606-017-0015-6
Northwestern University “Purpose in Life by Day Linked to Better Sleep at Night.” NeuroscienceNews. NeuroscienceNews, 10 July 2017.
<http://neurosciencenews.com/sleep-day-purpose-7055/>.
<http://neurosciencenews.com/sleep-day-purpose-7055/>.
Abstract
Is purpose in life associated with less sleep disturbance in older adults?
Background
Previous work has shown that purpose in life can be protective against numerous negative health outcomes including sleep disturbances. Given that sleep disturbances are common among older adults and African Americans, the aim of the present study was to examine the relationship between purpose in life, overall sleep quality, and the presence of sleep disorders in a community-based bi-racial sample of older adults.
Methods
Participants were 825 non-demented older African Americans (n = 428) and Whites (n = 397) from two cohort studies, the Minority Aging Research Study (MARS) and the Rush Memory and Aging Project (MAP). Participants completed a 32-item questionnaire assessing sleep quality and symptoms of Sleep Apnea, Restless Leg Syndrome (RLS) and REM Behavior Disorder (RBD). Purpose in life was assessed with a 10-item measure modified from Ryff & Keyes’s scales of Psychological Well Being.
Results
In a series of hierarchical multiple linear regressions controlling for the demographic covariates of age, sex, race, and education, higher levels of purpose in life were associated with better sleep quality at baseline. Using longitudinal follow-up data, higher levels of purpose in life was associated with lower risk of sleep apnea at baseline, 1-year follow-up, and 2-year follow-up, as well as reduced symptoms of RLS at 1-year and 2-year follow-up.
Conclusions
These findings provide support for the hypothesis that a higher level of meaning and purpose in life among older adults is related to better sleep quality and appears to be protective against symptoms of sleep apnea and RLS.
“Reduced Mastication Impairs Memory Function” by Y. Fukushima-Nakayama, Takehito Ono, M. Hayashi, M. Inoue, H. Wake, Takashi Ono, and T. Nakashima in Journal of Dental Research. Published online June 16 doi:10.1177/0022034517708771