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Melatonin and reduction in risk of youth Self harm.

Melatonin and reduction in risk of youth Self harm.

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Researchers examined how melatonin consumption affected children’s and teenagers’ self-harm. They discovered that melatonin consumption reduced self-harm in children and adolescents. Particularly in adolescent girls who were depressed and anxious.

These findings and the potential advantages of melatonin for mental health and wellbeing require further research to be confirmed. Young people frequently experience sleep difficulties including insomnia, particularly those who have psychiatric issues.

Some estimates place the number of young people who self-harm at roughly 17%. There aren’t many treatments for the disease among young people that have empirical backing right now.

According to a recent meta-analysis, addressing the root reasons of self-harm may lower its prevalence. Hence, some have proposed that correcting sleep issues may lower the frequency of self-harm.

Melatonin is the most frequently prescribed medication in Sweden for treating sleep disorders in kids and teenagers. A hormone that occurs naturally, melatonin supports a healthy sleep-wake cycle as well as other biological functions.

Treatment options for the habit might be improved by learning more about how melatonin influences self-harm in children and teenagers. Recently, researchers looked at the risk of self-harm and unintentional injuries in young people with and without psychiatric problems before and after melatonin administration.

They discovered that taking melatonin was associated with lower rates of self-harm, particularly among adolescent girls who were depressed and anxious. Journal of Child Psychology and Psychiatry published the paper.

Why Do Young People Self Harm?

There are several reasons why kids and teenagers self-harm. A traumatic event, like abuse, or a mental illness, like anxiety or depression, are frequently to blame.

Youth who self-harm may also be unable to articulate their emotions or feel like they have no control over their lives. Self-harm is not a healthy behaviour and should be seen as a cry for help rather than a coping mechanism for uncomfortable emotions.

It’s possible that kids and teenagers have trouble expressing their emotions. You can encourage kids to start talking about what’s going on in their lives by paying attention to what they are saying and doing.

Decreased risk of self-harm with melatonin

For the study, the researchers analyzed public healthcare data from 25,575 youths in Sweden who began melatonin treatment between ages 6 and 18.

The children and adolescents were followed for a year prior to melatonin prescription and a year following. They began treatment at an average of age 13 years old, and most commonly initiated treatment in November. Treatment lasted for an average of 6.4 months.

The researchers found that 87.2% of melatonin users received at least one psychiatric diagnosis by age 18. Over 50% received an ADHD diagnosis. Self-harm was around five times more common in girls than boys.

In the end, the researchers found that melatonin use decreased the risk of self-harm by 42% and poisoning risk by 41%. Effects were especially prevalent among girls and adolescents with depression and or anxiety.

They noted, however, that melatonin use did not decrease rates of bodily injuries, falls, or transport accident rates.

Limitations

Even though he was not engaged in the study, Dr. Lokesh Shahani, an associate professor of psychiatry at UTHealth Houston’s McGovern Medical School, commented:

“Some cases were overlooked since the study employed a national registration to obtain patient diagnosis, prescription, and death records. Moreover, no research was done in this city on the impact of various sleep aids on suicidal behaviour.

As several of the study participants also took antidepressants, Dr. McGrath continued, it’s probable that their use had an impact on the study’s findings.

Dr. Johnson-Arbor cautioned that the findings might not be applicable to other nations. Where melatonin is sold as a dietary supplement rather than a prescription, is less strictly regulated. This may be tainted with other drugs.

How melatonin may help mental health?

Dr. Kelly Johnson-Arbor, a medical toxicologist, co-medical director, and interim executive director of the National Capital Poison Center who was not involved in the study, responded to a question on how melatonin can decrease self-harm in young people by saying:

Melatonin, a hormone naturally produced by the brain, aids in controlling circadian rhythm and sleep-wake cycles. Young persons with psychiatric disorders frequently experience sleep disruptions, and childhood emotional and behavioural problems have also been linked to sleep issues.

It’s feasible that changes in sleep quality will lead to gains in emotional stability and behavioural control given that sleep issues can affect mood and conduct, said Kelly Johnson-Arbor, M.D.

Because of this, she explained, the authors of the study “sought to explore if management of the sleep cycle, through the use of melatonin, might potentially help avoid self-harm, body injuries, and falls in young individuals between the age of 6 and 18 years old.”

Melatonin during puberty

Depending on the animal species, melatonin administration was found to either hasten or postpone the onset of puberty in animal studies. Gonadotropin-releasing hormone, which controls puberty in humans, is produced by the brain. It may be altered by melatonin treatment, according to Dr. Johnston-Arbor.

“The development of female reproductive organs may be affected by melatonin as well. Yet, numerous human trials including kids who received melatonin for extended periods of time did not reveal any negative impacts on puberty, she continued.

Dr. Michael J. McGrath, a board-certified psychiatrist and medical director of The Ohana Luxury Alcohol Rehab who was also not engaged in the study, responded when asked the same question by saying:

Melatonin should be used with caution in prepubescent children because there is conflicting information and no conclusive evidence linking it to changes in the timing of puberty.

Melatonin dosage recommendations are still unclear.

The results “suggest that children with sleep disorders may experience additional benefits, other than sleep control, after the use of melatonin,” Dr. Johnson-Arbor stated in response to a question regarding the study’s implications.

“More studies are needed to confirm the appropriate amount and duration of usage of melatonin needed to achieve the effects discovered in this analysis,” she said. “This study’s results may not generalise to other populations, and these findings warrant further exploration.”

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Higher magnesium intake linked to lower dementia risk.

Higher magnesium intake linked to lower dementia risk.

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Researchers looked into the effects of magnesium consumption on dementia risk variables. They discovered that a higher magnesium intake is associated with a lower risk of dementia. The findings need to be confirmed by other research.

Globally, 57.4 million people suffered from dementia in 2019. This number is projected to increase to 152.8 million by 2050.

Many researchers focus on preventative measures, such as diet, as there is presently no cure for dementia. According to certain research, consuming magnesium supplements may lower the chance of developing dementia and improve cognitive performance.

Reports

According to one study that tracked 1,000 middle-aged adults for 17 years, those who consumed the most magnesium had a 37% lower risk of developing dementia than those who consumed the least.

Further investigation on the relationship between magnesium and cognitive function may help develop dementia prevention measures.

Several studies looked into how long-term magnesium intake impacts dementia risk. They discovered that improved brain health—especially in women—is associated with higher magnesium intake.

The National Capital Poison Center’s Dr. Kelly Johnson-Arbor, a medical toxicologist, co-medical director, and interim executive director who was not involved in the study, said, “Although more research is needed on this subject, the results of this study suggest that higher magnesium intake is associated with improved brain health and may conceivably also be linked to preserved mental function and a reduced or delayed risk of developing dementia.”

Published in the European Journal of Nutrition was the study. Further investigation on the relationship between magnesium and cognitive function may help develop dementia prevention measures.

Several studies looked into how long-term magnesium intake impacts dementia risk. They discovered that improved brain health—especially in women—is associated with higher magnesium intake.

The National Capital Poison Center’s Dr. Kelly Johnson-Arbor, a medical toxicologist, co-medical director, and interim executive director who was not involved in the study, said, “Although more research is needed on this subject, the results of this study suggest that higher magnesium intake is associated with improved brain health and may conceivably also be linked to preserved mental function and a reduced or delayed risk of developing dementia.”

Published in the European Journal of Nutrition was the study.

350 vs. 550 mg of magnesium daily

The researchers used 6,001 people’ medical records from the UK Biobank, aged 40 to 73, for the study. Measurements of blood pressure, an MRI scan, and dietary magnesium consumption over a 24-hour period five times during a 16-month period were all included in the data.

Almost 95% of individuals maintained consistent magnesium intake throughout the research period. Yet, some people over time increased their intake while others decreased it.

Finally, they discovered that, in MRI scans, increased dietary magnesium intake was associated with larger brain volumes and smaller white matter lesions (WML), both of which are signs of dementia.

Also, they discovered that magnesium intake exceeding 550 mg per day is associated with a brain age by 55 years old that is roughly one year younger than intake of 350 mg per day, which is close to the daily recommended amount.

They pointed out that this indicates a 41% increase in magnesium intake could enhance brain health, maintain cognitive function, and reduce the incidence of dementia.

They also discovered that post-menopausal women compared to pre-menopausal women had higher levels of neuroprotective magnesium intake than men. However, they pointed out that bigger brain sizes in women were associated with lower magnesium intake over time.

Most correlations between blood pressure measurements and magnesium consumption were insignificant.

How magnesium lowers dementia risk?

According to Dr. Howard Pratt, D.O., psychiatrist and Mental Health Medical Director at Community Health of South Florida, Inc., who was not involved in the study, magnesium is known to be a neuroprotector and to have favourable effects on blood pressure.

“High blood pressure is a documented dementia risk factor in and of itself. The study later showed a decrease in white matter lesions in medium to early old age, indicating that increasing dietary magnesium consumption can have beneficial benefits on cardiovascular health,” he noted.

Magnesium, according to Dr. Johnson-Arbor, may aid in reducing inflammation.

Chronic medical disorders that lead to magnesium deficiency are more likely to occur as we age, including renal disease and vitamin D deficiency. Several studies have suggested that magnesium may be implicated in the development of dementia and other neurologic diseases because magnesium deficiency may result in reduced cellular communications and increased inflammation inside the brain,” stated Dr. Johnson-Arbor.

Magnesium’s effects on women’s health

The University of California, Irvine, Program in Public Health’s Dr. Bruce Albala, an environmental and occupational health professor who was also not involved in the study, is trying to figure out what might be to blame for the enhanced effects of magnesium on post-menopausal women.

The authors suggest that the older women’s lower levels of chronic inflammation may have been a result of their higher magnesium consumption. At this time, these findings should be treated with caution, especially for the smaller magnesium dietary subgroups, the author advised.

The fact that oestrogen is a vasodilator, which means that it can assist lower blood pressure, is one of the interesting things about it. Post-menopausal women’s lower oestrogen levels can actually lead to greater blood pressure.

Study restrictions

Dr. Albala cited a number of the study’s limitations. The individuals’ average age was 55, thus it is unknown whether magnesium is beneficial later in life because the researchers did not include a follow-up MRI scan.

More than 95% of the subjects had steady magnesium intake during a 16-month period, he continued, therefore there was no information available on how variations in magnesium intake over time increase the risk of dementia.

He added that the amount of magnesium consumed is not always related to the body’s actual amounts of the mineral or how it affects tissues like the brain. Dr. Pratt stated that rather than making dementia diagnosis, the study looked into risk factors.

The fact that a person can have numerous dementia risk factors but not actually get the disease restricts this study. Also, there are limits in our knowledge of the timing and scope of magnesium’s neuroprotective effects on the brain, the author pointed out.

Dr. Johnson-Arbor continued, “Although the study authors considered elements like triglyceride levels, tobacco use history, history of diabetes, physical activity, and alcohol intake when they created their analysis, they did not collect data on other conditions—such as other cancer, kidney disease, or other neurologic conditions—that may have affected the findings in this study.

Magnesium to ward off dementia

Board-certified emergency medicine specialist Dr. Naomi Jean-Baptiste was not involved in the study. She advised people to avoid consuming too much magnesium.

“Like all nutrients in the body, magnesium has a recommended range and too much of it might be bad for you. Magnesium excess can result in mortality due to muscle weakness, exhaustion, low blood pressure, and dyspnea. Hence, before include additional magnesium in your diet, use caution and see your doctor, advised Dr. Naomi Jean-Baptiste.

Dr. Jason Krellman is an assistant professor of neuropsychology at Columbia University Medical Center and a neuropsychologist who was not engaged in the study.

“Further research is required to investigate the possible neurological and cognitive benefits of a magnesium-rich diet utilising carefully controlled, experimental circumstances and a study design that tracks people’s neurocognitive health over time,” he said.

However, the study’s encouraging results show that there are a number of dementia risk factors that people can identify and minimise through healthy lifestyle choices, such as heart-healthy eating habits, aerobic exercise as tolerated, and engaging in enjoyable cognitive and socially stimulating activities.

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How Bone Density May Be Linked to Dementia Risk?

How Bone Density May Be Linked to Dementia Risk?

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According to researchers, a decline in bone density may be associated with a higher risk of dementia.

Low bone density and dementia tend to develop at later age, but the researchers caution that they are unsure of why there may be a connection.

A nutritious diet and regular exercise, according to experts, are two strategies to enhance overall bone health.

A study was published in Neurology, the official journal of the American Academy of Neurology. People with low bone density may be more likely to develop dementia. 3,651 individuals with an average age of 72 whose medical histories and X-rays were examined by Dutch researchers.

Everybody underwent physical exams, including X-rays and dementia screenings, as well as interviews every four to five years.

Prior to the trial, none of the subjects had dementia. Among the conclusions were:

  • Dementia affected 688 people (19%) over an average of 11 years.
  • 90 of the 1,211 individuals with the lowest bone density who lived the longest had dementia.
  • During a decade, 57 of the 1,211 individuals with the highest bone density had dementia.

The researchers found that those with lower bone density were 42% more likely to develop dementia than those with higher bone density. Even after controlling for age, sex, education, other illnesses, medicinal use, and family history of dementia.

The study only demonstrates a connection, not cause and effect, the researchers noted.

Bone density and dementia

According to the researchers, bone density loss may occur in the early stages of dementia and, if it does, may be a sign of risk.

With that information, healthcare providers may focus on providing earlier and more regular screenings. Also, a better care to those who have bone loss.

The researchers also stated that little was known about a potential connection in the years preceding dementia and that inactivity and poor nutrition. Both of which are present in dementia patients, both cause bone loss, which is accelerated by inactivity.

The majority of the individuals in the study were Europeans over the age of 70. They poses a drawback in that the findings may not be generalizable to other races, ethnicities, and age groups.

Dr. Joel Salinas, is a behavioural neurologist, researcher at NYU Langone Health and the chief medical officer at Isaac Health in New York. He stated that he always believes that additional research is necessary to determine why there may be a relationship.

According to Salinas, “In this scenario, there could be a few reasons why there is an association between dementia and bone loss.”

He listed a few potential explanations:

  • These two illnesses have a strong connection to ageing.
  • Both disorders may be influenced by inflammation in some way.
  • nutrition, diet, and way of life.

Salinas continued, “Improving lifestyle factors like nutrition and activity levels can never be too late. Even if there are already symptoms of cognitive deterioration, putting out a conscious effort in these areas can help prevent the progression of dementia.

Common Bed Partners

In the elderly population, Low bone mineral density (BMD) and dementia frequently co-occur, with bone loss accelerating in dementia patients as a result of inactivity and poor nutrition. It’s unknown, though, how much bone loss already exists before dementia manifests.

The new findings are based on 3651 seniors (mean age 72 years, 58% women). These were dementia-free between 2002 and 2005 and participated in the Rotterdam Study.

Dual-energy radiography absorptiometry (DXA) was used to measure BMD at the femoral neck, lumbar spine, and overall body at that time. The trabecular bone score, which provides additional information like bone microarchitecture, was also calculated. Up to January 1st, 2020, participants were monitored.

Age, sex, education, physical activity, smoking status, body mass index, blood pressure, cholesterol, history of comorbidities (stroke and diabetes), and apolipoprotein E genotype were all taken into account while doing the analyses.

In the 688 people who underwent follow-up who got dementia, the majority (77%), had Alzheimer’s disease.

Preventing bone loss

Dr. Nahid Rianon, a professor of general medicine at McGovern Medical School at UTHealth Houston who was not involved in the study, responded to Medical News Today when asked what would account for the connection between poor bone density and dementia risk:

Although this is a very useful study, it is impossible to determine if low bone density causes dementia, whether dementia causes low bone density, or whether low bone density and dementia share a risk factor.

The findings are significant because each of the three hypotheses has a critical role to play. To prevent both fatal diseases, it is imperative to find out if they share a common cause.

According to Rivadeneyra, “Dementia and bone health are two typical diseases we all struggle with to some extent as we age, so it’s no surprise there would be a correlation.” “We are aware that smoking increases the risk of dementia, low bone density, and cardiorespiratory problems. As we age, alcohol misuse is also linked to weak bones and dementia. Many of these ‘age-related’ diseases we frequently see are caused by heart disease, prolonged pharmaceutical usage (for some medications), injuries and trauma, metabolic issues like thyroid disease or diabetes, and a strong family history (genetics).

Consuming a diet high in calcium and vitamin D is also essential.

Osteoporosis and women

Osteoporosis is a prominent factor in broken bones in older men and postmenopausal women. Although each bone in the body has the potential to fracture, hip, vertebral, and wrist fractures are the most common in older people.

According to Dr. Gayatri Devi, a neurologist at Lenox Hill Hospital in New York, “women have a higher risk of osteoporosis and dementia, which could be related to decrease of oestrogen after menopause.”

According to Devi, those who engage in less physical activity—often older adults due to conditions like heart disease, diabetes, and stroke—have lower bone density and, thus, are at a greater risk for dementia.

The crucial conclusion, she continued, is that treating low bone density can lower the risk of dementia, fractures, and hospitalisation. “I think that everyone over the age of 50 should get a baseline bone density test because there is a good treatment, either through medication or exercise.”

Study limitations and implications

Dr. Wiggins noted that although other studies have described such relationships, since the majority of the patients in this study were in their 70s and of European heritage, they might not apply to other populations.

We must be careful not to conclude that lower bone density directly causes dementia, he cautioned, since this study merely found a link between bone and brain health.

Board-certified neuropsychologist Dr. Karen D. Sullivan, who runs the Pinehurst, North Carolina-based practise I CARE FOR YOUR BRAIN and was not engaged in the study, said:

The results of this study suggest that dementia may be more likely to strike those with inadequate bone density. According to Dr. Sullivan, this study “adds to the persuasive body of literature that demonstrates that maintaining bone health integrity is a crucial component of successful ageing.

“Evidence-based techniques for enhancing bone health after age 50 include putting a premium on high-quality animal/plant protein, polyunsaturated fatty acids, fruits and vegetables high in potassium, fibre, and foods high in calcium and vitamin D having the greatest study backing. In order to maintain strong, healthy bones as we age, frequent weight-loading and resistance exercises are also necessary, the expert concluded.

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Focused ultrasound can improve Parkinson’s symptoms?

Focused ultrasound can improve Parkinson’s symptoms?

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In a recent study, a novel, non-invasive method of using focused ultrasound to lessen Parkinson’s disease symptoms was presented. In order to disrupt the neural network that causes uncontrolled movement and motor dysfunction, the approach entails deleting a tiny neuron cluster.

Twice as many research participants received the new treatment than those who received sham care, and these improvements in symptoms frequently sustained for at least a year.

An innovative, noninvasive strategy for lowering dyskinesia, or uncontrollable movements, and motor impairment in Parkinson’s disease patients is presented in a recent study. Focused ultrasound is used in the novel technique.

When compared to trial participants who underwent a sham, or placebo, therapy, twice as many people reported improvement in dyskinesia and motor impairment three months after undergoing the incision-less procedure.

In 77% of individuals who responded to the medication, the gains persisted for up to a year. Patients who receive focused ultrasound therapy often return home the same day.

Gait issues, speaking difficulty, and eye disruption were among the infrequently reported negative effects by the researchers. The group that received the treatment experienced more severe adverse effects than the group that received a placebo.

Focused ultrasound

Focused ultrasound is a minimally invasive, non-surgical technique that causes an ablation in a region that reduces Parkinson’s and tremor symptoms. To produce a clear thermal lesion deep into the brain without harming nearby structures, we use focused ultrasonic waves. The basal ganglia are what we are primarily aiming for. A set of brain regions are involved in the coordination and control of movement. We employ a thermal imaging equipment for magnetic radiofrequency imaging (MRI) during the procedure. This gauges alterations in the skull’s temperature and enables us to guarantee the patient’s security.

The treatment is fantastic because it allows us to work on really delicate places securely, effectively, and with very minimal adverse effects.

Dopamine and L-DOPA

Parkinson’s disease is caused by low levels of the neurotransmitter dopamine in the substantia nigra of the brain. This is brought on by the death of neurons that produce dopamine.

The predominant idea holds that autophagy, the brain’s housekeeping mechanism, has failed, causing an accumulation of waste that impairs brain function.

Dopamine synchronises various brain regions so that they are communicating with one another at the same frequency, according to Dr. Jean-Philippe Langevin, director of the Pacific Neuroscience Institute’s Restorative Neurosurgery and Deep Brain Stimulation Program, who was not involved in the study.

“Consider all these parts of the brain as walkie-talkies or phones trying to communicate, but the frequency at which they’re trying to communicate is off,” said Dr. Langevin. Movements become stiff, hesitant, and tremble as a result, and are no longer flowing.

Dr. Langevin stated that the absence of dopamine causes the motor system of the brain, which regulates movement, to be “quite noisy.” Researchers can actually recognise electrical noise as this “noise.” According to recent research, Parkinson’s disease actually causes some neuronal frequencies to rise.

Levodopa, also known as L-DOPA, which replenishes dopamine in the brain, is the most widely used medication for the illness.

Yet, for many people, the dyskinesia and motor dysfunction they encounter are genuine side effects of L-DOPA therapy. Over time, the medication’s effectiveness deteriorates as well.

New treatment

The novel method examined in the trial is based on an essential tremor medication that was previously authorised in 2016.

A small group of neurons in the globus pallidus area of the brain are removed or ablate during focused ultrasound therapy. By leaving scarring on the tissue, ablation causes tissue destruction.

Dr. Howard M. Eisenberg, co-author of the study and professor of neurosurgery at the University of Maryland Medical System, with the following explanation of how a little more than 1,000 sound energy beams ablate the target tissue:

“Like light, sound can be concentrated. Imagine you had a magnifying glass when you were a child. If you focused the sun’s rays on a piece of paper, you would receive a tiny dot of light that would then transform into heat and burn a hole in the paper. With sound, we may achieve the same results.

When the beams are concentrated and the intensity is strong enough, “you can burn a little hole in the brain” precisely at the target location without harming surrounding tissue, he told us.

In essence, Dr. Eisenberg said, “that’s how it works: Back to the future, similar to ablation that was done years ago for essential tremor, but using different technology.”

According to Dr. Eisenberg, the dyskinesia and motor dysfunction are not always brought on by the ablated neurons. Instead, “it’s a system of targets that are interconnected nuclei, and you’re interrupting that system,” he said.

Motives for excitement

If the procedure enables Parkinson’s patients to take less L-DOPA medication, then there are many reasons to be optimistic, according to Dr. Langevin.

According to Dr. Eisenberg, based on prior experience with essential tremor ablation, we can anticipate benefits in roughly 80% of patients, and they might last at least five years.

However, not every participant in the research benefited from this treatment. A few participants, according to Dr. Eisenberg, might have skulls that are less effective at transmitting acoustic energy.

The reason for this is that the skull is made up of two hard layers of bone sandwiched by a softer layer, “like an Oreo biscuit,” rather than being one solid piece of bone.

Focused ultrasound vs. DBS

Dr. Eisenberg pointed out that deep brain stimulation is thought to be more successful for treating essential tremors than ablation (DBS). DBS stimulates tissue rather than destroying it. Furthermore, Parkinson’s dyskinesia and motor disability are treatable by DBS.

DBS, however, necessitates creating one or more tiny holes in the skull through which a wire is placed and directed to the desired location in the brain. The wire is then attached to a tiny neurostimulator that has been inserted into the chest.

“They won’t consider it even though we always explain that deep brain stimulation has advantages over focused ultrasound,” Dr. Eisenberg said of individuals who would prefer it instead. Hence, it’s beneficial for individuals who simply don’t want deep brain stimulation, which is understandable.

Yet, he added, the advantages provided by the new focused ultrasound approach are still potent enough to be life-altering.

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Could matcha tea have anti-depressant properties?

Could matcha tea have anti-depressant properties?

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In the US, major depressive disorders are thought to affect 21 million persons. According to Japanese researchers, matcha tea powder may be able to reduce symptoms of sadness while also enhancing mood and cognitive function.

According to reports, the powder improves mental wellness by stimulating dopaminergic cerebral pathways. Further research involving human people is required, experts believe. Their study was conducted on mice.

A recent study in the journal Nutrients found that matcha tea powder can aid people in managing stress and depression. According to research, the traditional Japanese tea can improve depressive symptoms in mice who have previously suffered stress from social isolation, activate dopaminergic brain networks, and improve mood and mental function.

The health advantages of matcha have been emphasised. But, additional mechanistic research is needed, which is why the study was conducted on mice, according to experts from Japan’s Kumamoto University. They claimed that more study could contribute in the creation of better antidepressants.

Depression and dopamine

A mood disorder called depression can make it difficult for a person to function in daily life. A continuous sense of emptiness is one of the many symptoms that someone with depression may experience.

Depression still doesn’t have a known specific cause. Yet, some risk factors, including as going through painful experiences or having depressed family members, might raise a person’s likelihood of getting depression.

Many of the basic elements of depression are still not fully understood, and researchers are continually trying to comprehend them. How neurotransmitters like serotonin and dopamine affect depression is one topic of investigation.

Dopamine, a chemical messenger that affects motivation and mood, is thought by some experts to play a role in depression.

How to treat depression?

The researchers made note of the fact that depression continues to afflict an increasing number of people and is the most common mental health disorder in the world.

Its onset varies, but it is thought to be caused by a decline in dopamine levels in the brain. Dopamine is an important neurotransmitter and hormone that helps people feel better.

Low dopamine levels can be treated with antidepressants, although many have negative effects. Antidepressant resistance can also develop in patients, necessitating increased dosages or drug adjustments.

Matcha tea and its impact on depression

Matcha, a type of tea that has been around for a while, is made from the Camellia sinensis plant, which has a lot of happy-making substances in its leaves.

Regular matcha drinking, according to researchers, has been shown to reduce anxiety-like behaviour in rats during prior experiments by triggering dopamine function via dopamine D1 receptor signalling.

Researchers lead by Dr. Yuki Kurauchi of Kumamoto University examined the impact of matcha tea powder on depression in socially isolated mice. The team stressed social isolation on both stress-tolerant BALB/c and stress-sensitive C57BL/6J mice.

They claimed that giving the stress-prone rats an oral dose of a matcha tea suspension appeared to lower their levels of depression. This was determined by how well the mice performed in tail suspension experiments, which are frequently used to gauge mouse sadness.

In contrast to stress-tolerant mice, matcha tea only decreased the immobility time in stress-susceptible mice who were more stressed out by social isolation and showed more depressive-like behaviour. stated Kurauchi in a statement.

The prefrontal cortex and nucleus accumbens were activated in the stress-susceptible mice following matcha consumption, according to a brain examination of the mice. These areas are vital for regulating dopamine levels in the brain as they represent a significant component of the dopaminergic circuit.

Their activation would normally enhance dopamine levels, improving mood, as shown by an increase in the number of cells expressing c-Fos, a critical marker of brain activity.

Experts on matcha tea study

Although there are differences between mice and humans, experts told Healthline they were optimistic about the findings.

Dr. Kelly Johnson-Arbor, a medical toxicologist and the director of the National Capital Poison Center, stated that there isn’t much data on how matcha might effect depression in people. Also, the best dose and time frame for using matcha to prevent or treat depression haven’t been determined.

It’s not yet clear whether matcha can affect people’s moods. According to Johnson-Arbor, Healthline. Matcha has not been clearly demonstrated to be useful in preventing the onset of depression in humans, despite the fact that most healthy people may be able to incorporate it into their daily routine as part of a healthy, balanced diet.

She continued, “Before adopting matcha or any other natural therapy to treat depression symptoms, people should always see their doctor.”

Experts Opinion

Matcha has high levels of L-theanine, an amino acid that relaxes the brain and nervous system, according to Victoria Chan, a licenced naturopathic doctor who specialises in integrative mental health and has medical training in pharmaceuticals. This lessens the jittery effects of the tea’s natural caffeine.

The root causes of depression are still being discovered by scientists, according to Chan. Contrary to common belief, ‘chemical imbalances’ or imbalanced neurotransmitters are not the exclusive cause of depression. Digestion, hormones, immune reactions, thyroid, detoxification, allergic responses, nutrition, liver, heredity, and stress responses are just a few of the many elements that might contribute to depression.

According to Chan, matcha reduces depression in ways other than via influencing neurotransmitters.

According to Chan, if antidepressant medicine is not successfully treating your depression, the underlying cause may not be entirely controlled by neurotransmitters, which antidepressant medications primarily target. If so, you might benefit from treating your depression with substances that support various biological pathways, such as matcha, and from employing methods that do so.

Some cautions on the study

According to Dr. Zeeshan Afzal, a dermatologist and medical advisor for the artificial intelligence healthcare platform Welzo, matcha’s L-theanine and caffeine can work together to enhance brain function.

Afzal cautioned against becoming overly euphoric, though. He stated that the study conducted on mice “may offer some insights into the potential antidepressant.” “It’s vital to keep in mind that the results might not apply to humans. Because of the physiological variations between mice and humans, there are frequently notable discrepancies in how medications and therapies affect the two species.

Further affective human studies, according to Afzal, are required.

“Matcha could potentially become a natural alternative or complementary treatment for depression,” he added. “If subsequent studies confirm the antidepressant effects of matcha.” To diagnose and treat depression, people with the condition should always seek the advice of a trained healthcare expert, it is crucial to note that there is still much research to be done in this area.

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Brain’s recycling system breaks down in Parkinson’s Disease

Brain’s recycling system breaks down in Parkinson’s Disease

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A recent study suggests that the usual house-cleaning activity of neuronal cells may fail in Parkinson’s disease. A buildup of damaged proteins in brain synapses, which may eventually result in patches of dead neurons, is one of the symptoms of Parkinson’s disease.

According to a study done on fruit flies called Drosophila, a calcium surge in healthy brain synapses starts the cleaning process by causing a protein that causes cells to throw away the waste. But, when a gene mutation known to cause Parkinson’s disease is present, the protein does not react to calcium’s signal as it should, and synaptic cleanup is not successful.

According to a recent study, the typical process for getting rid of broken-down proteins in brain cells is disrupted by a gene mutation linked to Parkinson’s disease. As a result, synapses may accumulate debris, which could lead to Parkinson’s symptoms.

Researchers used Drosophila, or fruit flies, to explore how calcium releases in neurons cause autophagy or cell cleaning, and how a gene mutation prevents this release.

In the synapses of persons with Parkinson’s disease, abnormal protein clumps called Lewy bodies are discovered. These Lewy bodies are mostly made up of clumps of the protein alpha-synuclein. Normally, alpha-synuclein participates in the communication between brain cells. Misfolded alpha-synuclein proteins, on the other hand, clump together and destroy neurons, leaving dead brain cells in their wake.

Dr. Warren D. Hirst of Biogen claims that the idea that Parkinson’s is brought on by a malfunction in autophagy is not new. The new study, however, meticulously outlines the potential culprits and underlying mechanisms of autophagy’s failure. (Dr. Hirst did not take part in the research.)

Parkinson’s disease

After Alzheimer’s disease, Parkinson’s disease is the neurodegenerative condition that is most frequently diagnosed. Parkinson’s disease affects almost one million Americans, and by 2030, that figure is projected to reach 1.2 million. Parkinson’s disease affects about 10 million individuals globally. In the United States, almost 90,000 new cases are diagnosed yearly.

Critical basal ganglia dopamine-producing neurons die in the disease’s advanced stages. This area of the brain regulates movement.

The primary signs of Parkinson’s disease are:

Parkinson’s disease may also result in skin concerns, bladder problems, constipation, trouble eating, chewing, and communicating, as well as sadness and other emotional disturbances.

The majority of Parkinson’s patients are over 60 years old, while 5% may be diagnosed earlier. The extent to which the condition may be inherited is unclear.

It’s crucial to remember that everyone is affected by the ailment differently; some people may have more severe symptoms, such as losing all mobility, while others may still just have mild symptoms. Although there is no known cure for Parkinson’s disease, there are treatment options that can help manage the symptoms, including drugs, deep brain stimulation (DBS), and treatments.

Parkinson’s disease may also result in skin concerns, bladder problems, constipation, trouble eating, chewing, and communicating, as well as sadness and other emotional disturbances. The majority of Parkinson’s patients are over 60 years old, while 5% may be diagnosed earlier. The extent to which the condition may be inherited is unclear.

It’s crucial to remember that everyone is affected by the ailment differently; some people may have more severe symptoms, such as losing all mobility, while others may still just have mild symptoms.

Although there is no known cure for Parkinson’s disease, there are treatment options that can help manage the symptoms, including drugs, deep brain stimulation (DBS), and treatments.

Calcium, autophagy, and Parkinson’s risk

It is “a basic mechanistic work taking a mutation that is known to raise the incidence of Parkinson’s, and investigating what that mutation does in a fruit-fly model of Drosophila,” according to neuroscientist Dr. Santosh Kesari, who was also not involved in the study.

The researchers discovered that the earliest indirect trigger of autophagy in Drosophila was an influx of calcium at brain synapses. Also, they found that these synaptic calcium surges can be brought on by either neuronal activity or by depriving cells of amino acids.

Associate Professor of Neurology Ian Martin, who was not involved in the study, stated, “The authors give considerable data suggesting a role for calcium in the onset of autophagy within Drosophila synapses.

According to Asst. Prof. Martin, “A variety of approaches, including biochemistry, genetics, synaptic physiology, and microscopy, are generally well-supportive in the study of the idea that synaptic autophagy could be coupled to neuronal activity, and that this autophagy is required for neuronal survival.” Autophagy, according to Dr. Kesari, “is the cell’s trash disposal.”

Parkinson’s disease and EndoA

The study then showed that a mutation in the Endophilin-A protein, also known as “EndoA,” which is linked to Parkinson’s disease, is responsible for the relationship between calcium and autophagy.

The endolysosomal system, which includes EndoA, has been linked in other research as a putative early pathomechanism causing Parkinson’s disease and alpha-synuclein aggregates.

Normally, the calcium influx increases EndoA’s flexibility, allowing for the creation of the autophagosomes that power autophagy. However, the study discovered that in those who have the Parkinson’s-related mutation, the calcium influx makes EndoA stiffen, and this stiffness prevents the creation of autophagosomes, which in turn prevents autophagy.

So, the new work is distinctive in two ways: it focuses on autophagy particularly at synaptic terminals and shows how the Parkinson’s disease-related gene mutation prevents the process from starting.

Making use of the study’s insights

According to studies from human post-mortem tissue, Asst. Prof. Martin said that the idea that autophagy failure plays a role in Parkinson’s is validated. Beside EndoA, Parkinson’s disease is also thought to be caused by pathogenic mutations in proteins including alpha-synuclein and LRRK2.

Autophagy abnormalities are frequently implicated in Parkinson’s disease-related neurodegeneration, according to genetic studies.

In conclusion, Dr. Kesari remarked, “We need to think about how we can use this information to improve autophagy.” The next phase of the research with human cells is still to be completed.

A crucial, $64,000 question, according to Dr. Hirst, is how to accomplish this. The field is still looking for agents that boost autophagy. This still presents difficulties.

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Latest kind of food that helps with anxiety.

Latest kind of food that helps with anxiety.

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The brain can benefit from some foods, like almonds, and herbs, like chamomile, which may also help with anxiety symptoms. With 7.3% of the world’s population experiencing anxiety, it is one of the most common mental health illnesses.

It’s an all-encompassing phrase used to describe a number of disorders. This includes social anxiety disorder, generalised anxiety disorder, and phobias. It is typically characterised by persistent feelings of tension, worry, and nervousness that can interfere with daily life.

Medication is frequently needed as the primary form of treatment in many situations. There are, however, a number of methods you can employ to lessen the symptoms of anxiety, from exercise to breathing exercises.

In addition, there are a variety of foods you may eat to boost brain health and lessen the severity of your symptoms, especially whole grains. Also, there are a variety of foods you can eat that, mostly because of their brain-boosting qualities. This may assist maintain brain function and lessen the severity of your symptoms.

Millions of individuals throughout the world suffer with anxiety, which is a common condition. There are many different symptoms, and some people only sometimes encounter them. Yet, a person may develop generalised anxiety disorder if they have symptoms for more than six months (GAD).

Physical and psychological signs of GAD include:

  • fear
  • tension
  • excessive anxiety about regular issues and events
  • irritability
  • having trouble concentrating
  • challenges with connections in work, in society, and personally
  • increased heart rate and chest pain
  • skeletal tension
  • chest constriction

Medications and talk therapy, such as cognitive behavioural therapy (CBT), are frequently used by doctors to treat GAD. Some traditional therapies occasionally have short-term success rates. Yet, some studies indicates that healthy eating may aid with symptom improvement.

Salmon

Salmon might help people feel less anxious. It contains nutrients, such as vitamin D and the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid. They supports brain function (DHA).

These nutrients might assist in regulating the sedative and calming neurotransmitters serotonin and dopamine.

A diet high in EPA and DHA in particular is linked to lower levels of anxiety. These fatty acids are thought to be able to prevent brain cell malfunction. This is frequent in anxious persons, as well as inflammation.

This may also help your brain adjust to changes, enabling you to deal with pressures that bring on anxiety feelings more effectively.

Chamomile

An herb called chamomile may help people feel less anxious. It has anti-oxidant and anti-inflammatory qualities, which might help reduce anxiety-related inflammation.

Although the exact mechanisms are unknown, chamomile is thought to assist in the regulation of neurotransmitters involved in mood. This includes serotonin, dopamine, and gamma-aminobutyric acid (GABA).

The hypothalamic-pituitary-adrenocortical (HPA) axis, a crucial component of the body’s stress response, may also be regulated by it. The relationship between chamomile extract and anxiety relief has been the subject of certain studies.

A 1,500 milligramme dose of chamomile extract taken daily in a 38-week randomised study of 179 patients with (GAD). This results in a considerably better improvement in symptoms than those who did not take it.

Similar findings were made in a previous 2012 study, which found that people who took chamomile extract for eight weeks reported fewer depressive and anxious feelings. However, due to the study’s small sample size, cause-and-effect could not be proved statistically with sufficient strength.

The majority of investigations have been done on chamomile extract, despite the fact that these results are encouraging. The anti-anxiety properties of chamomile tea, which is most frequently drank, need to be evaluated by more recent studies.

Turmeric

Curcumin, a substance researched for its function in supporting brain health and reducing anxiety disorders, is present in the spice turmeric.

Curcumin, which has a high level of antioxidant and anti-inflammatory characteristics. This may aid in preventing brain cell deterioration brought on by oxidative stress and chronic inflammation.

It may also improve the conversion of alpha-linolenic acid (ALA), an omega-3 present in plants, to DHA. Also, it can raise DHA levels in the brain, according to animal research.

A daily intake of nano-curcumin, a smaller, more accessible version of curcumin, for 8 weeks led to considerably lower anxiety scores when compared to a placebo. Tis is as per double-blind, randomised research of 80 diabetics.

Anxiety levels were shown to be significantly reduced when 1 gram of curcumin was taken daily for 30 days instead of a placebo. This is as per another small, randomized crossover research. Although encouraging, the majority of studies focused on the effects of curcumin supplements rather than turmeric-derived curcumin. As a result, more study in this area is required.

Having said that, include turmeric in your diet is unquestionably worthwhile. Try combining curcumin with black pepper to improve absorption.

Dark chocolate

Moreover, adding some dark chocolate to your diet may reduce anxiety. Flavonols, which are plant-based chemicals with antioxidant properties like epicatechin and catechin, are found in dark chocolate.

According to certain studies, the flavonols in dark chocolate may have neuroprotective and beneficial effects on brain health. In instance, flavonols may improve cell-signaling pathways and boost blood flow to the brain.

Your ability to cope with stressful conditions that can cause anxiety and other mood disorders may improve as a result of these effects. Moreover, some studies contend that the benefits of dark chocolate for brain health may simply be a result of the substance’s comforting flavor for people. This refers to people who suffer from mood disorders.

One cross-sectional study with 13,626 participants discovered that those who ingested dark chocolate had significantly fewer depressive symptoms than those who ate little to no dark chocolate. Also, a review of nine studies found that consuming goods high in cocoa could elevate mood and affect in the short term.

This is encouraging, but more analysis of the long-term benefits of dark chocolate on anxiety and mood is required. Also, since it has a lot of calories and is simple to overeat, dark chocolate is best enjoyed in moderation. Enjoy a 1- to 1.5-ounce serving at a time for optimal results.

Yogurt

Certain yogurt varieties contain probiotics or good bacteria. This may enhance your physical and mental health among other elements of your wellbeing.

Probiotics may help the gut-brain axis, a complex connection connecting the gastrointestinal tract and the brain. Although, the fact that this area of study is still in its infancy. In example, evidence indicates that favourable gut flora may be associated with improved mental health.

Moreover, probiotic foods like yoghurt may improve mental health and cognitive performance by lowering inflammation and raising the production of neurotransmitters that improve mood, like serotonin.

Anxiety, stress, and quality of life were all found to be enhanced in one research of postmenopausal ladies who ate probiotic yoghurt every day for six weeks. Further human studies are required to investigate the precise link between yoghurt eating and anxiety, despite the field of study being quite promising.

The presence of probiotics in yoghurt varies widely, which is another key distinction. Choose a yoghurt with live active cultures stated as an ingredient for the probiotics advantages. Further human studies are required to investigate the precise link between yoghurt eating and anxiety, despite the field of study being quite promising.

The presence of probiotics in yoghurt varies widely, which is another key distinction. Choose a yoghurt with live active cultures stated as an ingredient for the probiotics advantages.

Green tea

The amino acid L-theanine, which is present in green tea, has been investigated for its potential benefits on anxiety and brain function.

Participants who drank a beverage containing L-theanine reported considerably lower subjective stress and lower levels of cortisol, a stress hormone associated to anxiety, in a double-blind, randomised research.

The ability of L-theanine to stop nerves from becoming overexcited may be the cause of these effects. Furthermore, GABA, dopamine, and serotonin may be increased by L-theanine; these neurotransmitters have been associated with anti-anxiety benefits.

The antioxidant epigallocatechin gallate (EGCG), which has been linked to improved brain function, is also found in green tea. Due to the fact that it raises GABA levels in the brain, it might help to lessen some symptoms.

It’s interesting to note that the combination of L-theanine, EGCG, and additional substances present in green tea appears to play a synergistic function in inducing serenity and reducing anxiety and may be more beneficial when combined than when used separately.

Almonds

Almonds are an excellent source of healthy fats and vitamin E, two nutrients considered to support brain function. In fact, several animal studies have discovered that almonds may lessen oxidative stress and inflammation, which may contribute to the emergence of anxiety.

Several potential mood-enhancing qualities of almonds exist. One study, for instance, discovered a link between higher nut consumption, particularly that of almonds, and a reduction in depressive symptoms.

Males who ingested the most nuts were 66% less likely to experience anxiety than those who consumed the least, according to a different research of 3,172 individuals. Females were not affected by this relationship, though.

In order to comprehend how almonds could affect mood and anxiety, further high-quality studies are required.

Blueberries

Vitamin C and other antioxidants like flavonoids, which have been examined for their potential to enhance brain function and reduce anxiety, are abundant in blueberries.

In a 4-week trial, it was discovered that giving 64 teenagers daily supplements of wild blueberries was associated with reduced self-reported depressive symptoms.

According to several animal studies, some chemicals in blueberries may also lessen the effects of oxidative stress and the symptoms of anxiety and depression.

Additionally, some studies have also suggested that consuming more fruits, such blueberries, may be associated with a decreased risk of anxiety. However, further research is required to assess how blueberries affect anxiety.

Eggs

Tryptophan, a neurotransmitter that may be helpful for anxiety symptoms, is a great source of nutrition in eggs. One study suggested that low amounts of tryptophan and insufficient protein intake, both of which are found in large quantities in eggs, may be linked to increased levels of anxiety.

Around 6% of the required Daily Value (DV) of vitamin D is found in one large egg, another nutrient found in eggs. Low vitamin D levels have been linked to increased symptoms of anxiety and sadness, according to several studies.

Even however, further research is required to fully understand the benefits of eggs specifically with regard to anxiety. Some of the nutrients in eggs may be advantageous.

Other meals that could reduce anxiety

Even though some of the foods on the following list have not been explicitly researched for their anti-anxiety benefits, they are full of nutrients that may help with related symptoms.

Tryptophan, an amino acid that the body converts to serotonin and may help with relaxation and anxiety alleviation, is present in foods including turkey, bananas, and oats.

Meat and dairy products: These are excellent sources of protein and provide necessary amino acids that help make the neurotransmitters dopamine and serotonin, which may help with mental wellness.

Chia seeds: Chia seeds are another another excellent source of anxiety-relieving omega-3 fatty acids, which are known to improve brain function.

Citrus fruits and bell peppers: These foods are high in vitamin C, which has antioxidant characteristics that may help reduce inflammation and shield cells from damage that can worsen anxiety. Citrus fruits and bell peppers also contain a lot of vitamin C.

Although these meals could help you maintain your mental health, they shouldn’t take the place of any prescription drugs or other treatments recommended by a doctor.

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Faster cognitive decline linked with food insufficiency

Faster cognitive decline linked with food insufficiency

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A recent study discovered that a lack of meals is linked to a quicker deterioration in cognitive function. Researchers examined information on thousands of people’s levels of food insecurity, cognitive health. Also, participation in the Supplemental Nutrition Assistance Program of the US federal government.

Those who don’t eat enough may have cognitive impairment due to poor nutrition or stress by significant financial difficulty. It prevents them from purchasing the food they require. Over the ten-year period from 2007 to 2016, the percentage of older persons in the United States who go without meals, frequently due to a lack of financial resources, more than doubled from 5.5% to 12.4%.

Number of young people going hungry has decreased because to initiatives like the U.S. Supplemental Nutrition Assistance Program (SNAP). According to study, older women who live alone in particular have had less success with their efforts than other senior people.

Age-related physical limitations and the risk of malnutrition and depression are more prevalent. This is among older adults who are food insecure. According to a recent review of SNAP data, there is also a link between older adults who are food insecure and cognitive impairment that happens more quickly.

A quicker rate of cognitive deterioration was observed in those who were SNAP qualified. It based on their income but did not take use of the programme. This pace was comparable to what would be anticipated if a person were 4.5 years older than they actually were.

Four years of brain ageing can be substantial for an older individual. When compared to individuals who had enough nourishment, those who did not showed a larger cognitive deterioration. This is equivalent to ageing by 3.8 years. The rate of mental decline was lowest in those who received enough meals.

Tying a lack of food to cognitive function

Data from 4,578 Medicare beneficiaries who were 65 years of age or older and took part in the National Health and Aging Trends Study (NHATS) from 2012 to 2020 were examined by the study’s authors.

As part of its yearly follow-up with participants, NHATS gathered data. Based on sociodemographic situation, social, physical, and technological settings, medical comorbidities, and cognitive function.

People’s responses to questionnaires about food insecurity were used as the basis for categorising them. As having enough food or not having enough, and their SNAP status was noted as part of NHATS. Participants in the new study were evaluated according to which of three groups they belonged to:

  • SNAP recipients
  • Non-participants who were SNAP-eligible, that is, non-participants who were making up to or less than 200% of the federal poverty threshold.
  • Non-participants who are SNAP-ineligible and make more over 200% of the federal poverty level.

Dr. Daniel P. Miller of Boston University, an expert on poverty and food insecurity who was not engaged in this study, clarified the critical distinction between “food insecurity” and “food insufficiency”.

Food insufficiency is just a statement about not having enough food to eat, as opposed to food insecurity, which is a condition of hardship where families struggle to put the correct kinds of food on the table due to a lack of money or other financial means.

He pointed out that, as opposed to food insecurity in the traditional sense, the focus of the current study was on food insufficiency.

Causes of food insecurity

According to Dr. Miller, economic hardship is mostly to blame for food insecurity. At an era of rising expenses for everything from food to health, he noted that older persons on fixed incomes are most at danger.

The definition of food insecurity according to the NHATS also included “non-financial constraints such as poor functional status, lack of social supports, and lack of access to food,” according to Dr. Colleen M. Heflin of Syracuse University, who was not engaged in this study.

Dr. Heflin stated that these access measures “are likely to be particularly significant for older persons who may need assistance acquiring food due to health restrictions, poor driving ability, and geographic isolation.”

Possible connection

Although the study found a link between dietary insufficiency and cognitive decline, because it was conducted over time, it was unable to determine whether a shortage of food causes cognitive impairment or the other way around.

Due to the challenging administrative procedures involved in proving programme eligibility, Dr. Heflin lamented that “my own data implies that cognitive impairment can function as a barrier to SNAP participation among older persons eligible for the programme.”

There are two likely causal mechanisms connecting food inadequacy to cognitive impairment, according to Drs. Heflin and Miller.

The first is a deficiency in crucial minerals and vitamins that support overall health, including brain function. Dr. Miller suggested that we should anticipate slower overall cognitive decline in elderly persons who are food insecure but instead expect greater reductions.

He did add, however, that research looking at the relationship between nutrition and cognitive decline have come to inconsistent results. Both experts agreed that long-term financial stress could be the second most likely causative mechanism. Dr. Heflin added that “stress exposure is linked to a higher rate of cognitive impairment.”

The importance of SNAP

A “electronic benefits transfer” card from SNAP allows users to make food purchases at approved retailers while also providing financial assistance. Dr. Heflin stated that SNAP participants consume more food at home and food of a higher quality than non-participants.

SNAP non-participation, according to Dr. Miller, is a “particularly important” indicator of future food insecurity. However, he continued, participation in the programme is lower than it could be, particularly among the elderly.

Dr. Miller pointed out that in 2020, just 47% of eligible older persons over the age of 60 joined in the programme, despite the fact that 78% of people of all ages who were eligible for SNAP did so.

A looming crisis?

Over 6 million Americans, according to the Centers for Disease Control and Prevention, suffer from Alzheimer’s and associated dementias. An estimated 14 million people will have Alzheimer’s by 2060, according to predictions.

The most vulnerable communities could be those of race. The number of cases among Latinos might rise seven times over current projections. There may be four times as many instances among African Americans as now anticipated.

In order to help prevent dementia, a new community-based programme in San Francisco will concentrate on established risk factors that may be changed. A model “Brain Health Program” being launched by Posit Science and the YMCA with funding from the National Institutes of Health.

Adults who are at risk for crime will be able to take classes through the initiative, which will launch in six months. The fundamentals of diet and nutrition the YMCA has been utilising in its Diabetes Prevention Program will be covered in some of the training.

REFERENCES:

  • https://www.healthline.com/health-news/how-ultra-processed-foods-hasten-cognitive-decline
  • https://www.medicalnewstoday.com/articles/dementia-and-diet-is-there-a-link
  • https://foodmatterslive.com/article/food-insufficiency-linked-to-faster-cognitive-decline-study-shows/
  • https://neurosciencenews.com/food-insecurity-cognition-aging-22532/

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Drinking good decaf coffee may reduce its symptoms.

Drinking good decaf coffee may reduce its symptoms.

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A recent study found that if decaffeinated coffee tastes close enough to the genuine thing, it may be able to lessen the negative effects of caffeine withdrawal.

A cup of premium decaf dramatically lessened the withdrawal symptoms individuals had been feeling 24 hours after their previous cup of caffeinated coffee, according to University of Sydney researchers.

While some participants in the study were not aware that they were drinking decaf, others were. It’s interesting to note that people who knew what they were consuming experienced less withdrawal symptoms.

The study is one of many that outline the frequently unexpected positive outcomes that placebos have in clinical studies.

Coffee and caffeine,

Everyone enjoys coffee. Many people rely on caffeine’s energy boost and believe that caffeine helps them stay focused and attentive. Yet according to research, coffee may have much more to give. Your chances of type 2 diabetes, heart failure, colon cancer, Parkinson’s disease, and Alzheimer’s disease may also be reduced.

The Food and Drug Administration (FDA) advises against exceeding the daily caffeine limit of 400 mg, or roughly four to five cups of coffee. Tea, energy drinks, and sodas all include caffeine as an additive. It is both a food additive and a medication, according to the FDA.

Despite the fact that caffeine is not actually addictive, quitting coffee can cause withdrawal symptoms such as headaches, exhaustion, drowsiness, irritability, melancholy, scattered attention, nausea, and muscle soreness or stiffness.

How much caffeine is in decaf coffee?

Even decaffeinated coffee contains some caffeine. In reality, it contains varied levels of caffeine, typically 3 mg per cup.

According to one study, there were 0–7 mg of caffeine in each 6 ounces (180 mL) cup of decaf coffee. Contrarily, the amount of caffeine in a typical cup of black coffee ranges from 70 to 140 mg, depending on the brand of coffee, how it is brewed, and the size of the cup.

Decaf generally contains extremely little caffeine, even if it does not contain no caffeine at all.

Caffeine withdrawal symptoms

The study did point out that fear of withdrawal symptoms is one of the major barriers, although prior research has shown that only a small percentage of people would actually experience withdrawal symptoms when they stop consuming caffeine.

According to earlier studies, these symptoms include headaches, feeling exhausted, having decreased alertness, drowsiness, and irritability, as well as having a negative mood.

When someone abruptly quits drinking coffee, caffeine withdrawal begins 12 to 24 hours later and peaks one to two days later. According to earlier studies, the effects can be lessened by progressively reducing the caffeine intake.

Reducing caffeine withdrawal symptoms

In the recent study, decaf minimised or improved these symptoms.

Lead researcher Dr. Llew Mills of the University of Sydney tells the University of Sydney News that a convincing cup of decaf has the ability to significantly lessen withdrawal symptoms even when the individual consuming it is ignorant that it is decaf. Yet according to our research, even if they are aware that it is decaf, they still stop withdrawing.

Decaf should be effective, according to Dr. Mills, as long as it “does not taste like decaffeinated coffee.” Major Dickason’s, a brand from the United States, was the brand used in the study. Despite Sydney residents’ well-known reputation as coffee snobs, Dr. Mills claimed that his participants were rather simple to deceive.

61 regular coffee consumers who consumed three or more cups daily for the study gave up their habit for a full day. Participants responded to a questionnaire about withdrawal symptoms after that time period.

The participants were sorted into three groups by the researchers. One group was told they would be sipping decaf, while the other was told they would be drinking coffee. Water was given to the third group, which served as the control. Participants completed the survey once more 45 minutes after finishing their beverage.

The amount of caffeine withdrawal in the group we lied to was significantly reduced, according to Dr. Mills. Surprisingly, however, the group to whom we revealed the truth also reported a decrease in their caffeine withdrawal, albeit a smaller one than the group to which we told a falsehood.

Decaf coffee is loaded with antioxidants and contains nutrients

Contrary to popular belief, coffee is not the devil. In reality, it is the Western diet’s main source of antioxidants. Antioxidants in decaf often equal those in regular coffee, though they may be up to 15% lower.

Most likely, the slight loss of antioxidants that occurred during the decaffeination procedure is what led to this disparity. The hydrocinnamic acids and polyphenols in regular and decaf coffee are the primary antioxidants.

Free radicals are reactive substances that can be neutralised by antioxidants very effectively. This lessens oxidative damage and could aid in the prevention of conditions including type 2 diabetes, cancer, and heart disease. Decaf also includes trace levels of several minerals in addition to the antioxidants.

Cause of effect

According to Dr. Kaptchuk:

“The mechanism of open-label placebo probably includes the body automatically and unconsciously reacting to the embodied ritual of coffee-taking that causes the central nervous system respond with similar reductions of symptoms as if it were taking a real cup of coffee,” according to the study.

This procedure in neuroscience is known as “prediction coding” (also known as “Bayesian Brain”) and is accepted as being crucial for symptom generation, according to Dr. Kaptchuk.

Dr. Kaptchuk made the following observations regarding the symptom decreases for the subjects who were aware they were consuming decaf:

Furthermore, the decaf effect did not entail expectations, supporting long-term clinical research on clinical patients that expectations do not contribute to genuine placebo effects.

REFERENCES:

  • https://www.medicalnewstoday.com/articles/caffeine-withdrawal-good-decaf-coffee-reduce-symptoms
  • https://www.healthline.com/nutrition/decaf-coffee-good-or-bad
  • https://www.foxnews.com/health/coffee-quitters-help-decaf-help-reduce-withdrawal-symptoms

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Could fructose contribute to development of Alzheimer?

Could fructose contribute to development of Alzheimer?

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An increased risk of neurological disorders, such as Alzheimer’s disease, is connected with the shift in the global age demographic towards older ages. Dementia risk profiles may also be evolving. Over the past 50 years, the frequency of obesity and type 2 diabetes has increased, and these conditions have been linked to a higher risk of dementia.

Certain dietary modifications could potentially pose a direct danger. From an estimated 8.1 kg/person/year at the start of the XIX century to an estimated 65 kg/person/year today, there has been a diet change in the United States with regard to the consumption of refined sugar, notably high-fructose corn syrup (HFCS).

With an estimated 6 million people living with it, Alzheimer’s disease continues to be a serious health issue. The hypothesis that fructose, a prevalent sugar present in packaged foods and fruits worldwide, may contribute to the disease’s development has recently put forth in a narrative review.

Alzheimer’s disease is characterised by the production of aberrant beta-amyloid and tau protein clumps. Treatments aimed at these aberrant protein aggregates, however, have had mixed results.

Conversely, other scientists have suggested that changes in brain metabolism that take place before the formation of these protein aggregates may be to blame for the onset of Alzheimer’s.

According to studies, diets that cause the body to produce a lot of fructose or foods that contain a lot of fructose might cause metabolic problems like obesity, diabetes, and high blood pressure.

Fructose survival pathway

A glucose and a fructose molecule make up each mole of table sugar, also known as sucrose. Most cell types and tissues in the body use glucose as fuel.

Despite the fact that fructose can be used as energy, the body prefers to store it as fat or as the storage carbohydrate glycogen.

The authors’ theory states that an animal can survive for extended periods of time without food or water by activating a survival response when it consumes fructose in excess. During migration or hibernation, the animal may be able to survive thanks to this survival reaction.

Consuming fructose results in an increase in thirst and hunger instead of fullness, which is produced by consuming glucose. Animals’ urge to forage is thereby stimulated by fructose ingestion. The fructose survival pathway, in particular, entails saving energy for just required actions, such as foraging, and minimising energy expenditure for body processes at rest.

Reducing the sensitivity of tissues to insulin, such as muscles, leads to a decrease in glucose absorption and consumption, which lowers energy expenditure. Moreover, the liver stores extra energy in the form of fat and glycogen.

The main mediators of the survival response include fructose, uric acid, and vasopressin. When this fructose survival route is activated for an extended period of time, the metabolism is disrupted, mimicking a number of the symptoms of metabolic syndrome.

They include persistent low-level inflammation, insulin resistance, high blood pressure, and weight gain. The fructose survival pathway can potentially affect the metabolism of the brain.

Impact on the brain

While making up only 2% of the overall mass of the body, the human brain consumes almost 20% of the total energy used while at rest. Furthermore, glucose is the only fuel that can be used by neurons, which make up the majority of brain cells.

The fructose survival pathway alters the metabolism of the brain at the regional level while reducing energy expenditure to conserve glucose for the brain.

In particular, the scientists believe that activating the fructose survival pathway causes the brain’s food-seeking areas to become active. An increase in impulsive and exploratory actions that enable the animal to quickly investigate risky locations promotes this foraging response.

Meanwhile, the foraging response is linked to the inhibition of brain regions, such as those involved in logic, memory, and impulse control, that may decrease foraging activity.

In other words, the aforementioned brain areas involved in cognitive function experience a drop in energy metabolism when the foraging response is activated.

Evidence supporting the role of fructose

The rise in fructose levels in the brain, according to the researchers’ theory, may play a role in the onset of Alzheimer’s disease.

Nevertheless, given that individual fruits only contain a modest amount of fructose and that only 1% to 2% of ingested fructose reaches the brain, this rise is most certainly not attributable to fruit consumption as a whole.

However, it appears that ingestion of foods high in glucose, glycemic index, and salt may be more relevant in raising fructose levels in the brain.

The levels of fructose in the brain could therefore be increased by a diet heavy in salt and carbohydrates. Moreover, the uric acid that is created when fructose breaks down in the periphery can encourage the creation of fructose in the brain.

According to studies, consuming more high-fructose corn syrup or table sugar, foods with a high glycemic index, and salty foods is linked to a higher risk of Alzheimer’s disease.

In line with this, metabolic diseases linked to increased consumption of certain foods, such as obesity, insulin resistance, and diabetes, are also risk factors for Alzheimer’s disease.

The fructose metabolism

According to Dr. Johnson, treating fructose metabolism may be essential for the management or prevention of Alzheimer’s.

The majority of the evidence, he continued, “suggests three characteristic findings in early Alzheimer’s that seem to precede the end-stage presentation: these are the presence of insulin resistance associated with reduced glucose uptake in the brain, the fact that there is mitochondrial dysfunction in the brain, and that there is local inflammation, or “neuroinflammation,” in the brain.

Others are still attempting to cure this condition by administering intranasal insulin or by reducing inflammation. Yet once more, this only addresses the symptoms and not the root problem, according to Dr. Johnson.

Moreover, the metabolism of fructose raises the amounts of uric acid in the brain, which on its own can cause inflammation and memory problems. For instance, memory impairments and hippocampal inflammation are seen in hyperuricemic rats that produce too much uric acid.

REFERENCES:

  • https://www.medicalnewstoday.com/articles/could-fructose-contribute-to-the-development-of-alzheimers
  • https://www.mindbodygreen.com/articles/this-type-of-sugar-could-be-linked-to-alzheimers-development
  • https://www.sciencedaily.com/releases/2023/02/230213113345.htm

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