Medical News Today: Eating out may mean eating more this Thanksgiving

If you’re shunning the stress of preparing a Thanksgiving dinner this year and eating out instead, you might want to approach the restaurant with caution; such an environment could cause you to eat more than you should.
Thanksgiving dinner
If you’re eating out for Thanksgiving, you could wind up eating more.

Research from the University of Michigan in Ann Arbor suggests that food-related cues, such as images of food and inviting aromas, might trick us into thinking that we are hungry, even if we have just eaten.

But the researchers found that these cues are unlikely to make food taste better, nor do they increase the pleasure of eating them.

Study leader Michelle Joyner, who works in the Department of Psychology at the University of Michigan, and colleagues have published the findings in the journal Clinical Psychological Science.

Thanksgiving is a time for reflection, gratitude, and a delicious meal, all while surrounded by family and friends. However, while the latter might provoke thoughts of a home-cooked feast, some of us prefer to enjoy the food but without all the hard work.

According to a recent survey from the National Restaurant Association, around 1 in 10 people in the United States will eat their Thanksgiving meal at a restaurant this year.

But the new study suggests that restaurant-goers should watch out, because the sight of food and its delicious aroma may trigger hunger pangs, even after a full-blown turkey dinner.

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Food cues lead to greater calorie intake

Joyner and her colleagues came to their findings by conducting a laboratory-based experiment in which they assessed how food-related cues impact feelings of hunger, food cravings, and food consumption.

The study included 112 college students, who were all randomly allocated to one of two groups.

One group was sent to a “fast-food laboratory,” where the laboratory was styled similar to a fast-food restaurant, with tables and chairs, or booths, images of food, and background music. The other group was sent to a “neutral” laboratory, with no food-related cues.

Both the groups were asked to eat lunch 1 hour before arriving at their designated laboratory. On arrival, they were given tokens that allowed them to purchase fast food such as cheeseburgers, French fries, and milkshakes. The tokens also allowed them to purchase time for activities unrelated to food, such as playing video games.

The team found that subjects who were exposed to food-related cues in the fast-food laboratory displayed more food cravings than those in the neutral laboratory, and they consumed 220 more calories.

Interestingly, there was no difference in how much the two groups liked the taste of the food that they consumed, or how much they enjoyed it.

“Food-related cues can make people want or crave food more, but don’t have as much of an impact on their liking, or the pleasure they get from eating the food,” says Joyner.

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Findings ‘have public health implications’

What is more, food-related cues were found to have no impact on participants’ purchasing of non-food-related activities, which indicates that the behavioral effects of food cues are food-specific.

Taken together, the researchers say that their findings suggest that food cues may “contribute to overconsumption through increased wanting and hunger. These findings have public health implications for overeating and obesity.”

So, you might want to stop and think before you go reaching for that extra slice of pumpkin pie: are you really still hungry? Or is the aroma of delicious food playing tricks on you?

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Medical News Today: Can you eat just one meal a day?

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    Aksungar, F.B., Sarikaya, M., Coskun, A., Serteser, M., & Unsal, I. (2017). Comparison of intermittent fasting versus caloric restriction in obese subjects: A two year follow-up [Abstract]. The Journal of Nutrition Health and Aging, 21(6), 681–685. Retrieved from

    Arnason, T. G., Bowen, M. W., & Mansell, K. D. (2017, April 15). Effects of intermittent fasting on health markers in those with type 2 diabetes: A pilot study. World Journal of Diabetes, 8(4), 154–164. Retrieved from

    Horne, B. D., Muhlestein, J. B., & Anderson, J. L. (2015, July 1). Health effects of intermittent fasting: Hormesis or harm? A systematic review. The American Journal of Clinical Nutrition, 102(2), 464–470. Retrieved from

    Tinsley, G. M., & La Bounty, P. M. (2015, October). Effects of intermittent fasting on body composition and clinical health markers in humans. Nutrition Reviews, 73(10), 661–674. Retrieved from

    Trepanowski, J. F., Canale, R. E., Marshall, K. E., Kabir, M. M., & Bloomer, R. J. (2011, October 7). Impact of caloric and dietary restriction regimens on markers of health and longevity in humans and animals: A summary of available findings. Nutrition Journal, 10, 107. Retrieved from

    Trepanowski, J.F., Kroeger, C. M., Barnosky, A. Klempel, M. C., Bhutani, S., Hoddy, K. K., … Varady, K. A. (2017, July). Effect of alternate-day fasting on weight loss, weight maintenance, and cardioprotection among metabolically healthy obese adults. A randomized clinical trial [Abstract]. JAMA Internal Medicine, 177(7), 930–938. Retrieved from

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Medical News Today: Immune cells cross blood-brain barrier in multiple sclerosis

Researchers probing the mechanisms of nerve tissue damage in multiple sclerosis have identified two ways in which white blood cells overcome the blood-brain barrier to wreak havoc in the highly protected environment of the brain and spinal cord.
doctor holding brain scans
How do white blood cells penetrate the blood-brain barrier in MS? A new study investigates.

In a paper published in the journal Cell Reports, first study author Sarah Lutz, assistant professor of anatomy and cell biology at the University of Illinois at Chicago, and colleagues describe how they studied mechanisms of immune attack on the central nervous system (CNS) in a mouse model of multiple sclerosis (MS).

Prof. Lutz explains that in MS, immune cells are able cause damage because they can gain entry to the brain and spinal cord from the bloodstream. “A better understanding of how these cells cross the blood-brain barrier,” she adds, “will aid our efforts to develop specific therapies to keep them out.”

The bloodstream carries essential nutrients, oxygen, cells, and other substances to all parts of the body, including the CNS, which comprises the brain, spinal cord, and optic nerves.

The blood-brain barrier and ‘tight junctions’

However, because of the delicate operations that go on in the CNS — such as the firing of neurons and passage of electrical signals that control movement and speech and carry information from the senses — it has a higher level of protection than the rest of the body.

One feature that can help the blood-brain barrier to restrict the movement of blood-borne cells, molecules, and ions into and out of the CNS is the close packaging of the endothelial cells that line the blood vessels that serve the CNS.

This close packing — which makes the blood vessels supplying the CNS virtually impermeable — comprises “tight junctions” of protein complexes that bolt the endothelial cells together.

In contrast, the junctions between endothelial cells in blood vessels that supply other organs and tissues are looser and can also be adjusted to allow a less restricted range of cells and other materials to pass through.

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An autoimmune disease of the CNS

MS is a persistent autoimmune disease in which cells of the immune system attack the fatty layer of tissue that surround the nerve fibers, or axons, in the CNS, mistaking it for a disease agent or other threat.

The fatty layer of tissue is known as myelin, and it protects the electrical impulses that carry messages between the CNS and other parts of the body — such as movement muscles and the senses. In MS, however, the immune system degrades not only the myelin but can also damage the exposed axons.

The myelin damage occurs at multiple places in the CNS. These become lesions that harden into scar tissue, or sclerosis, hence the name of the disease.

MS has many different symptoms depending on which parts of the CNS are affected. They include, but are not limited to: impaired vision; blindness; difficulty remembering and concentrating; poor coordination; problems with balance; extreme fatigue; tremors; slurred speech; numbness; and paralysis.

Symptoms can flare up, go away, and then come back again, or they can stay and progressively worsen.

The disease is commonly diagnosed in people aged 20–50, but it can affect any person of any age. In the United States, there are thought to be around 1 million people living with MS.

Damaged ‘tight junctions’

Scientists who are looking for MS’s causes have discovered that two types of white blood cell, the lymphocytes Th1 and Th17, are involved in destroying the myelin sheath that protects the axons of the CNS. But until now, it was not clear how these immune cells managed to get across the blood-brain barrier into the CNS.

For their investigation, Prof. Lutz and her colleagues studied the blood-brain barrier of both healthy mice and mice with autoimmune encephalomyelitis (EAE). Mice with EAE are often used as animal models in the study of MS.

To find out how the Th1 and Th17 immune cells get across the blood-brain barrier in MS, the team genetically labeled the tight junctions in the blood vessels using a fluorescent protein.

The scientists found that the tight junctions in the blood-brain barrier of the MS mice were much more damaged when Th17 cells were present, and that this damage seemed to occur in the very early stages of the disease.

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Traveling through endothelial cells

Around 3 days after observing the damage that occurred in the presence of the Th17 immune cells, the researchers saw that the Th1 cells were attacking the myelin and damaging neurons.

However, these cells did not gain access to the CNS through the damaged tight junctions, but did so through another mechanism that involved passing through the endothelial cells themselves.

It appeared that the Th1 cells were able to use small pits, or “caves,” called “caveolae.” These are found on the surfaces of cells — including endothelial cells — that are used to transport materials into and out of cells.

The researchers confirmed their findings by breeding MS mice without caveolae; they found hardly any Th1 immune cells in the CNS of these mice.

They concluded that the Th1 immune cells need the caveolae of the endothelial cells in the blood vessels that serve the CNS in order to cross the blood-brain barrier.

Prof. Lutz explains that that this was the first time that they had ever seen the different mechanisms through which the two types of immune cell got across the blood-brain barrier to reach the myelin and the axons “in live animals in real-time.”

Now that we know how these cells get to neurons, drugs or small molecules can be designed that interfere with or block each of these processes to help treat and possibly prevent multiple sclerosis.”

Prof. Sarah Lutz

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Medical News Today: Metastatic prostate cancer: What you need to know

Prostate cancer occurs when the cells in the prostate begin to grow uncontrollably.

Sometimes, prostate cancer develops quickly and spreads to other organs. This is known as stage IV prostate cancer and is said to be metastatic.

What is the prostate?

Prostate highlighted in 3D model of male anatomy.
The prostate is a small organ that plays a role in protecting sperm and producing semen.

The prostate gland is a small, walnut-shaped organ that sits between the bladder and rectum in men.

During ejaculation, sperm cells travel from the testicles through the seminal vesicles to the prostate gland. The prostate secretes special fluids that help the sperm cells survive.

This combination of fluid and sperm cells is known as semen, and it exits the body through the urethra.

What is metastatic prostate cancer?

In many cases, prostate cancer grows very slowly; so slowly in fact, that many men do not even know that they have the disease. In other men, however, the disease metastasizes — spreads to organs outside of where it originated.

There are two types of metastatic prostate cancer:

  1. Local metastasis: Prostate cancer with local metastasis means that the cancer has spread to other organs within the pelvis. This usually means the local lymph nodes, but can include any organ or structure in the pelvis.
  2. Distant metastasis: Distant metastasis means that the prostate cancer has spread beyond the pelvis. The bones, spine, brain, liver, and lungs are common sites of cancer metastasis.

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Man experiencing painful urination because of a prostate problem.
Potential symptoms of prostate cancer include difficulty urinating, pain during urination, and a sense of needing to urinate urgently.

Symptoms of prostate cancer can include:

  • urinary urgency
  • difficulty starting or stopping urination
  • weak or interrupted urine flow
  • painful or burning urination
  • erectile dysfunction
  • painful ejaculation
  • blood in the urine or semen

Anyone experiencing these symptoms should consult with their doctor as soon as possible. While many other conditions can cause similar symptoms, it is important to rule out prostate cancer.

Once a person has been diagnosed with prostate cancer, the signs of metastasis will vary depending on the where the cancer spreads and how quickly it is growing.

For example, a person with prostate cancer and local metastasis to nearby lymph nodes may not experience any change in symptoms.

However, a person with metastasis to the bones may experience bone pain.

Other symptoms of metastasis may include:

  • fatigue
  • feeling unwell
  • reduced appetite
  • weight loss
  • swelling in the legs or feet


Advanced prostate cancer can cause many other health problems depending on where the cancer has spread to and how quickly it is spreading.

  • Urinary problems: Cancerous growths can press on the bladder, urethra, or other pelvic organs. Prostate cancer can also spread to those organs and cause urinary retention, blood in the urine, incontinence, and difficulties emptying the bladder.
  • Bowel problems: Advanced prostate cancer can cause bowel problems, such as constipation, diarrhea, urgency, obstruction, and incontinence. This is often due to the use of pain medications, or the spread of prostate cancer to the bowel or rectum. Dietary changes, dehydration, and inactivity can also cause bowel problems.
  • Sexual problems: It is not uncommon for men with advanced prostate cancer to have difficulties getting or maintaining an erection. Some men also have decreased libido or an inability to ejaculate.
  • Bone pain or fractures: Prostate cancer that has spread to the bones can cause significant bone pain. It can also weaken the bones, making a person susceptible to breaks and fractures.
  • Hypercalcemia: Calcium is stored in the bones but can leak out into the blood if prostate cancer spreads to the bones. High levels of calcium in the blood can cause fatigue, increased thirst or need to urinate, nausea and vomiting, constipation, and loss of appetite.
  • Anemia: Anemia means a decrease in the number of red blood cells that are available to carry oxygen throughout the body. This can lead to severe fatigue, shortness of breath, and looking pale. It is usually caused by cancer that has spread to the bone marrow but can also be a side effect of cancer treatments.
  • Lymphedema: Prostate cancer that has spread to the lymph nodes can cause blockages within the vessels that transport lymph around the body. This causes swelling in the legs or scrotum.


There are many types of treatments available for advanced prostate cancer. A doctor or oncologist will develop a treatment plan that takes into account the individual’s symptoms, prognosis, goals for treatment, age, and general health.

Hormone therapy

Hormone therapy for advanced prostate cancer shuts down the production of male sex hormones. This can help prevent the cancer from continuing to grow. Common drugs include abiraterone (Zytiga) and enzalutamide (Xtandi).


Chemotherapy is a type of medication that destroys cancer cells or prevents them from multiplying. People are usually given chemotherapy once the prostate cancer has stopped responding to hormone therapy.

Chemotherapy is usually a combination of two or more drugs that are administered intravenously, injected, or taken as a pill.


Immunotherapy is a type of medication that modifies the body’s immune system to find and destroy cancer cells.

Treatment for prostate cancer that has spread to the bones includes drugs such as zoledronic acid (Zometa) and denosumab (Xgeva). Treatment for local metastatic cancer may also include radiation therapy.

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Side effects of prostate cancer treatment

Prostate cancer treatment can cause some serious side effects, including:

Senior male patient speaking to young male doctor.
Prostate cancer treatments may cause a number of side effects that should be outlined by a medical professional beforehand.
  • infertility
  • urinary incontinence
  • urinary retention
  • diarrhea
  • erectile dysfunction
  • pain
  • fatigue
  • hair loss
  • loss of appetite
  • nausea and vomiting

Luckily, there are many medications available to treat the side effects of cancer treatment.

A person should not feel the need to “power through” or suffer from uncomfortable symptoms. It is important for anyone undergoing treatment to communicate with their healthcare team about any side effects they are experiencing.


The prognosis for advanced prostate cancer depends on where the cancer has spread and how aggressively it is growing.

According to the American Cancer Society, survival rates are as follows:

  • Local prostate cancer without spread has a 5-year survival rate at nearly 100 percent.
  • Prostate cancer with local spread also has a 5-year survival rate at nearly 100 percent.
  • Prostate cancer with distant metastasis has a 5-year survival rate of around 29 percent.

These are general statistics; it is important for a person with prostate cancer to speak to their doctor about their specific case.


If prostate cancer is diagnosed before it has spread, or if it has only spread to nearby structures, the survival rate is excellent.

This makes routine screening and early diagnosis essential in the fight against prostate cancer.

Men over the age of 50 should speak to a healthcare professional about the different screening options and which one is most appropriate for them.

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Medical News Today: How do cancer cells start to spread? Study sheds light

Metastatic cancer is responsible for the vast majority of cancer deaths, but our limited understanding of how metastasis begins makes finding ways to stop it hugely challenging. A new study may provide some insight, however.
a cancer cell
Researchers have found that a tumor’s surrounding environment influences the spread of cancer cells.

Researchers from the University of California, San Diego (UCSD) have discovered how the surrounding environment of a tumor can cause cancer cells to metastasize.

Put simply, metastatic cancer occurs when cancer cells break away from a primary tumor and move to other areas of the body — most commonly the bones, liver, and lungs.

Once cancer cells have metastasized, controlling them becomes much more difficult. While current treatments such as chemotherapy and radiotherapy can help to slow the spread of cancer cells, they are not always successful.

It is estimated that around 90 percent of cancer-related deaths are a result of metastatic cancer, highlighting the need for more effective strategies to combat the disease.

But, as study leader Stephanie Fraley — a professor of bioengineering at UCSD — notes, “We are good at targeting tumor growth, but we do not know enough about metastasis.”

The new research, however, has uncovered further information about what triggers metastatic cancer, a discovery that could lead to more successful treatments.

The researchers recently reported their findings in the journal Nature Communications.

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Gene modules and vascular mimicry

For their study, Fraley and colleagues built a 3-D collagen matrix, which enabled them to get an in-depth look at the migration activity of various types of human cancer cell.

“It’s critical to have the cells surrounded by a 3-D environment that mimics what happens in the human body,” notes Fraley.

The researchers found that a condensed environment caused the cancer cells to activate a distinct set of genes, or a “gene module,” which the researchers named collagen-induced network phenotype (CINP).

The team found that the activation of this gene module prompted a phenomenon known as vascular mimicry, which is the formation of blood vessel-like structures.

These structures promote cancer metastasis; they supply the tumors with blood and help to provide cancer cells with the “nutrients” they need to survive.

“We thought that putting cells into this more constrained environment would prevent their spread,” says first study author Daniel Ortiz Velez, of the Department of Bioengineering at UCSD. “But the opposite happened.”

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Gene module predicts cancer metastasis

Next, the team searched for the CINP gene module across a range of cancer types.

They found that they were able to use the CINP to predict metastasis in nine different cancers, including breast cancer, lung cancer, and pancreatic cancer. They were also able to use the gene module to predict patient survival.

The researchers now plan to see whether they can replicate their findings in more cancer cell types and animal models, and they hope that their research will uncover a way to stop CINP activation and halt cancer metastasis.

“It is possible that gene expression analysis of additional cancer cell types induced into [vascular mimicry]-like behavior by our 3-D collagen system could help to further refine the conserved CINP gene module,” they say.

“This would facilitate prioritization of the genes for targeted functional studies to identify key regulators and potential therapeutic targets.”

“Validation of the prognostic value of this gene module could help patients avoid the long-term side effects of aggressive radiation and chemotherapy if the likelihood of metastasis is very low,” the researchers conclude.

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Medical News Today: How cinnamon can help you to burn holiday fat

As you make that pumpkin pie for Thanksgiving, consider adding an extra pinch of cinnamon; a study shows that cinnamaldehyde, the organic compound that gives cinnamon its flavor, helps you to burn fat.
Cinnamon is a common holiday spice with surprising fat-burning properties, new research suggests.

Pumpkin pie, mulled wine, hot chocolate, and eggnog — these are just a handful of the foods and drinks that make the holidays such a truly delicious time.

But if you’re worried that such yummy treats could make you pack on the extra pounds, worry no more! These enticing foods also contain cinnamon, and new research bears some good news: the common holiday spice could help you to burn fat.

The new study comes from the University of Michigan (UM) Life Sciences Institute (LSI) in Ann Arbor, and the research was led by Jun Wu, a research assistant professor at the LSI and an assistant professor of molecular and integrative physiology at the UM Medical School.

Wu and colleagues set out to examine the effect of cinnamaldehyde on human fat cells. Speaking about the motivation for her study, Wu says, “Scientists were finding that this compound affected metabolism.”

Previous studies in mice had already shown that cinnamaldehyde helps to fight off obesity and hyperglycemia. “So,” Wu continues, “we wanted to figure out how — what pathway might be involved, what it looked like in mice, and what it looked like in human cells.”

To do this, the researchers treated adipocytes, or fat cells, from both mice and humans with the compound. Their findings were published in the journal Metabolism.

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Cinnamon triggers fat-burning process

The experiments revealed that cinnamaldehyde has a direct effect on fat cells. In a process known as thermogenesis, the compound makes the adipocytes start burning the fat that they had been storing.

Adipocytes store lipids, which can then be burned for energy. The cells evolved to help our bodies use energy resources effectively during times when such resources might be scarce, such as through a cold winter or famine.

“It’s only been relatively recently that energy surplus has become a problem. Throughout evolution, the opposite — energy deficiency — has been the problem. So any energy-consuming process usually turns off the moment the body doesn’t need it,” Wu explains.

Getting the body to turn the energy-consuming process, or thermogenesis, back on has been the focus of recent research, especially in light of the so-called obesity epidemic.

The study authors think that cinnamon might be one such way to turn thermogenesis on. In their research, they found a higher expression of certain genes and enzymes that boost lipid metabolism in the adipocytes treated with cinnamaldehyde.

Additionally, they found a higher level of Ucp1 and Fgf21, which are regulatory proteins that help to induce thermogenesis.

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Cinnamon may be better than drugs

In the study paper, Wu and team conclude, “Given the wide usage of cinnamon in the food industry, the notion that this popular food additive, instead of a drug, may activate thermogenesis, could ultimately lead to therapeutic strategies against obesity that are much better adhered to by participants.”

The lead researcher emphasizes this conclusion.

Cinnamon has been part of our diets for thousands of years, and people generally enjoy it […] So if it can help protect against obesity, too, it may offer an approach to metabolic health that is easier for patients to adhere to.”

Jun Wu

So, this holiday season, we’re probably safe to add a bit more cinnamon — but not a massive amount — to our festive food.

The researchers caution that more research is needed to figure out the perfect way to use cinnamaldehyde to trigger thermogenesis without causing any side effects.

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Medical News Today: Blood blister in mouth: Pictures and treatment

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Medical News Today: Could vitamin D help to keep rheumatoid arthritis at bay?

After studying immune cells taken from the joints of people with rheumatoid arthritis, scientists have found that once the disease sets in, some types of cell lose their sensitivity to vitamin D.
old woman's hands
Researchers explore vitamin D’s role in rheumatoid arthritis.

The team — which comprised researchers from University College London and the University of Birmingham, both in the United Kingdom — reports the new findings in the Journal of Autoimmunity.

Rheumatoid arthritis is an autoimmune disease that arises because the immune system attacks healthy tissue — usually the joints — by mistake, leading to painful inflammation and swelling.

The disease often affects several joints at the same time, such as the knees, hands, and wrists. It inflames the lining of the joint and eventually damages the joint itself. This can lead to long-lasting pain, problems with balance, and deformity.

Estimates suggest that approximately 1 percent of the world’s population has rheumatoid arthritis, including around 1.3 million adults in the United States. It affects women more often than men, raising the question of whether hormonal factors may be involved.

Study examined cells from inflamed joints

In their journal paper, the researchers explain that previous studies have revealed that vitamin D has “potent anti-inflammatory effects,” including the ability to suppress activity in some types of immune system T cell that are known to be active in rheumatoid arthritis.

However, those studies have only used immune cells isolated from blood, and so the impact of vitamin D on immune cells “at the site of active disease is unclear.”

A significant feature of the new study is that it is the first to use immune cells taken from both the blood and from the inflamed joints of people with rheumatoid arthritis.

“Unlike previous studies,” explains senior study author Karim Raza, a professor in the Institution of Inflammation and Ageing at the University of Birmingham, “we isolated different immune cell types from the actual site of disease to determine whether specific subsets of immune cells (specific T cell groups) have equal sensitivity to vitamin D.”

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Immune cells lost sensitivity to vitamin D

For the investigation, the scientists used samples of synovial fluid taken from the joints of 15 people with rheumatoid arthritis aged between 40 and 85. Synovial fluid is a thick, sticky liquid that acts as a lubricant to reduce friction between bones that meet at joints.

They also examined blood samples taken from those with rheumatoid arthritis, and from individuals without rheumatoid arthritis — matched for the same age and gender — who had donated to a blood bank (the controls).

When they tested how immune cells in the different samples reacted to vitamin D, they found that some types of immune cell responded differently.

In particular, they found that some types of T cell taken from inflamed joints were less sensitive to the anti-inflammatory effects of vitamin D than those taken from the blood of the same people.

Corresponding study author Martin Hewison, a professor in the University of Birmingham’s Institute of Metabolism and Systems Research, explains, “This appears to be because immune cells from the joints of rheumatoid arthritis patients are more committed to inflammation, and therefore less likely to change, even though they have all the machinery to respond to vitamin D.”

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Can vitamin D prevent rheumatoid arthritis?

Although the study was limited to investigating cells in the laboratory, the findings would appear to support the idea that maintaining vitamin D levels might help to prevent rheumatoid arthritis and other inflammatory diseases.

However, they would also suggest that simply taking vitamin D supplements is unlikely to help people with rheumatoid arthritis because their immune cells are already desensitized.

“Instead,” notes study co-author Dr. Louisa Jeffery, also from the University of Birmingham, “much higher doses of vitamin D may be needed, or possibly a new treatment that bypasses or corrects the vitamin D insensitivity of immune cells within the joint.”

The researchers now want to take the research further and find out why rheumatoid arthritis causes immune cells to become insensitive to vitamin D, and how this might be prevented. They also want to find out if there are similar effects in other inflammatory conditions.

Our findings were unexpected as we initially thought that cells from the inflamed rheumatoid joint would respond just as well to vitamin D as cells from the blood.”

Prof. Karim Raza

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Medical News Today: What you need to know about PRP

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    Anitua, E., Pino, A., Martinez, N., Orive, G., & Berridi, D. (2017, May). The effect of plasma rich in growth factors on pattern hair loss: A pilot study [Abstract]. Dermatologic Surgery, 43(5), 658-670. Retrieved from

    Braun, H. J., Kim, H. J., Chu, C. R., & Dragoo, J. L., (2014, March 14). The effect of platelet-rich plasma formulations and blood products on human synoviocytes [Abstract]. The American Journal of Sports Medicine, 42(5), 1204–1210. Retrieved from

    Charousset, C., Zaoui, A., Bellaiche, L., & Bouyer, B. (2014, April 1). Are multiple platelet-rich plasma injections useful for treatment of chronic patellar tendinopathy in athletes? A prospective study. The American Journal of Sports Medicine, 42(4), 906–911. Retrieved from

    Filardo, G., Di Matteo, B., Di Martino, A., Merli, M. L., Cenacchi, A., Fornasari, P., … Kon, E. (2015, May 7). Platelet-rich plasma intra-articular knee injections show no superiority versus viscosupplementation. The American Journal of Sports Medicine, 43(7), 1575–1582. Retrieved from

    Kang, J. S., Zheng, Z., Choi, M. J., Lee, S. H., Kim, D. Y., & Cho, S. B. (2014, January). The effect of CD34+ cell-containing autologous platelet-rich plasma injection on pattern hair loss: A preliminary study. Journal of the European Academy of Dermatology and Venereology, 28(1), 72–79. Retrieved from

    Patel, S., Dhillon, M. S., Aggarwal, S., Marwaha, N., & Jain, A. (2013, February). Treatment with platelet-rich plasma is more effective than placebo for knee osteoarthritis: A prospective double-blind, randomized trial [Abstract]. The American Journal of Sports Medicine, 41(2), 356–364. Retrieved from

    Gentile, P., Garcovich, S., Bielle, A., Scioli, M. G., Orlandi, A., & Cervelli, V. (2015, November). The effect of platelet-rich plasma in hair regrowth: A randomized placebo-controlled trial. Stem Cells Translational Medicine, 4(11), 1317–1323. Retrieved from

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Medical News Today: Cancer cell growth halted with cold and flu drug

“Feed a cold, starve a fever,” so the saying goes. The results of a new study, however, suggest that “treat a cold, starve cancer cells” might be a more appropriate motto.
illustration of a cancer cell
Researchers suggest that NAC could be used to halt cancer cell growth.

Researchers found that a medication used to ease symptoms of the common cold — called N-Acetylcysteine (NAC) — could also help to prevent the growth of cancer cells by depriving them of proteins that are important for their survival.

Study co-author Prof. Federica Sotgia, of the School of Environment and Life Sciences at the University of Salford in the United Kingdom, and colleagues recently reported their findings in the journal Seminars in Oncology.

Cancer remains one of the biggest health challenges of our time. In the United States, more than 1.6 million new cancer cases were diagnosed last year.

In terms of cancer treatment, we have come a long way over recent years. This is reflected in death rates from the disease, which fell by 13 percent between 2004 and 2013.

Still, cancer continues to the take the lives of more than half a million people in the U.S. every year, highlighting the need for new, more effective therapies.

Prof. Sotgia and colleagues hope that their new research will bring us closer to such treatments, after discovering how NAC could help to halt the spread of cancer cells.

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NAC, oxidative stress, and cancer cells

NAC — sometimes referred to as acetylcysteine — is an over-the-counter medication and dietary supplement commonly used to help alleviate some cold and flu symptoms, such as coughing, wheezing, and thick mucus.

NAC may also be used in the treatment of acetaminophen overdose, cystic fibrosis, and chronic obstructive pulmonary disease.

The medication also has antioxidant properties. This means that it has the ability to reduce cell damage caused by oxidative stress, which is an imbalance between potentially harmful reactive oxygen species and levels of detoxifying molecules.

Prof. Sotgia and team note that previous research has identified high levels of oxidative stress in the stromal cells of tumors, particularly breast cancer tumors. Stromal cells are cells that comprise connective tissue.

The researchers explain that when the stromal cells of tumors are exposed to oxidative stress, they release lactate and other “nutrients” that the cancer cells need to thrive.

With this in mind, the team hypothesized that the antioxidant properties of NAC might help to “starve” cancer cells of these nutrients.

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‘Encouraging results’

To test their theory, the researchers conducted a trial on 12 women who had recently received a diagnosis of stage 0 or stage 1 breast cancer, and who were awaiting surgery for the disease.

For 3 weeks between their breast cancer diagnosis and surgery, each woman received NAC. The medication was administered intravenously at a dose of 150 milligrams per kilogram once weekly. On days when the subjects did not receive NAC intravenously, they received a twice-daily oral dose of 600 milligrams.

Biopsies of each woman’s breast cancer tumor were taken both prior to and during surgery, and the researchers analyzed them for levels of three biomarkers of cancer aggressiveness: MCT4, CAV1, and Ki67.

The study revealed that levels of Ki67 in the tumors had reduced by 25 percent, while levels of MCT4 were reduced by a whopping 80 percent.

These findings indicate that treatment with NAC could be an inexpensive, non-toxic way to stop cancer cell growth and division.

“High levels of stromal MCT4 are extremely worrying,” notes study co-author Prof. Michael Lisanti, also of the School of Environment and Life Sciences at the University of Salford, “as they are linked to aggressive cancer behavior and poor overall survival, so this is very encouraging result.”

Our idea was to repurpose an inexpensive FDA-approved drug, to examine if its antioxidant properties could target the feeding behavior of cancer cells. To be able to inhibit MCT4 protein expression, in a non-toxic way, is huge step forward.”

Prof. Michael Lisanti

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