Those polar plunge nuts—you know, the people who strip to their skivvies in February and jump into freezing water—might be on to something.
According to doctors from the United Kingdom, a 28-year-old man who had been complaining of persistent, post-operative pain was cured after jumping into incredibly cold water for a vigorous 60-second, intense swim. Roughly two months prior to his swim, the man had undergone an endoscopic thoracic sympathectomy procedure to treat his severe facial blushing. In this procedure, a portion of the sympathetic nerve trunk is destroyed to treat excessive sweating, blushing and Raynaud’s disease.
The operation went smoothly, but nagging, sharp pain in his chest continued for 10 weeks after the operation. Exercise and movement tended to make things worse, which was bad news for the patient, who has a devoted triathlete. Doctors tried analgesics and other means to control pain with limited success, and when things didn’t work, the patient took a leap of faith.
In a bold attempt to take his mind of pain, the patient decided to go for a swim in the coastal waters of a past triathlon competition. His route was along a rocky, jagged coastline; therefore, there was no dipping his toes in to acclimate to the water. The man had to jump from a rocky outcrop.
“I wasn’t sure if it would help the pain—I just wanted to do it—I thought at best it was a long-shot, but I was desperate to get some relief,” the man told doctors.
When his body slapped into seawater that was 52 degrees Fahrenheit, he had no choice but to swim for safety, or risk hypothermia. He told doctors:
“I initially thought, ‘Damn this is so cold I’m going to die!’ I just swam for my life. Once I was in the water, I had tunnel vision. For the first time in months, I completely forgot about the pain or the fear of shooting pains in my chest if I moved. My entire body tingled with the cold. I just knew if I didn’t keep swimming, I’d soon freeze. After a few moments I actually enjoyed it – it was just an immersive rush of adrenaline. I bet I couldn’t have felt my pain, even if I tried.”
The funny thing is, his pain never returned.
Doctors, of course, dug into the man’s case to see if there was any precedent, but they couldn’t find any in their survey of medical literature. No doubt, ice baths and pool therapy are commonplace in rehabilitation regimens, but swimming in bitter cold water to manage pain appears to be a new one.
The authors considered that this could just be a coincidence, and that there isn’t enough evidence to build a causal relationship between swimming, cold water and pain relief. Maybe it was the placebo effect. Maybe the shock of the water overwhelmed his persistent pain. But if that’s the case, why did the pain remain in remission long after the initial shock of jumping in the water passed? The doctors say they don’t have a clear explanation for why this man’s unorthodox therapy session worked. In a report published Monday in the British Medical Journal, doctors wrote:
“It is possible that the high range of movement involved in swimming manipulated tissues surrounding peripheral nerves in such a way as to mechanically free adhesions and resolve pain. Psychologically, ‘flooding’ with intense activity may have abruptly broken maladaptive cycles of movement avoidance and withdrawal from exercise and its associated pain relieving properties.”
This case, though it may be an outlier, challenges conventional thinking about postoperative treatment and pain management. The doctors say the takeaway here is that more physically aggressive rehabilitation programs may be warranted for certain patients; of course, not everyone can or should jump into bone-chilling water to alleviate postoperative pain. Of course, they’d like to conduct more research into the analgesic effects of forced, cold-water swimming.
10 Ways Space Changes the Body
Former astronaut Mark Kelly (left) poses with his identical twin brother, astronaut Scott Kelly (right). As part of NASA’s Twins Study, Scott spent nearly a year in space, while Mark stayed here on Earth. This gave researchers a chance to study the health effects of long-term spaceflights. (Credit: NASA)
Scott and Mark Kelly are identical twin brothers. Though that alone does not make them unique, what does is the fact that they are also both astronauts. In order to take advantage of the Kellys’ unique situation, NASA scientists decided to conduct a detailed study on the twins, aimed at unraveling how nature versus nurture plays out in space.
As part of NASA’s Twins Study, researchers collected biological samples from each of the Kellys before sending Scott to the International Space Station for a year starting in March 2016. Meanwhile, his brother Mark, who retired as an astronaut in 2011, remained on Earth to serve as the control subject. By analyzing how each twins’ biological markers evolved during the mission, the researchers learned a great deal about how the human body reacts — both physically and mentally — to extended periods of spaceflight.
The NASA Twins Study is made up of ten distinct research projects, which all focus on different aspects of the human body. And last month, after nearly two years of study, the ten separate research teams confirmed their preliminary findings (which were initially released in 2017), as well as presented details on their postflight follow-up results.
Later this year, the findings for each of the various projects will be integrated together and released as one summary paper, which will be followed by several companion papers focusing on the individual studies. In the meantime, here is a summary of the most recent findings for each of the research projects that were carried out as part of the Twins Study.
#1 – Telomeres get longer during spaceflight
Telomeres are the caps that shield the ends of our chromosomes, protecting DNA strands from damage and degradation. In a study led by Susan Bailey of Colorado State University, researchers tracked the length of each twins’ telomeres before, during, and after Scott’s yearlong spaceflight.
The researchers found that Scott’s telomeres significantly increased in length while he was in space, which was not the case with his Earth-bound brother Mark, whose telomeres remained relatively stable. Previous research has shown that longer telomeres are associated with fewer age-related problems.
Though Scott’s telomeres were found to lengthen while he was in space, postflight measurements showed that the telomeres underwent rapid shortening within about 48 hours of landing back on Earth. Eventually, they returned to their preflight lengths. The team believes that the temporary lengthening of Scott’s telomeres could be a side effect of his rigorous exercise routine and restricted, low-calorie diet.
#2 – Decreased body mass and increased folate in orbit
A study conducted by Scott M. Smith of the NASA Johnson Space Center monitored the biochemical profiles of each twin to identify any changes. To do this, his team tracked the brothers’ heights and weights and analyzed their blood and urine samples throughout the duration of the mission.
The researchers not only found that Scott’s body mass noticeably dropped during his time in space, but also that his levels of folate — a beneficial form of folic acid often used to treat anemia — significantly increased.
Much like Bailey’s findings on telomere lengthening, Smith believes the drop in body mass and increase in folate could simply be a result of eating healthier and exercising more often.
#3 – Mentally fit in space, foggy back on Earth
Mathias Basner of the University of Pennsylvania conducted a study that monitored the cognition of both twins over the duration of the mission. By requiring each twin to perform ten different cognitive tests multiple times (preflight, inflight, and postflight), the researchers were able to track how spacefaring Scott’s mental faculties were affected by microgravity.
Using the preflight test results as a baseline, Basner found that Scott’s yearlong mission aboard the ISS did not significantly impair his cognitive abilities while inflight. However, when Scott returned to Earth, the researchers did detect a more pronounced decrease in his speed and accuracy on cognitive tests.
The researchers believe that readjusting to Earth’s gravity may be the cause of Scott’s postflight cognitive decline, but further study is needed to confirm. They also point out that Scott’s performance could have suffered when returning to Earth as the result of a very hectic postflight schedule.
#4 – Flu vaccine stimulates immune system, even in space
To investigate how space affects a human body’s immune system, Emmanuel Mignot of Stanford University conducted a study that introduced the flu vaccine to Scott and Mark on two separate occasions spaced one year apart — during preflight and postflight.
On both occasions, after the vaccines were administered, the twins displayed similar increased immune cell responses to the flu. When the human body is vaccinated against the flu, weakened or dead flu virus cells are injected into the bloodstream. This triggers the body to produce antibodies that seek out and destroy the viral cells, thus preventing any healthy flu cells from multiplying and overwhelming the body’s defenses.
Because the twins showed similar immune responses to both vaccinations, the researchers concluded that being in space does not prevent the flu vaccine from producing the desired immune response.
#5 – Inflammation increases while in space
Mike Snyder of Stanford University carried out a study that investigated whether or not space affects inflammation in the human body. Using blood tests to measure lipids (fats) and cytokines (proteins in the blood that serve as well-known indicators of inflammation), Snyder was able to compare how the inflammatory responses of the brothers differed while Scott was in space.
In this study, the researchers found multiple lines of evidence suggesting that Scott’s body was more prone to inflammation in a microgravity environment than Mark’s was on Earth. For one, the researchers found that Scott had altered levels of a lipid panel taken in space, indicating increased inflammation in his body. The researchers also noted that a certain group of Scott’s cytokines were found to be elevated before the flight, and they remained elevated throughout the mission. Furthermore, another group of Scott’s cytokines spiked just after he returned to Earth. This group of cytokines remained elevated for six months.
Additionally, the study showed that Scott’s body experienced an increase in some proteins that are known to help regulate normal insulin activity. Since inflammation can cause insulin resistance, the increase in Scott’s proteins may have been a counter-measure executed by his body to help combat the insulin resistance associated with inflammation.
#6 – Space affects the microbiome
Inside of each of our guts lives a vast community of microorganisms, known as the microbiome, which plays an important role in our overall health. To study how living in a microgravity environment impacts the microbiome, Fred Turek of Northwestern University monitored the state of each twin’s microbiome before, during, and after the yearlong mission.
The researchers found that the microbiomes of both Scott and Mark were drastically different at all times throughout the project, but the differences were somewhat expected considering microbiomes are very sensitive to environmental variances such as diet and individual immunity. However, the researchers point out that Scott’s microbiome was different in space than it was preflight, displaying a decreased presence of one branch of bacteria known as Bacteroidetes. However, these changes did not persist upon Scott’s return to Earth.
Even though the study showed that Scott’s microbiome changed when switching settings between Earth and space, the changes that were observed were similar to those that would be expected if someone on the ground significantly modified their diet or was exposed to a new environment.
#7 – Spaceflight can trigger gene mutations
Chris Mason of Weill Cornell Medicine used the Twins Study as an opportunity to investigate how space travel can influence genetics. By looking for chemical changes in RNA and DNA through the use of whole-genome sequencing, the researchers showed that Scott experienced hundreds of unique gene mutations compared with his twin.
Though some distinct gene mutations were to be expected, even in twins, the sheer amount of changes surprised the researchers. A few of the gene changes, which were discovered only after Scott returned to Earth, were even found on cell-free DNA and RNA that was circulating in his bloodstream. The researchers believe that these gene changes resulted from the stresses of space travel, which can alter the biological pathways within cells, causing them to eject DNA and RNA. These free-floating DNA and RNA molecules can then trigger the production of new fats or proteins, or even turn specific genes on and off. Though 93 percent of the genes that expressed themselves differently while Scott was in space returned to normal postflight, the researchers found a subset of several hundred “space genes” that remained disrupted after his return.
Of the many gene-induced changes Scott’s body experienced, the researchers found five to be of particular relevance for future missions: (1) Hypoxia, which was likely caused by a lack of oxygen and a surplus of carbon dioxide; (2) Mitochondrial stress and increased levels of mitochondria in the blood, which suggests damage was done to the “power plants” of cells; (3) Telomere lengthening, DNA repair, and DNA damage, which could be a result of living a healthy lifestyle while constantly exposed to radiation; (4) Decreased collagen production, blood clotting, and bone formation, which was likely a combined result of living in microgravity and of fluids shifting around within the body; and (5) Hyperactive immune activity, which may be an effect of living in a new environment.
#8 – Living in space changes how genes are expressed
Similar to the previous project, Andy Feinberg of Johns Hopkins University conducted a study that tracked how each of the twins’ epigenetics (the way that genes express themselves) differed based on their environment.
In two separate populations of white blood cells, Feinberg found multiple regions of the genome where DNA methylation — the process responsible for turning genes on and off — had occurred. These chemical modifications to Scott’s genome were found near two interesting regions. One was close to a gene known to help regulate telomere growth, and another was found near a gene related to collagen production.
Although Scott did experience epigenetic changes during his time in space, the researchers found that the majority of changes were within the expected range of variability for his twin on Earth. However, the results related to telomere growth and collagen production are consistent with the findings of other Twins Study projects.
#9 – Artery walls thicken while in space
Stuart Lee of KBRWyle at NASA Johnson Space Center’s Cardiovascular and Vision Lab performed a study on how inflammation and oxidative stress (damage by free radicals in the air) can impact the structure and effectiveness of arteries. To do this, the researchers examined the twins’ arteries using ultrasound, as well as collected blood and urine samples throughout the mission.
Both during and immediately after the mission, the researchers found that Scott’s inflammation biomarkers were elevated and that the wall of his carotid artery was thicker than it was preflight. Neither of these changes were seen in Mark during his stay on Earth.
At this point, the researchers do not know whether the thickening of Scott’s carotid artery is a temporary and reversible adaptation to living in space, or if it is evidence of permanent and premature arterial aging. Further study is needed to put these findings into clearer focus.
#10 – Proteins that regulate fluids increase while in space
In order to investigate how spaceflight impacts the body’s ability to form and modify proteins, Brinda Rana of the University of California carried out a study that collected urine samples from Scott and Mark before, during, and after the mission. This allowed Rana to identify certain biomarker proteins that are associated with space-related bodily changes, such as muscle and bone loss, metabolic and cardiovascular changes, and the altered regulation of fluids within the body.
The researchers found that while Scott was in space, he excreted some proteins at different concentrations than his Earth-bound brother Mark. In particular, Scott had elevated levels of a protein called aquaporin 2, which helps form the pathways used to carry water through cell membranes in the kidneys. Because aquaporin 2 helps regulate how water is transported within the body, it also serves as a valuable indicator of a body’s overall hydration status.
Notably, the researchers also found that Scott’s increase in aquaporin 2 during spaceflight was correlated with higher levels of plasma sodium — an indicator of dehydration. Though further study is needed, the researchers believe that the increase in aquaporin 2 and plasma sodium may be tied to fluids shifting throughout Scott’s body while he was in a microgravity environment. This is important because, as has been documented with other space-bound astronauts, fluids tend to migrate to the head, causing visual impairment and intracranial pressure.
By taking advantage of an extremely unique opportunity, NASA’s Human Research Program has carried out the first genomic evaluation of the potential risks the human body faces during extended periods of spaceflight. While the results of NASA’s Twins Study are far from conclusive — the sample size is one set of twins and not every variable was strictly controlled for — the study does provide researchers with a wealth of data to guide future studies on the risks of human spaceflight.
As NASA said in a press release, “observations guide development of future hypotheses,” and NASA’s Twins Study has taken the first step to observing how our genomic blueprint is affected by long-term exposure to microgravity and an increased radiation environment. With the information collected as part of this medley of studies, NASA has the preliminary data it needs to inform countless more projects for years to come.
In the meantime, make sure to check back later this year when NASA releases its Twins Study summary paper, which will integrate the results from all ten of the individual studies. Shortly thereafter, each individual study will be releasing its own companion paper.
This post originally appeared in Astronomy.com.
Chemicals in Non-Stick Pans May Contribute to Weight Gain
Uhoh: Those non-stick pans you love cooking with are often made with a chemical that could contribute to weight gain. (Credit: Shutterstock)
More than 38 percent of American adults and 17 percent of American children are obese. And while there are numerous ways to shed pounds, it’s often difficult for many people to keep them off. It turns out some common items regularly used by people across the world could be the culprit.
A study released Tuesday in PLOS Medicine suggests that perfluoroalkyl substances (PFASs) could be contributing to weight gain and lead to obesity. Since the 1950s, these environmental chemicals have been used in food packaging, non-stick cookware, stain resistant fabrics and carpets, water-repellent clothing, and even some cosmetics. These manmade compounds’ effects on humans aren’t well known, but past studies on animals have shown they may disrupt the endocrine system, or the collection of glands that produce hormones. PFASs have also been linked to cancer, immune issues and high cholesterol.
Down and Up
Over the course of two years, researchers put 621 obese and overweight men and women on energy-restricted diets and tracked their weights. Measuring the plasma concentrations of PFASs, they were able to gather metabolic information including body weight and resting metabolic rate (RMR).
Researchers found that those with higher levels of PFASs at the beginning of the experiment were associated with regaining the pounds they lost, especially in women. Participants lost on average 14 pounds (6.4 kg) in the first six months, regaining almost half of the weight throughout the study. The weight gain could be due to a decline of RMR over the first six months.
“These chemicals may lead to more rapid weight gain after dieting,” Qi Sun, co-author of the study, told the Guardian. “It is very hard to avoid exposure to PFASs, but we should try to. It’s an increasing public health issue.”
With that said, the authors can’t definitively link PFAS chemicals to the weight regain. Some potentially important influences weren’t measured including socioeconomic and psychosocial factors and potential relapses to prior diets weren’t considered. Still, the authors hope this study will lead to further research of environmental chemicals and their possible impact on obesity.
Huntington's Disease Reveals a New Weapon to Fight Cancer
Scientists have found a silver lining to Huntington’s disease.
The malady causes nerve cells in the brain to break down; there is no cure. But if there’s one redeeming quality to this fatal genetic illness it’s this: Medical data has shown that people with Huntington’s are 80 percent less likely to develop cancer than the general population. But why?
Building off of previous experiments and related studies conducted over several years, Marcus Peter and his colleagues at Northwestern University in Chicago say they have successfully pinpointed the link between Huntington’s and cancer cells: RNA interference.
Peter, a professor of cancer metabolism at Northwestern’s Feinberg School of Medicine, said that there’s a system built into every cell that allows for it to kill itself at the detection of any serious defects. It’s been coined the “kill-switch” mechanism, and it involves the function of the RNA interference system, which is used in body cells to silence certain gene expressions.
“It’s a fantastic tool to interrogate the genome by selectively silencing individual genes and asking what happens to the cell,” says Peter.
Peter’s team can apply a cell silencer by either completely destroying the messenger RNAs (the instructions for building proteins), or by simply masking the mRNA and making it unreadable, thus stopping it at the protein production level. The first method involves small interfering RNAs (siRNAs), which cut up the mRNA, while the second relies on regulation help from a family of small RNAs called microRNAs. Both siRNAs and microRNAs are being heavily investigated for their role in cancer treatment.
Peter and his team found that they could induce inevitable cell death in cancer cells with siRNAs containing certain sequences. They called this system DISE: death induced by survival cell elimination.
“When we induce this particular form of cell death with siRNAs, we noticed that multiple, I mean many, cell death pathways are activated in parallel, and the fascinating part was that the cells could not become resistant to this,” says Peter.
Cancer cells are masters of resistance. Over time, most treatment therapies fail because cancer cells adapt and mutate components of the pathway so it can no longer accept or deliver signals. But by attacking an entire network of survival genes, the cell simply becomes overloaded. Better yet, the sensitivity to this treatment does not change with repeated exposure.
The Next Logical Step
Andrea Murmann, a research assistant professor at Northwestern and first author on the study, discovered the next steps to take with this powerful tool.
Murmann proposed that if this kill-switch was a fundamental biological mechanism, then there must be people with an overactive system which would result in the loss of certain tissues. In turn, these people would also have a lower prevalence of cancer. Her search narrowed to trinucleotide repeat diseases, of which Huntington’s is one of many.
Huntington’s disease is caused by over-amplification of nucleotide repeat sequence CAG (cytosine-adenine-guanine) in the the gene huntingtin, causing the pathology. While normally, everyone has around 30 repeats of this sequence, those afflicted by Huntington’s could have hundreds. The overabundance of the sequence, which codes for the protein glutamine down the line, results in a toxic buildup in the cell. The longer the length of the repeat, the earlier the onset of the disease.
These CAG repeats in huntingtin can be folded and processed to form small siRNAs active in RNA interference, and resulting small CAGs (sCAGs) have been shown in the past to kill cells—you might call these assassin molecules.
Peter and colleagues tested the cancer-fighting qualities of CAG-based siRNAs by delivering them—via nanoparticles—into mouse models with preclinical ovarian cancer.
“We developed natural nanoparticles that allow it to couple to siRNAs, and when the nanoparticles encounter a cancer cell, the cancer cells take up the nanoparticle without any further treatments…It just internalizes them, and release the cargo inside the cell,” says Peter. The team published results of their study Monday in the journal EMBO Reports.
In tests, the mice tumors regressed, and were still fully sensitive after treatment. Still, there’s more work to do.
“We just have to find a better way of formulating this for administering to the mice, and hopefully, to the people; but there’s a lot of technological components required to get better reagents to deliver siRNA to cells,” commented Peter. “Of course, all these steps need improvement, from the delivery to the stability, because we’re working on all these various aspects.”
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