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The link between insomnia and cardiovascular disease


Sleeping problems can affect both mental and physical health. Now, a large-scale analysis in China highlights how insomnia might lead to potentially life threatening cardiovascular diseases.

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New research points to concerning links between insomnia and cardiovascular problems.

Insomnia is a relatively widespread problem. When a person has insomnia, they often struggle to fall asleep or stay asleep. Some people experience both.

Around 1 in 4 adults in the United States experience short-term, or acute, insomnia every year, according to research carried out at the University of Pennsylvania, PA. Acute insomnia typically means that a person experiences sleep problems for just a short period, perhaps due to stress or worry.

Approximately three-quarters of these people return to their regular sleeping patterns. Others, however, go on to develop chronic insomnia.

Chronic insomnia refers to a person who experiences problems sleeping for at least 3 nights a week for no less than 3 months.

Both acute and chronic insomnia can result in daytime drowsiness, concentration and memory problems, and a lack of energy.

But studies have found more worrying links. One recent analysis, appearing in Sleep Medicine Reviews, linked insomnia to the onset of depression, anxiety, and alcohol misuse. Other studies have found a relationship between insomnia and heart disease.

Now, authors of a new study, published in Neurology, point out that previous research has failed to define insomnia correctly and has included people who may not have the disorder. So they set out to find a stronger association.

Tracking insomnia

The results of the new paper suggest that identifying insomnia, particularly in young people, may reduce cardiovascular disease risk later on in life.

The researchers used data from the China Kadoorie Biobank, which investigates and tracks the leading causes of chronic diseases in China.

The participants, aged between 30 and 79, had no history of heart disease or stroke when the study commenced.

In the new study, the researchers analyzed three symptoms of insomnia, where the symptoms lasted at least 3 days a week. The symptoms were: problems falling asleep or staying asleep, waking too early, or struggling to focus during the day because of disrupted sleep.

The data show that 11% of the participants reported trouble falling or staying asleep, and 10% had problems with waking up early. Only 2% of the participants reported having focusing issues during the day.

The researchers followed all of the volunteers for about a decade. During that time, they identified 130,032 incidences of heart attack, stroke, and comparable diseases.

A higher chance of cardiovascular disease

After taking into account other risk factors, such as smoking and alcohol consumption, researchers identified several significant findings.

The new study identified that the participants who reported experiencing all three insomnia symptoms had an 18% increased chance of developing cardiovascular diseases compared with those who did not experience the symptoms.

Those who reported trouble focusing during the day were 13% more likely to develop heart attack, stroke, and comparable diseases than people who did not have problems focusing.

Researchers identified that the people who found it difficult to fall asleep or stay asleep had a 9% higher chance of developing these diseases, while those who woke up too early were 7% more likely to experience a stroke, heart attack, or similar.

Despite these results, the researchers point out that they have not established a cause and effect between insomnia and cardiovascular illnesses. The findings simply highlight an association between the two.

Notably, this link “was even stronger in younger adults and people who did not have high blood pressure at the start of the study,” says study author Dr. Liming Li of Beijing’s Peking University in China.

The researchers note that the participants in the study self-reported their symptoms of insomnia, which may mean the data are not entirely accurate. However, further analyses, enlisting medical professionals to track symptoms of insomnia rather than relying on self-reporting, would strengthen the relationship.

These results suggest that if we can target people who are having trouble sleeping with behavioral therapies, it’s possible that we could reduce the number of cases of stroke, heart attack, and other diseases later down the line.”

Dr. Liming Li



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Targeting one gut bacterium may treat alcoholic liver disease


Precision targeting of bacteria in a different way to antibiotics shows promise as a treatment for alcoholic liver disease, according to new research in mice.

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Targeting a specific bacterium has helped scientists eliminate alcoholic liver disease in mice.

A recent Nature study paper describes how an international team of scientists used bacteriophages, which are viruses that kill bacteria, to eradicate alcoholic liver disease in mice.

They used a particular mixture of phages to selectively eliminate Enterococcus faecalis, a gut bacterium that releases a toxin that kills liver cells.

They found that people with alcoholic liver disease had more E. faecalis in their guts than people without this condition.

In addition, they saw that levels of the bacterium correlated with disease severity.

“We not only linked a specific bacterial toxin to worse clinical outcomes in [people] with alcoholic liver disease, we found a way to break that link by precisely editing gut microbiota with phages,” says senior study author Bernd Schnabl, a professor of medicine and gastroenterology at the University of California San Diego School of Medicine.

Alcoholic liver disease on the rise in the US

Alcoholic liver disease is a major global public health concern. In fact, it is the leading cause of death in people with liver conditions worldwide.

The cause of this disease is damage to the liver from drinking high amounts of alcohol. Disease severity can range from mild to life threatening.

Fatty liver, which can develop after a few days of heavy alcohol use, is the first stage of alcoholic liver disease.

After decades of heavy drinking, alcohol-related fatty liver usually progresses to fibrosis, and then to cirrhosis. The disease can also take on a very severe form called alcoholic hepatitis.

Alcoholic hepatitis and other severe forms of alcoholic liver disease are on the rise in the United States. According to the Centers for Disease Control and Prevention (CDC), they were responsible for around 22,246 deaths in the U.S. in 2017.

Doctors usually treat alcoholic hepatitis with corticosteroids, but these drugs are not very effective. In fact, up to three-quarters of people with this severe form of alcoholic liver disease usually die within 3 months of receiving a diagnosis.

Currently, the only cure is to receive an early liver transplant. However, these operations are not widely available, and there is a long waiting list.

Previous studies have demonstrated that gut microbes can promote alcohol-induced liver disease in mice, but as the recent study authors explain, “little is known about the microbial factors that are responsible for this process.”

Phage treatment abolished disease in mice

In the new study, the researchers identified cytolysin, which is a toxin that E. faecalis produces, as a cause of injury and cell death in the liver. They investigated this further in samples from people with alcoholic hepatitis.

They found that the vast majority of people with alcoholic hepatitis who tested positive for cytolysin died within 180 days of being admitted to the hospital. In contrast, of those who tested negative for cytolysin, only a small minority died within 180 days.

In the next stage of the study, the team demonstrated that treatment with bacteriophages could abolish alcohol-induced liver disease in mice.

They first isolated four bacteriophages that can target cytolysin-secreting E. faecalis bacteria.

When they treated mice with these phages, they eradicated the animals’ alcoholic-induced liver disease. Treatment using phages that target other strains of bacteria, or those that target E. faecalis that does not release cytolysin, had no such effect.

The team suggests that these findings also highlight the potential for using cytolysin as a predictor of alcoholic hepatitis.

Phage therapy as a new approach

The idea of using viruses that kill bacteria as a way to treat bacterial infections is not new. In fact, scientists were experimenting with phage therapy about 100 years ago, but they seemed to lose interest when antibiotics came along.

However, because of the rising problem of antibiotic resistance, researchers are looking again at phage therapy as an alternative approach to treating bacteria-related illness.

It is likely to be a while before phage therapy is ready as a treatment for alcoholic liver disease, however.

Much more research is necessary, particularly into safety; phages can trigger a strong immune response in people with this type of disease.

“This novel avenue of research now needs to be expanded to test the safety and effectiveness of phage therapy in human clinical trials in [people] with alcohol-related disease,” says study co-author Debbie L. Shawcross, a professor of hepatology and chronic liver failure at King’s College London in the United Kingdom.

It is also likely that other forms of chronic liver disease associated with changes in the gut microbiome will also benefit from this novel approach, such as fatty liver disease.”

Prof. Debbie L. Shawcross



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New blood test marks progress in battle against sepsis


A new blood test could save lives in the treatment of sepsis. It assesses five markers in the blood to predict who is at low, medium, and high risk of death. With this knowledge, doctors could start treating the serious condition much earlier and with more precision.

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New research details how a blood test could help predict and prevent sepsis.

Researchers from several children’s hospitals in the United States have been developing the test – which they call PERSEVERE – for more than 10 years. They recently evaluated it in two ways.

First, they used the test to predict the risk of death in more than 400 children severely ill with sepsis. They then used it on mice with experimental sepsis to compare treatment decisions.

A recent paper in Science Translational Medicine gives a full account of the study and its findings.

Dr. Hector Wong, a director of Critical Care Medicine at Cincinnati Children’s Hospital Medical Center in Ohio, is the study’s senior investigator and first author.

He says that PERSEVERE not only puts patients into groups according to the deadliness of the sepsis but that it also enables doctors to decide which treatments to give to specific patients, such as picking the right drugs and dosages.

Unpredictable and challenging to treat

Sepsis is a serious condition in which the immune system launches an overwhelming response to infection. The cause of the infection can be any type of microbe, including fungi, bacteria, and viruses, but usually, it is bacteria.

The immune response releases inflammatory proteins into the bloodstream, causing blood clots to form and vessels to leak. This impedes blood flow and leads to organ damage.

The progress of sepsis is often unpredictable and rapid. It is a significant cause of hospital deaths and readmissions.

While anyone can develop sepsis, older adults, children, and babies are among those most at risk. People with serious injuries, cancer, AIDS, diabetes, and other medical problems are also more susceptible.

According to the National Institute of General Medical Sciences, which is one of the National Institutes of Health (NIH), sepsis affects at least 1.7 million adults and is responsible for 270,000 deaths every year in the U.S.

Despite significant progress in modern medicine, sepsis remains a challenge for doctors and carries a high risk of death.

Five biomarkers for sepsis prognosis

Over the 10 years or more that the researchers have been developing PERSEVERE, they have evaluated it using information from more than 1,000 children.

They started with a panel of 80 biomarkers and progressively reduced it to five.

According to the team, five is a manageable number for bringing together various advanced methods for searching and then choosing treatments.

In their study paper, the authors list the five PERSEVERE biomarkers as: “C-C chemokine ligand 3 (CCL3), interleukin 8 (IL8), heat shock protein 70 kDa 1B (HSPA1B), granzyme B (GZMB), and matrix metallopeptidase 8 (MMP8).”

Each biomarker is a protein that “reflects sepsis biology,” they note.

In the new study, the team evaluated the latest version of PERSEVERE using blood samples from 461 critically ill children with sepsis who were under care at several pediatric hospitals in the U.S. They also tested the tool in mouse models of sepsis.

As regulators have not yet approved the tool for clinical use, the researchers did not allow the results to inform decisions about patient care and treatment. All they did was check its accuracy and evaluate its potential.

High prognostic reliability

The results showed that PERSEVERE predicted with high reliability which children would develop severe sepsis and which would not.

The researchers then used the same five biomarkers in a mouse model of sepsis. The test accurately predicted which animals were at high and low risk of death.

In addition, compared with mice at low risk, those at high risk had much greater quantities of bacteria in their blood than those at low risk and needed much higher doses of antibiotics to tackle the infection.

The researchers then went back to the children’s samples and confirmed that those individuals at higher risk of death from sepsis also had much greater quantities of bacteria in their blood.

PERSEVERE can also give useful clues about the biological origins of the sepsis and the mechanisms that drive its rapid progress. This information could aid in the development of new treatments.

The researchers are continuing to develop and refine PERSEVERE as a prognostic tool and to discover more about the underlying biology of sepsis. They are also working on an adult version.

Dr. Wong points out that the main focus of PERSEVERE is not diagnostic but “prognostic enrichment.” Its purpose is to help doctors better predict the course of sepsis in individuals and tailor treatments accordingly.

Prognostic enrichment is a fundamental tool of precision medicine.”

Dr. Hector Wong



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Retinal imaging shows promise in early detection of Alzheimer’s


An analysis of how the retina of the eye scatters light shows promise as an aid for the early diagnosis of Alzheimer’s disease.

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Examining how the retina disperses light can provide insight into Alzheimer’s disease.

Scientists from the University of Minnesota in Minneapolis came to this conclusion after carrying out a recent study, the findings of which appear in ACS Chemical Neuroscience.

The researchers investigated retinal hyperspectral imaging (HSI) as a potential technique for early Alzheimer’s detection in 35 people.

HSI is an emerging imaging method in medicine. As a diagnostic aid, it can provide valuable information about tissue composition and structure.

Scientists can take HSI scans of the retina using a special camera that attaches to a spectral imaging system.

The method, which takes about 10 minutes to administer, is noninvasive and does not require the injection of tracer substances.

Need for biomarkers of early Alzheimer’s

Alzheimer’s disease is responsible for 60–80% of cases of dementia, an incurable condition that progressively impairs memory and thinking to the point that independent living is no longer possible.

The presence of toxic clumps of beta-amyloid protein in the brain is an established hallmark of Alzheimer’s disease.

If there was a way to detect the toxic beta-amyloid clumps in their early stages, this could greatly improve early diagnosis and increase the potential for treatment to delay disease progression.

As the retina is an extension of the brain, it is possible for these toxic protein clumps to form there as well.

This knowledge has spurred scientists to look for Alzheimer’s biomarkers in the retina, which is easy to examine noninvasively.

Retinal HSI uses light scattering

Retinal HSI applies the principle of Rayleigh scattering, which is the dispersion of electromagnetic radiation by particles that are much smaller than the wavelength of the radiation.

In their study paper, the authors explain that because of this principle, they would expect retinas with small, early clusters of beta-amyloid to scatter the light in a different way than retinas that either lack the protein clumps or have clumps that are more developed.

The team had already demonstrated the effectiveness of the technique in mouse models of Alzheimer’s disease.

The new study “concerns the translation of our [retinal HSI] technique from animal models to human [Alzheimer’s disease] subjects,” write the authors.

In the new investigation, the team compared retinal HSI results from 19 people at different stages of Alzheimer’s with those of 16 controls who did not have the disease and also had no family history of it.

Retinal HSI picks out MCI stage

For each participant, the team took HSI scans from different parts of the retina, including the optic disc, the perifoveal retina, and the central retina.

The results showed that individuals whose retinal light scatter had the “largest spectral deviation from control subjects” were those whose memory tests indicated that they were at the mild cognitive impairment (MCI) stage.

In addition, the researchers found that the amount of spectral deviation correlated with the memory test scores of those at the MCI stage.

They suggest that these results indicate that the technique’s sensitivity is higher in the early stages of Alzheimer’s disease.

Age and certain eye conditions, such as glaucoma and cataracts, appeared to have little or no effect on the results.

The study’s first and corresponding author, Swati S. More, Ph.D., who is an associate professor in the Center for Drug Design at the University of Minnesota, envisages retinal HSI becoming part of annual eye tests that could help identify individuals who might need a further exam or treatment.

The preliminary results from this study are promising and have laid the foundation for next steps involving rigorous validation of the technique in a clinical setting.”

Swati S. More, Ph.D.



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Scientists propose new theory of Parkinson’s disease


As scientists delve deeper into the nature of Parkinson’s, the more it appears that it is highly varied, suggesting numerous subtypes. A new review proposes that Parkinson’s falls into one of two main categories, depending on whether it originates in the central nervous system (CNS) or the peripheral nervous system (PNS).

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New research redefines Parkinson’s disease.

In a recent Journal of Parkinson’s Disease paper, scientists from Denmark argue how results from imaging and tissue studies fit with a theory of Parkinson’s that divides the condition “into a PNS-first and a CNS-first subtype.”

Parkinson’s disease principally destroys dopamine cells in the brain’s substantia nigra area. This is the part that controls movement.

This damage gives rise to the most common symptoms, including tremors, rigidity, and balance difficulties.

Parkinson’s disease may also cause emotional changes, depression, constipation, sleep disruption, and urinary problems.

The pattern of symptoms and their rate of progression can vary widely among individuals.

A distinguishing feature of Parkinson’s, however, is the accumulation and spread of toxic clumps of alpha-synuclein protein called Lewy bodies. These clumps are also hallmarks of dementia with Lewy bodies.

Debating the origins of Parkinson’s

Some scientists have proposed that the toxic alpha-synuclein forms in the PNS of the gut and spreads to the brain, which is part of the CNS, via the vagus nerve.

“However, not all autopsy studies agree with this interpretation,” says Dr. Per Borghammer, who works in the Department of Nuclear Medicine & PET at Aarhus University Hospital in Denmark.

“In some cases,” he adds, “the brains do not contain pathology at the important ‘entry points’ into the brain, such as the dorsal vagus nucleus at the bottom of the brainstem.”

Dr. Borghammer and his colleague Nathalie Van Den Berge, Ph.D. — of the Department of Clinical Medicine at Aarhus University — are the two authors of the new review.

They discuss and evaluate the results of imaging studies from people with Parkinson’s disease and tests on human and animal model tissues.

In differentiating between a PNS-first and a CNS-first subtype theory of Parkinson’s, they focus on a symptom called REM sleep behavior disorder (RBD).

RBD and the two types of Parkinson’s

People with RBD appear to be acting out their dreams while in REM sleep. This can result in violent behavior that can harm the individual or their bed partner.

RBD affects up to 0.5% of adults, with older adults among those most likely to experience the condition. The rate is much higher, however, among those with Parkinson’s disease and dementia with Lewy bodies.

Dr. Borghammer and Van Den Berge suggest that the distinguishing feature of the PNS-first subtype of Parkinson’s is the presence of RBD in the early, or prodrome, phase of disease — before the classic movement-related symptoms emerge.

“It is a central component of this hypothesis,” they write, “that the PNS-first phenotype appears to be strongly associated with the presence of [RBD] during the prodrome of [Parkinson’s disease], whereas the CNS-first phenotype is more often RBD-negative during the prodromal phase.”

The distinction between the two types, which affects the timing of RBD emergence, has to do with which part of the nervous system first shows signs of toxic alpha-synuclein damage.

New theory explains several discrepancies

In addition to a strong link with RBD during the early phase, in the PNS-first subtype, the disease damages the autonomic PNS before it affects the brain’s dopamine system.

In contrast, in the CNS-first subtype — which typically has no RBD in the early phase — the disease damages the dopamine system in the substantia nigra before it affects the autonomic PNS.

The autonomic PNS largely controls functions of the body that do not require conscious attention, such as digestion, breathing, heart rate, pupil dilation, and urination.

One area that appears to require further clarification is how the olfactory bulb, which is the organ in the nose that gives us our sense of smell, fits into the hypothesis.

Dr. Borghammer and Van Den Berge concede that the review only offers a brief discussion on this point. They suggest that the PNS-first subtype covers the olfactory bulb in the sense that it offers two entry points for toxic protein to reach the brain.

One entry point is directly through the nerve that links the olfactory system to the brain, and the other is via the gut, and then along the vagus nerve, due to the swallowing of nasal fluids.

In conclusion, the authors suggest that their hypothesis “seems capable of explaining a number of discrepant findings” in the literature and offers a new direction for further exploration into the origins and progression of Parkinson’s disease.

It is probable that these different types of [Parkinson’s disease] need different treatment strategies.”

Dr. Per Borghammer



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