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Friday, April 19, 2024
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Humans first drank caffeinated tea more than 4,000 years ago in China. Since then, it has become one of the most popular drinks worldwide, second only to water.

Both green and black teas are brewed from the leaves of the same shrub, Camellia sinensis, but green tea, which is made from unfermented leaves, contains more antioxidants.

Oxidation during the fermentation process of black tea reduces its antioxidant levels.

Several studies have found that green tea inhibits the formation of cancers, lowers high blood pressure, and reduces the risk of heart disease.

However, the molecular mechanism responsible for the effect on blood pressure has been unclear until now.

Scientists at the University of California, Irvine (UCI) and the University of Copenhagen, in Denmark, have found that antioxidants in tea open ion channels and can relax the muscles that line blood vessels.

They report their findings in the journal Cellular Physiology & Biochemistry.

Preventable risk factor

The discovery could guide the design of more effective antihypertensive drugs, which could potentially improve the health of millions of people around the world.

According to the National Heart, Lung, and Blood Institute, controlling or lowering high blood pressure can help prevent chronic kidney disease, heart attacks, heart failure, and possibly dementia.

The Centers for Disease Control and Prevention (CDC) report that almost half of all adults in the United States have hypertension. It estimates that in 2018, the condition played a role in the deaths of nearly half a million people in the country.

The World Health Organization (WHO), meanwhile, estimate that more than 1 billion people worldwide have hypertension.

The new study first shows that two antioxidants in tea, known as catechins, open a protein channel in the membranes of the smooth muscle cells that line blood vessels. This allows positively charged potassium ions to leave the cells.

Channels in nerve and muscle cells maintain voltages across their membranes by allowing negative and positive ions to pass in and out in a controlled way. They are “voltage-gated,” which means that they respond to changes in this voltage by opening or closing.

The researchers found that the catechins in green tea activate a particular type of potassium ion channel, called KCNQ5.

Previous work by some of the same scientists suggests that this protein channel may underlie the antihypertensive effects of several plants used as folk medicines for millennia.

Voltage sensor

For the new study, the researchers used computer modeling and mutated versions of the channel protein to show that the two catechins bind to a section that senses voltage changes.

“This binding allows the channel to open much more easily and earlier in the cellular excitation process,” explains senior study author Prof. Geoffrey Abbott, of the Department of Physiology & Biophysics at the UCI School of Medicine.

In theory, this should make the muscle cells less “excitable” and therefore less likely to contract. They should instead relax, dilating the blood vessel and reducing blood pressure.

To test this theory, Prof. Abbott’s co-authors at the University of Copenhagen measured changes in tension in the walls of arteries from rats. Their findings confirmed that the two catechins from tea relax and dilate arteries by activating the KCNQ5 ion channel.

Milky tea

The authors are confident that adding a dash of milk to black tea does not reduce its antihypertensive effects.

Milky tea, applied directly to cells in the lab, failed to activate their KCNQ5 channels. But this is likely not the case when a person drinks it.

Prof. Abbott explains:

“We don’t believe this means one needs to avoid milk when drinking tea to take advantage of the beneficial properties of tea. We are confident that the environment in the human stomach will separate the catechins from the proteins and other molecules in milk that would otherwise block [the] catechins’ beneficial effects.”

The scientists also discovered that warming green tea to 35°C increased the activation of KCNQ5.

However, lovers of iced tea need not be concerned.

“Regardless of whether tea is consumed iced or hot, this temperature is achieved after tea is drunk, as human body temperature is about 37°C,” says Prof. Abbott. “Thus, simply by drinking tea, we activate its beneficial, antihypertensive properties.”

Electrical activity in the brain

KCNQ5 also exists in the membranes of nerves in the brain, where it helps regulate electrical activity and signal transmission.

People with a disorder called epileptic encephalopathy have a version of the channel protein that does not respond effectively to voltage changes, which leads to frequent seizures.

The study authors point out that catechins can cross the blood-brain barrier, which prevents larger molecules, including some drugs, from entering the brain.

In theory, drugs modeled on catechin molecules could, therefore, help correct the cause of epileptic encephalopathy.

“Discovery of their ability to activate KCNQ5 may suggest a future mechanism to fix broken KCNQ5 channels to ameliorate brain excitability disorders stemming from their dysfunction,” the researchers conclude.

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Around 1 million people in the United States and 10 million people worldwide have Parkinson’s. It is the second most common neurodegenerative disorder after Alzheimer’s disease.

Parkinson’s disease is a progressive brain disorder that affects dopamine-producing neurons. It causes tremors, muscular stiffness or rigidity, and slowness of movement, among other symptoms.

Loss and degeneration of dopamine-producing neurons in a specific region of the brain called the substantia nigra causes the movement-related, or “motor,” symptoms that can characterize Parkinson’s.

There is no cure for Parkinson’s disease, though several drug treatments can help alleviate the symptoms. The most commonly prescribed medication for this purpose is levodopa (Sinemet), which replenishes dopamine levels.

“Currently, there is no preventive medicine for Parkinson’s disease,” notes Dr. Akiko Kojima-Yuasa, an associate professor at the Graduate School of Human Life Science at Osaka City University, in Japan, “we only have coping treatments.”

One cause of cell loss in the substantia nigra is oxidative stress. This led Dr. Kojima-Yuasa and colleagues to investigate whether sesaminol, a powerful antioxidant, could prevent nerve cell death in a model of Parkinson’s.

Sesaminol is found in abundance in sesame seed husks, which are a waste product from the industrial extraction of sesame oil.

Oxidative damage

The researchers used a toxic chemical called 6-hydroxydopamine to model the oxidative damage that occurs in Parkinson’s.

When they applied the chemical to human nerve cells growing in lab cultures, the concentration of damaging reactive oxygen species increased, and the cells began to die off.

Adding sesaminol to the cultures significantly reduced the concentration of reactive oxygen species and prevented cell death. Sesaminol appeared to shield the cells from oxidative damage by increasing their production of two protective proteins: Nrf2 and NQO1.

Next, the researchers turned to a standard animal model of Parkinson’s disease, which involves dosing mice with the neurotoxin rotenone.

The toxin reduces dopamine production in the animals’ brains. This impairs their motor abilities and reduces their gut motility, which are both classic symptoms of Parkinson’s in humans. In fact, people with the disease might experience constipation decades before difficulties with movement become apparent.

Mice that ate a diet containing sesaminol for 36 days had higher dopamine levels and performed better on a standard test of motor abilities than control-group mice that ate a normal diet. The gut motility of the mice in the test group was also normal.

In addition, the mice that ate sesaminol had lower levels of alpha-synuclein in their substantia nigras. Alpha-synuclein is a protein that clumps together to form larger structures called Lewy bodies, which are a characteristic feature of neurodegeneration in Parkinson’s.

The research has been published in the journal Heliyon.

Preventive treatment?

In their paper, the scientists conclude:

“Notably, the protective effect was observed with the feeding of a small amount of sesaminol. These results show that sesaminol is very suitable for use as a preventive treatment of [Parkinson’s disease]. Further detailed elucidation of the mechanism of action will be necessary for practical application.” Dr. Kojima-Yuasa and her team are keen to start clinical trials of the extract.

The authors suggest that sesaminol may be able to cross the blood-brain barrier in humans. This barrier prevents pathogens and large molecules from entering the brain. Further investigation, however, is needed to support the findings.

Overall, it is worth keeping in mind that results of studies in cell cultures and animal models do not always reflect what happens in the human body.

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Researchers have found that aerobic exercise may reduce cognitive decline in people with Alzheimer’s disease.

The research, published as a pilot study in the Journal of Alzheimer’s Disease, supports aerobic exercise as an intervention for people with this condition and lays the ground for future, larger studies to corroborate the initial findings.

Alzheimer’s treatments

According to the National Institute on Aging (NIA), Alzheimer’s disease is an irreversible and progressive neurological disorder.

At its mildest, it can affect a person’s ability to think or remember things. Moderate forms of the condition can affect a person’s brain areas and impair language, reasoning, sensory processing, and conscious thought.

When the disease progresses to become severe, it can stop a person from performing basic, everyday tasks and recognizing or communicating with friends or family.

According to the NIA, researchers estimate Alzheimer’s disease affects over 5.5 million people in the United States. It typically first appears in people in their mid-60s.

The Alzheimer’s Association highlight that there is no known cure for the condition, with treatments instead focusing on easing the symptoms of the disease or slowing its progression.

While various drugs are available in the treatment of Alzheimer’s disease, there is an emerging body of evidence suggesting that aerobic exercise may also be effective in reducing the progression of the disease.

However, as the authors of the present study note, randomized controlled trials that have put this to the test have produced inconsistent findings.

To begin to resolve this problem in existing research, the present authors devised a randomized controlled trial to act as a pilot study.

This study examined whether a group of older adults with Alzheimer’s disease would have less cognitive decline following 6 months of aerobic exercise compared with the expected level of cognitive decline they would experience if the disease progressed naturally.

Pilot study

The study involved 96 participants aged 66 years or older with Alzheimer’s disease.

Researchers randomly split these participants into two groups. One group of 64 people took part in supervised cycling exercise classes three times a week for 6 months.

The remaining 32 participants took part in supervised stretching and range of motion exercise classes, which the scientists matched to the cycling group in terms of the regularity of the classes and their length of time, but at low intensity. This latter group also acted as a control.

Researchers continually monitored participants’ heart rates in both groups. The team also supported the cycling group to achieve 50–75% heart rate reserve while helping the control group maintain less than 20% heart rate reserve.

In addition, the scientists measured participants’ cognition at the beginning of the intervention, as well as at months 3, 6, 9, and 12.

Exercise reduced cognitive decline

The researchers found that both the cycling group and the stretching or range of motion group scored significantly better than would have been predicted if they had continued with treatment as normal.

The researchers used the Alzheimer’s Disease Assessment Scale-Cognitive Subscale, a scaling system where a greater number reflects worse cognition.

According to this scale, after 6 months, the cycling group scored 1.0±4.6, and the control group 0.1±4.1. This compares with a score of 3.2±6.3, which would be in line with expectations given the natural progression of Alzheimer’s disease.

According to Prof. Fang Yu, Edson Chair in Dementia Translational Nursing Science at the Arizona State University Edson College of Nursing and Health Innovation, and corresponding author of the study, “our primary finding indicates that a 6-month aerobic exercise intervention significantly reduced cognitive decline in comparison to the natural course of changes for Alzheimer’s dementia.”

“However, we did not find a superior effect of aerobic exercise to stretching, which is likely due to the pilot nature of our trial. We do not have the statistical power to detect between-group differences, there was a substantial social interaction effect in the stretching group, and many stretching participants did aerobic exercise on their own.”

As a consequence, scientists need to conduct further research to corroborate these initial encouraging findings.

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Although obesity is common, there are many misconceptions associated with it — and these myths often fuel social stigma. In this edition of Medical Myths, we tackle five of the most common misunderstandings about obesity.

According to the Centers for Disease Control and Prevention (CDC), in the United States, 42.4% of adults have obesity. Globally, the World Health Organization (WHO) estimate that around 650 million adults have obesity.

People are growing increasingly aware of the health issues associated with obesity. However, despite public health campaigns, myths continue unabated. Many of the most common myths drive stigma that can impact the mental health of people with obesity.

For instance, the results of one 2020 meta-analysis on the subject indicate “a stronger association between weight stigma and diminished mental health with increasing body mass index [BMI].”

Addressing the myths that surround obesity is important. With this in mind, this article will tackle five of the most prevalent misunderstandings around this condition.

1. To reduce obesity, just eat less and move more

In many cases, consuming more calories than the body needs for a prolonged amount of time is the direct cause of obesity. Indeed, the vast majority of measures for reducing obesity aim to lower caloric intake, increase physical activity, or both.

Although diet and exercise are important factors, several unrelated factors can also play a significant part in obesity.

These factors, which people often forget about, include insufficient sleep, psychological stress, chronic pain, endocrine (hormone) disruptors, and the use of certain medications.

In these cases, overeating, for instance, may be a symptom rather than a cause.

Also, some of these factors work together to increase the chance of obesity. As an example, stress can increase the chance of obesity. Due to the prevalence of weight stigma, obesity can be stressful for some people, thereby increasing stress levels and sparking a negative feedback loop.

Added to this, stress can impact sleep quality, and this, in turn, might cause sleep deprivation, which is another factor in the development of obesity. Sleep deprivation also appears to increase stress levels. As one paper explains, “stress hormone levels correlate positively with decreased sleep duration.”

Sleep apnea, wherein a person stops breathing for short periods during sleep, is more prevalent in people with overweight or obesity. Again, a cycle can form: As they gain weight, their sleep apnea may worsen, which can lead to sleep deprivation, which can lead to further weight gain.

As another example, there appears to be an association between chronic pain and obesity. The reasons for this relationship are sure to be complex and differ from person to person, but they likely include chemical factors, sleep, depression, and lifestyle.

It is not difficult to see how chronic pain would both increase stress levels and impact sleep, adding to the negative loops outlined above.

Stress, sleep, and pain are just three interlinking factors that can drive obesity. Each person’s case will be different, but simply receiving an instruction to “move more and eat less” might not be an adequate intervention.

As this article will continue to reiterate, calorie intake and exercise are vital factors in reducing obesity, but they do not tell the whole tale.

2. Obesity causes diabetes

Obesity does not directly cause diabetes. It is a risk factor for type 2 diabetes, but not everyone with obesity will develop type 2 diabetes, and not everyone with type 2 diabetes has obesity.

Obesity is also a risk factor for gestational diabetes, which occurs during pregnancy, but it is not a risk factor for type 1 diabetes.powered by Rubicon Project

3. People with obesity are lazy

An inactive lifestyle is a factor in obesity, and becoming more active can aid weight loss, but there is more to obesity than inactivity.

One 2011 study used accelerometers to measure the activity levels of 2,832 adults, aged 20–79 years, for 4 days. Their step counts reduced as their weight increased, but the differences were not as significant as one might predict, particularly for women.

The list below shows the women’s weights and how many steps they took per day during this study:

  • those with a “healthy” weight: 8,819 steps
  • those with overweight: 8,506 steps
  • those with obesity: 7,546 steps

When one considers that someone with overweight or obesity expends more energy with each step, the difference between the groups’ overall energy expenditures may be even more slight.

This does not mean that physical activity is not essential for good health, but the story is more complex.

Another factor to consider is that not all people are able to perform physical activity. For instance, some physical disabilities can make moving challenging or impossible.

Also, certain mental health issues can severely impact motivation — and there appears to be a relationship between depression and obesity, which further deepens the complexity.

Aside from physical and mental health issues, some people with obesity may also have a negative body image, which might make leaving their home a more daunting prospect.

4. If your close relatives have obesity, so will you

The relationship between obesity and genetics is complex, but someone whose relatives have obesity will not necessarily develop the condition themselves. However, their chance of doing so is higher.

Understanding the role of genes and the environment in isolation is difficult; people who share similar genes often live together and, therefore, may have similar dietary and lifestyle habits.

In 1990, a group of researchers published a study that helped split genes from the environment. The results appeared in The New England Journal of Medicine.

The scientists investigated twins who had been brought up apart and compared them with twins who had been brought up together. In this way, they hoped to tease apart the impact of genetics and the environment. Overall, they conclude:

“[G]enetic influences on [BMI] are substantial, whereas the childhood environment has little or no influence.”

One twin study from 1986 reached similar conclusions. The researchers found that the weights of adopted children correlated with the weights of their biological parents, but not with those of their adoptive parents.

Although more recent studies have identified a more significant role for the environment, genetics do appear to play an important part in obesity.

In recent years, scientists have searched for the genes that influence the chance of obesity. As the CDC explain, in most people with obesity, “no single genetic cause can be identified. Since 2006, genome-wide association studies have found more than 50 genes associated with obesity, most with very small effects.”

One gene that is linked to obesity is a variant of a gene called FTO. This variant, according to one 2011 study, is associated with a 20–30% increased chance of obesity.

Although genetics are important, this does not mean that obesity is inevitable for someone whose relatives have the condition. The above study, which involved individuals with the FTO gene variant, looked at the role of exercise. As the paper explains:

“Using data from over 218,000 adults, the authors found that carrying a copy of the susceptibility gene increased the odds of obesity by 1.23-fold. But the size of this influence was 27% less in the genetically susceptible adults who were physically active.”

A review and meta-analysis that investigated the same gene variant came to a similar conclusion. The authors explain that people with the FTO variant “respond equally well to […] weight loss interventions and thus genetic predisposition to obesity associated with the FTO minor allele can be at least partly counteracted through such interventions.”

However, it is important to reiterate the point that these interventions alone may not be helpful for some people.

5. Obesity does not impact health

This is a myth. There are several conditions associated with obesity. For instance, obesity increases the risk of diabetes, high blood pressure, cardiovascular disease, osteoarthritis, sleep apnea, and some mental health conditions.

That said, even modest weight loss can provide health benefits. According to the CDC, “weight loss of 5–10% of your total body weight is likely to produce health benefits, such as improvements in blood pressure, blood cholesterol, and blood sugars.”

Also, a review of existing literature in the BMJ concludes that weight loss interventions “may reduce premature all-cause mortality in adults with obesity.”

Obesity is highly prevalent. Currently, the stigma surrounding the condition is unhelpful and can be damaging. We need to address it whenever we encounter it.

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In today’s turbulent political climate, hostility is becoming an increasingly familiar part of everyday life. This negative environment not only makes it uncomfortable to socialize, but prolonged, cynical hostility may pose a serious health issue.

According to a Baylor University-led study that appeared in the September 2020 issue of Psychophysiology, cynical hostility may cause an increased risk of developing cardiovascular disease.

The findings resulted from data collected from 196 participants in a stress test conducted by the Laboratory for the Study of Stress, Immunity, and Disease at Carnegie Mellon University in Pittsburgh, PA.

Participants took part in two lab sessions, 7 weeks apart. Sessions consisted of establishing a 20-minute baseline and a 15-minute psychological stress test.

Researchers recorded each person’s heart rate and blood pressure, and the participants completed a standard psychological scale to determine their personality and temperament.

The sessions involved placing participants in reasonably stressful situations, for example, asking them to take 5 minutes to prepare and then deliver a speech defending themselves from traffic violations or shoplifting accusations. All participants knew that the researchers would record and evaluate them.

As Alexandra T. Tyra, a doctoral candidate in psychology and neuroscience and the lead study author, explains, “These methods of social and self-evaluation are designed to increase the experience of stress and have been validated in prior research.”

Tyra’s team looked at three types of hostility: cognitive, which includes cynical hostility; emotional hostility, which links to chronic anger; and behavioral hostility, which involves verbal and physical aggression.

The researchers found that stress responses had no relationship to emotional or behavioral hostility.

“This does not imply that emotional and behavioral hostility are not bad for you,” says Tyra, “just that they may affect your health or well-being in other ways.”

The prolonged harm of cynical hostility

Cognitive hostility’s impact on the cardiovascular system ultimately comes down to how a person deals with repeated exposure to stress triggers.

Tyra explains how a typical reaction to repeated stress normally plays out, “When you’re exposed to the same thing multiple times, the novelty of that situation wears off, and you don’t have as big of a response as you did the first time.” This is a healthy reaction to stress.

With cynical hostility, a person continues to react to stressful circumstances with a similar intensity level, no matter how much exposure they have to similarly stressful situations.

Consistent arousal of this nature causes a strain on the cardiovascular system over time.

The Baylor University study represents the latest of its kind linking cynicism with adverse health problems. A 2014 study appearing in Neurology found that those with higher levels of cynical distrust in later life might be more likely to develop dementia.

The study author, Anna-Maija Tolppanen, Ph.D., of the University of Eastern Finland in Kuopio, believed her team’s findings showed a person’s “view on life and personality may have an impact on their health.”

Although it is more common to probe the harm caused by cynicism and negative thinking, some researchers try to find a positive outcome for less positive mindsets.

One such study looked at pessimism in particular. The research suggested “defensive pessimism” might be useful for developing actionable strategies in the face of the worst possible outcome.

Still, research has repeatedly linked suspicious thoughts and a hostile disposition with poor health.

Timely findings

Following the study, the Baylor University team believes the outcome of its research is very timely. It comes near the end of a year of extremes, dominated end-to-end by intense political debates and social commentary.

Some might find it natural to approach each adverse circumstance with excessive cynical hostility. However, these harsh stances might not be worth the added risk to a person’s cardiovascular health. With this in mind, the study authors offer a word of caution:

“Perhaps the next time someone thinks a negative thought about the motives, intentions or trustworthiness of their best friend, a co-worker or even a politician, they will think twice about actively engaging with that thought.”

Even as they weigh the immediate implications of their research, the study team hopes that future research will give more insight into how cynical hostility affects one’s health across an entire life span. What can we learn from following more cynically hostile test participants as they age?

For now, a crucial takeaway of this study, especially in such a tense political climate, is to keep an open mind and a cool head.

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In a small clinical trial, patients with major depressive disorder (MDD) who were given two doses of psilocybin along with psychotherapy showed a reduction in depressive symptoms. The psychedelic’s therapeutic effects persisted for up to 4 weeks with minimal side effects.

Psychedelics are known for their hallucinogenic properties, but their mind-altering effects may also benefit people with depression.

According to the National Institute of Mental Health, about 17.3 million adults in the United States have experienced at least one depressive episode.

Currently, the gold standard for treating MDD is psychotherapy or antidepressant medication. A 2014 study in World Psychiatry found that psychotherapy combined with antidepressants was more effective than the former alone.

Replacing antidepressants with hallucinogenic mushrooms

New antidepressants are ketamine-like drugs that show a high therapeutic response. A 2014 meta-analysis in Psychopharmacology reports that roughly 0.5 milligrams per kilogram of ketamine effectively reduced depressive symptoms. These effects also lasted 2–3 days after treatment. However, there are some drawbacks.

While currently approved by the Food and Drug Administration (FDA), there are some short-term side effects to consider when using ketamine, such as feeling strange or bizarre, numbness, and difficulties speaking.

Ketamine has a high liability for addiction and may have a large potential for abuse. A 2018 study in Neurobiology of Stress found that repeated low-dose ketamine treatments for treatment-resistant depression resulted in cognitive impairments and potential for abuse.

To avoid people abusing their medication, alternative treatments to support psychotherapy are needed — enter psilocybin.

There is growing evidence of psilocybin’s antidepressant properties. A study in the Journal of Psychopharmacology demonstrateda single psilocybin dose that produced an antidepressant and anxiolytic response in cancer patients, which lasted for 5 years.

Compared with ketamine, psilocybin has lower addictive properties, which would be beneficial as a potential add-on for current treatments. However, clinical research evaluating this substance in combination therapies is limited.

Recently, researchers at Johns Hopkins University published an article contributing to the research investigating the effectiveness of psilocybin-assisted therapy for depression.

“These data expand the findings of previous studies involving patients with cancer and depression, as well as patients with treatment-resistant depression, by suggesting that psilocybin may be effective in the much larger population of MDD,” write the study authors.

Their clinical trial results appear in JAMA Psychiatry.

Johns Hopkins clinical trial

From August 2017 to April 2019, the researchers of the current study recruited adults with MDD who were not taking antidepressant medications and had no history of psychotic disorder, suicide attempts, or hospitalizations. The scientists randomly assigned a total of 24 participants to an immediate or a delayed treatment group.

The psychedelic-assisted therapy lasted for 8 weeks, with 18 in-person visits and 2 days for psilocybin treatment.

Participants in the immediate treatment group began the psilocybin treatment during an 11-hour supportive psychotherapy session. The researchers allowed for a 1.6-week break between the first and second doses. In contrast, the delayed treatment group waited 8 weeks before receiving psilocybin-assisted therapy.

Reduction in severity of depression

At the time of enrollment, participants had a score of 23 in the GRID-Hamilton Depression Rating Scale (GRID-HAMD), which indicates moderate depression. After a 1-week and 1-month follow-up, participants in the immediate treatment group dropped to a score of 8, indicating mild depression.

In the entire cohort, 67% reduced the severity of their depressive symptoms 1 week after psilocybin treatment. This percentage grew to 71% when researchers followed up after 4 weeks.

After 1 week, the researchers found that 58% of the cohort were no longer classified as clinically depressed. By week 4, they found that 54% of the participants were no longer classified as depressed.

Limitations from the clinical trial design

Several limitations exist that could challenge the usefulness of the study results. The research had insufficient minority representation, as recruitment leaned towards non-Hispanic whites.

This is important because while white people typically report more cases, the American Psychiatric Association note that Black and Hispanic Americans are more likely to experience depression for more extended periods. In response, the researchers acknowledge the need for future studies to validate this proof of concept in more representative populations.

The study also fails to address the long-term effects of psilocybin treatment. Unlike the investigation on cancer patients, which had a 5-year follow up, the current research followed up after only 1 month.

There were also variables in the study design that could question psilocybin’s effectiveness as an antidepressant drug. One comes from a lack of a placebo group. Placebos are essential in determining whether a person truly benefitted from the drug and not from outside factors. For this reason, the safety of using psilocybin remains unknown.

Final thoughts

Overall, the authors find their clinical trial supports the use of psilocybin-assisted therapy for MDD.

“Although the rapid antidepressant effects of psilocybin are similar to those reported with ketamine, the therapeutic effects are different. Ketamine effects typically last for a few days to 2 weeks, whereas the current study showed that clinically significant antidepressant response to psilocybin therapy persisted for at least 4 weeks, with 71% of the participants continuing to show a clinically significant response (≥50% reduction in GRID-HAMD score) at week 4 of follow-up.”

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A study finds that social anxiety and depression lead to a greater use of dating apps and affect what people hope to gain from them.

Pew Research Center data released in February this year indicate that, in the United States, as many as 30% of adults have used a dating site or app.

According to a Statista survey, in the first quarter of 2020, Tinder, the most popular of these apps, had more than 6 million subscribers.

There are numerous reasons for using a dating app. Now, a new study from Ryerson University in Toronto, Canada, looks specifically at the link between social anxiety, depression, and dating apps.

According to this research, there is a link between social anxiety and depression and a more extensive use of dating apps.

“With increased symptoms of social anxiety and depression, women may be even more likely to turn to technology for social connection, especially if alternative forms of social contact are reduced due to social avoidance.” – Senior author Martin Antony, from Ryerson University in Toronto, Canada

The study appears in Cyberpsychology, Behavior, and Social Networking.

Why do people use dating apps?

Previous research suggests there are six things people who use Tinder hope to attain. These “Tinder motives” are:

  • love
  • casual sex
  • ease of communication
  • self-worth validation
  • thrill of excitement
  • trendiness

The prevailing theory tested in the new research is the positive link between social anxiety and depression with a greater use of dating apps. In addition, the researchers predicted positive associations between social anxiety and depression and a desire for:

  • ease of communication for men, due to the anxiety associated with asking potential partners for a date, traditionally perceived as a male responsibility
  • love, equally for both genders
  • self-worth validation, equally for both genders
  • the thrill of excitement, especially for men
  • casual sex, especially for men

The study authors also predicted a negative association between social anxiety, depression, and contacting dating app matches equally for both genders.

The study’s findings

A total of 374 individuals who use dating apps were recruited for the study and responded to questions posed through Amazon’s Mechanical Turk platform.

There were no inclusion or exclusion criteria, and each person received $1 for taking part in the study.

The researchers asked participants to fill out the 17-question Social Phobia Inventory (SPIN), in which a person describes the anxiety they have experienced in social situations over the past week. Researchers recognize the SPIN survey for its usefulness as a psychometric measure.

In addition, individuals completed the equally well-regarded 21-question Depression Anxiety Stress Scales survey for measuring anxiety, depression symptoms, and stress.

Participants also completed the Tinder Motives Scale survey that tracked the importance of five of the six Tinder motives to the individual. The research team did not include trendiness because they considered the survey ineffective for measuring its significance.

The scientists measured individuals’ use of dating apps through the Online Dating Inventory questionnaire to assess their use and behavior.

The researchers found that social anxiety and depression are not interchangeable, and were variously linked, or not, with different motives for using dating apps.

The researchers’ general hypothesis was deemed correct: social anxiety and depression do appear to be associated with greater dating app use. Beyond that, the authors of the study drew a variety of conclusions.

They found that:

  • Social anxiety and depression are associated with the use of dating apps for ease of communication by both genders, though the effect is more pronounced for women.
  • Women with social anxiety are more likely to be interested in obtaining love through dating apps. Depression did not affect whether people were looking for this, for either men or women.
  • Dating apps are used for self-worth validation by people of both genders with social anxiety. This was also true of people with depression, with a stronger effect in women than men.
  • Contrary to the researchers’ expectations, there was a positive link between social anxiety and the thrill of excitement for women, though not for women living with depression, and not for men.
  • There was an association between social anxiety in men and women with an effort to obtain casual sex. This was also true in people living with depression, with a stronger effect in women.

The researchers also discovered a negative correlation between social anxiety and depression in men and the likelihood that they would actually contact a person who turned out to be a match. The likelihood a woman would initiate contact was not affected at all by their level of depression.

The study authors point out that they cannot know whether social anxiety and depression lead to greater dating app use or the other way around, suggesting this open question would benefit from further research.

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Asian female buying some wine at a supermarket

Doctors have warned that people in the United States may be drinking excessively as a way to cope with the COVID-19 pandemic.

In a new viewpoint article, two doctors have warned that more people in the U.S. may be turning to alcohol as a way of coping with the “myriad stressors” of the COVID-19 pandemic.

The article, published in the Journal of General Internal Medicine, proposes a series of interventions to try to minimize this behavior and better support people with alcohol use disorder.

Coping strategy

It is well documented that drinking alcohol is one way that people cope with stressful situations. For example, research has shown that in the U.S., people tend to drink more alcohol following terrorist attacks.

Furthermore, if a person has alcohol use disorder, they are more likely to use alcohol to cope with the stress of a traumatic event.

In this context, the current COVID-19 pandemic is a particular cause for concern. The authors of the current article point out that rather than being a single event, the effects of the COVID-19 pandemic are prolonged over time, potentially exposing people to ongoing trauma.

Further, the pandemic has caused various potential stressors that a person may cope with by drinking alcohol.

As well as the catastrophic effect on people’s health and the loss and grief experienced by many, the pandemic has also disrupted economies and social and cultural life, threatening people’s jobs, disrupting their interpersonal support structures, increasing barriers to health care, and forcing many people into isolation.

Before the pandemic, researchers had noted that people in the U.S. were tending to drink more. This was particularly the case for females.

Recent research suggests that people in the U.S. increased their alcohol consumption in the early phase of the pandemic. This is in line with similar findings from studies in the United Kingdom and Australia.

Alcohol health effects

This matters because well-documented links exist between increased alcohol consumption and adverse health outcomes.

As the National Institute on Alcohol Abuse and Alcoholism point out, alcohol consumption can change mood and behavior, damage a person’s heart, liver, and pancreas, increase the risk of several types of cancer, and weaken a person’s immune system.

Research has also linked excessive alcohol consumption to mental health disorders, such as anxiety and depression, which may worsen during the pandemic.

Consequently, it is important to encourage people to find alternative coping strategies in response to the stressors of the pandemic. Effective support should also be available for people experiencing the effects of increased alcohol consumption or people with alcohol use disorder.

Interventions

The authors of the present study offer various suggestions for interventions that may help reduce people’s dependence on alcohol during the pandemic. Other suggestions focus on better preparing clinical services to support people with substance abuse issues.

According to Dr. Shelly F. Greenfield, director of the Alcohol, Drug, and Addiction Clinical and Health Services Research Program at McLean Hospital in Belmont, MA, “[i]ncreasing identification of harmful alcohol use in patients and intervening early are key components of addressing this problem.”

“In addition, recognition of the problem from policymakers could lead to changes in federal regulations — such as we have seen with telehealth — and improvements in access to healthcare,” she notes.

The authors suggest that public health messaging should raise awareness of the potential for increased drinking during the pandemic, as well as giving advice on alternative coping strategies for the stressors of the pandemic.

They also suggest that primary care practitioners should offer increased screening for alcohol use disorder when people contact primary care services.

Technologies, such as telehealth — that enable clinical information to pass between doctors and individuals at a distance — may also be valuable for people who are isolating or where the pandemic has forced a reduction in the enrolment for some face-to-face clinical services.

Finally, the authors highlight that ensuring people have access to health insurance to cover medical treatment costs is crucial. This is particularly important given the number of people who depend on work-place health insurance and the significant number of people who have lost their jobs during the pandemic.

Co-author Dr. Dawn E. Sugarman, a research psychologist in the Center of Excellence in Alcohol, Drugs, and Addiction at McLean Hospital, notes that:

“We hope this article will call attention to the pandemic’s effects on alcohol use and offer mitigating approaches to this under-recognized public health concern.”

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Nerve damage from neurodegenerative conditions, traumatic injuries, and certain eye conditions leads to disability and death for millions of people in the United States. Currently, doctors consider such damage irreversible.

However, researchers at The Ohio State University Wexner Medical Center have discovered a new type of human immune cell that appears to prevent and reverse nerve damage in the optic nerve and spinal cord.

This finding could allow researchers to create more advanced neurodegenerative immunotherapies.

These therapies might offer fresh hope to people with currently incurable neurological conditions, including Alzheimer’s disease, multiple sclerosis, stroke, and Parkinson’s disease. They might also help treat central nervous system (CNS) damage from injury or infection.

“I treat patients who have permanent neurological deficits, and they have to deal with debilitating symptoms every day, “says Dr. Benjamin Segal, professor and chair of the Department of Neurology at The Ohio State College of Medicine and co-director of the Ohio State Wexner Medical Center’s Neurological Institute.

“So the idea of being able to restore neurological function and take that burden away from my patients is really amazing.”

Funded by the National Eye Institute (NEI), the National Institutes of Health (NIH), the Wings of Life Foundation (C.Y.), and the Dr. Miriam and Sheldon G. Adelson Research Foundation, the study appears in the journal Nature Immunology.

The emerging field of immunotherapy

Immunotherapy therapies alter the immune response by stimulating it or using the body’s own immune cells to treat disease. Over the past few decades, scientists have begun developing them to tackle a wide range of medical conditions.

Doctors already use immunotherapies to treat certain types of cancer. They help the immune system to recognize and destroy cancer cells.

Other researchers are investigating whether immunotherapy could help prevent or treat neurological disease.

Researchers have been extensively testing immunotherapies that increase the clearance rate of certain proteins whose accumulation has links with neurological diseases, such as Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, and dementia with Lewy bodies.

Scientists have already created T-cell mediated immunotherapy approaches that target proteins linked with these neurological diseases, such as amyloid-beta, tau, and alpha-synuclein proteins.

Immunotherapy may also present opportunities to prevent and treat nerve damage by activating alternative immune pathways in response to CNS damage.

A 2014 study found that anti-inflammatory or immunoregulating (M2) macrophages are critical for remyelination, which is a form of nerve repair.

The study

The researchers examined immune cells in fluids and spinal cord tissues collected from mice with optic and spinal nerve damage.

Within these fluids and tissues, the team found a unique type of granulocyte. Granulocytes are a category of white blood cells. Neutrophils are the most common kind of granulocytes.

Neutrophils are scavengers that help destroy pathogens or other unwanted particles in the body. The new type of granulocyte that the scientists identified behaved like an immature neutrophil.

This newly discovered granulocyte helped protect neural cells and tissues from damage in the mice. It also encouraged nerve cell regeneration by secreting a mix of beneficial growth compounds. The team also found a human cell line with similar neuroprotective properties.

“This type of cell actually secretes growth factors to rescue dying nerve cells. It can also stimulate the surviving nerve cells to grow new fibers once they’re severed or damaged in the [CNS], which is really unprecedented,” says Dr. Segal. “This can potentially lead to therapeutic breakthroughs for a wide range of conditions by repairing these nerve pathways.”

However, researchers have a long way to go before doctors can use immune cells, such as this newly discovered granulocyte, to treat humans.

The team’s first major hurdle will be figuring out how to harness the power of this new immune cell and enhance its natural healing effects by growing it in a laboratory setting. Next, they’ll have to prove their newly proposed therapy is both effective and safe in humans.

In the future, the team hopes that doctors can inject these novel cells into people with chronic cognitive deficits to slow down or halt degenerative decline.

Dr. Segal concludes that they have got a lot of work left to do to make their laboratory findings relevant in a clinical setting, but says he is optimistic about the road ahead:

“There’s so much that we’re learning at the bench that has yet to be translated to the clinic, but I think there’s huge potential for the future.”

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A small observational study has found no evidence that osteoporosis drugs increase the risk of getting COVID-19. The research hints that some of the drugs may even reduce the risk.

In people with osteoporosis, progressive reductions in bone density increase the risk of fractures. The condition tends to affect older people, and its incidence among females increases following menopause.

Researchers have yet to directly test the possible effect of drug treatments for osteoporosis on a person’s risk of developing COVID-19. Influential health organizations, such as the American College of Rheumatology, recommend that people continue taking their medications as usual.

Now, researchers led by a team from the Hospital del Mar Medical Research Institute, in Barcelona, Spain, have analyzed data from 2,102 patients who received treatments for osteoporosis, osteoarthritis, and fibromyalgia at the hospital.

The mean age of the patients was 66.4 years, and 80.5% were female. Around 64% had osteoarthritis, 44% had osteoporosis, and 27% had fibromyalgia.

The researchers compared the incidence of COVID-19 in these patients between March 1 and May 3, 2020, with the incidence in Barcelona as a whole over the same period, during the first wave of infections in Spain.

The age-adjusted incidence rate for COVID-19 was 3.7% in the general population of Barcelona, compared with 4.7% for this group of patients. However, when the researchers focused on the subset of 914 patients with osteoporosis, they found a lower rate of infection: around 3%.

The data appeared to show that some drugs increased COVID-19 risk, some decreased it, and others had no effect. However, this was an observational study, rather than a clinical trial, and the group sizes were too small to draw any definitive conclusions.

The researchers report their findings in the journal Aging.

Statistical models

The physicians and scientists used a statistical modeling technique called Poisson regression to estimate the relative risk of COVID-19 associated with particular treatments.

After adjusting for factors already known to affect the risk, including age, sex, and health conditions such as diabetes and cardiovascular disease, their models suggested that most of the treatments had no influence on the incidence of infection.

These included drugs that directly target osteoporosis, such as oral bisphosphonates or vitamin D, as well as nonsteroidal anti-inflammatory drugs that target chronic pain caused either by fractures from weakened bones or coexisting musculoskeletal conditions.

Antihypertensive drugs, used to treat the common comorbidity of high blood pressure, also showed no influence on COVID-19 infection rates.

According to the models, three osteoporosis treatments were potentially associated with a reduced risk of COVID-19.

Denosumab, a monoclonal antibody treatment, was associated with a 42% reduced risk. There was a considerable degree of uncertainty about this value — it could range from a 72% reduced risk to a 22% increased risk.

Intravenous zoledronate was associated with a 38% reduced risk, with a range of 73% reduction to 41% increase. Meanwhile, calcium showed a 36% reduced risk, with a range of 63% reduction to 12% increase.

“The study suggests that some of these treatments may protect patients against infection by [SARS-CoV-2, the virus that causes] COVID-19, although further studies still need to be conducted on more patients to prove it,” says the study’s first author, Dr. Josep Blanch-Rubió.

Both denosumab and zoledronate are known to modify the immune system, and they do so in different ways.

Denosumab decreases the activity of immune signalling molecules called cytokines, which are involved in the excessive immune reaction that characterizes severe COVID-19.

The authors speculate that zoledronate, meanwhile, may protect the lungs from the infection by stimulating T cells and natural killer cells.

Musculoskeletal conditions such as osteoarthritis and fibromyalgia can cause chronic pain, and fractures resulting from osteoporosis can also be painful. Some pain medications commonly prescribed to people with these health issues appeared to increase the risk of COVID-19.

This was particularly true for pregabalin, which was associated with a 55% increased risk of COVID-19, with a range of estimates of 14% reduced pain to 280% increased pain.

People with these conditions also frequently experience mood disorders, such as depression. Most of the antidepressants in the analysis were associated with an increased risk, apart from duloxetine, which was associated with a 32% reduced risk, with a range of 66% decrease to 34% increase.

Dr. Alba Gurt, a study author and primary care physician at the Pere Virgili Hospital Center, in Barcelona, concludes:

“The data from the study would indicate that the [osteoporosis] treatments and duloxetine administered to our primary care patients are safe against infection by [the virus that causes] COVID-19 and could even reduce its incidence. However, studies with a higher number of patients are required to verify this.”

Important limitations

The analysis had some important limitations that are common to all observational studies. The associations identified may result from hidden “confounders” — other influences on the risk of developing COVID-19 that the researchers did not take into account.

The statistical power of the study was limited due to the relatively small numbers of patients with osteoporosis taking each medication and the possibility of complex drug interactions.

Also, the estimates of relative risk have wide confidence intervals — a term that describes the level of certainty about the risk. As a result, it is possible that denosumab, zoledronate, and calcium could all increase the risk of COVID-19, though the estimates veered more toward the drugs having a protective effect.

Overall, the actual risks or benefits of these osteoporosis treatments with regard to COVID-19 may be very different from what the team has found.

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