Regular NSAID Use Linked to Erectile Dysfunction

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J Urology. Published online February 21, 2011. Abstract

Regular NSAID Use Linked to Erectile Dysfunction


Laurie Barclay, MD
Authors and Disclosures

Review Updated Criteria March 7, 2011 — Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with erectile dysfunction (ED), according to the results of a prospective cohort study reported online February 21 and in the April print issue of the Journal of Urology.

"This study is a great example of how we work to understand the safety and effectiveness of what we recommend for our patients," said senior author Steven J. Jacobsen, MD, PhD, an epidemiologist and director of research for Kaiser Permanente Southern California in San Diego, in a news release.

"We went into this study thinking we would find the opposite effect: that NSAIDs would have a protective effect because they protect against heart disease, which is also linked to ED. The next step is to dive a bit deeper to understand the underlying physiology of what might be happening with these drugs."

Beginning in 2002, the California Men's Health Study enrolled a large, ethnically diverse cohort of male members of the Kaiser Permanente managed care plans who were 45 to 69 years old. A questionnaire evaluated ED, and automated pharmacy data and self-reported use allowed evaluation of NSAID exposure.

NSAID use was present in 47.4% of the 80,966 participants, and moderate or severe ED was reported in 29.3%. NSAID use and ED correlated strongly with age. Regular NSAID use increased from 34.5% in men aged 45 to 49 years to 54.7% in men aged 60 to 69 years, and ED increased from 13% to 42% in these age groups.

Without adjustment for potentially confounding variables, the odds ratio (OR) for the association of NSAIDs and ED was 2.40 (95% confidence interval [CI], 2.27 - 2.53). A positive association persisted after adjustment for age, race/ethnicity, smoking status, diabetes mellitus, hypertension, hyperlipidemia, peripheral vascular disease, coronary artery disease, and body mass index (adjusted OR, 1.38). A positive association also was evident when a stricter definition of NSAID exposure was used.

"There are many proven benefits of non steroidals in preventing heart disease and for other conditions," Dr. Jacobsen said. "People shouldn't stop taking them based on this observational study. However, if a man is taking this class of drugs and has ED, it's worth a discussion with his doctor."

Limitations of this study include cross-sectional design, potential participation bias, and low original participation rate.

"These data suggest that regular NSAID use is associated with ED even after extensive adjustment for age and potentially confounding factors or comorbidities," the study authors write.

"While this raises the question of the role of inflammation and COX [cyclooxygenase] pathways in ED etiology, we cannot exclude alternative explanations. However, if this is a direct relationship, the current strategy of using NSAIDs for cardiovascular disease protection as well as other common uses of NSAIDs should be weighed against the potential side effects of ED. Studies are needed to elucidate this association in more detail."

The California Cancer Research Program and Kaiser Foundation Community Benefit Program supported this study. Some of the study authors have disclosed various financial and/or other relationships with Takada, GlaxoSmithKline, Kaiser Permanente, and/or Merck.

Children with attention-deficit/hyperactivity disorder and autistic features

From :
Psychiatry Res. 2011 Jan 30;185(1-2):225-31. Epub 2010 May 23.


Children with attention-deficit/hyperactivity disorder and autistic features: EEG evidence for comorbid disorders.

Clarke AR, Barry RJ, Irving AM, McCarthy R, Selikowitz M.

Brain & Behaviour Research Institute and School of Psychology, University of Wollongong, Wollongong 2522, Australia. adam_clarke@uow.edu.au

Abstract
Attention-deficit/hyperactivity disorder (AD/HD) is the most common psychiatric disorder of childhood, although AD/HD is rarely the only diagnosis given to these children. Within the literature there is some debate as to whether it is valid to diagnose AD/HD with autism as a comorbid disorder, since the present diagnostic systems exclude the diagnosis of both disorders in the same child. The aim of this study was to determine whether electroencephalography (EEG) differences exist between two groups of children diagnosed with AD/HD, one scoring high (AD/HD+) and one scoring low (AD/HD-) on a measure of autism. The EEG was recorded during an eyes-closed resting condition from 19 electrodes, and Fourier transformed to provide absolute and relative power estimates in delta, theta, alpha and beta bands. Compared to age- and sex-matched controls, the AD/HD- group had increased absolute power in all frequency bands, somewhat higher relative theta activity and decreased relative delta. In comparison to the AD/HD- group, patients with autistic features (AD/HD+) had a number of qualitative differences in the beta and theta bands. These results indicate the presence of two comorbid conditions in the AD/HD+ group, which suggests that AD/HD and autism can occur in the same individual.

Copyright © 2009 Elsevier Ltd. All rights reserved.

Effects of a restricted elimination diet on the behaviour of children with attention-deficit hyperactivity disorder

Effects of a restricted elimination diet on the behaviour of children with attention-deficit hyperactivity disorder (INCA study): a randomised controlled trial


The Lancet, Volume 377, Issue 9764, Pages 494-503

Lidy M. Pelsser, Klaas. Frankena, Jan. Toorman, Huub F. Savelkoul, Anthony E. Dubois, Rob Rodrigues. Pereira, Ton A. Haagen, Nanda N. Rommelse, Jan K. Buitelaar


Original Text

Dr Lidy M Pelsser MSc a , Klaas Frankena PhD b, Jan Toorman MD c, Prof Huub F Savelkoul PhD b, Prof Anthony E Dubois MD d, Rob Rodrigues Pereira MD e, Ton A Haagen MD f, Nanda N Rommelse PhD g, Prof Jan K Buitelaar MD g

Summary

Background

The effects of a restricted elimination diet in children with attention-deficit hyperactivity disorder (ADHD) have mainly been investigated in selected subgroups of patients. We aimed to investigate whether there is a connection between diet and behaviour in an unselected group of children.

Methods

The Impact of Nutrition on Children with ADHD (INCA) study was a randomised controlled trial that consisted of an open-label phase with masked measurements followed by a double-blind crossover phase. Patients in the Netherlands and Belgium were enrolled via announcements in medical health centres and through media announcements. Randomisation in both phases was individually done by random sampling. In the open-label phase (first phase), children aged 4—8 years who were diagnosed with ADHD were randomly assigned to 5 weeks of a restricted elimination diet (diet group) or to instructions for a healthy diet (control group). Thereafter, the clinical responders (those with an improvement of at least 40% on the ADHD rating scale [ARS]) from the diet group proceeded with a 4-week double-blind crossover food challenge phase (second phase), in which high-IgG or low-IgG foods (classified on the basis of every child's individual IgG blood test results) were added to the diet. During the first phase, only the assessing paediatrician was masked to group allocation. During the second phase (challenge phase), all persons involved were masked to challenge allocation. Primary endpoints were the change in ARS score between baseline and the end of the first phase (masked paediatrician) and between the end of the first phase and the second phase (double-blind), and the abbreviated Conners' scale (ACS) score (unmasked) between the same timepoints. Secondary endpoints included food-specific IgG levels at baseline related to the behaviour of the diet group responders after IgG-based food challenges. The primary analyses were intention to treat for the first phase and per protocol for the second phase. INCA is registered as an International Standard Randomised Controlled Trial, number ISRCTN 76063113.

Findings

Between Nov 4, 2008, and Sept 29, 2009, 100 children were enrolled and randomly assigned to the control group (n=50) or the diet group (n=50). Between baseline and the end of the first phase, the difference between the diet group and the control group in the mean ARS total score was 23·7 (95% CI 18·6—28·8; p<0·0001) according to the masked ratings. The difference between groups in the mean ACS score between the same timepoints was 11·8 (95% CI 9·2—14·5; p<0·0001). The ARS total score increased in clinical responders after the challenge by 20·8 (95% CI 14·3—27·3; p<0·0001) and the ACS score increased by 11·6 (7·7—15·4; p<0·0001). In the challenge phase, after challenges with either high-IgG or low-IgG foods, relapse of ADHD symptoms occurred in 19 of 30 (63%) children, independent of the IgG blood levels. There were no harms or adverse events reported in both phases.

Interpretation

A strictly supervised restricted elimination diet is a valuable instrument to assess whether ADHD is induced by food. The prescription of diets on the basis of IgG blood tests should be discouraged.

Funding

Foundation of Child and Behaviour, Foundation Nuts Ohra, Foundation for Children's Welfare Stamps Netherlands, and the KF Hein Foundation.

A Comprehensive Study of Whole-Brain Functional Connectivity in Children and Young Adults

Current research further confirms the idea of "Functional Connection" within the brain. This is why our functional appraoch to the treatment of Childhood Developmental Disorders such as ADD, ADHD, and ASD is specifically designed to correct for "Functional Dysconnections" between the right and left hemispheres.

If you or someone you know has a child with ADD, ADHD, or ASD, or if you suspect your child has one of these conditions, please call the office (919) 562-5355 or visit my website http://www.drdanechiro.com/ to schedule a consultation. Be looking in the News & Observer North Raleigh Community Paper for a schedule of our Free Workshops.

Abstract (http://cercor.oxfordjournals.org/content/21/2/385.abstract)

Over the past decade, examination of functional connectivity using functional magnetic resonance imaging has become an important tool to investigate functional changes in patient populations, healthy aging, and recently also child development. Most prior developmental studies focused on functional connectivity between brain regions important for cognitive or emotional control and the so-called “default-mode network.” In the present study, we investigated whole-brain functional connectivity in children (11–13 years; N = 19) and young adults (19–25 years; N = 29), without a priori restrictions to specific regions. We found similar patterns of functionally connected regions in children and young adults, but there were differences in the size of functionally connected regions (i.e., the number of voxels), as well as in the strength of functional connectivity (i.e., the correlation value) between brain regions. This indicates that functional connectivity continues to change during adolescence. Developmental differences were found across the whole brain, but the effects differed for functional connectivity patterns associated with higher cognitive or emotional functions and functional connectivity patterns associated with basic visual and sensorimotor functions. Finally, we showed that the majority of functional connectivity differences could not be explained on the basis of gray matter density alone.


Dietsje D. Jolles1,2,3, Mark A. van Buchem1,3, Eveline A. Crone1,2 and Serge A.R.B. Rombouts1,2,3
+ Author Affiliations

1. Leiden Institute for Brain and Cognition, Leiden University, 2300 RC Leiden, the Netherlands

2. Institute of Psychology, Leiden University, 2333 AK Leiden, the Netherlands

3. Department of Radiology, Leiden University Medical Center, 2300 RC Leiden, the Netherlands

Address correspondence to Dietsje Jolles, Department of Radiology, Leiden University Medical Center, Postzone C2-S, PO Box 9600, 2300 RC Leiden, the Netherlands. Email: d.d.jolles@lumc.nl.

The presence of common GI symptoms in non-Celiac patients confirms other mechanisms besides Celiac Disease.

American Journal of Gastroenterology Validates non-Celiac Gluten Sensitivity


The presence of common GI symptoms in non-Celiac patients confirms other mechanisms besides Celiac Disease.

January 18, 2011

Phoenix, Arizona______ The American Journal of Gastroenterology’s January 11, 2011 issue published the report of a highest-standards-in-research study (double-blind, randomized, placebo-controlled rechallenge trial) in patients diagnosed with Irritable Bowel Syndrome who claim considerable improvement in gut symptoms with the institution of a gluten-free diet. The study had a specific goal according to the authors “The aims of this study were to examine the hypotheses that gluten can cause gastrointestinal symptoms in patients without celiac disease and to preliminary screen for potential mechanisms of whether gluten does so by causing intestinal injury and / or inflammation in such subjects.”

The Authors acknowledged “Gluten intolerance in individuals without celiac disease is a controversial issue and has recently been described as the “no man’s land of gluten sensitivity.” In this study, patients with irritable bowel syndrome in whom celiac disease was excluded and who were symptomatically controlled on a gluten-free diet received either gluten or placebo in the form of two bread slices plus one muffin per day with a gluten-free diet for up to 6 weeks. Symptoms were evaluated using a visual analog scale and markers of intestinal inflammation, injury, and immune activation were monitored. The Authors concluded that in some individuals ‘Non-celiac gluten intolerance’ may exist.”

Am J Gastroenterol. 2011 Jan 11

Autistic Mannerisms Reduced By Sensory Treatment

Autistic Mannerisms Reduced By Sensory Treatment

The brain is so very complex! In children with developmental disorders, whether ASD, AD/HD, Dylexia or other learning disabilites, paramount to effective treatment is identifying which hemisphere of the brain is not maturing as fast as the other hemisphere. When one side of the brain is immature as compared wiht the other, sensory issues arise.

Functional neurology seeks to identify the weaknesses associated with a brain that is not maturing normally and then provides the specific stimulation to prompt development. The brain is very plastic, meaning it is changeable. Functional healthcare services for childhood developmental disorders are available at our office!

Visit us on the web at http://www.drdanechiro.com/

From the August 2010 Scientific American Magazine

How Acquired Diseases Become Hereditary Illnesses:

New understanding of epigenetics, or the molecular processes that control genes, show how it underlies hereditary forms of obesity and cancer.
By JR Minkel


One of the primary goals of genetics over the past decade has been to understand human health and disease in terms of differences in DNA from person to person. But even a relatively straightforward trait such as height has resisted attempts to reduce it to a particular combination of genes. In light of this shortcoming, some investigators see room for an increased focus on an alternative explanation for heritable traits: epigenetics, the molecular processes that control a gene’s potential to act. Evidence now suggests that epigenetics can lead to inherited forms of obesity and cancer.

The best-studied form of epigenetic regulation is methylation, the addition of clusters of atoms made of carbon and hydrogen (methyl groups) to DNA. Depending on where they are placed, methyl groups direct the cell to ignore any genes present in a stretch of DNA. During embryonic development, undifferentiated stem cells accumulate methyl groups and other epigenetic marks that funnel them into one of the three germ layers, each of which gives rise to a different set of adult tissues. In 2008 the National Institutes of Health launched the $190-million Roadmap Epigenomics Project with the goal of cataloguing the epigenetic marks in the major human cell types and tissues. The first results could come out later this year and confirm that different laboratories can get the same results from the same cells, says Arthur L. Beaudet of the Baylor College of Medicine, the project’s data hub. “One couldn’t automatically assume it would be so nice,” he says.

Up to this point, the best way to study epigenetic effects has been a strain of mice known as agouti viable yellow. In these mice, a retro¬transposon—a bit of mobile DNA—has inserted itself in a gene that controls fur color. Mice bearing the identical gene can be yellow or brown depending on the number of methyl groups along the retrotransposon. Such methylation marks would normally be erased in the reproductive cells of an animal. But in 1999 a group led by geneticists at the University of Sydney in Australia discovered that methylation of the fur color genes persists in the female germ line, allowing it to be passed down to offspring like a change in the DNA.

Agouti viable yellow mice might have something to say about the human obesity epidemic. The animals have a tendency to overeat and become obese. In 2008 Robert A. Waterland, also at Baylor, discovered that this trait gets passed down and amplified from one generation of agouti to the next, so that “fatter mothers have fatter offspring,” he says. He is investigating whether the effect can be explained in terms of methylation patterns in the hypothalamus, the part of the brain that regulates appetite.

Retrotransposons could lead to other epigenetic effects. In the early 2000s geneticist David Martin of Children’s Hospital Oakland Research Institute in California reasoned that the silencing mechanism that keeps retrotransposons inactive might randomly shut down genes that are supposed to be left on. If the silencing occurred in a gene responsible for suppressing tumor formation, the result would appear the same as genetic mutations that predispose people to cancer.

Working with colleagues at St. Vincent’s Hospital in Sydney, Martin identified two individuals who had the characteristics of hereditary nonpolyposis colorectal cancer, which is usually caused by a mutation that inactivates one of a person’s two copies of the tumor suppressor gene MLH1, but who showed no signs of mutation. Instead the MLH1 of both was methylated in cells of the blood, hair follicles and inner cheek—all derived from different embryonic layers.

In Martin’s view, the result strongly suggested that the patients had inherited the silenced gene from one of their parents, like the case with agouti mice. Although some researchers have suggested that a genetic mutation in the fertilized egg cell could be responsible for the methylation pattern, Martin says the simplest explanation is an inherited epimutation. “Nobody has been able to explain why these things aren’t actually germ-line epimutations,” he says.

If epimutations can happen, the same effect should turn up in other genes. Martin’s colleague Catherine Suter of the Victor Chang Cardiac Research Institute in Sydney is studying whether melanoma patients have epimutations in genes associated with the cancer. It is also conceivable that epimutations could play a role in some cases of autism, Beaudet says.
Researchers agree they are just scratching the surface of understanding the role of epigenetics in health and disease. The NIH Roadmap Project should help by allowing them to compare models of disease with reference samples. In effect, “we’re trying to figure out how we work,” says epigenetics researcher Randy Jirtle of Duke University. “It’s an amazingly huge project, and it’ll never go away.”