Health and Me

Tanya Dutt

Medical Memoir: Before COVID, Hepatitis Was The Mystery Virus That Haunted Generations

<em>'<span rel="noindex">Medical Memoir</span>' is a Health &amp; Me series that delves into some of the most intriguing medical histories and unveils how medical innovations have evolved over time. Here, we trace the early stages of all things health, whether a vaccine, a treatment, a pill, or a cure.</em>

You think this is a history lesson, but let’s do some math. What does Hepato‑ (“liver”) + ‑tropic (“infecting and replicating in the liver”) + DNA (HBV genome) equal? That spells hepatitis—a mystery virus long misunderstood, long before COVID dominated headlines.

This isn’t just linguistic trivia. It’s a journey through centuries of medical detective work, flawless missteps, and public health triumphs—all centered on one family of viruses that quietly reshaped liver medicine and modern virology.

<h2>Early Clues in Jaundice and Contagion</h2>

Hepatitis didn’t appear on a microscope slide in the 20th century—it was described millennia earlier. Ancient Greek physician Hippocrates observed jaundice as a distinctive yellowing of skin and eyes. By the 8th century, medical writers suspected jaundice was contagious, hinting at an infectious agent at work in the liver.

Between the 17th and 19th centuries, dramatic epidemics of jaundice spread through soldiers and navies. Shared living quarters, contaminated water, and later, mass inoculation campaigns and reused syringes during wars linked the outbreaks to bloodborne transmission. By 1885, physicians recognized that transfused blood could carry the mysterious jaundice-causing pathogen. And when measles and yellow fever vaccinations during World War II triggered outbreaks, it became clear: an unseen virus replicated in bloodstreams—and in the liver.

This early history underscored two enduring facts: hepatitis came in different forms, and it was stealthy, delayed, and extremely hard to track.

By mid-century, researchers sought to categorize the illness. In 1947, MacCallum introduced a dual classification that would shape all future work: Viral Hepatitis A (infectious, via contaminated food or water) and Viral Hepatitis B (serum-borne, via blood and body fluids). That breakthrough turned a single symptom—jaundice—into a family of diseases with different transmission pathways and prevention needs.

Modern hepatitis history truly began in the 1960s. In 1963, Baruch Blumberg identified the Australia antigen (HBsAg) in Aboriginal Australians and hemophiliac blood donors using immunologic screening. It was the first direct marker for Hepatitis B virus, revealing a virus that lay dormant in carriers, often for decades.

1970 – The Dane particle (complete HBV virus) was visualized, proving the viral identity.

Early 1970s – Researchers described the HBeAg, another disease marker.

1973 – Hepatitis A virus (HAV) was isolated, confirming two different viruses.

Suddenly, hepatitis was no longer a vague syndrome—it was a family of identifiable pathogens. That scientific clarity laid the foundation for prevention and treatment.

<h2>Finding a Cure Before HCV With Plasma‑Derived Vaccines</h2>

The early HBV vaccine story is unique. Developed from human plasma, it became the first vaccine not produced via tissue culture, licensed under the name Heptavax in 1981. That innovation paved the way for recombinant vaccines, but the achievement stood alone for a time. Taiwan’s national HBV vaccination program, launched in 1984, offered powerful proof of impact:

HBV carrier rate dropped from 9.1% to 2.7% among children.

Rates of pediatric hepatocellular carcinoma plummeted from 27% to 17%.

Effectively, this was the world’s first anti-cancer vaccine. The vaccine didn’t just stop liver infection—it significantly reduced childhood liver cancers in real populations.

<h2>The C Virus and the Molecular Breakthrough of 1989</h2>

In 1989, the hepatitis world shifted again. A team led by Choo, Kuo, and Houghton unveiled Hepatitis C virus (HCV) using molecular cloning techniques—no tissue culture, electron microscope, or serology required. It was the first virus discovered solely via genetic methods.

That breakthrough explained persistent post‑transfusion hepatitis cases, intravenous drug-user outbreaks, and a heavy burden of global liver disease. It was the start of a new era: molecular virology, where pathogens were identified by their RNA alone.

Soon came discoveries of HDV (delta virus), HEV, and GBV‑C/HGV (hepatitis G virus). This growing catalog of viral types clarified why <span>hepatitis symptoms</span> varied and why prevention needed multiple strategies.

<h2>From Unproven Remedies to Modern Antivirals</h2>

Mid-20th-century treatment was often worse than the disease: prolonged bed rest and steroids were used for acute hepatitis until controlled trials in the ’60s showed they caused harm. In chronic cases, steroids lingered until the 1980s, when researchers clearly proved they worsened outcomes.

By the early 1990s, interferon alpha offered the first real antiviral option. In 1998, lamivudine appeared, followed by more potent nucleoside analogues in the 2000s. For chronic HBV, these drugs allowed suppression of the virus with daily pills—a huge leap in quality of life. HCV treatment advanced spectacularly:

<ul><li>Pegylated interferon plus ribavirin drove cure rates into the 40–60% range.</li><li>Protease inhibitors like boceprevir and telaprevir added another 30%+ success.</li><li>By the 2010s, direct-acting antivirals (DAAs) offered cure rates above 85–90% within a few months, without interferon.</li><li>Chronic HCV became the only curable chronic viral infection—a feat comparable in scope to eradication campaigns for smallpox or polio.</li></ul>

Globally today, over 300 million people live with chronic HBV or HCV and over 1.3 million die annually from liver cirrhosis, cancer, or hepatitis complications.

In response, the World Health Organization’s 2022–2030 strategy aims to reduce new infections by 90% and deaths by 65%. It underscores the urgent need for universal vaccinations, access to testing, and treatment—especially in low-income settings across Asia and Africa, without coordinated action, projections warn:

<ul><li>9.5 million new infections,</li><li>2.1 million liver cancer cases,</li><li>2.8 million deaths by 2030.</li></ul>

Yet history offers reason for optimism: the leaps science made over just a few decades show what’s possible—with political will, investment, and global partnerships.

HBV opened new pathology understanding by linking to polyarteritis nodosa. HCV revealed risks beyond the liver: cryoglobulinemia, non-Hodgkin lymphoma, metabolic disorders like Type II diabetes, and altered lipid profiles. Hepatitis viruses reshaped fields ranging from rheumatology to oncology.

The discoveries required collaboration—and some competition—across labs and continents. The story of hepatitis is one of scientific rivalry, teamwork, serendipity, and intellectual persistence. That blend of curiosity and rigor transformed a family of mysterious illnesses into preventable and treatable diseases.

Long before COVID captured global focus—before masks, PCR tests, and lockdowns—hepatitis was a mystery virus that haunted generations. It caused jaundice, silent liver failure, and cancer. It eluded diagnosis, lacked vaccines, and spread undetected.

Yet through a combination of linguistic insight, molecular science, epidemiology, and public health action, the world unraveled its secrets—one virus at a time.

Today, hepatitis is no longer an invisible threat. It's a medical triumph—because when science is patient, and public health persistent, even the most elusive pathogens can be conquered. The story isn't over, but it's a testament to what decades of dedication and discovery can achieve.

Health Conditions A-Z

health

hepatitis a to e

hepatitis symptoms

liver infection

hepatitis transmission

viral hepatitis types

hepatitis vaccine

hepatitis prevention

Medical memoir

Not Just Face, 'Ozempic Hair' Is The Latest Side Effect Everyone’s Talking About

A Strain Of Typically Harmless HPV Caused 40 Skin Cancer Lesions In A 34-Year-Old Woman

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'Medical Memoir' is a Health & Me series that delves into some of the most intriguing medical histories and unveils how medical innovations have evolved over time. Here, we trace the early stages of all things health, whether a vaccine, a treatment, a pill, or a cure.You think this is a history lesson, but let’s do some math. What does Hepato‑ (“liver”) + ‑tropic (“infecting and replicating in the liver”) + DNA (HBV genome) equal? That spells hepatitis—a mystery virus long misunderstood, long before COVID dominated headlines.This isn’t just linguistic trivia. It’s a journey through centuries of medical detective work, flawless missteps, and public health triumphs—all centered on one family of viruses that quietly reshaped liver medicine and modern virology.Early Clues in Jaundice and ContagionHepatitis didn’t appear on a microscope slide in the 20th century—it was described millennia earlier. Ancient Greek physician Hippocrates observed jaundice as a distinctive yellowing of skin and eyes. By the 8th century, medical writers suspected jaundice was contagious, hinting at an infectious agent at work in the liver.Between the 17th and 19th centuries, dramatic epidemics of jaundice spread through soldiers and navies. Shared living quarters, contaminated water, and later, mass inoculation campaigns and reused syringes during wars linked the outbreaks to bloodborne transmission. By 1885, physicians recognized that transfused blood could carry the mysterious jaundice-causing pathogen. And when measles and yellow fever vaccinations during World War II triggered outbreaks, it became clear: an unseen virus replicated in bloodstreams—and in the liver.This early history underscored two enduring facts: hepatitis came in different forms, and it was stealthy, delayed, and extremely hard to track.Naming a Virus in Two PartsBy mid-century, researchers sought to categorize the illness. In 1947, MacCallum introduced a dual classification that would shape all future work: Viral Hepatitis A (infectious, via contaminated food or water) and Viral Hepatitis B (serum-borne, via blood and body fluids). That breakthrough turned a single symptom—jaundice—into a family of diseases with different transmission pathways and prevention needs.Modern hepatitis history truly began in the 1960s. In 1963, Baruch Blumberg identified the Australia antigen (HBsAg) in Aboriginal Australians and hemophiliac blood donors using immunologic screening. It was the first direct marker for Hepatitis B virus, revealing a virus that lay dormant in carriers, often for decades.The story advanced quickly:1970 – The Dane particle (complete HBV virus) was visualized, proving the viral identity.Early 1970s – Researchers described the HBeAg, another disease marker.1973 – Hepatitis A virus (HAV) was isolated, confirming two different viruses.Suddenly, hepatitis was no longer a vague syndrome—it was a family of identifiable pathogens. That scientific clarity laid the foundation for prevention and treatment.Finding a Cure Before HCV With Plasma‑Derived VaccinesThe early HBV vaccine story is unique. Developed from human plasma, it became the first vaccine not produced via tissue culture, licensed under the name Heptavax in 1981. That innovation paved the way for recombinant vaccines, but the achievement stood alone for a time. Taiwan’s national HBV vaccination program, launched in 1984, offered powerful proof of impact:HBV carrier rate dropped from 9.1% to 2.7% among children.Rates of pediatric hepatocellular carcinoma plummeted from 27% to 17%.Effectively, this was the world’s first anti-cancer vaccine. The vaccine didn’t just stop liver infection—it significantly reduced childhood liver cancers in real populations.The C Virus and the Molecular Breakthrough of 1989In 1989, the hepatitis world shifted again. A team led by Choo, Kuo, and Houghton unveiled Hepatitis C virus (HCV) using molecular cloning techniques—no tissue culture, electron microscope, or serology required. It was the first virus discovered solely via genetic methods.That breakthrough explained persistent post‑transfusion hepatitis cases, intravenous drug-user outbreaks, and a heavy burden of global liver disease. It was the start of a new era: molecular virology, where pathogens were identified by their RNA alone.Soon came discoveries of HDV (delta virus), HEV, and GBV‑C/HGV (hepatitis G virus). This growing catalog of viral types clarified why hepatitis symptoms varied and why prevention needed multiple strategies.From Unproven Remedies to Modern AntiviralsMid-20th-century treatment was often worse than the disease: prolonged bed rest and steroids were used for acute hepatitis until controlled trials in the ’60s showed they caused harm. In chronic cases, steroids lingered until the 1980s, when researchers clearly proved they worsened outcomes.By the early 1990s, interferon alpha offered the first real antiviral option. In 1998, lamivudine appeared, followed by more potent nucleoside analogues in the 2000s. For chronic HBV, these drugs allowed suppression of the virus with daily pills—a huge leap in quality of life. HCV treatment advanced spectacularly:Pegylated interferon plus ribavirin drove cure rates into the 40–60% range.Protease inhibitors like boceprevir and telaprevir added another 30%+ success.By the 2010s, direct-acting antivirals (DAAs) offered cure rates above 85–90% within a few months, without interferon.Chronic HCV became the only curable chronic viral infection—a feat comparable in scope to eradication campaigns for smallpox or polio.Globally today, over 300 million people live with chronic HBV or HCV and over 1.3 million die annually from liver cirrhosis, cancer, or hepatitis complications.In response, the World Health Organization’s 2022–2030 strategy aims to reduce new infections by 90% and deaths by 65%. It underscores the urgent need for universal vaccinations, access to testing, and treatment—especially in low-income settings across Asia and Africa, without coordinated action, projections warn:9.5 million new infections,2.1 million liver cancer cases,2.8 million deaths by 2030.Yet history offers reason for optimism: the leaps science made over just a few decades show what’s possible—with political will, investment, and global partnerships.HBV opened new pathology understanding by linking to polyarteritis nodosa. HCV revealed risks beyond the liver: cryoglobulinemia, non-Hodgkin lymphoma, metabolic disorders like Type II diabetes, and altered lipid profiles. Hepatitis viruses reshaped fields ranging from rheumatology to oncology.The discoveries required collaboration—and some competition—across labs and continents. The story of hepatitis is one of scientific rivalry, teamwork, serendipity, and intellectual persistence. That blend of curiosity and rigor transformed a family of mysterious illnesses into preventable and treatable diseases.Long before COVID captured global focus—before masks, PCR tests, and lockdowns—hepatitis was a mystery virus that haunted generations. It caused jaundice, silent liver failure, and cancer. It eluded diagnosis, lacked vaccines, and spread undetected.Yet through a combination of linguistic insight, molecular science, epidemiology, and public health action, the world unraveled its secrets—one virus at a time.Today, hepatitis is no longer an invisible threat. It's a medical triumph—because when science is patient, and public health persistent, even the most elusive pathogens can be conquered. The story isn't over, but it's a testament to what decades of dedication and discovery can achieve.

medical memoir: before covid, hepatitis was the mystery virus that haunted generations

Science of Hair Serums: Do They Really Repair Damaged Hair?

science of hair serums: do they really repair damaged hair?

Health News

Demand For Weight Loss Injections Now ‘Unsustainable’, Experts Say Most Don’t Qualify

demand for weight loss injections now ‘unsustainable’, experts say most don’t qualify ozempic mounjaro wegovy glp-1 drugs

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Celebrity Nutritionist Shares 2 Foods For Lunch That Help Avoid Afternoon Slump

celebrity nutritionist shares 2 foods for lunch that help avoid afternoon slump

New Sweat-Sensing Wearable Could Help Monitor And Improve Bipolar Disorder Treatment

new sweat-sensing wearable could help monitor and improve bipolar disorder treatment

<span>Ozempic</span>, once known mainly for helping people manage type 2 diabetes, is now practically a household name for another reason: weight loss. The drug—and its semaglutide siblings like Wegovy, Mounjaro, Rybelsus, and Zepbound—has become a go-to for those looking to shed pounds fast but the rise of Ozempic has come with side effects that users didn’t quite see coming.

It started with the Ozempic face—that sunken, aged look from rapid weight loss. Then came the Ozempic butt, Ozempic hands, and even reports of changes to genital appearance like the so-called Ozempic penis. As more people turn to semaglutide drugs like Ozempic and Wegovy for weight loss, a surprising list of aesthetic side effects is emerging. Social media is full of before-and-after images not just of trimmed waists, but of gaunt cheeks, drooping skin, sagging arms, and visible bones in places people never expected. These aren't just cosmetic concerns—they raise important questions about how these drugs reshape the body in unintended ways. Curious where the science stands? Let’s break it all down.

Across social media and Reddit threads, people are asking- Why is my hair thinning since I started this medication? Is it the drug? Or is it the weight loss?

<h2>What Is Ozempic Hair?</h2>Here’s the thing: there’s no clear-cut evidence that Ozempic (or semaglutide itself) directly causes hair loss. In fact, during initial clinical trials for both Ozempic and Wegovy, hair loss wasn’t even reported as a side effect. Still, anecdotal accounts tell a different story—and science may explain why.

<span>Telogen effluvium</span> is the most likely explanation. This is a condition where large numbers of hair follicles enter a “resting” phase at the same time and shed together, leading to noticeable thinning. It typically starts about three months after a stressful event—and yes, that includes rapid weight loss.

<h2>Why Rapid Weight Loss Triggers Hair Loss?</h2>

Hair growth follows a cycle. It includes a growth phase, a rest phase, and a shedding phase. Normally, these cycles are staggered so you’re not losing all your hair at once. But major physiological stress—like surgery, trauma, or drastic weight loss—can throw this rhythm off. When too many follicles hit the rest phase at once, hair falls out in clumps.

This doesn’t mean it’s permanent. In most cases, hair does grow back over several months. But the emotional and psychological toll during the shedding period can be significant.

<h2>What Else Might Be Reason for Hair Thinning And Hair Loss?</h2>

Ozempic suppresses appetite. That’s one of the reasons it works so well for weight loss. But eating less food also means fewer nutrients—especially if your diet wasn’t balanced to begin with. Deficiencies in iron, biotin, zinc, and protein can impair hair growth. Women, in particular, are at higher risk of iron deficiency, which is tightly linked to hair thinning.

Semaglutide mimics GLP-1, a hormone that helps regulate insulin and blood sugar levels. Hormonal changes, especially those involving insulin or cortisol, can affect hair cycles. We see similar shifts during menopause, thyroid imbalances, or postpartum—each of which is linked to hair loss.

<h4>3. Stress—Physical and Emotional</h4>

Whether it’s the underlying condition (like diabetes), the rapid change in body weight, or the stress of seeing more hair in the drain each morning, stress itself is a well-documented hair loss trigger. And once stress hits, it can form a vicious cycle—more shedding, more stress, more shedding.

<h2>How Common Is Ozempic-Linked Hair Loss?</h2>

Right now, we don’t have exact numbers. In Wegovy’s clinical trials, about 3% of participants reported increased shedding—compared to 1% in the placebo group. That 2% margin might sound small, but given the millions now using semaglutide-based drugs, it adds up. In 2023 alone, nearly 2% of the U.S. population was prescribed Ozempic or similar GLP-1 agonists.

That’s a huge number of people and even a small side effect becomes a big deal when the user base is massive.

On Reddit, one longtime type 2 diabetic described their three-year experience on Ozempic. They didn’t notice sudden hair fallout, but gradually saw thinning over time—alongside other gastrointestinal side effects like sulfur gas and diarrhea. When they stopped taking the medication, their gut issues resolved and their hair began growing back. Interestingly, their weight stayed off even without the drug.

While anecdotal, stories like this point to the need for deeper research and more personalized monitoring.

<h2>What To Do If You're Experiencing Hair Loss on Ozempic</h2>

If your hair is thinning after starting Ozempic, don’t panic—but don’t ignore it either. Here's what to do:

First, rule out other medical causes. Thyroid disorders, hormonal imbalances, autoimmune conditions, or nutrient deficiencies may be the real culprits. Don’t self-diagnose.

Sometimes, the combination of medications can amplify hair loss risks. A review with your provider can identify if alternatives might work better for you—without compromising your health goals.

Even if your appetite is low, aim for nutrient-dense meals. Include lean protein, leafy greens, fruits, whole grains, and supplements if necessary. Consider bloodwork to check iron, B12, and zinc levels.

Avoid tight hairstyles, heat tools, and harsh chemical treatments. Your follicles need time to recover. Switch to gentle hair products and wide-tooth combs.

Chronic stress prolongs telogen effluvium. Explore stress-management tools like mindfulness, therapy, walking outdoors, or journaling.

Some dermatologists recommend treatments like PRP (platelet-rich plasma) therapy, which uses your own blood’s growth factors to promote regrowth. While not FDA-approved for all types of hair loss, it's increasingly popular and worth exploring with a specialist.

Hair loss tied to Ozempic isn’t inevitable, and it doesn’t happen to everyone. For many, the benefits of GLP-1 medications—weight loss, improved blood sugar control, reduced risk of heart disease—far outweigh the risks but side effects like hair thinning remind us that no drug is free from trade-offs.

ozempic

ozempic hair loss

semaglutide side effects

glp 1 drugs

ozempic face

telogen effluvium

wegovy hair shedding

weight loss medication effects

Skin & Hair

Ozempic, once known mainly for helping people manage type 2 diabetes, is now practically a household name for another reason: weight loss. The drug—and its semaglutide siblings like Wegovy, Mounjaro, Rybelsus, and Zepbound—has become a go-to for those looking to shed pounds fast but the rise of Ozempic has come with side effects that users didn’t quite see coming.It started with the Ozempic face—that sunken, aged look from rapid weight loss. Then came the Ozempic butt, Ozempic hands, and even reports of changes to genital appearance like the so-called Ozempic penis. As more people turn to semaglutide drugs like Ozempic and Wegovy for weight loss, a surprising list of aesthetic side effects is emerging. Social media is full of before-and-after images not just of trimmed waists, but of gaunt cheeks, drooping skin, sagging arms, and visible bones in places people never expected. These aren't just cosmetic concerns—they raise important questions about how these drugs reshape the body in unintended ways. Curious where the science stands? Let’s break it all down.Across social media and Reddit threads, people are asking- Why is my hair thinning since I started this medication? Is it the drug? Or is it the weight loss?What Is Ozempic Hair?Here’s the thing: there’s no clear-cut evidence that Ozempic (or semaglutide itself) directly causes hair loss. In fact, during initial clinical trials for both Ozempic and Wegovy, hair loss wasn’t even reported as a side effect. Still, anecdotal accounts tell a different story—and science may explain why.Telogen effluvium is the most likely explanation. This is a condition where large numbers of hair follicles enter a “resting” phase at the same time and shed together, leading to noticeable thinning. It typically starts about three months after a stressful event—and yes, that includes rapid weight loss.Why Rapid Weight Loss Triggers Hair Loss?Hair growth follows a cycle. It includes a growth phase, a rest phase, and a shedding phase. Normally, these cycles are staggered so you’re not losing all your hair at once. But major physiological stress—like surgery, trauma, or drastic weight loss—can throw this rhythm off. When too many follicles hit the rest phase at once, hair falls out in clumps.This doesn’t mean it’s permanent. In most cases, hair does grow back over several months. But the emotional and psychological toll during the shedding period can be significant.What Else Might Be Reason for Hair Thinning And Hair Loss?1. Nutrient DeficienciesOzempic suppresses appetite. That’s one of the reasons it works so well for weight loss. But eating less food also means fewer nutrients—especially if your diet wasn’t balanced to begin with. Deficiencies in iron, biotin, zinc, and protein can impair hair growth. Women, in particular, are at higher risk of iron deficiency, which is tightly linked to hair thinning.2. Hormonal ShiftsSemaglutide mimics GLP-1, a hormone that helps regulate insulin and blood sugar levels. Hormonal changes, especially those involving insulin or cortisol, can affect hair cycles. We see similar shifts during menopause, thyroid imbalances, or postpartum—each of which is linked to hair loss.3. Stress—Physical and EmotionalWhether it’s the underlying condition (like diabetes), the rapid change in body weight, or the stress of seeing more hair in the drain each morning, stress itself is a well-documented hair loss trigger. And once stress hits, it can form a vicious cycle—more shedding, more stress, more shedding.How Common Is Ozempic-Linked Hair Loss?Right now, we don’t have exact numbers. In Wegovy’s clinical trials, about 3% of participants reported increased shedding—compared to 1% in the placebo group. That 2% margin might sound small, but given the millions now using semaglutide-based drugs, it adds up. In 2023 alone, nearly 2% of the U.S. population was prescribed Ozempic or similar GLP-1 agonists.That’s a huge number of people and even a small side effect becomes a big deal when the user base is massive.On Reddit, one longtime type 2 diabetic described their three-year experience on Ozempic. They didn’t notice sudden hair fallout, but gradually saw thinning over time—alongside other gastrointestinal side effects like sulfur gas and diarrhea. When they stopped taking the medication, their gut issues resolved and their hair began growing back. Interestingly, their weight stayed off even without the drug.While anecdotal, stories like this point to the need for deeper research and more personalized monitoring.What To Do If You're Experiencing Hair Loss on OzempicIf your hair is thinning after starting Ozempic, don’t panic—but don’t ignore it either. Here's what to do:First, rule out other medical causes. Thyroid disorders, hormonal imbalances, autoimmune conditions, or nutrient deficiencies may be the real culprits. Don’t self-diagnose.Sometimes, the combination of medications can amplify hair loss risks. A review with your provider can identify if alternatives might work better for you—without compromising your health goals.Even if your appetite is low, aim for nutrient-dense meals. Include lean protein, leafy greens, fruits, whole grains, and supplements if necessary. Consider bloodwork to check iron, B12, and zinc levels.Avoid tight hairstyles, heat tools, and harsh chemical treatments. Your follicles need time to recover. Switch to gentle hair products and wide-tooth combs.Chronic stress prolongs telogen effluvium. Explore stress-management tools like mindfulness, therapy, walking outdoors, or journaling.Some dermatologists recommend treatments like PRP (platelet-rich plasma) therapy, which uses your own blood’s growth factors to promote regrowth. While not FDA-approved for all types of hair loss, it's increasingly popular and worth exploring with a specialist.Hair loss tied to Ozempic isn’t inevitable, and it doesn’t happen to everyone. For many, the benefits of GLP-1 medications—weight loss, improved blood sugar control, reduced risk of heart disease—far outweigh the risks but side effects like hair thinning remind us that no drug is free from trade-offs.

not just face, 'ozempic hair' is the latest side effect everyone’s talking about

Ishita Roy

Hepatitis A To E: How Each Virus Affects Your Liver?

hepatitis a to e: how each virus affects your liver?

Why Do Some Cancer Patients Respond Better To Treatment Than Others? Answer Lies In Body’s Defense Mechanism

why do some cancer patients respond better to treatment than others? the answer lies in our body’s natural defense

What Is The 'Asian Glow'? Is It Just Body's Reaction To Alcohol Or Something More Dangerous?

what is the 'asian glow'? is it just body's reaction to alcohol or something more dangerous?

What Is Metastatic Cancer? How It Spreads, What It Means And Why Chemotherapy Isn’t Always Enough

what is metastatic cancer? how it spreads, what it means and why chemotherapy isn’t always enough

In a breakthrough that has the potential to reshape how we understand some forms of <span>skin cancer</span>, doctors at the U.S. National Institutes of Health (NIH) have identified a strain of <span>human papillomavirus</span> (<span>HPV</span>), commonly found on the skin, as the direct cause of cutaneous squamous cell carcinoma in a woman with a rare immune disorder.

The findings, published in the <em>New England Journal of Medicine </em>this week, challenge long-held assumptions about the role of HPV in skin <span>cancer</span> and spotlight the risks faced by immunocompromised individuals.

The discovery came during treatment of a 34-year-old woman, who was suffering from a rare genetic condition that severely weakened her immune system. 

Over time, she developed more than 40 skin cancer lesions across her face, hands, and legs, all diagnosed as cutaneous squamous cell carcinoma, the second most common form of skin cancer after melanoma.

Despite undergoing multiple surgeries and immunotherapy, her cancer kept returning. 

That’s when a team of doctors, led by Dr. Andrea Lisco from NIH’s National Institute of Allergy and Infectious Diseases, decided to dig deeper. What they found was shocking: her tumors were being driven by beta HPVs, a group of viruses typically seen as harmless.

“The virus replicated in a somewhat uncontrolled manner and ended up integrating into the skin cells,” said Dr. Lisco. “Once they did that, they became cancerous.”

Until now, HPV’s link to skin cancer was considered indirect at best. Scientists believed the virus might weaken skin cells or make them more vulnerable to UV damage, but not directly cause cancer.

This case flips that understanding on its head.

Unlike alpha HPVs, which are known to cause cervical, anal, and throat cancers and are targeted by the Gardasil vaccine, beta HPVs live on the skin and usually stay dormant. In healthy people, they don’t integrate into DNA or cause illness.

But in this woman’s case, a weakened immune system, specifically impaired T-cells, allowed the virus to behave aggressively and hijack her skin cells’ DNA, turning them malignant.

<h4>A Life-Saving Treatment and New Insights</h4>

With her immune system unable to fight the virus, doctors decided a stem cell transplant to replace her malfunctioning immune cells. Three years after the procedure, she remains cancer-free.

“This case gives us valuable insight into how the immune system interacts with HPV,” said Dr. Anthony Rossi, a dermatologist at Memorial Sloan Kettering Cancer Center, who was not involved in the study. “What’s novel is that it’s the first time beta HPV has been directly linked to human skin cancer.”

Dr. Lisco noted that while the finding is important, it doesn’t suggest that everyone with beta HPV is at risk. “We shake hands and we pick up those viruses,” he said. “But if our immune systems are intact, we’re fine.”

<h4>A Warning for the Immunocompromised</h4>

Doctors emphasize that this case highlights a very specific risk, one that primarily applies to people with compromised immune systems, including those with HIV, organ transplants, long-term immunosuppressive medications, or rare genetic conditions.

“Immunocompromised people are up to 100 times more likely to develop this type of skin cancer,” said Dr. Rossi. “HPV can integrate and disrupt the cell cycle more easily in these individuals.”

Dr. Anthony Oro, professor of dermatology at Stanford Medicine, added, “It suggests that beta HPVs could contribute to cancers in patients where the immune defense, especially T-cells, is impaired.”

While Gardasil protects against nine strains of alpha HPV, it’s unclear whether it offers any protection against beta strains.

“There is some theory that cross-protection may exist,” said Dr. Rossi, “but we need more research to know for sure.”

Studies in mice had long hinted at a potential link between beta HPV and cancer, but this is the first human case to show such a direct cause-and-effect relationship.

Experts say the general population is not at risk from beta HPV-related skin cancer, at least not based on current evidence. Most skin cancers are still caused by sun exposure, and the best prevention is still protecting your skin.

Use sunscreen daily, even on cloudy days.

Wear protective clothing when outdoors, especially during peak sun hours.

Get regular skin checks, particularly if you’re immunocompromised or have a history of skin cancer.

Consult your doctor about HPV vaccines and whether they may benefit you.

“This case serves as a reminder,” said Dr. Oro, “that even viruses we thought were harmless can become dangerous in the wrong context. And that context is often an immune system not doing its job.”

skin cancer

health and wellness

cancer

skincare

human papillomavirus

In a breakthrough that has the potential to reshape how we understand some forms of skin cancer, doctors at the U.S. National Institutes of Health (NIH) have identified a strain of human papillomavirus (HPV), commonly found on the skin, as the direct cause of cutaneous squamous cell carcinoma in a woman with a rare immune disorder.The findings, published in the New England Journal of Medicine this week, challenge long-held assumptions about the role of HPV in skin cancer and spotlight the risks faced by immunocompromised individuals.A Case That Changed EverythingThe discovery came during treatment of a 34-year-old woman, who was suffering from a rare genetic condition that severely weakened her immune system. Over time, she developed more than 40 skin cancer lesions across her face, hands, and legs, all diagnosed as cutaneous squamous cell carcinoma, the second most common form of skin cancer after melanoma.Despite undergoing multiple surgeries and immunotherapy, her cancer kept returning. That’s when a team of doctors, led by Dr. Andrea Lisco from NIH’s National Institute of Allergy and Infectious Diseases, decided to dig deeper. What they found was shocking: her tumors were being driven by beta HPVs, a group of viruses typically seen as harmless.“The virus replicated in a somewhat uncontrolled manner and ended up integrating into the skin cells,” said Dr. Lisco. “Once they did that, they became cancerous.”HPV’s Role in Skin CancerUntil now, HPV’s link to skin cancer was considered indirect at best. Scientists believed the virus might weaken skin cells or make them more vulnerable to UV damage, but not directly cause cancer.This case flips that understanding on its head.Unlike alpha HPVs, which are known to cause cervical, anal, and throat cancers and are targeted by the Gardasil vaccine, beta HPVs live on the skin and usually stay dormant. In healthy people, they don’t integrate into DNA or cause illness.But in this woman’s case, a weakened immune system, specifically impaired T-cells, allowed the virus to behave aggressively and hijack her skin cells’ DNA, turning them malignant.A Life-Saving Treatment and New InsightsWith her immune system unable to fight the virus, doctors decided a stem cell transplant to replace her malfunctioning immune cells. Three years after the procedure, she remains cancer-free.“This case gives us valuable insight into how the immune system interacts with HPV,” said Dr. Anthony Rossi, a dermatologist at Memorial Sloan Kettering Cancer Center, who was not involved in the study. “What’s novel is that it’s the first time beta HPV has been directly linked to human skin cancer.”Dr. Lisco noted that while the finding is important, it doesn’t suggest that everyone with beta HPV is at risk. “We shake hands and we pick up those viruses,” he said. “But if our immune systems are intact, we’re fine.”A Warning for the ImmunocompromisedDoctors emphasize that this case highlights a very specific risk, one that primarily applies to people with compromised immune systems, including those with HIV, organ transplants, long-term immunosuppressive medications, or rare genetic conditions.“Immunocompromised people are up to 100 times more likely to develop this type of skin cancer,” said Dr. Rossi. “HPV can integrate and disrupt the cell cycle more easily in these individuals.”Dr. Anthony Oro, professor of dermatology at Stanford Medicine, added, “It suggests that beta HPVs could contribute to cancers in patients where the immune defense, especially T-cells, is impaired.”Does the HPV Vaccine Help?While Gardasil protects against nine strains of alpha HPV, it’s unclear whether it offers any protection against beta strains.“There is some theory that cross-protection may exist,” said Dr. Rossi, “but we need more research to know for sure.”Studies in mice had long hinted at a potential link between beta HPV and cancer, but this is the first human case to show such a direct cause-and-effect relationship.What This Means for YouExperts say the general population is not at risk from beta HPV-related skin cancer, at least not based on current evidence. Most skin cancers are still caused by sun exposure, and the best prevention is still protecting your skin.Here’s what you can do:Use sunscreen daily, even on cloudy days.Wear protective clothing when outdoors, especially during peak sun hours.Get regular skin checks, particularly if you’re immunocompromised or have a history of skin cancer.Consult your doctor about HPV vaccines and whether they may benefit you.“This case serves as a reminder,” said Dr. Oro, “that even viruses we thought were harmless can become dangerous in the wrong context. And that context is often an immune system not doing its job.”

a strain of typically harmless hpv caused 40 skin cancer lesions in a 34-year-old woman

Aarushi Bhadury

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When we think of public heroes, people we look for when things go wrong, we find military, police and firefighters in our corners. Firefighters have one of the at-risk jobs and face many dangers to save other people. They are not just trained to bring people to safety, but also how to control a dangerous situation, immediate medical care which goes beyond just first aid as well as investigating possible threats. 

We are all aware of how they put their lives on the line to save others from dangerous situations whether it is jumping in to save people from burning buildings or, helping people escape from potentially dangerous situations. However, this is not the only way they are risking their own lives for us. 

A recent study by the <span>American Cancer Society</span> (ACS) highlights a serious health concern for firefighters: their job significantly increases their chances of developing various cancers, including skin and kidney cancer. This discovery sheds light on the long-term health challenges these essential workers face, which extend far beyond the immediate dangers of battling fires. It's a stark reminder that the bravery of firefighters comes with a hidden cost to their health over time.

<h2>Why Firefighters Need Protection and Screening </h2>

This study's findings are a crucial wake-up call, even if they're not pleasant to hear. The research emphasizes that the health risks firefighters encounter go beyond the immediate dangers of their profession. It's incredibly important to step up efforts to protect firefighters' health. This means making sure they have better access to cancer screenings, ensuring early detection, and implementing stronger prevention strategies. By doing so, we can help safeguard the well-being of those who put their lives on the line for us. 

For this study, researchers looked at a vast amount of health data collected over 36 years. They focused on individuals who were cancer-free at the beginning of the study in 1982. Specifically, they examined information from over 470,000 firefighters and compared their rates of cancer-related deaths to those of men in other professions. The overall conclusion strongly supports what other research has suggested: being a firefighter is linked to an increased risk of developing cancer. 

<h2>Specific Cancer Risks Identified </h2>

The study identified the highest increased risks for specific types of cancer: 

Firefighters had a significantly higher chance (72% more) of developing skin cancer. This might be because they often work outdoors without enough sun protection. Taking better precautions against sun exposure could help reduce this risk. There was also a 39% higher risk of kidney cancer among firefighters. The study also found smaller, but still notable, increases in risk for other cancers: 

<ul><li>Firefighters who had been on the job for 30 years or more showed an 8% higher risk of Lung cancer</li><li>There was a 14% higher risk of prostate cancer</li><li>Firefighters had a 15% higher risk of colon cancer.</li></ul>

When we think of public heroes, people we look for when things go wrong, we find military, police and firefighters in our corners. Firefighters have one of the at-risk jobs and face many dangers to save other people. They are not just trained to bring people to safety, but also how to control a dangerous situation, immediate medical care which goes beyond just first aid as well as investigating possible threats. We are all aware of how they put their lives on the line to save others from dangerous situations whether it is jumping in to save people from burning buildings or, helping people escape from potentially dangerous situations. However, this is not the only way they are risking their own lives for us. A recent study by the American Cancer Society (ACS) highlights a serious health concern for firefighters: their job significantly increases their chances of developing various cancers, including skin and kidney cancer. This discovery sheds light on the long-term health challenges these essential workers face, which extend far beyond the immediate dangers of battling fires. It's a stark reminder that the bravery of firefighters comes with a hidden cost to their health over time. Why Firefighters Need Protection and Screening This study's findings are a crucial wake-up call, even if they're not pleasant to hear. The research emphasizes that the health risks firefighters encounter go beyond the immediate dangers of their profession. It's incredibly important to step up efforts to protect firefighters' health. This means making sure they have better access to cancer screenings, ensuring early detection, and implementing stronger prevention strategies. By doing so, we can help safeguard the well-being of those who put their lives on the line for us. For this study, researchers looked at a vast amount of health data collected over 36 years. They focused on individuals who were cancer-free at the beginning of the study in 1982. Specifically, they examined information from over 470,000 firefighters and compared their rates of cancer-related deaths to those of men in other professions. The overall conclusion strongly supports what other research has suggested: being a firefighter is linked to an increased risk of developing cancer. Specific Cancer Risks Identified The study identified the highest increased risks for specific types of cancer: Firefighters had a significantly higher chance (72% more) of developing skin cancer. This might be because they often work outdoors without enough sun protection. Taking better precautions against sun exposure could help reduce this risk. There was also a 39% higher risk of kidney cancer among firefighters. The study also found smaller, but still notable, increases in risk for other cancers: Firefighters who had been on the job for 30 years or more showed an 8% higher risk of Lung cancerThere was a 14% higher risk of prostate cancerFirefighters had a 15% higher risk of colon cancer.Why Are Firefighters More At-Risk For Cancer? The Leukemia & Lymphoma Society explains that beyond the immediate dangers of putting out fires, they face a hidden threat: an increased risk of various cancers. This is due to the smoke and harmful chemicals they encounter while on duty. Modern homes and buildings are full of synthetic and plastic materials. When these burn, they create a lot more smoke than natural materials. This smoke contains carcinogens, which are substances that can cause cancer. One common type is polycyclic aromatic hydrocarbons (PAHs), a group of over 100 different chemicals. Being exposed to some PAHs can lead to cancer. Firefighters might also come across other known cancer-causing agents like asbestos and diesel exhaust. These harmful substances can be breathed in or soaked up through the skin. Filling Gaps in Cancer Research Earlier studies from the International Agency for Research on Cancer (IARC) hinted that firefighting could increase the risk of cancers like mesothelioma and bladder cancer. However, these studies weren't clear about other types of cancer. This new research helps fill in those missing pieces. It's especially important because it provides fresh evidence linking firefighting to skin, kidney, prostate, and colorectal cancers. These were types of cancer where the connection to firefighting wasn't strong or clear before. This new study gives us a much better understanding of the cancer risks firefighters face because of what they're exposed to on the job. 

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Not Just Face, 'Ozempic Hair' Is The Latest Side Effect Everyone’s Talking About

A Strain Of Typically Harmless HPV Caused 40 Skin Cancer Lesions In A 34-Year-Old Woman

Firefighters May Be Putting Their Lives At Risk In More Ways Than We Realize - Study Finds

Health Conditions A-Z

Not Just Face, 'Ozempic Hair' Is The Latest Side Effect Everyone’s Talking About

A Strain Of Typically Harmless HPV Caused 40 Skin Cancer Lesions In A 34-Year-Old Woman

Firefighters May Be Putting Their Lives At Risk In More Ways Than We Realize - Study Finds