If you are dealing with excessive daytime sleepiness, gain an extra boost of alertness with tips from these recent research studies.... Read more »
Reid, K., Baron, K., Lu, B., Naylor, E., Wolfe, L., & Zee, P. (2010) Aerobic exercise improves self-reported sleep and quality of life in older adults with insomnia. Sleep Medicine, 11(9), 934-940. DOI: 10.1016/j.sleep.2010.04.014
Snap! Ouch! That’s from my head doing a double take. All these years, I thought the calcium vs heart disease thing was a conspiracy arranged by one researcher and publication. However, 3 months ago, I stumbled upon some corroborating studies by other researchers in other journals. Even the US Preventive Services Task Force recently came out against low dose calcium (less than 1,000mg/d) in post-menopausal women because they could not find conclusive evidence of benefit in the face of a small risk of harm from kidney stone... Read more »
Bolland, M., Grey, A., Avenell, A., Gamble, G., & Reid, I. (2011) Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women's Health Initiative limited access dataset and meta-analysis. BMJ, 342(apr19 1). DOI: 10.1136/bmj.d2040
Langsetmo, L., Berger, C., Kreiger, N., Kovacs, C., Hanley, D., Jamal, S., Whiting, S., Genest, J., Morin, S., Hodsman, A.... (2013) Calcium and Vitamin D Intake and Mortality: Results from the Canadian Multicentre Osteoporosis Study (CaMos). Journal of Clinical Endocrinology . DOI: 10.1210/jc.2013-1516
--> The mycobiome is starting to get a little traction!When will we know the weight of the fungi on and in our bodies? The human microbiota has been recognized as hugely important in the last few years, but that has almost entirely focused on bacteria. I’ve been interested in the mycobiome of the human built environment for a while, and I certainly haven’t been alone. People tend to think of fungi as a problem in buildings, on or in plants, and in the outside air. However, there is still so much unknown about the mycobiota of animals including humans. Only last year, there was a key discovery about mammal-fungal interactions in the gut that may drive some rather sever disease in humans (ulcerative colitis)*, and it appears things are starting to pick up pace for the mycobiome, largely with the help of sequencing technology.Using over 5 million sequences of a standard fungal ID rDNA fragment, Findley et al. show specific fungal communities on human skin that shift with location on the body while bacteria shift depending on the site physiology. They also found startling fungal commensal diversity on the skin. Most of the identification they did was only to genus level, but for the predominant fungal genus, Malassezia, they identified species. Unlike Candida, which I think is basically a single species of human commensal out of a diverse group of environmental Saccharomycetales yeasts, Findley et al. found 11 of the 14 described species of Malassezia species consistently on the body. More interestingly it was mostly in the distribution of these species that the structure of the fungal community over the core body emerged. Different core body locations were dominated by different Malassezia species. The feet were another thing altogether. The fungal community on feet was vastly different from the core body and much more diverse. The fungal communities also differed from each other depending on site on the foot (toe nail, toe web, heel), but only really in feet showing clinical signs of infection (skin flaking etc.).They also found a kind of outlier individual who had a short course of treatment oral antifungal treatment months previous to the study. This individual had vastly different fungal community composition than the others but the bacterial community was not different.Having seen this I wonder how much abundance plays a role. Sometimes when abundance is high communities are less diverse. I think there could be parallels in other kinds of mycobiomes for what they’ve found on humans. Another clear thing to think about is the long-term effect on fungal communities of application of antifungals/fungicides. It’s exciting to see this level of detail in a study, but obviously, with only ten people studied, the Findley et al. work is small scale and a lot more patterns could emerge with new studies. Let’s get sequencing the Tube fungal community!*As an aside, I have often wondered how much the amphibian disease community cares about the immune response effects of Basidiobolus on amphibians infected with Batrachochytrium. Iliev, I., Funari, V., Taylor, K., Nguyen, Q., Reyes, C., Strom, S., Brown, J., Becker, C., Fleshner, P., Dubinsky, M., Rotter, J., Wang, H., McGovern, D., Brown, G., & Underhill, D. (2012). Interactions Between Commensal Fungi and the C-Type Lectin Receptor Dectin-1 Influence Colitis Science, 336 (6086), 1314-1317 DOI: 10.1126/science.1221789Findley, K., Oh, J., Yang, J., Conlan, S., Deming, C., Meyer, J., Schoenfeld, D., Nomicos, E., Park, M., Becker, J., Benjamin, B., Blakesley, R., Bouffard, G., Brooks, S., Coleman, H., Dekhtyar, M., Gregory, M., Guan, X.,... Read more »
Iliev, I., Funari, V., Taylor, K., Nguyen, Q., Reyes, C., Strom, S., Brown, J., Becker, C., Fleshner, P., Dubinsky, M.... (2012) Interactions Between Commensal Fungi and the C-Type Lectin Receptor Dectin-1 Influence Colitis. Science, 336(6086), 1314-1317. DOI: 10.1126/science.1221789
Findley, K., Oh, J., Yang, J., Conlan, S., Deming, C., Meyer, J., Schoenfeld, D., Nomicos, E., Park, M., Becker, J.... (2013) Topographic diversity of fungal and bacterial communities in human skin. Nature. DOI: 10.1038/nature12171
Picking up on my infatuation with all things Hsp, today more on the effects of two of the large Hsps on Candida albicans biofilm formation and virulence in mice and worms.Ssa1, a member of the Hsp70 family, is traditionally implicated in protein folding and entwining. Following heat shock, Ssa1 expression increases, which is a hallmark of heat shock proteins. Recently, Ssa1’s role in Candida albicans’ virulence has been extensively characterized. A series of experiments involving C. albicans mutant strains demonstrated that deletion of SSA1 (i) has no effect on survival in the mouse model of candidiasis of the bloodstream, (ii) leads to reduced fungal burden in mouse organs, (iii) results in significantly smaller lesions on the tongues of infected mice, (iv) yields less damage to endothelial and epithelial cells, and (v) causes less endocytosis. These effects are due to Ssa1 localizing to the outermost part of the cell wall where it governs binding to cadherins. Thus, lack of Ssa1 results in poor adherence, endocytosis and invasion, all of which are determinants of virulence in C. albicans. Interestingly though, filaments of SSA1 deletion strains are of comparable length to those of wild type cells.On the note of Hsp redundancy, Ssa1 has a paralog, a second copy in the genome so to speak, which is 98% identical. Yet, SSA2deletion mutants resemble the wild type. This is probably due to increased SSA1 expression levels that compensate for the lack of SSA2. Though, why then does SSA2 not make up for SSA1 deletion?Hsp104also entwines damaged proteins and cooperates with Ssa1 in refolding and reactivating them. Its expression is not just induced in response to heat but several other stresses, such as ethanol and arsenite, highlighting its role as a general anti-stress chaperone. Fungal virulence is contingent on stress responses thus suggesting a role for this chaperone in virulence, which was characterized most recently by studying the effect of HSP104deletion on survival of heat shock, biofilm formation, a critical virulence trait, and killing of worms, an invertebrate model host. Not too surprising, Hsp104 is required for thermotolerance, biofilm formation and structure as well as virulence in the worm model. Furthermore, Hsp104 appears to be haploinsufficient, which means that the phenotype of the HSP104/hsp104 is intermediate between the wild type and the null.Curiously, expression of Hsp70/Ssa1, Hsp90, and Hsp104 is induced by the one and only Hsf1.... Read more »
Fiori, A., Kucharikova, S., Govaert, G., Cammue, B., Thevissen, K., & Van Dijck, P. (2012) The Heat-Induced Molecular Disaggregase Hsp104 of Candida albicans Plays a Role in Biofilm Formation and Pathogenicity in a Worm Infection Model. Eukaryotic Cell, 11(8), 1012-1020. DOI: 10.1128/EC.00147-12
Sun JN, Solis NV, Phan QT, Bajwa JS, Kashleva H, Thompson A, Liu Y, Dongari-Bagtzoglou A, Edgerton M, & Filler SG. (2010) Host cell invasion and virulence mediated by Candida albicans Ssa1. PLoS pathogens, 6(11). PMID: 21085601
Take Home Message: Evidence of increased alpha angles has been shown in ice hockey players as compared to non-hockey playing matched controls. Even at young ages, signs of bony abnormality linked to femoroacetabular impingement are present.
Femoroacetabular impingement (FAI) is a common radiographic finding among athletes participating in sports requiring hip flexion, hip internal rotation, and repetitive cyclic motions. Cam-deformity FAI is marked by the aspherical shape of the femoral head, and is radiographically defined by an alpha angle 55˚. Hockey players employ a skating pattern that is suspected to cause cam-deformity but it remains unclear how common cam-deformities are among asymptomatic young ice hockey players. Therefore, Philippon and colleagues conducted a cohort study to determine how common a large alpha angle was among 61 youth hockey players and 27 youth skiers.... Read more »
Philippon, M., Ho, C., Briggs, K., Stull, J., & LaPrade, R. (2013) Prevalence of Increased Alpha Angles as a Measure of Cam-Type Femoroacetabular Impingement in Youth Ice Hockey Players. The American Journal of Sports Medicine. DOI: 10.1177/0363546513483448
The ‘actuator lugs’ on the Newton Running Shoes... Read more »
Moran, M., & Greer, B. (2013) Influence of midsole ‘actuator lugs’ on running economy in trained distance runners. Footwear Science, 5(2), 91-99. DOI: 10.1080/19424280.2013.792878
Drinking pruno is a risky endeavor, both in terms of its offense to culinary sensibilities and to one's health. However, turned stomachs are not the only hazard here; you may add a desire to avoid botulism to your list of reasons to shy away from you'r mates latest batch of prison hooch. The soil-dwelling bacterium Clostridium botulinum can contaminate fruits and veggies, and, in warm, oxygen-deprived conditions, produces the neuroparalytic toxin botulinum. Even more wholesome DIY endeavors, such as canning fruits and crafting jams, can create an excellent staging ground for growing one's own C. botulinum.... Read more »
Centers for Disease Control and Prevention (CDC). (2013) Notes from the field: botulism from drinking prison-made illicit alcohol - Arizona, 2012. MMWR. Morbidity and mortality weekly report, 62(5), 88. PMID: 23388552
Since my last blog post, where I shared my thoughts on BRCA1, BRCA2, and preventive mastectomies, I've been asked what else can a woman do to reduce her risk of breast cancer. I've heard a big deal about vitamin D, so I did a bit of research on the matter. As a disclaimer, I should tell you up front that, though many correlations between vitamin D deficiency and cancer risk have been found, just as many have been refuted or found inconclusive. You can read more about it on the wikipedia page.What is vitamin D? The name "vitamin D" includes a group of steroid-like molecules (they are similar to steroids, but not quite steroids) that help our intestine absorb calcium and phosphates. Since calcium is essential in bone development, vitamin D deficiency has been most commonly associated to osteoporosis and other bone-related diseases. There aren't many foods rich in vitamin D, however, vitamin D can be endogenously synthesized when the skin is exposed to sunlight. Unfortunately, modern lifestyle keeps us cooped up many hours in office cubicles, or in the house during chores, or in malls. When we're out enjoying the sunshine we cover up with hats and super-protective sunscreens because we've been told that the sun is bad for the skin and can cause malignancies. As a consequence, vitamin D deficiency is increasing world-wide. There is a foundation for all the studies that have analyzed correlations between several diseases, including cancers, and vitamin D: (i) several ecological studies have found a trend for an increase in incidence of certain cancers at higher latitudes, suggesting that longer exposures to the sun may have a protective effect. (ii) The vitamin D receptor (VDR) is expressed in many cells of the immune system, and mouse models have shown that vitamin D deficiency can promote certain auto-immune diseases. In a recent review, Sundaram and Coleman examine the link between vitamin D and influenza [Adv. Nutr. 2012 3: 517-525]. (iii) "VDR regulates a wide range of cellular mechanisms central to cancer development, such as apoptosis (cell death), cell proliferation (uncontrolled cell growth), differentiation, angiogenesis, and metastasis ". In line with this observation, Pereira, Larriba, and Munoz published a review on the evidence that vitamin D plays a protective role in colon cancer [Endocr. Relat. Cancer 2012 19: R51-R71].In , Crew discusses the use of vitamin D supplementation as part of breast cancer prevention. She presents many interesting findings, for example:"Colon, breast, and lung cancer have all demonstrated downregulation of expression of VDR when compared to normal cells and well-differentiated tumors have shown comparably more VDR expression as measured by immunohistochemistry when compared to their poorly differentiated counterparts. Higher tumor VDR expression has also been correlated with better prognosis in cancer patients ."Crew looks at different types of studies: some suggest beneficial effects from using vitamin D (calcitriol) in combination with other anti-cancer treatments; some found an inverse association with mammography density, a biomarker for breast cancer (supposedly high density increases the risk of cancer); some found an inverse association between better breast cancer prognosis and vitamin D deficiency. However, many of these studies have limitations. For example, some only assess the levels of vitamin D through dietary intake, which is not a good measure of the circulating levels because it doesn't account for vitamin D synthesized through sun exposure. Some were confounded by obesity since fat is known to sequestrate vitamin D and also raise breast cancer risk. In light of all these considerations, Crew concludes:"Even with substantial literature on vitamin D and breast cancer, future studies need to focus on gaining a better understanding of the biologic effects of vitamin D in breast tissue. Despite compelling data from experimental and observational studies, there is still insufficient data from clinical trials to make recommendations for vitamin D supplementation for breast cancer prevention or treatment ."As I often do in my posts, rather than giving you answers, I make an effort to provide you with pointers and food for thought: in the end you have to make your own decisions about your health and the wellbeing of your family. As a personal note, I'll add that on my last blood report my vitamin D circulating levels were undetectable. I had no symptoms whatsoever, but I am now taking a vitamin D supplement. I'm also much less paranoid about smothering my kiddos with sunscreen when they play outside (which has made them much happier, two birds with one stone).  Crew, K. (2013). Vitamin D: Are We Ready to Supplement for Breast Cancer Prevention and Treatment? ISRN Oncology, 2013, 1-22 DOI: 10.1155/2013/483687... Read more »
Crew, K. (2013) Vitamin D: Are We Ready to Supplement for Breast Cancer Prevention and Treatment?. ISRN Oncology, 1-22. DOI: 10.1155/2013/483687
Depression or Major Depressive Disorder (MDD) has multiple genetic and environmental causes. Genetic factors are hard to find and the discovered factors usually are also associated with other mood disorders. Furthermore, twin studies reveal that genetics can predict 37% of the depressions, which is a much lower heritability than in bipolar disorder, a comparable mood disorder (reviewed in Belmaker et al., 2008). ... Read more »
Papakostas, G., Shelton, R., Kinrys, G., Henry, M., Bakow, B., Lipkin, S., Pi, B., Thurmond, L., & Bilello, J. (2011) Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a Pilot and Replication Study. Molecular Psychiatry, 18(3), 332-339. DOI: 10.1038/mp.2011.166
Pariante, C., & Lightman, S. (2008) The HPA axis in major depression: classical theories and new developments. Trends in Neurosciences, 31(9), 464-468. DOI: 10.1016/j.tins.2008.06.006
Raison, C. (2012) A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist Infliximab for Treatment-Resistant DepressionThe Role of Baseline Inflammatory BiomarkersInfliximab for Treatment-Resistant Depression. Archives of General Psychiatry, 1. DOI: 10.1001/2013.jamapsychiatry.4
Nibuya M, Morinobu S, & Duman RS. (1995) Regulation of BDNF and trkB mRNA in rat brain by chronic electroconvulsive seizure and antidepressant drug treatments. The Journal of neuroscience : the official journal of the Society for Neuroscience, 15(11), 7539-47. PMID: 7472505
classical music and intense sensory exercises produced improvements in autism symptoms in children after just six months, scientists have found.... Read more »
Woo, C., & Leon, M. (2013) Environmental Enrichment as an Effective Treatment for Autism: A Randomized Controlled Trial. Behavioral Neuroscience. DOI: 10.1037/a0033010
An episode of the BBC program Horizon on 'Big Data' recently caught my attention. The content was a fascinating insight into how we are living in a data-rich age and how trawling/mining/dredging such data has the ability to advance medicine, predict crime and even make someone a few quid/dollars/euros on the stock market.Gone (data) fishing @ Wikipedia I'm a big believer in big data. In particular how, with the right sources, technology, techniques and people, big data might be able to open up some real insights into many important areas including mental health research* and very possibly autism research with a specific focus on the science of biomarkers to aid things like early diagnosis. Indeed, I'm not the only one talking about this (see here).I've spoken before on this blog about biomarkers for autism and other conditions - the promises, the problems, the future - and how alongside the various autism research banks (genes, brains, etc.) and systems biology chatter, we are just starting to understand the value of those big data resources such as the archived bloodspot samples which so many neonates provide these days.Indeed with the greatest appreciation for pioneers like Robert Guthrie, I offer a post on an interesting paper by Gerald Mizejewski and colleagues** discussing results suggestive of potential candidate biomarkers for autism based on archived bloodspot samples. I should point out that this is not the first time that Dr Mizejewski has talked about the feasability of biomarkers for autism as per this article*** (open-access) as part of quite a distinguished research career it has to be said (see here) with a specific focus on an interesting molecule called alpha-fetoprotein****.The most recent paper is unfortunately not at the time of writing open-access, so I'll just go through a few summary points about the work:This was a retrospective study based on that tantalising resource of archived bloodspot cards which sit in many a hospital basement. Out of a total case group of 200 families with a child with autism, 40 families with children aged between 3-5 years old were initially contacted for participation. This was eventually whittled down to 16 participants (all diagnosed with autism by the same clinician with the same diagnostic manual) for whom archived neonatal bloodspot cards were available. Two age-matched control specimens located immediately before and after the dried bloodspot card in question in the filing system were also chosen.A small 3mm punch of the Guthrie cards was analysed by immunoassay which in this case, probed for 90 potential biomarkers covering everything from neurotrophins to cytokines, immunoglobulins to more direct inflammatory markers (including C-reactive protein).Some fancy statistical modelling was applied to the obtained results - including Bayesian information criterion (BIC) - which eventually resulted in three models of best-fit based on findings from the bloodspots of those who went to be diagnosed with an autism spectrum disorder (ASD). The 'best model' of five compounds included some familiar names to this blog: glutathione-S-transferase (GST), IL-7, IL-5, TNF-beta and something called Lp(a) (lipoprotein a). Most were increased in quantity in the autism samples aside from GST which was decreased.There is a very nice illustration in the paper (Figure 3) showing how the potential connections between the biomarkers identified and some of the more biomedical themes of autism research might fit. So we have methionine metabolism mentioned (see here and here), oxidative stress (see here), gastrointestinal comorbidity (see here) and immune activation (see here) to name a few. It's all very systems biology.The authors caution that their results are preliminary and that although said biomarkers were modelled as being related to autism they "have not been confirmed to be causative with autism".Before I get too carried away with this research, there are a few issues worth mentioning. Yes, the sample size was small in this preliminary communication and indeed very little information is provided about participants outside of just them fulfilling the DSM-IV criteria for autism in terms of things like comorbidity. Also why out of 200 families such a small number of participants were eventually included for study.Indeed there is also an assumption from this study that a biomarker for autism is present in the neonatal phase which for example, might not take into account the issue of behavioural regression that seems to cover quite a percentage of cases.Whilst the identified best-fit biomarkers are of potentially real interest to autism research as per other similar studies (see here), it is the method and resources used in this paper which is the real 'big data' story allied to all those lovely -omics which reign supreme these days. Parents in many countries will be acquainted with that bloodspot taken during the earliest days of infancy to test for various inborn errors of metabolism such as phenylketonuria (PKU). Many people don't however give a second thought to what happens to those bloodspot cards, and how valuable a resource they might constitute. Although not usually in the business of crystal-ball gazing, I would hazard a guess that we are one day going to hear big news about the big data from those archived bloodspot cards; if not with autism in mind, then something else. ----------* Ayers JW. et al. Seasonality in seeking mental health information on Google. Am JPrev Med. April 2013.** Mizejewski GJ. et al. Newborn screening for autism: in search of candidate biomarkers. Biomark Med. 2013; 7: 247-260.*** Mizejewski GJ. Biomarker testing for suspected autism spectrum disorder in early childhood: is such testing now feasible? Biomark Med. 2012; 6: 503-506.**** Mizejewski GJ. Biological roles of alpha-fetoprotein during pregnancy and perinatal development. Exp Biol... Read more »
Mizejewski GJ, Lindau-Shepard B, & Pass KA. (2013) Newborn screening for autism: in search of candidate biomarkers. Biomarkers in medicine, 7(2), 247-60. PMID: 23547820
The carbon footprint from running shoes... Read more »
Cheah, L., Ciceri, N., Olivetti, E., Matsumura, S., Forterre, D., Roth, R., & Kirchain, R. (2013) Manufacturing-focused emissions reductions in footwear production. Journal of Cleaner Production, 18-29. DOI: 10.1016/j.jclepro.2012.11.037
Teasing out the insulin effect.
On the face of it, the study seems to come out of left field: A group of researchers claimed that marijuana smokers showed 16 per cent lower fasting insulin levels than non-smokers. The study, called “The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults,” is in press for The American Journal of Medicine. The authors are a diverse group of medical researchers from Harvard, Beth Israel Deaconess Medical Center, and the University of Nebraska College of Medicine. The study concluded: “We found that marijuana use was associated with lower levels of fasting insulin and HOMA-IR [a measure of insulin resistance], and smaller waist circumference.”
Of course, it was that last tidbit about waist circumference that was picked up by the media. “Why Pot Smokers Are Skinnier,” headlined the Atlantic. However, the important implications are not so much for weight control, or the discovery of some built-in offsetting mechanism for the marijuana munchies, but rather for insulin control and the treatment of diabetes.
But in a clinical study, remarkable observations require remarkable documentation. What does the research actually say?
There are problems with the study worth noting. While researchers took blood samples after a 9-hour fast to determine insulin and glucose levels, they relied on self-reporting for marijuana use data. And self-reporting for alcohol and drug use has its limitations as an investigative tool. Namely, lack of honesty. But let’s get beyond that for a moment: From a database of 4, 657 men and women who participated in the National Health and Nutrition Examination Survey, the researchers determined that 579 were current marijuana users, while 1, 975 were pot smokers in the past.
The marijuana-smoking cohort tended to be young males who also smoked cigarettes. After running everything through a series of complicated multivariable-adjusted models, marijuana came out associated with lower insulin levels, and “lower waist circumference” than those who reported never using marijuana. And the results didn’t change much after adjusting for BMI numbers and excluding participants who actually had diabetes. Furthermore, the association was strongest in current smokers, “suggesting that the impact of marijuana use on insulin and insulin resistance exists during periods of recent use.” (It should also be noted that other health habits can effect glucose and insulin activity, including cigarettes, alcohol, and lack of physical activity.)
The investigators don’t offer a solution to the increased appetite/decreased waistline conundrum they claim to have identified. “We did not find any significant associations between marijuana use, and triglyceride levels, systolic blood pressure, or diastolic blood pressure,” they concluded.
We know marijuana has a complicated relationship with appetite mechanisms, as evidence by its use with chemotherapy patients who need to eat. The theory is that the metabolic effects are mediated by a complex mix of cannabinoid type 1 and type 2 receptor interactions, since type 1 receptor antagonists like rimonabant improve insulin resistance in humans, and type 1 knockout mice also show resistance to diet-induced obesity.
Does marijuana smoking protect against diabetes? Wisely, the researchers don’t go that far, on the basis of this one uncontrolled study. The researchers’ conclusions neatly hedge the bets, suggesting that with recent trends in the direction of marijuana legalization, “physicians will increasingly encounter patients who use marijuana and should therefore be aware of the effects it can have on common disease processes, such as diabetes mellitus.”
As it happens, the findings aren’t entirely new. Anecdotal reports abound. Back in 2010, on the Diabetes Daily support board, there was a long discussion of marijuana’s effect on blood glucose levels in diabetics. And there are several mouse models showing the same effects. In a prepared statement, lead investigator Murray A. Mittleman of Beth Israel Deaconess Medical Center in Boston conceded that previous epidemiological studies have found “lower prevalence rates of obesity and diabetes mellitus in marijuana users compared to people who have never used marijuana, suggesting a relationship between cannabinoids and peripheral metabolic processes.” However, he believes that “ours is the first study to investigate the relationship between marijuana use and fasting insulin, glucose, and insulin resistance.”
Perhaps so. A 2011 study in the American Journal of Epidemiology concluded that “the prevalence of obesity is lower in cannabis users than in nonusers.” And the British Medical Journal featured a finding in 2012 by Los Angeles researchers that marijuana use was “independently associated with a lower prevalence of diabetes mellitus.” But the online patient guide for marijuana offered by Mayo Clinic says without equivocation that “cannabis may lower blood sugar. Caution is advised in patients with diabetes or hypoglycemia, and in those taking drugs, herbs, or supplements that affect blood sugar.” In fact, Mayo Clinic advises that patients may want to monitor their blood glucose levels if they smoke medical marijuana.
Regarding the current study, the editor-in-chief of the American Journal of Medicine said in a statement that there is a need for “a great deal more basic and clinical research into the short- and long-term effects of marijuana in a variety of clinical settings such as cancer, diabetes, and frailty of the elderly.” Editor Joseph S. Alpert also called on the National Institutes of Health (NIH) and the Drug Enforcement Administration (DEA) to collaborate in “developing policies to implement solid scientific investigations that would lead to information assisting physicians in the proper use and prescription of THC in its synthetic or herbal form.”
Penner E.A., Buettner H. & Mittleman M.A. (2013). The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults, The American Journal of Medicine, DOI: 10.1016/j.amjmed.2013.03.002
Photo Credit: http://www.herbalmission.org/
... Read more »
Penner Elizabeth A., Buettner Hannah, & Mittleman Murray A. (2013) The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults. The American Journal of Medicine. DOI: 10.1016/j.amjmed.2013.03.002
Take Home Message: High adherence to a neuromuscular injury prevention program like the FIFA 11 decreases the risk of injury.
Injury prevention programs typically are multifaceted warm-up programs that focus on neuromuscular recruitment. Although various programs aim to improve performance and decrease injury risk no investigation has shown a link between improved physical performance and the quality and adherence of neuromuscular injury prevention training. Therefore, Steffen and colleagues completed a cluster-randomized trial to assess the influence of player adherence and delivery method of the FIFA 11 injury prevention program (approximately 20 minutes, 15 exercises) on injury risk among females.... Read more »
Steffen K, Emery CA, Romiti M, Kang J, Bizzini M, Dvorak J, Finch CF, & Meeuwisse WH. (2013) High adherence to a neuromuscular injury prevention programme (FIFA 11 ) improves functional balance and reduces injury risk in Canadian youth female football players: a cluster randomised trial. British Journal of Sports Medicine. PMID: 23559666
Newly discovered papers have shed light on a fascinating episode in the history of neuroscience: Weighing brain activity with the balance The story of the early Italian neuroscientist Dr Angelo Mosso and his ‘human circulation balance’ is an old one – I remember reading about it as a student, in the introductory bit of a [...]... Read more »
Sandrone S, Bacigaluppi M, Galloni MR, Cappa SF, Moro A, Catani M, Filippi M, Monti MM, Perani D, & Martino G. (2013) Weighing brain activity with the balance: Angelo Mosso's original manuscripts come to light. Brain : a journal of neurology. PMID: 23687118
Last February, Dr. Sam Parnia, an intensive care physician who has been researching near-death experiences for the past 15 years, published his new book ‘Erasing death: The Science That is Rewriting the Boundaries Between Life and Death’. Following the release of that book, Dr. Parnia was interviewed on National Public Radio in the US. It wasn’t so much this interview that sparked my interest, as much as the comments that followed. “It’s hard to believe that this guy is actually a doctor based on the junk he presents here,” commenter ‘Joe MARTYN’ says. And another user, ‘Steven Kay’, adds: “Oh, please.. Not this guy again. Why not interview the last person who claims to have seen the Virgin Mary?”
To be fair, many other commenters did appreciate the interview and the work that Dr. Parnia had done. But still, the virulent dismissiveness related to this subject baffled me. Why is research on near-death experiences received with such hostility?... Read more »
van Lommel P, van Wees R, Meyers V, & Elfferich I. (2001) Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands. Lancet, 358(9298), 2039-45. PMID: 11755611
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
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
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
Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.
If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.
Research Blogging is powered by SMG Technology.
To learn more, visit seedmediagroup.com.