Health and Me

Ishita Roy

Oxford University Scientists Have Found The Reason Behind The Need To Sleep

We’ve long thought that the need for sleep begins and ends in the brain. But a new study by scientists at the University of Oxford flips this notion on its head, or rather, down to a cellular level. According to research published in Nature, the mitochondria within specific sleep-regulating neurons may be the ones quietly counting the minutes we stay awake and deciding when it’s time to shut down.

The study, led by neuroscientist Gero Miesenböck, used Drosophila melanogaster (fruit flies) as the model species to explore this phenomenon. The team’s data suggests that after prolonged periods of wakefulness, mitochondria in certain neurons accumulate oxidative stress, and that stress appears to be the trigger for sleep.

Mitochondria are often described as the powerhouses of the cell, responsible for producing ATP, the molecule that stores and transports energy. But the Oxford team discovered that these tiny structures do more than keep the lights on. In the sleep-regulating neurons of the fly’s dorsal fan-shaped body, a known sleep center, mitochondria remained active even when the neurons themselves were idle.

This constant mitochondrial activity causes a slow leak of electrons from the respiratory chain, leading to the production of reactive oxygen species (ROS). These unstable molecules can damage cell membranes if they build up unchecked.

According to Miesenböck, the sleep-inducing neurons appear to use this oxidative stress as a kind of internal clock. Once the ROS level passes a certain threshold, the brain flips the switch for sleep, triggering a period of rest and recovery.

<h4>Sleep Is for Repair, Not Just Rest</h4>

Crucially, the researchers observed that when the flies were allowed to sleep, their mitochondrial shape and function quickly returned to normal, a strong indication that the primary purpose of sleep, at least on a cellular level, may be repair rather than simply energy conservation.

“When these unstable molecules pile up, the only fix is to shut the system down,” Miesenböck said. “The sleep homeostat is actually looking at its own mitochondria to estimate the need for sleep.”

To test whether wakefulness alone, rather than stress or injury, triggered this mitochondrial activity, the researchers kept one group of flies awake using non-harmful methods like gentle shaking or activating arousal neurons. Both methods led to the same signature of mitochondrial stress, strengthening the argument that sleep need is directly linked to time spent awake.

Further experiments showed that flies with fragmented (damaged) mitochondria in their sleep neurons slept less and were unable to recover lost sleep. However, when the researchers forced mitochondrial fusion, essentially improving the cells’ repair tools, the flies slept longer and bounced back better after deprivation.

An especially clever twist involved optogenetics. By installing a light-sensitive proton pump into the mitochondria, the researchers were able to trigger sleep with just an hour of green light exposure, increasing rest time by 25 percent.

While the study was conducted in fruit flies, its implications could extend to humans. Mitochondrial proteins are highly conserved across species, and fatigue is a hallmark symptom of many mitochondrial disorders. Ryan Mailloux of McGill University, who wasn’t involved in the research, noted the potential of targeting mitochondrial stress pathways to treat human sleep issues, as reported by Earth.com.

Previous rodent studies have shown similar patterns, forced wakefulness raises ROS levels, which can lead to cell damage and even death if the stress isn’t alleviated with sleep. A 2023 review also identified mitochondrial redox shifts as a possible master regulator of sleep homeostasis.

<h4>Implications for Human Sleep Disorders</h4>

The findings could pave the way for novel sleep therapies. If mitochondria truly act as internal sleep meters, then tweaking electron flow within sleep neurons might help manage insomnia or shift-work fatigue.

That said, targeting mitochondria must be done with precision. Drugs that broadly affect electron transport could generate excess heat and deplete energy, not an ideal outcome for patients. More targeted approaches, like modulating lipid repair enzymes or focusing only on specific brain regions, may offer a safer route.

Wearable diagnostics could also emerge from this research. If circulating markers of mitochondrial ROS correlate with sleep need, a blood or breath test might one day tell people when their bodies are approaching critical rest thresholds, a potential game-changer for shift workers or pilots.

Ultimately, the study challenges the idea of sleep as passive downtime. Instead, it presents a view of sleep as a metabolically driven maintenance window, one commanded not from the whole brain, but from microscopic sentinels inside individual neurons.

In aging studies, preserving mitochondrial health has already been shown to protect cognitive function. This new research ties those dots even closer together, showing that sleep, aging, energy balance, and cellular repair may all be chapters in the same story.

As science digs deeper, it appears that sleep may not be a simple “off switch”, but rather, a strategic and necessary pause, dictated by the fiery engines within us all.

Health Conditions A-Z

health

health and wellness

oxford university

oxford university study

sleep health

oxford university study sleep

sleep cycle

Loni Anderson Dies Day Before Her 80th Birthday: Remembering Her Crusade Against COPD

Jessie J Health Update: Hospitalized Weeks After Cancer Surgery Due To Lung Infection

Health & Wellness

What Should Fitness Look Like For A 13-18 Year Old

Food For Diabetes: What Should A Diabetic Diet Contain

You Don’t Always Need Weights For Strength Training

Feel Sleepy After Lunches - Light And Healthy Office Lunches

Positive Thinking Practice – How Does It Help You?

MIND Diet – Is This A Healthy Diet Or Another Trend?

Yoga Prop Essentials To Improve Your Exercise Session

Should Potatoes Be The Part Of A Healthy Diet?

Best And Worst Foods To Lower Blood Pressure

Low-Impact Cardio Workouts You Should Try

10 Healthy Pasta Salad Dressing For Weight Loss

Breathing Exercise You Should Do To Relieve Stress

Headache vs. Migraine: Difference Explained In 60 Seconds

High Carb Foods That Are Actually Healthy

How Many Times Do You Need To Wash Your Face?

Hypothyroidism Diet – What To Eat And What You Should Avoid

Stretches To Relieve Leg Pain And Numbness After Sitting For Too Long

No-Cook Healthy Meals For Lazy Days At Home

Easy Breakfast Options To Try During Calorie Deficit

How To Stop Muscle Cramps Immediately

Why You Should Go For An Anti-Inflammatory Diet

Foods To Lower Cortisol Levels In Your Body

High-Fiber Dips You Can Make At Home For The Week

Weekend Warrior Exercises To Makeup For Stressful Week

Experiencing Headaches At Word? Natural Remedies To Try

Yoga Poses That Enhance Digestion

Health Benefits of Walking Backwards

No Eggs? Egg-Alternatives You Can Add To Your Diet

Savory And Smart Ways To Add Broccoli To Your Diet

Calorie Burning Habits That Can Help You Shed Extra Pounds

Yoga Poses That Can Help With Bloating

Fiber-Rich Oatmeal Dishes You Can Have For Breakfast

Signs You Must Visit A Doctor For Your Back Pain

Avocado Meal Prep Ideas To Increase Healthy Fat In Your Diet

Arm Exercises You Can Do At Home

Quick-Office Lunches That Can Keep You Full-Longer

How Increased Screen Time Affects Children's Health

Homemade Recipe To Make Protein-Rich Pancakes With Healthy Alternatives

Push-Up Variations You Can Do At Home

Common Mistakes Running Mistakes People Make

We’ve long thought that the need for sleep begins and ends in the brain. But a new study by scientists at the University of Oxford flips this notion on its head, or rather, down to a cellular level. According to research published in Nature, the mitochondria within specific sleep-regulating neurons may be the ones quietly counting the minutes we stay awake and deciding when it’s time to shut down.The study, led by neuroscientist Gero Miesenböck, used Drosophila melanogaster (fruit flies) as the model species to explore this phenomenon. The team’s data suggests that after prolonged periods of wakefulness, mitochondria in certain neurons accumulate oxidative stress, and that stress appears to be the trigger for sleep.Mitochondria as Sleep SensorsMitochondria are often described as the powerhouses of the cell, responsible for producing ATP, the molecule that stores and transports energy. But the Oxford team discovered that these tiny structures do more than keep the lights on. In the sleep-regulating neurons of the fly’s dorsal fan-shaped body, a known sleep center, mitochondria remained active even when the neurons themselves were idle.This constant mitochondrial activity causes a slow leak of electrons from the respiratory chain, leading to the production of reactive oxygen species (ROS). These unstable molecules can damage cell membranes if they build up unchecked.According to Miesenböck, the sleep-inducing neurons appear to use this oxidative stress as a kind of internal clock. Once the ROS level passes a certain threshold, the brain flips the switch for sleep, triggering a period of rest and recovery.Sleep Is for Repair, Not Just RestCrucially, the researchers observed that when the flies were allowed to sleep, their mitochondrial shape and function quickly returned to normal, a strong indication that the primary purpose of sleep, at least on a cellular level, may be repair rather than simply energy conservation.“When these unstable molecules pile up, the only fix is to shut the system down,” Miesenböck said. “The sleep homeostat is actually looking at its own mitochondria to estimate the need for sleep.”Shaking Flies, Testing TheoriesTo test whether wakefulness alone, rather than stress or injury, triggered this mitochondrial activity, the researchers kept one group of flies awake using non-harmful methods like gentle shaking or activating arousal neurons. Both methods led to the same signature of mitochondrial stress, strengthening the argument that sleep need is directly linked to time spent awake.Further experiments showed that flies with fragmented (damaged) mitochondria in their sleep neurons slept less and were unable to recover lost sleep. However, when the researchers forced mitochondrial fusion, essentially improving the cells’ repair tools, the flies slept longer and bounced back better after deprivation.An especially clever twist involved optogenetics. By installing a light-sensitive proton pump into the mitochondria, the researchers were able to trigger sleep with just an hour of green light exposure, increasing rest time by 25 percent.Not Just a Fly ProblemWhile the study was conducted in fruit flies, its implications could extend to humans. Mitochondrial proteins are highly conserved across species, and fatigue is a hallmark symptom of many mitochondrial disorders. Ryan Mailloux of McGill University, who wasn’t involved in the research, noted the potential of targeting mitochondrial stress pathways to treat human sleep issues, as reported by Earth.com.Previous rodent studies have shown similar patterns, forced wakefulness raises ROS levels, which can lead to cell damage and even death if the stress isn’t alleviated with sleep. A 2023 review also identified mitochondrial redox shifts as a possible master regulator of sleep homeostasis.Implications for Human Sleep DisordersThe findings could pave the way for novel sleep therapies. If mitochondria truly act as internal sleep meters, then tweaking electron flow within sleep neurons might help manage insomnia or shift-work fatigue.That said, targeting mitochondria must be done with precision. Drugs that broadly affect electron transport could generate excess heat and deplete energy, not an ideal outcome for patients. More targeted approaches, like modulating lipid repair enzymes or focusing only on specific brain regions, may offer a safer route.Wearable diagnostics could also emerge from this research. If circulating markers of mitochondrial ROS correlate with sleep need, a blood or breath test might one day tell people when their bodies are approaching critical rest thresholds, a potential game-changer for shift workers or pilots.Is Sleep A Strategic Shutdown?Ultimately, the study challenges the idea of sleep as passive downtime. Instead, it presents a view of sleep as a metabolically driven maintenance window, one commanded not from the whole brain, but from microscopic sentinels inside individual neurons.In aging studies, preserving mitochondrial health has already been shown to protect cognitive function. This new research ties those dots even closer together, showing that sleep, aging, energy balance, and cellular repair may all be chapters in the same story.As science digs deeper, it appears that sleep may not be a simple “off switch”, but rather, a strategic and necessary pause, dictated by the fiery engines within us all.

oxford university scientists have found the reason behind the need to sleep

Heavy Weed Usage Could Increase Your Chances Of Cancer By 3 Times

heavy weed usage could increase your chances of cancer by 3 times

Parenting

To Be A Mother With Multiple Sclerosis: Actor Christina Applegate Gets Candid About Her Diagnosis And How It Changed Motherhood

to be a mother with multiple sclerosis: actor christina applegate gets candid about her diagnosis and how it changed motherhood

Understanding Chronic Regional Pain Syndrome: When Pain Persists Beyond Injury

understanding chronic regional pain syndrome: when pain persists beyond injury

Inner Child: How ‘Be a Good Girl’ and ‘Boys Don’t Cry’ Create Adults Who Struggle to Say What They Really Feel

inner child: how ‘be a good girl’ and ‘boys don’t cry’ create adults who struggle to say what they really feel

For many, <span>Loni Anderson</span> is remembered as the glamorous Jennifer Marlowe from the hit sitcom <span>WKRP in Cincinnati</span>. Right before her 80th birthday, she passed away following a "prolonged" illness, as per her longtime publicist, Cheryl J Kagan. 

“We are heartbroken to announce the passing of our dear wife, mother and grandmother,” Anderson’s family said in a statement.

However, beyond the spotlight, the actress waged a far more personal battle, one that profoundly reshaped her life and purpose

Anderson became a caregiver to both of her parents as they battled <span>Chronic Obstructive Pulmonary Disease</span> (<span>COPD</span>), a progressive and debilitating lung condition primarily caused by smoking. Watching them suffer changed everything for her.

“I would have thought they would have thrown those cigarettes away immediately,” she once said in an interview. “My mom would say, ‘I can’t breathe,’ and my dad said, ‘I feel like I’m drowning.’ And yet, they still reached for another cigarette. That was really shocking to me.”

Although she never smoked herself, Anderson came to understand just how gripping cigarette addiction can be, often likened to the difficulty of quitting heroin. But for her, the pain wasn’t theoretical. It was daily, emotional, and lived.

<h4>Spreading the Message Before COPD Even Had a Name</h4>

Even before the term COPD became widely recognized, Anderson was advocating for awareness when it was still largely referred to as “emphysema.” 

She spoke out passionately about the disease’s connection to smoking and long-term lung damage, not just in interviews, but through action.

COPD is not just a smoker’s cough. It’s a chronic condition that narrows the airways, causes irreversible damage to lung tissue, and raises the risk of heart disease, lung cancer, and early death. Both of Anderson’s parents died from the disease, and far too young.

<h4>How Did Anderson Work Towards Its Awareness?</h4>

Determined to raise public awareness, Anderson began visiting senior living facilities, speaking at health conferences, and even reaching out to youth. “It takes all your breath to shower,” she said, describing what she saw in late-stage COPD patients. “That should be enough to make someone want to quit.”

For Anderson, one of the most defining moments in her advocacy journey came when her son was just 10 years old. One day, he walked into the room dressed up like a character from TV, complete with a fake cigarette, emulating someone he admired.

“And I thought, ‘Oh my God,’” Anderson recalled. She knew that moment was a crossroads. She sat him down and explained that he never got to meet his grandparents, her parents, because smoking had taken them too soon.

“I said, ‘Will you help me to make sure that other kids get to have their moms and dads and grandmas and grandpas?’” That moment turned her son into a partner in her mission and made her advocacy even more urgent.

Anderson didn’t just focus on the elderly or the ill. She also took her message to high schools, hoping to reach young people before they made smoking a lifelong habit. “Even high school may not be early enough,” she said. “You have to start talking to junior high kids.”

While quitting smoking can stop further damage, the lung destruction caused by COPD is largely irreversible. Her message was simple but powerful: don’t start, and if you already have, quit now.

Anderson reflected often on the years lost. Her parents died in their 50s and 60s, decades earlier than they might have if not for smoking. “They never got to meet my children. They missed weddings, birthdays, graduations. They should have had 30 more years.”

Though Loni Anderson has now passed away, her legacy in health advocacy continues. She used her platform not just for fame, but to fight for awareness of a disease that remains one of the leading causes of death globally.

Her personal loss became a national message: Smoking isn’t just a bad habit, it’s a killer. COPD is often preventable. And every cigarette not smoked is a chance to live longer, breathe easier, and be there for the moments that truly matter.

Loni anderson

loni anderson illness

lonnie anderson

loni anderson cause of death

loni anderson death

wkrp in cincinnati

loni anderson children

copd

Chronic Obstructive Pulmonary Disease

For many, Loni Anderson is remembered as the glamorous Jennifer Marlowe from the hit sitcom WKRP in Cincinnati. Right before her 80th birthday, she passed away following a "prolonged" illness, as per her longtime publicist, Cheryl J Kagan. “We are heartbroken to announce the passing of our dear wife, mother and grandmother,” Anderson’s family said in a statement.However, beyond the spotlight, the actress waged a far more personal battle, one that profoundly reshaped her life and purposeA Caregiver, A Health AdvocateAnderson became a caregiver to both of her parents as they battled Chronic Obstructive Pulmonary Disease (COPD), a progressive and debilitating lung condition primarily caused by smoking. Watching them suffer changed everything for her.“I would have thought they would have thrown those cigarettes away immediately,” she once said in an interview. “My mom would say, ‘I can’t breathe,’ and my dad said, ‘I feel like I’m drowning.’ And yet, they still reached for another cigarette. That was really shocking to me.”Although she never smoked herself, Anderson came to understand just how gripping cigarette addiction can be, often likened to the difficulty of quitting heroin. But for her, the pain wasn’t theoretical. It was daily, emotional, and lived.Spreading the Message Before COPD Even Had a NameEven before the term COPD became widely recognized, Anderson was advocating for awareness when it was still largely referred to as “emphysema.” She spoke out passionately about the disease’s connection to smoking and long-term lung damage, not just in interviews, but through action.What Is COPD?COPD is not just a smoker’s cough. It’s a chronic condition that narrows the airways, causes irreversible damage to lung tissue, and raises the risk of heart disease, lung cancer, and early death. Both of Anderson’s parents died from the disease, and far too young.How Did Anderson Work Towards Its Awareness?Determined to raise public awareness, Anderson began visiting senior living facilities, speaking at health conferences, and even reaching out to youth. “It takes all your breath to shower,” she said, describing what she saw in late-stage COPD patients. “That should be enough to make someone want to quit.”A Wake-Up Call Through Her SonFor Anderson, one of the most defining moments in her advocacy journey came when her son was just 10 years old. One day, he walked into the room dressed up like a character from TV, complete with a fake cigarette, emulating someone he admired.“And I thought, ‘Oh my God,’” Anderson recalled. She knew that moment was a crossroads. She sat him down and explained that he never got to meet his grandparents, her parents, because smoking had taken them too soon.“I said, ‘Will you help me to make sure that other kids get to have their moms and dads and grandmas and grandpas?’” That moment turned her son into a partner in her mission and made her advocacy even more urgent.It’s Never Too Late to QuitAnderson didn’t just focus on the elderly or the ill. She also took her message to high schools, hoping to reach young people before they made smoking a lifelong habit. “Even high school may not be early enough,” she said. “You have to start talking to junior high kids.”While quitting smoking can stop further damage, the lung destruction caused by COPD is largely irreversible. Her message was simple but powerful: don’t start, and if you already have, quit now.Anderson reflected often on the years lost. Her parents died in their 50s and 60s, decades earlier than they might have if not for smoking. “They never got to meet my children. They missed weddings, birthdays, graduations. They should have had 30 more years.”Leaving a Legacy of PreventionThough Loni Anderson has now passed away, her legacy in health advocacy continues. She used her platform not just for fame, but to fight for awareness of a disease that remains one of the leading causes of death globally.Her personal loss became a national message: Smoking isn’t just a bad habit, it’s a killer. COPD is often preventable. And every cigarette not smoked is a chance to live longer, breathe easier, and be there for the moments that truly matter.

loni anderson dies day before her 80th birthday: remembering her crusade against copd

What Does Retracted Eardrum Mean? Here's All That You Need To Know About

Health News

Dizzy Spells Misread as Vertigo Led to Brain Tumour Diagnosis for 63-Year-Old

dizzy spells misread as vertigo led to brain tumour diagnosis for 63-year-old

What Makes Flu Season 2025 Different? Unique Symptoms Of Flu In 2025 And How Long The Infection Lasts

unique symptoms of flu in 2025 and how long the infection lasts

Hearing Loss Can Cost Young Adults Their Livelihood Or Education

hearing loss can cost young adults their livelihood or education

World Alopecia Day: Experts Bust Popular Myths and Reveal Hidden Health Issues Behind Hair Loss

world alopecia day: experts bust popular myths and reveal hidden health issues behind hair loss

A retracted <span>eardrum</span>, also called tympanic membrane atelectasis, is a condition where the eardrum gets pulled inward toward the middle ear. Normally, the eardrum (or tympanic membrane) acts as a boundary between the outer and middle ear, transmitting sound vibrations to tiny bones that help us hear. But when it collapses inward, that delicate process can be disrupted.

The condition is often silent at first, meaning people may not realize they have it. But in some cases, it can escalate, causing discomfort or even permanent <span>hearing</span> damage.

In most cases, a retracted eardrum doesn’t cause any noticeable symptoms. But when the retraction becomes severe enough to affect structures inside the ear, individuals may experience:

<ul><li>Earache</li><li>Temporary hearing loss</li><li>Fluid discharge from the ear</li></ul>

If left untreated, a chronic retracted eardrum can lead to permanent hearing loss.

The most common cause of a retracted eardrum is Eustachian tube dysfunction. These narrow tubes connect the middle ear to the back of the nose and help regulate ear pressure.

When they don’t work properly, pressure inside the ear drops, effectively pulling the eardrum inward.

<ul><li>Recent or recurring ear infections</li><li>Cleft palate</li><li>A poorly healed eardrum after rupture</li><li>Enlarged tonsils or adenoids</li></ul>

Upper respiratory infections, such as the common cold

Diagnosis typically begins with a discussion about symptoms and any recent infections. A doctor will then use an otoscope, a tool with a light, to look into the ear canal. This allows them to visually confirm if the eardrum is abnormally positioned or collapsed.

<h4>Treatment Options: When to Wait and When to Act</h4>

Not all <span>retracted eardrums</span> require immediate treatment. In mild cases, doctors often recommend a “watch and wait” approach, as pressure may normalize naturally over a few months.

For more advanced cases, several interventions are possible:

<strong>Decongestants or nasal steroids: </strong>These can improve airflow in the ear and relieve pressure.

<strong>The Valsalva maneuver:</strong> This self-administered technique involves closing your mouth, pinching your nose, and gently blowing as if trying to pop your ears. It should be performed under medical guidance.

If the condition begins to affect hearing or causes persistent pain, surgical options may be considered.

<strong>Tube Insertion (Myringotomy):</strong>

Often used in children with recurring ear infections, this procedure involves placing small tubes into the eardrum to help ventilate the middle ear.

In more severe cases, part of the damaged eardrum may be removed and replaced with cartilage from the outer ear. This stiffens the eardrum, preventing future collapses.

The outlook largely depends on the severity. Minor retractions usually resolve without intervention and don’t cause long-term damage. However, more serious cases, especially those that persist or press against ear bones, may result in hearing loss and need medical or surgical correction.

Experts recommend seeking medical attention if you notice ear discomfort, hearing changes, or frequent infections. Early diagnosis can prevent long-term issues and protect one of your most important senses, your hearing.

retracted eardrums

hearing

eardrum

hearing health

A retracted eardrum, also called tympanic membrane atelectasis, is a condition where the eardrum gets pulled inward toward the middle ear. Normally, the eardrum (or tympanic membrane) acts as a boundary between the outer and middle ear, transmitting sound vibrations to tiny bones that help us hear. But when it collapses inward, that delicate process can be disrupted.The condition is often silent at first, meaning people may not realize they have it. But in some cases, it can escalate, causing discomfort or even permanent hearing damage.Spotting the SymptomsIn most cases, a retracted eardrum doesn’t cause any noticeable symptoms. But when the retraction becomes severe enough to affect structures inside the ear, individuals may experience:EaracheTemporary hearing lossFluid discharge from the earIf left untreated, a chronic retracted eardrum can lead to permanent hearing loss.Why Does It Happen?The most common cause of a retracted eardrum is Eustachian tube dysfunction. These narrow tubes connect the middle ear to the back of the nose and help regulate ear pressure.When they don’t work properly, pressure inside the ear drops, effectively pulling the eardrum inward.Some common triggers include:Recent or recurring ear infectionsCleft palateA poorly healed eardrum after ruptureEnlarged tonsils or adenoidsUpper respiratory infections, such as the common coldHow Doctors Diagnose ItDiagnosis typically begins with a discussion about symptoms and any recent infections. A doctor will then use an otoscope, a tool with a light, to look into the ear canal. This allows them to visually confirm if the eardrum is abnormally positioned or collapsed.Treatment Options: When to Wait and When to ActNot all retracted eardrums require immediate treatment. In mild cases, doctors often recommend a “watch and wait” approach, as pressure may normalize naturally over a few months.For more advanced cases, several interventions are possible:Decongestants or nasal steroids: These can improve airflow in the ear and relieve pressure.The Valsalva maneuver: This self-administered technique involves closing your mouth, pinching your nose, and gently blowing as if trying to pop your ears. It should be performed under medical guidance.If the condition begins to affect hearing or causes persistent pain, surgical options may be considered.Surgical InterventionsTwo common surgical treatments are:Tube Insertion (Myringotomy):Often used in children with recurring ear infections, this procedure involves placing small tubes into the eardrum to help ventilate the middle ear.Tympanoplasty:In more severe cases, part of the damaged eardrum may be removed and replaced with cartilage from the outer ear. This stiffens the eardrum, preventing future collapses.What’s the Prognosis?The outlook largely depends on the severity. Minor retractions usually resolve without intervention and don’t cause long-term damage. However, more serious cases, especially those that persist or press against ear bones, may result in hearing loss and need medical or surgical correction.Experts recommend seeking medical attention if you notice ear discomfort, hearing changes, or frequent infections. Early diagnosis can prevent long-term issues and protect one of your most important senses, your hearing.

what does retracted eardrum mean? here's all that you need to know about

Could Millipedes Help Treat Pain And Parkinson’s?

Nutrition

Food Myth Debunked - Eating Sugar Doesn't Make You Crave It More

food myth debunked - eating sugar doesn't make you crave it more

Could This New Alzheimer’s Drug Buy Patients Four More Good Years? Here Is What We Know

could this new alzheimer’s drug buy patients four more good years? here is what we know

In a surprising discovery that bridges the gap between creepy crawlies and cutting-edge neuroscience, researchers at Virginia Tech have identified unique compounds in millipede secretions that could pave the way for future treatments for pain and neurological diseases like Parkinson’s, depression, and schizophrenia.

Led by chemist Emily Meyers, the research team uncovered naturally occurring alkaloids in the defensive secretions of the Andrognathus corticarius, a species known colloquially as the Hokie millipede. The millipede, which lives under decomposing leaves and branches on the university’s Blacksburg campus, produces a chemical cocktail that not only deters predators but may influence neuroreceptors in the brain.

“These compounds are quite complex, so they’re going to take some time to synthesize in the lab,” said Meyers, who specializes in studying underexplored ecological sources for potential new drugs.

The compounds, dubbed andrognathanols and andrognathines by Meyers’ team, belong to a class of complex alkaloids. They were discovered after researchers collected several millipedes from wooded areas on campus and analyzed the contents of their defensive glands using a suite of chemical tools.

The results were striking: some of these secretions had a disorienting effect on ants, one of the millipede’s presumed predators. But that’s not all, several of the compounds were found to interact with a neuroreceptor known as Sigma-1. This receptor has been linked to multiple brain disorders, including schizophrenia, depression, Lou Gehrig’s disease (ALS), and Parkinson’s disease.

In addition to warding off predators, the researchers discovered that the compounds may also serve a social function, possibly helping millipedes signal their location to family members in leaf-littered environments.

This study, recently published in the Journal of the American Chemical Society, is not Meyers’ first foray into studying arthropod chemistry. She has been collaborating with entomologist Paul Marek, and together, they have previously suggested that the family of alkaloids found in millipede secretions could have significant therapeutic potential.

“Millipedes have been around for hundreds of millions of years. They’ve developed these intricate chemical defense systems, and we’re only beginning to understand their value,” said Meyers.

While the compounds show promise, the next hurdle is a familiar one in drug discovery: scalability. The compounds exist in trace amounts in the wild, and researchers need larger quantities for in-depth testing and potential pharmaceutical development.

The team is now exploring partnerships with laboratories that can synthesize the compounds in bulk, which would allow for further testing on their biological activity and medicinal properties. Meyers emphasized that while the research is still in its early stages, the potential applications are broad, from pain management to novel treatments for complex neurological conditions.

“Nature has always been a wellspring of inspiration for medicine,” said Meyers. “And sometimes, the most powerful solutions come from the smallest and most unexpected creatures, like a tiny millipede under a log.”

With this groundbreaking discovery, scientists are reminded once again that the natural world may hold secrets that, once unlocked, could transform human health in unimaginable ways.

millipedes pain killer

parkinsons

millipedes as pain killer

natures pain killer

In a surprising discovery that bridges the gap between creepy crawlies and cutting-edge neuroscience, researchers at Virginia Tech have identified unique compounds in millipede secretions that could pave the way for future treatments for pain and neurological diseases like Parkinson’s, depression, and schizophrenia.Led by chemist Emily Meyers, the research team uncovered naturally occurring alkaloids in the defensive secretions of the Andrognathus corticarius, a species known colloquially as the Hokie millipede. The millipede, which lives under decomposing leaves and branches on the university’s Blacksburg campus, produces a chemical cocktail that not only deters predators but may influence neuroreceptors in the brain.“These compounds are quite complex, so they’re going to take some time to synthesize in the lab,” said Meyers, who specializes in studying underexplored ecological sources for potential new drugs.A Hidden Chemical ArsenalThe compounds, dubbed andrognathanols and andrognathines by Meyers’ team, belong to a class of complex alkaloids. They were discovered after researchers collected several millipedes from wooded areas on campus and analyzed the contents of their defensive glands using a suite of chemical tools.The results were striking: some of these secretions had a disorienting effect on ants, one of the millipede’s presumed predators. But that’s not all, several of the compounds were found to interact with a neuroreceptor known as Sigma-1. This receptor has been linked to multiple brain disorders, including schizophrenia, depression, Lou Gehrig’s disease (ALS), and Parkinson’s disease.In addition to warding off predators, the researchers discovered that the compounds may also serve a social function, possibly helping millipedes signal their location to family members in leaf-littered environments.From Defense to Drug DiscoveryThis study, recently published in the Journal of the American Chemical Society, is not Meyers’ first foray into studying arthropod chemistry. She has been collaborating with entomologist Paul Marek, and together, they have previously suggested that the family of alkaloids found in millipede secretions could have significant therapeutic potential.“Millipedes have been around for hundreds of millions of years. They’ve developed these intricate chemical defense systems, and we’re only beginning to understand their value,” said Meyers.While the compounds show promise, the next hurdle is a familiar one in drug discovery: scalability. The compounds exist in trace amounts in the wild, and researchers need larger quantities for in-depth testing and potential pharmaceutical development.The Road AheadThe team is now exploring partnerships with laboratories that can synthesize the compounds in bulk, which would allow for further testing on their biological activity and medicinal properties. Meyers emphasized that while the research is still in its early stages, the potential applications are broad, from pain management to novel treatments for complex neurological conditions.“Nature has always been a wellspring of inspiration for medicine,” said Meyers. “And sometimes, the most powerful solutions come from the smallest and most unexpected creatures, like a tiny millipede under a log.”With this groundbreaking discovery, scientists are reminded once again that the natural world may hold secrets that, once unlocked, could transform human health in unimaginable ways.

could millipedes help treat pain and parkinson’s?

About Us

Contact Us

Terms & Conditions

Privacy Policy

Company

Health and Me is a premium website with content written and curated to function as a handbook for all Health concerns.

Oxford University Scientists Have Found The Reason Behind The Need To Sleep

Quick Stories

Loni Anderson Dies Day Before Her 80th Birthday: Remembering Her Crusade Against COPD

Low Grade Prostate Cancer Could Be Increasing Health Risks By 30%

Hearing Loss Can Cost Young Adults Their Livelihood Or Education

Health Conditions A-Z

Loni Anderson Dies Day Before Her 80th Birthday: Remembering Her Crusade Against COPD

Oxford University Scientists Have Found The Reason Behind The Need To Sleep

Jessie J Health Update: Hospitalized Weeks After Cancer Surgery Due To Lung Infection