Is cracking your knuckles a bad idea?

Cracking sounds on your joints can definitely sound—if not feel—alarming. It's probably happened to all of us, though, whether from cracking knuckles on purpose or just hearing popping sounds when stretching. I talked to a few medical experts to find out what's going on and whether or not all this noise is a sign of a medical issue. Here's what they said.

It's Usually Harmless The common misconception that cracking your joints will cause arthritis is just that—a misconception. Dr. Levi Harrison, an orthopedic surgeon and the author of The Art of Fitness, says he's often asked this question. He explains:

Commonly, joints make an audible cracking sound when the joint is stretched or manipulated due to gas inside the joint fluid or synovial fluid. Common gases in the joint are O2 (Oxygen) and N (Nitrogen). When you flex and stretch your fingers in order to "crack your knuckles", the capsule around the joint which contains this gas filled fluid causes the bubbles to burst which causes that sound. The sound may be loud or dull. Often, you have to wait a period of time before the sound can be heard again, if you manipulate the joint. It takes time for the gas bubbles to reform in the joint.

Dr. Michael Haley, owner of Agape Chiropractic, offers a few more insights —and strange medical terms (joint mice? crepitus?!) that describe the issue:

Sometimes the sounds are coming from muscle bellies. Other times they are coming from the deeper joint structures - tendons, ligaments, and discs. Sometimes the sounds aren't "cracking sounds" at all, but rather, inflammation in the joints that is "squishing around" with movement. These are the noises someone might hear continuously when they turn their heads side to side. Ideally, turning your head does not make any noise. Joint mice may contribute to the sounds. These sounds are collectively usually referred to as "crepitus".

Based on clinical experience, it seems that tension builds up and allows for the joints to "crack" or release. Inactivity seems to increase the need... whereas frequent movement and stretching seems to not only decrease the need, but also even the possibility of of cracking the joints.

An interesting observation is that humans learn to disobey their need for movement. Cats and dogs seem to stretch out their bodies, with an emphasis on their spines, after every period of inactivity. Kids seem to stretch after inactivity too. But adults tend to get up and go about their sedentary days. No wonder their joints crack... or need cracking…

In other words, it's a good idea to fit more movement into your day, if you're not already doing so.

When You Might Want to Consult a Doctor Those assurances aside, there are times cracking joints is more ominous. If you experience any pain with the cracking, it could be a sign of a medical problem. Dr. Harrison says:

Individuals who have painful grinding and creaking joints that started after an injury or trauma to their joints may have arthritis. This is not a good thing. Arthritis occurs when the protective cartilage lining of a joint has been damaged or eroded. This can occur from an injury, age, or an even inflammatory condition like rheumatoid arthritis.

If you have had an injury, for example to your hips or knee and experience significant hip and or knee pain, as well as popping of your joints, you may have arthritis in these areas. I recommend an evaluation by your healthcare practitioner. After an appropriate history and physical exam, they may order the necessary radiographic tests to evaluate the joint. Arthritis is common and pain with creaking and popping in any joint warrants proper evaluation by your doctor.

In the absence of pain, though, you probably don't have to worry (but can check with your doctor if you're still anxious about this). Dr. Harrison doesn't recommend cracking your knuckles, neck, or anything else, but it's still probably harmless. Consider this research noted by Dr. Amy Baxter, CEO of MMJ Labs (which makes a really cool pain blocker, Buzzy):

One really fun paper was what we call an "n of 1" study - some guy (Dr. DL Unger) decided to only crack one hand his whole life, and see what happened. He then published the result. Bottom line: the cracked knuckle was bigger, but none the worse for wear.

I also asked my sister, a family physician in Arizona, about this, and she said she gets this question a lot—strangely from young teenage patients. Her advice? It's probably nothing...but if it bothers you, stop cracking your knuckles or neck. So there you go.

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Study suggests we're all susceptible to false memories

Researchers from UC Irvine have found that people with extraordinarily accurate memory are as vulnerable to the inception of fake memories as others, indicating that perhaps nobody is protected from memory distortion. The study, published last month in Proceedings of the National Academy of Sciences, focused on people with highly superior autobiographical memory (HSAM), who are able to recall highly specific facts about their lives, like what they ate for lunch, going all the way back to their childhood.

In one test, subjects were falsely told that news footage captured the plane crash of United 93 in Pennsylvania on September 11th, 2001. The researches found that when asked if they had seen the footage before, 20 percent of subjects with HSAM said they had, compared to 29 percent of people with normal memory. In other tests including false narratives, people with HSAM said they remembered the false facts about as much as people with normal memory.

The results echo earlier scientific studies about the implantation of false memories. The consequences are far reaching and impact our ability to trust things like eyewitness reports, which are vital for historical, journalistic, and legal matters. The Innocence Project claims that the leading cause of wrongful conviction in the United States is improper identification in eyewitness testimony; the Project says that of the 311 convicts who've been exonerated by DNA since 1989, 72 percent of those cases involved false eyewitness testimony.

"Even though this study is about people with superior memory, this study should really make people stop and think about their own memory," researcher Lawrence Pathis told The Atlantic . "Gone are the days when people thought that [only] maybe 20, 30, or 40 percent of people are vulnerable to memory distortions."

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BREAST CANCER SPREADS WHEN TUMORS CAN’T ‘BREATHE’

Lack of oxygen inside a breast cancer tumor can trigger the chain of events that spreads the disease throughout the body, biologists say.

The discovery explains how tumors produce two proteins that transform breast cancer cells from rigid and stationery to mobile and invasive—and may lead to new strategies for interrupting the spread of tumors, the process called metastasis.

“High levels of RhoA and ROCK1 were known to worsen outcomes for breast cancer patients by endowing cancer cells with the ability to move, but the trigger for their production was a mystery,” says Gregg Semenza, professor of medicine at Johns Hopkins University School of Medicine.

“We now know that the production of these proteins increases dramatically when breast cancer cells are exposed to low-oxygen conditions.”

To move, cancer cells must make many changes to their internal structures, says Semenza. Thin parallel filaments form throughout the cells, allowing them to contract. Cellular “hands” rise up allowing cells to “grab” external surfaces to pull themselves along. The proteins RhoA and ROCK1 are known to be central to the formation of these structures.

The genes that produce RhoA and ROCK1 are known to be turned on at high levels in metastatic breast cancers. In a few cases, those increased levels can be traced back to a genetic error in a protein that controls them, but not in most. This led Semenza to search for another cause for the high levels.

The study, published in the Proceedings of the National Academy of Sciences, shows that low-oxygen conditions, common in breast cancers, serve as the trigger for increased production of RhoA and ROCK1.

MASTER CONTROL PROTEINS

“As tumor cells multiply, the interior of the tumor begins to run out of oxygen because it isn’t being fed by blood vessels,” Semenza explains. “The lack of oxygen activates the hypoxia-inducible factors, which are master control proteins that switch on many genes that help cells adapt to the scarcity of oxygen.”

While that response is essential for life in normal cells, hypoxia-inducible factors also turn on genes that help cancer cells escape from the oxygen-starved tumor by invading blood vessels, through which they spread to other parts of the body.

Daniele Gilkes, a postdoctoral fellow and lead author of the report, analyzed human metastatic breast cancer cells grown in low oxygen conditions in the laboratory. She found that the cells were much more mobile in the presence of low levels of oxygen than at physiologically normal levels. They had three times as many filaments and many more “hands” per cell.

When the hypoxia-inducible factor protein levels were knocked down, though, the tumor cells hardly moved at all. The numbers of filaments and “hands” in the cells and their ability to contract were also decreased.

PREVENTING METASTASES

When Gilkes measured the levels of the RhoA and ROCK1 proteins, she saw a big increase in the levels of both proteins in cells grown in low oxygen.

When the breast cancer cells were modified to knock down the amount of hypoxia-inducible factors, however, the levels of RhoA and ROCK1 decreased, indicating a direct relationship between the two sets of proteins. Further experiments confirmed that hypoxia-inducible factors actually bind to the RhoA and ROCK1 genes to turn them on.

The team then took advantage of a database that allowed them to check whether having RhoA and ROCK1 genes turned on in breast cancer cells affected patient survival. They found that breast cancer patients with high levels of RhoA or ROCK1, and especially those with high levels of both, were much more likely to die of breast cancer than those with low levels.

“We have successfully decreased the mobility of breast cancer cells in the lab by using genetic tricks to knock the hypoxia-inducible factors down,” Gilkes says.

“Now that we understand the mechanism at play, we hope that clinical trials will be performed to test whether drugs that inhibit hypoxia-inducible factors will have the double effect of blocking production of RhoA and ROCK1 and preventing metastases in women with breast cancer.”

The National Cancer Institute, Johns Hopkins Institute for Cell Engineering, the American Cancer Society, and the Susan G. Komen Breast Cancer Foundation supported the research.

Source: Johns Hopkins University

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How a retrovirus can kick-start brain repair

Researchers used a retrovirus to regenerate neurons after a brain injury and in Alzheimer’s models. The method may lead to therapies for an array of neurological disorders.

Gong Chen, a professor of biology, the Verne M. Willaman Chair in Life Sciences at Penn State, and the leader of the research team, calls the method a breakthrough in the long journey toward brain repair.

“This technology may be developed into a new therapeutic treatment for traumatic brain and spinal cord injuries, stroke, Alzheimer’s disease, Parkinson’s disease, and other neurological disorders,” Chen says. The research appears in the journal Cell Stem Cell.

When the brain is harmed by injury or disease, neurons often die or degenerate, but glial cells increase and branch out. These “reactive glial cells” initially build a defense system to prevent bacteria and toxins from invading healthy tissues, but this process eventually forms glial scars that limit the growth of healthy neurons.

“A brain-injury site is like a car-crash site,” Chen explains. “Reactive glial cells are like police vehicles, ambulances, and fire trucks immediately rushing in to help—but these rescue vehicles can cause problems if too many of them get stuck at the scene. The problem with reactive glial cells is that they often stay at the injury site, forming a glial scar and preventing neurons from growing back into the injured areas.”

Reviving Scar Tissue

Several years ago, Chen’s lab tested new ways to transform glial scar tissue back to normal neural tissue.

“There are more reactive glial cells and fewer functional neurons in the injury site,” Chen says, “so we hypothesized that we might be able to convert glial cells in the scar into functional neurons at the site of injury in the brain. This research was inspired by the Nobel prize-winning technology of induced pluripotent stem cells (iPSCs) developed in Shinya Yamanaka’s group, which showed how to reprogram skin cells into stem cells.”

Chen and his team began by studying how reactive glial cells respond to a specific protein, NeuroD1, which is known to be important in the formation of nerve cells in the hippocampus area of adult brains. They hypothesized that expressing NeuroD1 protein into the reactive glial cells at the injury site might help to generate new neurons—just as it does in the hippocampus.

To test this hypothesis, his team infected reactive glial cells with a retrovirus that specifies the genetic code for the NeuroD1 protein.

“The retrovirus we used is replication-deficient and thus cannot kill infected cells like other viruses found in the wild,” Chen says. “More importantly, a retrovirus can infect only dividing cells such as reactive glial cells, but it does not affect neurons, which makes it ideal for therapeutic use with minimal side effect on normal brain functions.”

In a first test, Chen and his team investigated whether reactive glial cells can be converted into functional neurons after injecting NeuroD1 retrovirus into the cortex area of adult mice. The scientists found that two types of reactive glial cells—star-shaped astroglial cells and NG2 glial cells—were reprogrammed into neurons within one week after being infected with the NeuroD1 retrovirus.

“Interestingly, the reactive astroglial cells were reprogrammed into excitatory neurons, whereas the NG2 cells were reprogrammed into both excitatory and inhibitory neurons, making it possible to achieve an excitation-inhibition balance in the brain after reprogramming,” Chen says.

His lab also performed electrophysiological tests, which demonstrated that the new neurons converted by the NeuroD1 retrovirus could receive neurotransmitter signals from other nerve cells, suggesting that the newly converted neurons had successfully integrated into local neural circuits.

Alzheimer’s model

In a second test, Chen and his team used a transgenic-mouse model for Alzheimer’s disease, and demonstrated that reactive glial cells in the mouse’s diseased brain also can be converted into functional neurons. Furthermore, the team demonstrated that even in 14-month-old mice with Alzheimer’s disease—an age roughly equivalent to 60 years old for humans—injection of the NeuroD1 retrovirus into a mouse cortex can still induce a large number of newborn neurons reprogrammed from reactive glial cells.

“Therefore, the conversion technology that we have demonstrated in the brains of mice potentially may be used to regenerate functional neurons in people with Alzheimer’s disease,” Chen says.

To ensure that the glial cell-to-neuron conversion method is not limited to rodent animals, Chen and his team further tested the method on cultured human glial cells. “Within 3 weeks after expression of the NeuroD1 protein, we saw in the microscope that human glial cells were reinventing themselves: they changed their shape from flat sheet-like glial cells into normal-looking neurons with axon and dendritic branches,” Chen says.

The scientists further tested the function of these newly converted human neurons and found that, indeed, they were capable of both releasing and responding to neurotransmitters.

“Our dream is to develop this in vivo conversion method into a useful therapy to treat people suffering from neural injury or neurological disorders. Our passionate motivation for this research is the idea that an Alzheimer’s patient, who for a long time was not able to remember things, could start to have new memories after regenerating new neurons as a result of our in vivo conversion method, and that a stroke victim who could not even move his legs might start to walk again.”

Penn State University and the National Institutes of Health funded the project.

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7 Fascinating Facts About Your Muscles

Your muscles aren't just fibers and nerves. They're complex tissues that help you move and, in the process, torch calories and fat to give you a lean, fit figure. So do yourself a favor and get to know them—they're a lot more interesting than you might think.

Your muscles can be up to 70 percent water, says Monica Nelson, American Council on Exercise-certified fitness expert. So when you work out, you should always carry some H2 O with you to keep them hydrated.

Muscle tissue makes up 35-40 percent of your body weight, says Nelson. So keep this mind before jumping to conclusions when you hop on the scale.

For every pound of muscle, the average person can burn up to 50 extra calories, says Nelson. Hmm, suddenly that number on the scale doesn't seem so bad…

Using heavier weights in your exercises won't necessarily make your muscles stronger. In order to make strength gains, practicing good form should be at the top of your get-fit list, says fitness expert Suzanne Bowen, creator of BarreAmped.

A single step uses almost 200 different muscles, says Nelson, including your hamstrings, quads, iliacus, and psoas major and minor.

Your muscles memorize movement patterns, says strength coach Lee Boyce , owner of Boyce Training Systems in Toronto, Canada. So if you end up taking a break from the gym—planned or unplanned—all your body needs is a few warm-up exercises to remember how to get into the swing of things.

Source: Women Health Magazine

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This Gene Helps Some of Us Never Forget a Face

The oxytocin receptor, a gene known to influence mother-infant bonding, also plays a role in the ability to remember faces.

The finding has important implications for disorders in which social information processing is disrupted—like autism spectrum disorder—and may lead to new strategies for improving social cognition in several psychiatric disorders.

According to study author Larry Young, of the department of psychiatry at Emory University, this is the first study to demonstrate that variation in the oxytocin receptor gene influences face recognition skills.

He and colleagues point out the implication that oxytocin plays an important role in promoting our ability to recognize one another, yet about one-third of the population possesses only the genetic variant that negatively impacts that ability.

The new finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.

For the study published in Proceedings of the National Academy of Sciences, researchers studied 198 families with a single autistic child because these families are known to show a wide range of variability in facial recognition skills. Two-thirds of the families were from the United Kingdom, and the remainder from Finland.

Researchers had previously found the oxytocin receptor is essential for olfactory-based social recognition in rodents, like mice and voles, and wondered whether the same gene could also be involved in human face recognition.

Familial face recognition They examined the influence of subtle differences in oxytocin receptor gene structure on face memory competence in the parents, non-autistic siblings, and autistic child, and discovered a single change in the DNA of the oxytocin receptor had a big impact on face memory skills in the families.

This finding implies that oxytocin likely plays an important role more generally in social information processing, which is disrupted in disorders such as autism.

Additionally, this study is remarkable for its evolutionary aspect. Rodents use odors for social recognition while humans use visual facial cues.

This suggests an ancient conservation in genetic and neural architectures involved in social information processing that transcends the sensory modalities used from mouse to man.

Skuse credits Young’s previous research that found mice with a mutated oxytocin receptor failed to recognize mice they previously encountered.

“This led us to pursue more information about facial recognition and the implications for disorders in which social information processing is disrupted.”

Researchers from University College London and University of Tampere in Finland contributed to the study, which was funded by grants from the US National Institute of Mental Health and the Office of Research Infrastructure Programs as well as the Nancy Lurie Marks Family Foundation and National Alliance for Autism Research.

Source: Emory University

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