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duminică, 5 august 2012

ADHD Linked With Slower Brain Development

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Editor's Choice
Main Category: ADHD
Also Included In: Neurology / Neuroscience;  Pediatrics / Children's Health
Article Date: 03 Aug 2012 - 8:00 PDT Current ratings for:
ADHD Linked With Slower Brain Development
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According to a study conducted by the National Institutes of Health, children with attention-deficit/hyperactivity disorder (ADHD) experience a developmental delay in frontal regions of the brain.

The study is published in Biological Psychiatry.

The team examined 234 children with ADHD and 231 normally developing children. Each child's brain was scanned up to four times from age 10 to 17. The team then used advanced neuroimaging technology in order to map the trajectories of surface area development at over 80,000 points across the brain.

The surface area of the cerebral cortex - the folded gray tissue that makes up the outermost part of the brain - grows during childhood. However, the researchers discovered that this process was delayed in frontal brain regions in children with ADHD.

According to the researchers, the normally developing children attained 50% peak area in the right prefrontal cortex at a mean of 12.7 years compared with 14.6 years for children with ADHD.

Dr. Phillip Shaw, a clinician studying ADHD at the National Institute of Mental Health explained: "As other components of cortical development are also delayed, this suggests there is a global delay in ADHD in brain regions important for the control of action and attention."

Dr. John Krystal, Editor of Biological Psychiatry, said: "These data highlight the importance of longitudinal approaches to brain structure. Seeing a lag in brain development, we now need to try to understand the causes of this developmental delay in ADHD."

Dr. Shaw explained that the study finding "guides us to search for genes that control the timing of brain development in the disorder, opening up new targets for treatment."

Further research expanding these measures into adulthood will also be vital. Such data would help determine whether or when a degree of normalization occurs, or if these delays translate into long-lasting cortical deficits.

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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posted by Alexander Nestoiter on 3 Aug 2012 at 7:30 pm

Review this statement from the article very carefully: "According to the researchers, the normally developing children attained 50% peak area in the right prefrontal cortex at a mean of 12.7 years compared with 14.6 years for children with ADHD."
This means that children attain 50% peak in the average of 12.7 years. Children with ADHD attain this point in the average of 14.6 years. The study was conducted on kids from 10 to 17 years of age. As you can see something is off with their figures.
What is even more bothersome, is that while they studied kids 10-17 years of age, they now pass the results of the study to all kids, including those who are only 4 years old.
Not in this article, but in others, they urge parents to monitor their kids for any signs of the broad ADD/ADHD spectrum of symptoms, get the kids diagnosed, and, of course, seek treatment = pills.

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'ADHD Linked With Slower Brain Development'

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joi, 15 decembrie 2011

Ability Of Brown Fat To Burn Calories Linked To Immune Cells

Main Category: Obesity / Weight Loss / Fitness
Article Date: 15 Dec 2011 - 0:00 PST

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Throughout the interior spaces of humans and other warm-blooded creatures is a special type of tissue known as brown fat, which may hold the secret to diets and weight-loss programs of the future.

Unlike ordinary "white" fat, in which the body stores excess calories, brown fat can burn calories to heat up the body. It's one of the things that helps keep wild critters warm on cold nights.

Investigating how brown fat works in mice, a team of researchers at the University of California, San Francisco (UCSF) has uncovered what may be a holdover from our evolutionary past: in response to cold, tiny immune cells known as macrophages can switch on the brown fat, inducing it to burn energy to make heat.

Prior to this research, published last month in the journal Nature, scientists had assumed that brown fat metabolism was completely controlled by the brain. But the UCSF research suggests that the immune system plays a backup role in this process - a legacy, perhaps, of some ancient ancestral creature whose metabolic and immune systems were much more intertwined.

"This is a very important secondary system that the body uses to provide a backup for the thermal stress response," said Ajay Chawla, MD, PhD, an associate professor at UCSF's Cardiovascular Research Institute who led the research. "It raises the possibility that we can perhaps modulate this program and enhance it in humans to rev up metabolism."

Immune Cells Found Inside Brow

The modern human immune system relies on these macrophages to gobble up bacteria, helping protect us against infection. Macrophages were never known to play a role in metabolism, but the evidence Chawla and his colleagues gathered suggests otherwise.

Using brown fat to burn calories and produce heat is one of the ways that mammals maintain thermoregulation - an essential adaptation that defines warm blooded creature and enables them to thrive in the face of challenging environmental extremes. Not all animals share this ability.

Many animals, like lizards, are "cold blooded" or exothermic. They maintain their body temperature through completely external means, sunbathing at certain times of the day and huddling in warm, protective places at night. This naturally limits their range and explains why lizards, so abundant in tropical climates, are far rarer in cold climates.

Mammals, on the other hand, are "warm-blooded" or endothermic. They produce heat internally by a variety of means: shivering, sweating, regulating the size of their blood vessels and burning off excess calories in brown fat.

Scientists have known for years that brown fat burns calories in response to signals from the brain. These signals cause break down of molecules known as triglycerides in white fat, which are then released into the bloodstream as fatty acids. These circulating fatty acids are taken up by brown fat and burned to generate heat. Brown fat is full of blood vessels, and the heat warms the blood, which in turn circulates and warms the body.

The brain controls this process by monitoring the body's temperature and, in face of extreme cold, releasing a hormone called norepinephrine, which kick-starts the brown fat.

The work of the UCSF team showed that macrophage cells within the brown fat can also do this directly. Macrophages residing in brown and white fat produce an enzyme that makes norepinephrine when mice are exposed to the cold. This leads to the production, the breakdown and mobilization of stored fat, which is then burned in brown fat to produce heat.

What these results suggest, Chawla said, is that immune cells help facilitate the function of brown fat.

Mammals today have evolved to have separate systems for immunity and metabolism. But flies, for instance, have combined the equivalent functions of the human liver, fat and immune system into one organ: a tissue referred to as its fat body. Mammalian macrophages may have some functions related to this shared origin.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our obesity / weight loss / fitness section for the latest news on this subject. The article, “Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis” by Khoa D. Nguyen, Yifu Qiu, Xiaojin Cui, Y. P. Sharon Goh, Julia Mwangi, Tovo David, Lata Mukundan, Frank Brombacher, Richard M. Locksley and Ajay Chawla appeared in the Nov. 20 issue of Nature.
In addition to UCSF, the authors of this study are affiliated with Stanford University and the University of Cape Town, South Africa.
This work was funded by grants from the National Institutes of Health and the Larry L. Hillblom Foundation; by an National Institutes of Health Director’s Pioneer Award; and by Stanford Graduate and
A-STAR Fellowships.
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marți, 13 decembrie 2011

Parkinsons' - Brain Volume Decrease And Cognitive Decline Linked

Editor's Choice
Academic Journal
Main Category: Parkinson's Disease
Also Included In: Neurology / Neuroscience
Article Date: 13 Dec 2011 - 9:00 PST

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According to a study published in the December issue of Archives of Neurology, one of the JAMA/Archives journals, individuals who suffer with Parkinson disease-related dementia seem to have increased brain atrophy in the parietal, hippocampal, temporal lobes, as well as decreased prefrontal cortex volume than individuals with Parkinson disease without dementia.

The researchers explain:

"Patients with Parkinson disease (PD) are at an increased risk of developing dementia (PDD), with cumulative prevalence rates of up to 80 percent.

Approximately 25 percent of non-demented PD patients meet neuropsychological criteria for mild cognitive impairment (PD-MCI), which converts to PDD in many cases, and even mild cognitive deficits in PD are associated with functional impairments and worse quality of life."

Daniel Weintraub, M.D., of the Perelman School of Medicine, University of Pennsylvania, Philadelphia, and colleagues, set out to evaluate the areas and patterns of brain atrophy in individuals with Parkinson disease with normal cognition (PD-NC), individuals with Parkinson disease with dementia-level cognitive deficits (PDD), as well as individuals with PD with mild cognitive impairment (PD-MCI).

The researchers enrolled 84 individual with Parkinson disease (61 PD-NC, 11 PDD, and 12 PD-MCI) and 23 healthy control individuals to participate in the study. All participants in the study underwent magnetic resonance imaging (MRI) of the brain. The team gathered data as part of the University of Pennsylvania Center of Excellence for Research on Neurodegenerative Diseases.

After the researchers adjusted for other factors, such as education level, sex, and age of the participant, they discovered no between-group differences in regional brain volumes for PD-NC participants compared with control group patients. The team found that among participants with Parkinson disease, there were cognitive group-level differences in medial temporal lobe and hippocampal volumes.

The hippocampal volumes among PD-MCI and PDD participants were smaller than PD-NC participants, although the team found no differences between participants in the PDD and PD-MCI groups. In addition, participants in the PDD group had medial temporal lobe atrophy compared with participants in the PD-NC group, but not those in the PD-MCI group. The researchers observed no between-group differences for other regions in the brain.

Patients in the PD-MCI group had a different pattern of brain atrophy than participants in the PD-NC group, although similar to that of PDD participants. The researchers characterized this pattern by atrophy in prefrontal cortex gray and white matter, hippocampal volume, parietal lobe white matter, and occipital lobe gray and white matter.

In Parkinson's disease patients without dementia, the team discovered an association between memory-encoding performance and hippocampal volume, "suggesting heterogeneity in the neural substrate of memory impairment."

The researchers conclude:

"With growing recognition of Parkinson disease with mild cognitive impairment as common and clinically significant, it will be important to develop consensus diagnostic criteria, validate assessment instruments for use in clinical care and research, and test treatments for their symptomatic and disease-modifying effects. Use of a pattern classification approach may allow identification of diffuse regions of cortical gray and white matter atrophy early in the course of cognitive decline."

Written by Grace Rattue
Copyright: Medical News Today
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Visit our parkinson's disease section for the latest news on this subject. Arch Neurol. 2011;[12]:1562-1568. Please use one of the following formats to cite this article in your essay, paper or report:

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luni, 12 decembrie 2011

Prostate Cancer - Cardiovascular Risks Linked To Androgen Suppression Therapy Ignored

Editor's Choice
Main Category: Prostate / Prostate Cancer
Also Included In: Cardiovascular / Cardiology;  Urology / Nephrology
Article Date: 12 Dec 2011 - 9:00 PST

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According to specialists' warnings published in Heart, it has been established that androgen suppression therapy (AST) drugs, that suppress testosterone production for the treatment of prostate cancer, can lead to complications in form of stroke and heart disease, yet standard management of the disease ignores this risk.

According to the authors, AST is the primary treatment for advanced prostate cancer and is evidently very efficient, however, mounting evidence indicates that these drugs also substantially raise the risk of heart disease and stroke, and may also be linked to a higher risk of mortality from these causes, the authors add referring to evidence of various published research.

They say that since the introduction of prostate specific antigen (PSA) tests, the number of men who have been started on AST at an earlier stage has risen significantly and will continue to do so. Other side effects of hormone suppression include thinning of the bones, a higher risk of fractures fatigue and less muscle function.

The authors state that even though it remains unclear whether there is a direct causal association between these drugs and cardiovascular disease, there are definitely plausible explanations for the impact these drugs have on increasing the risks for stroke and heart disease. This is a fact that has not been overlooked by various initiatives, such as the American Heart Association, the American Cancer Society, and the American Urological Association, who have issued a joint statement to this effect.

The authors point out that one study estimates that for every 1,000 men who underwent AST therapy for five years the result will be an additional 360 extra cases of diabetes, 315 cases of heart disease, 42 more strokes and 28 additional heart attacks, which equates to £700 million to £2 billion ($1.1 billion to $3 billion) in NHS (National Health Service, UK) costs between 2004 and 2009 alone.

They argue:

"The concept of incorporating cardiovascular disease management into AST as standard has not yet percolated into clinical practice."

They add that due to the fact that cancer and heart disease are managed separately, there is hardly any coordination between doctors. Current guidelines on prostate cancer have not accounted for management of cardiovascular disease and neither do they clarify who should be taking the lead they write, stating:

"Presently, we are unaware of any current local or national management plans that attempt to address the increased risk of cardiovascular disease associated with androgen suppressant therapy or recognize these men in screening procedures."

They concluded:

"The current status quo of no action is, in our view, unsatisfactory for the patient and unlikely to be cost effective," and continue suggesting that the solution of the problem may be cancer nurse specialists, who are highly efficient and relatively cost-effective.

Written by: Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our prostate / prostate cancer section for the latest news on this subject. Cardiovascular risk in androgen suppression: underappreciated, under-researched, and unresolved Online First 2011; doi 10.1136/heartjnl-2011-300893 Please use one of the following formats to cite this article in your essay, paper or report:

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In Newly Diagnosed Inflammatory Breast Cancer, Circulating Tumor Cells Not Linked To Survival

Main Category: Breast Cancer
Also Included In: Medical Devices / Diagnostics
Article Date: 12 Dec 2011 - 1:00 PST

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The presence of circulating tumor cells in the blood appears to have no relationship to survival in women who have just been diagnosed with inflammatory breast cancer, according to new research from Fox Chase Cancer Center. However, the research shows that these stray tumor cells may signal that the disease has spread to other parts of the body, even before imaging reveals any metastases. The results were presented at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium.

If a woman is diagnosed with inflammatory breast cancer, a particularly fast-growing form of the disease, doctors should consider close imaging to monitor and possibly continue aggressive treatment if she also has circulating tumor cells (CTCs), regardless of what imaging shows, recommends study author Massimo Cristofanilli, M.D., F.A.C.P., chair of the department of medical oncology at Fox Chase. "You should be carful before stopping treatment in someone who has evidence of circulating cells, particularly when dealing with a disease like inflammatory breast cancer, which can progress rapidly."

Previous research by Cristofanilli and his colleagues found that the number of stray cancer cells circulating in the blood is the best predictor of both how long a woman with metastatic breast cancer will live and the amount of time until her cancer progresses. But the researchers have also found that the presence or lack of CTCs has little to say about prognosis in women with metastatic inflammatory breast cancer, an aggressive disease with extremely poor outcomes in spite of multidisciplinary modality treatment.

During the current study, Cristofanilli and his team reviewed the records of 84 women who had just learned they have inflammatory breast cancer, either in stage III or stage IV. A total of 64 (76.2%) women had at least 1 CTC and 29 (34.5%) had at least 5. The researchers found that women with no CTCs had comparable survival and spent the same amount of time progression-free as women with one or more CTCs. The results suggest that there is little prognostic value in measuring CTCs in women newly diagnosed with inflammatory breast cancer.

It's not clear why CTCs appear to be linked to prognosis in some forms of cancer but not others, says Cristofanilli. Inflammatory breast cancer is already an aggressive disease, he says, so compared to other forms of breast cancer whether or not cells have broken off and entered the blood may say little more about an otherwise already aggressive disease.

Inflammatory breast tumors are typically fast-growing, and travel quickly to lymph nodes and the brain. During follow-up in the current study, which lasted more than 22 months for half of patients, more than 30% of the entire group had died.

Perhaps "the most important finding from the study," says Cristofanilli, is that more than three-quarters of women who just learned they have inflammatory breast cancer had CTCs that can be detected in the blood. In comparison, he adds, only 15% of women with non-inflammatory breast cancer typically have CTCs. "So there is a huge difference in inflammatory breast cancer and other forms of breast cancer." These stray tumor cells, therefore, may indicate something about inflammatory breast cancer, he reasons, perhaps serving as an early sign that it has already spread. Indeed, only approximately one-third of women with inflammatory breast cancer have detectable metastases at diagnosis, but 60% will eventually develop them.

Currently, says Cristofanilli, doctors primarily measure CTCs in women with metastatic disease, since a decrease in CTCs can signal that treatment is working. But given that most women with inflammatory breast cancer are likely metastatic at the time of diagnosis, this test could serve another purpose - to guide doctors towards more aggressive and prolonged forms of treatment, says Cristofanilli. "If women with inflammatory breast cancer have CTCs, perhaps we should continue to treat them as if they have already established metastatic breast cancer, even if imaging does not show metastases."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. Co-authors include Michal Mego, Antonio Giordano, Ugo De Giorgi, Limin Hsu, Anthony Lucci, Shaheenah Dawood, Wendy A. Woodward, Naoto T. Ueno, Vicente Valero, Eleni Andreopoulou, Gabriel N. Hortobagyi, and James M. Reuben.
Fox Chase Cancer Center Please use one of the following formats to cite this article in your essay, paper or report:

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duminică, 11 decembrie 2011

Unpleasant Smell Linked To Gonorrhea In Men

Editor's Choice
Academic Journal
Main Category: Sexual Health / STDs
Also Included In: Men's health
Article Date: 09 Dec 2011 - 18:00 PST

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A much higher percentage of men with an unpleasant smell were found to have gonorrhea compared to other men, researchers from the Institute of Cytology and Genetics in Novosibirsk, Russia revealed in the Journal of Sexual Medicine. The authors explained that adult males with gonorrhea had a putrid smell, as far as many adult females were concerned.

As background information, the authors explained that animal research had demonstrated that rats and mice pick up on chemical signals to avoid sexual contact with infected potential mates. However, studies into body odor in humans have so far been limited to medical diagnostics. No studies had ever looked into smell modifications in humans, due to infection, and what impact that might have in choosing a sexual partner.

As STDs or STIs (sexually transmitted infections) have no clear visible external signs, the researchers wondered whether odor might be a sign that has been overlooked.

Mikhail Moshkin and team set out to determine whether odor unpleasantness in young adult males might be linked to infection with Neisseria gonorrhoeae (gonorrhea).

The researchers collected saliva and armpit samples from 16 healthy, 13 gonorrhea infected, and 5 other men who had recovered from gonorrhea after medical treatment. Healthy young female volunteers then assessed the sweat samples for odor (smell). With the saliva samples, the researchers measured for concentrations of testosterone, cortisol, immunoglobulin G (IgG), and immunoglobulin A (IgA). All the male participants were aged from 17 to 25 years and the female ones from 17 to 20.

Their aim was to determine whether the females could distinguish pleasant and unpleasant armpit sweat smells, and whether the differences might be linked to gonorrhea infection, no infection, or recent infection.

They found that: The women described the odor from infected individuals as less pleasant compared to the healthy and recently recovered men. A very high proportion of samples from the infected men were rated as putrid (rotten, rancid).There was a negative correlation between odor pleasantness and concentrations of nonspecific salivary IgA and IgC.In an Abstract in the journal, the authors wrote:

"Perhaps, the immune-dependent reduction of the scent pleasantness in the acute phase of STI is part of an evolutionary mechanism ensuring, unconsciously, avoidance of a risky romantic partner."

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our sexual health / stds section for the latest news on this subject. "Scent Recognition of Infected Status in Humans"
Mikhail Moshkin DrSci, Nadezhda Litvinova DrSci, Ekaterina A. Litvinova PhD, Alena Bedareva PhD, Andrey Lutsyuk MD, and Ludmila Gerlinskaya DrSci
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joi, 8 decembrie 2011

Endurance Exercise Linked To Damage In The Right Ventricle Of The Heart

Main Category: Sports Medicine / Fitness
Also Included In: Cardiovascular / Cardiology
Article Date: 08 Dec 2011 - 1:00 PST

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Researchers have found the first evidence that some athletes who take part in extreme endurance exercise such as marathons, endurance triathlons, alpine cycling or ultra triathlons may incur damage to the right ventricles of their hearts - one of the four chambers in the heart involved in pumping blood around the body.

The research, published online in the European Heart Journal [1], found that although the damage was reversed within a week of a competitive event in most of the 40 athletes studied, five of them (13%) showed evidence of more permanent damage, with magnetic resonance imaging (MRI) showing scarring of the heart muscle (known as fibrosis). These five had been competing in endurance sports for longer than those who did not show the same damage.

Dr André La Gerche (MD, PhD), a postdoctoral research fellow at St Vincent's Hospital, University of Melbourne, Australia, but who is currently based at the University Hospitals Leuven, Belgium, said: "It is most important that our findings are not over-extrapolated to infer that endurance exercise is unhealthy. Our data do not support this premise."

However, he said that the findings did suggest that there might be some athletes who might have been born with a susceptibility to develop damage as a result of long-term endurance exercise.

"Virtually all of the changes in the athletes' hearts had resolved one week after having taken part in a competitive event. In most athletes, a combination of sensible training and adequate recovery should cause an improvement in heart muscle function; that is, the heart rebuilds in a manner such that it is more capable of sustaining a similar exercise stimulus in the future. This positive training response can be over months rather than weeks," he explained. "The question from our research is whether there are some athletes in whom extreme exercise may cause injury from which the heart does not recover completely. If this occurs, affected athletes may be at risk of reduced performance - a cardiac 'over-training' syndrome - or it may cause arrhythmias. If this occurs, it is likely to affect only a minority of athletes, particularly those in whom more intense training fails to result in further improvements in their performance."

Dr La Gerche and his colleagues in Australia and Belgium recruited 40 elite athletes in Australia who were planning to compete in one of the four endurance events [2]. The athletes were already well trained (training intensely for more than 10 hours a week), performing well (having finished within the first 25% of the field in a recent event), and had no known heart problems.

The researchers studied the athletes, using echocardiography, MRI, and blood tests, at three time points: two to three weeks prior to the race, immediately after the race (within one hour), and 6-11 days after the race.

Results showed that immediately after the race the athletes' hearts had changed shape, with the volume increasing, while the function of the ventricle decreased. Levels of a chemical called B-type natriuretic peptide (BNP), which is secreted by the ventricles in response to excessive stretching of heart muscle cells, increased. Right ventricle function recovered in most athletes after one week, but in the five who had been training and competing for longer than the others, MRI detected signs of scarring (fibrosis). The researchers also found that the post-race changes to the function of the right ventricle increased with the duration of the race.

In contrast, the left ventricle, which, up to now has been the most studied in athletes, showed no changes.

Dr La Gerche said: "Our study identifies the right ventricle as being most susceptible to exercise-induced injury and suggest that the right ventricle should be a focus of attention as we try to determine the clinical significance of these results. Large, prospective, multi-centre trials are required to elucidate whether extreme exercise may promote arrhythmias in some athletes. To draw an analogy, some tennis players develop tennis elbow. This does not mean that tennis is bad for you; rather it identifies an area of susceptibility on which to focus treatment and preventative measures."

He concluded: "It is important to note that this is one component of an evolving understanding of how the right ventricle is the 'Achilles heel' of heart function during exercise. We previously studied heart function during intense exercise and demonstrated that the load on the right ventricle (stress, work and oxygen demand) increases to a greater extent than in any of the other heart chambers. Professor Hein Heidbuchel, who I work with, has shown that the source of ventricular arrhythmias in affected athletes is almost always the right ventricle. Finally, it has been shown that intense exercise in rats causes inflammation, fibrosis and arrhythmias in the right but not the left ventricle. Hence, there are consistent messages, all implicating the right ventricle and yet it has been neglected in the vast majority of studies regarding cardiac changes in athletes. Now there is sufficient evidence to invest in the long-term prospective studies that are required."

In an accompanying editorial [3], Professor Sanjay Sharma, of St George's University London (UK), who is medical director of the London Marathon, writes that although the study is small, "the results provide food for thought and the data should be embraced to galvanise more detailed and longitudinal assessment of large groups of endurance athletes. The potential for such projects is enormous considering the colossal increase in participation rates in endurance events such as the marathon. The long-term conclusions of the authors may appear preposterous to some, but could prove to be the retrospective 'elephant in the room'."

In a statement for this press release, Prof Sharma said: "My personal feeling is that extreme endurance exercise probably does cause damage to the heart in some athletes. I don't believe that the human body is designed to exercise at full stretch for as long as 11 hours a day, so damage to the heart is not implausible. It is too early to say that taking part in endurance sports causes long-term damage to the right ventricle, but this study is an indication that it might cause a problem in some endurance athletes with a predisposition and, therefore, it should be studied further."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our sports medicine / fitness section for the latest news on this subject. [1] "Exercise induced right ventricular dysfunction and structural remodelling in endurance athletes". European Heart Journal. doi:10.1093/eurheartj/ehr397
[2] The distances for each event are as follows: marathon = 42.2 kms; endurance triathlon = 1.9km swim, 90 kms cycle, 21.1 kms run; alpine cycling = 207 kms; ultra triathlon = 3.8 kms swim, 180 kms cycle, 42.2 kms run.
[3] "Exercise-induced arrhythmogenic right ventricular cardiomyopathy: fact or fallacy?". European Heart Journal. doi:10.1093/eurheartj/ehr436
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Obesity Linked To Worse Outcomes In Early Breast Cancer Treatment

Main Category: Breast Cancer
Also Included In: Obesity / Weight Loss / Fitness
Article Date: 08 Dec 2011 - 3:00 PST

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Obesity is associated with worse outcomes overall in early-stage breast cancer, researchers reported at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium, held Dec. 6-10, 2011.

Obesity was linked to shorter time to recurrence (TTR), disease-free survival (DFS) and overall survival (OS). The exception was treatment with endocrine therapy (mainly tamoxifen), in which obesity was associated with a protective effect.

"The findings add to the body of evidence indicating that obesity, in general, increases a patient's chance for having a worse prognosis," said lead researcher Sao Jiralerspong, M.D., Ph.D., an assistant professor of medicine at Baylor College of Medicine.

"Obesity is a probable risk factor for worse breast cancer outcomes, and ours is the latest study to suggest it has an effect on treatment outcome as well," Jiralerspong said.

Using data from the Lester and Sue Smith Breast Center at Baylor, Jiralerspong and colleagues examined the link between weight and treatment modality in 4,368 patients treated between 1970 and 1995.

For the group as a whole, data revealed that overweight patients had similar outcomes to normal-weight patients, but obese patients had an increased risk for worse TTR, DFS and OS.

Among patients who received no adjuvant chemotherapy or endocrine therapy, there was a trend for worse survival outcomes in obese patients compared with normal-weight patients.

Obese patients who received chemotherapy fared significantly worse compared with normal-weight patients, "with the magnitude of this effect approaching that of the degree of benefit expected from chemotherapy," Jiralerspong said.

In contrast, overweight patients who received endocrine therapy, predominantly tamoxifen, fared significantly better compared with normal-weight patients.

"Finding that overweight patients have a better outcome than normal-weight patients after tamoxifen treatment is surprising. We are examining the possible reasons for this," Jiralerspong said.

He said that obesity could contribute to worse outcomes because of biological factors associated with excess weight, such as higher blood insulin and estrogen levels, inflammation and growth factors secreted by fat cells. But Jiralerspong also added that more research is needed to understand the effect of body mass on adjuvant treatment because of the unexpected findings and because additional agents are in use today compared with the time period studied.

The study was funded by the Lester and Sue Smith Breast Center at Baylor College of Medicine.

Article adapted by Medical News Today from original press release. Source: American Association for Cancer Research
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