Tag Archives: clinical

The FDA finally approved a condom for anal sex. Here’s why it’s a good thing

Whether you’re in a committed relationship or prone to the throws of lust (or both, we’re not judging), you need to protect yourself and your partner — which usually means using a condom.

Still, as humans tend to be, we’re not always careful. We like to experiment, we sometimes falter — and pick up sexually-transmitted diseases (STDs). Whatever the reason, condoms are a great way to stay safe and can be used by people of the appropriate age just about anywhere–and they can also be lots of fun. Now, there’s a new type of condom on the block.

A victory for all genders and denominations

There’s never been an approved condom specifically for anal intercourse. Until now, condoms on the market were only approved for vaginal intercourse, which omits a large section of our society.

Condoms for vaginal sex currently on the market are recommended for use during anal or oral intercourse by the Center for Disease Control – meaning they’re legally backed by a drug agency for one activity and informally deemed effective for another in what is known as ‘off-label’ use. But the US Food and Drug Administration (USFDA) has finally approved the first condom for anal sex: the ONE Male Condom.

The approval is seen as a victory for sexual health and especially important for the LGBTQ community, who, until now, have not had a condom aimed specifically at them. Courtney Lias, director of the USFDA’s Office of GastroRenal, Obstetrics-Gynecological, General Hospital, and Urology Devices, says:

“The risk of STI transmission during anal intercourse is significantly higher than during vaginal intercourse. The FDA’s authorization of a condom that is specifically indicated, evaluated, and labeled for anal intercourse may improve the likelihood of condom use during anal intercourse.” 

What’s different with this condom

The newly approved condom is a natural rubber latex sheath that covers the penis. It’s available in three different versions: standard, thin and fitted. The fitted condoms, available in 54 different sizes, incorporate a paper template to find the best condom size for each user to minimize leakage. Global Protection Corp, which makes the condom, stresses that during anal intercourse, users should employ a compatible lubricant with their condom and all other brands.

“We want people to have lots of sex — but we also want them to be empowered and informed,” said Davin Wedel, president of Global Protection Corp.

Scientists studied the safety and efficacy of the condom in a clinical trial comprised of 252 men who prefer sex with men and 252 men who prefer intercourse with women. All volunteers were between 18 and 54 years of age. 

Results show the total condom failure rate was 0.68% for anal sex and 1.89% for vaginal intercourse. Researchers defined the condom failure rate as the number of slippages, breakage, or both slippage and breakage events over the total number of sex acts recorded in a diary by participants.

Disappointingly, the trial didn’t calculate the STD baseline as too many variables (such as not wearing a condom) could cause infection during the trial. Therefore, the rate of STDs was not measured at the beginning of the study and compared with later data. Despite this, the trial center did allow participants to self-report any genital-based infections which could have resulted from the use of a different condom brand before or during tests.

The researchers from Emory University who were behind the study said an essential reason for the trial’s success was that volunteers used lubricant, which prevents slippage and breakage, and the inclusion of instructions.

Taken together, these findings suggest that health bodies should provide lubricant along with the billions of condoms distributed as part of HIV and STD prevention efforts to minimize failure. 

The USFDA will help get more condoms like these on the market

The USFDA is responsible for controlling and supervising food, tobacco, dietary supplements, prescription drugs, blood transfusions, medical devices, cosmetics, and animal & veterinary products. They achieve this by inspecting manufacturing premises and reviewing the safety and effectiveness of a product before a business can sell it on the market after it has undergone extensive clinical trials that can last for over a decade.

A rigid classification, under the terms of a De Novo, the submitting company, must prove that their product presents a ‘medium risk’ to humans. In contrast, under the 510(k) submission, an organization only has to show their device presents no more risk to human health than the approved equivalent product – even where the marketed product has been deemed dangerous. De Novo submissions are also more expensive than the cheaper 510(k).

Surprisingly, even though the ONE condom is already approved by the USFDA using the flexible 510(k) category for vaginal sex, the agency has cleared the new product for anal sex through the De Novo pathway. This fact certainly raises questions regarding the lack of equivalency between condoms used for vaginal sex and anal sex.

On a positive note, they have established special controls so that other devices can now show equivalence to the ONE condom using a 510(k) classification to receive quicker clearance without the need for clinical trials. 

In its press release, the USFDA said the green light could pave the way for more condom makers to apply for faster approval if they show equivalent results. They add that they expect authorization of the ONE Male Condom to help reduce the transmission of STDs, including HIV/AIDS in both anal and vaginal intercourse.

All approved condoms are an easy way to protect yourself

Experts remind all sexually-active couples that they can still use other approved condoms on the market during anal sex:

“This isn’t a groundbreaking advancement in my opinion. All condoms can (and should!) be used to make anal sex safer, so just because this one brand has FDA approval doesn’t make it any better than other condom brands on the market,” says obstetrician-gynecologist and author Jennifer Lincoln who wasn’t part of the trial, for PopSci. “Don’t let the ‘FDA approved’ label sway you when you are at the grocery store—the best condom to use for safe sex is the one you have access to and the one you will actually use.”

Still, this is a galvanizing moment for the LGBTQ movement.

“This authorization helps us accomplish our priority to advance health equity through the development of safe and effective products that meet the needs of diverse populations. This De Novo authorization will also allow subsequent devices of the same type and intended use to come to the market through the 510k pathway, which could enable the devices to get on the market faster,” Lias added in the USFDA statement.

It remains to be seen whether this will trigger a longer-term movement. In the meantime, stay safe.

The fascinating science behind the first human HIV mRNA vaccine trial – what exactly does it entail?

In a moment described as a “potential first step forward” in protecting people against one of the world’s most devastating pandemics, Moderna, International AIDS Vaccine Initiative (IAVI), and the Bill and Melinda Gates Foundation have joined forces to begin a landmark trial — the first human trials of an HIV vaccine based on messenger ribonucleic acid (mRNA) technology. The collaboration between these organizations, a mixture of non-profits and a company, will bring plenty of experience and technology to the table, which is absolutely necessary when taking on this type of mammoth challenge.

The goal is more than worth it: helping the estimated 37.7 million people currently living with HIV (including 1.7 million children) and protecting those who will be exposed to the virus in the future. Sadly, around 16% of the infected population (6.1 million people) are unaware they are carriers.

Despite progress, HIV remains lethal. Disturbingly, in 2020, 680,000 people died of AIDS-related illnesses, despite inroads made in therapies to dampen the disease’s effects on the immune system. One of these, antiretroviral therapy (ART), has proven to be highly effective in preventing HIV transmission, clinical progression, and death. Still, even with the success of this lifelong therapy, the number of HIV-infected individuals continues to grow.

There is no cure for this disease. Therefore, the development of vaccines to either treat HIV or prevent the acquisition of the disease would be crucial in turning the tables on the virus.

However, it’s not so easy to make an HIV vaccine because the virus mutates very quickly, creating multiple variants within the body, which produce too many targets for one therapy to treat. Plus, this highly conserved retrovirus becomes part of the human genome a mere 72 hours after transmission, meaning that high levels of neutralizing antibodies must be present at the time of transmission to prevent infection.

Because the virus is so tricky, researchers generally consider that a therapeutic vaccine (administered after infection) is unfeasible. Instead, researchers are concentrating on a preventative or ‘prophylactic’ mRNA vaccine similar to those used by Pfizer/BioNTech and Moderna to fight COVID-19.

What is the science behind the vaccine?

The groundwork research was made possible by the discovery of broadly neutralizing HIV-1 antibodies (bnAbs) in 1990. They are the most potent human antibodies ever identified and are extremely rare, only developing in some patients with chronic HIV after years of infection.

Significantly, bnAbs can neutralize the particular viral strain infecting that patient and other variants of HIV–hence, the term ‘broad’ in broadly neutralizing antibodies. They achieve this by using unusual extensions not seen in other immune cells to penetrate the HIV envelope glycoprotein (Env). The Env is the virus’s outer shell, formed from the cell membrane of the host cell it has invaded, making it extremely difficult to destroy; still, bnAbs can target vulnerable sites on this shell to neutralize and eliminate infected cells.

Unfortunately, the antibodies do little to help chronic patients because there’s already too much virus in their systems; however, researchers theorize if an HIV-free person could produce bnABS, it might help protect them from infection.

Last year, the same organizations tested a vaccine based on this idea in extensive animal tests and a small human trial that didn’t employ mRNA technology. It showed that specific immunogens—substances that can provoke an immune response—triggered the desired antibodies in dozens of people participating in the research. “This study demonstrates proof of principle for a new vaccine concept for HIV,” said Professor William Schief, Department of Immunology and Microbiology at Scripps Research, who worked on the previous trial.

BnABS are the desired endgame with the potential HIV mRNA vaccine and the fundamental basis of its action. “The induction of bnAbs is widely considered to be a goal of HIV vaccination, and this is the first step in that process,” Moderna and the IAVI (International AIDS Vaccine Initiative) said in a statement.

So how exactly does the mRNA vaccine work?

The experimental HIV vaccine delivers coded mRNA instructions for two HIV proteins into the host’s cells: the immunogens are Env and Gag, which make up roughly 50% of the total virus particle. As a result, this triggers an immune response allowing the body to create the necessary defenses—antibodies and numerous white blood cells such as B cells and T cells—which then protect against the actual infection.

Later, the participants will also receive a booster immunogen containing Gag and Env mRNA from two other HIV strains to broaden the immune response, hopefully inducing bnABS.

Karie Youngdahl, a spokesperson for IAVI, clarified that the main aim of the vaccines is to stimulate “B cells that have the potential to produce bnAbs.” These then target the virus’s envelope—its outermost layer that protects its genetic material—to keep it from entering cells and infecting them.  

Pulling back, the team is adamant that the trial is still in the very early stages, with the volunteers possibly needing an unknown number of boosters.

“Further immunogens will be needed to guide the immune system on this path, but this prime-boost combination could be the first key element of an eventual HIV immunization regimen,” said Professor David Diemert, clinical director at George Washington University and a lead investigator in the trials.

What will happen in the Moderna HIV vaccine trial?

The Phase 1 trial consists of 56 healthy adults who are HIV negative to evaluate the safety and efficacy of vaccine candidates mRNA-1644 and mRNA-1644v2-Core. Moderna will explore how to deliver their proprietary EOD-GT8 60mer immunogen with mRNA technology and investigate how to use it to direct B cells to make proteins that elicit bnABS with the expert aid of non-profit organizations. But readers should note that only one in every 300,000 B cells in the human body produces them to give an idea of the fragility of the probability involved here.

Sensibly, the trial isn’t ‘blind,’ which means everyone who receives the vaccine will know what they’re getting at this early stage. That’s because the scientists aren’t trying to work out how well the vaccine works in this first phase lasting approximately ten months – they want to make sure it’s safe and capable of mounting the desired immune response.

And even though there is much hype around this trial, experts caution that “Moderna are testing a complicated concept which starts the immune response against HIV,” says Robin Shattock, an immunologist at Imperial College London, to the Independent. “It gets you to first base, but it’s not a home run. Essentially, we recognize that you need a series of vaccines to induce a response that gives you the breadth needed to neutralize HIV. The mRNA technology may be key to solving the HIV vaccine issue, but it’s going to be a multi-year process.”

And after this long period, if the vaccine is found to be safe and shows signs of producing an immune response, it will progress to more extensive real-world studies and a possible solution to a virus that is still decimating whole communities.

Still, this hybrid collaboration offers future hope regarding the prioritization of humans over financial gain in clinical trials – the proof is that most HIV patients are citizens of the third world.

As IAVI president Mark Feinberg wrote in June at the 40th anniversary of the HIV epidemic: “The only real hope we have of ending the HIV/AIDS pandemic is through the deployment of an effective HIV vaccine, one that is achieved through the work of partners, advocates, and community members joining hands to do together what no one individual or group can do on its own.”

Whatever the outcome, money is no longer a prerogative here, and with luck, we may see more trials based on this premise very soon.

Study on mice: Exercising later in life can keep your muscles young

Exercising can not only make you feel younger, but it can also actually keep you younger as well. A study on mice suggests that exercising, even later in life, can do wonders for your muscles. In addition to underscoring the importance of staying active, the study could also help us uncover some of the secrets of rejuvenation.

Even though some diseases are inherited, we can still improve our overall health through lifestyle choices such as diet and exercise. Still, whatever the reason, the genes related to some of these conditions must be expressed for them to develop. So how does this happen?

A new study has brought us closer to an answer by mapping the genetic changes involved in rejuvenating the muscle cells of elderly mice put on an exercise program.

Turning genes on and off

The analysis centers on DNA, the “blueprint” for our bodies. DNA consists of four bases, called cytosine, guanine, adenine, and thymine, and the process used to help manage these massive helixes: a methyl molecule composed of one carbon and three hydrogen atoms. These atoms attach themselves to one of the four bases (cytosine) to form what’s known as a CpG site.

When this occurs, the CpG becomes methylated and the site produces proteins to regulate something in the body — whatever that something may be. In contrast, the region becomes unmethylated when you lose that methyl group, turning that gene off. In this way, a process called DNA methylation can promote or inhibit the expression of specific genes — whether it’s stopping a tumor, preventing cancer, or activating genes responsible for causing wrinkles in old age. This process is constant, occurring billions of times a second in every cell throughout the body, and we’re just starting to understand it.

DNA methylation is one of the many mechanisms of epigenetics, where inborn or acquired changes in DNA don’t touch the actual sequence – meaning a person can potentially reverse things like fat deposits through diet or exercise. More and more studies are starting to suggest that this is an unharnessed and robust process, linked to longevity and the regulation of lifespan in most organisms on earth.

The current study attempts to further this theory using lifestyle interventions such as exercise to roll back genetic aging in skeletal muscle – measuring the animal’s ‘epigenetic clock’ for accuracy. This clock is measured via methylation levels in the blood to reflect exposures and disease risks independent of chronological age, providing an early-warning system and a true representation of a period of existence.

Kevin Murach, an assistant professor at the University of Arkansas, says, “DNA methylation changes in a lifespan tend to happen in a somewhat systematic fashion. To the point, you can look at someone’s DNA from a given tissue sample and with a fair degree of accuracy predict their chronological age.”

Using exercise to turn back the clock

The study design was relatively simple: mice nearing the end of their natural lifespan, at 22 months, were given access to a weighted exercise wheel to ensure they built muscle. They required no coercion to run on the wheel, with older mice running from six to eight kilometers a day, mostly in spurts, and younger mice running up to 10-12 kilometers.

Results from the elderly mice after two months of weighted wheel running suggested they were the epigenetic age of mice eight weeks younger, compared to sedentary mice of the same maturity.

The team also used the epigenetic clock to map a multitude of genes involved in the formation and function of muscles, including those affected by exercise. Blood work indicated that the genes usually over methylated (hypermethylated) in old age resumed normal methylation in the active aged mice, unlike those mapped in their sedentary counterparts.

For instance, the rbm10 gene is usually hypermethylated in old age, disrupting the production of proteins involved in motor neuron survival, muscle weight & function, and the growth of striated muscle. Here it was shown to undergo less methylation in older mice who exercised, improving its performance. Normal methylation levels also resumed across the Timm8a1 gene, keeping mitochondrial function and oxidant defense at workable levels – even where neighboring sites exhibited dysfunctional epigenetic alterations.

More work is needed to harness DNA methylation

Murach notes that when a lifespan is measured incrementally in months, as with this mouse strain, an extra eight weeks — roughly 10 percent of that lifespan — is a noteworthy gain, further commending the importance of exercise in later life.

He adds: that although the connection between methylation and aging is clear, methylation and muscle function are less clear. Despite these sturdy results, Murach will not categorically state that the reversal of methylation with exercise is causative for improved muscle health. “That’s not what the study was set up to do,” he explained. However, he intends to pursue future studies to determine if “changes in methylation result in altered muscle function.”

And, “If so, what are the consequences of this?” he continued. “Do changes on these very specific methylation sites have an actual phenotype that emerges from that? Is it what’s causing aging or is it just associated with it? Is it just something that happens in concert with a variety of other things that are happening during the aging process? So that’s what we don’t know.”

He summarizes that once the medical community has mapped the mechanics of dynamic DNA methylation in muscle, their work could provide modifiable epigenetic markers to improve muscle health in the elderly. 

Electric knee implants could help millions of arthritis patients

An answer could be on the horizon for millions of people living with arthritis after scientists have found a way to repair joints using electrical implants. The implants work by producing a current every time the person moves their joint to regrow the protective cartilage that cover the ends of bones .

Bioengineers from the University of Connecticut developed a biodegradable mesh implant, about half a millimeter thick, which generated tiny electrical signals to repair arthritic joints in rabbits. The study, published in Science Translational Medicine, saw the team successfully regrow cartilage in rabbits’ knees without using potentially toxic growth factors or stem cells. Crucially, the cartilage that grows back is mechanically robust, with further plans to trial the implant in larger animals and humans.

In their white paper, the team states that although more work is needed to improve the scaffold, this study provides evidence that biodegradable implants that produce electricity independently can use exercise to treat arthritis.

No cure for arthritis despite tens of millions of sufferers

According to the CDC, 58.5 million people currently have arthritis in the United States, which costs the American people $303.5 billion annually. While there are treatments, arthritis technically has no cure.

It is a widespread and painful disease caused by damage to joints formed between the body’s bones. One of the subtypes of this disease, called osteoarthritis, attacks the cartilage at the end of bones in the joint. As this buffer deteriorates, bones begin to rub against each other so that everyday activities like walking become agonizingly painful – making the growth of new cartilage highly desirable. 

Sufferers face years of pain without surgical or pharmaceutical intervention, but these treatments can only slow down the damage instead of repairing damage to the joint. However, even this process involves taking healthy cartilage from the patient or a donor and comes with inconveniences and risks.

Therefore, regrowing healthy cartilage in the damaged joint itself would be very helpful. Some researchers have investigated chemical growth factors to induce the body to regrow it; other attempts rely on a bioengineered scaffold to promote tissue growth. But, neither of these approaches works-even in combination-with the regrown cartilage breaking under the everyday stresses of the joint.

Your joints can generate electricity to heal you

The new breakthrough involves a tissue scaffold made out of poly-L lactic acid (PLLA) nanofibers, a material often used to stitch surgical wounds that dissolve after the person heals. The scaffold produces a little burst of electrical current when squeezed in a process known as piezoelectricity. In this case, the joint’s regular ‘squeezing’ is provided by walking, which generates a weak electrical field that encourages cells to colonize the implant and grow into cartilage.

“Piezoelectricity is a phenomenon that also exists in the human body. Bone, cartilage, collagen, DNA, and various proteins have a piezoelectric response. Our approach to healing cartilage is highly clinically translational, and we will look into the related healing mechanism”, says Dr. Yang Liu, a postdoctoral fellow in Nguyen’s group and the lead author of the published work.

Nguyen’s group implanted their scaffold in the knee of injured rabbits. After a month in recovery, the rabbits were encouraged to walk for 20 minutes a day on a slow-moving treadmill to exercise their legs and generate the electric current. The charge encouraged the regrowth of fresh, mechanically robust cartilage, making the knee as solid and functional as before it was injured. Whereas rabbits treated with nonpiezoelectric scaffold and exercise treatment still had a hole in this protective sheath and limited healing.

In an interview with New Scientist, Thanh Nguyen, an assistant professor in the department of mechanical engineering, says, “If used in people, the material used to make the implant would dissolve after about two months – although it could be tweaked to make it last longer.”

What next for this promising implant?

Nguyen states that the results are exciting but cautions that further tests need to be carried out on larger animals that bear more similarities to humans.

His lab now plans to observe the treated animals for 1-2 years to ensure the cartilage is durable and wants to test the PLLA scaffolds in older animals as arthritis usually affects the elderly. He concludes by saying that if the scaffolding helps older animals heal, it indeed could be a bioengineering breakthrough.