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Are brain fog, sleep, and pain improved by Cannabis?

Are brain fog, sleep, and pain improved by Cannabis?

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Cannabis, according to researchers, may be able to lessen the negative effects of chemotherapy as well as cancer discomfort. In a recent study, cancer patients said that using cannabis helped them feel less pain, sleep better, and think more clearly.

According to experts, federal rules need to be altered so that more studies may be done on cannabis’ advantages and impacts on medical ailments.

According to a study conducted at the University of Colorado at Boulder and published in the journal Exploration in Medicine, people with cancer who use cannabis to alleviate symptoms experience less pain, sleep better, and have clearer thinking.

This is one of the first observational studies to examine the potential effects of cannabis products obtained from a dispensary on chemotherapy side effects and cancer symptoms.

University researchers are only permitted to possess and distribute cannabis products that are authorized by the government or that meet pharmaceutical standards in the United States, which makes it challenging to conduct studies on dispensary goods.

The researchers at the University of Colorado, however, developed a novel strategy. When 25 cancer patients bought their products, they watched how they responded.

During a baseline visit, the researchers evaluated the patient’s pain tolerance, sleep quality, and cognitive function. After that, the participants went to a dispensary and bought a cannabis edible product of their choice. They selected several different products, such as:

  • Chocolates
  • Gummies
  • Tinctures
  • Pills
  • a baked good

Additionally, the THC and CBD potencies varied widely.

Information from the cannabis and cancer pain study

The researchers traveled to each person’s residence in a mobile lab.

Before being asked to consume the cannabis product they had chosen at home, each person had their physical and mental capabilities evaluated in the van. After consuming medical marijuana, they completed another test.

Within an hour of using the items, the patients claimed that their pain levels had greatly decreased. Additionally, it made them feel “high” and affected their cognitive function. They claimed to feel higher the more THC was present.

After two weeks of consistent use, the individuals underwent a follow-up examination. At that time, the patients indicated that their pain, sleep, and cognitive abilities had all decreased. Improvements were evident in various cognitive domains, including reaction times, according to objective measurements.

The researchers found that lower levels of pain led to an improvement in cognitive performance. The improvement in cognition increased as the discomfort decreased.

Patients who consumed more CBD reported significant reductions in pain and better sleep. CBD reduces inflammation. The authors of the study point out that while cognition was temporarily reduced, it can be enhanced by treating pain.

How cannabis might benefit cancer patients

Some dosages and cannabis types, according to experts, may be beneficial for persons receiving cancer therapy.

Dr. Wael Harb, a hematologist and medical oncologist at Memorial Care Cancer Institute at Orange Coast Medical Centre in California who was not involved in the study, said, “This study adds to the growing body of research that examines the potential benefits of cannabis use in cancer patients.”

According to Harb, “the results highlight the potential for cannabis to reduce pain, enhance cognition, and improve the overall quality of life for patients.” These findings have important therapeutic ramifications since they imply that cannabis may be used as an auxiliary or alternative therapy for cancer patients, particularly those who are in pain or have cognitive deficits.

However, “it is important to note that the study has limitations, such as a relatively small sample size, which may not represent the larger population of cancer patients,” the author continued.

The study also uses self-reported information, which is prone to bias. To validate these results and investigate any potential hazards or negative consequences related to cannabis usage in cancer patients, additional research with bigger, more diverse samples and more objective assessment technologies is required.

What do you need to understand about medical marijuana?

The director of the UCI Centre for the Study of Cannabis, Daniele Piomelli, Ph.D., stated that “this small study supports what oncologists have known for a long time: many cancer patients (half of them, according to some surveys) use cannabis to cope with nausea, pain, and sleeplessness caused by cancer drugs“.

He informed us that the National Cancer Institute, a division of the National Institutes of Health, is aware of this and that urgently required larger investigations are about to begin.

According to the National Institutes of Health, the cannabis plant has two major compounds (cannabinoids) that are employed in medical procedures. THC and CBD are these.

These have not been given use approval by the Food and Drug Administration. The group has, however, approved a small number of drugs that do:

  • Cannabidiol (Epidolex)
  • Dronabinol (Marinol, Syndros)
  • Nabilone

Currently, marijuana use is either decriminalized or legal in 46 states. Anyone considering using medical items should first examine the regulations in their locality as each state has different legislation.

Dr. Olivia Seecof, clinical assistant professor of medicine and attending physician in supportive oncology at NYU Langone Perlmutter Cancer Centre in New York, said she was “very excited” about the study because it was “one of the first studies to address some of the issues surrounding recommending medical cannabis products in an evidence-based way.”

During outpatient supportive oncology appointments, I do certify patients for medical cannabis. I had to enroll in the New York State Medical Cannabis Programme and complete further training/certification to be able to do that,” she explained to us.

The market for medical marijuana is expanding.

Its US market value in 2021 was close to $27 billion. Market Research Future estimates that by 2030, it would reach $248 billion.

According to a Reuters article, some proposed measures in Congress would decriminalize or legalize marijuana.

It would be decriminalized under one statute, leaving state regulation to their discretion. More research will be possible thanks to the regulation reform, giving doctors and other healthcare providers the data they need to treat patients.

Because of cannabis’ murky legal status and negative connotations, many doctors are still uneasy about marijuana, according to Piomelli. “But the profession can no longer bury its head in the sand with so many patients using it. To better meet the requirements of their patients, doctors, nurses, and other medical professionals need to have more knowledge about the advantages and drawbacks of cannabis.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Detect the Cognitive ability by a test before its arrival.

Detect the Cognitive ability by a test before its arrival.

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According to researchers, a quick card memory test can identify cognitive decline years before symptoms appear. According to experts, the test would make it possible for those who are more likely to develop dementia to receive treatment and preventative measures sooner.

One specialist advocates administering the test to everyone over 45. Researchers claim to have created an easy test that can forecast a person’s future risk of developing cognitive impairment.

The test only applies to persons without pre-existing cognitive and memory impairments, the researchers write in their study, which was just published in the journal Neurology.

The study’s lead author and clinical professor at the Albert Einstein College of Medicine in New York City, Ellen Grober, Ph.D., said in a statement that there is “increasing evidence” that some people who appear to be healthy and have no cognitive or memory issues may fact be displaying very mild indicators of early cognitive impairment. In our study, a quick and accurate memory test indicated the likelihood that individualsnormally thought to have normal cognition will experience cognitive impairment.

Cognitive impairment study

969 participants in the study, whose average age was 69, took a basic memory test and then underwent follow-up exams over ten years.

There were two phases of the test.

The participants were first instructed to examine four cards, each of which had four drawings of various objects.

Then, the respondents were required to identify each item as a member of a specific category. For instance, when asked to name a fruit, participants might respond “grape.”

In the following stage, participants were required to recall the things to gauge their memory capacity. They were given category cues, which calculated the amount of memory storage, for the items they couldn’t recall.

Result of the tests for cognitive impairment

Using the Stages of Objective Memory Impairment (SOMI) approach, researchers categorized the participants into five groups with stages zero through four based on their test results.

Stage 0 was for patients with no memory issues (47% of cases).

Memory retrieval problems, which researchers noted can occur five to eight years before dementia, were more difficult to recall in stages one (35%) and two (13%) of the disease. When given indications, these participants could recall information.

The individuals in the third and fourth stages (5% overall) had trouble remembering all the objects, even with hints. These stages, according to the researchers, occur 1 to 3 years before dementia.

234 of the 969 subjects experienced cognitive impairment in the end.

Subjects at stages one and two were twice as likely to experience cognitive impairment compared to those at SOMI stage zero, even after accounting for factors such as age, gender, education level, and the APOE4 gene, which affects a person’s chance of developing Alzheimer’s disease.

Cognitive impairment was three times as likely to develop in those in stages three and four.

The significance of testing for cognitive impairment

The SOMI method continues to forecast an elevated risk of cognitive impairment even after accounting for indicators of Alzheimer’s disease including amyloid plaques and tau protein tangles.

According to research, 72% of people in the third and fourth stages will have cognitive impairment after ten years, compared to 57% of people in the second stage, 35% of people in the first stage, and 21% of people in stage zero.

Our findings confirm the SOMI system’s application in locating those most at risk for cognitive decline, according to Grober. “Researchers looking for remedies can benefit from spotting cognitive impairment early on. By working with their doctor and implementing strategies to support healthy brain aging, those persons who are discovered to be at elevated risk may also benefit.

Neura Health’s virtual headache and migraine clinic’s medical director, Dr. Thomas Berk, a neurologist, pointed out that present testing only reflect the brain’s current condition.

“Predicting neurological change years later is very difficult,” said Berk. When someone has neurological testing, “we are getting a snapshot of their current brain function, not what their brain will look like years later,”

“This does give some evidence for being able to assess the future risks of developing memory issues,” he continued.

There is unquestionably a need for “a simple and fairly rapid test,” particularly in light of the growing body of evidence that early intervention can have a positive impact, according to Dr. Dale Bredesen, head of the University of California Los Angeles’ Easton Centre for Alzheimer’s Disease Research.

Standard neurocognitive tests can take hours, making them impractical for screening, and common quick tests like the MMSE aren’t sensitive enough to catch these early alterations, according to Bredesen.

Using fresh memory tests

According to Bredesen, the subjects of present testing are those who already have cognitive problems.

“Simple tests like the one described in this report should be included for everyone over the age of 45, to identify those who should be evaluated further, and potentially treated,” he advised.

One physician claimed that the SOMI system made him think of a well-known kid’s game.

According to Dr. Clifford Segil, a neurologist at Providence Saint John’s Health Centre in California, “I advise my patients to make a mental image of a scene with all three words to help in their recall when they have to recall the three words.” “I would suggest the same for this proposed card cognition exam. Currently used cognitive exams include additional memory tests.“

“Go Fish,” which is utilised as a learning tool for children rather than a cognitive exam for senior people, is similar to the suggested test to be employed in my elderly population, which interests me as a parent and a practising adult neurologist, Segil added.

“When you start to worry that you might be losing your memory, you should be evaluated by a neurologist to see if your complaints are generally age-appropriate normal or something else,” he said.

REFERENCES:

For Cognitive disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Atrial fibrillation catheter therapy and dementia risk.

Atrial fibrillation catheter therapy and dementia risk.

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Researchers looked into how medications and catheter ablation for atrial fibrillation affected people’s risk of developing dementia.

They discovered that catheter ablation therapy lowered the risk of dementia more effectively than medicine alone.

For the correlation to be verified and the cause of it to be understood, more research is required.

Atrial fibrillation (Afib)

A cardiac disorder called atrial fibrillation (Afib) is characterised by erratic beating in the upper chambers of the heart, which restricts blood flow to the lower chambers. Patients who have afib may experience discomfort and have a five-fold increased risk of stroke.

183,321 death certificates in the US in 2019 listed AFib as a cause of death. By 2030, 12.1 million persons in the United States are predicted to be affected by the illness.

AFib has been linked in studies to dementia and cognitive decline. Additionally, studies have shown that patients with dementia and cognitive impairment who also have AFib suffer from a greater rate of cognitive decline than those who do not.

Understanding whether treating Afib patients lowers their likelihood of developing dementia may improve patient outcomes.

Recent studies evaluated the effects of Afib medication versus catheter-based therapy on the risk of dementia. They discovered that compared to medicine alone, catheter-based Afib therapy was associated with improved cognitive function.

“Despite having negative brain imaging results, I have encountered multiple patients with long-term persistent atrial fibrillation who had cognitive impairment, decreased swallowing capacity, and slower motor performance.

Based on this, I do not find [the results] surprising,” Dr. Vicken Zeitjian, a San Antonio, Texas-based cardiologist board-certified in nuclear cardiology and echocardiography who was not involved in the study, told.

He went on to say that “these results further demonstrate that catheter ablation is a superior method of atrial fibrillation management than medical management alone.” The research will be presented at the 75th Annual Meeting of the American Academy of Neurology.

Medicine versus catheter ablation

887 Afib patients with an average age of 75 were included in the study by the researcher. Before enrollment, 193, or 21.8%, of the participants got catheter ablation, whereas the remaining patients just received Afib medication.

Catheter ablation is the process of utilising radiofrequency to remove tiny patches of cardiac tissue that may be the source of an irregular heartbeat.

The individuals’ cognitive function was evaluated at baseline, one year later, and two years later. Out of a possible 30, a 23 or below score indicated cognitive impairment.

The study’s findings showed that those who underwent catheter ablation had an average cognitive score of 25, compared to those who did not, who had a score of 23.

The researchers discovered that those who received catheter ablation were 36% less likely to experience cognitive impairment than those who were just given medication after controlling for conditions like heart disease, kidney disease, and sleep apnea.

However, they pointed out that there were no appreciable variations in the incidence of heart attacks between patients who underwent catheter ablation or medication alone.

They also discovered that using warfarin and other anticoagulants had no appreciable impact on cognitive deterioration.

The risk of dementia and catheter ablation

We enquired about how catheter ablation might lower the risk of dementia from Dr. Aaron Ritter, director of the Memory & Cognitive Disorders Programme at Hoag Hospital in Newport Beach, California, who was not involved in the study. Although the study doesn’t say how, he pointed out that there could be a number of causes.

“For me, ablation may be a more conclusive or long-lasting therapy than pharmaceutical management, which necessitates a commitment to a daily prescription schedule, perhaps twice daily. We have to wonder if the compliance issue is important to the outcome in those with memory issues, he said.

“Furthermore, we may also hypothesise that ablation may be more a successful treatment for atrial fibrillation, and as a result, individuals may have fewer blood clots or better consistent delivery of blood and oxygen to the brain,” he added.

Future research should, he hoped, incorporate measurements of blood flow, which would help researchers understand why ablation performed better in this trial.

less cognitive impairment overall

In the recent study, data for 887 older persons with AFib were analysed. Participants were 75 years old on average, about half were women, and more than 87% were white.

Approximately 22% of patients underwent catheter ablation. Compared to those who just received medicine for their AFib, these individuals were more likely to have both a persistent AFib and an implantable cardiac device.

Before the study began, participants performed cognitive function tests that evaluated their short-term memory, attention, concentration, and language skills. One and two years later, they conducted similar tests once more.

These tests merely evaluated whether a person had problems completing particular mental activities; they did not determine whether a person had dementia.

In contrast to individuals who only received pharmacological treatment during the two-year research, those who underwent catheter ablation had a 36% lower chance of experiencing cognitive impairment.

Dementia is caused by many things.

The results of the current study should not be taken too seriously because they have not yet undergone peer review, said Dr. Keith Vossel, a neurologist and the director of UCLA’s Mary S. Easton Centre for Alzheimer’s Research and Care in Los Angeles.

Additionally, the study must be published before its influence on clinical practise can be evaluated, the researcher added.

However, “it does this add to other research supporting the possible use of certain treatments for reducing dementia risk,” he said to Healthline.

The fact that blood flow to the brain was not measured in the present study’s limitations to determine if patients treated with catheter ablation or medication had different blood flow patterns to the brain.

Limitations

Additionally not engaged in the study, Dr. Fanny Elahi, a physician-scientist who is an assistant professor of neurology, neuroscience, pathology, molecular, and cellular-based medicine at Mount Sinai, stated:

“Although these findings are intriguing, more investigation is required to determine the connection between catheter ablation (CA) and dementia. With cognition as a co-primary endpoint and the study appearing to be observational rather than randomised, I wonder if the study is tainted by the baseline health of individuals who receive CA.

The main drawback is that cerebral blood flow measurements were not provided to go along with the cognitive testing. The authors’ use of a 30-point cognitive test, a somewhat constrained measure of cognition, is another drawback, says Dr. Ritter added.

Implications

cardiologist at Staten Island University Hospital, Dr. Rina Shah, who was not involved in the study, stated:

“It is significant to note that dementia and the prevalence of AFib both rise with ageing. AFib, however, can result in a variety of other medical issues, including hemodynamic deterioration and cardiomyopathies if rates are difficult to manage. We can assist prevent or delay the harmful effects of AFib by administering catheter ablation to patients earlier.

The study, according to Dr. Elahi, emphasises the significance of connections between the brain and the body.

“We must care for the whole person if we want to increase brain health. Implementing molecular and imaging biomarkers may help to further define the impact if there is one, she said.

“I am a strong believer in knowing the biological impacts of such therapies since we probably need several shots on goal to battle brain ageing and cognitive loss. Finding out why something works allows us to use synergistic methods to enhance the intervention, she added.

REFERENCES:

For Cardiovascular medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=11

Researchers identify potential new stroke treatment targets

Researchers identify potential new stroke treatment targets

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When blood flow to a portion of the brain is stopped or reduced by a hemorrhage or obstruction, a stroke results. Although some stroke survivors recover completely, many still struggle with long-term repercussions and are at increased risk of having another stroke.

Brain damage following a stroke is thought to be a result of changes in small blood arteries that exist in addition to the blockage.

In the injured small blood arteries in the brain, a recent study identified multiple changes in gene activity that may serve as targets for pharmacological therapy to enhance stroke recovery.

An artery in the brain becomes clogged or bursts, resulting in a stroke. Beyond the blockage or bleeding, the brain cells are starved of oxygen and nutrients and suffer damage or degeneration. Researchers have been looking for strategies to lessen damage after a stroke and hasten recovery.

Researchers from Weill Cornell Medicine have now discovered alterations in gene activity in small blood arteries after a stroke. The results imply that these alterations could be targeted with current or upcoming medications to lessen brain damage or enhance stroke recovery.

The research was released in PNAS. Weill Cornell Medicine assistant professor of pathology and laboratory medicine and the lead author, Dr. Teresa Sanchez, told:

“By providing a knowledge platform of the molecular alterations in the cerebral microvasculature, our study has improved our understanding of the pathophysiology of stroke. This is critical to developing novel therapeutic strategies for this devastating condition.”

Stroke symptoms

The majority of strokes are ischemic strokes, in which a blood clot obstructs a blood vessel leading to the brain. This prevents nutrition and oxygen from reaching brain cells.

Immediate signs could be:

  • bewilderment and difficulty speaking
  • Headache, maybe accompanied by dizziness or nausea
  • numbness or a lack of movement in certain body areas, especially on one side
  • vision issues
  • Walking difficulties, a loss of coordination, and vertigo.

It’s crucial to get therapy and a diagnosis right away to reduce long-term damage. Many stroke victims, however, continue to experience physical and psychological after effects.

Over 795,000 people experience a stroke each year in the United States. Also, the condition is one of the main causes of long-term disability. This is according to the Centres for Disease Control and Prevention (CDC).

Long-term damage from a stroke

Despite the fact that only 10% of stroke survivors experience a near-complete recovery, survivors frequently experience a variety of symptoms, such as:

  • weakness or paralysis on one side of the body.
  • thinking, memory, and speaking issues.
  • difficulty swallowing and chewing.
  • issues controlling one’s bowels and bladder.
  • Depression.

Inflammation and long-term alterations in the brain’s small blood arteries, result in constrained blood flow to brain cells and leaking over the blood-brain barrier. They are the root of many of these symptoms.

In a recent study, gene activity in mouse cerebral microvasculature after a stroke was observed to vary. Similar modifications were found in stroke patients from people as well.

Gene activity changes following a stroke

The researchers discovered 541 genes whose activity was altered similarly in mice and people after stroke, and they also discovered many clusters of genes with various roles.

According to Dr. Teresa Sanchez, “Our work has also clarified the shared transcript alterations between human and mouse stroke and identified common changes in pathways associated with vascular/endothelial dysfunction, sphingolipid metabolism, and signalling.“

They discovered genes linked to vascular disease, general inflammation, brain inflammation, and the specific form of vascular malfunction. This results in leaky cerebral microvessels. The blood-brain barrier, which controls the flow of chemicals between the blood and brain cells, is weakened as a result of these leaky arteries.

The activity of molecules that regulate the blood-brain barrier was shown to vary after stroke, according to the researchers.

Dr. Sanchez stated that a stroke causes “robust changes in the genes regulating the blood-brain barrier and endothelial activation, i.e. upregulation of genes causing blood-brain barrier leakage and downregulation of genes protecting the blood-brain barrier.“

Additionally, they found that after a stroke, there was a disruption in the activity of genes that regulate sphingolipid levels, which are fat molecules involved in a broad variety of biological activities, including inflammation.

Potential therapeutic routes

Some of these molecular alterations, according to the researchers, might make for fresh medication therapy targets. They draw attention to the elevated sphingolipid concentrations in the cerebral microvasculature and hypothesize that sphingolipid targeting may be therapeutic after stroke.

We questioned Dr. Sanchez on the possibility of using medicines to either prevent these changes or undo the harm already done.

“Since endothelial dysfunction is a major contributor to stroke and, concurrently, stroke-induced cerebral ischemia causes additional injury to the endothelium, which further compromises cerebral blood flow and exacerbates brain injury,” she said.

According to Dr. Allder, the discoveries could influence research into other neurological conditions:

“I can see how it might make post-stroke treatments more accessible, but I also see how it might open up new treatment options for dementia and post-brain injuries, particularly repetitive brain injuries.”

More research is required

Therefore, the results may possibly suggest novel therapeutic avenues, but Dr. Iyer emphasised the need for more study:

The key drawback of this research is that human genome and transcriptome models aren’t usually transferable from mouse models. However, this study reveals a hitherto unrecognised cellular signalling route that is unquestionably ready for further study.

Preclinical research is currently being conducted by Dr. Sanchez and her team to see whether it would be advantageous for stroke patients to reverse some of the specific microvascular abnormalities that were observed in their study. They are doing this by employing candidate medications or genetic techniques.

REFERENCES:

For Stroke medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_99

Possible link between migraine and carpal tunnel syndrome.

Possible link between migraine and carpal tunnel syndrome.

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Researchers looked into the prevalence of migraine headaches in patients who have nerve decompression surgery.

They discovered that people who have surgery to decompress a nerve at particular points on their bodies may be up to 70% more likely to get migraines than others who have the procedure elsewhere.

To determine whether nerve decompression can treat migraines, more research is required.

There may be pain and a loss of function when the nerves in the hands and arms contract around muscles and soft tissues. Between 5% and roughly 9% of the population are affected by various types of nerve compression in these places.

Surgery is frequently used to treat the illness and might result in full or partial symptom relief.

The muscles, blood arteries, and bone in the vicinity of the head’s surrounding nerves can also compress those nerves. Improvement or alleviation from migraine and headaches may result by decompressing these nerves.

What is Carpal tunnel syndrome?

Carpal tunnel syndrome is caused by compression of the median nerve. On the hand’s palm side, the carpal tunnel is a small opening encircled by bones and ligaments. Numbness, tingling, and weakness in the hand and arm are signs of median nerve compression.

Carpal tunnel syndrome can be caused by repetitive hand motions, health issues, and wrist morphology.

The tingling and numbness are typically reduced with appropriate care, and wrist and hand function is recovered.

Symptoms

The following list of signs and symptoms of carpal tunnel syndrome includes:

Feeling tingly or numb. Numbness and tingling in the fingers or hand may be apparent. Normal afflicted fingers include the thumb, index, middle, and ring fingers, but not the little finger. In certain fingers, you might experience something like to an electric jolt.

The wrist may feel the sensation before it moves up the arm. These symptoms may awaken you from sleep and frequently happen while you are holding the phone, newspaper, or steering wheel.

To try to alleviate their symptoms, many people “shake out” their hands. Over time, the numb sensation could persist continuously.

Weakness. You can feel weak in your hands and drop things. This can be because the thumb’s pinching muscles, which are similarly regulated by the median nerve, are weak or because the hand is numb.

Migraine and carpal tunnel syndrome

When the nerve that travels from the forearm to the palm of the hand is squeezed at the wrist, carpal tunnel syndrome develops.

In comparison to 16% of those without carpal tunnel syndrome, 34% of those with the condition get migraines, according to a cross-sectional study with 25,880 participants. It might be more effective to screen patients for the disorders if it is known whether nerve compression around the head is related to nerve compression in the hands and arms.

Researchers looked at how frequently people who had nerve decompression surgery for the hands and arms were diagnosed with migraines.

According to their findings, people who have particular types of nerve compression are more prone to suffer from migraine headaches. Not a part of the study, Dr. Chantel Strachan is an internist at ColumbiaDoctors and an assistant professor of medicine at Columbia University Irving Medical Centre in New York. She said.

“I wouldn’t jump to advise carpal tunnel release in every migraine patient. The choice to proceed with surgical treatment for nerve compression is specific to the patient and should be carefully considered with the patient’s medical care team.

Journal of Plastic and Reconstructive Surgery published the findings.

Most likely to experience migraine

Data from 9,558 patients who underwent nerve decompression surgery of the hands and arms between 2009 and 2019 were analysed for the study.

Participants were also evaluated by the researchers for the presence of migraine.

Of the subjects, the median nerve was decompressed in about 71% of cases. Surgery is done on the wrist to release pressure on the nerve, which lessens carpal tunnel syndrome symptoms.

A decompression of the ulnar nerve was done on about 14% of subjects. That is an elbow nerve decompression. 6.5% of patients underwent decompression procedures at various body locations.

In the end, the researchers discovered that people with multiple nerve decompression and median nerve decompression were respectively 30% and 70% more likely to experience migraines than people with ulnar nerve decompression.

Nerve compression and migraine

Dr. Sean Ormond, a specialist in anesthesiology and interventional pain management, did a study to learn more about the potential connection between nerve decompression and migraine.

He mentioned that there are a number of possibilities, but that the causes of nerve compression in the arms and hands and migraine are not entirely known.

“Both upper extremity nerve compression syndromes and migraine may share common risk factors, such as obesity, sedentary lifestyle, poor posture, or repetitive stress injuries,” stated Dr. Ormond.

The affected area may experience inflammation as a result of nerve compression. It is also recognised that inflammation contributes to the pathophysiology of migraines. The presence of inflammation in one place of the body may cause inflammation to spread throughout the body, potentially aggravating migraines, the doctor added.

Ormond observed that although further research is need to establish this, some people may be more prone to higher nerve compression and migraine due to a hereditary tendency.

According to Dr. Strachan, migraine sufferers may become more sensitive to pain due to nerve damage.

Limitations of the migraine study

Dr. Strachan pointed out that because the study was retrospective in nature, the results suggest association rather than causality.

She stated that different providers and their subspecialties, such as primary care, neurology, and pain, may have utilised different criteria to diagnose migraine.

The association between migraine and pain from nerve compression may be the consequence of other variables, as the researchers stated in their report that there is a general overlap across chronic pain disorders.

REFERENCES:

For Migraine disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=17

Analyze the links between BMI, obesity & cognitive ability.

Analyze the links between BMI, obesity & cognitive ability.

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According to the World Health Organisation (WHO), there were more than 650 million obese adults in the world as of 2016. Obesity has been linked in the past to an increased risk of cognitive deterioration.

Evidence from University College London researchers challenges the idea that fat and cognitive capacity are causally related.

Around the world, more than 1.9 billion adults were obese in 2016, with more than 650 million of those adults suffering from obesity, a disease in which a person’s weight is over normal ranges and may lead to various health issues.

According to current estimates, 167 million adults and children will be overweight or obese by 2025. A multitude of disorders, including diabetes, cardiovascular disease, hypertension, osteoporosis, rheumatoid arthritis, and cancer, have been linked to obesity in previous studies, including these.

Furthermore, previous research has connected obesity to a higher risk of cognitive deterioration.

The causal relationship between obesity and cognitive performance has now been called into question by University College London academics. They contend that common family variables have tainted the research linking cognitive aptitude and BMI.

Obesity

If a person’s present weight is excessive for their height, they are considered obese. The body mass index (BMI) is the most popular metric for determining a person’s level of obesity.

This tool determines if an adult is obese or not based on their height and current weight:

  • BMI less than 18.5 indicates underweight.
  • Suitable BMI range: 18.5-24.9
  • BMI of 25 to 29.9 indicates obesity
  • obesity: a BMI of 30 or above

Children and teenagers need a different BMI calculator, which considers height, age, and gender to evaluate obesity because they are still developing.

The BMI measurement is not without problems, though. It is unable to distinguish between muscle and fat when weighing someone. Additionally, it disregards a person’s race, overall body composition, or bone density.

Cognitive function and obesity

Lead author of this study and senior research fellow at the Centre for Longitudinal Studies at University College London in the U.K., Dr. Liam Wright, Ph.D., states that there are several reasons why the research team decided to investigate the causal relationship between cognitive capacity and obesity:

“Over the past forty years, there has been a significant rise in the prevalence of obesity, but BMI hasn’t increased uniformly throughout the population. Therefore, it is crucial to understand why some people are more predisposed to obesity than others.

Additionally, there is a substantial body of research in the field of cognitive epidemiology that demonstrates a connection between cognitive function and practically every measure of health and health behaviour, including obesity.

Unfortunately, the majority of the cognitive epidemiology literature employs observational research designs that may be biassed and fail to show causal effects, according to Dr. Wright. “There are some compelling theoretical arguments for why cognitive ability might have a causal effect on health, but regrettably, these arguments are based on observational research designs,” she said. Because a sibling design could take into account some of the variables that can skew relationships found in previous research, we felt it was crucial to investigate for a relationship between cognitive capacity and BMI.

Examining siblings to reduce bias

Dr. Wright and his research group evaluated data from four distinct young population cohort studies carried out in the United States that included 12,250 siblings from 5,602 homes. Each participant’s data were tracked from youth to age 62.

The scientists were able to take into consideration unobserved characteristics associated with family background by analysing the relationship between cognitive capacity and BMI among families.

“Sibling designs account for factors that are shared between siblings by design,” Dr. Wright said. They don’t require the measurement of these factors, which is both a benefit and a drawback because it is difficult to determine which common factors actually contribute.

With this qualification, he continued, “There are four main factors that we thought might be significant: genetics (siblings share 50% of DNA), parental socioeconomic class (wealth, location, etc.), parenting styles (particularly regarding dietary choices), and parental cognitive ability (cognitive ability could operate indirectly!). “Once more, we didn’t directly examine these.”

According to Dr. Wright, they predicted that these variables would make general population studies more biassed and lead to weaker relationships than in earlier studies, which is exactly what they found.

However, he cautioned, “remember that sibling designs have their own flaws, including the ability for siblings to influence one another, for example, by modelling one another’s behaviour. This may imply that our findings are also skewed, albeit downwardly and smaller than the actual causal effect.

Association between BMI and cognitive ability

When the researchers evaluated the data from study participants who were not related, they discovered that, after accounting for family socioeconomic status, the change in teenage cognitive capacity from the 25th to the 75th percentile was associated with an estimated 0.61 kg/m drop in BMI.

And when the researchers analyzed the information from siblings, they discovered that the change in BMI from the 25th to the 75th percentile of teenage cognitive ability was only correlated with a 0.06 kg/m drop in cognitive capacity.

The relationship between cognitive capacity and BMI was less pronounced when siblings were compared than when the entire population was, according to Dr. Wright, but he was not surprised by this given the overall characteristics he mentioned.

However, he noted, “I was shocked at how little of an association there was when comparing siblings. As said, there are strong arguments to support the idea that cognitive ability has an impact on health and health-related decision-making“.

“Two possibilities for this small association are that one, our results were biassed towards finding smaller associations (e.g., by siblings influencing each other), and two, reflective decision-making isn’t as important in determining BMI as other factors like satiety, etc.,” Dr. Wright continued. Both of these are hypothetical.

Unproven causality

As a parent and a neurologist, Dr. Segil claimed that he has never observed a connection between obesity or a healthy weight and cognitive aptitude in people.obese

The purpose of this study, according to Dr. Segil, “is to argue that people with higher cognitive abilities, who have a higher socioeconomic position, have made healthier decisions.” Additionally, it’s possible that people’s cognitive function increases as their BMI decreases when they make healthier decisions.

He continued, “I do not believe that there is any evidence linking obesity to cognitive function. And I believe that their research’s use of siblings or other family members who are in a similar social economic situation to real-life situations such as brothers or sisters or siblings is realistic.”

After reading this study, Dr. Segil stated that he would be curious to know whether maternal or paternal obesity had a greater impact on adolescent cognitive development.

As a result of reading this, they claimed that adolescent cognition is linked to a lower adult BMI, he continued. So I’m keen to know if stronger adolescent cognitive abilities are related to the maternal and paternal BMI. Does having a thin or fat parent, using the same dataset, alter their children’s cognitive ability?I was shocked, though, by how little of an association there was when comparing siblings. As mentioned, there are strong arguments to support the idea that cognitive ability has an impact on one’s health and decision-making in relation to their health.

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New clues about how ketamine could lead to psychosis.

New clues about how ketamine could lead to psychosis.

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Researchers looked into whether ketamine could cause mental changes like psychosis. They discovered that ketamine increases ambient noise, which may obstruct the brain’s ability to process sensory signals.

As rats were used in the study, more research is required to determine whether the results apply to people. Changes in reality perception, such as persistent delusions, hallucinations, and disorganized thought, are characteristics of schizophrenia. Almost 24 million people around the world are affected by the illness.

There is still no known cause for schizophrenia. Yet, research points to environmental, psychological, and genetic variables as potential causes of the illness.

By blocking NMDA receptors in the brain, the drug ketamine causes a mental state resembling psychosis in healthy humans. As a result, the central nervous system develops an imbalance of excitatory and inhibitory signals, which impacts sensory experience.

According to experts, schizophrenia-related perception abnormalities may be related to similar changes in NMDA receptors. Yet, it hasn’t been made clear how this might be the case.

Ketamine and psychosis

Recently, scientists investigated how ketamine alters sensory perception in rat brains.

They discovered that ketamine increased “background noise” in the brain, which reduced the clarity or intensity of sensory information. They remarked that this might help to explain why persons with schizophrenia or psychosis experience reality differently. The European Journal of Neuroscience published their findings.

These results, according to Dr. Sam Zand, a Las Vegas-based psychiatrist who was not involved in the study, “indicate that malfunction in NMDA receptors may play a role in the development of psychosis.”

“The work offers fresh understandings into the process by which ketamine may cause psychotic symptoms. The results might influence the creation of novel medications for psychosis that target NMDA receptors or brain noise, the researcher continued.

Study design

Seven male lab rats were used in the study to examine how ketamine affected their ability to perceive sensory information. To do this, they first implanted electrodes into rats’ brains to capture electrical activity.

They then recorded the brain’s reactions before and after administering ketamine while simulating their own whiskers. To be more precise, the scientists studied how ketamine affected beta and gamma oscillations in a neuronal network. They carries messages from sensory organs to the brain.

Gamma waves have a frequency range of 30-80 Hz, while beta oscillations have a frequency range of 17-29 Hertz (Hz). Processing sensory data requires the use of frequencies.

In the end, the scientists discovered that even before they stimulated the rats’ whiskers, ketamine enhanced power in both beta and gamma oscillations.

However, they also discovered that the amplitude of the rats’ beta and gamma oscillations dropped post-stimulus and after ketamine administration, which is associated with hampered perception.

They also observed that ketamine enhanced gamma frequency noise, which is related to a reduced capacity for sensory signal processing.

The researchers hypothesised that their findings suggest that increased background noise, which in turn may be brought on by damaged NMDA receptors leading to an imbalance of inhibition and excitation in the brain, may be a trigger for the distorted reality experienced in psychosis and schizophrenia.

According to Dr. Sofya Kulikova, senior research fellow at the HSE University in Perm, Russia, and one of the study’s authors, “The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders.”

Research limitations

The study was not conducted by Dr. Howard Pratt, a psychiatrist and mental health medical director at Community Health of South Florida. He made it clear that:

The main drawback of these results is that, although a strong association, causation has not yet been shown. There are many potential explanations for conditions like psychosis, including increases in dopamine, which is the focus of treatment for those with a diagnosis of schizophrenia. I’m interested to see what happens as the investigation expands past animal studies.

We also discussed the study’s shortcomings with Dr. James Giordano, the Pellegrino Institute professor of neurology and biochemistry at Georgetown University Medical Center who was not engaged in the study.

The fact that the study solely looked at ketamine-induced effects, he said, “is a key limitation. While valuable and practical for understanding ketamine’s activity in a rat model, it may not provide direct translation to comprehend non-drug-induced dissociative, and psychotic states in humans.”

Dr. Giordano went on to say that it is possible that the effects of ketamine on humans, while undoubtedly dissociative and exhibiting some psychotic traits, are not entirely representative of or identical to the neurological mechanisms underlying other forms of psychosis and schizophreniform disorders.

Possible clinical repercussions

The study’s ramifications, according to Dr. Giordano, are that “[t]hese findings are useful in that evidence of ketamine’s actions at defined brain networks may enable better understanding— and improved clinical applications—of its effects in humans.”

The researcher added, “In addition, by highlighting the functions of these brain nodes and networks involved in mediating dissociative experiences, we may create improved understanding — and possibly treatments for — specific types of drug-induced psychoses, and perhaps other psychotic illnesses, such as forms of schizophrenia, as well.

Larger Trials Needed

Dan Iosifescu, MD, MSc, associate professor of psychiatry at New York University School of Medicine in New York City, commented on the study and said that if the results “were based on a larger study” it would be very important because such patients are currently being denied access to a beneficial treatment due to a theoretical risk of psychosis.

A low risk of psychosis exacerbation following IV ketamine, according to Iosifescu, who is also the director of clinical research at the Kline Institute for Psychiatric Research in Orangeburg, New York, and was not involved in the study, is still possible given that the review is based on a small sample.

Veraart concurred, stating that “well-designed randomised controlled trials should be conducted to ascertain the efficacy, safety, and tolerability of ketamine in depressed individuals with a propensity to psychosis before administration on a large scale is pushed.”

The study received no particular funding. Outside of the submitted work, Veraart has received speaker honoraria from Janssen. Disclosures from the other authors are provided in the original publication. Iosifescu has advised clinics on the most effective ways to administer IV ketamine therapy as a consultant to the Centers of Psychiatric Excellence.

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Common Dry-Cleaning Agent May lead to Parkinson’s Disease

Common Dry-Cleaning Agent May lead to Parkinson’s Disease

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Trichloroethylene (TCE), a chemical, has been linked by some researchers to Parkinson’s disease. Dry cleaning, degreasing, and even decaffeinating coffee have all been common uses for TCE.

According to recent study, the chemical’s capacity to reach the brain and harm cell mitochondria may be the root of the problem.

The authors claim that the chemical’s influence might be “enormous” given how commonplace it is in the environment. TCE should be outlawed, and people should be shielded from more exposure, as suggested alternatives.

According to the Parkinson’s Foundation, the substania nigra, a region of the brain that includes cells that create the neurotransmitter dopamine, is affected by Parkinson’s disease, a neurodegenerative condition.

Parkinson’s disease patients endure tremors, slowness of movement, limb stiffness, and balance issues.

Muhammed Ali and Michael J. Fox are two well-known public celebrities who suffer with the illness.

According to the authors, up to a third of the groundwater in the United States has TCE pollution. The chemical is additionally present in Camp Lejeune, a Marine Corps base, and 15 Superfund sites in Silicon Valley.

What is trichloroethylene (TCE)?

TCE is a chemical that is a colourless liquid that does not exist in nature. It is well known to smell like chloroform.

This substance can be found in a wide range of goods and businesses, such as:

  • industry-wide dry cleaning
  • metal scrubbing
  • wiping cloths
  • carpet and garment stain removers
  • lubricants
  • aerosol adhesives

Using TCE-containing products or working in a TCE-containing plant are two ways that people can be exposed to the chemical.

TCE can also contaminate our air, water, and food and drink by leaking into the soil, water, and air near where it is used or disposed of. High levels of TCE exposure can cause the following symptoms:

  • dizziness
  • headaches
  • confusion
  • nausea
  • facial paralysis

Link between TCE and Parkinson’s disease

According to the study, which was published in the Journal of Parkinson’s Disease, there may be a “invisible” cause of Parkinson’s disease that is related to the widespread use of TCE.

Dr. James Beck, Chief Scientific Officer of the Parkinson’s Foundation, commented on the study, saying, “We have known for some years that TCE exposure and Parkinson’s disease are related. I believe that this opinion piece effectively highlights the risks associated with TCE exposure.

The researchers’ findings are discussed in the study together with the evidence tying TCE to Parkinson’s disease.

TCE is lipophilic, as the scientists explain in their research, which means that it has a propensity to dissolve in fatty tissues. This makes it simple for it to enter the brain and other bodily tissues where it can wreck havoc with cell mitochondrial function. This sort of toxin is extremely toxic to dopamine-producing cells, which may help to explain how exposure to TCE might cause Parkinson’s disease.

Seven other people, including the late Senator Johnny Isakson, are also profiled. Isakson employed TCE to degrease aircraft during his time in the military; as a result, he eventually developed Parkinson’s disease as well as renal cell carcinoma, a cancer associated to TCE exposure.

The matter was initially brought to his notice, according to co-author Dr. Ray Dorsey, when his colleague, Dr. Caroline Tanner, told him about the exposures at Camp Lejeune.

TCE poses a “enormous” risk to the general public’s health, he claimed. “At one time, it was used by 10 million Americans, including printers, embalmers, mechanics, dry cleaners, chip manufacturers, engineers, painters, metal workers, pilots and others. It has been absorbed into the environment by millions more people.

Avoiding exposure to TCE

The issue of TCE contamination, according to Dorsey, requires a few actions. It must be prohibited first, along with tetrachloroethylene (PCE), another industrial solvent.

Second, home remediation systems such to those used for radon must be deployed to alert and protect persons who are at danger of exposure.

The connection between TCE and Parkinson’s disease, he added, has to be explored further through research. People can be exposed to TCE through contaminated soil, food, water, air, or direct skin contact, according to the U.S. Centers for Disease Control and Prevention.

You are most likely to become exposed by drinking polluted water, but you can also become exposed through the air as it is released from contaminated water, as a third of all groundwater may be affected.

Working in a sector where TCE is manufactured or utilised, like the degreasing business, is a significant additional method that you could be exposed to it. It can enter the body by coming into direct touch with the skin or by inhaling the vapours.

You may also be exposed through contaminated soil, such as that found in landfills. Moreover, TCE can enter your body through the consumption of contaminated foods or contact with consumer products that contain it.

According to the CDC, TCE is a common solvent used in a variety of products, including cold metal cleaners, adhesives, lubricants, paints, varnishes, paint strippers, and paints. Labels for these goods should include instructions on how to reduce exposure.

The Occupational Safety and Health Administration (OSHA) also mandates that your company give you a material safety data sheet (MSDS) outlining the dangers and proper handling techniques for any chemicals you use at work.

When exposed to TCE

A doctor can check for TCE in your blood, breath, or urine if you’ve recently been exposed to the substance, according to the Agency for Toxic Substances and Disease Registry (ATSDR).

It can also be tested for in the environment you have visited. But, once you’ve been exposed, there is no cure to get it out of your system. Either your breath will expel it or your kidneys will excrete it into your urine.

They advise avoiding any known toxic regions, such as those with tainted water, soil, or air.

You should always use items containing TCE in well-ventilated areas with the appropriate personal protective equipment, such as chemical-protection gloves, safety goggles, and respirators, in addition to adhering to any safety advice on such products.

High TCE exposure can, in the short term, irritate people and even make them pass out or become fatally ill. If you have been exposed to the chemical extensively, it is crucial to seek immediate medical care.

The individual should also be transferred to clean air, and any contaminated clothing should be taken off, if it’s safe to do so. If the skin or eyes have been exposed, thoroughly rinse them with water.

Kidney cancer and Parkinson’s disease have both been associated with long-term TCE exposure. The ATSDR advises that the greatest form of protection is to shield yourself from exposure altogether.

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Explore the latest link between MS and Your Gut.

Explore the latest link between MS and Your Gut.

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The central nervous system is impacted by the chronic disease known as multiple sclerosis (MS). When the immune system targets the outer layer of nerve cells, symptoms including weakness in the muscles and visual issues appear.

MS’s precise causation is unknown, however scientists believe that a number of variables may be involved. A recent study discovered that MS may be brought on in persons with a genetic predisposition by a toxin produced by a common gut bacterium.

Multiple sclerosis (MS) is a persistent nerve system disease. Young adults between the ages of 20 and 40 are the most frequently affected, and women are more likely than males to experience it.

There are around 2.8 million MS sufferers worldwide, and the number is growing, according to the Multiple Sclerosis International Federation (MSIF).

Symptoms of Multiple Sclerosis

The immune system of the affected person destroys the myelin sheath that protects the nerve fibers in this autoimmune illness. Sclerosis is a scar or lesion that results from damage. These lesions, which most frequently affect the central nervous system, can cause a variety of symptoms, such as:

Relapsing-remitting MS, the most prevalent type of MS that accounts for 85% of cases, is characterised by episodes of new or worsening symptoms and intervals during which symptoms subside or go away.

Scientists believe that environmental variables and genetic vulnerability may play a role in the development of the illness, while the specific reason is yet unknown. MS is riddled with many mysteries.

Epsilon toxin, which is produced by a bacteria that may be found in the small intestine, has now been linked to the development of MS and the maintenance of symptoms, according to study conducted by researchers at Weill Cornell Medicine’s Brain and Mind Research Center.

How the gut microbiota affects MS?

The trillions of bacteria that reside in your digestive system make up the gut microbiota. The majority of microbes are bacteria, but they can also include viruses, fungi, and the microscopic, single-celled creatures known as protozoa.

In general, these bacteria are beneficial and even essential to our health. Yet, dysbiosis, or an out-of-balance microbiota, can cause issues. According to studies, alterations in the microbiota may be a factor in various autoimmune diseases.

In MS patients, changes to the gut flora are frequent. According to this recent study, patients with MS are more likely than healthy controls to carry the pathogen Clostridium perfringens. Epsilon toxin, which is produced by C. perfringens, opens the blood arteries in the brain and permits inflammatory cells to enter the central nervous system (CNS).

What is the epsilon toxin?

Dr. Barbara Giesser stated that the researchers “investigated how the toxin induced an MS-like condition in a mouse model using unique and sensitive techniques to determine the presence of the bacterium.

The scientists collected faeces from both MS patients and healthy controls. They used polymerase chain reaction (PCR) analysis to examine these samples in order to find the epsilon toxin (ETX) gene, which is only present in C. perfringens.

They discovered that the ETX gene was present in 61% of samples from MS patients but only in 13% of those from healthy controls. Also, they discovered that compared to age- and sex-matched healthy controls, MS patients had a higher likelihood of having ETX-positive C. perfringens invade their gut microbiome.

Treatments to target this toxin

The current amount of knowledge regarding the gut microbiome in MS patients is expanded upon by this study. It has been demonstrated to respond to treatment with various disease-modifying treatments and is known to differ from those of non-MS controls, according to Dr. Barbara Giesser.

Epsilon toxin is only produced by C. perfringens during the rapid development phase. The researchers hypothesise that ETX is the cause of MS lesions, which would explain why the illness is episodic and manifests less symptoms when the toxin-producing bacteria are absent.

They draw the conclusion that the bacterium, its toxin, and MS exhibit a robust clinical connection. According to Dr. Giesser, this finding raises the prospect of therapies that target this pathway:

“The toxin facilitates central nervous system access for immune cells. This implies that medications that target the bacterium or the toxin may be effective in treating the condition.

The researchers point out that clinical trials would be required to see whether this could result in MS treatments.

Healthy microbiome

The development of MS may be significantly influenced by the gut microbiome, according to studies. An analysis of multiple research published in 2017 discovered that nutrition might be used to alter the gut flora and alter the course of MS.

The advantages of keeping a healthy gut microbiota are becoming more widely understood, and this study provides more proof that an unbalanced microbiota may lead to the onset of disease.

A healthy diet and lifestyle that promote the growth of advantageous gut flora may potentially lower the risk of MS as well as the risk of many other illnesses.

Improve gut health

Some elements, such as genetics and environment, are beyond your control. Although our gut microbiota is set up early in life, there are some things that can change it.

Certain modifications enhance the diversity and health of our microbiome. Alterations may be harmful.

These are some actions you may do to encourage a balanced, healthy gut microbiome:

  • Consume more fibre. All of the little microorganisms in your gut can eat fibre. Fruits, vegetables, beans, lentils, nuts, seeds, and whole grains all contain fibre.
  • Drink less alcohol. There is evidence that alcohol causes dysbiosis. You might want to think about reducing your drinking if you do.
  • Consume fermented food. Foods that have been fermented are sources of good bacteria and may be beneficial to health. Among the foods that are fermented include kimchi, tempeh, yoghurt, kefir, miso, and sauerkraut.
  • Stress management. Your gut microbiota’s state of health can be impacted by stress. To manage tension, try some stress-relieving exercises like yoga or meditation.
  • Don’t overuse antibiotics. Antibiotics can kill some of the helpful bacteria in addition to the harmful ones. Dysbiosis may result from this. Antibiotics should only be used as necessary, and they should be taken exactly as prescribed. Some of the beneficial bacteria may be restored by taking a probiotic supplement.
  • Look into probiotic dietary supplements. Supplements with probiotics may be beneficial. To determine the appropriate dosage and strain for particular ailments, more research is required. Start with the US Probiotic Guide if you want to.

Conclusive note

  • The human body is home to trillions of microorganisms. The gut contains the majority of them.
  • The possibility that the sorts of bacteria in our guts may have an impact on our health is intriguing.
  • Dysbiosis is more likely to occur in MS patients. When the gut microbiota is out of equilibrium, it is called dysbiosis. Inflammation and autoimmune illnesses are now more likely as a result.
  • A healthy gut microbiota can be supported by consuming fermented foods and a high-fiber diet.
  • There is continuing research into the potential benefits of altering the gut microbiome for MS patients.

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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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