Can we finally reverse balding with these new experimental treatments?

Male pattern baldness could soon be a thing of the past, with new hair loss treatments beginning to show tantalising results

By Joshua Howgego

26 September 2023


baytunc/Getty Images

I’LL level with you: a part of me didn’t want to write this story. When I first realised that I was losing my hair, I found it important to mention it often in conversation. I was so embarrassed about it that I was trying some sort of reverse psychology. But I soon realised that if there was one thing less attractive than my balding head, it was how much I was talking about it. I am joking, of course: there is nothing wrong with being bald. Still, for me, the prospect is terrifying. My hair is a big part of my identity, so to lose it is crushing.

I’m not alone. By the age of 50, between 30 and 50 per cent of men have begun to experience male pattern baldness . Despite there being plenty of handsome hairless men out there – I’m looking at you, Thierry Henry – studies suggest that people tend to perceive bald men as less attractive and less friendly . And we don’t need science to tell us that this can be deeply upsetting.

So although I have dialled down the discussion of my growing bald patch, I have been quietly digging into the science of hair loss – and what I found is worth shouting about. It is common knowledge that some treatments can slow hair loss. What is less known is that as we are coming to understand the reasons why male pattern baldness causes people to lose their hair, we are finding new strategies to restore it. There may soon be a way to not just slow balding, but reverse it.

In a field…

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Fda approves second yale-researched treatment for alopecia areata.

A side by side comparison of the same patient before and after treatment.

A side by side comparison of the same patient before and after treatment.

Just a year after the U.S. Food and Drug Administration (FDA) approved the first treatment for severe alopecia areata, the federal agency has approved a second treatment for the disfiguring skin disease — both the result of pioneering research by the same Yale dermatologist.

On June 23, the FDA announced its approval for the use of ritlecitinib — a Janus kinase (JAK) inhibitor — to treat alopecia areata in both adolescents and adults. The medicine, taken orally, goes by the product name Litfulo.

Alopecia areata is an autoimmune disease characterized by sudden, often disfiguring, loss of hair. It is the second most common cause of hair loss, affecting up to 7 million people in the United States.

Dr. Brett King , an associate professor of dermatology at Yale School of Medicine, worked with pharmaceutical company Pfizer to conduct a series of clinical trials with ritlecitinib. He worked with Eli Lilly and Company on clinical trials for the earlier medicine — baricitinib (which goes by the product name Olumiant), approved as a treatment for patients with severe alopecia areata in June 2022 .

King’s groundbreaking work with JAK inhibitors, which were originally designed to treat rheumatoid arthritis and myelofibrosis (a rare blood cancer), has shown significant potential to treat an array of intractable skin diseases, including eczema, erosive lichen planus, vitiligo, granuloma annulare, and sarcoidosis.

King spoke with Yale News about this latest FDA approval.

How does FDA approval for ritlecitinib change the treatment landscape for people with alopecia areata?

Brett King: Ritlecitinib [Litfulo] changes the treatment landscape for people with alopecia areata enormously. Last year, history was made when baricitinib [Olumiant] was FDA approved for the treatment of adults with severe alopecia areata. But alopecia areata affects people of all ages and, indeed, it commonly affects children of all ages. Ritlecitinib is approved in patients ages 12 years and older.

Childhood and adolescence are such vulnerable times, and children and adolescents have so much to do and learn and become during these years. It is challenging enough to be a kid, but when alopecia areata happens and suddenly one has big bald spots or is completely bald and missing eyebrows, the normal trajectory of that kid’s life, and the family’s life, too, can be derailed. Kids withdraw from sports and other social activities, and even from school. Extreme sadness and anxiety are common. It is awful. There is a way out of the darkness, however, and that is to regrow the hair that was lost, to restore the person as they had been prior to alopecia areata.

Normalcy is so important for everybody, but especially when we are developing. So it is easy to understand what a monumental breakthrough it is to have a medicine, ritlecitinib, approved for adolescents. Ritlecitinib restores normalcy and will make life better — literally will change life — for so many people.

When can patients in the U.S. expect ritlecitinib to be available for use?

King: Hopefully in the days or weeks ahead.

You have been at the center of two FDA approvals for major treatments of alopecia areata in two years. Has that sunk in yet — and how does that make you feel?

King: These new medicines for alopecia areata are historic, and I feel super fortunate to be a part of their development. Being a doctor is amazing because I get to share in the lives of others, hopefully making those lives better. It happens one person at a time, though. To have played a central role in the development of treatments for alopecia areata and other diseases — treatments that doctors around the world will give to thousands and thousands (or even millions) of people to make their lives better — is really incredible. We are all a part of something bigger than ourselves, and for me this experience highlights that as well as the possibility that we can change the world.

What are you working on next?

King: The next horizon is approval of these and other treatments for younger patients. Remember, alopecia areata is not uncommon in pre-adolescents. Also, JAK inhibitors do not work for everybody with alopecia areata, and so work needs to be done both to understand why that is and to develop treatments other than JAK inhibitors. The goal is for everybody to be able to have effective treatment. We have come so, so far but we still have a ways to go. It’s exciting.

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Growing back stronger … the hope is that injecting the cells returns hair to a more youthful state.

‘We’re not making new hairs, we’re rescuing’: could scientists reverse male pattern baldness?

The onset of hair loss can be devastating for some men. But research into experimental cell therapy is offering hope of keeping baldness at bay

P aul Kemp’s introduction to the issue of baldness came as a rude awakening while getting a haircut at the age of 20. “I remember my hairdresser looking down and saying ‘Oh my God, you’re going bald on top’.”

Kemp, now in his 60s, was dismayed at the discovery, but it also marked the beginning of a lifelong professional interest in the science of hair loss and how to stop it. Kemp is the co-founder and chief executive officer of HairClone, a company that is developing an experimental cell therapy treatment for male pattern baldness and whose tagline is “making hair loss history”.

Male pattern baldness affects around 85% of men by the age of 50 and losing hair can be a source of anxiety and low self-esteem . There are drugs that can slow hair loss, transplants to redistribute hair around the head, or strategic hairstyles to disguise receding hairlines and bald spots. Nothing exists to reverse the process, but that could be set to change.

Male pattern baldness affects around 85% of men by the age of 50.

In recent years, scientists have discovered that baldness has its origin in the loss of specialised skin cells, called dermal papillae, that line the base of hair follicles. These cells are crucial for regulating hair thickness, growth, texture and possibly even colour. But in some men, these cells are progressively killed off by dihydrotestosterone, the hormone that causes the male body to mature during puberty.

“You have about 1,000 of these dermal papilla cells per hair,” says Kemp. “The more dermal papilla cells, the thicker the hair shaft. When you get down to around half that number, you’ll notice the hair thinning.”

Baldness implies a lack of hair, but, technically, bald heads are not hairless. As dermal papilla cells are lost, the follicle shrinks and the hair shaft it produces becomes finer and spends longer in the dormant state. Eventually, the hairs become so fine and grow so slowly that they are effectively invisible.

HairClone is aiming to reverse this so-called miniaturisation process by allowing people to bank 100 or so youthful follicles or follicles from parts of the head that still have hair. After being taken from a patient’s head, the follicles are placed in a deep freeze container at -150C. Then, as and when required, the hair can be thawed and the dermal papilla cells can be cloned and multiplied in the laboratory to provide an almost unlimited supply.

The hope, based on experiments in mice and previous tests in people by an earlier company, is that injecting the cells back into the scalp will plumpen the follicles and return hair to a more youthful state.

“We’re not making new hairs, we’re rescuing miniaturising hairs,” says Kemp.

Around 200 clients have already banked hair, although none have yet been treated. The efficacy of the approach has not yet been established in a clinical trial, but the company is in the process of establishing quality controls that will allow it to manufacture cells to clinical standards. At that point – and the company is hoping that will be within the next 12-18 months – doctors will be able to offer it on an experimental basis to patients who they think could benefit.

One of those to have banked his hair is Tommy Smith, a 65-year-old planning consultant, who lives in Red Oak, North Carolina. Smith initially began losing hair in his 20s, possibly as a side-effect of powerful acne medications, including high dosages of prescription vitamin A.

He had a hair transplant in 1988, aged 30, which he says had “outstanding” results until he began to lose both his transplanted hair and original hair in 2015. He sees hair cloning as an insurance against further hair loss. “The concept of having hair follicles stored to address the potential of additional hair loss in the future is very encouraging,” he says. “I also think this could provide young men who have hair loss history in their family the opportunity to address future hair loss in a much less painful and complicated manner.”

Smith’s experience highlights the dilemma that hair surgeons and their patients are faced with when planning a transplant. Once transplanted, follicles retain their original identity and so need to be taken from a safe zone of the scalp that is not destined to go bald in future. Transplanting before the hairline has stabilised can lead to a “hair island” effect, requiring further transplants – and there’s also a question of whether the hairline will recede so far that there won’t be sufficient hair to spread over the whole head. “You’re chasing a moving target,” says Kemp.

However, scientists believe it may be possible to predict a man’s eventual hairline by analysing genetic markers hidden inside dermal papilla cells, meaning that in future men could make more informed choices about the most appropriate treatment.

“There’s always been this clear pattern of male hair loss, but no one’s really explained why it’s like that,” says Dr Claire Higgins, a lecturer in tissue regeneration at Imperial College London and scientific adviser to HairClone.

In a paper published in May , Higgins described evidence that the hairline of a middle-aged man could be traced back to the earliest stages of embryonic development. Around the third week of an embryo’s life, cells form three layers called the ectoderm, mesoderm and endoderm. Most organs in the body contain cells that derive from just one of these lineages: the endoderm gives rise to the internal organs, the mesoderm becomes the muscle and connective tissues, and the ectoderm becomes the central nervous system. “Normally a tissue is one lineage, but the [skin] is a bit of an enigma,” says Higgins. “The dermis [the skin’s lower layer] on the face is ectoderm and the dermis on your body is mesoderm, but the top of your head is not really known.”

Higgins argues that male pattern baldness traces out the boundary between skin cells that have taken two very different paths during development. This, she says, could explain why the cells on only certain parts of the head are oversensitive to dihydrotestosterone.

Kemp and colleagues are working to develop a test, based on the gene expression of dermal papilla cells, to establish whether the part of the scalp they come from is balding, destined to bald or will always retain its hair. “Ideally you want to be able to map the head,” he says. “We’re finding genetic differences between the hairs and we’re in the preliminary phases of doing that.”

Kemp says that after years of living with hair loss, he is comfortable with his appearance – and treatment is not for everyone. “At this stage, I’m used to looking like this,” he says. “But when I was 20, had they said, there’s something we can do about that, I would’ve done it. Our targets are younger people.”

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Cure for hair loss? Breakthrough study may pave the way for new treatment

A single molecule may hold the key to battling male- and female-pattern hair loss, recent research suggests.

In mouse experiments, scientists showed that the molecule, dubbed SCUBE3, could spark hair growth in dormant mouse follicles, and even in human ones that had been grafted onto mice. The research was described in a study published in Developmental Cell.

Hair follicles in people who are bald still have the machinery to sprout new strands, study co-author Maksim Plikus, Ph.D., professor of developmental and cell biology at the University of California, Irvine, told TODAY.

All follicles have stem cells at their base that work together to produce strands of hair, Plikus said. In people who are bald or have thinning hair , some of those stem cells don’t seem to be working, he added.

“When it comes to growing hairs, follicle stem cells need to become activated,” Plikus said. “Once activated, they divide into daughter cells that mature and come together to form a strand.”

“Most people when they lose their hair wonder if the follicles are gone,” Plikus said. “They are there, but they are dormant. The reason they are inactive is that they are not hearing signaling molecules.”

That's where SCUBE3 comes in: The molecule carries the message that tells the follicles to activate. Plikus and his colleagues showed in their experiments that when mice were given microinjections of SCUBE3, their hair grew in thick . Even human follicles that were transplanted into the mouse skin turned on when exposed to SCUBE3. The findings suggest that, in people with thinning hair, there isn’t enough SCUBE3 present.

Plikus compares a head covered with dormant follicles to a huge factory filled with 3D printers that are idling and ready to print, but are waiting for someone to push their start buttons.

It’s likely, Plikus said, that it would take very small amounts of SCUBE3 to activate dormant human hair follicles. Moreover, he suspects that treatments would need to be given only two or three times a year.

While the research on SCUBE3 is promising, getting from mouse experiments to a human treatment for baldness isn’t guaranteed, and even if SCUBE3 turns out to grow hair in people, it takes a long time to take a treatment through all of the clinical trials needed to get Food and Drug Administration approval, Plikus said.

“Right now, we are very excited about it,” Dr. Brian Abittan, director of skin and hair rejuvenation at the Mount Sinai Health System, told TODAY. “With this SCUBE3 molecule, we’re hoping to have a more precise understanding of the signaling that controls hair growth. It would be great to have another pathway to treatments.”

But, Abittan said, this is still in the preclinical stage of development.

There is still a long way to go before this could become a baldness treatment, Rui Yi, Ph.D., professor of pathology and dermatology at Northwestern University's Feinberg School of Medicine, told TODAY. “There is a big difference between a human and a mouse. Mice have short hair that grows just long enough to cover their bodies.”

Before doing a clinical trial, the researchers probably will need to do more safety testing, Yi said.

new research for baldness

Linda Carroll is a Peabody Award-winning journalist who is a contributing health and medicine writer for NBC News and TODAY. She is co-author of three books: “The Concussion Crisis: Anatomy of a Silent Epidemic”, “Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings” and “Duel for the Crown: Affirmed, Alydar, and Racing’s Greatest Rivalry”.  

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Going bald? Lab-grown hair cells could be on the way

These biotech companies are reprogramming cells to treat baldness, but it’s still early days.

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mouse engineered to grow human hair

Biologists at several startups are applying the latest advances in genetic engineering to the age-old problem of baldness, creating new hair-forming cells that could restore a person’s ability to grow hair.

Some researchers tell MIT Technology Review they are using the techniques to grow human hair cells in their labs and even on animals. A startup called dNovo sent us a photograph of a mouse sprouting a dense clump of human hair—the result of a transplant of what the company says are human hair stem cells.

The company’s founder is Ernesto Lujan, a Stanford University–trained biologist. He says his company can produce the components of hair follicles by genetically “reprogramming” ordinary cells, like blood or fat cells. More work needs to be done, but Lujan is hopeful that the technology could eventually treat “the underlying cause of hair loss.”

We’re born with all the hair follicles we’ll ever have—but aging, cancer, testosterone, bad genetic luck, even covid-19 can kill the stem cells inside them that make hair. Once these stem cells are gone, so is your hair. Lujan says his company can convert any cell directly into a hair stem cell by changing the patterns of genes active in it.

In biology, we “now understand cells as a ‘state’” rather than a fixed identity, says Lujan. “And we can push cells from one state to another.” 

Reprogramming cells

The chance of replacing hair is one corner in a wider exploration of whether reprogramming technology can defeat the symptoms of aging. In August, MIT Technology Review reported on a stealthy company, Altos Labs , that plans to explore whether people can be rejuvenated using reprogramming. Another startup, Conception , is trying to extend fertility by converting blood cells into human eggs.

A key breakthrough came in the early 2000s, when Japanese researchers hit on a simple formula to turn any type of tissue into powerful stem cells, similar to ones in an embryo. Imaginations ran wild. Scientists realized they could potentially manufacture limitless supplies of nearly any type of cell—say, nerves or heart muscle.

In practice, though, the formula for producing specific cell types can prove elusive, and then there’s the problem of getting lab-grown cells back into the body. So far, there have been only a few demonstrations of reprogramming as a way to treat patients. Researchers in Japan tried transplanting retina cells into blind people. Then, last November, a US company, Vertex Pharmaceuticals, said it might have cured a man’s type 1 diabetes after an infusion of programmed beta cells, the kind that respond to insulin.

The concept startups are pursuing is to collect ordinary cells such as skin cells from patients and then convert these into hair-forming cells. In addition to dNovo, a company called Stemson (its name is a portmanteau of “stem cell” and “Samson”) has raised $22.5 million from funders including from the drug company AbbVie. Cofounder and CEO Geoff Hamilton says his company is transplanting reprogrammed cells onto the skin of mice and pigs to test the technology.

Both Hamilton and Lujan think there is a substantial market. About half of men undergo male-pattern baldness, some starting in their 20s. When women lose hair, it’s often a more general thinning, but it’s no less a blow to self-image.

These companies are bringing high-tech biology to an industry known for illusions. There are plenty of bogus claims about both hair-loss remedies and the potential of stem cells. “You’ve got to be aware of scam offerings,” Paul Knoepfler, a stem-cell biologist at UC Davis, wrote in November .

new research for baldness

Tricky business

So is stem-cell technology going to cure baldness or become the next false hope? Hamilton, who was invited to give the keynote at this year’s Global Hair Loss Summit , says he tried to emphasize that the company still has plenty of research ahead of it. “We have seen so many [people] come in and say they have a solution. That has happened a lot in hair, and so I have to address that,” he says. “We’re trying to project to the world that we are real scientists and that it's risky to the point I can’t guarantee it’s going to work.”

Right now, there are some approved drugs for hair loss, like Propecia and Rogaine, but they’re of limited use. Another procedure involves cutting strips of skin from someplace where a person still has hair and surgically transplanting those follicles onto a bald spot. Lujan says in the future, hair-forming cells grown in the lab could be added to a person’s head with a similar surgery.

“I think people will go pretty far to get their hair back. But at first it will be a bespoke process and very costly,” says Karl Koehler, a professor at Harvard University.

Hair follicles are surprisingly complicated organs that arise through the molecular crosstalk between several cell types. And Koehler says pictures of mice growing human hair aren't new. “Anytime you see these images,” says Koehler, “there is always a trick, and some drawback to translating it to humans.”

Koehler’s lab makes hair shafts in an entirely different way—by growing organoids. Organoids are small blobs of cells that self-organize in a petri dish. Koehler says he originally was studying deafness cures and wanted to grow the hair-like cells of the inner ear. But his organoids ended up becoming skin instead, complete with hair follicles.

Koehler embraced the accident and now creates spherical skin organoids that grow for about 150 days, until they are around two millimeters across. The tube-like hair follicles are clearly visible; he says they are the equivalent of the downy hair that covers a fetus.

One surprise is that the organoids grow backwards, with the hairs pointing in. “You can see a beautiful architecture, although why they grow inside out is a big question,” says Koehler.

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New research shows promise for reversing baldness

A breakthrough technique that can generate human hair growth shows promise for treating baldness in men and women, a new study suggests.

“If it works in humans, it actually opens up the possibility of hair restoration for many more patients than are currently available,” study co-leader Angela Christiano, a dermatology professor at Columbia University Medical Center, told NBC News.

In the study, Christiano and colleagues took dermal papillae — cells inside the base of human hair follicles — from seven donors and cloned the cells in tissue culture. After a few days, the cells were transplanted onto human skin that had been grafted onto the backs of mice.

The transplants resulted in new hair growth lasting at least six weeks in five of the seven tests, according to the findings. DNA analysis confirmed that the new hair follicles genetically matched the human donors.

The research is in its early stages, so it may be years before this science makes its way to the marketplace to help men and women with notable hair loss by age 60. 

The study was published Monday in the online edition of the Proceedings of the National Academy of Sciences.

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  • Published: 12 September 2023

Hair loss treatments take aim at the immune system

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Nature Biotechnology volume  41 ,  pages 1179–1181 ( 2023 ) Cite this article

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Drugs commonly used in rheumatology, the JAK inhibitors, are opening up treatment options for people with autoimmune-driven hair loss, and new mechanistic knowledge is also helping scientists tackle androgenic alopecia, the commonest cause of baldness.

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The Key to Locks: Columbia Team’s Breakthrough Led to Hair Loss Treatment

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For over a decade, Columbia geneticist Angela Christiano , PhD, has attended the annual meeting of the National Alopecia Areata Foundation, where hundreds of individuals affected by the hair loss disorder gather to support one another and learn about the latest scientific research. The meeting is a safe space where patients with alopecia, many of whom have lost all their hair, joyfully remove their wigs and head coverings for the three-day celebration, without fear of shame or judgment.

But this year’s meeting was a bit different. Christiano had trouble recognizing conference attendees she’s known and worked with for years, because many of them now have full heads of hair.

For people with alopecia areata, an autoimmune disease that can cause hair loss so complete that people even lose their eyebrows, the change in appearance was dramatic.


It was also a direct result of Christiano’s groundbreaking research on the condition, which led the FDA in June to approve the first systemic treatment specifically developed for severe alopecia areata.

“It’s a strange feeling. It’s what every geneticist dreams of, to find the genes for a condition and develop a treatment that can directly benefit patients. But it’s extremely rare that it actually works out that way,” says Christiano, who has studied alopecia areata for more than 20 years, motivated by her own bout with the disease.

Mysterious origins

Unlike hormone-driven male pattern baldness, alopecia areata is an autoimmune disease in which the body’s own immune system mistakenly attacks the hair follicle and shuts down hair production.

When Christiano began working on it, though, nobody knew exactly what caused the problem.

Starting with a series of basic research studies on the genetics and cell biology of hair growth, Christiano and a multidisciplinary team of collaborators produced a steady stream of advances, first in the lab and then in the clinic.

The first major clue came in 2010, from a study led by Christiano’s team that looked through the genomes of a thousand patients. The study, published in Nature, uncovered a gene that, when abnormally expressed, produces a known "danger signal" that causes the body to recognize the hair follicle as foreign. 

The genome study was also crucial since the findings also explained why previous efforts to treat the condition hadn’t worked.

“Drugs for other autoimmune skin diseases had been tested in alopecia, but they had largely failed,” Christiano says.

“At that point, we realized that was because alopecia doesn’t share genetic pathways with other autoimmune skin diseases.”

Taming killer T cells

The genome study led the team to focus on investigating a particular kind of "killer" T cell recruited by the danger signal, which became central to understanding the mechanism of hair follicle destruction.

Columbia alopecia team . Dermatologist Julian Mackay-Wiggan (left), immunologist Raphael Clynes (center), and geneticist Angela Christiano (right) made key discoveries that have led to a new drug for alopecia areata, an autoimmune disease that can cause severe hair loss. Photo: Columbia University Irving Medical Center.

Christiano is not an immunologist, so she needed to enlist an expert to help make inroads into understanding the behavior of these cells. She approached Raphael Clynes, MD, PhD, at that time a faculty member in the Department of Medicine, who was an expert in studying the same kinds of killer T cells in type 1 diabetes and in cancer. 

Clynes looked at the list of genes from the genome study and images of the "swarm" of killer T cells surrounding the hair follicle and suggested that inhibiting enzymes known as JAK kinases might be one way to treat the disease.

The team showed that small molecule drugs called JAK inhibitors could shut down signaling inside the killer T cells. Amazingly, by inhibiting the JAK pathway, the team found they could reverse alopecia areata in a mouse model of the disease.

Dramatic regrowth of hair

Armed with photos of mice with alopecia that had regrown all their hair, Christiano next approached her colleague Julian Mackay-Wiggan, MD, a Columbia dermatologist who specialized in hair disorders and had an interest in early-stage clinical research.  

Excited by the early results in the mice, Mackay-Wiggan began treating a few patients with alopecia areata using JAK inhibitors that were already FDA-approved for other disorders. The first few patients experienced dramatic regrowth of their hair, just as the researchers had observed in the mice. Christiano’s team reported these groundbreaking studies in 2014.

Building on these early results, Mackay-Wiggan conducted additional Columbia clinical studies that showed that 75% of patients experienced significant hair regrowth after treatment with two different JAK inhibitors.

Pharma attention

Soon after the Columbia team reported its findings, additional case reports began appearing in the published literature that replicated the results in alopecia patients from around the world.

Because there were no FDA-approved drugs for alopecia when their work began, it didn’t take long for pharmaceutical companies to turn their attention to developing JAK inhibitors specifically for alopecia treatment. These efforts led to newly approved Olumiant from Eli Lilly, Incyte (previously approved for rheumatoid arthritis and hospitalized patients with COVID-19), and two additional JAK inhibitors being developed by Pfizer and Concert Pharmaceuticals and now in late-stage clinical trials.

Christiano welcomes the pharmaceutical companies’ new attention to alopecia areata after the condition had long been neglected and was frequently dismissed as a cosmetic problem.

For patients with complete hair loss, the barrage of stares and intrusive questions can be demoralizing and psychologically devastating. “It’s the stigma of unwanted attention; how do you quantify that?” says Christiano. “The impact of this treatment on patients has been truly transformative.”

Male pattern baldness next?

While Olumiant and other new JAK inhibitors are often life-changing for patients who respond well to them, the treatments are still far from perfect.

“These are potent immunosuppressive drugs, so there are safety considerations to be taken into account when assessing the risk/benefit ratio for individual patients,” says Christiano. After the treatment ends, some patients’ alopecia relapses for reasons the researchers don’t fully understand. In addition, about a third of patients don’t respond to the drugs.

Fortunately, Christiano has no intention of resting on her laurels. Her lab is hoping to understand what causes the condition to relapse after JAK inhibitor treatment.

And by continuing to investigate alopecia areata with new tools and techniques, her team is developing both new biological insights and more potential ways to attack the disease process. “We’re now looking upstream of the JAK signaling pathway to see if other mechanisms can lead to the common endpoint of alopecia areata,” she says.

Christiano’s team also hopes to extend these insights and apply the same approaches to treat other types of hair loss.

Hair follicles grown in a dish in the Christiano lab. Made possible with 3D printing technology, engineered human hair follicles created in this way could generate an unlimited source of new hair follicles for patients undergoing robotic hair restoration surgery. Read more .

In one recent study, for example, Christiano’s team found that JAK inhibitors also reawaken dormant hair follicles , a problem common to male and female pattern baldness.

They also discovered a previously unknown type of immune cell that puts hair follicles into a dormant state by secreting a substance called oncostatin M and that the hair cycle can be reactivated by blocking this pathway.

While translating these results into effective treatments for hair loss will likely take years, it’s a process Christiano now knows well.

More information

Angela M. Christiano, PhD, is the Richard and Mildred Rhodebeck Professor of Dermatology, vice chair of research in the Department of Dermatology, and professor of genetics & development at Columbia University Vagelos College of Physicians and Surgeons. She also serves as an Advisory Dean for Basic Science Faculty. In 2020, Christiano was elected to the National Academy of Sciences.

Raphael Clynes, MD, PhD is currently vice president of translational biology at Xencor Inc.

Julian Mackay-Wiggan, MD, MPH, is currently in practice in the Siperstein Dermatology Group. 

Angela Christiano and Raphael Clynes are co-inventors on several patents filed by Columbia University on the use of JAK inhibitors in treating hair loss disorders, which have been licensed to Aclaris Therapeutics, Inc. Angela Christiano is a shareholder of Aclaris Therapeutics, Inc. and has served as a consultant/scientific advisor for Arcutis Biotherapeutics, Inc., Almirall, S.A., Aclaris Therapeutics, Inc., Bioniz Therapeutics, Inc., Dermira, Inc., Intrinsic Medicine, Inc., Janssen Pharmaceuticals, Inc., and Pfizer, Inc. She is a shareholder of Intrinsic Medicine, Inc., has received research grant support from Bristol-Myers Squibb, Inc., Pfizer, Inc., and Sanofi Genzyme S.A. and serves on/chairs the scientific advisory boards for the Dystrophic EB Research Association of America and the National Alopecia Areata Foundation. She previously served as president of the Society for Investigative Dermatology and currently serves as president of the American Hair Research Society. She is a scientific co-founder of Rapunzel Bioscience.

To revisit this article, visit My Profile, then View saved stories .

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Simar Bajaj

This Follicle-Hacking Drug Could One Day Treat Baldness

Alopecia Areata

Denise Jones quit her job because she was losing her hair. Diagnosed with the autoimmune disease alopecia areata , she saw her hair falling out in patches, bald spots dotting her scalp. The snarky comments and backhanded compliments had already started at her workplace, and she wasn’t sure how much more she could take. So she left.

According to her physician, Luis Garza, a professor of dermatology at Johns Hopkins University School of Medicine in the US, Denise (whose name has been changed to protect her privacy) is far from alone in experiencing stress and anxiety over hair loss. Hair, he explains, is a fundamental aspect of identity, deeply intertwined with our body image and sense of self. That’s why baldness can, quite literally, change a person’s life.

Yet despite more than 50 percent of women and 85 percent of men in the US experiencing balding during their lives, there still aren’t effective treatments for hair loss. “None of them work really well,” Garza says. For common baldness, the two drugs approved by the US Food and Drug Administration (FDA)—finasteride and minoxidil—promote hair growth only slightly, must be used daily, and can cause side effects like depression and decreased libido . Another popular option is hair transplantation, where hair follicles are moved from one part of the scalp to another. But the procedure is invasive, expensive (costing $4,000 to $15,000 out of pocket in the US), and limited by how much hair can be moved. Given these lackluster options, most people can’t do anything meaningful about their hair loss.

But that may soon change. In a study published in Developmental Cell last month, Maksim Plikus, professor of developmental and cell biology at the University of California, Irvine, and chief scientific officer of hair biotech company Amplifica, uncovered the role of a potent signaling molecule called SCUBE3. This protein might reshape how physicians approach baldness.

With its roughly half a million hair follicles, you can think of your scalp as a gigafactory of 3D printers. According to Plikus, nearly all these follicles need to be constantly “printing” in order to create a full mop of hair. But in common baldness, these printers start shutting down, leading to hair thinning (if roughly 50 percent have switched off) and balding (when more than 70 percent are off). By activating stem cells present in people’s scalps, SCUBE3 hacks hair follicles to restart the production line and promote rapid growth.

Plikus’ research began because he wanted to better understand dermal papilla cells, which are located at the bottom of hair follicles. It’s notoriously difficult to experiment with them, so to learn more about how they work, his team used a genetic tool to target a signaling pathway (a series of molecular reactions that involve certain proteins) that these cells use to drive hair growth. The goal was to get this pathway, in a set of hairless mice, to stay always switched on. Once he and his team got the tool to work, the genetically modified mice started rapidly growing hair.

But Plikus and his team didn’t know what exactly in this pathway was driving growth, so using single-cell RNA sequencing—a technique that lets you see what genes are active in a cell, and thus what proteins are being created—they compared cells from the genetically modified mice and control mice. They found that SCUBE3 was being expressed in the mutant mice but not in the controls. That didn’t mean anything on its own, however, because SCUBE3 could’ve just been a bystander molecule. So they performed a series of experiments with this protein, first deleting it from mice, then injecting it into normal mice, and then injecting it into mice with human hair follicles grafted to their skins. These all showed that SCUBE3 drives hair growth and, crucially with the last experiment, human hair growth.

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Blue microbeads soaked in SCUBE3 protein induce new hair growth in mice . No hair growth is seen around microbeads...

While Plikus recognizes that much work is needed to go from mouse models to an FDA-approved treatment, he’s already envisioning a future in which patients might go to their dermatologist to get SCUBE3 microinjected into their scalps. “You have a patient sitting in a dentist-like chair, they close their eyes, and then you go tch, tch, tch, tch ,” Plikus says as he mimics a syringe being pressed into the patient’s head. SCUBE3 would be dispensed less than a millimeter deep, with only micrograms needed, so the procedure would be short (under 20 minutes) and fairly painless, he predicts.

The cost might be similar to Botox, so not cheap, but certainly less expensive than a hair transplant. In addition, the therapy would probably need to be repeated two or three times a year to ensure continued hair growth. “Pharma would love the model,” Plikus says, because booster therapy is an attractive mix of real efficacy and repeat customers; the popularity of Botox and dermal fillers demonstrates this well. If things take off, SCUBE3 would also be easy to scale, given that culturing proteins is cheap and already widely done, as it is for insulin.

“I think it’s a realistic vision,” says Maria Kasper, associate professor of cell and molecular biology at the Karolinska Institute in Sweden. However, she emphasizes that it’s too early to say whether Plikus’ findings will lead to a new treatment for hair loss and notes that alternative therapeutic approaches are being developed as well.

Turn Biotechnologies, for instance, is developing a treatment that uses messenger RNA (mRNA), following the same basic principles as the Pfizer and Moderna Covid vaccines—delivering genetic instructions to our cells to have them build useful substances. According to cofounder Vittorio Sebastiano, an associate professor of obstetrics and gynecology at Stanford University in the US, Turn’s goal is to deliver mRNA encoding for a cocktail of proteins that can turn back the clock on hair follicles. Their treatment, TRN-001, would be delivered to follicles inside liquid nanoparticles and help reset stem cells there, making the follicles functionally younger. “I would be happy to get my hair back to when I was 30,” Sebastiano jokes, “so that would be 15 years of rejuvenation.”

Sebastiano is hoping to start clinical trials in humans by the end of next year or early 2024, envisioning a future in which TRN-001 is applied topically with microinjections, much like Plikus imagines for SCUBE3. But while an mRNA-based approach might be more potent, since it forces cells to make relevant proteins themselves, Sebastiano recognizes that this technology’s newness makes the cost and periodicity of treatment difficult to predict and the regulatory landscape more challenging.

In fact, Kevin McElwee, associate professor of dermatology at the University of British Columbia in Canada and chief scientific officer of hair biotech company RepliCel, says that’s why his team isn’t going down the mRNA route: “the regulatory issues with the FDA are huge.” Instead, RepliCel—and a competitor, HairClone—are working on a cell-based approach to baldness, where hair cells from one part of the scalp are moved to another in order to kickstart growth. First, hair follicles are harvested from the back of a person’s scalp, then the relevant cells (dermal papilla cells for HairClone, dermal sheath cup cells for RepliCel) are dissected out and cultured, and finally these multiplied cells are microinjected into a person’s balding head. Some of these cells are also cryopreserved for future injections.

“The problem with hair transplantation is that it’s one for one; you still have the same number of hairs, just spread out,” says HairClone CEO Paul Kemp. With these multiplying techniques, you can instead increase the volume of hair. However, Kemp and McElwee both estimate that for the patient, the process might take one to two months from start to finish and, at least initially, cost more than hair transplants, given the manual labor involved. But this treatment might also be more successful, Kemp says, because “it’s a personalized cell therapy, unlike Plikus’ approach, which is a one-size-fits-all.” RepliCel’s therapy has begun to be tested in patients in Japan, while HairClone hopes to start human trials in the UK by early 2023; both countries have more flexible clinical trial requirements than the US.

Nonetheless, whether it’s with molecular, RNA, or cell-based approaches, new hair-loss treatments are coming soon. It’s just impossible to know when. “Despite decades of trying, it’s always that the next therapy for hair loss is five years away,” Garza jokes. The problem is the “valley of death” between preclinical studies and commercialization, where hair biotech companies have long crashed and burned, he says, because baldness is so poorly understood—to this day. “They’re trying to build skyscrapers in a swamp.”

Kasper emphasizes the need for basic scientific research to establish a stronger foundation. Her lab at the Karolinska Institute, for instance, studies how to make new hair follicles inside skin—from scratch—which is an admittedly more challenging question than how to hack existing follicles. Beyond offering opportunities to better understand hair biology, this research emphasizes the complexity of hair loss: SCUBE3, TRN-001, and cloned cells can’t help patients who don’t have hair follicles in the first place. The only way to help such patients, who may have burns, large wounds, or scarring alopecia , is with new follicles.

In all likelihood, none of these are going to be a magic bullet. Instead, the future is probably one of multiple treatments used together, each with complementary strengths and limitations. But Garza would be happy with even just one, because in the therapeutic black hole of baldness, his patients are becoming increasingly desperate and helpless. “The state of art is terrible right now,” he says.

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Researchers develop a new way to safely boost immune cells to fight cancer

Researchers in Virginia Tech’s College of Engineering have developed a new cancer immunotherapy to localize cancer-killing cytokines in tumors to improve treatment effectiveness.

  • Hailey Wade

19 Apr 2024

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Five researchers looking at results on a computer.

Cancer is the monster of our society. Last year alone, more than 600,000 people in the United States died from cancer, according to the American Cancer Society . The relentless pursuit of understanding this complex disease has shaped medical progress on developing treatment procedures that are less invasive while still highly effective. 

Immunotherapy is on the rise as a possible solution. Immunotherapy involves harnessing the power of the body’s immune system to fight against cancer cells. Researchers in the College of Engineering have found a way to revamp a treatment procedure into a groundbreaking practice.

Rong Tong , associate professor in  chemical engineering , has teamed up with Wenjun "Rebecca" Cai , associate professor in  materials science and engineering , to explore a cancer immunotherapy treatment that has long been of interest to researchers. In their newly published article in the journal Science Advances , Tong and Cai detailed their approach, which involves activating the immune cells in the body and reprogramming them to attack and destroy the cancer cells. This therapeutic method is frequently implemented with the protein cytokine. Cytokines are small protein molecules that act as intercellular biochemical messengers and are released by the body's immune cells to coordinate their response.

“Cytokines are potent and highly effective at stimulating the immune cells to eliminate cancer cells,” Tong said. “The problem is they’re so potent that if they roam freely throughout the body, they’ll activate every immune cell they encounter, which can cause an overactive immune response and potentially fatal side effects.”

Tong and Cai, in collaboration with chemical engineering and materials science and engineering graduate students, have developed an innovative approach to employ cytokine proteins as a potential immunotherapy treatment. Unlike previous methods, their technique ensures that the immune cell stimulating cytokines effectively localize within the tumors for weeks while preserving the cytokine’s structure and reactivity levels. 

Combining forces to take down cancer cells

Current cancer treatments, such as chemotherapy, cannot distinguish between healthy cells and cancer cells. When someone with cancer is treated with chemotherapy, the treatment attacks all of the cells in their body, which can lead to side effects such as hair loss and fatigue. Stimulating the body’s immune system to attack tumors is a promising alternative to treat cancer. The delivery of cytokines can jump-start immune cells in the tumor, but overstimulating healthy cells can cause severe side effects.

“Scientists determined a while ago that cytokines can be used to activate and fight against tumors, but they didn’t know how to localize them inside the tumor while not exposing toxicity to the rest of the body,” said Tong. “Chemical engineers can look at this from an engineering approach and use their knowledge to help refine and elevate the effectiveness of the cytokines so they can work inside the body effectively.” 

The research team’s goal is to find a balance between killing cancer cells in the body while sparing healthy cells. 

To accomplish this goal, Tong and his students used their expertise to create specialized particles with distinctive sizes that help determine where the drug is going. These microparticles are designed to stay within the tumor environment after being injected into the body. Cai and her students worked on measuring these particles’ surface properties.

“In the field of materials science and engineering, we study the surface chemistry and mechanical behavior of materials, such as the specialized particle created for this project,” Cai said. “Surface engineering and characterization, along with particle size, play important roles in controlled drug delivery, ensuring prolonged drug presence and sustained therapeutic effectiveness.”

To ensure successful drug delivery, Tong and his chemical engineering students designed a novel strategy that: 

  • Anchors cytokines to these new microparticles, limiting the harm of cytokines to healthy cells
  • Allows the newly particle-anchored cytokines to jump-start immune systems and recruit immune cells to attack cancer cells

“Our strategy not only minimizes cytokine-induced harm to healthy cells, but also prolongs cytokine retention within the tumor,” Tong said. “This helps facilitate the recruitment of immune cells for targeted tumor attack.”

The next step in the process involves combining the new, localized cytokine therapy method with commercially available, Food and Drug Administration (FDA)-approved checkpoint blockade antibodies, which reactivate the tumor immune cells that have been silenced so they can fight back the cancer cells. 

“When there is a tumor inside the body, the body’s immune cells are being deactivated by the cancer cells,” Tong explained. “The FDA-approved checkpoint blocking antibody helps “take off the brakes” that tumors put on immune cells, while the cytokine molecules “step on the gas” to jump-start the immune system and get an immune cell army to fight cancer cells. These two approaches work together to activate immune cells.”

Combining the checkpoint antibodies with the particle-anchored cytokine proved to successfully eliminate many tumors in their study.

Five researchers posing together in a lab.

Engineering an impact on cancer treatment

Team members hope their impact on immunotherapy treatment is part of a greater movement toward cancer treatment approaches that are harmless to healthy cells. The new approach of attaching cytokines to particles also could be used in the future to deliver other types of immunostimulatory drugs, according to the team.

“Researchers are still looking for safer and more effective cancer treatments,” said Tong. “This motivation is what drives us to develop new technologies in the field. The whole class of drugs that are employed to jump-start the immune system to fight cancer cells has largely not yet succeeded. Our goal is to create novel solutions that allow researchers to test these drugs with existing FDA-approved therapeutics, ensuring both safety and enhanced efficacy.”

Cai said the nature of cancer treatment research requires expertise across engineering disciplines. 

“I view this project as a perfect marriage between chemical engineering and materials science,” Cai said. “The former focuses on the synthesis and drug delivery part, the latter on applying advanced materials characterization. This collaboration not only accelerates immunotherapy research, but also has the ability to transform cancer treatment.”

Chelsea Seeber


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Baldness Breakthrough: microRNA Stimulates Hair Growth in Aging Follicles

By Northwestern University June 8, 2023

Northwestern Medicine scientists found that the stiffness of aging hair follicle stem cells hinders hair growth. They discovered that softening these cells using a tiny RNA, miR-205, stimulates hair growth in mice. Future experiments will test whether topically delivered miR-205 can promote hair growth potentially in humans.

Softening stiff hair follicle stem cells with a microRNA regrows hair.

  • Regulating cell mechanics stimulates hair growth in mice
  • Next step will be testing if delivering microRNA via nanoparticles grows hair
  • Potential for human hair growth

Just as people’s joints can get stiff as they age and make it harder for them to move around, hair follicle stem cells also get stiff, making it harder for them to grow hair, reports a new Northwestern Medicine study.

But if the hair follicle’s stem cells are softened, they are more likely to produce hair, the scientists found.

Northwestern scientists discovered how to soften up those stem cells to enable them to grow hair again. In a study in mice published recently in the journal PNAS , the investigators report that they can soften the stem cells by boosting the production of a tiny RNA , miR-205, that relaxes the hardness of the cells. When scientists genetically manipulated the stem cells to produce more miR-205, it promoted hair growth in young and old mice. 

“They started to grow hair in 10 days,” said corresponding author Rui Yi, the Paul E. Steiner Research Professor of Pathology and professor of dermatology at Northwestern University Feinberg School of Medicine. “These are not new stem cells being generated. We are stimulating the existing stem cells to grow hair. A lot of times we still have stem cells, but they may not be able to generate the hair.

“Our study demonstrates the possibility of stimulating hair growth by regulating cell mechanics. Because of the potential to deliver microRNA by nanoparticles directly into the skin, next we will test whether topically delivered miR-205 can stimulate hair growth first in mice. If successful, we will design experiments to test whether this microRNA can promote hair growth potentially in humans.”

This study was conducted in genetically engineered mouse models. The scientists used advanced microscopy tools, including atomic force microscopy, to measure the stiffness and two- photon microscopy to monitor cell behaviors in live animals.

Reference: “MicroRNA-205 promotes hair regeneration by modulating mechanical properties of hair follicle stem cells” by Jingjing Wang, Yuheng Fu, Wenmao Huang, Ritusree Biswas, Avinanda Banerjee, Joshua A. Broussard, Zhihai Zhao, Dongmei Wang, Glen Bjerke, Srikala Raghavan, Jie Yan, Kathleen J. Green and Rui Yi, 22 May 2023, Proceedings of the National Academy of Sciences . DOI: 10.1073/pnas.2220635120

Other Northwestern authors include Jingjing Wang, Yuheng Fu, and Kathleen Green.

This study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases grants AR066703, AR071435, AR043380, AR041836, and P30AR075049 of the National Institutes of Health .

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13 comments on "baldness breakthrough: microrna stimulates hair growth in aging follicles".

new research for baldness

So there is hope for me I am 73 yrs old totally bald exactly like Benjamin Franklin.

new research for baldness

If one wants his hair grow again after developing baldness,what does he need to overcome this and how long does it last without again having same occurrence.

And how much it costs ?

new research for baldness

So they show a guy with a full head of shortly cut hair “regrow” his hair. Ok. Whatever.

new research for baldness

It’s a bad choice for a visual aid seeing as how it hasn’t been tested on humans yet but, obviously, it’s because they haven’t tested it on humans yet. Didn’t you read the article you’re commenting on?

new research for baldness

I would like more information on any products or procedures that help men with baldness

new research for baldness

Same thing happens when you push a turd out real hard…

new research for baldness

why are we testing it on mice? They are physiologically different. This isn’t even available for humans so why publish it? what about head injury follicles Or follicles that have been damaged by surgery? Can’t grow that back. I’d rather be bald than regrow grey hair. In my case silver. I blame the sugar industry!

new research for baldness

Im m2f 44 year old was bold at 28 started hrt my 2013 surgery 2018. I use finasteride estradiol17valerat divigel and spironololactone, wich made my hair perfect, as i was 16

new research for baldness

My hair just won’t grow since I was a child and if it grow it broke off an makes holes here and there can u please help me

Who cares I’ve never had a woman ask me for more hair

new research for baldness

BS. Mice !!

new research for baldness

Sure,Mam;I would like to have someone contact me at# 843-227-3307, thank you.

new research for baldness

Would like to join the study

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Male baldness is often trivialised – our research shows it should be taken seriously

new research for baldness


new research for baldness

By Paul Hodkinson , Matthew Hall3

Friday, April 26, 2024 1:29 AM UTC

Male pattern baldness, or hereditary hair loss, has not always been taken seriously. Celebrity hair loss and transplants are greeted with fascinated amusement while, in popular media, bald men have often been absent , mocked or maligned .

The everyday lives of ordinary balding men are often punctuated by comments, jokes and an expectation to laugh along.

Hereditary hair loss can occur any time after puberty and two thirds of men are affected by the time they’re 60. Social pressures and beauty ideals prompt many to turn to the multi-billion dollar hair loss industry, amid moves to medicalise baldness . But studies that examine the detail of men’s experiences of going bald remain sparse.

Our Journeys of Hair Loss research involved in-depth interviews with 34 men of different ages and backgrounds. It highlights why the challenges balding men can face should be taken seriously — and not only by those seeking to profit from them.

Negative emotions

Experiences varied among the men we interviewed, but it was clear that most felt hair loss had been negative overall, and many described moments or periods of emotional struggle.

upset middle aged man with alopecia looking at mirror

Most interviewees felt hair loss had been negative experience overall. cunaplus/Shutterstock

Balding could often be accompanied by a sense of loss, or the development of social anxieties. The process could be particularly challenging for younger men, those who were single, those experiencing other life struggles, or those connected to cultures that placed high value on appearance and grooming, including some gay participants.

Sometimes, attempts to hide hair loss came to dominate everyday life. Constant adjusting of hair, avoiding being viewed from particular angles, and careful negotiating of weather and lighting conditions could be accompanied by ever present worry. As Nick* explained:

If it’s windy, I’m thinking I need to have a look … I’ve not looked at my hair for a little while, is there a mirror? It’s something I’m looking at more and more.

Hair loss treatment

Encounters with the hair loss industry were mixed. Some pointed towards the hope or relief that medical treatments, such as finasteride or hair transplants, could provide. Many, though, regarded this level of intervention as unfeasible, or undesirable.

Topical treatments such as oils and caffeinated shampoos were more commonly tried, but many struggled with cycles of false hope. Ishaan* said he was “fooling himself” into thinking it was actually helping" and that checking for results “becomes obsessive because you want to see a difference”.

Advertising for treatments could also contribute to anxiety, particularly where men found themselves repeatedly targeted by algorithmic ads. Awareness about baldness and treatments varied strikingly, with reliable, non-commercial information sometimes difficult to find.

Talk and humour

“Serious” talk with others about the emotional challenges of hair loss was unusual. This may partly have reflected longstanding masculine difficulties with opening up about struggles. However, some men conveyed a more specific sense that baldness was not a legitimate subject for seeking support.

Marcus* explained how baldness struggles “are not a thing we are open about”, noting that “if somebody was to talk about depressive thoughts, anxiety, self-harm, these are all things that are accepted…but I’d never lump baldness into that”.

Interaction with others about hair loss, then, more often took the form of jokes and teasing. Some welcomed how jokes could bring their hair loss into the open, and even made self-depreciating jokes themselves. Others, though, found jokes hurtful, or felt under pressure to laugh at themselves.

Bald men can receive comments, nicknames or even unwanted physical attention.

Many men felt they had come to accept their hair loss over time, whether through gradual adjustment or dramatic moments of intervention. For some, shaving their head for the first time felt like a key moment where struggles or worries were brought under control.

David* was left wondering why he hadn’t taken the step earlier: “I remember seeing the results and I was like, why did I not do this five years ago? It was just relief.”

Acceptance of baldness often entailed genuine relief from struggles to live up to dominant beauty ideals, and could act as a form of resistance against the hair loss industry discourse and medicalisation . Acceptance often had limits, though; feelings could fluctuate and many noted that, were a cost-free “magic solution” to appear, they still might be tempted.

Moving forward, men experiencing hair loss would benefit from compassion, support and trustworthy information as they navigate competing social pressures. Taking their experiences seriously might offer a valuable starting point.

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new research for baldness

Are you losing your hair? A dermatologist breaks down some FAQs.

If you’ve noticed an excessive amount of hair shedding , a receding hairline, or that the hair on the crown of your head becoming increasingly sparse, you’re probably experiencing a form of hair loss. Losing your hair can be a distressing experience, but you’re not alone.

Understanding the underlying cause of your hair loss is absolutely necessary in determining the best approach to halt and reverse any further damage to your hair and scalp. Individualized treatment is key, and to break down the reasons you might be experiencing hair loss, USA TODAY spoke with Dr. Oma Agbai , MD, a board-certified dermatologist and director of Multicultural Dermatology and Hair Loss Disorders at UC Davis.

Why am I losing my hair?

According to the American Academy of Dermatology, it’s completely normal to shed anywhere between 50 to 100 strands of hair per day. However, if you’ve noticed more strands falling out of your head than normal, you may be experiencing alopecia , the medical term for hair loss. Common diagnoses include androgenetic alopecia, alopecia areata, telogen effluvium, and lymphocytic scarring alopecia, Agbai tells USA TODAY.

There are several reasons why you might be losing your hair. According to Agbai, genetics, hormonal shifts, stress, underlying medical conditions, nutritional deficiencies, and scalp inflammation are notable factors. 

What is baldness?

Androgenetic alopecia, also known as male pattern or female pattern baldness, is one of the most common types of hair loss, Agbai says. “The term ‘baldness’ implies that hair has thinned to the point of having an abnormally-visible scalp.” she says. “Not everyone with hair loss experiences baldness,” but “baldness can occur in severe cases.”

Baldness is often hereditary, and is activated by a shift in your hormones. If you’re experiencing elevated levels of the hormone dihydrotestosterone (DHT), your body will respond by shrinking your hair follicles and reducing the length of the hair growth cycle, according to Cleveland Clinic.

Agbai further explains that the “miniaturization” of hair follicles contributes to the “thinning of the hair shaft and eventual hair loss.” Male pattern baldness is typically characterized by a receding hairline, and the thinning of hair on the crown. People experiencing female pattern baldness may also notice a general thinning of hair on the top of your head, but hair loss typically won’t occur on the front of your scalp, per Harvard Health. 

What other common types of hair loss are there?

According to Healthline, other common types of alopecia include traction alopecia, telogen effluvium, alopecia areata, central centrifugal cicatricial alopecia (CCCA), and lichen planopilaris (LPP). 

Traction alopecia is the result of environmental factors, such as wearing your hair in tight hairstyles, Agbai says. Telogen effluvium refers to the excessive shedding of hair follicles, and it occurs when hair follicles prematurely skip to the end of the hair growth cycle, she adds. 

Alopecia areata is an autoimmune condition that is characterized by “round patches of hair loss on the scalp,” although it can occur elsewhere on the body, Agbai says. While the exact reason for this type of hair loss is unknown, it is generally understood that “the immune system mistakenly attacks hair follicles, leading to hair loss,” she adds.

CCCA and LPP fall under the umbrella of lymphocytic scarring alopecia. The telltale signs of  these conditions are chronic inflammation of the scalp and the scarring of hair follicles, which can result in irreversible hair loss, Agbai notes.  

How do I know which type of hair loss I have?

Hair loss is often the result of both genetic and environmental factors, so “understanding the complexities of hair loss means realizing the different types of hair loss may not fit neatly into categories,” Agbai says. It’s also possible to experience two forms of alopecia at the same time. “Each type of hair loss needs its own diagnosis and treatment, even if they're happening in the same person.”

Got thin hair? You're not alone. A primer on how to get thicker hair.

On the whole, it’s important that you speak with your doctor about any symptoms you’re experiencing. A dermatologist can provide a proper diagnosis, and select a personalized treatment that will help restore health to you hair and scalp. 

New study offers hope for a rare and devastating eye cancer

new research for baldness

After more than a decade studying a rare eye cancer that produces some of the hardest-to-fight tumors, researchers from University of Pittsburgh Medical Center have found a treatment that works on some patients and, more importantly, a tool that can predict when it is likely to succeed.

The work, published in Nature Communications, is being validated in a clinical trial involving at least 30 patients. It could pave the way for similar methods designed to overcome one of the enduring frustrations of cancer care.

Because tumors differ, not only between patients but even inside the same patient, a treatment that works on one mass may fail on another, even when both are of the same cancer type.

The researchers in Pittsburgh tackled this problem in uveal melanoma, an eye cancer that afflicts only 5 people in a million, but that half the time spreads to other parts of the body, often the liver. The median survival once uveal melanoma has spread has been less than seven months, according to a 2018 study in the journal JAMA Ophthalmology.

“We chose this because it was one of the only cancers that 10 years ago when we started, there was nothing approved for it,” said Udai Kammula, who led the study and directs the Solid Tumor Cell Therapy Program at UPMC Hillman Cancer Center in Pittsburgh.

Scientists had long speculated that the reason uveal melanoma is so tough to fight is that something helps the tumor keep out T cells, a key part of the body’s immune system that develops in bone marrow. However, previous studies by Kammula and his colleagues showed that uveal melanoma tumors actually have T cells inside, and they are turned on.

The problem? The cells lie dormant instead of multiplying and reaching numbers large enough to overwhelm the tumor.

The culprit appears to reside somewhere inside the tumor’s ecosystem of cells, molecules and blood vessels, known formally as the tumor’s “microenvironment.” Kammula compares this ecosystem to the infrastructure that supports a city. Something in that infrastructure helps protect uveal melanoma tumors by preventing the critical T cells from multiplying.

“Ultimately, if we’re going to get rid of cancer, we have to get rid of this infrastructure,” Kammula said.

A tool for predicting success

He and his colleagues have had some success using a treatment known as adoptive cell therapy, which was developed in the 1980s by Steven Rosenberg at the National Institutes of Health.

The treatment involves removing the T cells from the tumor, where they have been unable to proliferate. Scientists then take those T cells and grow them outside the body in a lab dish. They treat patients with chemotherapy to kill off the last of their old immune systems. Finally, they reinfuse the lab-grown T cells into the patient’s blood stream and the cells, now in much greater numbers, go on to attack the tumor.

In this treatment, the T cells are often referred to as tumor-infiltrating leukocytes, or TILs.

Kammula said his team has found that tumors shrink partially or completely in about 35 percent of patients who receive the treatment. But they wanted to know why it doesn’t work in the majority of cases, and whether there might be some way to predict beforehand when it will succeed.

To find out, the researchers analyzed samples from 100 different uveal melanoma tumors that had spread to different parts of the body in 84 patients, seeking to examine all of the tumors’ genetic material.

“We basically put the tumor biopsy in a blender that had the stroma [supportive tissue], the blood vessels, the immune cells, the tumor cells. It had everything,” Kammula said, explaining that they then analyzed all of the tumor’s genetic material.

They found 2,394 genes that could have helped make the tumor susceptible to treatment, some of them genes that experts would regard as “the usual suspects” and others that were unexpected. Using this long list of genes, the scientists searched for characteristics that they shared.

The genes were predominantly involved in helping the body defend itself against viruses, bacteria and other foreign invaders by removing the invaders and helping tissue heal. Kammula and the study’s lead author, Shravan Leonard-Murali, a postdoctoral fellow in the lab, used the different activity levels of these genes to develop a clinical tool.

The tool, known as a biomarker, assigns a score to a uveal melanoma tumor based on the likelihood that it will respond well to the treatment ― removing T cells, growing them outside the body, then reinfusing them.

So far, Kammula said, the biomarker has been “extremely good,” in predicting when the treatment will be effective, though he added, “these findings will need confirmation in the current ongoing clinical trial.”

“I thought it was somewhat of a tour de force, honestly,” said Eric Tran, an associate member of the Earle A. Chiles Research Institute, a division of Providence Cancer Institute in Portland, Ore. Tran did not participate in the study.

He said that while it will be important to validate these results, “I was certainly encouraged by their studies. And from my perspective, I wonder if that sort of strategy can be deployed in other cancers.”

Ryan J. Sullivan, an oncologist at Massachusetts General Hospital and associate professor at Harvard Medical School who was not involved in the study, called the team’s work “timely” and said “it is even more significant that they appear to have a [tool] that appears to predict which patients will benefit.”

The team at UPMC is already investigating possible wider application of both the treatment and the biomarker in a second clinical trial that involves a dozen different cancers.

new research for baldness


Breakthrough in brown fat research: Researchers have found brown fat's 'off-switch'

Brown fat, also known as brown adipose tissue (BAT), is a type of fat in our bodies that's different from the white fat around our belly and thighs that we are more familiar with. Brown fat has a special job -- it helps to burn calories from the foods that we eat into heat, which can be helpful, especially when we're exposed to cold temperatures like during winter swimming or cryotherapy. For a long time, scientists thought that only small animals like mice and newborns had brown fat. But new research shows that a certain number of adults maintain their brown fat throughout life. Because brown fat is so good at burning calories, scientists are trying to find ways to activate it safely using drugs that boost its heat-producing abilities.

A new study from the research groups of Prof. Jan-Wilhelm Kornfeld from the University of Southern Denmark/the Novo Nordisk Center for Adipocyte Signaling (Adiposign) and Dagmar Wachten from the University Hospital Bonn and the University of Bonn (Germany) has found that brown fat has a previously unknown built-in mechanism that switches it off shortly after being activated. This limits its effectiveness as treatment against obesity. According to first author of the study, Hande Topel, who is a Senior Postdoc at the University of Southern Denmark and the Novo Nordisk Center for Adipocyte Signaling (Adiposign), the team has now discovered a protein responsible for this switching-off process. It is called 'AC3-AT'.

Blocking the "off switch" opens up a new strategy

"Looking ahead, we think that finding ways to block AC3-AT could be a promising strategy for safely activating brown fat and tackling obesity and related health problems," Hande Topel says. The research team found the switch-off protein using advanced technology predicting unknown proteins. Hande Topel explains: "When we investigated mice that genetically didn't have AC3-AT, we found that they were protected from becoming obese, partly because their bodies were simply better at burning off calories and were able to increase their metabolic rates through activating brown fat."

Two groups of mice were fed a high-fat diet for 15 weeks, which rendered them obese. The group that had their AC3-AT protein removed, gained less weight than the control group and were metabolically healthier. "The mice that have no AC3-AT protein, also accumulated less fat in their body and increased their lean mass when compared to the control mice," says co-author, Ronja Kardinal, who is a PhD student at the University of Bonn in the lab of Dagmar Wachten at UKB, continuing: "As AC3-AT is found not only in mice but also in humans and other species, there are direct therapeutic implications for humans."

Hope for strategies that support weight loss

Although the prevalence of brown fat decreases as humans age, and despite grown-ups not having as much brown fat as newborns, it can still be activated, for instance by cold exposure. When it gets activated, it enhances the rate of metabolism of these individuals, which again may help to stabilize weight loss in conditions where calorie intake is (too) high.

Intriguingly, this study not only identified AC3-AT, which is a shorter, previously unknown form of the AC3protein. The researchers also identified other unknown protein/gene versions, that respond to cold exposure, similar to AC3-AT.

"However, further research is needed to elucidate the therapeutic impact of these alternative gene products and their regulatory mechanisms during BAT activation," says co-corresponding author Prof. Dagmar Wachten, Co-Director of the Institute of Innate Immunity at the UKB and member of the Cluster of Excellence ImmunoSensation2 and the Transdisciplinary Research Areas (TRA) "Modelling" and "Life & Health" at the University of Bonn.

"Understanding these kinds of molecular mechanisms not only sheds light on the regulation of brown fat but also holds promise for unraveling similar mechanisms in other cellular pathways. This knowledge can be instrumental in advancing our understanding of various diseases and in the development of novel treatments," says co-corresponding author Prof. Jan-Wilhelm Kornfeld, University of Southern Denmark.

This study was conducted in the context of the DFG Collaborative Research Center Transregio-SFB 333 "Brown and Beige Fat -- Organ Interactions, Signaling Pathways and Energy Balance (BATenergy)," which is pursuing a better understanding of the different types of adipose tissue and their role in metabolic diseases and the Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign) at University of Southern Denmark that aims to understand fat cell dysfunction in model organisms and obese patients.

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Story Source:

Materials provided by University of Southern Denmark . Original written by Birgitte Svennevig. Note: Content may be edited for style and length.

Journal Reference :

  • Sajjad Khani, Hande Topel, Ronja Kardinal, Ana Rita Tavanez, Ajeetha Josephrajan, Bjørk Ditlev Marcher Larsen, Michael James Gaudry, Philipp Leyendecker, Nadia Meincke Egedal, Aylin Seren Güller, Natasa Stanic, Phillip M. M. Ruppert, Isabella Gaziano, Nils Rouven Hansmeier, Elena Schmidt, Paul Klemm, Lara-Marie Vagliano, Rainer Stahl, Fraser Duthie, Jens-Henning Krause, Ana Bici, Christoph Andreas Engelhard, Sabrina Gohlke, Peter Frommolt, Thorsten Gnad, Alvaro Rada-Iglesias, Marta Pradas-Juni, Tim Julius Schulz, Frank Thomas Wunderlich, Alexander Pfeifer, Alexander Bartelt, Martin Jastroch, Dagmar Wachten, Jan-Wilhelm Kornfeld. Cold-induced expression of a truncated adenylyl cyclase 3 acts as rheostat to brown fat function . Nature Metabolism , 2024; DOI: 10.1038/s42255-024-01033-8

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