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Focused ultrasound can improve Parkinson’s symptoms?

Focused ultrasound can improve Parkinson’s symptoms?

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?

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

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.

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 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.


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.


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.


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 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.


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.


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

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.



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Drinking good decaf coffee may reduce symptoms.

Drinking good decaf coffee may reduce symptoms.

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.



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Could fructose contribute to development of Alzheimer?

Could fructose contribute to development of Alzheimer?

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.



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Are Exercise helpful in managing parkinson’s symptoms.

Are Exercise helpful in managing parkinson’s symptoms.

According to the Parkinson’s Foundation, a charity that supports research and disseminates information about the condition, Parkinson’s disease is the second most prevalent neurological illness after Alzheimer’s disease.

It is unclear to experts what causes Parkinson’s. Nonetheless, a lot of people think that a hereditary and environmental combination of factors may be to blame. Parkinson’s patients frequently have a decrease of dopaminergic neurons, or brain cells that produce dopamine, in the substantia nigra, a region of the brain.

In a recent study, researchers discovered that every year, roughly 90,000 Individuals 65 years of age or older are given a Parkinson’s disease diagnosis. In comparison to earlier projections, this is a 50% increase.

Symptoms of Parkinson’s disease

Typical signs of Parkinson’s disease include:

  • tremors
  • slow motion
  • limb rigidity
  • balance and gait issues.

Parkinson’s disease can be treated with drugs and surgery even though there is presently no cure. Experts concur that altering one’s lifestyle may be beneficial.

Recently, the Cochrane Database of Systematic Reviews published a systemic review and network meta-analysis on the advantages of Parkinson’s patients engaging in exercise routines to manage the condition.

Exercise as treatment

Exercise has been regarded by specialists as a type of treatment for people with Parkinson’s disease for more than 60 years.

The Parkinson’s Outcomes Study, a clinical trial of over 13,000 Parkinson’s patients from five different countries that was started in 2009, discovered that engaging in at least 2.5 hours of exercise per week can reduce the disease’s impact on a person’s quality of life.

Further research is being done to understand the mechanisms through which exercise benefits people with Parkinson’s.

For instance, a 2022 study discovered that a hormone released during exercise lowers the amounts of a protein responsible for the symptoms of Parkinson’s disease.

Different types of exercise

The goal of this systematic review and network meta-analysis was to assess how various forms of physical activity affected persons with Parkinson’s disease.

The studies that were considered as part of the analysis focused on the advantages of exercise regimens that the researchers categorised into ten, more general categories, including:

  • dance
  • an aquatic workout
  • gait, equilibrium, and functional training
  • multi-domain instruction
  • mind-body conditioning
  • endurance exercises
  • flexibility exercises
  • resistance and strength training
  • gaming
  • Parkinson’s patients that participate in the physical therapy programme LSVT BIG learn to move their bodies more easily.

According to Dr. Giselle Petzinger, a neurologist and associate professor of neurology at the Keck School of Medicine at the University of Southern California, “they really did try to cover, I think, truly the gamut of the different types of activities.” She wasn’t a part of this study.

She continued, “I think the breadth is quite broad. The effects of these various forms of exercise on motor symptoms and quality of life were examined by the researchers. They also looked at the negative outcomes that various study investigators reported.

Studies selected for research

Starting with trial registries, conference proceedings, reference lists of identified studies, and eight databases (including Embase), the researchers conducted a systematic search for articles. This search covered the period from May 2021.

RCTs were a part of the systemic review conducted by the researchers. They examined the effectiveness of several forms of organised physical activity for Parkinson’s disease in adults by contrasting them with one another, a control group, or both.

In the end, the researchers enrolled 7,939 people from 156 RCTs, the majority of whom had mild to severe Parkinson’s disease but no significant cognitive impairment.

The trials included a median of 51 participants. The included studies were carried out in a variety of nations, but the nation with the greatest number of included cases was the United States.

Analysis of the effects of exercise

Network meta-analysis, which is defined as “a meta-analysis in which multiple treatments (that is, three or more) are being compared using both direct comparisons of interventions within randomised controlled trials and indirect comparisons across trials based on a common comparator,” was used by researchers to analyse the effects of the exercises.

The investigation specifically looked at how different types of exercise affected the severity of motor symptoms and quality of life. The negative consequences of exercise were also examined.

On 71 trials with 3,196 people that assessed the severity of motor symptoms and on 55 trials with 3,283 participants that assessed quality of life, network meta-analyses were performed. 5192 participants and 85 studies provided safety information.

Beneficial effects of exercise

The Unified Parkinson Disease Rating Scale (UPDRS)-M scores are used by the researchers to express the effects of various forms of exercise on the severity of motor symptoms in Parkinson’s patients.

The following is evidence from network meta-analyses on the effect of various types of exercise on the severity of motor signs:

  • Dance may have a mildly positive effect, according to the findings.
  • Evidence suggests that aqua-based exercise “may have a moderately positive effect.”
  • Gait, balance, and functional exercise may “may have a moderately positive effect,” according to the data.
  • Evidence indicates that multi-domain training “may have a moderate favourable effect.”
  • Evidence indicates that mind-body training “may have a small beneficial effect”
  • Data suggests that endurance training “may have a slight beneficial effect.”
  • Training your flexibility may “have a modest or no effect,” according to the evidence.
  • Evidence for strength/resistance training is somewhat speculative.
  • LSVT BIG: Evidence is highly speculative.

The Parkinson’s Disease Questionnaire scores were used by the researchers to categorise the impact of various forms of exercise on people with Parkinson’s quality of life.

They discovered what follows:

  • Evidence suggests that aquatic training “probably has a considerable beneficial effect.”
  • Evidence suggests that endurance training “may have a moderate favourable effect.”
  • According to the available data, functional exercise “may have a small beneficial effect” on gait and balance.
  • Evidence suggests that multi-domain training “may have a slight favourable effect.”
  • Evidence for mind-body training is highly speculative.
  • gaming: extremely shaky evidence
  • Strength-resistance training: Very unclear evidence
  • Dance: pretty shaky evidence
  • LSVT BIG: Very shaky evidence
  • Evidence for flexibility training is highly speculative.

Just 85 of the chosen studies offered any sort of safety information. In 40 of the RCTs that were examined, no negative occurrences happened. 28 studies did find adverse effects.

Participants in 18 research reported having fallen, and 10 studies said they had hurt themselves. The results of the analysis stated that the “impact of physical activity on the risk of adverse events” is “extremely questionable” in light of the accumulated information.

The researchers did highlight that there was not much data to suggest that the various types of exercise had varied detrimental consequences.



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Type 2 diabetes drug may help lower rose dementia risk.

Type 2 diabetes drug may help lower rose dementia risk.

According to new research, older persons with newly diagnosed type 2 diabetes mellitus (T2DM) who have a history of stroke or ischemic heart disease may benefit most from treatment with the thiazolidinedione pioglitazone.

In general, over the course of an average of 10 years, patients who took pioglitazone had a 16% lower risk of dementia. This compares to the people who take medication, according to a large cohort study from Korea.

However, the risk of dementia was decreased by 54% and 43%, respectively, among people with ischemic heart disease and stroke histories.


There will be 139 million cases of dementia worldwide by 2050, with the number continuing to rise. Dementia is more likely to affect some people, particularly those with type 2 diabetes.

Researchers have shown that persons with type 2 diabetes who used the diabetic medication pioglitazone had a lower risk of dementia in old age.

Dementia affects an estimated 55 million individuals worldwide, and by 2050, that figure is anticipated to rise to 139 million.

Type 2 diabetes and dementia

Why would someone with type 2 diabetes have a higher chance of getting dementia?

At Pinehurst, North Carolina, Dr. Karen D. Sullivan, a board-certified neuropsychologist and proprietor of I CARE FOR YOUR BRAIN, claims that diabetes has a detrimental effect on nearly every system of the body, including the brain.

“Compared to people without diabetes, people with type 2 diabetes have a 50–60% increased risk of developing dementia. She stated in an interview with Medical News Today that this is one of the most potent modifiable risk factors for dementia.

She said: “The insulin resistance we detect in diabetes increases atherosclerosis and alters energy metabolism. This results in microvascular alterations in the brain and ultimately a decrease of blood supply to networks of neurons.”

16% lower risk with pioglitazone

Researchers used information on newly diagnosed type 2 diabetics without dementia from the National Korean Health Database for their investigation. The average follow-up period for the more than 91,000 participants was 10 years. 3,467 of the individuals received the medication pioglitazone.

Following examination, researchers discovered that 8.3% of those taking pioglitazone experienced dementia. This is opposed to 10% of those with type 2 diabetes who did not take the medication.

Scientists discovered that persons with type 2 diabetes who took pioglitazone were 16% less likely to acquire dementia later in life after controlling for a number of lifestyle factors. This study was limited by the fact that it was based on data from insurance claims. Therefore it is possible that some participants did not even take pioglitazone.

The study contains no data on the severity of the illness, the participants’ glycemic control, or their genetic susceptibility to dementia.

How blood vessels may play a role

Dr. Eosu Kim is a professor in the Department of Psychiatry in the College of Medicine at Yonsei University in Seoul, Republic of Korea, and the lead author of this study responded when asked how pioglitazone helps reduce the risk of a person with type 2 diabetes developing dementia by pointing out that this study was to investigate the association between pioglitazone use and incidence of dementia, not how — with what mechanisms — this drug can suppress dementia pathology.

Nonetheless, he told Medical News Today, “Several could be recommended based on [the] basic pharmacological activities of this medicine and findings from past studies.”

“First of all, maintaining healthy blood sugar levels is advantageous for brain activities. Also, this medication enhances cells’ capacity for metabolism and encourages them to use bioenergy more effectively. This helps the brain’s insulin resistance.

“Second, certain studies have demonstrated that pioglitazone removes harmful beta-amyloid proteins from the brain. One of the main causes of Alzheimer’s disease is the buildup of beta-amyloid in the brain, he continued.

“Lastly,” he continued, “we hypothesise that pioglitazone’s anti-dementia action may be related to increasing blood vessel health as we found that this medication is more beneficial in diabetic patients who have blood circulation difficulties in the heart or brain than in those without such problems.

Strongest defence in people with heart illness

Speaking about the heart, Dr. Kim and his team discovered that individuals with type 2 diabetes who had previously experienced an ischemic stroke or ischemic heart disease benefited from pioglitazone the most in terms of dementia protection.

Researchers discovered that dementia risk was lowered by 54% in people with ischemic heart disease. Also, by 43% in people with ischemic stroke. Dr. Kim claimed that these outcomes astounded him and his team. It was a surprising discovery, he added.

“Ischemic heart or brain disorders are key risk factors for dementia, thus it would have made sense if pioglitazone’s effects were found to be less effective in those with these conditions. The outcome, though, was the exact reverse of what was anticipated, he said.

Anti-diabetic drugs against dementia

Dr. Kim stated that the next stage of this research is looking at how current anti-diabetic medications or potential medications. These meds enhance cell energy metabolism can inhibit dementia pathogenesis in animal models.

To confirm this medication’s anti-dementia properties and the risk-benefit ratio of using it, prospective trials are required in clinical research. That is, [a] balance between adverse symptoms and advantageous long-term consequences of this medication in terms of dementia prevention,” he said.

Dr. Sullivan replied that the next stage for pioglitazone would be to evaluate long-term safety in people and determine the ideal dose that minimises side effects while maintaining the desired results.

Due to safety concerns, pioglitazone is presently only used as a second-line medication for type 2 diabetes. It is well recognised to raise the risk of fractures, weight gain, and heart failure hospitalisation.

Until then, Dr. Sullivan advised persons with type 2 diabetes to focus on stabilising their blood glucose levels because both high blood sugar (hyperglycemia) and low blood sugar (hypoglycemia) might harm brain blood vessels.

According to her, brain damage occurs when people experience extreme highs and lows.



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Explore the easy hacks to deal with depression.

Explore the easy hacks to deal with depression.

As sneaky as it is unpredictable, depression may be. You could be surprised by it at any time. even when everything appears to be going according to plan and when everything is “wonderful.”

You might be asking yourself, “How can I feel so horrible when I have so much to be grateful for?” while you try to make sense of this. Worst yet, “I have no business feeling depressed,” Such ideas are not constructive. These just serve to reinforce guilt feelings, which are depression’s best buddy and partner.

Your relationships, your job, and your entire feeling of self-worth can all be affected by clinical depression. It has a powerful punch. Fortunately, there are resources out there that can aid in your resistance.

Preventative care is of course the most significant (therapy, a positive support system, getting enough sleep and exercise, etc.). But, the following are some spot-on, urgent steps you can take if you find yourself in the middle of a depressive episode. All of these “tools” won’t be able to cure depression, but they might at least help clear things up a little.

Symptoms of depression

In a depressive episode, the individual experiences significant difficulties in personal, family, social, educational, occupational, and/or other important areas. The symptoms generally differs in terms of severity and natured which is based on individual occupation, gender, and age group. Depression symptoms can vary from mild to severe and can include:

  • Changes in appetite
  • Loss of energy or increased fatigue
  • Increase in purposeless physical activity or slowed movements or speech
  • weight loss or weight gain
  • Trouble sleeping or sleeping too much
  • Feeling sad or having a depressed mood
  • Feeling worthless or guilty
  • Difficulty thinking, concentrating or making decisions
  • Thoughts of death or suicide
  • Loss of interest or pleasure in activities once enjoyed

Furthermore, medical conditions such as thyroid problems, brain tumors, and vitamin deficiencies can mimic depression symptoms, so it is important to rule out general medical causes.

Hacks to relieve depression

Activate your body.

Moving your body is the fastest technique to combat depression feelings right now. Of course, exercising may be the last thing you feel like doing when you’re depressed. It need not be difficult, though; any kind of physical exercise will do.

Just performing 20 jumping jacks or shaking your body for a minute or more can have an impact. Our thoughts and bodies are intertwined; if we let our bodies take the lead, the mind will probably follow.

Answer the phone.

Dial a number. a buddy. an associate. With one exception, any kind of social connection can be extremely therapeutic. Make sure the individual you are connected with is a positive support who feeds you rather than drains you.

If you are unable to phone, you can still text someone to feel connected. If you have no one to contact or text, go online and pick one of the many support groups or chat rooms to meet people going through similar experiences to you. Human connection has the ability to heal.

Determine possible triggers.

Even though a depressed episode can appear to occur suddenly and without “good reason,” there usually is an outside trigger. It could be a difficult conversation or experience that you haven’t yet processed, or it could be a self-defeating mindset, which is more harder to recognise.

You can respond, “But nothing happened, and I wasn’t even thinking about anything at the time,” in response to this. The second is impossible. We are constantly thinking. Our thoughts never go away, whether we are debating the meaning of existence or choosing which shoes to wear.

Negative ideas might blend in with the background. Like the sirens you hear so frequently, you stop noticing them. Worst-case scenarios involve these pessimistic thoughts developing into strongly held self-beliefs. For instance, skewed, unfavourable thoughts may surface if you failed a test or lost your job, such as “I failed because I’m not smart enough” or “I’ll never find another job again.” It doesn’t matter what you believe or feel, it still might not be real. It is our responsibility to recognise these thoughts before they take control and to resist them.

Reject the provoking thought.

Lies are one of depression’s greatest strengths. Never trust them.

Once the negative concept has been located, question its veracity. Ask yourself: How do you know that, for instance, when you tell yourself, “I’ll never find another work again”? The future cannot be predicted. Instead, in response to the statement, “I’m not smart enough,” you might provide evidence to the contrary, such as a list of all the times you performed well or your accomplishments to date.

Also, avoid generalising. Simply because you lost one job or failed one test does not mean that you will never find another one or pass another test. Whatever depression tells you, ignore it!

Remain in the current moment.

When depression has you in its tight grip, it might be difficult to think clearly. The prefrontal cortex, a better developed region of the brain that governs cognitive processes like rational thought, can frequently lose control to the limbic system, which governs emotions.

Here, mindfulness can be useful. This does not imply that you must sit and practise meditation for 20 minutes (although practising meditation is one of the best ways to cultivate mindfulness). Catching a negative idea and immediately changing your attention to something physical in the present, like your breath or the noises or odours around you, sometimes be all it takes. Being aware is more than just a trendy concept; it will benefit you all your life.

Take refuge in a good movie.

We all need to occasionally step outside of our thoughts. Of course, in a non-destructive manner. One of the things to do is to watch a fantastic movie. Avoid tearjerkers and instead pick a comedy or at least an upbeat movie. Only a few examples of comedic and/or lighter movies that you can add to your toolkit for battling sadness are provided below.



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