tumblr: bellapaige88On average, 9.5/1000 population has epilepsy in Low and Middle Income Countries (LAMIC). A research which has resulted in the global campaign against epilepsy has shown, the gap between treatment need and the treatment provision worldwide is approximately 70% . This large ‘treatment gap’, i.e., lack of appropriate treatment for a large number of patients with epilepsy, due to a number of causes including inability to identify cases, inability to deliver adequate treatment, people’s attitudes and perception, availability of anti-epileptic drugs and finally, health policies of individual countries and the priority given to epilepsy. The first step towards narrowing the treatment gap is improving diagnosis. Clinical investigations that help in the diagnosis of epilepsy include electroencephalography (EEG), neuro-imaging techniques such as computed axial tomograpy (CT) and magentic resonance imaging (MRI). Simple blood tests, including haematological, liver and kidney function profiles can reveal treatable causes of epilepsy, such as parasitic infections. Neuropsychological evaluation identifies areas of function and dysfunction. Long term video monitoring can greatly improve the diagnosis of epilepsy. Therapeutic drug monitoring can ensure that patients are receiving optimal doses of medication and can help greatly in avoiding toxicity. However, the availability of investigative procedures varies greatly, from 82.4% for EEG, 70.5% for CT, 45% for therapeutic drug monitoring to only 20.6 % for MRI, 21.7% for long-term video monitoring and in LAMICs. Special investigations of brain function such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) are not available in most LAMIC centres.Epilepsy services in low and middle income countries are almost non-existent and service organization is a challenge. Epilepsy services should be community based and it is important to integrate these services into the primary health care structure to ensure sustainability. The Indian model is one such example, where epilepsy care has been incorporated into programmes for poverty alleviation . Public-private partnerships and non-governmental organizations (NGO) are also important components of the Indian model. The ultimate goal of all workers in the epilepsy field is to improve the quality of the life of people with epilepsy and their families. The prime manner in which this is aimed for is by the provision of good medical care.Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM, & Sander JW (2003). The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60 (9), 1544-5 PMID: 12743252Mbuba CK, Ngugi AK, Newton CR, & Carter JA (2008). The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49 (9), 1491-503 PMID: 18557778 Pal, D., Das, T., & Sengupta, S. (2000). ... Read more »
Mbuba CK, Ngugi AK, Newton CR, & Carter JA. (2008) The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49(9), 1491-503. PMID: 18557778
Pal, D., Das, T., & Sengupta, S. (2000) Case-control and qualitative study of attrition in a community epilepsy programme in rural India. Seizure, 9(2), 119-123. DOI: 10.1053/seiz.1999.0357
Mani KS, Rangan G, Srinivas HV, Srindharan VS, & Subbakrishna DK. (2001) Epilepsy control with phenobarbital or phenytoin in rural south India: the Yelandur study. Lancet, 357(9265), 1316-20. PMID: 11343735
Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM.... (2003) The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60(9), 1544-5. PMID: 12743252
Staying hydrated is good advice for men who’ve had kidney stones before, but sugar-sweetened sodas and fruit punch may not be the best choice of fluids.... Read more »
Ferraro, P., Taylor, E., Gambaro, G., & Curhan, G. (2013) Soda and Other Beverages and the Risk of Kidney Stones. Clinical Journal of the American Society of Nephrology. DOI: 10.2215/CJN.11661112
Researchers have found that the cancer patients in America are more than two times more likely to go bankrupt than the healthy people. I think this is the case not only in America but everywhere in the world.
Researchers collected data in Washington State from about 400,000 adults and found that the patients of cancer have more chances of bankruptcy, i.e. 2.65 times more chances, even if they have the health insurance as the high cost of cancer treatment is really high.
“Younger cancer patients had 2–5 times higher rates of bankruptcy than cancer patients age sixty-five or older, which indicates that Medicare and Social Security may mitigate bankruptcy risk for the older group,” Researchers wrote.
“People who have fewer assets, less income and less generous insurance because of entry-level jobs or no insurance are more vulnerable to severe financial distress,” lead author, Dr. Scott Ramsey, said in a statement.
These financial crises could be solved by the help from the governments and employers.
“The findings suggest that employers and governments may have a policy role to play in creating programs and incentives that could help people cover expenses in the first year following a cancer diagnosis,” Researchers wrote.
Think Progress, NBC News
Ramsey, S., Blough, D., Kirchhoff, A., Kreizenbeck, K., Fedorenko, C., Snell, K., Newcomb, P., Hollingworth, W., & Overstreet, K. (2013). Washington State Cancer Patients Found To Be At Greater Risk For Bankruptcy Than People Without A Cancer Diagnosis Health Affairs DOI: 10.1377/hlthaff.2012.1263... Read more »
Ramsey, S., Blough, D., Kirchhoff, A., Kreizenbeck, K., Fedorenko, C., Snell, K., Newcomb, P., Hollingworth, W., & Overstreet, K. (2013) Washington State Cancer Patients Found To Be At Greater Risk For Bankruptcy Than People Without A Cancer Diagnosis. Health Affairs. DOI: 10.1377/hlthaff.2012.1263
The U.S. Centers for Disease Control has published a comprehensive summary of the epidemiology of childhood brain disorders in the most recent Morbidity and Mortality Weekly Report.This report produced some sensationalized headlines that up to 20% of children suffer from a mental disorder. However, I was more interested in looking at the prevalence estimates for some of the individual disorders from the report.The report collates data collected from a variety of surveys and data sets including the NHANES, NHIS and the National Survey of Children's Health (NSCH). These surveys typically use parental report to estimate prevalence ratesFor the purposes of this post, I will focus on two childhood brain disorders: attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).The key findings from the report in ADHD include:7.6% of parents reported their child between 3-17 years had received a diagnosis of ADHD in the NHIS8.9% of parents reported their child received a diagnosis of ADHD in the NSCH study9.6% to 12.3% of boys had received a diagnosis of ADHD3.8% to 5.4% of girls had received a diagnosis of ADHDA diagnosis of ADHD was more with older age, in children with health insurance and higher income groupsA diagnosis of ADHD was not related to parental education level The key findings from the report for autism and autism spectrum disorder include:.8% to 1.1% of parents reported their child between 3-17 years had received a diagnosis of autism1.8% of parents reported their child had received a diagnosis of ASDSurveys consisted noted a male predominance with boys having an estimated 3.5 to 4.5 times higher rate of autism and ASD diagnosisAgain having health insurance increased the rate of autism or ASD diagnosis by around two foldAutism and ASD prevalence rates were somewhat higher in the Northeast region of the U.S. and in white, non-Hispanic childrenIn contrast to ADHD, ASD rates were similar across parental income categoriesThe report notes in the discussion section: "Substantial but not insurmountable challenges to surveillance of mental disorders in children exists." They note current methods focus on parental reports and are biased by variability in access to health and mental health providers. The also note the imperfect diagnostic approach to childhood mental disorders and the need for more consistent diagnostic approaches.This report is a good comprehensive summary of what we know about these childhood brain disorders in the United States. Readers with more interest in this topic can access the free full text report in the citation below. In the next two posts, I will summarize key findings in the conduct disorder and affective disorder categories.Photo of clown fish from the Oklahoma Aquarium is from the author's files.Perou R, Bitsko RH, Blumberg SJ, Pastor P, Ghandour RM, Gfroerer JC, Hedden SL, Crosby AE, Visser SN, Schieve LA, Parks SE, Hall JE, Brody D, Simile CM, Thompson WW, Baio J, Avenevoli S, Kogan MD, Huang LN, & Division of Human Development and Disability, National Center on Birth Defects and Developmental Disabilities, CDC, Atlanta, Georgia (2013). Mental health surveillance among children - United States, 2005-2011. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002), 62 (2), 1-35 PMID: 23677130... Read more »
Perou R, Bitsko RH, Blumberg SJ, Pastor P, Ghandour RM, Gfroerer JC, Hedden SL, Crosby AE, Visser SN, Schieve LA.... (2013) Mental health surveillance among children - United States, 2005-2011. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002), 62(2), 1-35. PMID: 23677130
CrossFit Nutrition: Cell Health and Telomeres. CrossFit Nutrition: you can only be as healthy as your cells. One marker of cell health is telomere length. Telomeres cap the ends ofThe post CrossFit Nutrition: Saturated Fat and Cell Health appeared first on WODMasters Stiff Competition.... Read more »
Song Y, You NC, Song Y, Kang MK, Hou L, Wallace R, Eaton CB, Tinker LF, & Liu S. (2013) Intake of Small-to-Medium-Chain Saturated Fatty Acids Is Associated with Peripheral Leukocyte Telomere Length in Postmenopausal Women. The Journal of nutrition. PMID: 23616516
FIFA discoverd that a lot of Mexican meat contains clenbuterol. A drug used to fatten cattle, enhance sportsperfomance, treat people with breathing disorders ánd to lose weight. So watch it with those tacos.... Read more »
Thevis, M., Geyer, L., Geyer, H., Guddat, S., Dvorak, J., Butch, A., Sterk, S., & Schänzer, W. (2013) Adverse analytical findings with clenbuterol among U-17 soccer players attributed to food contamination issues. Drug Testing and Analysis. DOI: 10.1002/dta.1471
I'm gonna try and be fairly brief in this post on the paper by Valerio Napolioni and colleagues* (open-access) looking at plasma cytokine profiles in cases of autism and their asymptomatic siblings. Brief because (a) the paper is open-access and (b) the participant groups (autism: n=25; sibling controls n=25) were relatively small so one has to be quite careful in extrapolating the findings with any large degree of confidence.Siblings by Paul Klee @ WikiPaintings Just in case you are new to cytokines, we are talking biological signalling and communication, and in particular, the language of inflammation both pro- and anti-inflammatory (see this post).With the autism spectrum conditions in mind, research into cytokines has filled quite a few peer-reviewed papers** from lots of different perspectives (see here and here for example). The main message so far is that it is complicated as per everything about autism and immune function.Despite the quite small participant group, the Napolioni paper does seem to be an important paper for a few reasons:They report no overall difference in cytokine profiles - measuring 40 cytokines - between cases of autism and their asymptomatic siblings. This despite the fact that autism symptoms and total IQ measures were different. That was the paper's headline.But.... "the cytokine/chemokine levels in our subjects did correlate with the quantitative clinical traits" or in other words, certain analysed parameters seemed to match with level of severity of autistic traits as measured by schedules such as VABS and SRS. "IL-1β appears to be the cytokine most involved in the quantitative traits".When looking at the children with autism according to various clinical subgroups - non-verbal, functional gastrointestinal (GI) issues, history of regression, history of allergies - a few correlations were noted. So, children who were non-verbal seemed to show higher levels of cytokines such as IL-10, one of the more anti-inflammatory cytokines. Children with accompanying GI issues seemed to show higher levels of more pro-inflammatory cytokines like IL-1β and IL-6 compared with those without GI problems. Reported regression as part and parcel of symptom onset also seemed to show some correlation with specific cytokines too.As the authors point out correlation does not imply causation. Such that just because they reported connections between cytokines and functioning and other factors does not necessarily mean that these observations are causative of autism (or anything else). That being said, as I hinted before, this is not the first time that cytokines and their connection to immune function have been discussed in the autism research literature (see yet another example of this here***); many correlations in similar directions makes for some interesting discussions at least.That headline that children with autism and their siblings did not significantly differ in their cytokine profile carries a few possibilities for interpretation. The authors suggest that this could be evidence of "an ‘autism endophenotype’ that expands immune dysfunction to family members who are seemingly unaffected by the core symptoms of autism". One might also say the same thing about the Gondalia paper**** on gut bacteria in cases of autism and siblings (see here).Assuming that the broader autism phenotype (BAP) does not come into play here, one might speculate that (a) cytokine profiles are not related to the presence of autism, or (b) that the manifestation of autism, some autism, is representative of cytokine involvement but in addition to other factors in terms of the affected sibling - "when an environmental stress (for example, prenatal exposure to environmental toxins, viral and bacterial infections, parental microchimerism, etc.) occurs during development". This last point takes me back to that 1971 John Money study on the appearance of familial autoimmune related conditions 'round about' the presence of autism and a similar correlation. Part of a predisposition to autism?I note from Figure 4 of the paper, that when it came to summarising the various associations across the groups (and sub-groups), quite a few of the very significant differences seemed to be due to differences in IQ, which was tested using the Stanford-Binet Intelligence Scales (fifth edition). Aside from previous messages of caution on the use of this measure in autism research*****, one has to wonder whether this might be a more pertinent variable when it comes to cytokines and autism. I don't know enough about cytokine profiles in intellectual disability in children for example, to make any novel claims about this, but certainly intellectual development has been mentioned in the research literature with certain cytokines in mind******.OK I said I would try and be brief with this post and have failed miserably. The Napolioni paper has though been worth it though for the potential insights that it might provide into the complex world of cytokines and immune function in relation to the presentation of autism.To close, and following yet more 'we'll win it next year' commentary with regards to the UK entry in the event that is the Eurovision Song Content, might I suggest a group for your serious consideration as a contender next year?-----------* Napolioni V. et al. Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder. Journal of Neuroinflammation 2013; 10: 38.** Goines PE. & Ashwood P. Cytokine dysregulation in autism spectrum disorders (ASD): Possible role of the environment. Neurotoxicol Teratol. 2013; 36: 67-81.*** Ricci S. et al. Altered cytokine and BDNF levels in autism spectrum disorder. Neurotox Res. April 2013.**** Gondalia SV. et al. Molecular characterisation of gastrointestinal microbiota of children with autism (with and without gastrointestinal dysfunction) and their neurotypical siblings. Autism Research. 2012; 5: 419-427.***** Coolican J. et al. Brief report: data on the Stanford-Binet Intelligence Scales (5th ed.) in children with autism spectrum disorder. J Autism Dev Disord. 2008; 38: 190-197.****** von Ehrenstein OS. et al. Child intellectual development in relation to cytokine levels in umbilical cord blood. Am J Epidemiol. 2012; 175: 1191-1199. ----------... Read more »
Napolioni V, Ober-Reynolds B, Szelinger S, Corneveaux JJ, Pawlowski T, Ober-Reynolds S, Kirwan J, Persico AM, Melmed RD, Craig DW.... (2013) Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder. Journal of neuroinflammation, 38. PMID: 23497090
Erin on the side of a river somewhere in western NC, hard at work study obviously.
Erin Abernethy is a Master’s student in the Odum
School of Ecology at the University of Georgia, where she is studying
scavenging ecology in Hawaii. Before coming to Athens, Erin lived in North
Carolina earning her BS in Biology at Appalachian State. For that degree,... Read more »
Guillette Jr., L., Pickford, D., Crain, D., Rooney, A., & Percival, H. (1996) Reduction in Penis Size and Plasma Testosterone Concentrations in Juvenile Alligators Living in a Contaminated Environment. General and Comparative Endocrinology, 101(1), 32-42. DOI: 10.1006/gcen.1996.0005
Blue Harvest @ Wikipedia @ Family GuyI need to create a suitable atmosphere for this post, so try this music for size and think Blue Harvest...Right. The wait is over. The discussions / arguments / objections / agreements are all confined to history. Drum roll, spotlight centre-stage... enter DSM-5 and into unknown territory we all go, particularly with autism, sorry.. autism spectrum disorders (ASDs) in mind.As you can see from the link above to the new diagnostic guidelines from the American Psychiatric Association (APA) the diagnosis of autism has, as was widely anticipated, changed somewhat to encompass quite a few adaptations (see this previous post).I'm not saying too much more on this at the present time, bearing in mind 'spectrum' is a word which seems to get more of a mention in this revision of the DSM; and not just with autism in mind (see here and here*).Obviously things aren't going to just change overnight with DSM-5 as it is eventally rolled out. Clinicians will need to learn some new diagnostic brushstrokes. Remember too that DSM is only one part of the diagnostic manuals currently in use (although even ICD is subject to revision in coming years already mentioning something called Social Reciprocity Disorder?). That being said, the implications of DSM-5 on issues like the autism numbers game - same as what happened across previous versions - are probably going to be subject to some pretty intense scrutiny over the coming years.Don't also be under any disillusion that the new changes are going to herald any giant leaps forward in autism research anytime soon. Interestingly, Dr Tom Insel, head of the US National Institute of Mental Health (NIMH) was recently quoted as saying that "NIMH will be re-orienting its research away from DSM categories", reported also by other authors** (open-access). In other words, even with the fresh smell of new DSM in the air, a new 'nosology' is already planned.To close, Peter 'Han Solo' Griffin on TIE fighters... dan-dan-da-dan, da-da-dan-dan-dan...---------* Adam D. Mental health: on the spectrum. Nature. 2013; 496: 416-418.** Lai M-C. et al. Subgrouping the autism “spectrum": reflections on DSM-5. PLoS Biol. 2013; 11: e1001544.----------Lai M-C, Lombardo MV, Chakrabarti B, & Baron-Cohen S (2013). Subgrouping the Autism “Spectrum": Reflections on DSM-5 PLoS Biology... Read more »
Lai M-C, Lombardo MV, Chakrabarti B, & Baron-Cohen S. (2013) Subgrouping the Autism “Spectrum": Reflections on DSM-5. PLoS Biology. info:/
by Andrea in Science of Eating Disorders
Navigating health service systems can seem daunting, to say the least. Making phone calls, getting doctor appointments and referrals, attending intake appointments, and preparing oneself for treatment can be both mentally and physically draining. When children and adolescents develop eating disorders, their parents become the main navigators in this scenario, making decisions and arrangements for their under-18-year-olds. But what happens when these adolescents reach the age of 18, and still require and/or desire treatment?
A recent Canadian qualitative study by Gina Dimitropoulos and colleagues (2013) explored the transition between pediatric and adult treatment for eating disorders to identify ways to facilitate smooth and effective transitions. To explore the tensions surrounding transitions, the authors conducted focus groups with service providers from both pediatric and adult treatment programs, as well as interviews with community practitioners.
This study used grounded theory (more in-depth discussion here), a qualitative approach that aims to develop a theory to explain a particular phenomenon based on an analysis of rich descriptions (Strauss & Corbin, 1998). As Strauss & Corbin articulate, this methodology aims to represent participants’ voices as accurately …
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Dimitropoulos, G., Tran, A., Agarwal, P., Sheffield, B., & Woodside, B. (2013) Challenges in Making the Transition Between Pediatric and Adult Eating Disorder Programs: A Qualitative Study From the Perspective of Service Providers. Eating Disorders, 21(1), 1-15. DOI: 10.1080/10640266.2013.741964
Hypnotherapy is the use of the hypnotic state in combination with other psychological strategies acquired from behavioural, cognitive and analytical therapy as well as from neuro linguistic programming (NLP). The main purpose of hypnotherapy is the achievement of your particular goal.... Read more »
Anna Pons. (2013) What is hypnotherapy?. Clinical Hypnotherapy. info:/
We love them and yet we hate them. They get censored, augmented, reduced, replaced, covered, exposed. They get grilled, occasionally, but those are not the ones I'm talking about. We want to see them and yet we pretend we don't. We criticize them and yet we forget what they are made for, the most beautiful thing of all: nourish a new life.Yes, I'm talking about breasts. Angelina Jolie's breasts have been extensively discussed this week, more now that they are reportedly gone than when they were around. Sort of ironic, if you thin about it. Angelina did the unthinkable: she had both her healthy breasts removed to prevent cancer. In a second phase of her preventive plan, she will have her ovaries removed, too. The tabloids will no longer be able to speculate on her possible new pregnancies, but they will have plenty to discuss on and around her missing body parts.Somehow the news left me a little puzzled, unable to share the views of those who praised Angelina for her bravery. Yes, it takes guts to do what she did. At the same time, the huge resonance she's been given seems blown out of proportion. Just another Hollywood thing. It reminds me of back when our mothers were told that formula was way better than breast milk. Are we facing a new era where silicon is better than milk ducts? Are they trying to convince us that fake is healthier than real? Well, of course it is. It's fake!So, before we go around demonizing breasts and invoking chopping off body parts in the name of longevity, I wanted to get some facts straight.First of all, I read over and over again, "Angelina Jolie carries the gene BRCA1 ..." Turns out, we all carry the gene. What makes us different is that there are distinct copies of this gene across individuals, and some copies (but not all) do raise the risk of breast and ovarian cancer. BRCA1 and BRCA2 are part of the so called tumor suppressor genes, genes that code for proteins that are in charge of repairing damaged DNA. Our cells undergo numerous cellular divisions during our lifespan, and every cell division carries a certain chance of damaging the DNA. Though rare, mutations can be introduced, which can either be lethal or create a cancerous cell. Tumor suppressor proteins make a first attempt to repair the damaged DNA. If the DNA cannot be repaired, they promote apoptosis, or cell death. Another example of tumor suppressor gene is TP53, which encodes the protein p53. The first link between BRCA1 and breast cancer was discovered in 1990 by Hall et al. . BRCA1 and BRCA2 are expressed mostly in breast tissue. Some mutations in these genes cause them to code proteins that are not fully functional. When this happens, a cell with damaged DNA has a higher chance to escape the "screening" and start dividing instead of undergoing apoptosis. Because BRCA1 and BRCA2 are expressed mostly in the breast tissue, by removing the breast tissue one gets rid of the majority of cells expressing the defective genes, which in turns significantly lowers the chance of developing breast cancer. While hundreds of mutations/variations in the BRCA1 and BRCA2 genes have been found, not all are linked to breast cancer, and the ones that are don't increase the risk in the same amount. Furthermore, the majority of breast cancers are not linked to mutations in these two genes. In other words, having the mutations raises the risk, but not having them does not lower it. So, let's get some numbers straight. According to the American Cancer Society about 15% of women diagnosed with breast cancer have a family member diagnosed with it. That leaves the majority of breast cancers unrelated to family history: "About 85% of breast cancers occur in women who have no family history of breast cancer. These occur due to genetic mutations that happen as a result of the aging process and life in general, rather than inherited mutations."It's a puzzle I've discussed before, the missing herediatbility. On the one hand we know genes play a large role in cancer and we spend all this research money into looking for genetic causes. Yet, the vast majority of cancers are non-hereditary. While women with certain mutations in either the BRCA1 or BRCA2 genes have up to 80% (the exact chance varies depending on the type of mutation they carry) increased risk of developing breast cancer, only between 5% and 10% of breast cancers are linked to deleterious mutations in the BRCA1 or BRCA2 genes. So, yes, get tested. But chances are, your copy of BRCA1 and BRCA2 are fine. So, what makes BRCA1 and bRCA2 so scary? The American Cancer Society reports that approximately 60% of women with one of the harmful mutations in BRCA1 or BRCA2 develop breast cancer during their lifetime, versus the 12% of women in the general population. Remember, though: these genes are not the only ones playing a role in cancer. Things like epistasis with other loci in the genome can deeply affect such risks and, unfortunately, we still don't know enough to quantify them. High levels of IGF-1, the insulin-like growth factor have also been linked to breast cancer. So while having those mutations raises the risk, it does not mean that the individual will develop breast cancer for sure as other factors are still unknown. Careful considerations should be made before making a drastic choice like Angelina's. These considerations should also include risks associated to a double mastectomy (infection, necrosis, etc.) and reconstruction surgery, neither one free of complications. I'm somehow reluctant to consider implants healthier than normal breasts, whether or not those breasts were expressing faulty genes. What about those 85% of breast cancers that are not linked to BRCA1 or BRCA2 mutations? Can we do anything to prevent those? When you look at the global population, the most common risk factors for breast cancer are not the mutations in BRCA1 and BRCA2, rather, as Bernstein reports in a 2009 review :"The most consistently acknowledged risk factors for breast cancer other than gender and race/ethnicity are age, family history of breast cancer, early menarche, late age at first birth, nulliparity, late age at menopause, high postmenopausal weight or substantial weight gain as an adult, exposure to high levels of ionizing radiation and a history of benign proliferative breast disease ."All these risk factors point at one common etiology, ovarian hormones (estradiol and progesterone), because they"promote cellular proliferation in the breast, providing greater opportunity for the accumulation of random errors, which may lead to tumor development ."Body weight and exercise can be linked to different levels of estradiol in the blood (high body weight is associated with higher levels, exercise is associated with lower levels), hence their correlation to breast cancer risk. Some studies found up to 40% reduction in risk in women who exercised in particular in their adolescence. Of all risk factors, these two, body weight and exercise, are the ones we can actually take control over and actively lower our risk of developing breast cancer. A diet rich in antioxidants may lower the risk of DNA damage during cellular division. Things we have less control over is the woman's age at the first pregnancy. One of my grad school professors used to say, "Having a baby as a teen may ruin your life, but it sure lowers your risk of developing breast cancer later in life." The risk keeps lowering for every additional pregnancy, though not as significantly as with the first one. What's not clear is the extent to which breastfeeding can lower the risk of breast cancer, as the American Cancer Society reports: "Research suggests that breastfeeding has only a slight effect on breast cancer risk and that effect is only among women who have breastfed for a long time. They also concluded that breastfeeding seems to be more protective against the most aggressive types of breast cancer, including tumors in women with mutations in the BRCA1 gene, basal-like cancers, hormone-receptor negative, and possibly triple negative tumors."And while we do the things that we can to lower our risks, I am hopeful that one day gene therapy will be perfected to the point that it will offer a better options than what, in gross terms, amounts to amputation.Thoughts? ... Read more »
Hall, J., Lee, M., Newman, B., Morrow, J., Anderson, L., Huey, B., & King, M. (1990) Linkage of early-onset familial breast cancer to chromosome 17q21. Science, 250(4988), 1684-1689. DOI: 10.1126/science.2270482
Bernstein, L. (2008) Identifying population-based approaches to lower breast cancer risk. Oncogene. DOI: 10.1038/onc.2009.348
I told you so.I'm talking about the paper by Pu and colleagues* who meta-analysed the currently available literature looking at two SNPs in everyone's favourite Scrabble classic gene, MTHFR in relation to autism spectrum disorders (ASDs). Said gene controls production of methylenetetrahydrofolate reductase (MTHFR) which fits very snugly into the whole one carbon metabolism cycle (see here).Love at first sight? @ Wikipedia Regular readers might know that I have a bit of a thing for MTHFR with autism in mind. And how MTHFR serves an important purpose in reducing the compound 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate and onward its links to homocysteine (see here) and methionine (see here) and all that methylation palava.For a good summary (well, at least I think so) you might also want to have a look at this older post detailing the process, complete with hand-drawn diagram by yours truly.In essence, Pu et al reiterated the important role than the MTHFR C677T SNP might have to some cases of autism; in particular how "the C677T polymorphism was found to be associated with ASD only in children from countries without [folic acid] food fortification" denoting the potentially important link with the vitamin of the hour, folate (folic acid, vitamin B9) (see here).There's little more for me to add to this post that hasn't already been said. MTHFR is probably not going to be an issue for everyone with autism, and indeed might also be potentially important to other conditions outside of the autism spectrum (see here for a discussion of that recent schizophrenia paper). Mmm... perhaps another part of that common ground and potential RDoC variable?The nutrition link is perhaps something which adds to the view that environment might be a modifier of risk of some ASDs bearing also in mind the overlap with things like vitamin B12 (see here). That being said I'm also going to draw your attention back to all that folate receptor autoantibody stuff too just to bear in mind.I told you so.----------* Pu D. et al. Association between MTHFR gene polymorphisms and the risk of autism spectrum disorders: a meta-analysis. Autism Res. May 2013.----------Pu D, Shen Y, & Wu J (2013). Association between MTHFR Gene Polymorphisms and the Risk of Autism Spectrum Disorders: A Meta-Analysis. Autism research : official journal of the International Society for Autism Research PMID: 23653228... Read more »
Pu D, Shen Y, & Wu J. (2013) Association between MTHFR Gene Polymorphisms and the Risk of Autism Spectrum Disorders: A Meta-Analysis. Autism research : official journal of the International Society for Autism Research. PMID: 23653228
Prohibition and the “tobacco control endgame.”
Despite all our efforts in recent years to reduce the percentage of Americans who smoke cigarettes—currently about one in five—the idea of full-blown cigarette prohibition has not gained much traction. That may be changing, as prominent nicotine researchers and public police officials start thinking about what is widely referred to as the “tobacco control endgame.”
Considering the new regulatory powers given the FDA under the terms of the Tobacco Control Act of 2009, as a commentary in Tobacco Control framed it, “will the government be a facilitator or barrier to the effective implementation of strategies designed to achieve this public health goal?”
Two newer approaches have gained some traction in the research community: Reduce the level of nicotine in cigarette products (the FDA is prohibited by law from reducing nicotine content to zero), and continuing to emphasize the non-combustible forms. Plus, everybody pretty much agrees on higher prices.
Here are the six arguments for going all the way:
1) Death. Six million of them a year, worldwide, a number that will grow before it starts shrinking. A billion deaths this century, compared to 100 million in the 20th Century. Robert Proctor, author of The Golden Holocaust and a professor of history at Stanford, whose six arguments these are, calls the cigarette “the deadliest object in the history of human civilization.” So there’s that.
2) Other product defects. The cigarette is defective, Proctor writes in defense of his six arguments in Tobacco Control, because it is “not just dangerous but unreasonably dangerous, killing half its long-term users.” Indeed, it is hard to imagine the FDA green-lighting a drug product like that today. In addition, Proctor claims cigarettes are defective because the tobacco has been altered by flue curing to make it far more inhalable than would otherwise be the case. “The world’s present epidemic of lung cancer is almost entirely due to the use of low pH flue-cured tobacco in cigarettes, an industry-wide practice that could be reversed at any time.”
3) Financial burdens. These can be reckoned principally in terms of the costs of treating smoking-related illnesses. This, in turn, leads to diminished labor productivity, especially in the developing world, a process that “in many parts of the world makes the poor even poorer,” Proctor observes.
4) Big Tobacco’s impact on science. By sponsoring shoddy and distracting research, by publishing “decoy” findings and by otherwise confusing and corrupting scientific discourse on the cigarette question in the advertising-dependent popular media. The tobacco industry has proved to everyone’s satisfaction that it can put politicians and regulators under intense pressure to see things its way. Not to mention other institutions that have been “bullied, corrupted or exploited,” according to Proctor: The AMA, The American Law Institute, sports organizations, Hollywood, the military, and the U.S. Congress, for starters. (Until 2011, American submarines were not smoke-free.)
5) Environmental harms. More than you might think falls into this category: Deforestation, pesticide use, loss of savannah woodlands for charcoal used in flue curing, fossil fuels for curing and transport, fires caused by burning cigarettes, etc.
6) Smokers want to quit. Smoking is not a recreational drug, as Proctor takes pains to point out. Most smokers hate it and wish they could quit. This makes cigarettes different from alcohol or marijuana, Proctor insists. He quotes a Canadian tobacco executive, who said that smoking isn’t like drinking; it’s more like being an alcoholic. This rings true to for the majority of addicted smokers I know, and was certainly true of me when I was a smoker.
So there it is, the case for tobacco prohibition. But hasn’t all this prohibition business been tried and found wanting? We know the results of drug and alcohol prohibition, whatever their rationales: Smuggling, organized crime, increased law enforcement, more money. This argument, says Proctor, has been central to the cigarette industry since forever: “Bans are ridiculed as impractical or tyrannical. (First they come for your cigarettes…)”
Proctor’s response is that smuggling is already common, and people should be free to grow tobacco for their personal use. He advocates a ban on sales, not possession.
There are at least two major obstacles to cigarette prohibition. First, an enormous amount of tax revenue is generated by the production and sale of cigarettes. And the troubling question of a steep rise in black marketeering goes largely ignored or unaddressed. In the same special issue of Tobacco Control, Peter Reuter has sobering thoughts on that front: “Cigarette black markets are commonplace in high tax jurisdictions. For example, estimates are that contraband cigarettes now account for 20-30% of the Canadian market, which has restrained government enthusiasm for raising taxes further. All the proposed ‘endgame’ proposals for shrinking cigarette prevalence toward zero run the risk of creating black markets.”
In the end, Proctor argues that the cigarette industry itself has repeatedly promised to quit the business if its products where ever found to be profoundly harmful to consumers. As recently as 1997, Philip Morris CEO Geoffrey Bible swore under oath that if cigarettes were found to cause cancer “I’d probably… shut it down instantly to get a better hold on things.” Incredible statements like this by company executives go back to the 1950s. Perhaps it’s time to let them stop lying. “The cigarette, as presently constituted,” writes Proctor, “is simply too dangerous—and destructive and unloved—to be sold.”
Proctor R.N. (2013). Why ban the sale of cigarettes? The case for abolition, Tobacco Control, 22 (Supplement 1) i27-i30. DOI: 10.1136/tobaccocontrol-2012-050811
Photo: AAP/April Fonti
... Read more »
Proctor R. N. (2013) Why ban the sale of cigarettes? The case for abolition. Tobacco Control, 22(Supplement 1). DOI: 10.1136/tobaccocontrol-2012-050811
A short wrap-up of the Cell Symposium on Microbiome and Host Health in Lisbon, Portugal, May 12-14, 2013.... Read more »
Koren O, Knights D, Gonzalez A, Waldron L, Segata N, Knight R, Huttenhower C, & Ley RE. (2013) A guide to enterotypes across the human body: meta-analysis of microbial community structures in human microbiome datasets. PLoS computational biology, 9(1). PMID: 23326225
Ivanov II, & Honda K. (2012) Intestinal commensal microbes as immune modulators. Cell host , 12(4), 496-508. PMID: 23084918
Blaser M, Bork P, Fraser C, Knight R, & Wang J. (2013) The microbiome explored: recent insights and future challenges. Nature reviews. Microbiology, 11(3), 213-7. PMID: 23377500
Researchers have found that the immune system of the women declines more slowly than men and this could be one of the reasons for the longer life of women - at least in Japan.
Immunity & Ageing
Immune system is the system that recognizes and opposes disease. In the new study, researchers have reported that with the passage of time, men’s ability to oppose the disease decrease more rapidly as compared to women, resulting in increased weaknesses with time.
Researchers from Japan analyzed blood samples of 356 healthy men and women in the age range of 20 and 90. They found that the two components of the immune system; T-cells, which protect the body from infection, and B-cells, which secrete antibodies, declined rapidly in men as compared to women.
Moreover, CD4 T-cells and natural killer cells, two specific types of immune system cells that attack invaders and usually increase with age, increase at a higher rate in women as compared to men.
“Age-related changes in various immunological parameters differ between men and women.” Researchers wrote, “Our findings indicate that the slower rate of decline in these immunological parameters in women than those in men is consistent with the fact that women live longer than do men.”
Hirokawa, K., Utsuyama, M., Hayashi, Y., Kitagawa, M., Makinodan, T., & Fulop, T. (2013). Slower immune system ageing in women versus men in the Japanese population Immunity & Ageing, 10 (1) DOI: 10.1186/1742-4933-10-19... Read more »
Hirokawa, K., Utsuyama, M., Hayashi, Y., Kitagawa, M., Makinodan, T., & Fulop, T. (2013) Slower immune system ageing in women versus men in the Japanese population. Immunity , 10(1), 19. DOI: 10.1186/1742-4933-10-19
Guest post by Patrick Rabbitt, commenting on an article that claimed that simple reaction time is slower now than in the Victorian era. Mundane differences in equipment sensitivity may be responsible... Read more »
Michael A. Woodley, Jan te Nijenhuis, & Raegan Murphy. (2013) Were the Victorians cleverer than us? The decline in general intelligence estimated from a meta-analysis of the slowing of simple reaction time. Intelligence. info:/http://dx.doi.org/10.1016/j.intell.2013.04.006
It may not be traditionally what you think of as flu season, but lately there’s been a great deal of talk about some viruses that are concerning public health officials and infectious disease specialists. You might have heard of the H7N9 situation in China, and the NCoV virus in France that made headlines. But researchers [...]... Read more »
Squires, R., Noronha, J., Hunt, V., García-Sastre, A., Macken, C., Baumgarth, N., Suarez, D., Pickett, B., Zhang, Y., Larsen, C.... (2012) Influenza Research Database: an integrated bioinformatics resource for influenza research and surveillance. Influenza and Other Respiratory Viruses, 6(6), 404-416. DOI: 10.1111/j.1750-2659.2011.00331.x
Pickett, B., Sadat, E., Zhang, Y., Noronha, J., Squires, R., Hunt, V., Liu, M., Kumar, S., Zaremba, S., Gu, Z.... (2011) ViPR: an open bioinformatics database and analysis resource for virology research. Nucleic Acids Research, 40(D1). DOI: 10.1093/nar/gkr859
Some people would think twice before buying a house next to high-voltage power line. Wasn’t there something in the news about these wires causing cancer? Indeed many media have elaborately cited people worrying about the risks of electricity. But often without offering a scientific view on the subject.... Read more »
Draper, G. (2005) Childhood cancer in relation to distance from high voltage power lines in England and Wales: a case-control study. BMJ, 330(7503), 1290. DOI: 10.1136/bmj.330.7503.1290
Having too much body fat makes arteries become stiff after middle age, a new study has revealed.
In young people, blood vessels appear to be able to compensate for the effects of obesity. But after middle age, this adaptability is lost, and arteries become progressively stiffer as body fat rises – potentially increasing the risk of dying from cardiovascular disease.... Read more »
Sam Wong. (2013) Body fat hardens arteries after middle age. Imperial College of London. info:/
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