Medical News Today: How calcium in coronary arteries can predict future heart health

According to one new study, having high levels of calcium in the coronary arteries could be responsible for detrimental changes to the structure of the heart.
Heart anatomy model
A new study investigates calcium and heart disease.

“Heart disease is the leading cause of death for men and women,” according to the Centers for Disease Control and Prevention (CDC).

Being able to identify people at risk is therefore a crucial public health issue.

One way to determine a person’s risk of heart disease, stroke, or heart attack is by looking at their coronary artery calcium (CAC) levels.

Calcium plays a number of roles in the body, including keeping bones healthy. However, calcium present in coronary arteries can lead to the accumulation of plaque.

Over time, this calcified substance can cause atherosclerosis, or a narrowing of the arteries. Atherosclerosis restricts blood flow and oxygen supply to vital organs, potentially resulting in a heart attack or stroke.

High cholesterol levels can indicate that a person is at risk; but scientists can also test CAC levels directly.

Using a CT scan to take numerous sectional pictures of the heart, doctors can see specks of CAC. A person’s scores tend to range from zero to over 400. The higher the score, the higher the risk of developing cardiovascular disease.

Cholesterol guidelines from 2018 recommend a CAC scan for people ages 40–75 whose risk status is “uncertain,” note the American Heart Association (AHA).

A new study, the results of which now appear in the journal Circulation: Cardiovascular Imaging, has examined the CAC scores of younger people and drawn some interesting conclusions.

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Heart abnormalities

The scientists used data from almost 2,500 people to track CAC and heart structure differences between young adulthood and middle age. Women made up 57% of the group, and 52% of participants were white.

They took data from participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study, which began in the 1980s with the aim of identifying young adult risk factors for cardiovascular disease.

“We looked at early adulthood to middle age because this is a window in which we can see abnormalities that might not be causing symptoms, but could later increase the risk of heart problems,” explains study co-author Dr. Henrique Turin Moreira.

The researchers compared test results from years 15 and 25 of the CARDIA study period. At the 25-year mark, the average age of the group was around 50.

When it came to their CAC results, 77% of participants had a score of zero in year 15 of the study. However, in year 25, this had dropped to 72%.

A number of factors were linked to a rise in CAC scores, including being older, being male, being black, smoking, having higher cholesterol levels, and having higher systolic blood pressure.

Middle-aged people who had higher CAC scores also showed a 9% increase in left ventricular volume and a 12% increase in left ventricular mass.

When the left ventricle changes in this way, the heart has to put more effort into pumping blood. This, in turn, leads to a thickening of the heart, which increases the risk of heart failure.

The study authors also note that these abnormalities were more significant among black people. For these people, every one-unit change in their CAC score correlated with quadruple the increase in their left ventricular mass.

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Future implications

It is unclear why people exhibited such differences depending on their race. Dr. Moreira explains that it could be “due to genetic factors or perhaps greater exposure to cardiovascular risk factors that usually appear earlier” in black people.

What that do already know, however, is that black people are already more likely to develop cardiovascular disease. Although just 43% of white women and 50% of white men have cardiovascular disease, it affects 57% of black women and 60% of black men.

Further research, explains Dr. Moreira, will be needed to “examine the link between coronary artery calcium and heart health” — especially in relation to race. However, documenting the relationship between CAC and heart failure risk factors in a younger age group is significant.

“Given the burden of morbidity and mortality associated with heart failure, these are important findings,” says Dr. Salim Virani, a co-author of the AHA’s 2018 cholesterol guidelines.

“Prior studies from this cohort have also shown that a better risk factors profile in young adulthood is associated with much lower CAC and therefore, these results further highlight the importance of primordial prevention and risk factor modification in early adulthood.”

Source Article from https://www.medicalnewstoday.com/articles/325509.php

Medical News Today: Hypertension treatment may slow down Alzheimer’s progression

Hypertension treatment may slow down Alzheimer’s progression

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Medical News Today: Researchers find protein that might prevent, reverse diabetes

A recent study finds that targeting a specific protein within the fat cells of mice reverses type 2 diabetes. The results also show that the protein can prevent the disease from developing.
Doctor and patient with diabetes
Could new findings lead the way to improved diabetes treatments?

Since the 1980s, the global prevalence of diabetes has almost quadrupled.

According to the Centers for Disease Control and Prevention (CDC), in the United States, around 1 in 10 people have type 2 diabetes (T2D), the most common form of diabetes.

A further 1 in 3 people has prediabetes — higher-than-normal blood sugar levels that increase the risk of T2D.

The steady rise in levels of T2D is largely due to the increase in obesity rates: Obesity is one of the primary risk factors for diabetes.

Insulin is a hormone that regulates the levels of sugar in the blood. In T2D, the body either does not respond to the hormone, or it does not produce enough of it.

Although medications and lifestyle changes can help to manage insulin levels and control diabetes, there is no cure, and researchers are keen to find better interventions.

Recently, a group of researchers — many of whom are from the University of British Columbia, in Canada, or the Karolinska Institute, in Sweden — examined the role of a specific protein in fat cells.

They recently published their findings in the journal EBioMedicine.

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White adipose tissue

When we eat more calories than our body needs, a type of fat called white adipose tissue (WAT) expands to store the excess energy as fat. However, if we take on more energy than we need for more extended periods, this system cannot cope, eventually leading to insulin resistance.

In particular, the researchers were interested in how a glycoprotein called CD248 might influence WAT and the eventual development of T2D.

Researchers have previously associated CD248 with tumor growth and inflammation, but no one had investigated its role in T2D.

First, the researchers analyzed the gene expression in WAT from humans who were thin, obese, had T2D, or did not have T2D.

In those who had obesity or were insulin resistant, they found that the CD248 gene was upregulated; in other words, the body was making more of the protein. This observation led the scientists to conclude that CD248 might work as a marker of insulin sensitivity that is more sensitive than current methods.

Next, the researchers artificially reduced the activity of CD248 in human WAT cells in the laboratory.

From these experiments, they concluded that CD248 in WAT plays a role in the cellular processes that lead to insulin resistance caused by long-term overconsumption of energy. Specifically, they found that CD248 is involved in how cells respond to hypoxia, which is a hallmark of obesity.

Moving to a mouse model

Then, the scientists moved to a mouse model. They used mice that lacked the gene that codes for CD248 in their WAT (although other cell types were still producing CD248). In these experiments, the researchers found that the mice were protected from developing insulin resistance and T2D.

The mice did not develop diabetes, even when they were fed a high-fat diet and became obese.

Importantly, the mice with reduced CD248 in their fat cells did not appear to experience any adverse events, suggesting that targeting this protein might be a useful therapy in the future.

Aside from the protective effects of reducing CD248, the scientists also demonstrated its potential as a therapy for those who already have T2D.

A most interesting finding was that the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese.”

Co-senior author Dr. Edward Conway

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Early days

Although these findings are fascinating and add to our understanding of how T2D develops, researchers will need to conduct a great deal of work before the results can make their way to the pharmacy.

Dr. Conway adds a note of caution, “While these discoveries are exciting, we are still some distance from a new treatment.” However, he plans to continue his investigations, explaining, “Our immediate goals are to understand how CD248 works so that safe and effective drugs that reduce the protein’s levels or that interfere with its function can be designed.”

The journey from research in cells and mice to treating human patients is a long, expensive, and often unsuccessful one.

The study suggests a new way to assess insulin resistance, prevent its progression, and even reverse T2D. Because diabetes is advancing at a worrying rate, chasing up these leads is now urgent.

Source Article from https://www.medicalnewstoday.com/articles/325519.php

Medical News Today: Gut bacteria can alter how well a medication works

Recent research has revealed that gut microbes can alter how a medication works in our bodies, sometimes with undesirable — or even toxic — results.
senior holding pills in one hand and a glass of water in the other
Our gut bacteria can influence the effectiveness of the drugs we take.

A healthy human gut microbiome is made up of over 1,000 species of bacteria that work to help break down food and keep the digestive system in functioning order.

Bacteria are an essential part of overall good health.

However, researchers at the University of California, San Francisco have found that sometimes, gut bacteria can interfere with the way a certain medication is supposed to work.

“[T]his kind of microbial metabolism can also be detrimental,” says Vayu Maini Rekdal, a graduate student in the laboratory of first study author Prof. Emily Balskus. Their paper now appears in the journal Science.

“Maybe the drug is not going to reach its target in the body, maybe it’s going to be toxic all of a sudden, maybe it’s going to be less helpful,” adds Maini Rekdal.

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Investigating a Parkinson’s disease drug

To understand how this can happen, Prof. Balskus and colleagues worked with levodopa (L-dopa), a medication that doctors commonly prescribe to treat Parkinson’s disease.

Parkinson’s disease interferes with dopamine production, so researchers are investigating L-dopa in the hope that it will counteract symptoms of this conditon. Only around 1–5% of this medication actually reaches the brain, with these results varying in patient populations.

Doctors also prescribe another drug, called carbidopa, in conjunction with L-dopa in the hope that it will counteract the way the body breaks it down, and in doing so, allow the drug to work better.

Although this method is effective for many people, the researchers note that there is still a lot of variation in its mode of action, as different people can have different responses.

There is another side to this problem: L-dopa can cause side effects such as gastrointestinal and cardiac issues.

These side effects can intensify when a person increases their dosage of L-dopa because they are not getting enough dopamine. This occurs because their body is breaking it down and not enough dopamine can reach the brain.

Solving the microbial puzzle

First, the researchers looked at the digestive enzymes that convert L-dopa into dopamine, noting there are only a few that can do this.

Using the Human Microbiome Project, the researchers sought bacteria that had the genes necessary to do the same thing; and in this research, they uncovered that there is only one specific bacterium that consumes the L-dopa. It is called Enterococcus faecalis.

This presented a new problem to solve, as the introduction of the other medication (carbidopa) is meant to stop this reaction — but it does not always work the way it is supposed to do.

Although researchers do not yet know why this occurs, they suggest that the two types of enzyme (human and bacterial) might not work in the same ways because they are slightly different.

The new study, however, has already resulted in at least one positive finding; the researchers have found a specific molecule that can inhibit the bacteria without completely destroying them.

“The molecule turns off this unwanted bacterial metabolism without killing the bacteria; it’s just targeting a nonessential enzyme,” says Maini Rekdal.

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Parkinson’s disease

Parkinson’s is a neurodegenerative condition that affects the cells in the brain area that is meant to produce dopamine. Parkinson’s has a number of symptoms, such as tremors, a loss of smell, difficulty moving, trouble sleeping, and constipation.

There is currently no cure for Parkinson’s, but treatment options are available. Therapies vary by person but can include medication and surgery.

Further research into the treatment of Parkinson’s is ongoing, and the hope is that this new study — which has uncovered why L-dopa does not work as well as it should — may lead to better treatments for Parkinson’s in the future.

Source Article from https://www.medicalnewstoday.com/articles/325527.php

Medical News Today: How strength training may help people with diabetes

How strength training may help people with diabetes

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Medical News Today: Intermittent fasting: How I got started

Intermittent fasting regimes are gaining traction as a way to manage weight and long-term health. This is how I got started.
Intermittent fasting
Watching the clock was part of my first month of intermittent fasting.

It’s Tuesday, midafternoon. I’ve felt my concentration slip more than usual in the last half an hour. I’m also feeling quite cold.

Armed with an extra layer, I’m making my way to daycare to pick up my youngest daughter. What to have for dinner?

Preparation is the key; I’ve read it many times. But I only made a firm decision about embarking on this intermittent fasting journey yesterday.

So, it’s going to be a carrot and red lentil soup with basmati rice. But when we arrive home, a quick look around the kitchen reveals a disappointing lack of red lentils and basmati rice.

With a hint of frantic, last-minute adjustments, dinner now consists of aubergine, canned tomatoes, steamed carrot, white beans, and long-grain rice. The baby ate 3 portions, and I made do with 300-ish calories. I certainly felt better and sort of full for about 30 minutes.

The usual evening madness of getting two small kids to bed is a good distraction from hunger pangs, and I am nursing a herbal tea as things begin to calm down. I’ve clocked in just shy of 700 calories for the day.

I am certainly looking forward to a coffee and a big bowl of porridge in the morning, but I’m proud to have made it through my first day.

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Why this type of fasting?

My mother is an avid fan of intermittent fasting. She likes to talk about it, and at great lengths.

Mama Martin started 3 years ago with a 5:2 regime that saw her eating around 500 calories on 2 days each week. She dropped down to 6:1 about 6 months ago and now fasts on 1 day a week.

During this time, her body mass index (BMI) has dropped from 24 to 21. Most importantly, she says that she doesn’t experience intense sugar cravings or the accompanying sugar crash that featured as a regular companion in much of her adult life.

I’ve been considering starting intermittent fasting for two reasons. The first one is a stubborn 15 pounds that I’ve not been able to shift after the birth of my second daughter. For the first time in my life, I find myself near the top end of what the United Kingdom National Health Service (NHS) call a healthy BMI.

“Don’t trust scales, trust how your body feels,” I hear my friends commenting. Well, the scales are saying the same thing that my feelings are saying.

But more than the weight, I’m interested in the long-term effects on our health that scientists have been uncovering in experimental studies of different fasting regimes.

This brings me to my second reason. I lost my dad due to bowel cancer just days before I turned 30; he was 57 years old.

Scientists have found that in animal studies, intermittent fasting leads to a reduction in the risk of obesity-related conditions, one of which is cancer.

While there is no evidence that fasting can prevent cancer in humans, maintaining a healthy weight and metabolic profile may lower my risk of developing bowel cancer.

After dabbling with overnight fasting for the past few weeks, it’s time to get serious.

I’m basing my fasting regime on a modified version of the 5:2 diet and have decided to aim for between 700 and 800 calories on Tuesdays and Thursdays.

My first week of intermittent fasting

After my impromptu start, I am much more ready on my second fasting day. After a morning espresso with lemon juice (mom’s tip), I break my fast with the obligatory British tea with milk at 11:30 a.m., making it a 14-hour overnight fast, which I follow with lunch at midday.

Lunch is a homemade beef and bean stew, which an online calculator helped me estimate at 296 calories per portion.

I felt hungry most of the morning, but concentrating on work helped me take my mind off the sensation.

Although lunch has put a stop to this feeling, I am noticing my concentration slipping — until I realize that I haven’t drunk any water since starting work.

After rectifying this cardinal mistake, I tell myself to keep my glass of water topped up AT ALL TIMES on fasting days from now on.

I continue with some homemade hummus with carrot and celery plus some salty popcorn in the afternoon, which together come to 145 calories. Then for dinner, there is a vegetable and falafel salad, clocking up a total of around 735 calories for the day.

As the evening continues, I am feeling hungry. My plan is to head to bed pretty soon after a warming, herbal tea.

Overall, the first week has gone OK. Picking 2 busy days in the office has helped me keep my mind off food, and being better prepared on day 2 also made it easier.

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Week 3 and the hardest so far

The first 2 days of fasting have not brought about any miracles. Chocolate still tempts me in the evenings, and the kids seem to have confused my intermittent fasting memo with a call to intermittent night wakings.

But perhaps most importantly, I don’t feel that the first 2 days were too uncomfortable.

On Tuesday, the feeling of hunger has been coming and going most of the morning, but it’s more of a dull ache rather than a sharp pang. After the usual coffee this morning, I’ve been drinking green tea and water. My concentration levels have been fine, although I do feel myself glancing at the clock quite frequently to check when it will be time to go for lunch.

Thursday has been the best day so far. I’ve cut right down to 2 meals after a 16-hour fast, and food has not been on my mind much.

After last week’s success, the third week turned out to be more challenging than I anticipated.

On Tuesday, I woke up with a cold. I seriously considered giving up the intermittent fasting and replacing my endless cups of water with copious amounts of tea with honey, accompanied by chocolate. Mama Martin came to the rescue with a supportive message that helped me pull through.

Yet, the next evening, with the remnants of the sore throat still vividly etched into my memory, the thought of not being able to snack in between meals and have a milky coffee in the morning did fill me with a certain amount of resentful dread.

Once I got going, though, I was actually fine. I made it to 14 hours — through a night that the children disrupted, and a morning that I managed to fuel with black coffee — to my lunch.

I’ve felt hungry but not debilitated. Plus, the thought of having breakfast on the following morning filled me with a great sense of joyous anticipation and fuelled my resolve.

By week 4, routine has taken over, and my weight has started to shift slowly.

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Biggest challenges and top 3 tips

The most difficult moments for me have been when I’ve not felt 100% and when especially delicious foods have confronted me on fast days. Luckily, my cold didn’t last long, and I’ve made sure to include tasty foods of all descriptions on my non-fasting days, at moderate levels.

Here are the three things I found most helpful to get me this far.

1. Organization

At the risk of sounding like a broken record, organization is key.

I use a calorie counting app on my phone to make sure I know how much I’m totting up on fast days. By now, I also know what 400-calorie lunch options I can get within walking distance of the office.

2. Cooking skills

Luckily, I’m reasonably proficient in this area. And I haven’t found adjusting our meals to include my requirements too tricky.

Soups work out well, as do stews and salads with legumes. I can also easily adapt pasta with vegetables, a firm kids’ favorite, by upping the amount of veg and reducing how much pasta ends up on my plate.

3. Attitude

How I feel about intermittent fasting is the biggest factor that has seen me through the first month. I am doing this for me, for my health, for my kids’ futures. No one is forcing me, and I don’t consider it a diet. It’s a change I am making to my lifestyle.

Small goals work well for me. Now I’ve got the first month behind me, I’m looking at 3 months as my next goal, with 6 months looming in the not-so-far distance.

At the half-year mark, I plan to take stock. Stay tuned for an update in 6-months’ time.

Source Article from https://www.medicalnewstoday.com/articles/325517.php

Medical News Today: An 8-hour work week could be ideal for mental health

How many paid hours per week does a person need to work to maintain good mental health? That is the question a new study aimed to answer, and the findings suggest that shorter work weeks and longer weekends could be most beneficial.
happy people working together
What is the ideal ‘dose’ of paid work time per week?

In many countries around the world, people in full-time employment work 40-hour weeks (typically 8 hours per day), Monday to Friday.

Some countries have shorter work weeks, however.

For instance, in Belgium, people typically work 38-hour weeks (7.7 hours per day), Monday to Friday. In Norway, there are 37.5-hour weeks.

Yet companies in some parts of the world are increasingly trialing short weeks to see how they affect employees’ productivity and overall sense of well-being.

For example, one company in New Zealand trialed a 4-day work week (32 hours) in 2018, and the results were so positive that they moved the company to consider switching to this model permanently.

However, despite the fact that such experiments appear to be successful, little research has looked into just how many hours of paid work per week would be beneficial for a person’s mental health.

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So, recently, researchers from Cambridge University in the United Kingdom launched the project Employment Dosage to investigate this subject.

“We have effective dosage guides for everything from vitamin C to hours of sleep in order to help us feel better, but this is the first time the question has been asked of paid work,” notes study co-author Brendan Burchell, Ph.D.

In a recent study that is part of the Employment Dosage research project, Burchell and colleagues focused on how changes in hours spent doing paid work impacted the mental health and levels of life satisfaction of 71,113 people in the U.K. in 2009–2018.

The investigators’ findings now appear in the journal Social Science & Medicine.

No extra health benefits over 8 hours

Previous research has shown that unemployment, and the lack of stability and security that comes with it, are directly linked to poor mental health and elevated levels of psychological distress.

However, if having no paid work is bad for mental health, how much paid work is necessary to bring about positive effects?

“We know unemployment is often detrimental to people’s well-being, negatively affecting identity, status, time use, and sense of collective purpose. We now have some idea of just how much paid work is needed to get the psychosocial benefits of employment — and it’s not that much at all,” says Burchell.

In the new study, the team analyzed data from the UK Household Longitudinal Study on more than 71,000 people ages 16–64.

They followed the participants’ mental health and well-being over a period of 9 years, throughout which they changed working hours.

To identify any developments in terms of mental health, the researchers asked the participants questions about dealing with anxiety and poor sleep.

They found that working up to 8 hours per week of paid work boosted the mental well-being of people who were leaving a period of unemployment. However, the study revealed that working a “standard” week of 37–40 hours brought no additional mental health benefits. This effect was the same for both women and men.

This led the researchers to believe that the most beneficial “dose” of paid work is approximately 1 day (8 hours) per week.

They explain that although men reported an increase of around 30% in levels of life satisfaction when they worked 16 or fewer hours of paid work per week, women only started reporting a similar increase when they worked more than 20 but under 24 hours per week.

The researchers also note that “the significant difference in mental health and well-being is between those with paid work and those with none,” so shortening the working week would not have “a detrimental effect on the workers’ mental health and well-being.”

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Importance for future work work landscape

The researchers also believe that their findings could have implications for a near future in which we can expect the work environment to change drastically with the advent of new inventions.

“In the next few decades we could see artificial intelligence, big data, and robotics replace much of the paid work currently done by humans,” says first study author Daiga Kamerāde, Ph.D, from Salford University in the U.K.

“If there is not enough for everybody who wants to work full-time, we will have to rethink current norms. This should include the redistribution of working hours, so everyone can get the mental health benefits of a job, even if that means we all work much shorter weeks,” she continues.

Our findings are an important step in thinking what the minimum amount of paid work people might need in a future with little work to go round.”

Daiga Kamerāde, Ph.D.

The study authors also note that drastically cutting down work hours has the potential to increase people’s productivity, as it improves life satisfaction and work-life balance. It could also help reduce pollution by eliminating the need to commute to work each day.

“The traditional model, in which everyone works around 40 hours a week, was never based on how much work was good for people,” says study co-author Senhu Wang.

“However, the quality of work will always be crucial. Jobs where employees are disrespected or subject to insecure or zero-hours contracts do not provide the same benefits to well-being, nor are they likely to in the future,” Wang concludes.

Source Article from https://www.medicalnewstoday.com/articles/325529.php

Medical News Today: How does your brain take out the trash?

In this Spotlight, we introduce the glymphatic system: the brain’s dedicated waste clearance system. Now implicated in various conditions, it is high time that we became acquainted.
Astrocyte and blood vessel
Astroglia (illustrated above) play a pivotal role in the brain’s trash collection service.

Many of us are relatively familiar with the lymphatic system; it performs a number of roles, one of which is clearing metabolic waste from the gaps between cells, referred to as the interstitial space.

However, the central nervous system (CNS), which comprises the brain and spinal cord, does not have any true lymphatic vessels.

Because the CNS is highly active, metabolic waste can build up quickly.

The CNS is also very sensitive to fluctuations in its environment, so the body needs to remove cellular garbage somehow, and that’s where the glymphatic system comes in.

Before the discovery of this brain-based garbage disposal system, scientists believed that each individual cell handled its own metabolic detritus.

If the cellular system became overloaded or slowed down as we aged, metabolic garbage would build up between the cells. This garbage includes products such as beta-amyloid — the protein associated with Alzheimer’s disease.

Astroglia

The term “glymphatic” was coined by Maiken Nedergaard, a Danish neuroscientist who discovered the system. The name is a reference to the glial cells, which are vital to this waste clearance system.

Glial cells get relatively little coverage, compared with neurons, despite being just as numerous in the brain. They were long considered little more than lowly support cells, but are now held in higher regard.

Glia protect, nourish, and insulate neurons. They also play a role in the immune system and, as we now know, the glymphatic system.

In particular, a type of glial cell known as astroglia are important. Receptors, called aquaporin-4 channels, on these cells allow cerebrospinal fluid (CSF) to move into the CNS, setting up a current that shunts fluid through the system.

CSF is a clear fluid that surrounds the CNS, providing it with mechanical and immunological protection, among other things.

The glymphatic system, which runs parallel to arteries, also harnesses the pulsing of blood in circulation to help keep things moving.

As the blood vessels expand rhythmically, they drive the exchange of compounds between the interstitial space and the CSF.

The glymphatic system connects with the lymphatic system of the rest of the body at the dura, a thick membrane of connective tissue that covers the CNS.

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The importance of sleep

Following Nedergaard’s discovery, she ran a series of experiments on mice to develop a better understanding of how this system worked and when it was most active. In particular, the team focused on sleep and Alzheimer’s.

Nedergaard and her team found that the glymphatic system was most busy as the animals slept. They showed that the volume of interstitial space increased by 60% while the mice were sleeping.

This volume increase also boosted the exchange of CSF and interstitial fluid, speeding up the removal of amyloid. They concluded that:

The restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake [CNS].”

This early work inspired a wave of new studies, the most recent of which was published this month. The researchers looked at the impact of high blood pressure on the function of the glymphatic system.

Over time, high blood pressure causes blood vessels to lose their elasticity, becoming increasingly stiff. Because the regular pulsing of arterial walls drives the glymphatic system, this stiffening impedes its function.

Using a mouse model of hypertension, the scientists demonstrated that high blood pressure-induced artery stiffening did interfere with the way that the garbage disposal system worked; it prevented it from efficiently getting rid of large molecules in the brain, such as beta-amyloid.

This finding might help explain why scientists have found links between elevated blood pressure and cognitive decline and dementia.

Parkinson’s disease

Parkinson’s disease is another condition characterized by the buildup of protein in the brain. In this case, the protein is alpha-synuclein.

This has led some researchers to wonder whether the glymphatic system might be implicated here, too.

In Parkinson’s disease, there is disruption in the dopamine pathways of the brain. These pathways play an important role in sleep-wake cycles and circadian rhythms; therefore, people with Parkinson’s often experience sleep disturbances.

A review published in Neuroscience & Biobehavioral Reviews proposes that the disrupted sleep patterns could hinder the glymphatic removal of debris, including alpha-synuclein, helping it build up in the brain.

Brain trauma

Chronic traumatic encephalopathy results from repeated blows to the head; it used to be called “punch-drunk” syndrome because it occurs in boxers.

Selection of brain scans
Brain injuries may interfere with glymphatic drainage.

Symptoms can include memory loss, mood changes, confusion, and cognitive decline.

Some researchers believe that disruptions to the glymphatic system caused by brain trauma may increase the risk of developing chronic traumatic encephalopathy.

The authors of the review write that, following a traumatic brain injury, “Difficulties with sleep onset and maintenance are among the most commonly reported symptoms.”

As we have seen, this interferes with the glymphatic clearance of proteins from the interstitial space during sleep.

At the same time, these types of injury can cause the relocation of aquaporin-4 channels — those important receptors on astroglia that are vital for glymphatic clearance — into a position that hinders the removal of junk proteins from the interstitial space.

The authors believe that the disruption of this system could “provide one link in the explanatory chain connecting repetitive [traumatic brain injury] with later neurodegeneration.”

Diabetes

Beyond a possible role in neurological conditions, some researchers have investigated how disturbances in the glymphatic system may be involved in the cognitive symptoms of diabetes.

Scientists have shown that diabetes can impact a range of cognitive functions, both early in the disease’s progression and further down the line.

Some researchers are asking whether the glymphatic system might be involved here, too. A study carried out in mice used MRI scans to visualize the movement of CSF in the hippocampus, a part of the brain involved in forming new memories, among other tasks.

The scientists found that in the mice with type 2 diabetes, clearance of CSF “was slowed by a factor of three.” They also found a correlation between cognitive deficits and impairment of the glymphatic system — if the trash was not getting cleared, thinking skills were hampered.

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Aging

As we age, a certain level of cognitive decline is almost inevitable. There is a wide range of factors involved, and some scientists believe that the glymphatic system could play a role.

A study published in 2014 investigated the efficiency of mice’s glymphatic systems as they aged; the authors found a “dramatic decline in the efficiency.”

In a review of the glymphatic system and its role in disease and aging, the authors write that reduced activity in the system as we age might “contribute to the accumulation of misfolded and hyperphosphorylated proteins,” increasing the risk of neurodegenerative diseases and, perhaps, exacerbating cognitive dysfunction.

We still know comparatively little about the glymphatic system. However, because it cleanses our most sensitive and complex organ, it is likely to influence our overall health to some degree.

The glymphatic system might not contain the answers to all of our questions about neurodegenerative diseases and beyond, but it could hold the key to some interesting new perspectives.

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