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Monday, December 26, 2016

Protein in Urine Linked to Increased Risk of Memory Problems, Dementia

By Turbotorque (Own work) [Public domain], via Wikimedia Commons

Newswise, December 26, 2016-- People who have protein in their urine, which is a sign of kidney problems, may also be more likely to later develop problems with thinking and memory skills or even dementia.

Researchers looked at all available studies on kidney problems and the development of cognitive impairment or dementia.

“Kidney dysfunction has been considered a possible risk factor for cognitive impairment or dementia,” said Kay Deckers, MSc, of Maastricht University in the Netherlands, author of the systematic review and meta-analysis.

“Chronic kidney disease and dementia share many risk factors, such as high blood pressure, diabetes and high cholesterol, and both show similar effects on the brain, so they may have shared vascular factors or there may even be a direct effect on the brain from kidney problems.”

A total of 22 studies on the topic were included in the systematic review. Five of the studies, including 27,805 people, were evaluated in the meta-analysis on protein in the urine, also called albuminuria or proteinuria. The analysis showed that people with protein in the urine were 35 percent more likely to develop cognitive impairment or dementia than people who did not have protein in their urine.

For another marker of kidney function, estimated glomerular filtration rate, the results were mixed and did not show an association. For three other markers of kidney function, cystatin C, serum creatinine and creatinine clearance, no meta-analysis could be completed because the few studies available did not use the same methods and could not be compared.

“Protein in the urine was associated with a modestly increased risk of cognitive impairment or dementia,” Deckers said.

“More research is needed to determine whether the kidney problems are a cause of the cognitive problems or if they are both caused by the same mechanisms.”

The study was supported by the In-MINDD (Innovative Midlife Intervention for Dementia Deterrence) project funded by the European Union’s Framework Program Seven.

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Researchers Add to Evidence That Common Bacterial Cause of Gum Disease May Drive Rheumatoid Arthritis

Newswise, December 26, 2016 — Investigators at Johns Hopkins report they have new evidence that a bacterium known to cause chronic inflammatory gum infections also triggers the inflammatory "autoimmune" response characteristic of chronic, joint-destroying rheumatoid arthritis (RA). The new findings have important implications for prevention and treatment of RA, say the researchers.

In a report on the work, published in the Dec. 14 edition of the journal Science Translational Medicine, the investigators say the common denominator they identified in periodontal disease (gum disease) and in many people with RA is Aggregatibacter actinomycetemcomitans.

An infection with A. actinomycetemcomitans appears to induce the production of citrullinated proteins, which are suspected of activating the immune system and driving the cascade of events leading to RA.

"This is like putting together the last few pieces of a complicated jigsaw puzzle that has been worked on for many years," says Felipe Andrade, M.D., Ph.D., the senior study investigator and associate professor of Medicine at the Johns Hopkins University School of Medicine, who also practices at Johns Hopkins Bayview Medical Center.

"This research may be the closest we've come to uncovering the root cause of RA," adds first author Maximilian Konig, M.D., a former Johns Hopkins University School of Medicine fellow now at Massachusetts General Hospital.

Medical investigators have observed a clinical association between periodontal disease and RA since the early 1900s, and over time, researchers have suspected that both diseases may be triggered by a common factor.

In the last decade, studies have focused on a bacterium known as Porphyromonas gingivalis, found in patients with gum disease. However, while major efforts are currently ongoing to demonstrate that this bacterium causes RA by inducing citrullinated proteins, all attempts by this research team have failed to corroborate such a link, says Andrade.

But his team has persisted on finding alternative bacterial drivers, he says, because of intriguing links between periodontal disease and RA.
For this study, the investigative team with expertise in periodontal microbiology, periodontal disease and RA began to search for a common denominator that may link both diseases.

Initial clues came from the study's analysis of periodontal samples, where they found that a similar process that had previously been observed in the joints of patients with RA was occurring in the gums of patients with periodontal disease. This common denominator is called hypercitrullination.

Andrade explains that citrullination happens naturally in everyone as a way to regulate the function of proteins.

But in people with RA, this process becomes overactive, resulting in the abnormal accumulation of citrullinated proteins. This drives the production of antibodies against these proteins that create inflammation and attack a person's own tissues, the hallmark of RA.

Among different bacteria associated with periodontal disease, the research team found that A. actinomycetemcomitans was the only pathogen able to induce hypercitrullination in neutrophils, an immune white blood cell highly enriched with the peptidylarginine deiminase (PAD) enzymes required for citrullination. Neutrophils are the most abundant inflammatory cells found in the joints and the gums of patients with RA and periodontal disease, say the researchers. These cells have been studied for many years as the major source of hypercitrullination in RA.Actinomycetemcomitans initiates hypercitrullination through the bacterial secretion of a toxin, leukotoxin A (LtxA), as a self-defense strategy to kill host immune cells. The toxin creates holes on the surface of neutrophils, allowing a flux of high amounts of calcium into the cell where concentrations are normally kept low.
Since the PAD enzymes are activated with calcium, the abrupt exposure to high amounts of calcium overactivates these enzymes, generating hypercitrullination.

The researchers previously found that a similar type of pore-forming protein that was produced to kill pathogens by host immune cells was driving hypercitrullination in the joints of patients with RA.

These findings point to a common mechanism that is poking holes on cells, which may be relevant to the initiation of RA when the disease is being established, says Andrade.

As part of its study, the team developed a test using the bacterium and LtxA to detect antibodies against A. actinomycetemcomitans in blood. Using 196 samples from a large study of patients with RA, the researchers found that almost half of the patients -- 92 out of 196 -- had evidence of infection by A. actinomycetemcomitans.

These data were similar to patients, with periodontal disease with approximately 60 percent positivity, but quite different in healthy controls, who only had 11 percent of people positive for A. actinomycetemcomitans. More strikingly, exposure to A. actinomycetemcomitans was a major determinant in the production of antibodies to citrullinated proteins in patients with genetic susceptibility to RA.
Andrade cautioned that more than 50 percent of the study participants who had RA had no evidence of infection with A. actinomycetemcomitans, which, he says, may indicate that other bacteria in the gut, lung or elsewhere could be using a similar mechanism to induce hypercitrullination.

Andrade further cautions that his team's study only looked at patients at a single point in time with established RA, and that to prove cause and effect of A. actinomycetemcomitans and RA, more research will be needed to track the potential role of the bacteria in the onset and evolution of the disease, which can span decades.

"If we know more about the evolution of both combined, perhaps we could prevent rather than just intervene."

An estimated 1.5 million people nationwide live with rheumatoid arthritis, according to the Centers for Disease Control and Prevention. Current treatments with steroids, immunotherapy drugs and physical therapy help some by reducing or slowing the crippling and painful joint deformities, but not in all patients. The exploration of alternative treatment options is necessary.

Additional Researchers from Johns Hopkins included Kevon Sampson and Antony Rosen, M.D.

This research was funded by the Jerome L. Greene Foundation, the Donald B. and Dorothy L. Stabler Foundation, Fundación Bechara, Rheumatology Research Foundation, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) under grant numbers R01AR069569 and AR050026-01, the National Institute of Dental and Craniofacial Research (NIDCR) under grant numbers DE021127-01 and R37 DE12354, and the Intramural Research Program of the NIDCR. 

Researchers Reveal How Cancer Can Spread Even Before a Tumor Develops

Newswise, December 26, 2016--Even before tumors develop, breast cancer cells with a few defined molecular alterations can spread to organs, remain quiet for long periods of time, and then awaken to form aggressive, deadly breast cancer metastasis, says a team of investigators led by researchers at Icahn School of Medicine at Mount Sinai and the University of Regensburg in Germany.

They say their finding, published in two papers in the journal Nature, and conducted in animal models and tested in human samples, now solves the mystery of how breast cancer metastasis forms without a primary tumor in this new model of early dissemination and metastasis. Furthermore, a clinical primary tumor may never develop, investigators say.

The University of Regensburg team had discovered that cancer cells could spread not only from a highly mutated, overtly evolved and pathologically-defined invasive tumors, but also from early stage cancers commonly considered incapable of spreading cells.

However, how these early cancer lesions could spawn cells with traits of malignant tumors was unknown.
In two papers published in the journal Nature, and conducted in animal models and tested in human samples, the two teams now have identified the first mechanisms that allow cells to spread early in cancer progression and contribute to metastasis.

In the study from Mount Sinai, two changes in mammary cancer cells — a switched-on oncogene and a turned-off tumor suppressor— motivated cells to travel from breast tissue to the lungs and other parts of the body. There, the cells stayed quiet until a growth switch was activated and metastases developed in lungs.

“This research provides insight into the mechanisms of early cancer spread and may shed light into unexplained phenomena — among them, why as many as 5 percent of cancer patients worldwide have cancer metastases but no original tumor, and most importantly, why it is so difficult to treat cancer that has spread,” says the study’s senior investigators, Julio A. Aguirre-Ghiso, PhD, Professor of Medicine, Hematology and Medical Oncology, Maria Soledad Sosa, PhD, Assistant Professor of Pharmacological Sciences, and graduate student Kathryn Harper of The Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai.

“Biologically, this new model of early metastasis challenges everything we thought we knew about how cancer spreads and forms metastasis. It feels like we are going to have to adjust our ideas about the subject of metastasis,” he says. “Our hope is that these findings will reshape the way we think about how metastasis should be treated.”

An important finding from the Mount Sinai team is that most early spread cells remain dormant and most chemotherapy and targeted therapies are aimed at those cells that are proliferative.

So early spread cancer cells would escape these conventional therapies even if it kills a primary tumor, Dr. Aguirre-Ghiso says. The work also poses new questions on how early spread cancer cells support metastasis development. Do they do it on their own, do they set the soil for later arriving cells from tumors not caught early, or do they cooperate with later arriving cells?

This study reveals a new biological mechanism of early dissemination that must be explored to fully understand how to target the seeds of metastasis.

The companion paper headed by Dr. Christoph Klein at the University of Regensburg in Germany, published in the same issue of Nature and co-authored by Dr. Aguirre-Ghiso and members of his team provides additional key mechanistic clues on how early spread is controlled and proof in human cancer cells and tumors of the preclinical findings in this study. Researchers from both teams arrived at their findings independently and then collaborated on the project.

Researchers from both teams studied very early stages of breast cancer including DCIS (ductal carcinoma in situ), a noninvasive breast lesion, since 2-3 percent of women who have been treated for DCIS die of metastasis without ever developing a primary tumor.

The best explanation for this phenomenon is that early metastasis occurs before or as DCIS develops. A key finding from this second paper is that in the mouse models, 80% of metastasis originated from the early spread cells and not from the large tumors.

In fact, the Klein group identified a mechanism by which spread is more efficient in early lesions than in large tumors.

In both studies, investigators found that early cancer cell spread is an extension of the normal process of creating a branching tree of breast milk ducts in females.
Two major pathways are activated in this ancient process — p38, a tumor suppressor, and HER2, an oncogene. Switching off p38 and turning on HER2 activates a module of the EMT (epithelial to mesenchymal transition) signaling pathway. EMT promotes movement of cells during embryogenesis and tissue development.

The Klein paper also shows that progesterone receptor signaling, which controls branching of the mammary tree, is important for this early spread by regulating cues involved in EMT and growth programs, a mechanism that was hinted in his earlier studies.

As a mammary tree develops, p38, HER2, and EMT are alternatively turned on and off. This, in cooperation with progesterone signaling, allows mammary cells to move through the mammary gland, hollow out a tubular, branching network of milk ducts that flow to the nipple.

“Tweaking these pathways are a normal way of forming hollow branching tubes,” Dr. Aguirre-Ghiso says.

But in their experiments, they found that if HER2 is over-activated (not switched off) or mutated, and p38 is permanently turned off, EMT was continually activated, allowing cells to move out of the mammary gland and into the animal’s body through the blood.

“We were able to use organoids in three-dimensional cultures, and high resolution imaging directly in the live animal models to actually see these cells enter the blood stream from the mammary tree and travel to the lung, the bone marrow, and other places,” he says.

“We hadn’t thought about oncogenes and tumor suppressors in this way before. This is a new function for these pathways.”

John S. Condeelis, PhD, co-Director of the Gruss Lipper Biophotonics Center and its Integrated Imaging Program at Einstein, where the high resolution intravital imaging was performed, noted that “We were surprised to learn that cancer cells from DCIS-like lesions could show such robust dissemination using similar machinery found in tumor cells from invasive carcinoma. This is a new insight with implications beyond our expectations.”

Also David Entenberg MSc, Director of Technological Development and Intravital Imaging who led the imaging efforts within the same Center said, “A few years ago, it would not have been possible to image these disseminating cells inside a living animal with this level of detail. We’re pleased that Einstein’s imaging technology could, through this collaboration, contribute to the definitive proof of early dissemination.”

And while both studies focus on the mechanisms of early dissemination in breast cancer, similar processes could control early dissemination and metastasis in other human cancers, including melanoma and pancreatic cancer. In fact, pancreatic cancer early dissemination has also been linked to an EMT process, Dr. Aguirre-Ghiso says.

Among the critical avenues they are investigating, Mount Sinai researchers are looking for the growth switch that pushes early spread of dormant cancer cells to form metastases. “While our findings add a whole new level of complexity to the understanding of cancer, they also add energy to our efforts to finally solve the big issue in cancer — stop the metastasis that kills patients,” Dr. Aguirre-Ghiso says.

Study contributors include lead co-authors Kathryn L. Harper, PhD, Maria Soledad Sosa, PhD, Julie F. Cheung, BSc, Rita Nobre MSc, Alvaro Avivar-Valderas, PhD, Chandandaneep Nagi, MD, and Eduardo F. Farias, PhD, from Icahn School of Medicine at Mount Sinai; Christoph Klein, MD and Hedayatollah Hosseini, PhD from the University of Regensburg, Germany; Nomeda Girnius, PhD and Roger J. Davis, PhD from Howard Hughes Medical Institute at the University of Massachusetts Medical School; and David Entenberg, MSc and John Condeelis, PhD from Albert Einstein College of Medicine in New York.

Monday, December 19, 2016

Aspirin Slows Growth of Colon, Pancreatic Tumor Cells

Aspirin slows growth of cancers
Newswise, December 19, 2016--Researchers from Oregon Health and Science University and Oregon State University have found that aspirin may slow the spread of some types of colon and pancreatic cancer cells. The paper is published in the American Journal of Physiology—Cell Physiology.

Platelets are blood cells involved with clotting. They promote the growth of cancerous cells by releasing growth factors and increasing the response of certain proteins that regulate tumor cell development (oncoproteins).

Low doses of aspirin, an anti-platelet drug, have been shown to reduce the risk of some types of gastrointestinal cancers, but the process by which aspirin hampers tumor growth has been unclear.

“The current study was designed to determine the effect of inhibition of platelet activation and function by aspirin therapy on colon and pancreatic cancer cell proliferation,” the researchers wrote.

The research team combined activated platelets primed for the clotting process with three groups of cancer cells:
• metastatic colon cancer (cells that have spread outside the colon),
• nonmetastatic colon cancer (cells that grow only within the colon) and
• nonmetastatic pancreatic cancer cells.

When they added aspirin to the mixture, they found that the platelets were no longer able to stimulate growth and replication in the pancreatic and nonmetastatic colon cancer cells.

The metastatic colon cancer cells continued to multiply when treated with aspirin.

In pancreatic cancer cells, low doses of aspirin stopped the platelets from releasing growth factor and hampered the signaling of the oncoproteins that cause cancer to survive and spread.

Only very high doses—larger than are possible to take orally—were effective in stopping growth in the metastatic colon cells, explained the researchers.

The findings detail the interaction among platelets, aspirin and tumor cells and are promising for the future treatment of nonmetastatic cancer, according to the researchers.

 “Our study reveals important differences and specificities in the mechanism of action of high- and low-dose aspirin in metastatic and nonmetastatic cancer cells with different tumor origins and suggests that the ability of aspirin to prevent platelet-induced c-MYC [an oncoprotein] expression might be selective for a nonmetastatic phenotype.”

Physiology is the study of how molecules, cells, tissues and organs function in health and disease. Established in 1887, the American Physiological Society (APS) was the first U.S. society in the biomedical sciences field. The Society represents more than 11,000 members and publishes 14 peer-reviewed journals with a worldwide readership.

Wednesday, November 30, 2016

Protecting Your Vision: An Overview Of Diabetes And Eye Health

Protecting blindness for diabetics
Blood sugar control is key for eye health in patients with diabetes, says David Benderson, M.D., an ophthalmologist with Valley Medical Group in Ridgewood, NJ.

Newswise, November 30, 2016 — Loss of vision is one of the many dreaded complications of diabetes. Over 5.3 million Americans suffer from diabetes-related retinal disease or diabetic retinopathy. After 20 years of living with diabetes, nearly all type 1 diabetics will have some degree of diabetic retinopathy, as will approximately 60 percent of type 2 diabetics. Some of these patients will experience significant vision loss.

If you think of the eye as a camera, the retina is the film. This important structure translates images into electrical signals, which are then sent to your brain for processing. High blood sugar levels associated with diabetes damage small blood vessels throughout the body, including the retina. Advanced diabetic retinopathy can cause a devastating form of glaucoma due to growth of unhealthy blood vessels on the iris (neovascular glaucoma). 

Elevated blood sugar can also result in swelling of the lens, which can temporarily change a patient’s glasses prescription, resulting in blurry vision.

Once the blood sugar is controlled, the lens swelling resolves. Additionally, diabetics are at a higher risk for developing cataracts, or permanent clouding of the lens.

A multi-pronged approach is necessary to prevent and treat diabetic eye disease. To begin with, it is essential that diabetics work closely with their primary care physician and, in many cases, endocrinologist, to keep their blood sugar under good control.

Other health care providers, such as nurse educators and nutritionists serve an essential role in diabetes management. Large studies have shown that tight control of blood sugar reduces the risk of diabetic complications, including retinopathy.

Furthermore, diabetics should undergo a complete eye examination, including dilation (in order to view the retina and other structures) on a yearly basis. If a diabetic patient develops diabetic retinopathy, more frequent examination may be necessary.

If macular edema or proliferative diabetic retinopathy develop, early diagnosis and treatment is essential to preserving vision. Conversely, if a diabetic patient waits until they have vision loss to visit the doctor, treatment may be less effective.

Ultimately, prevention is the best tool to combat diabetic eye disease. Effective control of blood sugar and blood pressure, maintaining a healthy and balanced lifestyle, and regular follow-up with a primary care physician and ophthalmologist are key elements in avoiding vision loss from diabetes.

Comparing Gait Parameters Can Predict Decline In Memory And Thinking

Walking gait can foretell decline in memoryNewswise, November 30, 2016 —— Walking is a milestone in development for toddlers, but it’s actually only one part of the complex cognitive task known as gait that includes everything from a person’s stride length to the accompanying swing of each arm. A Mayo Clinic study recently published in the Journal of Alzheimer’s Disease found that problems associated with gait can predict a significant decline in memory and thinking.

Using the Rochester Epidemiology Project, Mayo Clinic researchers examined medical records of Olmsted County, Minnesota, residents, who were between ages 70 to 89 as of Oct. 1, 2004. The analysis included 3,426 cognitively normal participants enrolled in the Mayo Clinic Study of Aging who had a complete gait and neuropsychological assessment.

Using computerized analyses, researchers measured gait parameters, such as:
• Stride length
• Ambulatory time
• Gait speed
• Step count
• Cadence
• Stance time
• Arm swing

Alterations in several gait parameters were associated with decline in memory, thinking and language skills, and visual perception of the spatial relationship of objects.

The study results also supported the role of computerized analysis because the computer tool detected modifications before impairment was detected with a standard neuropsychological test.

“The presence of gait disturbances increases with advancing age and affects the independence of daily living, especially in the elderly,” says neurologist Rodolfo Savica, M.D., lead author on the study. “Computerized gait analysis is a simple, noninvasive test that potentially could be used to identify patients at high risk for cognitive decline and to target appropriate therapies.”

In addition to Dr. Savica, Mayo Clinic study co-authors are:
• Alexandra Wennberg, Ph.D.
• Clinton Hagen
• Kelly K. Edwards
• Rosebud Roberts, M.B., Ch.B.
• John Hollman, Ph.D.
• David Knopman, M.D.
• Bradley Boeve, M.D.
• Mary Machulda, Ph.D.
• Ronald Petersen, M.D., Ph.D.
• Michelle Mielke, Ph.D.

About Mayo Clinic
Mayo Clinic is a nonprofit organization committed to clinical practice, education and research, providing expert, whole-person care to everyone who needs healing. For more information, visit or

Medicare Beneficiaries Face High Out-Of-Pocket Costs For Cancer Treatment

Those without supplemental insurance incur expenditures averaging a quarter of income
High out of pocket costs for cancer treatment
Newswise, November 30, 2016 — Beneficiaries of Medicare who develop cancer and don’t have supplemental health insurance incur out-of-pocket expenditures for their treatments averaging one-quarter of their income with some paying as high as 63 percent, according to results of a survey-based study published Nov. 23 in JAMA Oncology.

Researchers at the Johns Hopkins Bloomberg School of Public Health and the Johns Hopkins Kimmel Cancer Center say their study shows that a cancer diagnosis can be a serious financial hardship for many elderly and disabled who receive Medicare, with annual out-of-pocket costs ranging from $2,116 to $8,115, on top of what they pay to have health insurance. The research shows that hospitalizations are a major driver of out-of-pocket costs.

Cancer treatment contributes more to health care costs in the United States than treatment for any other disease, say the researchers.

“The spending associated with a new cancer diagnosis gets very high quickly, even if you have insurance,” says one of the study’s authors, Lauren Hersch Nicholas, PhD, MPP, an assistant professor in the Department of Health Policy and Management at the Bloomberg School. 

“The health shock can be followed by financial toxicity. In many cases, doctors can bring you back to health, but it can be tremendously expensive and a lot of treatments are given without a discussion of the costs or the financial consequences.”

For their study, Nicholas and Amol K. Narang, MD, an instructor in the Department of Radiation Oncology and Molecular Radiation Sciences at the Johns Hopkins University School of Medicine and member of the Kimmel Cancer Center, examined data from more than 18,000 Medicare beneficiaries who were interviewed biennially between 2002 and 2012 for the Health and Retirement Survey. 

The survey is funded by the National Institute on Aging and includes data from seniors in the U.S. with wide geographic, socioeconomic and ethnic representation. Over the course of the study period, more than 1,409 people received a cancer diagnosis.

Medicare covers just 80 percent of outpatient health costs and has co-pays of $1,000 for each hospital visit. In the study, 15 percent of participants had Medicare alone. 

Others had some type of supplemental insurance: 50 percent had a Medigap plan or were still receiving employer or retiree benefits; 20 percent participated in a Medicare HMO; nine percent received Medicaid (the federal plan for the poorest Americans); and six percent got benefits from the Veteran’s Administration (VA). Each type of insurance covers a varying amount of the costs that Medicare doesn’t cover.

The researchers found that the average annual out-of-pocket costs associated with a new cancer diagnosis were $2,116 for Medicaid beneficiaries; $2,367 for the VA; $5,492 for those with employer-sponsored plans; $5,670 for those with Medigap; $5,976 for those with a Medicare HMO; and $8,115 for those without supplemental insurance of any kind. There are no caps on how much Medicare beneficiaries can be asked to pay.

Survey respondents without supplemental insurance reported that their average annual out-of-pocket costs were one-quarter of their annual income and, of those, 10 percent reported that those costs were at least 63 percent of annual income.

“Cancer costs are high, and a significant segment of our seniors who don’t have adequate insurance coverage can be hit hard by this,” Narang says. “In addition to efforts aimed at lowering cancer costs, we need to think about how to offer our seniors better insurance coverage.”

The researchers say one solution, though expensive, would be to cap the amount of out-of-pocket costs a patient can be charged each year. Many private insurance plans have such caps, known as catastrophic coverage. Congress would need to enact such a reform.

Narang and Nicholas found that inpatient hospitalizations accounted for between 12 percent and 46 percent of out-of-pocket cancer spending depending on whether and what type of supplemental insurance a patient had. Inpatient care can be necessary for surgical procedures and to handle severe side effects of treatment.

Narang says that doctors can help avoid hospitalizations with more intensive outpatient management of common side effects. 

He also points to the Kimmel Cancer Center’s urgent care clinic which has reduced hospitalization rates in patients undergoing cancer therapy. For example, among those undergoing radiation, the average number of patients who were hospitalized during their course of treatment or within 60 days decreased from 35 per month to 18 per month after the clinic opened. Of note, 10 percent of hospitalizations over this time resulted in patient liabilities of more than $2,000; among Medicare patients without supplemental insurance, 10 percent of their hospitalization-associated patient liabilities exceeded $10,000.

The researchers say that the study’s limitations include the potential for inaccuracies in survey respondents’ answers, misclassification of data or incomplete reporting. For the study, the researchers provided ranges within certain survey questions when respondents could not identify a specific value.

Because the study did not identify specific information on the type of hospitalizations among survey respondents, Narang says that more research is needed to understand which of these hospitalizations are truly preventable.

“We should expect to spend some of our income on health care,” Nicholas says. “But many people are unprepared to spend more than a quarter of their income treating a single disease. The physical disease is terrible and then you have to figure out how to deal with the economic fallout associated with paying to treat it.”

“Out-of-pocket spending and financial burden among Medicare beneficiaries with cancer” was written by Amol K. Narang and Lauren Hersch Nicholas.
The study was supported by a grant from the National Institute on Aging (K01AG041763).

Saturday, November 19, 2016

Is More, Better? Finding The Balance Between Nutritional Supplements And Eye Health

Nutritional Supplements and Vision Loss
Excess Lutein Supplements Linked to Formation of Crystal Deposits in the Eyes
Newswise, November 19, 2016— In the past decade, ophthalmologists have been prescribing nutritional supplements to be taken daily to prevent or slow vision loss from age-related macular degeneration (AMD). Now, using nutritional supplements for eye health has become more common. But does increasing the recommended dose increase your protection? 
A case report appearing online in JAMA Ophthalmology from the Moran Eye Center at the University of Utah reveals what can happen when a patient takes more of a supplement than their body needs.
In the article, Crystalline Maculopathy Associated with High-Dose Lutein Supplementation, principal investigator Paul Bernstein, M.D., Ph.D., describes a patient with no AMD or vision problems who was referred to the retinal clinic for crystal deposits in the macular region of the retina in both eyes.

With physician follow-up, it was learned that for the past eight years, the patient took a daily lutein supplement (20 mg) in addition to a diet rich in lutein, which included a broccoli, kale, spinach, and avocado smoothie every morning; she was therefore consuming much more than twice the recommended dose of lutein for an AMD patient (10 mg per day).
Lutein is part of the AMD prevention supplement regimen that was created based on results from the AREDS2 (Age-Related Eye Disease Study 2) clinical trial.
In that trial, researchers found that patients at high risk for visual loss from AMD who took lutein (10 mg) and zeaxanthin (2 mg) supplements reduced their risk of progressing to late stage AMD. Lutein and zeaxanthin are carotenoids—antioxidants made by plants—that are believed to neutralize light-induced damage in the eye.
Humans don’t make carotenoids, so they can only be added to the body by eating plants or taking supplements.
“When we looked at the patient’s carotenoid levels in serum, skin, and the retina, all measurements were at least two times greater than carotenoid levels in patients not taking nutritional supplements,” said Bernstein.
 “The patient quit taking the lutein supplement, but maintained her diet rich in lutein, and, after seven months, the crystals in the right eye disappeared.”
While AREDS2 supplements are recommended to patients at higher risk for AMD, there has also been increased use in the general population. Bernstein’s advice for his patients is that “everyone should eat an ‘eye-healthy’ diet rich in colorful fruits and vegetables, and individuals should take an AREDS2 supplement if their ophthalmologist detects signs of AMD.”
This case report must followed up by a larger clinical trial before the results can be considered conclusive but it serves as an indicator that there may be negative effects from consuming lutein considerably higher than the recommended AREDS2 dose.

  High Blood Pressure Can Impair Cognitive Function, Pose Risk For Alzheimer’s

Newswise, November 19, 2016 - High blood pressure in middle age can lead to impaired cognition and is a potential risk factor for Alzheimer’s disease, according to a statement from the American Heart Association co-authored by Loyola Medicine neurologist José Biller, MD.

Dr. Biller is a member of the multidisciplinary panel of experts that wrote the statement, published in the heart association journal Hypertension. Dr. Biller is chair of the department of neurology of Loyola University Chicago Stritch School of Medicine.

 The panel is chaired by Constantino Iadecola, MD, of Weill Cornell Medicine and co-chaired by Kristine Yaffe, MD, of the University of California San Francisco.

Dementia affects an estimated 30 to 40 million people worldwide, and the number is expected to triple by 2050 due to an aging population and other factors.

An estimated 80 million people in the United States have hypertension, and the brain is among the organs most affected. Except for age, hypertension is the most important risk factor for vascular problems in the brain that lead to stroke and dementia.

There is consistent evidence that chronic high blood pressure during middle age (40 to 64) is associated with altered cognitive function in both middle age and late life (65 to 84).

Cognitive abilities that are affected include memory, speed of processing and executive function (ability to organize thoughts, manage time, make decisions, etc.)

The effect of high blood pressure in late life is less clear. Some studies suggest it’s harmful, while other research suggests it may improve cognition.

This highlights “the complexities of recommending uniform levels of blood pressure across the life course,” the expert panel wrote.

Observational studies have demonstrated that high blood pressure causes atherosclerosis (hardening of the arteries) and other damage to the brain’s blood vessels, leading to reduced blood flow to brain cells. But evidence from clinical trials that treating blood pressure improves cognition is not conclusive.

After carefully reviewing available studies, the panel concluded there are not enough data to make evidence-based recommendations.

However, judicious treatment of high blood pressure, taking into account goals of care and the patient’s individual characteristics, “seems justified to safeguard vascular health and, as a consequence, brain health,” the panel concluded.

Saving Sight In Glaucoma: Why The Brain May Hold The Key

Retinal fibers from ganglion cell neurons (circles) stream through the optic nerve head on their way to brain.

Newswise, November 19, 2016 — What causes vision loss in glaucoma? There are two common answers that at first may seem disparate: the first is pressure, as in elevated ocular pressure, and the second is damage to the optic nerve, which is the structure that sends visual information to the brain. Both answers are correct.

Glaucoma involves sensitivity to ocular pressure (not just elevated pressure) that is translated or transduced to stress that degrades the optic nerve over time.

Current glaucoma therapies lower pressure using eye drops, surgery, or both in order to reduce stress transduced to the optic nerve. This approach is effective for many patients. But for those who continue to lose vision, where should we turn for new clinical therapies?

One idea is to consider where ocular pressure exerts its influence: the optic nerve head. This structure in the back of the eye defines where nerve fibers leave the retina and enter the optic nerve.

The nerve head contains lateral structures that support these fibers but also couple the nerve to the rest of the eye. In this way, pressure in the front of the eye can cause stress to the optic nerve.

While we do not understand precisely how this stress is conveyed, we do know that aging of the nerve head is likely to contribute to its susceptibility. By addressing age-related factors, new research might reveal therapies based on reducing the sensitivity of the nerve head to pressure.

What about the optic nerve itself? Like the brain, the optic nerve and retina are part of the central nervous system. Once damaged beyond a certain point, these structures cannot heal.

For patients who have lost substantial optic nerve tissue in glaucoma, the hope of regenerative medicine is to restore connectivity with the brain by introducing new nerve fibers or inducing damaged ones to regrow.

Another area of promise that may be forthcoming leverages the idea that increasing brain activity in some cases increases its resistance to stress. Catalyst for a Cure (CFC) research has demonstrated a "window of structural persistence" in which connectivity between the optic nerve and brain remains even when glaucoma affects visual function.

During this "window," optic nerve fibers attempt to boost their electrical activity through natural self-repair mechanisms.

New research by CFC investigators shows that enhanced activity can also help optic nerve fibers regenerate. Perhaps the best approach to a new type of nerve-based glaucoma treatment would combine optic nerve regenerative techniques with those that promote intrinsic repair in the brain.

Article by David J. Calkins, PhD, the Director of Vanderbilt Vision Research Center, Vice-Chairman and Director for Research at The Vanderbilt Eye Institute, and the Denis M. O'Day Professor of Ophthalmology and Visual Sciences at The Vanderbilt University Medical Center.

Tuesday, November 15, 2016

Act Your Age When It Comes To Skin Care

 Dermatologists share tips for women 
Dermatologists share skin care tips for women as they age

Newswise, November 15, 2016— People experience many changes as they age, and that includes changes in their skin. The body’s largest organ evolves over time, so it’s important for one’s skin care routine to evolve with it.

Although dermatologists’ skin care recommendations for each patient will depend on that patient’s age, there are a few core steps dermatologists advise virtually every woman to take:

1. Select products tailored to your skin type — for example, special formulations for sensitive skin, moisturizing products for dry skin, and oil-free or noncomedogenic options for oily skin.
2. Protect your skin from exposure to ultraviolet radiation from the sun and indoor tanning beds, which can lead to skin cancer and early skin aging. The American Academy of Dermatology recommends that you shield yourself from the sun’s harmful UV rays by seeking shade, wearing protective clothing and using a broad-spectrum, water-resistant sunscreen with an SPF of 30 or higher.
3. Use a retinoid, unless it dries out or irritates your skin. Retinoids increase cell turnover to exfoliate clogged pores and reduce the appearance of fine lines, which means they can effectively treat both acne and wrinkles.

While these steps form the foundation of most skin care regimens, each individual’s skin care routine should be based on her age and her skin’s specific needs. To kick off National Healthy Skin Month, three board-certified dermatologists discuss the top skin care concerns of women in their 20s, 30s and 40s, and provide skin care tips for each age group.

Women in their 30s: At the crossroads of prevention and treatment

Dark spots
When women in their 30s come into her Augusta, Ga., private practice to seek treatment for dark spots, board-certified dermatologist Lauren Eckert Ploch, MD, MEd, FAAD, always provides them with tips for prevention. “If you have dark spots at this point in your life, you’re at risk for getting more as you grow older,” she says.

Because UV exposure causes dark spots, Dr. Ploch reminds her patients in their 30s about the importance of sun protection. When applying their SPF 30 sunscreen each morning, she says, it’s vital for women in this age group to make sure they cover their neck and chest in addition to their face, especially if they commute.

“Because UVA rays can travel through window glass, you need to make sure you’re protected if you’re spending a lot of time in the car or on a train,” she says.

Women who received unprotected UV exposure when they were younger may start to see dark spots on their temples and cheeks when they reach their 30s, Dr. Ploch says, and these spots may be mistaken for melasma, a condition that causes brown patches to appear on the face.

While lightening agents like hydroquinone are a good option for melasma, she says, they usually aren’t effective in treating dark spots.

Instead, Dr. Ploch recommends that patients with dark spots follow a multipronged treatment plan. In addition to sun protection, she says, topical vitamin C and retinoids may be used for both treatment and prevention.

 Laser surgery and cryosurgery are also options for reducing the appearance of dark spots, she says, but these procedures should only be performed by a dermatologist or another experienced medical professional.

Dr. Ploch estimates that about half of her patients in their 30s are dealing with both wrinkles and acne.

As a result, she says, many patients in this age group may not be able tolerate wrinkle treatments designed for more mature skin because these heavier formulas can aggravate acne or cause milia, small cysts that occur when dead skin cells become trapped at the surface of the skin.

Dr. Ploch recommends women in their 30s use a retinoid to address both wrinkles and acne.

“Retinoids are my go-to wrinkle treatment for women in this age group,” she says. “In addition to improving your skin’s current appearance, they also help build collagen, which can lead to more voluminous skin in your 40s and 50s.”

Dr. Ploch also suggests that women in their 30s use a light antioxidant serum to protect their skin from the elements and improve signs of early skin aging, and she says those who are concerned about wrinkles also may want to consider botulinum toxin and hyaluronic acid fillers.

A low dose of botulinum toxin can minimize muscle movements that lead to future wrinkles, she says, and hyaluronic acid fillers can restore volume loss, reducing the appearance of lines around the mouth.

Spider veins
While spider veins are one of the most common problems for women in their 30s, Dr. Ploch says, they’re also one of the least-addressed problems in this age group.

Many women believe that treatment would be too invasive or expensive, she says, so they leave the condition unaddressed, allowing it to get worse as they get older.

According to Dr. Ploch, however, laser surgery and sclerotherapy are two accessible and noninvasive treatment options that women in their 30s may want to consider if they have spider veins. She also suggests that women in this age group take preventive measures against the emergence and progression of this condition.

Pregnancy and frequent standing are two risk factors for spider veins, Dr. Ploch says, and the condition takes several years to develop, which is why it often appears in women when they reach their 30s.

To help relieve the pressure that causes spider veins, she recommends that women wear compression socks, elevate their legs when possible and exercise, especially if they work in a field that requires prolonged standing, like health care or education.

Women in their 40s: Improvement through noninvasive interventions

Skin laxity
As people age, their skin begins to lose collagen and elastin, making it thinner and looser, without the resilient, springy quality of youthful skin, says board-certified dermatologist Anne M. Chapas, MD, FAAD, a clinical instructor of dermatology at Mount Sinai Medical Center in New York.

Skin laxity is most prevalent on the face and neck, she says, but it can occur anywhere on the body, including the arms, abdomen and thighs.

Everyone will experience some amount of skin laxity as they get older, Dr. Chapas says, but the degree of laxity depends on many factors, including sun damage, exposure to pollution, diet, weight fluctuations and lifestyle factors such as smoking.

“Women likely will start to notice skin laxity in their 40s, but they may not want to undergo an invasive procedure to correct it,” she says. “Fortunately, there are noninvasive options ideally suited for women in this situation.”

According to Dr. Chapas, energy-based treatments such as microfocused ultrasound and radiofrequency microneedling can help improve skin laxity by promoting the production of collagen and elastin to create firmer skin.

 “Imagine wrapping your loose skin in shrink wrap to pull everything tighter — that’s the kind of effect these energy devices can have,” she says.

Dr. Chapas says filler injections also can improve skin laxity by replacing lost collagen and elastin. “If you picture your skin as a tablecloth, then you can think of fillers as a sturdier table for it to rest on,” she says.

Volume changes
In addition to losing collagen and elastin as they age, Dr. Chapas says, women also lose fat in areas like the face and hands, resulting in a loss of skin volume. As a result, she says, women in their 40s may experience sagging skin, as well as prominent bones and veins.

According to Dr. Chapas, noninvasive treatments with dermal fillers and energy devices can help restore lost volume in addition to improving skin laxity. These treatments also may be combined to provide the best possible results, she says.

In addition to seeking treatment for lost collagen, Dr. Chapas also recommends that women in their 40s take steps to preserve the collagen they still have.

“It’s important to continue protecting your skin from the sun and the elements as you age,” she says, “and you also should consider incorporating topical growth factors and peptides into your skin care routine.”

Unwanted fat
Women in their 40s may have unwanted body bulges as the result of a slowing metabolism, pregnancy or other lifestyle changes, Dr. Chapas says. Even if women exercise regularly and are otherwise fit, she says, it may be difficult for them to eliminate fat in areas where the body is designed to store it, including the torso and the legs.

According to Dr. Chapas, women in their 40s who have isolated pockets of fat are ideal candidates for noninvasive body sculpting procedures like focused ultrasound, thermal energy treatment and cryolipolysis, all of which create areas of damaged fat that the body gradually removes.

While these treatments can be performed anywhere on the body, the waistline and thighs are the most commonly treated areas, Dr. Chapas says, while the neck and bra spillover area are currently gaining popularity.
Dr. Chapas says interest in these body sculpting treatments has surged in recent years because the procedures are noninvasive, quick and effective, with little downtime for patients.

Although liposuction remains the gold standard for fat removal, she says, other body sculpting procedures can provide subtle results for women who want to address problem areas without undergoing an invasive procedure.
No matter your age or skin concern, a board-certified dermatologist can answer your questions about skin health and help you develop a skin care plan that’s right for you.

In their own words: Dermatologists share their skin care secrets
Dr. Nada Elbuluk
“I wash my face twice a day with a mild cleanser and use a morning moisturizer with SPF 30 or higher. If I’m having an acne breakout, I use an acne spot treatment, typically with benzoyl peroxide and clindamycin. I also avoid the urge to pick or squeeze at any acne, as I know this will cause more inflammation and subsequent scarring. In the evening after cleansing, I use an eye cream and facial cream with retinol and antioxidants. During the day, if I know I will be outside for extended periods, I carry sunscreen in my bag so I can reapply. I also keep an eye out for any new growths or changes I see on my skin. Following these guidelines has helped my skin stay healthy, acne free, skin cancer free, youthful and radiant.”

Dr. Lauren Ploch
“Each morning, I apply an antioxidant serum that contains vitamin C. I follow this with a zinc oxide-containing sunscreen. I apply a retinoid product three to four nights per week, which is as often as I can tolerate it without irritation. I attribute my even, acne-free complexion to my retinoid — it’s the one skin care product I could not go without.

“I have treated my dark spots with various lasers and found them to be very effective as long as I protect myself from the sun after treatment. For wrinkles, botulinum toxin has ensured that I don’t have any! I started getting the occasional botulinum toxin injection in my mid 20s but began regularly injecting myself every four to six months in my early 30s. I prefer injecting smaller doses over the span of a few weeks to ensure that I always retain some natural expression. I also had a hyaluronic acid filler treatment last year and plan to follow up with additional treatments as necessary to restore volume lost over the past decade.

“Because I work long hours on my feet, compression socks are a must. I also wear them when traveling long distances, as sitting on a plane can lead to swelling and increased pressure in the legs. I prefer laser therapy to sclerotherapy for my small spider veins, and I elevate my legs at rest whenever possible to prevent their recurrence.”

Dr. Anne Chapas
“I’ve had noninvasive radiofrequency tightening treatments and dermal fillers regularly over the last few years. I also really like laser resurfacing, which removes damaged skin cells and replaces them with new ones. I think that smaller, regular, preventive in-office treatments, in addition to sun protection and topical retinoid use, have helped to maintain my youthful, healthier looking skin.

“Patients always comment on how ‘natural’ I look after I explain the treatments that I’ve personally received. I think it serves as an example that aesthetic treatments should look natural and healthy, not like you’ve had a lot of ‘work done.’ As dermatologists, we are experts in what healthy skin should look like and are the best-trained physicians to help patients to achieve this goal.”