Saliva gland test for Parkinson's shows promise

Described as a "big step forward" for research and treatment of Parkinson's disease, new research from Mayo Clinic in Arizona and Banner Sun Health Research Institute suggests that testing a portion of a person's saliva gland may be a way to diagnose the disease. The study was released today and will be presented at the American Academy of Neurology's annual meeting in San Diego in March.

11 jan 2013--"There is currently no diagnostic test for Parkinson's disease," says study author Charles Adler, M.D., Ph.D., a neurologist with Mayo Clinic in Arizona. "We have previously shown in autopsies of Parkinson's patients that the abnormal proteins associated with Parkinson's are consistently found in the submandibular saliva glands, found under the lower jaw. This is the first study demonstrating the value of testing a portion of the saliva gland to diagnose a living person with Parkinson's disease. Making a diagnosis in living patients is a big step forward in our effort to understand and better treat patients."

The study involved 15 people with an average age of 68 who had Parkinson's disease for an average of 12 years, responded to Parkinson's medication and did not have known saliva gland disorders. Biopsies were taken of two different saliva glands: the submandibular gland and the minor saliva glands in the lower lip. The surgical team was led by Michael Hinni, M.D., and David Lott, M.D., at Mayo Clinic in Arizona, and the biopsied tissues were tested for evidence of the abnormal Parkinson's protein by study co-author Thomas Beach, M.D., with Banner Sun Health Research Institute.

"This procedure will provide a much more accurate diagnosis of Parkinson's disease than what is now available," Dr. Beach says. "One of the greatest potential impacts of this finding is on clinical trials, as at the present time some patients entered into Parkinson's clinical trials do not necessarily have Parkinson's disease and this is a big impediment to testing new therapies."

The abnormal Parkinson's protein was detected in nine of the 11 patients who had enough tissue to study. While still being analyzed, the rate of positive findings in the biopsies of the lower lip glands appears much lower than for the lower jaw gland.

"This study provides the first direct evidence for the use of submandibular gland biopsies as a diagnostic test for living patients with Parkinson's disease," Dr. Adler. "This finding may be of great use when needing definitive proof of Parkinson's disease, especially when considering performing invasive procedures such as deep brain stimulation surgery or gene therapy."

Parkinson's disease is a progressive disorder of the nervous system that affects movement. It develops gradually, sometimes starting with a barely noticeable tremor in just one hand. But while tremor may be the best-known sign of Parkinson's, the disorder also commonly causes stiffness or slowing of movement. Currently, diagnosis is made based on medical history, a review of signs and symptoms, a neurological and physical examination, and by ruling out other conditions. Up to 30 percent of patients may be misdiagnosed early in the disease.

Although Parkinson's disease can't be cured, medications may markedly improve symptoms.

Provided by Mayo Clinic

First Alzheimer's case has full diagnosis 106 years later

10 jan 2013—More than a hundred years after Alois Alzheimer identified Alzheimer's disease in a patient an analysis of that original patient's brain has revealed the genetic origin of their condition.

The brain specimen tested was discovered in a university basement late last century after a search by rival teams of academics.

"It is extremely satisfying to place this last piece in the medical puzzle that Auguste Deter, the first ever Alzheimer patient, presented us with," said Professor Manuel Graeber, from the University of Sydney.

"It is not only of historical interest, however, as it ends any speculation about whether the disease is correctly named after Alois Alzheimer. Alzheimer's ability to recognise this dementia more than a century ago provides compelling support for specialisation in medicine. Alzheimer was a founding father of neuropathology, an important medical specialty that is still underrepresented."

Professor Graeber, from the University's Brain and Mind Research Institute, Sydney Medical School and the Faculty of Health Sciences, collaborated with Professor Ulrich Müller's team from the Institute of Human Genetics of the University of Giessen in Germany to produce themolecular diagnosis recently published in Lancet Neurology.

For years scientists have been wondering whether the first case of Alzheimer's disease had a genetic cause. In 1901 Auguste Deter, a middle-aged female patient at the Frankfurt Asylum with unusual symptoms, including short-term memory loss, came to the attention of Dr Alzheimer. When she died, Dr Alzheimer examined her brain and described the distinctive damage indicating a form of presenile dementia.

For decades the more than 200 slides that Alzheimer prepared from Deter's brain were lost. Then in 1992, after Professor Graeber uncovered new information pointing to their location, two teams of medical researchers began a dramatic race to find them.

One team searched in Frankfurt but it was a team headed by Professor Graeber, then working at the Max Planck Institute for Neurobiology that finally located the material at the University of Munich in 1997.

The slides were examined and confirmed beyond doubt that Deter was suffering from Alzheimer's disease, with large numbers of amyloid plaques and neurofribrillary tangles in the brain that are hallmarks of the disease. Until now a more sophisticated DNA analysis of the small amount of fragile material in single slides has not been possible.

Since their rediscovery, a significant number of brain slides have been under the official custodianship of Professor Graeber who has been at the University of Sydney since 2010. He is preparing a book on the material.

"We found a mutation whose ultimate effect is the formation of amyloid plaques. These plaques, which form between nerve cells and seem to suffocate them are the key diagnostic landmark of the disease."

Alzheimer's disease represents one of the greatest health problems in industrialised societies today. An estimated 100 million dementia sufferers are predicted worldwide by 2050, the vast majority of whom will have Alzheimer's disease. 
95 percent of Alzheimer's patients suffer late onset of the illness after they turn 65. Five percent fall ill before that age (early onset) and Auguste Deter belongs to this group.

"We have revealed that Auguste Deter is one of those in which early onset of the disease is caused by mutation in a single gene," said Professor Graeber.

More information: www.lancet.com/jou… 7-1/fulltext

Provided by University of Sydney

Cancer screening unlikely to benefit patients with a short life expectancy

Breast and colorectal cancer screening should be targeted towards patients with a life expectancy greater than 10 years: for any shorter life expectancy the harms are likely to outweigh the benefits, concludes a study published in BMJ today.

09 Jan 2013--The authors stress that their results "should not be used to deny screening for patients with limited life expectancy" but "should inform decision making which aims to account for patient preferences and values while maximising benefits and minimising risks."

Guidelines recommend screening healthy older patients because complications from screening can harm patients immediately while the benefits of screening are not seen for many years.

What still remains unclear, however, is how long a patient needs to live to benefit from cancer screening. Previous trials have focused on the size of benefit rather than when those benefits occur.

Researchers from the University of California in San Francisco therefore analysed the results of five breast and four colorectal cancer screening trials focusing on patients aged over 50.

Their goal was to estimate the time-lag to benefit (the time between screening and when the benefits of screening are seen) to determine whether an individual patient is likely to benefit from screening.

The trials were published between 1986 and 2008 and ranged in size from just under 40,000 people to just over 150,000 people. Follow-up ranged from 8-20 years.

Results showed that at five years, an average 2.8 colorectal cancer deaths were prevented for every 10,000 people screened. This benefit steadily increased with longer follow-up, reaching 23 colorectal cancer deaths prevented for every 10,000 people screened at 15 years.

In absolute terms, it took an average of 4.8 years to prevent one colorectal cancer death for 5,000 people screened and 10.3 years to prevent one death for 1,000 people screened.

For breast cancer, at five years an average of 5.1 deaths were prevented for every 10,000 women screened. By 15 years, this mortality benefit had increased to 19 breast cancer deaths prevented for every 10,000 women screened.

In absolute terms, it took an average of three years to prevent one breast cancer death for 5.000 women screened and 10.7 years to prevent one death for 1,000 women screened.

However, the researchers say that in both colorectal and breast cancer, approximately one in ten people screened will have a false positive result and many more will be subject to possibly unnecessary treatment.

Based on these results, they suggest that patients with a life expectancy greater than ten years "should be encouraged to undergo colorectal and breast cancer screening" but patients whose life expectancy is 3-5 years "probably should be discouraged from screening since the potential risks likely outweigh the very small probability of benefit."

They conclude that incorporating time lag estimates into screening guidelines "would encourage a more explicit consideration of the risks and benefits of breast and colorectal cancer screening, likely resulting in a more individualised decision making process for the heterogeneous population of older adults."

More information: Time-lag to benefit after screening for breast and colorectal cancer: meta-analysis of survival data from the United States, Sweden, United Kingdom and Denmark, BMJ, 2013.

Provided by British Medical Journal

Expert suggests top four reasons why diets fail

The battle of the bulge is on—any movement on the scale yet? "Losing weight is one of the top resolutions made every year, yet only 20 percent of people achieve successful weight-loss and maintenance," says Jessica Bartfield,MD, internal medicine who specializes in nutrition and weight management at the Loyola Center for Metabolic Surgery & Bariatric Care.

08 Jan 2013--Despite that fact that two-thirds of Americans say they are on a diet to improve their health, very few are actually decreasing in size. "Dieting is a skill, much like riding a bicycle, and requires practice and good instruction, " says Dr. Bartfield. "You're going to fall over and feel frustrated, but eventually you will succeed and it will get easier."

According to Dr. Bartfield, here are the top four reasons why many dieters fail to lose weight:

1. Underestimating Calories Consumed

"Most people (even experts!) underestimate the number of calories they eat per day. Writing down everything that you eat- including drinks and "bites" or "tastes" of food - can help increase self-awareness. Pay attention to serving sizes and use measuring cups and spoons as serving utensils to keep portions reasonable. Food eaten outside of the home tends to be much larger portion sizes and much higher in calories. Try to look up nutrition information of your favorite take-out meal or restaurant and select a healthy meal before picking up the phone or going out to eat.

2. Overestimating Activity and Calories Burned

"Typically you need to cut 500 calories per day to lose 1 lb per week. This is very difficult to achieve through exercise alone, and would require 60 minutes or more of vigorous activity every day. A more attainable goal would be to try to increase activity throughout the day and get a total of 30 minutes of moderate to vigorous exercise most days of the week. Buy a pedometer and track your steps; try to increase to a goal of 10,000 steps per day. But be careful- exercise is not an excuse to eat more!"

3. Poor Timing of Meals

"You need a steady stream of glucose throughout the day to maintain optimal energy and to prevent metabolism from slowing down. Eat breakfast every day within one hour of waking up, then eat a healthy snack or meal every three to four hours. Try not to go longer than 5 hours without eating a healthy snack or meal to keep your metabolism steady."

4. Inadequate Sleep

"Studies have shown that people who get fewer than six hours of sleep have higher levels of ghrelin, which is a hormone that stimulates appetite, particularly for high- carbohydrate/high- calorie foods. In addition, less sleep raises levels of cortisol, a stress hormone, which can lead to weight gain."

Dr. Bartfield regularly counsels patients through the Loyola Center for Metabolic Surgery & Bariatric Care, which offers surgical as well as non-surgical weight loss programs. "A registered dietitian, behavioral psychologist, exercise physiologist and a physician plus a surgeon if appropriate, all partner one-on-one with patients," said Bartfield. "Good health practices are more than just learned, they become a regular habit and a way of life."

Provided by Loyola University Health System

Dopamine-receptor gene variant linked to human longevity

07 Jan 2013—A variant of a gene associated with active personality traits in humans seems to also be involved with living a longer life, UC Irvine and other researchers have found.

This derivative of a dopamine-receptor gene – called the DRD4 7R allele – appears in significantly higher rates in people more than 90 years old and is linked to lifespan increases in mouse studies.

Robert Moyzis, professor of biological chemistry at UC Irvine, and Dr. Nora Volkow, a psychiatrist who conducts research at the Brookhaven National Laboratory and also directs the National Institute on Drug Abuse, led a research effort that included data from the UC Irvine-led 90+ Study in Laguna Woods, Calif. Results appear online in The Journal of Neuroscience.

The variant gene is part of the dopamine system, which facilitates the transmission of signals among neurons and plays a major role in the brain network responsible for attention and reward-driven learning. The DRD4 7R allele blunts dopamine signaling, which enhances individuals' reactivity to their environment.

People who carry this variant gene, Moyzis said, seem to be more motivated to pursue social, intellectual and physical activities. The variant is also linked to attention-deficit/hyperactivity disorder and addictive and risky behaviors.

"While the genetic variant may not directly influence longevity," Moyzis said, "it is associated with personality traits that have been shown to be important for living a longer, healthier life. It's been well documented that the more you're involved with social and physical activities, the more likely you'll live longer. It could be as simple as that."

Numerous studies – including a number from the 90+ Study – have confirmed that being active is important for successful aging, and it may deter the advancement of neurodegenerative diseases, such as Alzheimer's.

Prior molecular evolutionary research led by Moyzis and Chuansheng Chen, UC Irvine professor of psychology & social behavior, indicated that this "longevity allele" was selected for during the nomadic out-of-Africa human exodus more than 30,000 years ago.

In the new study, the UC Irvine team analyzed genetic samples from 310 participants in the 90+ Study. This "oldest-old" population had a 66 percent increase in individuals carrying the variant relative to a control group of 2,902 people between the ages of 7 and 45. The presence of the variant also was strongly correlated with higher levels of physical activity.

Next, Volkow, neuroscientist Panayotis Thanos and their colleagues at the Brookhaven National Laboratory found that mice without the variant had a 7 percent to 9.7 percent decrease in lifespan compared with those possessing the gene, even when raised in an enriched environment.

While it's evident that the variant can contribute to longevity, Moyzis said further studies must take place to identify any immediate clinical benefits from the research. "However, it is clear that individuals with this gene variant are already more likely to be responding to the well-known medical adage to get more physical activity," he added.

Provided by University of California, Irvine

When will genomic research translate into clinical care—and at what cost?

Genomic research is widely expected to transform medicine, but progress has been slower than expected. While critics argue that the genomics "promise" has been broken – and that money might be better spent elsewhere—proponents say the deliberate pace underscores the complexity of the relationship between medicine and disease and, indeed, argues for more funding.

06 jan 2013--But thus far, these competing narratives have been based mostly on anecdotes. Ramy Arnaout, MD, DPhil, a founding member of the Genomic Medicine Initiative at Beth Israel Deaconess Medical Center (BIDMC), decided it was time to look at genomics from a new perspective. So he turned to quantitative modeling, a numerical forecasting approach used to predict everything from weather events to the outcomes of political elections, and an extremely useful way to both set expectations and assist in decision-making.

Arnaout and colleagues knew that drug-related adverse outcomes cost the health-care system upwards of $80 billion a year, and that many such cases should be avoidable by choosing and dosing drug prescriptions according to a person's genome. So they developed a quantitative model to estimate how much time and money would be required to use genomics, specifically pharmacogenomics, to cut these adverse outcomes in half. Their findings, currently published online in the journal Clinical Chemistry, provide one of the first examples of data-driven estimates being applied to genomic medicine and offer a template for the use of quantitative modeling in this field.

How do the numbers add up? After analyzing their model for a range of situations, the research team found that the cost can be expected to be less than $10 billion, spread out over approximately 20 years.

"If you look across medicine, you can see specific places here and there where genomics is really starting to change things, but it's been hard to know how it all adds up in the big picture," explains Arnaout, who is also an Assistant Professor of Pathology at Harvard Medical School (HMS) and Associate Director of Clinical Microbiology at BIDMC. "Quantitative modeling is a standard approach for forecasting and setting expectations in many fields as we all remember from the recent presidential election and from the hurricane season. Genomics is so important and is so often on the minds of our patients, students and staff, that it seemed like a good idea to use modeling to get some hard numbers on where we're headed."

The idea for the study originated nearly two years ago, while Arnaout (whose laboratory studies genomics) and Sukhatme, BIDMC's Chief Academic Officer, were attending a lecture, shortly after the 10-year anniversary of the sequencing of the genome. "Vikas asked me, 'So when is genomics really going to change medicine?'" remembers Arnaout. "I realized I didn't know. And that got me thinking."

Arnaout and Sukhatme, together with coauthors Thomas Buck, MD, and Paulvalery Roulette, MD, of BIDMC and HMS, decided to try and answer this question by applying forecasting methods to a big clinical problem – drug-related adverse outcomes. "We know that preventable causes of these adverse outcomes—patients' non-adherence, interactions between multiple drugs, and medical error, for example—account for only a fraction of the millions of adverse outcomes that patients experience each year," explains Arnaout. "This leaves a significant number that are currently considered non-preventable and are thought to be caused by genomic variation."

By way of example, Arnaout explains that 30 million Americans currently use the blood-thinning drug warfarin. But because, in some cases, patients' genomes contain variants that make the standard dose of warfarin too high for them, these individuals are likely to experience bleeding, an extremely dangerous side effect. In fact, researchers now estimate that three-quarters of the variability in warfarin dosing requirement is due to these genomic variants, and they have already identified a set of variants in six specific genes that explain two-thirds of the variability.

"This kind of progress suggested an interesting thought experiment," says Arnaout. "What if we took existing examples in which there appears to be a carefully vetted, clinically useful connection between a specific adverse outcome and a specific genetic variant, found out how much it cost and how long it took to discover, and applied that model to all drugs? How much would it cost and how long would it take to cut adverse outcomes by 25 percent? How about by half?"

As data for the model, the authors selected eight associations involving six prescription drugs (clopidogrel, warfarin, escitalopram, carbamazepine, the nicotine-replacement patch and abacavir) and one drug class, the statin class of anticholesterol drugs.

Using an approach called Monte Carlo modeling, the team ran simulations to forecast the research investment required to learn how to cut adverse outcomes by meaningful amounts, and how long that research work would be expected to take. For statistical confidence, they ran their simulations thousands of times and explored a wide range of assumptions. "The results were surprising," says Arnaout. "Before we did this work, I couldn't have told you whether it would take a million dollars or a trillion dollars or whether it would take five years or a hundred years. But now, we've got a basis for thinking that we're looking at single-digit billions of dollars and a couple of decades. That may sound like a lot or a little, depending on your point of view. But with these numbers, we can now have a more informed conversation about planning for the future of genomic medicine."

The most important determinant of the numbers is the extent to which the examples used in the model will turn out to be representative of drugs as a whole. "It's a broad set of drugs that were used, but we know how the genome can surprise us," says senior author Sukhatme. "For example, you won't be able to use genomics to cut adverse outcomes in half if genomics turns out to explain less than half of the adverse outcomes. But even in that case, we found that pharmacogenomics will be able to make a significant dent in adverse outcomes – cutting them by a quarter – for multi-billion-dollar investments."

Also surprising, say the authors, was the timing. "As a rule, the fruits of research come only after research dollars have already been spent," points out Arnaout. This means that, in this case, hundreds of millions of dollars will be spent for "pump-priming" long before the public can expect to see any meaningful clinical impact. "It's one thing to say, 'Be patient,' based on just faith," he adds. "It's another to be able to say so based on data and a model. We now have that. This enables the conversation to shift to which indicators of progress to look for, over the five or so years of pump-priming, to make sure we're on track."

Can we go faster? "If we could enroll an ethnically diverse set of patients who are taking each of the 40 or 50 most commonly prescribed drugs, get their blood samples, and keep track of the adverse outcomes that some of them are bound to experience, we should be able to move faster, for less money," adds Arnaout, who describes this idea as a "50,000 Pharmacogenomes Project," a pursuit along the lines of the 1,000 Genomes Project, the UK10K or the Veteran's Association Million Veteran Program.

"This model provides the start of a provocative conversation and illustrates the value of quantitative modeling in this very practical and publically relevant aspect of genomics," adds BIDMC Chief of Pathology Jeffrey Saffitz, MD, PhD. "Such models should help both decision makers and the public set expectations and priorities for translating genomic research into better patient care."

Provided by Beth Israel Deaconess Medical Center

Why good resolutions about taking up a physical activity can be hard to keep

Physical inactivity is a major public health problem that has both social and neurobiological causes. According to the results of an Ipsos survey published on Monday 31 Dec., the French have put "taking up a sport" at the top of their list of good resolutions for 2013. However, Francis Chaouloff, research director at Inserm's NeuroCentre Magendie (Inserm Joint Research Unit 862, Université Bordeaux Ségalen), Sarah Dubreucq, a PhD student and François Georges, a CNRS research leader at the Interdisciplinary Institute for Neuroscience (CNRS/Université Bordeaux Ségalen) have just discovered the key role played by a protein, the CB1 cannabinoid receptor, during physical exercise. In their mouse studies, the researchers demonstrated that the location of this receptor in a part of the brain associated with motivation and reward systems controls the time for which an individual will carry out voluntary physical exercise. These results were published in the journal Biological Psychiatry.

05 jan 2013--The collective appraisal conducted by Inserm in 2008 highlighted the many preventive health benefits of regular physical activity. Such activity is limited, however, by our lifestyle in today's industrial society. While varying degrees of physical inactivity may be partly explained by social causes, they are also rooted in biology.

"The inability to experience pleasure during physical activity, which is often quoted as one explanation why people partially or completely drop out of physical exercise programmes, is a clear sign that the biology of the nervous system is involved", explains Francis Chaouloff.

But how exactly? The neurobiological mechanisms underlying physical inactivity had yet to be identified.

Francis Chaouloff (Giovanni Marsicano's team at the NeuroCentre Magendie; Inserm joint research unit, Université Bordeaux Ségalen) and his team have now begun to decipher these mechanisms. Their work clearly identifies the endogenous cannabinoid (or endocannabinoid) system as playing a decisive role, in particular one of its brain receptors. This is by no means the first time that data has pointed to interactions between the endocannabinoid system, which is the target of delta9-tetrahydrocannabinol (the active ingredient of cannabis), and physical exercise. It was discovered ten years ago that physical exercise activated the endocannabinoid system in trained sportsmen, but its exact role remained a mystery for many years. Three years ago, the same research team in Bordeaux observed that when given the opportunity to use a running wheel, mutant mice lacking the CB1 cannabinoid receptor, which is the principal receptor of the endocannabinoid system in the brain, ran for a shorter time and over shorter distances than healthy mice. The research published in Biological Psychiatry this month seeks to understand how, where and why the lack of CB1 receptor reduces voluntary exercise performance (by 20 to 30%) in mice allowed access to a running wheel three hours per day.

The researchers used various lines of mutant mice for the CB1 receptor, together with pharmacological tools. They began by demonstrating that the CB1 receptor controlling running performance is located at the GABAergic nerve endings. They went on to show that the receptor is located in the ventral tegmental area of the brain (see diagram below), which is an area involved in motivational processes relating to reward, whether the reward is natural (food, sex) or associated with the consumption of psychoactive substances.

Based on the results of this study and earlier work, the Bordeaux team suggests the following neurobiological explanation: at the beginning and for the duration of physical exercise, the CB1 receptor is constantly simulated by the endocannabinoids, lipid molecules that naturally activate this receptor in response to pleasant stimuli (rewards) and unpleasant stimuli (stress). Endocannabinoid stimulation of the CB1 receptor during physical exercise inhibits the release of GABA, an inhibitory neurotransmitter that controls the activity of the dopamine neurons associated with the motivation and reward processes. This stimulation of the CB1 receptor "inhibits inhibition", in other words, it activates the dopaminergic neurons in the ventral tegmental area. The CB1 receptor must therefore be stimulated before the exercise can go on for longer and the body must receive the necessary motivation.

Longitudinal section of the mouse brain (top) and diagram of interactions between the endocannabinoid, GABAergic and dopaminergic systems during voluntary physical exercise (bottom) ©Inserm/F. Chaouloff

Conversely, without these CB1 receptors, the "GABAergic brake" continues to act on the dopaminergic neurons in the ventral tegmental area, leading to the reduced performance levels observed above.

It is already known that CB1 receptors play a regulatory role in the motivation to consume rewards, whether natural or not. What is original about this research is that it shows that physical exercise can be added to the array of natural rewards regulated by the endocannabinoid system. "If confirmed, this motivational hypothesis would imply that the role played by the CB1 receptor has more to do with 'staying power' in the exercise than with actual physical performance levels" explain the researchers.

This work reveals that the endocannabinoid system plays a major role in physical exercise performance through its impact on motivational processes. It thus opens up new avenues of research into the mediators of pleasure – and even addiction – associated with regular physical exercise. "After endorphins, we now need to consider endocannabinoids as another potential mediator of the positive effects that physical exercise has on our mood," the researchers conclude.

More information: "Ventral Tegmental Area Cannabinoid Type-1 Receptors Control Voluntary Exercise Performance" Biological Psychiatry, 12 December 2012

Provided by Institut National de la Sante et de la Recherche Medicale

Smoking cessation expert offers tips for smokers trying to quit

04 jan 2013—With a New Year approaching and healthy lifestyle choices topping the list of personal resolutions, millions of smokers across New York State and more throughout the U.S. will attempt to quit smoking. Making an effort to stop smoking is an appropriate one given World Health Organization estimates that smoking contributes to five million deaths each year.

Smokers who are considering quitting as part of a new year's resolution may also be giving the most precious gift possible to their children and grandchildren. A recent study in Great Britain revealed that of those children who have parents that smoke, more than 50 percent say their one wish for Christmas is for their parents to stop smoking. In addition, more than 73 percent of those children frequently worry about their parent(s) dying.

"Quitting smoking is the best decision anyone can make to improve their overall health," said Scott McIntosh, Ph.D., director of the Greater Rochester Area Tobacco Cessation Center and associate director of the Smoking Research Program at  the Department of Public Health Sciencesat the University of Rochester Medical Center (URMC). But McIntosh stresses that having a plan in place is essential to being successful to one's smoking cessation efforts.

"Research shows that if a person makes a plan, builds a support system of family, friends and professionals, that they have a greater chance of successfully quitting smoking and beating nicotine addiction," said McIntosh, who also serves as an Associate Professor in the Department of Public Health Sciences and URMC's James P. Wilmot Cancer Center.

McIntosh offers 12 simple tips for quitting:

1.      Make a plan for quitting. Talk to your doctor about strategies such as quitting "cold turkey" versus nicotine replacement or other medication therapies.

2.      If you can give up cigarettes for 24 hours, you may learn something important to help you when you plan to quit for good.

3.       Tell your friends, family and co-workers that you plan to quit and rally them to help you stick with it.

4.      Consider using approved medications – nicotine gum, patch, lozenges, spray, inhaler, Chantix or Zyban – to help you quit.

5.      Use resources available from the New York State Smokers' Quitline:  1-866-NY-QUITS ( 1-866-697-8487) and www.nysmokefree.com, the New York Smokers' Quitsite.

6.      Use local resources (covered by Medicaid and many insurance plans) at the Healthy Living Center, which provides individual counseling and a quitting plan with tobacco dependence counselors and medical staff:  (585) 530-2050.

7.      Remove all ashtrays, lighters, matches and cigarettes from the house. Just seeing them can make you want to smoke.

8.      Start eating sugarless hard candy or chewing crunchy vegetables – like carrot sticks – to keep your mouth busy. Consider using cinnamon candy, because its "burning" sensation mimics the feeling of smoking and kills the craving.

9.      Drink a lot of water. It helps keep you feeling "full," and prevents you from overeating and gaining weight. It also helps "cleanse" your body of the toxins from years of smoking.

10. Practice breathing deeply or take a walk when you're craving a cigarette. Smoking involves taking long deep breaths, but now it'll be fresh air rather than chemicals entering your lungs.

11. Remind yourself why you are quitting - and reward yourself every day you make it without smoking cigarettes.

12. Age doesn't matter - older smokers are less likely to try to quit, but when they do try, they are more likely to succeed.

"Using approved medicines can help and talking to experts can help – and using both strategies can even further improve your chances of quitting for good," McIntosh said. "Within just 24 hours, the carbon monoxide – which hinders blood from bringing oxygen to your cells, tissues and organs – will be removed from your body, and the mucus and smoking debris will start to clear from your lungs, making breathing easier.

The New York State Smokers' Quitline  is also prepared to assist the more than two million smokers in New York State who say they want to quit. 

The Quitline offers smokers a free nicotine patch starter kit, coaching tips for quitting, self-help materials, and motivational messages. The Quitline can be reached at 1-866-NY-QUITS ( 1-866-697-8487) Monday through Thursday, 9:00 a.m. – 9:00 p.m., and Friday through Sunday, 9:00 a.m. – 5:00 p.m.  Additional support is available through a 24/7  online smoke-free community at http://www.nysmokefree.org , and additional tips and resources can be found at http://www.facebook.com/NYQuits and https://twitter.com/nysmokefree .

Top ten tips to combat diabetes this New Year

03 jan 2013—Getting your family and friends to support you in being physically active and setting yourself physical activity goals are among the top ten tips scientifically proven to help combat Type 2 diabetes.

Newcastle University researchers carried out a large-scale review of all randomised controlled trials examining changing physical activity and Type 2 diabetes. They analysed the ways people were encouraged to change their behaviour and linked them to whether it changed the control of their diabetes. From this analysis they devised a list of the successful strategies which help people become more active and improve their glucose control.

Publishing today in Diabetes Care, author Professor Mike Trenell who specialises in physical activity and metabolic research at Newcastle University said: "The message that we have known for a while is that people with Type 2 diabetes can benefit significantly by moving more and sitting less. What we have now shown is how people can best help themselves to be physically active.

"While being more physically active often conjures up images of hours on a treadmill or competitive marathon running - walking, using the stairs and just moving more in everyday life can be effective in helping manage diabetes.

"So this New Year, before reaching for the remote and yet another leftover Christmas treat, people should look at how they can move more and sit less. This list provides some useful tips on how to make those New Year's Resolutions a reality. Aside from general improvements in health, its likely that you will look and feel better too."

The Newcastle University team have pulled together the research on the topic and come up with the top ten tips to combat Type 2 diabetes:

• Set physical activity goals – make them specific, measurable and time dependent (such as walking 10,000 steps a day).

• Review your goals – and it doesn't matter if they're short or long-term activity goals.  Make time to think about whether you are achieving what you want.

• Plan in advance a time in your day to be active either at home or at work.

• Get friends or family members involved in your activity, walking with you or helping set or monitor goals.

• Build on your activity success – if you're more active in one area of your daily life such as taking the stairs, then build on that to increase activity in another such as walking to a bus stop further away.

• Get support – phone calls from your GP practice work as well as face-to-face sessions.

• Find out what activities are going on in your local area and when they take place – research shows that just having that information galvanises people into action.

• Build on past success - motivate yourself by thinking of a time where you were more active and how it made you feel.

• What might stop you? - Think what might get in the way of you reaching your activity goal and plan ways around it.

• How is this going to make you healthier? - Seek out information specifically about the benefits of physical activity for you. This might not be just improved diabetes control but looking better, feeling more energetic and meeting people.

Between 2006 and 2011, the number of people diagnosed with diabetes in England has increased by 25 per cent, from 1.9 million to 2.5 million. It's estimated that up to 850,000 people have diabetes but don't know it. The cost of treating diabetes is a staggering £10.3 billion a year – around 10% of the entire NHS budget.

However, as previous Newcastle University research has shown, patients with Type 2 diabetes can walk 45 minutes every day and get the same improvement in blood glucose control as from a major class of drugs.

But getting people with Type 2 diabetes to be more active can prove difficult.

The Newcastle team carried out a systematic review of over 8000 studies and examined 17 studies in depth to understand how health professionals helped support people with Type 2 diabetes to become more physically active and in turn improve their diabetes control. A total of 21 behaviours were identified which had a positive impact on people's health.

Moving more helps improve glucose control by keeping blood flowing to the muscles, maintaining the uptake of sugar from the blood into the muscles where it can be stored or burnt. The increase in energy expenditure also helps prevent weight gain, a major driver for the worsening of diabetes over time.

Professor Mike Trenell adds: "There's growing evidence that moving more and keeping active not only prevents Type 2 diabetes but is critical in protecting us as we grow older.

"The science is clear about the benefits of a moving more and sitting less to diabetes control. But, making the advice into action is much more difficult – we hope that these tips will help people with diabetes improve self management through being more physically active and possibly look and feel better too."

Provided by Newcastle University

Higher levels of obesity associated with increased risk of death

In an analysis of nearly 100 studies that included approximately 3 million adults, relative to normal weight, overall obesity (combining all grades) and higher levels of obesity were both associated with a significantly higher all-cause risk of death, while overweight was associated with significantly lower all-cause mortality, according to a study in the January 2 issue of JAMA.

02 jan 2013--"Estimates of the relative mortality risks associated with normal weight, overweight, and obesity may help to inform decision making in the clinical setting," according to background information in the article.

Katherine M. Flegal, Ph.D., of the National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, Md., and colleagues conducted a study to compile and summarize published analyses of body mass index (BMI) and all-cause mortality that provide hazard ratios (HRs) for standard BMI categories. For the review and meta-analysis, the researchers identified 97 studies that met inclusion criteria, which provided a combined sample size of more than 2.88 million individuals and more than 270,000 deaths. Regions of origin of participants included the United States or Canada (n = 41 studies), Europe (n = 37), Australia (n = 7), China or Taiwan (n = 4), Japan (n = 2), Brazil (n = 2), Israel (n = 2), India (n = l), and Mexico (n = l).

All-cause mortality HRs for overweight (BMI of 25-<30 18.5-="18.5-" 1="1" 2="2" 30-="30-" 3="3" and="and" calculated="calculated" grade="grade" grades="grades" normal="normal" obesity="obesity" of="of" p="p" relative="relative" to="to" weight="weight" were="were">

The researchers found that the summary HRs indicated a 6 percent lower risk of death for overweight; a 18 percent higher risk of death for obesity (all grades); a 5 percent lower risk of death for grade 1 obesity; and a 29 percent increased risk of death for grades 2 and 3 obesity.

The authors note that the finding that grade 1 obesity was not associated with higher mortality suggests that that the excess mortality in obesity may predominantly be due to elevated mortality at higher BMI levels.

The researchers add that their findings are consistent with observations of lower mortality among overweight and moderately obese patients. "Possible explanations have included earlier presentation of heavier patients, greater likelihood of receiving optimal medical treatment, cardioprotective metabolic effects of increased body fat, and benefits of higher metabolic reserves."

The use of predefined standard BMI groupings can facilitate between-study comparisons, the authors conclude.

More information: JAMA. 2013;309(1):71-82

Editorial: Does Body Mass Index Adequately Convey a Patient's Mortality Risk?

"Can overweight as defined by BMI actually have a protective association with mortality?" write Steven B. Heymsfield, M.D., and William T. Cefalu, M.D., of the Pennington Biomedical Research Center, Baton Rouge, La., in an accompanying editorial.

"The presence of a wasting disease, heart disease, diabetes, renal dialysis, or older age are all associated with an inverse relationship between BMI and mortality rate, an observation termed the obesity paradox or reverse epidemiology. The optimal BMI linked with lowest mortality in patients with chronic disease may be within the overweight and obesity range. Even in the absence of chronic disease, small excess amounts of adipose tissue may provide needed energy reserves during acute catabolic illnesses, have beneficial mechanical effects with some types of traumatic injuries, and convey other salutary effects that need to be investigated in light of the studies by Flegal et al and others."

"Not all patients classified as being overweight or having grade 1 obesity, particularly those with chronic diseases, can be assumed to require weight loss treatment. Establishing BMI is only the first step toward a more comprehensive risk evaluation."

JAMA. 2013;309(1):87-88

Provided by JAMA and Archives Journals

Smartphone apps for health and fitness an exploding craze

When Jon Mead, a devoted cyclist, visits a new city, he goes right to his smartphone app Strava to find the best bike routes. In Sacramento, Calif., where he works at a Fleet Feet running-gear shop, the 24-year-old uses MapmyRide to track his course in an archive.

01 jan 2013--Bethany Scribner, a runner who also works at the fitness gear retailer, likes the apps MapmyRun and Livestrong, which tracks nutrition in a daily pie chart showing fat, protein and carbs. Saucony Run4Good is a favorite, too, said Scribner, 21, because the company donates to anti-obesity programs for kids if enough runners cover enough miles.

MapMyRide, MapMyRun, Livestrong, Run4Good, MyFitnessPal – they're all part of an exploding arena of health and fitness applications for smartphones. The trend, which falls under the umbrella of Health 2.0, an international tech movement grounded in San Francisco, is proving an obsession for programmers at code-a-thons, as well as users who get hooked on tracking their workouts, calorie intake and weight loss.

Among users, a pinch of competition - a social network of friends who sign up to share fitness scores - is all you need to make this an activity as additive as Twitter is for some and Facebook is for others.

The Pew Research Center, in a new report titled Mobile Health 2012, found smartphone owners in the vanguard, with 52 percent gathering health information on their palm-sized, micro-computers. That compares to 6 percent of owners of regular cellphones, the report said.

In addition, Pew found, 19 percent of smartphone owners have at least one health app on their devices - with exercise, diet, and calorie-counting programs the most popular.

Overall, the proportion of cellphone owners who use their phones to access health data nearly doubled from 17 percent two years ago to 31 percent today, according to the report.

Ale Lauth is a senior health educator for Kaiser Permanente in the North Sacramento Valley region. She has witnessed the trend first-hand in her role as wellness guru for hundreds of Kaiser employees and physicians.

"We've definitely seen their usage increase," Lauth said. "The apps have come a long way, and they're constantly upgrading."

They are also proliferating. Click on Apple's health and fitness apps page and you'll find iRunner, Fitocracy, Fitter Fitness, Fitness Buddy, Fitbit, Fitness Pro, miCoach, Abs Workout, RunKeeper, Virtual Trainer - and about 250 more.

And it's not just fitness. There's a parallel world of apps geared to other aspects of health and wellness: iTriage, iFirstAidLite, InstantHeartRate, CuresA-Z, not to mention a host of downloadable apps such as OvulationCalendar that help women track their menstrual and fertility cycles. And, yes, there are apps with tips for carrying on when that fertility cycle is spot on.

The medical community is embracing the trend, holding contests to encourage programmers to design disease-specific apps that doctors can "prescribe" to patients with heart disease, diabetes and other chronic conditions.

The American Medical Association has launched its own consumer weight app, and the U.S. Department of Health and Human Services Office of the National Coordinator of Health Information Technology held a contest in July for the best app to help consumers identify and reduce their risk of heart disease.

The next phase is already in the works: apps that will transform your smartphone into a regulated medical device. Think phones as electrocardiography, or ECG, machines that can detect abnormal heart rhythms and determine if a patient is having a heart attack.

Such clinical apps will not go forward without approval from the federal Food and Drug Administration. Already, U.S. Rep. Mike Honda, D-San Jose, is working on a bill to establish a new FDA Office of Mobile Health designed to regulate health apps.

In the meantime, the private sector is leading the charge at Health 2.0-inspired code-a-thons, live events where developers gather to build apps and tools for improved health care. A topic getting prime billing at the International Consumer Electronics Show in Las Vegas this January: "The Human Body: The Next Digital Revolution."

For now, most physicians are happy to see patients using simple apps to motivate them to exercise, eat well and lose weight.

MyFitnessPal has emerged as one of the more popular apps in this category, allowing users to set weight loss goals then diligently chart calories consumed, calories burned and poundage. Lauth, of Kaiser Permanente, said dozens of her charges use MyFitnessPal, getting into the swing of competition when they add friends to their wellness social network who can track each other's progress - or lack thereof.

"These are great motivators," said Lauth. "When you hit your goals, you and your friends see the results."

Others in this category flash smiley-faces or other positive on-screen icons as rewards. They also offer pre-programmed verbal pats-on-the-back.

Says Lauth, "It's like they are saying, 'You are fantabulous!'"

Scribner, who helps Fleet Feet customers gear up for their runs, says she likes the social network aspect of workout apps.

"You can compete with your friends over your course, and it shows your elevation," she said. "Simply hit go."