Monday, May 9, 2011

Association between adolescent emotional problems and metabolic syndrome: The modifying effect of C-reactive protein gene (CRP) polymorphisms

Abstract
Depression is associated with the development of the metabolic syndrome, and both depression and metabolic syndrome are associated with markers of systemic inflammation, such as C-reactive protein (CRP). We examined associations between affective status in adolescence and adulthood, and the metabolic syndrome at age 53 years in a large representative British birth cohort. We also investigated whether two CRP gene polymorphisms (rs1205 and rs3093068) were associated with affective status and the metabolic syndrome, and whether the association between affective status and the metabolic syndrome was modified by these CRP polymorphisms. Women, but not men, with emotional problems in adolescence were more likely to have the metabolic syndrome (OR = 1.53, 95% CI: 1.04, 2.26), although this sex difference was not statistically significant (p = 0.22). The CRP SNPs were not associated with affective status or the metabolic syndrome, but the association of adolescent emotional problems with the metabolic syndrome was stronger in those who were homozygous for the major allele (C) of rs1205 (OR = 1.83, 95% CI: 1.17, 2.86) than in carriers of the T allele (OR = 1.01, 95% CI: 0.66, 1.55) (p = 0.05 for gene by affective status interaction). This interaction was stronger when considering adolescent emotional problems as a continuous variable (p = 0.003). Adolescent emotional problems play an important role in the development of the metabolic syndrome later in life, particularly in those homozygous for the major allele of CRP rs1205. These findings may highlight new ways of identifying people with emotional problems at high risk of developing the metabolic syndrome, which is of great importance for the management of the physical health of these patients.
Abstract
Depression is associated with the development of the metabolic syndrome, and both depression and metabolic syndrome are associated with markers of systemic inflammation, such as C-reactive protein (CRP). We examined associations between affective status in adolescence and adulthood, and the metabolic syndrome at age 53 years in a large representative British birth cohort. We also investigated whether two CRP gene polymorphisms (rs1205 and rs3093068) were associated with affective status and the metabolic syndrome, and whether the association between affective status and the metabolic syndrome was modified by these CRP polymorphisms. Women, but not men, with emotional problems in adolescence were more likely to have the metabolic syndrome (OR = 1.53, 95% CI: 1.04, 2.26), although this sex difference was not statistically significant (p = 0.22). The CRP SNPs were not associated with affective status or the metabolic syndrome, but the association of adolescent emotional problems with the metabolic syndrome was stronger in those who were homozygous for the major allele (C) of rs1205 (OR = 1.83, 95% CI: 1.17, 2.86) than in carriers of the T allele (OR = 1.01, 95% CI: 0.66, 1.55) (p = 0.05 for gene by affective status interaction). This interaction was stronger when considering adolescent emotional problems as a continuous variable (p = 0.003).

Adolescent emotional problems play an important role in the development of the metabolic syndrome later in life, particularly in those homozygous for the major allele of CRP rs1205. These findings may highlight new ways of identifying people with emotional problems at high risk of developing the metabolic syndrome, which is of great importance for the management of the physical health of these patients.

Brain, Behavior, and Immunity
Volume 25, Issue 4, May 2011, Pages 750-758

Monday, November 15, 2010

Eat dark chocolate ‘to control hypertension’

Suffering from hypertension? Fret not, for a new study has found that dark chocolate could control one’s high blood pressure levels and thus keep one's heart in good shape.

Dark chocolate is already known to contain high levels of antioxidants which are thought to be beneficial to health.

Now, a team from Sweden has revealed that dark chocolate works on the body in the same way as blood pressure pills -- in fact, researchers have discovered that it inhibits an enzyme that raises blood pressure.

Lead researcher Ingrid Persson said that the dark chocolate, which contains large amounts of cocoa, has high levels of compounds called catechins and procyanidines, both of which have been shown to affect blood pressure.

She added that with other factors such as a balanced diet and not smoking, dark chocolate could be a good way to lower risk of heart disease and stroke. But, milk chocolate contains too much sugar and not enough cocoa to offer the same health effects, the ‘Daily Express’ reported.

In their study, 10 men and six women had blood samples taken before and after eating 75 grams of dark chocolate - a large piece. Within three hours, the team saw a blood pressure enzyme known as ACE had been inhibited by up to 18 per cent.

This is as effective as ACE inhibitor drugs currently given to the millions of patients with high blood pressure.

Dr. Perrson was quoted by the British newspaper as saying, “We have previously shown that green tea inhibits the enzyme ACE, which is involved in the body’s fluid balance and blood pressure regulation.”

Other studies have shown that dark chocolate may also reduce stress levels and boost mood.

Wednesday, September 15, 2010

Differently regulated proteins in sera of breast cancer patients and healthy donors

Abstract

e21022

Background: Breast cancer is the most common cancer type in women worldwide. Its early detection is a crucial step for the successful treatment. Although many serum biomarkers were described for breast cancer, all of them still lack of clinical specificity and sensitivity for the early detection. Therefore, we developed and evaluated a proteomics-approach for detection of biomarkers in serum of breast cancer patients and tried to identify differently regulated proteins.

Methods: Blood samples of 50 women with breast cancer (CA) and 50 age-matched healthy women (CTRL) were drawn prior to surgery and respective sera were obtained. We used surface-enhanced laser desorption/ionisation time-of-flight mass spectrometry (SELDI-TOF-MS) for protein profiling with three active surfaces of the protein chips with different binding properties. Data was analyzed by multivariate statistical techniques and artificial neural networks.

Results: We obtained a protein profile with 15 differently regulated proteins. Ten of them were upregulated in sera of breast cancer patients. The diagnostic pattern could discriminate CA from CRTL with specificity of 77% and sensitivity of 85%, the area under curve (AUC) of 0.85 was achieved. Two of upregulated proteins in breast cancer sera are Inter-a (globulin) inhibitor H4 (ITIH4) and Apolipoprotein C-I (ApoC-1).

Conclusions: SELDI-TOF-MS is a promising, non-invasive tool for detection of breast cancer biomarkers with low sample amounts and high sensitivity and specificity. The next step of this project is the identification of all obtained biomarkers from our protein profiles and a validation serum study in a larger study population. The knowledge of different regulated proteins can help to understand the development of cancer, possibly leading to its early detection.

Journal of Clinical Oncology, 2010 ASCO Annual Meeting Proceedings (Post-Meeting Edition).
Vol 28, No 15_suppl (May 20 Supplement), 2010: e21022


K. Keller, D. Boehm, A. Lebrecht, M. Schmidt, J. Pieter, H. Koelbl and F. Grus
Department of Obstetrics and Gynecology, Johannes Gutenberg University, Mainz, Germany; Department of Experimental Ophthalmology, Johannes Gutenberg University, Mainz, Germany

Lifetime care for patients with autism

Anton R. Miller
University of British Columbia, Division of Developmental Pediatrics, BC Children’s Hospital, Vancouver, BC

The model of care in Nova Scotia proposed by Casey 1 is spot on, but the scope of the project is faulty.

The unrelenting pressure for resources for autism services and research tends to bury at least two important facts. First, many children are challenged by complex neurodevelopmental disorders, and all would benefit from a properly coordinated and accessible system of intervention and support services. It would be unconscionable if discrepancies existed among children with different kinds of cancer — full support for those with bone cancer but meagre support for those with kidney cancer.

Second, it is true that autism and related disorders are diagnosed in more and more children, but the spectrum is broad. The needs of some children and families are complex, but others have fewer needs. Allocation of resources based on a medical diagnosis ignores this crucial fact.

Many professionals involved in the support of children with neurodevelopmental disorders are advocating for child and family support based on need rather than diagnosis. What we really need are regional total care centres for children with complex neurodevelopmental disorders — all those with complex learning and behavioural problems that elude a simple diagnosis.

Thursday, January 28, 2010

Oral health and risk for head and neck squamous cell carcinoma: the Carolina Head and Neck Cancer Study.

OBJECTIVE: Recent reports have linked oral health and periodontal disease indicators with increased risk of squamous cell carcinoma of head and neck (SCCHN). Thus far, evidence has been inconclusive; our objective was to study the association between oral health and SCCHN risk in the context of a large population-based study.

METHODS: A population-based case-control study of incident SCCHN, the Carolina Head and Neck Cancer Study was carried out in 2002-2006 in 46 counties in North Carolina. Controls (n = 1,361) were frequency matched with cases (n = 1,289) on age, race, and gender. Oral health was assessed using interview data on tooth loss and mobility, mouthwash use, and frequency of dental visits.

RESULTS: Subjects were 26-80 years old (median age = 61). The distribution of tooth loss among controls was 0-5 teeth = 60%; 5-14 = 15%; and 16-28 = 25%. After controlling for covariates, tooth loss did not yield any notable association with SCCHN (16-28 vs. 0-5 lost teeth: OR: 1.21, 95% CI: 0.94, 1.56). Self-reported history of tooth mobility was moderately associated with increased SCCHN risk (OR: 1.33, 95% CI: 1.07, 1.65); however, the association did not persist among never smokers. Routine dental visits were associated with 30% risk reduction (OR: 0.68, 95% CI: 0.53, 0.87).

CONCLUSIONS: These data provide support for a possible modest association of periodontal disease, as measured by self-reported tooth loss indicators, but not tooth loss per se, with SCCHN risk.

Divaris K, Olshan AF, Smith J, Bell ME, Weissler MC, Funkhouser WK, Bradshaw PT.

Tuesday, November 24, 2009

Nicotine induces DNA damage in human salivary glands

Abstract
The tobacco alkaloid nicotine is responsible for addiction to tobacco and supposed to contribute to tobacco carcinogensis, too. Recently, genotoxic effects of nicotine have been reported in human cells from blood and upper aerodigestive tract. Because of nicotine accumulation in saliva, the study of possible in vitro genotoxic effects of nicotine have been extended to human salivary gland cells. Specimens of parotid glands of 10 tumor patients were obtained from tumor-free tissue. Single cells were prepared by enzymatic digestion immediately after surgery and exposed for 1 h to 0.125–4.0 mM of nicotine. Possible genotoxic effects were determined by the Comet assay using the % DNA in tail (DT) as a reliable indicator of DNA damage. Nicotine induced a significant dose-dependent increase of DNA migration in parotid gland single-cells. The mean DT was 1.12-fold (0.125 mM) to 2.24-fold (4.0 mM) higher compared to control. The lowest concentration eliciting significant DNA damage within 1 h, 0.25 mM nicotine, is only 10-fold higher than maximal concentrations of nicotine reported in saliva after unrestricted smoking. Although conclusive evidence for a carcinogenic potential of nicotine is still lacking, the safety of long-term nicotine replacement therapy should be carefully monitored.

Toxicology Letters
Volume 184, Issue 1, 10 January 2009, Pages 1-4

Wednesday, November 18, 2009

Is running marathons damaging your health?

There is speculation from the scientific literature that marathon runners may be more susceptible to chronic inflammation and caradic events such as artrial fibrillation (abnormal heart rhythms). The research indicates that there is an association to artrial fibrillation and endurance running.

Furthermore, research demonstrates an interesting correlation between inflammation and artrial fibrillation in chronic endurance training and racing. The researchers believe that high levels of C-reactive protein(s) could be a risk factor for developing artrial fibrillation. C-reactive protein are produced in the liver or present in the blood in an inactive form that are turned on during times of inflammation such as running a marathon.

In addition, research published in the American Society for Clinical Research investigated elevations of an enzyme called myeloperoxidase (MPO) in runners that completed the Boston Marathon in 2005. The researchers looked at myeloperoxidase as a means to detect inflammation after endurance racing, which was statistically elevated after the race in 22 of the 24 runners. Interestingly enough, myeloperoxidase has been associated with coronary artery disease and atherosclerosis.

Systemic inflammation in respect to marathon running may contribute to a compromised cardiovascular system that may lead to chronic injuries and oxidative stress.

Seattle Budget Fitness Examiner Dave Guevara