COVID-19: What do we know about the C.1.2 variant?

• Researchers have identified a new SARS-CoV-2 variant, which they refer to as C.1.2.
• C.1.2 contains mutations associated with increased transmissibility and ability to evade antibodies than other variants.
• However, experts say the public should not panic about the C.1.2 variant.
• They add that public health protocols, such as vaccinations, wearing a mask, and social distancing, are effective ways to prevent infection.

The more viruses spread, the more likely they are to mutate and form different variants. Variants that become more transmissible, resistant to current treatment options and vaccines, or cause more severe disease, are called Variants of Concern (VOC).

The World Health Organization (WHO)Trusted Source currently recognizes four SARS-CoV-2 VOCs:

• Alpha B.1.1.7, first detected in September 2020 in the United Kingdom
• Beta B.1.351, first detected in May 2020 in South Africa
• Gamma P.1, first detected in November 2020 in Brazil
• Delta B.1.617.2, first detected in October 2020 in India

Viruses need a host to replicate and mutate. The only way to stop new and more dangerous variants of SARS-CoV-2 from emerging is to prevent transmission and infection.

SARS-CoV-2 replicates quicker in unvaccinated people and, therefore, the virus has more opportunity to mutate. As these individuals have not already developed an immune response to the virus, it can survive and multiply for longer periods of time in their bodies.

The more opportunity SARS-CoV-2 has to cause infection in unvaccinated individuals, the higher the chance for new VOCs to emerge.

In recent research, scientists from the National Institute for Communicable Diseases (NICD) in Johannesburg, South Africa, alongside other institutions in the country, identified and discussed a new potential Variant of Interest called C.1.2.

Since its initial discovery in May 2021, scientists have detected the C.1.2 variant in seven other countries, including New Zealand, the U.K., and China. While it has some characteristics that may cause concern, experts are still gathering data.

A recent study investigating the variant appears on the preprint server, medRxiv.

Mutations

Using genetic analysis, the study authors note that C.1.2 contains many mutations also present in the Alpha, Beta, Delta, and Gamma variants of SARS-CoV-2. The researchers state these mutations make it easier for the virus to enter target cells, resist current treatments and vaccines, and pass from one person to another.

“​​Scientists are concerned about the variant, because of how quickly it has mutated: it is between 44 and 59 mutations away from the original virus detected in Wuhan, [China] making it more mutated than any other WHO-identified VOC or Variant of Interest,” said Dr. Vinod Balasubramaniam, senior lecturer at Monash University of Malaysia, who was not involved in the study.

“It also contains many mutations that have been associated with increased transmissibility and a heightened ability to evade antibodies in other variants,” the scientists said, “though they occur in different mixes, and their impacts on the virus are not yet fully known,” he added.

As the variant has had just a few months to circulate, knowledge on how it works is limited. However, the researchers reported that cases of the variant have increased in recent months at a similar rate to the Beta and currently dominant Delta variants as they began to spread in South Africa.

In May, C.1.2 accounted for 0.2% of genomes sequenced, in June, 1.6%, and in July, 2.0%.

The researchers also note there is usually a delay of 2–4 weeks between sampling and data being publicly available. This, alongside limitations in their sampling capacity, may mean the variant is more common than current data suggests.

Where did C.1.2 come from? 

“Viruses mutate in part as a result of an immune attack,” Dr. Cathrine Scheepers, first author of the study and senior medical scientist at the NICD in South Africa, told Medical News Today, “When someone [acquires an infection] with a virus, our antibodies bind onto this virus to kill it and prevent it from getting into our cells.

“During infection, the virus will mutate randomly. If these random mutations confer a benefit, such as the ability to evade these immune attacks by preventing antibody binding, that mutation will increase in number, as viruses with that mutation have a competitive advantage,” she continued.

“The longer somebody [has an infection] with a particular virus, the more chance it has to accumulate a lot of mutations. Since this lineage (C.1.2) is so highly mutated, we hypothesize it is a result of a prolonged infection allowing the virus to accumulate many mutations before being transmitted to others,” she added.

Source: Medical News Today

COVID-19: Why the Omicron variant has scientists worried

 Scientists have detected cases of a new variant of SARS-CoV-2, which is the virus that causes COVID-19, in a number of countries. Omicron (B.1.1.529) has an unprecedentedly large number of mutations in the part of its genome that encodes a key section of its spike protein, which the virus uses to infect host cells. This suggests that Omicron may be able to evade some of the immune protection afforded by vaccines, many of which are based on the original spike protein, and past infections.

On November 16, 2021, there were 136 daily recorded cases of COVID-19 in South Africa. By November 25, 2021, that number had risen to over 1,200.

More than 80% of these cases were in the densely populated province of Gauteng, which includes Johannesburg and Pretoria.

Researchers estimated that the R-value, which is the average number of new cases caused by each infection, was 1.47 for South Africa as a whole.

If R is more than 1, an outbreak will grow exponentially. In Gauteng province, R was 1.93.

Scientists at the Centre for Epidemic Response and Innovation (CERI) in Stellenbosch, South Africa, believe that a new variant of the virus known as Omicron (B.1.1.529) is responsible for these worrying figures.

There have been three previous peaks of infection in South Africa during the course of the pandemic, with the third due to the Delta variant. The latest surge coincides with the first detection of Omicron by scientists.

Scientists have sequenced around 100 confirmed cases of Omicron infection in South Africa. Most of the cases have been in Gauteng.

The new variant is also present in Botswana, Hong Kong, Europe, Canada, Israel, Japan, the United States, and elsewhere.

News briefing from South Africa

“The main message today is that you have to know the enemy in order to fight,” said Prof. Tulio de Oliveira, Ph.D., the director of CERI, at a virtual news briefing on November 25, 2021.

He went on to say that the variant’s genome contains “a very unusual constellation of mutations.” Many of these are confirmed or predicted to either help the virus evade the immune system or increase its transmissibility.

He said that there are around 50 mutations across the entire genome of the virus and more than 30 in the part that codes for its spike. This is the protein that allows the virus to invade its host cells.

A particular part of the spike called the receptor-binding domain (RBD) binds to a receptor called ACE2Trusted Source in the membrane of human cells.

Prof. Oliveira said that there is an exceptionally large number of changes within the RBD of the new variant.

Antibodies that bind to the RBD can prevent the virus from infecting cells. So, the RBD is a crucial target for COVID-19 vaccines, which provoke the immune system to make antibodies against particular protein sequences.

The Beta variant has three mutations in the RBD part of its genome, and the Delta variant has two, said Prof. Oliveira. However, according to the European Centre for Disease Prevention and Control, Omicron has 15 mutations there.

The concern among scientists is that the changes due to the mutations may prevent antibodies, which are generated through vaccination or an encounter with an older variant of the virus during an infection, from neutralizing the virus.

Source: Medical News Today

Drinking coffee may reduce the risk of developing Alzheimer’s disease

 

• There is currently no cure for Alzheimer’s disease, although treatment and lifestyle changes can slow its progression.
• A new Australian study suggests that higher coffee intake might be linked to a slower rate of cognitive decline.
• There was also an association between higher coffee intake and slower accumulation of amyloid deposits in the brain.

More than 55 million people worldwide are living with dementia. The most common type of dementia is Alzheimer’s disease (AD), which experts believe accounts for 50–75% of dementia cases. In an aging population, AD cases are expected to increaseTrusted Source.

AD is a complicated disease and not a normal part of aging. It causes complex brain changes that can lead to memory loss and cognitive decline.

A new study in Australia has uncovered evidence to suggest that there is a link between the amount of coffee people drink and their rate of cognitive decline. The study recently appeared in the journal Frontiers in Aging Neuroscience.

Previous research has suggested that coffee might reduce the incidence of cognitive disorders. The authors of this new study set out to explore this further.

Dr. Samantha Gardener, the lead author of the paper, says that if additional research confirms this link, “coffee intake could one day be recommended as a lifestyle factor aimed at delaying the onset of [AD].”

She continues: “It’s a simple thing that people can change […]. It could be particularly useful for people who are at risk of cognitive decline but haven’t developed any symptoms.”

Investigating the link

The research team is based at the Edith Cowan University in Perth, Western Australia. The scientists used data from the Australian Imaging, Biomarkers, and Lifestyle (AIBL) longitudinal study and followed the participants for more than a decade.

The study involved 227 adults aged 60 years or over, who did not have cognitive decline at the start of the study. The team used a questionnaire to gather information from the participants about the amount and frequency of coffee they consumed.

They then performed cognitive assessments using a selection of psychological measures at baseline and 18-month intervals. These assessments measured six cognitive areas: episodic recall memory, recognition memory, executive function, language, attention and processing speed, and the AIBL Preclinical Alzheimer Cognitive Composite (PACC).

PACC is a composite score, combining tests for memory, executive function, and cognition. ResearchTrusted Source has shown that it can reliably measure the first signs of cognitive decline.

A subset of 60 participants underwent PET brain scans to assess the accumulation of beta-amyloid in the brain. A further subset of 51 participants had MRI scans to assess their brain volume atrophy.

Findings

Analysis of the data showed that habitual coffee drinking was positively associated with the cognitive areas of executive function, attention, and the PACC score. Drinking higher amounts of coffee was associated with slower cognitive decline in these areas over the course of the study.

Higher baseline coffee consumption was also linked to a slower accumulation of amyloid protein over the 126 months.

There did not seem to be a link between coffee intake and brain volume atrophy in this study.

The observed results suggest that increasing coffee intake from 1 to 2 cups per day could potentially reduce cognitive decline by up to 8% after 18 months. There could also be up to a 5% decrease in cerebral beta-amyloid accumulation over the same period.

Dr. Gardener told MNT, “[h]igher coffee intake was associated with slower accumulation of the sticky protein called beta-amyloid, which clumps together in the brains of those with Alzheimer’s disease.”

“This was really interesting to us to establish a potential mechanism, especially as the recently approved medication designed to treat Alzheimer’s disease in the United States, Aduhelm [aducanumab], also works by targeting this protein to reduce its buildup but has been quite controversial and hasn’t shown effects on reducing cognitive decline, which coffee intake has.”

Limitations

It is important to consider the limitations of the study. These include the fact that self-reported dietary data could be subject to recall bias. However, the authors do note that coffee intake is less prone to reporting errors because of its long-term habitual nature.

Secondly, this is quite a small sample size of just 227 people. With a small number of participants, it is harder to draw conclusions about the general population.

Also, the data were not able to show a difference between drinking caffeinated or decaffeinated coffee or to confirm whether the preparation method had any effect.

Dr. Sara Imarisio, head of research at Alzheimer’s Research UK, told MNT, “Studies like this one can provide useful clues about the effects of diet on our brain health, but we must be careful when interpreting the results, as we know many other factors are at play when it comes to dementia risk.”

MNT asked Dr. Gardener about the generalizability of the results. She said: “The vast majority of our study cohort are [white], and, therefore, generalizability regarding similar effects in other populations may be limited. Additional studies in more varied groups will be required to confirm results are transferable.”

“Our study did not have data on midlife coffee consumption — consequently, potential positive or negative effects of coffee intake at midlife cannot be assessed in the current study.”

Future research 

The authors say that more long-term observational and intervention studies are necessary to confirm these findings.

Dr. Gardener told MNT, “Additional studies with participants followed for [more than] 10 years in a range of different groups of participants, and intervention studies where participants are assigned a specific amount and type of coffee to drink are required to confirm our preliminary findings.”

Source: Medical News Today

‘Flimsy’ evidence for social media worsening adult mental health

 

• Researchers investigated the link between social media use and depression in adults, including older adults.
• They found that the use of some social media, but not all, has associations with an increased risk of depressive symptoms.
• Alongside expert commentators, the team asks for caution when interpreting the results due to study limitations and uncertainty around causation.

The use of social media has correlations with reduced well-being and increased anxiety and depression among adolescents and young adultsTrusted Source.

One reviewTrusted Source highlighted a study that found using the internet to communicate and play games for more than 4 hours a day predicts depressive symptoms 1 year later. The research also found that depressive symptoms predict increased internet use and decreased participation in nonscreen activities.

Another study involving 990 participants in the United States found a link between social media use and the development of depression. However, preexisting depression did not predict social media use.

However, how accurate these studies are may be questionable because many of them rely on self-reported social media use. A reviewTrusted Source of 47 studies investigating the accuracy of self-reported digital media use raised a concern that self-reported measurements rarely correlate with logged measurements.

Furthermore, studies often do not include adults in their samples, so the effects of social media on older age groups are relatively unknown.

Lastly, whether there is a causal relationship between social media use and depression — and which comes first — is still unknown.

Recently, researchers conducted a survey study investigating the link between social media use and the development of depressive symptoms.

The results suggest certain social media use preceded the worsening of depressive outcomes. The findings appear inJAMA Network OpenTrusted Source.

However, some experts doubt the extent to which these findings can be interpreted.

Surveys 

The researchers analyzed results from survey data taken between May 2020 and May 2021 from individuals aged 18 years and above. The survey sample included quotas for sex, age, and race and ethnicity from each of the 50 states in the U.S. to ensure it was representative of the country’s population.

Survey questions included the nine-item Patient Health Questionnaire (PHQ-9) to assess for depressive symptoms. Questions examined whether participants had “little interest or pleasure in doing things” and whether they were “feeling down, depressed, or hopeless” on a four-point scale.

The researchers also queried participants on:

• their use of social media, such as Facebook, Instagram, and TikTok
• whether they consumed any sources of COVID-19-related news in the last 24 hours
• the number of social supports they have available to discuss problems
• the number of face-to-face meetings they had with nonhousehold members in the previous 24 hours

For the data analysis, the team included participants who had filled out the surveys at least twice and had an initial PHQ-9 score of less than 5, indicating less than mild depression.

Overall, 5,395 people completed two surveys. Their average age was 55.8 years old, while 65.7% were female, 4.7% Hispanic, 10.6% Black, and 76.3% white.

From their analyses, the researchers noted that Snapchat, Facebook, and TikTok use in the first survey had associations with a significantly greater risk of an increase in self-reported depressive symptoms.

They also noted that COVID-19-related news participants consumed in the last 24 hours alongside the number of social supports and daily face-to-face interactions only impacted results linked to Snapchat.

While TikTok and Snapchat use had correlations with depressive symptoms among those aged 35 years and older, but not those younger than 35, Facebook use had associations with depressive symptoms among those under 35, but not those older than 35.

Unknown mechanisms

The researchers say that due to the observational nature of their study, they cannot ascertain why social media use may have links to depression. However, they identify possible mechanisms.

“One possible explanation for our results is that people who are at risk for depression, even if they’re not currently depressed, are more likely to use social media,” Roy H. Perlis, M.D., M.Sc., lead author of the study, told Medical News Today.

“Another is that social media actually contributes to that increased risk. With our study design, we can’t distinguish between the two. What we can exclude is the possibility that depressed people are more likely to report social media use, which was a limitation of some previous studies,” he added.

When asked to explain what might be behind this association, Sara Makin, M.S.Ed. NCC., LPC., and founder and CEO of Makin Wellness, who was not involved in the study, highlighted that when isolated, people may turn to social media as a way to feel more connected. However, this may have an inverse effect and therefore result in depressive symptoms.

She also noted the effect of social comparison: “Social media often only shows people ‘living their best lives’ or the positive things that are happening like purchasing a new house, getting a new job, graduating from college, etc. Most people compare their failures to others’ successes, which can make us have negative thoughts about ourselves.”

Questionable causation

While it seems as though rates of depression increased during the COVID-19 pandemic, some question whether social media use had a casual role at all.

“Big limitations make it difficult, if not impossible, to conclude anything worthwhile from the findings, “ Craig J. R. Sewall, a postdoctoral fellow at the University of Pittsburgh, who was not involved in the study, told MNT.

“The item they used to measure use of [social media] platforms is a simple ‘yes/no’ response to this question: ‘do you ever use any of the following social media sites or apps?’ So a person [who] used Instagram, for example, 5 years ago and a person [who] used Instagram 5 hours ago would both answer ‘yes.’”

“That’s a big problem and renders this finding practically meaningless: In adjusted regression models, Snapchat, Facebook, and TikTok use at first survey were significantly associated with greater risk of increase in self-reported depressive symptoms,” he continued.

“Because the question about [social media] use was phrased the way it was, even if they found an association between [social media] use and depression, they would have no way to ascertain whether that [social media] use was recent or a long time ago, whether they frequently visited the [social media] platform or whether it was a ‘one-and-done’ situation [or both]. As a result, it’s a big stretch to conclude that participants’ increase in depression between May 2020 and May 2021 had anything to do with whether they used certain [social media] platforms,” he explained.

“At the same time, people had to rely more on digital technology like [social media] to connect with friends, colleagues, and loved ones. So people who became more depressed due to the pandemic may have relied on [social media] more as a coping mechanism,” he concluded.

“Explaining the links between social media use and depression requires a lot of careful thought and precise methodology, “ said Dr. Fisher. “In my personal opinion, this should be done in a way that moves away from cross-sectional, self-report measures like are employed in this study and toward measures that consider the individual (sometimes called idiographic methods), and those which measure social media use in a more objective fashion (like using device logs or a data donation framework).”

“I just don’t know that we have enough evidence from this paper to decisively conclude that there is a link between social media use and depression, much less that the causal directionality here is that social media use [leads to] depression. It’s also possible that those who were more depressed during the pandemic happened to use social media more (e.g., to connect with friends). The methods used here don’t let us conclude either way,” he added.

The researchers conclude that we need to understand the relationship between social media use and mental health better.

“Even if social media use is only telling us about underlying risk, rather than causing it, can we understand why?” said Dr. Perlis. “Might we be able to intervene to prevent depression and anxiety? We hope that our work will inform both mental health researchers and policymakers in thinking about how to study and potentially act on this relationship. What we can’t​ continue to do is simply ignore this association or try to wave it away as a statistical artifact.”

The researchers note that their study has several limitations. Firstly, they say they could not properly control for all factors that may have influenced their results. They stress that their research does not prove causation and that social media use may “simply be a marker of underlying vulnerability to depression.”

Implications for public health?

When asked how these findings should influence public health, Ms. Makin said: “For one, limits for the amount of social media that one consumes should be set. This can be easily done by going into your settings on your [smartphone], so once you have reached your limit for the day, you can no longer access the app.”

“Likewise, research may need to be done to determine what is an appropriate amount of time to spend on social media where it makes us feel good but does not cause us to become fixated on the lives of others and cause feelings of depression. It may also be helpful to suggest changes about the way that we interact and react on social media with others. Teenagers and adolescents who have social media accounts may need to be monitored more closely to make sure they are not victims or perpetrators of cyberbullying,” she added.

However, Dr. Sewall believes these findings should not influence public health recommendations, given the “flimsy” evidence:

“If the hope is to help people improve their well-being during these very difficult times, I believe it would be a waste of time and resources to focus on people’s [social media] use. [It would be] much better to focus on some of the myriad other issues that have been impacted by the pandemic — like financial security.”

Dr. Fisher agreed that these findings should not directly influence public health recommendations, “at least not in an extreme way.”

Dr. Fisher added: “I do hope that findings like these generate some momentum toward pressuring social media companies to share their data with independent researchers, because this is likely the only way for us to come up with evidence that is actually conclusive with regard to the links between social media use and depression.”

“I am all for increased accountability for social media platforms, but the fact is that social media use is very idiosyncraticTrusted Source, and for some people, it’s positive, and for others, it’s negative, just like many other behaviors.”

“There is by no means a consensus in the academic community that ‘social media,’ or even particular social platforms are harmful to mental health in a general sense and [we] need much better data to be more sure about these links, and even more so to understand which direction the causal order flows,” Dr. Fisher concluded.

Source: Medical News Today

Exercise may lower Alzheimer’s risk by reducing inflammation

 

• Physical activity may reduce the risk of Alzheimer’s disease and all-cause dementia and slow age-related cognitive decline.
• Aging and neurodegenerative conditions, such as Alzheimer’s disease, have associations with increased inflammation in the brain.
• Animal studies have shown that physical activity may lead to cognitive benefits by reducing the activation of microglial cells, the primary immune cells in the brain.
• A new study involving older adults reports that reducing microglial activation may help support the protective effects of physical activity on cognitive functioning.

A decline in certain cognitive abilities, such as memory and attention, is typical with aging. However, some individuals may experience dementia, which involves a severe decrease in cognitive abilities that impair daily functioning.

Studies show that individuals who exercise regularly have a lower risk of Alzheimer’s disease and all-cause dementia. Moreover, physical activity can slow down the progression of cognitive decline.

Scientists do not fully understand the mechanisms through which physical activity produces these cognitive benefits in humans.

A recent study led by researchers at the University of California San Francisco (UCSF) shows that reducing inflammation in the brain may mediate the cognitive benefits of physical activity.

Specifically, the researchers found that physical exercise had associations with reduced activation of microglia, the primary immune cells in the brain.

The study’s co-author, Dr. Kaitlin Casaletto, a professor at UCSF, told Medical News Today, “Many studies show that physical activity relates to better brain and cognitive health (e.g., estimates indicate that inactivity alone accounts for 13% of Alzheimer’s disease cases worldwide). Yet, we still do not fundamentally understand the mechanisms linking physical activity to cognition in humans. Our study is the first human data showing that microglial activation (“brain inflammation”) may be a meaningful mechanism.”

The study appears in the Journal of Neuroscience.

Physical activity and microglia

The nervous system consists of two major cell types: neurons and glial cells. Neurons are primarily involved in transmitting electrical and chemical signals, whereas glial cells protect and support neurons. More recently, scientists have discovered that glial cells can modulate signal transmission between neurons.

Animal studies suggest that the glial cells in the brain may mediate the beneficial effects of physical activity on cognitive function. Specifically, physical activity is known to alter the activity of microglia, a sub-type of glial cells.

Microglia are the brain’s immune cells and become activated in response to an infection or neuron damage.

Activation of microglia can benefit the immune system as it mounts an inflammatory response against an infection. But an abnormal increase in the activation of microglia can damage neurons.

Chronic low-grade inflammation in the brain is a characteristic of aging and neurodegenerative disorders such as Alzheimer’s disease. Moreover, studies show that these conditions involve an abnormal increase in the number of activated microglia in the brain.

Scientists know that physical exercise in animals reduces the activation of microglia and other brain markers of inflammation.

Microglia can also modulate the structure and function of synapses, which are specialized contact sites through which neurons communicate with each other. Microglia play an important role in the formation and elimination of synapses.

Moreover, they can modulate the strength of these synapses, thus influencing signal transmission between neurons.

StudiesTrusted Source in animals show that the cognitive benefits of physical activity have associations with improvements in synaptic health or integrity. Furthermore, these studies suggest that microglia may mediate the effects of physical activity on synaptic integrity and cognitive function.

The present study investigated the relationship between physical activity and microglial activation in older adults. Given the association between physical activity and improvements in cognitive function and synaptic health, the study estimated the extent to which changes in microglial activity may support these effects of physical activity.

The study found that, as in animals, physical activity had associations with reduced microglial activation in older adults. Moreover, the study’s results suggest that reduced microglial activation could be one of the brain pathways through which physical activity protects individuals from cognitive decline, especially in Alzheimer’s disease.

Measuring physical activity

The present study consisted of 167 deceased individuals enrolled in the Rush Memory and Aging Project (MAP). The Rush MAP is a longitudinal study that aims to identify risk factors associated with the development of Alzheimer’s disease.

The Rush MAP includes older adults without dementia at enrollment and involves annual assessments for dementia risk factors. The participants in the project had agreed to donate their brains and other organs for post-mortem analysis.

The present study consisted of individuals with an average age of 87 years at the time of the first physical activity test and 90 years at their death.

The researchers assessed daily physical activity using a wearable sensor called actigraph. Actigraphy provides an objective measure of physical activity by continuously tracking periods of motor activity and rest over multiple days.

In the current study, the researchers conducted actigraphy assessments continuously for up to 10 days. They also conducted yearly tests to assess cognitive function and the ability of the participants to perform various motor tasks.

After the participants’ death, the researchers analyzed the brain tissue to determine the number of activated microglia in four brain regions. They also assessed the levels of proteins associated with synaptic health and brain markers for Alzheimer’s disease, Lewy body dementia, stroke (infarcts), and other conditions.

Physical activity and microglial activation

The researchers found that higher physical activity levels measured using actigraphy had associations with a lower proportion of activated microglia when they considered all four brain regions together.

Factors such as limited motor function and cognitive impairment could potentially restrict the ability of the participants to engage in physical activity.

Consequently, the researchers adjusted their analysis for age, sex, motor, and cognitive function. They found that the association between the proportion of activated microglia and physical activity was independent of these variables.

The researchers then examined this association in individual brain regions. They found that the association between higher physical activity levels and reduced microglial activation reached statistical significance only in two brain regions — the ventromedial caudate and the inferior temporal gyrus.

Furthermore, the relationship between physical activity and reduced microglial activation was stronger in individuals with higher levels of brain pathologies in these two brain regions.

The brain pathologies found in the ventromedial caudate and inferior temporal gyrus consisted of microinfarcts (or mini-stroke) and Alzheimer’s disease-related pathologies, respectively.

In other words, individuals with higher levels of brain pathologies who regularly engaged in physical activity showed lower microglial activation than their counterparts with similar brain pathology levels but lower physical activity levels.

These data suggest that the effects of physical activity on microglial activation were specific to certain brain regions. These results are consistent with data showing that microinfarcts and brain pathologies associated with Alzheimer’s disease tend to be more common in the two brain regions.

Association with cognition and synaptic integrity

The researchers then examined the association between microglial activation and clinically meaningful markers for dementia, namely cognition and the integrity of the synapses.

Microglial activation in the inferior temporal gyrus, but not the ventromedial caudate, had associations with a decline in cognitive functioning and lower levels of synaptic health markers.

Next, the researchers examined the extent to which reduced microglial activation associated with physical activity could improve cognition and the integrity of synapses.

Using a statistical method called mediation analysis, the researchers estimated that the decrease in the proportion of activated microglial in the inferior temporal gyrus contributed to over 30% of the effects of physical activity on cognition and synaptic markers.

Significantly, changes in microglial activation in the inferior temporal gyrus in individuals with higher levels of Alzheimer’s disease-related brain pathologies mediated more than 40% of the effects of physical activity on cognition and synaptic health.

In contrast, in individuals with lower Alzheimer’s disease-related pathologies, changes in microglial activity contributed to only 10% of the effects of physical activity.

Study strengths and limitations

One of the study’s strengths included the use of actigraphy, which provides an objective assessment of physical activity levels. This is in contrast to other studies that often estimate physical activity levels using self-reports, which are prone to biases and inaccuracies.

This is the first human study to show that physical activity may improve cognitive functioning by reducing microglial activation.

Dr. Casaletto noted that the study had a few limitations. She said, “A major limitation of this work is the observational design. We cannot determine the directionality of effects, and it is likely that at least some of the relationship between physical activity and brain inflammation is bidirectional (i.e., brain inflammation leading to reductions in physical activity).”

Dr. Casaletto said that her research group intends to address this shortcoming in subsequent studies. She said, “We have a physical activity intervention study ongoing in which we hope to capture complementary markers of in-vivo inflammatory markers to help support causality of effects.”

Among other limitations, Dr. Casaletto noted, “We captured physical activity and cognition in life but brain inflammation and pathology at death. These are likely dynamic processes, and understanding the temporal link between lifestyle behaviors and biological changes is needed.”

Lastly, Dr. Casaletto noted that the study participants were primarily white and from Northeastern Illinois. Thus, the researchers do not know whether they can generalize the findings to a diverse population.

Source: Medical News Today

1 in 5 people with hypertension take drugs that increase blood pressure

 

• Most people with hypertension in the United States have not managed to lower their blood pressure to recommended levels with treatment.
• There are many causes of high blood pressure, and some drugs can contribute to this.
• Researchers have shown that many individuals with hypertension are taking medications that could raise their blood pressure.
• There are often alternatives to these drugs that healthcare professionals should consider for those individuals.

Nearly half of adults in the U.S. have high blood pressure, or hypertension. Yet only 1 in 4Trusted Source of them have managed to reduce their blood pressure to the recommended levels with treatment, according to the Centers for Disease Control and Prevention (CDC).

It is important to keep blood pressure within the recommended levels of under 120/80 millimeters of mercury (mm Hg). Hypertension increases the risk of developing a heart attack and stroke, which are leading causes of death in the U.S.

The causes of high blood pressure vary, with genetics, diet, exercise, lifestyle, and some medical conditions all playing a role. Certain medications for a number of different conditions can also raise blood pressure.

Researchers from Beth Israel Deaconess Medical Center in Boston, a Harvard-affiliated teaching hospital, have examined existing survey data to determine how many people with hypertension are taking medication that may raise blood pressure.

Their results appear in a research letter in the journal JAMA Internal MedicineTrusted Source.

Letter co-author Dr. Timothy Anderson spoke with Medical News Today. He explained that sometimes, there is no choice but to give some people with hypertension drugs that can raise their blood pressure; however, other times, there may be other options:

Analyzing survey data

The researchers analyzed data from the National Health and Nutrition Examination SurveyTrusted Source collected between 2009 and 2018. The dataset consisted of information about people over the age of 18 who were not pregnant.

In total, there were 27,599 adults, of whom 11.3% were Black, 14.8% were Hispanic, and 65.3% were non-Hispanic white.

Data for the survey were generated by home interviews. Among other details, information about prescription medications was obtained.

The researchers identified antihypertensive medications, which people take for hypertension, and medications that may cause elevated blood pressure.

Hypertension was defined as systolic blood pressure of 130 mm Hg or higher, diastolic blood pressure of 80 mm Hg or higher, or if a person answered “yes” to the question, “Have you ever been told by a doctor or other healthcare professional that you had hypertension, also called high blood pressure?”

The prevalence of hypertension and uncontrolled hypertension was 49.2% and 35.4%, respectively.

While the researchers had expected to find that some of the individuals would be taking prescription medications that could raise blood pressure, they were surprised to find that there were so many.

Their analysis shows that nearly 1 in 5 adults in the United States with hypertension were on medication that could raise their blood pressure. The authors found that a total of 15% of all adults were on these medications.

Dr. Anderson told MNT: “It certainly is a higher proportion than I might have guessed starting out, though we see this scenario often in our primary care clinics. We also anticipate this is an understatement, as our study does not include over-the-counter [(OTC)] medications that were not prescribed, and many [OTC] medications, including anti-inflammatories and decongestants, may raise blood pressure.”

Increasing risk

The researchers also observed an association between these medications and increased risk of uncontrolled hypertension in people who were not receiving antihypertensives, but not among those who were receiving them.

They also found that “The use of medications that may raise [blood pressure] was associated with greater use of antihypertensives among both adults with controlled hypertension […] and adults with uncontrolled hypertension.”

The most commonly prescribed medications that cause a rise in blood pressure are antidepressants, nonsteroidal anti-inflammatory drugs, steroids, and estrogen.

MNT also spoke with Dr. Dave Dixon, an associate professor from the Virginia Commonwealth University School of Pharmacy, who was not involved in the study.

Reducing or eliminating the use of some of the prescribed medications could cause different challenges, and Dr. Dixon pointed out it was unclear in the paper for how long the individuals were taking these medications.

He advised, “Regardless, patients with hypertension should monitor their blood pressure closely at home with a validated home blood pressure monitor and report changes to their [doctor].”

Source: Medical News Today