Thursday, June 29, 2017

Why does hair turn gray?


As you look in the mirror in the morning, you see that inevitable fate has struck: your first gray hair! Whether you are in your 20s or your 50s, gray hair catches up with all of us eventually.

During hair growth, melanocytes make pigment and pass it to hair progenitor cells at the base of the hair follicle. These cells, in turn, transform into the various components of the growing hair.
When our hair grows, pigments are continuously being incorporated, which results in our unique hair color. The cells responsible for this process are the pigment-producing melanocytes at the base of the hair follicle.
In normal hair growth, the follicle produces hair at a rate of around 1 centimeter per month for several years.
But all the cells in our body become increasingly damaged during our lifetime, and these melanocytes are eventually lost. When all the melanocytes are lost in a particular hair follicle, the next hair that grows will be gray or white.
The biology of hair growth is rather complex, with a multitude of specialized cells involved in hair follicle structure and function. Scientists continue to unravel the process of human hair growth and pigmentation.

What controls pigmentation?

Humans have two different types of pigment. Eumelanin is responsible for black and brown colors, while pheomelanin is responsible for orange and yellow.
Genes determine the mixture of pigments that each individual produces, which is why hair color is often similar within families.
The exact mechanisms that control pigmentation are not yet clear. However, recent research points to a finely tuned interplay between several cells in the hair follicle.
Hair progenitor cells are reported to release a protein called stem cell factor, which is a requirement for the production of pigment by melanocytes. In mouse studies, the researchers showed that if this protein is absent, hair color is lost.
Once the hair stops growing, the hair follicle undergoes dramatic structural changes and enters a rest period. During this process, melanocytes naturally die.
However, melanocyte stem cells in the hair follicle normally produce a new set of melanocytes at the start of the next hair growth cycle.
Once the new hair starts to grow, these melanocytes once again ensure that pigmentation is available. But when the melanocytes are damaged or absent, the hair that is produced lacks color and can look gray or white.

Hair growth after damage

Research has shown that human hair follicles that produce gray or white hair have higher levels of cellular damage caused by free radicals. In these follicles, melanocytes and melanocyte stem cells are absent.
In mice, when the DNA of melanocyte stem cells in the hair follicle were damaged, it resulted in permanent cell damage. These stem cells were then unable to reproduce.
Without the pool of stem cells, the next round of hair growth proceeds without melanocytes, resulting in gray hair.
Although it has not yet been possible to fully establish cause and effect during hair graying in humans, the accumulation of damage in melanocyte stem cells over time most likely leads to a loss of this cell population. Each hair follicle will eventually be unable to produce colored hair.
So, while it is inevitable that we will all lose our hair pigment one day, why do some of us go gray in our 20s, while some of us hold on to our colorful locks until our 50s? Research from 2016 showed that individuals with a certain variant of the gene interferon regulatory factor 4 are prone to earlier graying.
As with many of our other traits, we can thank our parents for passing their propensity for graying along to us.

Inflammatory bowel disease: Scientists zoom in on genetic culprits

Scientists have closed in on specific genes responsible for Inflammatory Bowel Disease (IBD) from a list of over 600 genes that were suspects for the disease. The team from the Wellcome Trust Sanger Institute and their collaborators at the Broad Institute of MIT and Harvard and the GIGA Institute of the University of Liège combined efforts to produce a high resolution map to investigate which genetic variants have a causal role in the disease.
In the new study, published today (28 June) in Nature, scientists examined the genome of 67,852 individuals and applied three statistical methods to zoom in on which genetic variants were actively implicated in the disease. Of the regions of the genome associated with IBD that were studied, 18 could be pin-pointed to a single genetic variant with more than 95 per cent certainty. The results form a basis for more effective prescription of current treatments for the disease as well as the discovery of new drug targets.
More than 300,000 people suffer from IBD in the UK. IBD is a debilitating disease in which the body's own immune system attacks parts of the digestive tract. The exact causes of this disease are unclear, and there currently is no cure.
To understand more about the genetics underlying IBD, researchers have conducted genome wide association studies and previously found hundreds of genetic variants linked to the disease. However, it was not certain which specific genes were actually implicated by those variants.
Dr Jeffrey Barrett, joint lead author from the Wellcome Trust Sanger Institute said: "We have taken the biggest ever data set for IBD and applied careful statistics to narrow down to the individual genetic variants involved. Now we have a clearer picture of which genes do and do not play a role in the disease. We are zooming in on the genetic culprits of IBD."
The high resolution map of the disease enabled scientists to see which variants directly influence disease, and to separate them from other variants which happen to be located near each other in the genome.
Dr Hailiang Huang, first author from the Massachusetts General Hospital and Broad Institute said: "An issue with studying complex diseases is that it can be hard to move from genetic associations, usually including many genetic variants of similar evidence, to knowing exactly which variants are involved. We need to be careful in deciding when we are sure we have the right variant. This new technique helps us to pinpoint which genetic variants are implicated in IBD with greater confidence."
Professor Michel Georges, joint lead author from the GIGA Institute of the University of Liège said: "These results will help towards rational drug discovery for complex human diseases like IBD, and possibly for the development of personalised medicine by finding biomarkers for more effective prescription of existing drugs."

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Materials provided by Wellcome Trust Sanger InstituteNote: Content may be edited for style and length.

A new weapon for the war on cancer

Cancerous tumors are formidable enemies, recruiting blood vessels to aid their voracious growth, damaging nearby tissues, and deploying numerous strategies to evade the body's defense systems. But even more malicious are the circulating tumor cells (CTCs) that tumors release, which travel stealthily through the bloodstream and take up residence in other parts of the body, a process known as metastasis. While dangerous, their presence is also a valuable indicator of the stage of a patient's disease, making CTCs an attractive new approach to cancer diagnostics. Unfortunately, finding the relative handful of CTCs among the trillions of healthy blood cells in the human body is like playing the ultimate game of needle-in-a-haystack: CTCs can make up as few as one in ten thousand of the cells in the blood of a cancer patient. This is made even more difficult by the lack of broad-spectrum CTC capture agents, as the most commonly used antibodies fail to recognize many types of cancer cells.
To address this problem, a group of researchers at the Wyss Institute at Harvard University has adapted an engineered human blood opsonin protein known as FcMBL, which was originally developed as a broad-spectrum pathogen capture agent, to target CTCs instead. Using magnetic beads coated with FcMBL, they were able to capture >90% of seven different types of cancer cells. "We were able to rapidly isolate CTCs both in vitro and from blood, including some which are not bound by today's standard CTC-targeting technologies," says Michael Super, Ph.D., Lead Senior Staff Scientist at the Wyss Institute and co-author of the paper. "This new technique could become useful in cancer diagnostics." The technology is described today in Advanced Biosystems.
Current CTC diagnostic systems frequently make use of a cancer cell marker, the epithelial cell adhesion molecule (EpCAM), which is highly expressed on the surface of tumor cells. However, EpCAM expression on cancer cells decreases when tumor cells transform into CTCs, ironically making EpCAM-based tests less useful precisely when it is most crucial to know that a patient's cancer has metastasized.
The Wyss Institute capture technology takes advantage of a protein naturally found in the body, mannose-binding lectin (MBL), which recognizes and binds to carbohydrates present on the surfaces of bacteria and other pathogens, marking them for destruction by the immune system. Healthy human cells have different carbohydrate patterns and are immune to MBL, but many cancer cells have aberrant carbohydrates that are similar to those found on pathogens and, therefore, are vulnerable to MBL binding.
The team previously developed a genetically engineered version of MBL in which the binding portion is fused to an antibody Fc fragment (FcMBL) to stabilize the molecule. Past studies showed that when tiny magnetic beads are coated with FcMBL and added to various pathogens, the FcMBL-coated beads attach to the surfaces of these cells like flies on flypaper so that, when a magnetic field is applied, the beads drag their bound cells along with them toward the magnet.
To evaluate whether this system could specifically target CTCs, the researchers implanted fluorescently-labeled human breast cancer cells in mice, let the tumors develop for 28 days, and then tested the blood to determine the number of CTCs present. They then mixed the blood with FcMBL-coated beads and pulled the beads out of suspension with a magnet. "The FcMBL-coated beads are unlikely to be bound to normal cells, and so when we measured the movement of cancer cells versus normal cells, the cancer cells moved much faster because they were being dragged to the magnet by the beads," explains first author Joo Kang, Ph.D., who was a Technology Development Fellow at the Wyss Institute while completing this study and is now an Assistant Professor at the Ulsan National Institute of Science and Technology. The concentration of CTCs present in the blood was also reduced by more than 93%, showing that FcMBL can effectively capture CTCs in the blood even after they have undergone the transitions that reduce EpCAM expression.
The team then tested their system against six additional cancer cell types, including human non-small cell lung cancer, lung carcinoma, and glioblastoma. The FcMBL-coated beads captured all six types of tumor cells with >90% efficiency -- which is comparable to EpCAM-targeting methods -- and were also able to capture two types that are not successfully bound by anti-EpCAM antibodies (lung carcinoma and glioblastoma). "Our results suggest that while the EpCAM marker can be useful for some tumors, it becomes less and less useful over time as EpCAM expression decreases and the cell becomes metastatic," says Super. "Our FcMBL system can either be used as an alternative to EpCAM-based diagnostics, or as a follow-up method once EpCAM ceases to be expressed."
The researchers hope to continue their studies to determine exactly which carbohydrate molecules FcMBL is targeting on CTCs, which could further improve the specificity and efficacy of capture. "The FcMBL opsonin technology has already been shown to be an extremely broad-spectrum capture agent for pathogens," says senior author of the study and Wyss Founding Director Donald Ingber, who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School (HMS) and the Vascular Biology Program at Boston Children's Hospital, as well as a Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. "This new finding that it has similar broad-spectrum binding activity for many different types of circulating cancer cells is equally exciting, and once again demonstrates the power of leveraging biological design principles when developing new medical innovations."

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Materials provided by Wyss Institute for Biologically Inspired Engineering at HarvardNote: Content may be edited for style and length.

Combating chronic kidney disease with exercise

A University of Delaware research team in the College of Health Sciences is combating chronic kidney disease (CKD) with exercise.
Dave Edwards, professor in UD's Department of Kinesiology and Applied Physiology, received a National Institutes of Health grant to investigate whether exercise training could improve the health of the blood vessels.
Edwards and postdoctoral researcher Danielle Kirkman invited early stage CKD patients to take part in a specially designed exercise program, all completed under the expert supervision of UD researchers.
The study showed the exercise program improved blood vessel health and exercise capacity. Equally as important, patients reported improvements in their everyday quality of life as a result of becoming more active.
More than 26 million American adults have CKD and, because of difficult-to-see warning signs, late detection is common. The leading cause of death in patients with CKD is cardiovascular disease.
The end of the study turned out to be just the beginning for participants. They wanted to continue exercising, but lacked a safe, supervised environment.
To meet the demand, Edwards' lab started a renal rehab exercise program for CKD patients in the community. The program is open to non-dialysis CKD, dialysis patients and those that have received a kidney transplant.
"There are two groups of patients that fall through the cracks -- those who have exercised with us and want to continue and those who didn't qualify for our studies, but wanted to start exercising," Edwards said.
The team works individually with each patient to reach their goals, whether it's controlling blood pressure or losing weight for a transplant.
"If you look at other areas like cardiac or pulmonary rehab, exercise training is well-integrated as part of routine care; that's not the case with kidney disease," Kirkman said. "Exercise may have an array of health benefits to these patients ranging from keeping their diabetes under control, maintaining healthy muscles and blood vessels to controlling weight gains after a transplant that are associated with prescribed medications."
Once word got out that UD was offering the program, the research team fielded a mini-explosion of interest. Transplant doctors and dialysis clinics began sending patients to the renal rehab program to work on their health and fitness. Soon groups of kidney disease patients were exercising together -- sometimes eight people per session in the friendly confines of the Kinesiology and Applied Physiology (KAAP) Exercise Intervention Lab.

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Materials provided by University of Delaware. Original written by Dante LaPenta. Note: Content may be edited for style and length.

Wednesday, June 28, 2017

Dairy: Is it good or bad for you?

Dairy is a controversial and confusing food group. Health organizations promote dairy as vital for improved bone health, yet other experts disagree and hail dairy as detrimental to health. Who is correct? Is dairy good or bad for your health? We examine the facts.
What do government health guidelines say? According to the United States Department of Agriculture (USDA) food MyPlate guidelines, to get all the nutrients you need from your diet, healthy food and beverage choices should be made from all five food groups, including fruits, vegetables, grains, protein foods, and dairy.
The dairy food group consists of all fluid milk products and many foods that are made from milk. The USDA recommend that food choices from the dairy group should retain their calcium content and be low-fat or fat-free. Fat in milk, yogurt, and cheese that is not low-fat or fat-free will count toward your limit of calories from saturated fats.
While calcium-fortified soymilk is included as part of the dairy group, food products such as butter, cream, sour cream, and cream cheese are not included due to their low calcium content.
Daily dairy recommendations depend on your age. Children 2-3 years old require two cups of dairy per day, 4-8 year-olds need 2.5 cups per day, and three cups per day are recommended for age 9 and upward.
For people who do not consume dairy products, the USDA mention the following foods to contribute toward calcium intake: kale leaves, calcium-fortified juices, breads, cereals, rice or almond milk, canned fish, soybeans, other soy foods, such as tofu, soy yogurt, and tempeh, and some leafy greens including collard and turnip greens, kale, and bok choy.
They point out that the amount of calcium that is absorbed from these foods varies.

MyPlate vs. Healthy Eating Plate

The USDA developed the MyPlate nutrition guide in 2011 as a replacement for their MyPyramid that was used for 19 years.
The Harvard T.H. Chan School of Public Health state that while the USDA MyPlate has been revised to reflect some key findings in nutritional scientific research, it does not offer a complete picture of basic nutrition advice.
The Harvard T.H. Chan School of Public Health created the Healthy Eating Plate to address the deficiencies they identified in the USDA's MyPlate.
One major alteration to the Healthy Eating Plate compared with MyPlate is the replacement of the dairy glass with a glass of water. The Healthy Eating Plate recommends drinking water, tea, or coffee and limiting dairy to one to two servings per day, since they say that high intakes are associated with a greater risk of prostate cancer and possibly ovarian cancer.
MyPlate recommends dairy with every meal to protect against osteoporosis. However, the Harvard T.H. Chan School of Public Health report that there is little to no evidence to support this statement and considerable evidence that too high an intake of dairy can be harmful.

Nutrients in milk

Milk is a good source of calcium, potassiumvitamin D, and protein.

Milk is an important source of calcium and may help maintain and improve bone health.
The USDA report that dairy products are the primary source of calcium in the American diet. They also say that calcium helps to build bones and teeth, maintain bone mass, improve bone health, decrease the risk of osteoporosis and, what is more, diets that have an intake of three cups of dairy products per day can improve bone mass.
Furthermore, they note that dairy intake is particularly important to bone health during childhood and adolescence - a time when bone mass is being built.
Potassium in milk may help with maintaining blood pressureVitamin D helps the body maintain the correct calcium and phosphorous levels, which, in turn, contributes to building and maintaining bones. Dairy intake is also associated with a reduced risk of cardiovascular disease, type 2 diabetes, and lower blood pressure.
The USDA highlight that it is important to choose low-fat or fat-free foods from the dairy group because foods high in saturated fats and cholesterol have adverse health implications. They say that diets high in saturated fats raise "bad" low-density lipoprotein (LDL) cholesterol in the blood. High LDL cholesterol increases the risk for coronary heart disease. Whole milk and many dairy products are high in saturated fat.
To help keep blood cholesterol levels healthy, the USDA recommend limiting the intake of foods high in saturated fat.
In summary, government guidelines say that milk is rich in nutrients. Calcium-rich low-fat or fat-free dairy products are essential for bone health, heart health, and type 2 diabetes, but full-fat dairy increases the risk for coronary heart disease. All sounds simple enough. So where does the controversy come in?

Is eating dairy 'natural'?

It is often argued that dairy products should not be consumed since it is not "natural" to do so.
Cow's milk is designed to provide all the protein, micronutrients, and fatty acids that calves need to grow in the same way that breast milk is designed to nurture human babies.
Not only are humans the only species that consumes milk as adults, but we are also the only species that drinks milk from other animals. Humans are not calves, and they have no need to grow, so why drink milk? Quite a convincing argument.
Dairy does not appear to be essential for humans from an evolutionary perspective and was not consumed until after the agricultural revolution. However, in some parts of the world, dairy has been consumed for thousands of years, and research has shown that genes have altered in humans to accommodate dairy consumption.
While consuming dairy may not have once been natural for humans, the evidence that shows that we have genetically adapted to eat dairy indicates that it may now be natural for us to eat and drink it.

Lactose intolerance

Another argument against dairy consumption is that around 75 percent of the world's population and about 25 percent of the people in the U.S. lose their ability to produce digestive lactase enzymes sometime after weaning.
Lactase enzymes are present in infants and young children to help them break down and digest lactose - a sugar present in milk. A lack of lactase enzymes means that lactose cannot be split into glucose and galactose for absorption into the bloodstream, which results in lactose intolerance.
After eating lactose-containing dairy products, people who are lactose intolerant experience abdominal bloating, pain, nausea, flatulence, and diarrhea. Some lactose intolerant individuals can eat fermented dairy, such as yogurt, or high-fat, dairy like butter.
Most people of Northern European ancestry can digest lactose with no problems whatsoever.

Full-fat dairy and cardiovascular disease

The USDA guidelines and conventional wisdom dictate that full-fat dairy increases the risk of heart disease due to its high saturated fat content.

Research investigating the link between dairy consumption and heart disease is conflicting.
The theory behind this idea is that saturated fat raises levels of LDL cholesterol in the blood, LDL cholesterol then lodges in the arteries, which causes atherosclerosis and eventually, heart disease. However, despite it being a dietary recommendation, this theory has never been proven and has been debunked in recent years.
systematic review and meta-analysis published in the Annals of Internal Medicine and a meta-analysis published in The American Journal of Clinical Nutrition found no link between dietary saturated fat and an increased risk of coronary heart disease, stroke, and cardiovascular disease.
A study that used data from the Nurses' Health Study - a long-term epidemiological study in the U.S. examining risk factors for major chronic disease in women - found that high intake of dairy fat is connected with a greater risk of coronary heart disease.
However, other studies have shown that full-fat dairy may protect against heart disease and stroke.
For example, research examining 10 studies that included full-fat dairy consumption showed that drinking milk might be associated with "a small but worthwhile reduction in heart disease and stroke risk."
In grass-fed cows, full-fat dairy has been linked with a reduced risk of heart disease and stroke. One study indicated that people who consumed the most full-fat dairy had a 69 percent lower risk of cardiovascular death than individuals who consumed the least.
Research examining the role of dairy in heart disease is conflicting. However, heart disease risk seems to be significantly lower when consuming full-fat dairy in countries with grass-fed cows.

Does dairy benefit bone health?

Most health organization guidelines recommend an intake of two to three servings of dairy every day to ensure adequate calcium for bone health.

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Some experts disagree with these guidelines because countries with higher dairy consumption have higher rates of osteoporosis than countries with lower intakes of dairy. However, it has to be noted that dairy consumption is not the only difference between these countries and does not conclude that dairy causes osteoporosis.
Two observational studies are often cited in the argument against consuming milk for bone health. The first study suggests that consumption of dairy products - particularly at the age of 20 years - is associated with a greater risk of hip fracture in old age. The second study found no evidence that intake of milk or calcium protects against hip or forearm fractures.
However, numerous studies support the benefits of dairy consumption for bone health. Research indicates that consuming dairy increases bone density and may prevent age-related bone loss and osteoporosis.
Randomized controlled trials are considered to be more reliable than observational studies and have shown in every age group that dairy improves bone health.
Dairy and calcium consumption leads to increased bone growth in children, decreases bone loss in adults, and improves bone density and lowers fracture risk in seniors.
Other than calcium, dairy provides other nutrients that are beneficial to bone health, such as protein and phosphorous, and Vitamin K-2 in full-fat dairy from grass-fed cows. Vitamin K-2 is a fat-soluble vitamin and is not present in low-fat and fat-free varieties of dairy products. Vitamin K-2 helps to regulate calcium metabolism, is vital for bone health, and may prevent heart disease.

Other conditions associated with dairy

Dairy has been linked to the development and prevention of many conditions and appears to cause and cure various diseases simultaneously. We check out the evidence behind these claims.

Obesity


Evidence suggests that dairy consumption lowers the risk of developing type 2 diabetes.
Dairy products, and full-fat dairy products in particular, might be avoided due to concerns that these foods are fattening and may lead to obesity.
However, a study published recently in the American Journal of Clinical Nutrition determined that children who drink whole milk are leaner and have higher levels of vitamin D than those who drink the low-fat or skimmed varieties.

Type 2 diabetes

While flavored milk should be avoided with diabetes, there is no reason that people with diabetes should not consume dairy products.
In fact, research by Dr. Ulrika Ericson, of the Lund University Diabetes Center in Malmö, Sweden, and colleagues found that people who consumed the highest amounts of high-fat dairy products had a 23 percent lower risk of developing type 2 diabetes than individuals who consumed the least amount of dairy per day.
Harvard University found that teenagers who drink milk are 43 percent less likely to develop type 2 diabetes as adults compared with non-milk drinkers.

Prostate cancer

Some studies have found that a high dairy intake is associated with an increased risk of prostate cancer. One study reported that having higher intake of dairy increased the risk of prostate cancer by 32 percent. This greater risk may be linked to calcium levels.
In contrast, a study published in the British Journal of Cancer does not support the theory that high calcium intake increases the risk of prostate cancer.

Parkinson's disease

Katherine C. Hughes, of the Harvard T.H. Chan School of Public Health, and collaborators have found an association between consuming at least three servings of low-fat dairy a day and risk of developing Parkinson's disease.
"The results provide evidence of a modest increased risk of Parkinson's with greater consumption of low-fat dairy products. Such dairy products, which are widely consumed, could potentially be a modifiable risk factor for the disease," said Hughes.
The study authors stress that the findings do not mean that dairy products cause Parkinson's disease, they just show a link between the two.

Depression

Opting for low-fat dairy rather than full-fat dairy reduces the risk of depression, according to Prof. Ryoichi Nagatomi, of Tohoku University in Japan, and team.
Adults who consumed low-fat milk and yogurt between one and four times per week were less likely to experience depression symptoms than those who reported no dairy consumption.

Brain health

People with higher intakes of dairy products have been shown to score significantly higher on memory and brain function tests than individuals who drink little or no milk.
The A2 type of beta-casein protein contained in cow's milk is suggested to increase the body's defenses against neurodegenerative diseases, pancreatitis, and cancer by raising an essential antioxidant in the body.
The jury is out on whether dairy is good or bad for you; the arguments for and against are ongoing, and the health effects vary between individuals. However, for the most part, evidence shows that dairy consumption has many benefits.

Why is osteoarthritis more common among women? Study sheds light

Osteoarthritis is more common in women than men in older age, but researchers have struggled to pinpoint precisely why this is. A new study may have shed light on the issue, after identifying differences in the synovial fluid of men and women with the disease.
Synovial fluid is the fluid that surrounds the joints. It helps to protect cartilage - which is the tissue that covers the ends of the bones - against damaged caused by friction during movement.
Synovial fluid is known to contain information that can be used to determine the health of a joint. For the new study, researchers set out to investigate whether there were differences in this information between men and women with osteoarthritis (OA).
Study co-author Dr. Monte Hunter, chair of the Department of Orthopedic Surgery at the Medical College of Georgia at Augusta University, and colleagues recently published their findings in the journal Scientific Reports.
For the study, the team analyzed samples of synovial fluid taken from the knees of men and women both with and without OA.
The researchers focused on the exosomes of synovial fluid, which are vesicles within the fluid that carry small molecules called microRNAs (miRNAs). These regulate gene expression.

Estrogen has a part to play

The analysis revealed significant differences in miRNA activity between men and women with OA.
Specifically, they found that the synovial fluid of men showed 69 downregulated and 45 upregulated miRNAs, while the the synovial fluid of women had 91 downregulated and 53 upregulated miRNAs.
This microRNA activity was associated with 70 altered biological processes among women, compared with approximately 50 altered biological processes among men.
Interestingly, the researchers found that women were more likely than men to show a deactivation or alteration of miRNAs that are important for estrogen signaling and collagen production.
The team notes that lower estrogen levels - which normally arise as a result of menopause - are associated with a greater production of bone-destroying cells. What is more, studies have linked hormone replacement therapy, which boosts estrogen levels, with a lower risk of OA.
Taking this information into account, the researchers believe that their findings indicate that estrogen influences miRNA levels within the exosomes of synovial fluid.
Further confirming their theory, the researchers found that blocking estrogen availability in exosomes using aromatase inhibitors led to a reduction in miRNAs.

Potential cause of OA uncovered

Additionally, the study may have shed light on a cause of OA in both sexes. The team identified one miRNA, called MiR-504-3p, that was upregulated in both men and women with OA.
While the researchers are unable to explain the exact role of MiR-504-3p in OA, they believe that it may be involved in cartilage degeneration, which is the root cause of the disease.
Based on this finding, Dr. Hunter and colleagues plan to conduct further studies, which will investigate the effects of MiR-504-3p inhibition on OA development.
In the meantime, the researchers believe that their current findings help to explain why women are at greater risk of OA than men.
"To conclude, this is the first study to demonstrate gender-specific miRNA profiling in EVs [extracellular vesicles] of synovial fluid in human OA," write the authors.
"Synovial fluid derived exosomes play an important role in the pathophysiology of OA. Furthermore, these differentially expressed female miRNAs might be estrogen-responsive and play a role in TLR [toll-like receptor] signaling during pathogenesis of OA."