Wellness Warriors

Wellness Warriors Health/beauty

Why do fingers get wrinkly after a long bath or swim? This expert explains
Recent research suggests blood vessels are the key to why fingers and toes turn pruny and pale after being submerged for a while.

Skin is an awesome and weird organ. As the body’s biggest organ, it does a lot to look after you, protecting you from the outside world of sunlight, harsh chemicals, nasty germs and severe cold. And it does all this while keeping water inside your body and enabling the sense of touch.

I’m a biomedical engineer. My research team and I try to better understand the mechanics and function of soft biological tissues.

We know skin wrinkles as you get older or when you pinch it between two fingers. But it’s been somewhat of a mystery why skin gets wrinkly and even sometimes changes color after you take a leisurely bath or spend too long in the swimming pool.

Often people assume that these wrinkles form because the skin absorbs water, which makes it swell up and buckle. To be honest, I did too for a long time.

But researchers back in the 1930s discovered that in people with nerve damage in their fingers, the post-bath wrinkles didn’t form. Wrinkly fingers can’t just be due to water absorption then, or this would be a universal phenomenon, no matter how well your nerves are or aren’t working.

So, if it isn’t swelling due to water, then what is behind pruny fingers and toes after a long swim? Scientists have recently discovered what they think is the answer.

A nerve signal for narrower blood vessels
To explain what is happening, first you need to know a bit about the autonomic nervous system – the involuntary part of how your body works. Functions like breathing, blinking, your heart pumping or your pupils constricting in the sun all happen without your needing to consciously control them, thanks to the autonomic nervous system.

It also automatically controls the expansion and contraction of your blood vessels. Typically, temperature, medications or what you eat or drink can cause your blood vessels to expand or contract. Think of how your skin may flush of its own accord when you go out into a hot day, exercise or even blush.

This contraction of your blood vessels is also what causes the skin to wrinkle after a lengthy swim.

When your hands and feet come into contact with water for more than a few minutes, the sweat ducts in your skin open, allowing water to flow into the skin tissue. This added water decreases the proportion of salt inside the skin. Nerve fibers send a message about lower salt levels to your brain, and the autonomic nervous system responds by constricting the blood vessels.

The narrowing of the blood vessels causes the overall volume of skin to reduce, puckering the skin into these distinct wrinkle patterns. It’s like how a dried-out grape becomes a wrinkled raisin – it’s lost more volume than surface area.

This constriction of blood vessels also causes the skin to become paler – it’s the opposite of what happens when your skin gets redder when you get into a really hot bath, due to your blood vessels dilating. The color change is a little more obvious in people with lighter complexions.

With nerve damage, this constriction doesn’t occur. The blood vessels never get a message to narrow, so the wrinkles never happen even if you stay in the bath for a really long time.

A vaccine against fentanyl and he**in overdose is close to clinical trials
Human trials for these vaccines will evaluate both their safety and effectiveness, with an emphasis on protecting vulnerable populations.

Researchers at the University of Montana are on the brink of human trials for vaccines aimed at curbing fentanyl and he**in drug overdoses. These vaccines could potentially save countless lives from accidental overdoses and provide a glimmer of hope for those struggling with drug addiction.

“We anticipate testing our vaccines in humans in early 2024. The first vaccine will target he**in, followed shortly thereafter with a fentanyl vaccine in Phase I clinical trials. Once we establish safety and early efficacy in these first clinical trials, we hope to advance a combined multivalent vaccine targeting both he**in and fentanyl,” said Dr. Jay Evans, who heads the University of Minnesota Center for Translational Medicine.

Fighting the opioid epidemic
According to the National Institutes of Health, over 106,000 drug overdose deaths were reported in the United States in 2021, with approximately 71,000 attributed to synthetic opioids such as fentanyl.

In the early 2000s, prescription painkillers used to be the leading cause of overdose deaths. But in the past ten years, he**in — which now kills at least four times more people than in 2000 — and then fentanyl, surpassed prescription opioid drugs as the main cause of overdose death.

Fentanyl is a synthetic opioid about 100 times stronger than morphine and 50 times stronger than he**in. Because it’s so strong yet cheap to make, fentanyl has flooded the drug black market. Many he**in users have switched to fentanyl and some drug dealers cut he**in with it to improve their bottom line, risking their customers’ lives.

Accidentally overdoing fentanyl is incredibly easy. Users who try it and have little to no opioid tolerance can die from ingesting just a dash of fentanyl. In 2018, the opioid crisis cost $700 billion (with a “B”), a staggering 3.4% of the United States’ GDP. Since 2015 when fentanyl really started to take off, the dreadful drug has caused trillions of dollars of damage.
The two highly awaited vaccines are the brainchild of Dr. Marco Pravetoni, a professor of psychiatry and behavioral sciences at the University of Washington who has worked on vaccines against opioids for more than a decade. Pravtoni and his team specialize in designing haptens — very small molecules that elicit an immune response by binding to proteins and pharmaceutical drugs in the body — and drug conjugate vaccines.

A drug conjugate vaccine is an innovative medical approach that combines the principles of vaccines and drug conjugates. It involves attaching specific antigens from a pathogen to a carrier molecule, which is then administered to stimulate the immune system. This unique combination enables the immune system to recognize and combat the pathogen while also delivering therapeutic drugs directly to the infection site, promising more effective and targeted treatment strategies against a range of diseases.

“Our vaccines are designed to neutralize the target opioid, while sparing critical medications such as methadone, buprenorphine, naltrexone and naloxone, which are used in treatment of opioid addiction and reversal of overdose,” said Pravetoni in a press release.

The vaccine developed at the University of Washington was combined with an adjuvant called INI-4001 developed by the University of Minnesota. Adjuvants are added to vaccine cocktails to enhance their effectiveness by stimulating a stronger and longer-lasting immune response.

The two anti-opioid vaccine candidates were tested on animal models (mice, rats, and pigs). The fentanyl vaccine was shown to be effective, whereas the results for the he**in vaccine are pending.

Nevertheless, the scientists hope to start clinical trials soon with both vaccine candidates. They expect to be granted FDA approval to commence these trials by the end of the year. The early trials are meant to gauge both vaccine safety and efficacy. Once this first step is cleared, the vaccines will be allowed to be tested on a broader number of volunteers, typically in the 1,000-participant range. There will be a long monitoring period to see how long the antibodies against the opioids will last.

He**in and fentanyl are both extremely addictive drugs, with relapse rates hovering at the 90% range. The idea of these vaccines is not only to protect users from overdosing but also to help them quit these drugs for good.

Scientists find dozens of genes linked to different types of epilepsy
The research could unveil new avenues for effective epilepsy treatments.

The largest-ever genetic study on epilepsy, a neurological disorder affecting approximately 50 million worldwide, has uncovered DNA changes that put people at risk of this condition. A whopping 26 distinct areas within our DNA seem to play a role in epilepsy.

Doctors have noticed for centuries that epilepsy can run in the family, thereby having a genetic component. But it’s only now that we’ve been privileged with a more in-depth look at these genetic components.

Epilepsy: A Complex Genetic Connection
The International League Against Epilepsy (ILAE) Consortium on Complex Epilepsies led the study, published in Nature Genetics. They examined genetic data from over 29,000 epileptics and compared it to genetic data from 52,538 control subjects without the condition.

The study is one of the largest of its kind. Over 150 scientists based across Europe, Australia, Asia, South America, and North America, contributed to the research. The ILAE Consortium was formed in 2010, recognizing that the complexity of genetic and environmental factors underlying epilepsy would require research across massive datasets and therefore unprecedented collaboration on an international scale.

Epilepsy, characterized by recurrent seizures, is a complex disorder with various manifestations and responses to treatment. The study’s findings offer a more nuanced understanding of the genetic factors contributing to epilepsy and hold promise for developing more tailored and effective treatments.

“Gaining a better understanding of the genetic underpinnings of epilepsy is key to developing new therapeutic options and consequently a better quality of life for the over 50 million people globally living with epilepsy,” said Gianpiero Cavalleri, professor of human genetics at the Royal College of Surgeons in Ireland’s School of Pharmacy and Biomolecular Science.

One key insight gleaned from the study is the importance of accurately classifying different subtypes of epilepsy based on their clinical presentation. This categorization can prove crucial in determining appropriate treatment strategies. This study demonstrated that focal epilepsy (FE) and genetic generalized epilepsy (GGE) have significantly different genetic mechanisms.

Twenty-six separate regions of human DNA were found to be potentially involved in epilepsy. Of these, 19 are unique to GGE. They also identified 29 genes within these regions of DNA that likely play a role in epilepsy. The findings also suggest that proteins involved in transmitting electrical impulses between brain cells contribute to the risk of developing epilepsy in its generalized form.

“This identification of epilepsy-associated genetic changes will allow us to improve diagnosis and classification of different epilepsy subtypes,” said Colin Doherty, consultant neurologist at St. James’s Hospital and co-author. “This in turn, will guide clinicians in selecting the most beneficial treatment strategies, minimizing seizures.”

The implications of these findings are substantial, potentially paving the way for personalized treatment approaches. The study suggests treatments targeting specific genetic factors could yield more favorable outcomes for certain epilepsy subtypes. The potential also extends beyond medication. The study highlighted alternative treatment avenues such as specialized diets, surgical interventions, and neuromodulation techniques.

For instance, dietary therapies like the well-known ketogenic diet have effectively reduced seizures for some individuals with epilepsy. With the knowledge gained from this study, medical professionals could better identify patients most likely to benefit from these dietary interventions.

Similarly, surgical procedures that involve removing specific brain areas, called focal resection, have proven effective in certain cases. Accurate classification of epilepsy subtypes becomes paramount in determining which patients could benefit the most from such interventions.

Additionally, the study highlighted neuromodulation techniques as potential treatment options. These approaches involve stimulating nerves to alleviate symptoms. The most notable are vagus nerve stimulation and deep brain stimulation. The study’s authors suggest that understanding how these techniques align with the genetic markers identified in the study could lead to more targeted and effective neuromodulation therapies.

The research represents a pivotal advancement in comprehending epilepsy’s genetic basis. For patients who have not responded to current treatments, tailored treatments based on subtype-specific genetic insights provide renewed hope.