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  • June 23, 2014
  • 12:28 AM

The rainbow diet pills: there and back again

by Shelly Fan in Neurorexia

* This post contains spoilers for Requiem for a Dream. Last night I re-watched Requiem for a Dream, a Darren Aronofsky masterpiece that is perhaps...... Read more »

Cohen PA, Goday A, & Swann JP. (2012) The return of rainbow diet pills. American journal of public health, 102(9), 1676-86. PMID: 22813089  

  • June 22, 2014
  • 04:02 PM

Microbiome, Obesity and Diet

by Bernadeta Dadonaite in The Question Gene

How microbiome is linked to obesity in humans and how the diet can affect gut communities.... Read more »

Ridaura VK, Faith JJ, Rey FE, Cheng J, Duncan AE, Kau AL, Griffin NW, Lombard V, Henrissat B, Bain JR.... (2013) Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science (New York, N.Y.), 341(6150), 1241214. PMID: 24009397  

  • June 22, 2014
  • 02:01 PM

Solution to alcoholism? Get sober friends!

by DJMac in Recovery Review

A solution to alcoholism? If you want to live long and healthily, get loads of friends. That was the finding of a massive meta-analysis of around 150 studies involving over a third of a million people. Good social connections predict longevity. Dependent drinking shortens lives. Is the process of finding sober friends helpful as a solution [...]
The post Solution to alcoholism? Get sober friends! appeared first on Recovery Review.
... Read more »

Litt, M., Kadden, R., Kabela-Cormier, E., & Petry, N. (2007) Changing network support for drinking: Initial findings from the Network Support Project. Journal of Consulting and Clinical Psychology, 75(4), 542-555. DOI: 10.1037/0022-006X.75.4.542  

Litt, M., Kadden, R., Kabela-Cormier, E., & Petry, N. (2009) Changing network support for drinking: Network Support Project 2-year follow-up. Journal of Consulting and Clinical Psychology, 77(2), 229-242. DOI: 10.1037/a0015252  

  • June 22, 2014
  • 10:23 AM

The Love Song of Philo T. Farnsworth

by Gabriel in Lunatic Laboratories

Philo Farnsworth, if the name sounds vaguely familiar than you might just be a Futurama watcher. If you don't watch and know who I'm talking about or even better are a fan then, "YAY!" and for those of you who don't know, don't sweat it you're not alone. One of the forgotten greats, Farnsworth should be a household name, namely because one of his biggest inventions is in practically every home.... Read more »

The associated press. (2006) Elma Gardner Farnsworth, 98, Who Helped Husband Develop TV, Dies. The New York Times. info:/

Edwin Cartlidge. (2007) The Secrete way of Amateur Fusion. Physics World. info:/

  • June 21, 2014
  • 10:50 PM

Meta-analysing cytokine involvement in autism

by Paul Whiteley in Questioning Answers

A fairly brief post today to draw your attention to the "systematic review and meta-analysis" paper by Masi and colleagues [1] on all-things cytokine in relation to autism. They concluded that there was "strengthening evidence of an abnormal cytokine profile in ASD [autism spectrum disorder] where inflammatory signals dominate". I should point out that other authors have reached similar conclusions in previous reviews [2] and here also [3]."The herring does not fry here" @ Wikipedia In case you didn't know, cytokines are the chemical messengers of the immune system (see here) and perform various important tasks in relation to processes such as inflammation (see here). Autism research has a growing respect for the role of cytokines in quite a few cases of autism as per the growth in the amount of research literature available in this area (see here). I've covered quite a few papers focused on cytokines and autism on this blog (see here and see here for example) down the years.The Masi paper is an important one because it gathered quite a bit of the peer-reviewed research literature mentioning cytokines and autism together and for want of better words, 'statistically spat' out the sum total of the findings from the various studies. A couple of old friends "were significantly higher in the participants with ASD" compared with control populations including interleukin 1-beta (IL-1β), IL-6, interferon-gamma (IFNγ) and monocyte chemotactic protein-1 (MCP-1) potentially indicative of a more pro-inflammatory state. A general reduction in the levels of more 'anti-inflammatory' molecules such as transforming growth factor-beta 1 (TGF-β1) [4] added to proceedings.It's perhaps slightly unfair to say that these and other cytokines noted to be generally elevated in relation to autism are solely pro-inflammatory cytokines (i.e. inducing or maintaining inflammation) because that's not necessarily the way they always work. IL-6 for example, is now realised as being both a pro-inflammatory and anti-inflammatory molecule [5]. That being said, the growing recognition that inflammation and inflammatory processes may have some bearing on brain and behaviour (see here) ties in well with the Masi findings and where science perhaps needs to start looking with greater vigour if one is going to understand the interplay between immune function and psychiatry. As the authors note: "A better understanding of the inflammatory biology of ASD and possible associations with behavioral impairments and non-diagnostic features warrants further investigation and may have significant therapeutic implications". I can't argue with those sentiments, although as per the recent paper by Careaga and colleagues [6] how science goes about looking at that relationship is going to be important.Oh, and on the topic of MCP-1, the paper by Zerbo and colleagues [7] observing elevations in the levels of this cytokine in newborn blood spots from those subsequently diagnosed with autism is indeed timely... (and again reiterates the potentially usefulness of those drops of blood which many children give in their earliest days welcomed into the big, wide world).Music now. Daft Punk, and before Get Lucky, they were already Around the World.----------[1] Masi A. et al. Cytokine aberrations in autism spectrum disorder: a systematic review and meta-analysis. Molecular Psychiatry. 2014. June 17.[2] Goines PE. & Ashwood P. Cytokine dysregulation in autism spectrum disorders (ASD): possible role of the environment. Neurotoxicol Teratol. 2013 Mar-Apr;36:67-81.[3] Onore C. et al. The role of immune dysfunction in the pathophysiology of autism. Brain Behav Immun. 2012 Mar;26(3):383-92.[4] Qian L. et al. Potent anti-inflammatory and neuroprotective effects of TGF-beta1 are mediated through the inhibition of ERK and p47phox-Ser345 phosphorylation and translocation in microglia. J Immunol. 2008 Jul 1;181(1):660-8.[5] Scheller J. et al. The pro- and anti-inflammatory properties of the cytokine interleukin-6. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 2011; 1813: 878-888.[6] Careaga M. et al. Inflammatory profiles in the BTBR mouse: How relevant are they to Autism Spectrum Disorders? Brain Behav Immun. 2014 Jun 14. pii: S0889-1591(14)00171-8.[7] Zerbo O. et al. Neonatal cytokines and chemokines and risk of Autism Spectrum Disorder: the Early Markers for Autism (EMA) study: a case-control study. Journal of Neuroinflammation 2014, 11:113----------Masi, A., Quintana, D., Glozier, N., Lloyd, A., Hickie, I., & Guastella, A. (2014). Cytokine aberrations in autism spectrum disorder: a systematic review and meta-analysis Molecular Psychiatry DOI: 10.1038/mp.2014.59... Read more »

  • June 21, 2014
  • 01:00 PM

Global Warming doesn’t actually benefit Plants

by Gabriel in Lunatic Laboratories

Things are heating up. It’s no secret that the mercury is rising and we are to blame. Sure, there is a lot of uncertainty, for example how long we have […]... Read more »

  • June 20, 2014
  • 01:00 PM

Haters gonna… hate?

by Gabriel in Lunatic Laboratories

Haters gonna hate, unless you’ve been hiding under a rock since the internet has been born you’ve probably heard this phrase. Well now there is a new study that shows […]... Read more »

  • June 20, 2014
  • 12:07 PM

Maternal Smoking and Child Conduct Disorder Risk

by William Yates, M.D. in Brain Posts

Conduct disorder is a serious behavioral disorder of childhood characterized by aggression, destruction of property, lying, theft and violation of rules.A significant number of children with conduct disorder go on to adult antisocial personality disorder.Conduct disorder is known to have genetic as well as environmental risk factors.Darya Gaysina from the United Kingdom and colleagues recently published a review of maternal smoking during pregnancy and offspring conduct problems.This review examined three independent studies including:The Christchurch Health and Development StudyThe Early Growth and Development StudyThe Cardiff Invitro Fertilization Study These studies combined adoption study designs with biological children designs to examine risk for childhood disorders.  This allowed for comparison of results for children raised by genetically related and genetically unrelated mothers.Maternal smoking status in these studies was grouped into three categories, 0 cigarettes/day, 1-9 cigarettes per day and 10 or more cigarettes per day.Children were rated for conduct problems between the ages of four and seven years.The research design of these studies included controlling for important covariates including child gender, ethnicity, birth weight, maternal age at birth, breast feeding status, maternal education, socioeconomic status and parenting style.Across all the three studies similar findings and strength of associations were found. Maternal smoking increased risk of childhood conduct disorder with odds ratios estimated of between 2 and 4 fold.This effect was found for both the children raised by their biological mother and those adopted children raised by mothers who were not there biological mothers.This last finding helps disentangle maternal smoking effects from maternal child rearing effects and supports a specific link to environmental effects from maternal smoking. The limitations of these studies include difficulty sorting out potential effects of maternal smoking during pregnancy versus effects of passive smoking ("second-hand smoke") exposure. Additionally genetic risk for maternal smoking may overlap with genetic risk for conduct disorder.I have previously collaborated with Dr. Remi Cadoret in adoption study design research on aggression and conduct disorder. We found significant contributions of genetic factors to conduct disorder.Additionally, our research found a significant interaction between genetic and environmental risk. Children with genetic risk for conduct disorder experienced the most negative effect of adverse home environment, i.e. marital discord, divorce, parental mental health or substance abuse diagnoses.It would be interesting to evaluate whether exposure to maternal smoking is more adverse for children who also have a genetic risk for conduct disorder.Readers with more interest in this research can access the free full-text article by clicking on the PMID link in the reference below.Photo of sculpture from the Illumnia collection outside the CenturyLink Arena in Omaha, Nebraska is from the author's files. Sculpture is by the artist Matthew Placzek.Follow the author on Twitter at WRY999Gaysina D, Fergusson DM, Leve LD, Horwood J, Reiss D, Shaw DS, Elam KK, Natsuaki MN, Neiderhiser JM, & Harold GT (2013). Maternal smoking during pregnancy and offspring conduct problems: evidence from 3 independent genetically sensitive research designs. JAMA psychiatry, 70 (9), 956-63 PMID: 23884431 Cadoret RJ, Yates WR, Troughton E, Woodworth G, & Stewart MA (1995). Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Archives of general psychiatry, 52 (11), 916-24 PMID: 7487340... Read more »

  • June 20, 2014
  • 06:40 AM

Diabetes update: positive new facts and the role of genes

by Patrícia Fonseca Pedro in United Academics

Even though it is agreed that genetic inheritance is a very important factor, it is widely acknowledged, nowadays, that eating habits have a far more prominent role in Type 2 Diabetes’ development.... Read more »

  • June 20, 2014
  • 04:59 AM

Vitamin D and autism: same old story?

by Paul Whiteley in Questioning Answers

I have to say that I wasn't all that surprised when I read the conclusions to the study by Eva Kočovská and colleagues [1] (open-access here) talking about significantly lower levels of 25-Hydroxyvitamin D3 (25(OH)D3) levels detected in their small cohort of young adults diagnosed with an autism spectrum disorder (ASD) compared with various control populations.A deficiency or insufficiency of vitamin D - the sunshine vitamin/hormone - in relation to quite a few cases of autism is something that has been talked about more than once on this blog (see here). The value-added bit to the Kočovská findings was the suggestion that lower levels were detected "in young adolescents/adults with ASD" based in the Faroe Islands, where a lack of UVB exposure as a function of geographic position is to some extent compensated by "a diet rich in large oily fish containing vitamin D". I might add that this authorship group have talked vitamin D and autism in a previous paper [2].The Kočovská paper is open-access but a few pointers might be in order:Young adults with autism, "their siblings and parents, and.. a typically-developing comparison group in the Faroe Islands" were the target populations under study as part of a wider investigation on the prevalence of autism in the Faroe Islands [3]. Blood draws "for [the] analysis of various environmental factors" enabled researchers to assay for vitamin D - 25(OH)D3 serum concentrations - by the gold standard that is mass spectrometry. The assay was apparently conducted here in Blighty.Results: "The ASD group had significantly lower levels of 25(OH)D3 [median (IQR) = 24.8 (27.5) nmol/L] compared to the healthy comparison group [median (IQR) = 37.6 (32.3) nmol/L], (95 % CI 5.0–22.5), p = 0.002 to their siblings [median (IQR) = 46.1 (28.3) nmol/L] (95 % CI 9.4–24.8), and parents [median (IQR) = 46.7 (36.2) nmol/L) (95 % CI 11.0–27.74], (p < 0.001 in both instances)". Of all participants in the ASD group, only 1 person had a result falling into the sufficiency range (≥75 nmol/L) and that seemed to be an outlier described as a female: "her 25(OH)D3 level was much higher than all other participants’ at 153 nmol/L".Quite a few participants from across the various control groups included for analysis were vitamin D deficient (58-65%). But: "In the ASD group, 88 % were vitamin D deficient". Insofar as possible correlates, well, there was a "slight over-representation of spring births among the ASD group (32.5 %) and corresponding lowest level of vitamin D in this group". There was also a trend towards lower levels of vitamin D in males with ASD and their siblings. But diagnosis within the autism spectrum and scores on the ADOS showed no significant correlation.The authors are rightly cautious about drawing too many conclusions from their results as they stand. They talk about low vitamin D levels in cases of autism potentially being linked to issues like being a picky eater [4] or "autism impacting on a family/child’s lifestyle" as per a preference for more indoor activities rather than those more likely to provide some sun exposure (see here). Body mass index (BMI) is also talked about as a function of the growing interest in vitamin D levels in those who are categorised as overweight or obese [5] which is something that continues to crop up in the autism research literature (see here). We can't also rule out some effect from comorbidity - ESSENCE as one of the Kočovská authors has described it - particularly in light of other research starting to talk about ADHD (attention-deficit hyperactivity disorder) and vitamin D deficiency (see here) and what seems to be emerging about the heightened comorbid prevalence of autism and ADHD (see here). Same also goes for something like depression too (see here) and its links with at least some autism [6]. Plenty of variables which have the ability to influence the Kočovská results.But... on the back of previous studies indicating that vitamin D levels might be perturbed in some cases of autism I find myself similarly drawn to another conclusion reached by the authors: "the low vitamin D levels could be an indication of life-long vitamin D deficiency in ASD, and this hormone deficiency could, at least theoretically, have been involved in early aberrant development of the brain in these individuals, leading to the development of ASD". I say this acknowledging that Kočovská et al only looked at a single measurement of vitamin D and the evidence that maternal or cord blood levels of vitamin D don't seem to have much of an effect in this process as per the findings from Whitehouse and colleagues (discussed here) and some more recent work [7]. I don't think though anyone has actually tracked vitamin D levels across the child- and adulthood with autism in mind...I might also draw your attention to a few other areas where vitamin D deficiency in cases of autism might also merit additional research... stop me if you've heard me talk about these before. So: autoimmunity and vitamin D levels as per the Mostafa findings (see here). GcMAF and vitamin D as per the Hornig/Lipkin patent application (see here). And then there is leaky gut and vitamin D (see here) in light of another area with some autism interest (see here); all worthy of further research consideration alongside further examination of those vitamin D receptors which are currently lacking in the autism research literature.The news recently of "a remarkably consistent" relationship between "the lowest quintile of serum 25(OH)D concentration.. associated with increased all-cause and cardiovascular mortality" based on the findings from Schöttker and colleagues [8] (open-access here) is potentially pertinent. Without using scare tactics or anything like that, such findings should perhaps have special meaning in light of the Kočovská results and the news that over half o... Read more »

Kočovská E, Andorsdóttir G, Weihe P, Halling J, Fernell E, Stóra T, Biskupstø R, Gillberg IC, Shea R, Billstedt E.... (2014) Vitamin D in the General Population of Young Adults with Autism in the Faroe Islands. Journal of autism and developmental disorders. PMID: 24927807  

  • June 19, 2014
  • 01:00 PM

Warning: Serious Side Effects may be Overstated

by Gabriel in Lunatic Laboratories

Black box warnings, I’m all too familiar with them. A quick look in the medicine cabinet and you would see why. In fact I’m surprised the door shuts some days. […]... Read more »

  • June 19, 2014
  • 11:20 AM

Smoking and Abnormal Brain Pleasure Response

by William Yates, M.D. in Brain Posts

Smoking cessation in those with nicotine dependence is one of the most difficult challenges for patients and their clinicians.Research targeting the neurobiology of smoking cessation provides hope for designing more effective treatments for nicotine dependence.Takeshi Isomura along with colleagues in the U.S. and Japan recently summarized recent findings in the brain pleasure response in nicotine dependence.The brain ventral striatum region is known to be key in nearly all sensations of pleasure.Isomura and colleagues note research supports specific changes in reward response among nicotine dependent individuals.During the process of developing nicotine dependence, the brain reward circuitry develops an adaptive drug-related brain response to cues.In smokers, this adaptation produces abnormally elevated responses to smoking cues in the pleasure circuitry involving the ventral striatum, orbitofrontal cortex (OFC) and ventromedial prefrontal cortex (VMPFC). This sensitization or turbocharging of the brain's response to a specific drug cue contributes to the difficulty in discontinuing drug use.However, another phenomenon appears to be important to developing nicotine and drug dependence. This phenomenon is the adaptation of the brain's pleasure response to non-drug related stimuli.Brain imaging studies using fMRI in adolescents show the potential for smoking only a few cigarettes to modify the pleasure response.Research by Peters and his group demonstrated a reduction in ventral striatum response to a monetary incentive reward in adolescents who had smoked compared to adolescents who had not smoked. The reduction in pleasure response to non-drug cues was greatest in those who smoked regularly but could be demonstrated even in those who had smoked as few as 5 to 10 cigarettes in their lifetime.There are two possible explanations for this finding. Either lowered non-drug pleasure response increases risk for smoking or smoking reduces the responsivity of the ventral striatum.The Isomura notes that heightened pleasure response to nicotine and reduced pleasure response to other rewards may contribute to a cognitive distortion in smokers.This distortion produces cognition that something like "Smoking is my only source of pleasure and things that others enjoy, for example hobbies are not pleasurable for me" This type of cognitive distortion is substance abusers has been described by Aaron Beck and other pioneers in the cognitive behavioral treatment of addiction.Isomura notes the effect of even small numbers of cigarettes in adolescents is like the "Paradise Lost" phenomenon described with the fall of Adam and Eve. Their analogy posits teenagers who begin smoking find lost pleasure (paradise) in typically pleasurable activities.  Like Adam and Eve, once the forbidden apple is is consumed, it is impossible for the teenage smoker to return to the Garden of Eden present before smoking.Smoking cessation treatments may need to focus more on re-establishing non-nicotine reward responses. This type of intervention, may provide greater chances for combating the addictive brain response to nicotine.Readers with more interest in this topic can find the free full-text manuscript by clicking on the link in the Isomura reference below.Photo of sculptures outside CenturyLink arena in Omaha, Nebraska is from the author's files.Follow the author on Twitter WRY999Isomura T, Suzuki J, & Murai T (2014). Paradise Lost: The relationships between neurological and psychological changes in nicotine-dependent patients. Addiction research & theory, 22 (2), 158-165 PMID: 24719610Peters J, Bromberg U, Schneider S, Brassen S, Menz M, Banaschewski T, Conrod PJ, Flor H, Gallinat J, Garavan H, Heinz A, Itterman B, Lathrop M, Martinot JL, Paus T, Poline JB, Robbins TW, Rietschel M, Smolka M, Ströhle A, Struve M, Loth E, Schumann G, Büchel C, & IMAGEN Consortium (2011). Lower ventral striatal activation during reward anticipation in adolescent smokers. The American journal of psychiatry, 168 (5), 540-9 PMID: 21362742... Read more »

Peters J, Bromberg U, Schneider S, Brassen S, Menz M, Banaschewski T, Conrod PJ, Flor H, Gallinat J, Garavan H.... (2011) Lower ventral striatal activation during reward anticipation in adolescent smokers. The American journal of psychiatry, 168(5), 540-9. PMID: 21362742  

  • June 19, 2014
  • 08:30 AM

Can Mindfulness Help You Shed Pounds?

by Pranita Sohony in Workout Trends

It is 8.30 in the morning. I have 12 Unread Mails, 5 files on my desk, 3 meetings to attend, 1 cheese wrap in my hand, and ‘Zero’ attention to what I am eating! How familiar is this story? Isn’t that your story at office every morning? Do you even remember what you had for […]
The post Can Mindfulness Help You Shed Pounds? appeared first on .
... Read more »

Framson, C., Kristal, A., Schenk, J., Littman, A., Zeliadt, S., & Benitez, D. (2009) Development and Validation of the Mindful Eating Questionnaire. Journal of the American Dietetic Association, 109(8), 1439-1444. DOI: 10.1016/j.jada.2009.05.006  

  • June 19, 2014
  • 04:26 AM

More suramin and autism [mouse] findings

by Paul Whiteley in Questioning Answers

The headline: 'Century-old drug reverses signs of autism in mice' brought the paper by Jane Naviaux and colleagues [1] (open-access) to my attention and some slightly familiar work (see here) on the use of suramin in a mouse model of autism, or rather a mouse model of maternal immune activation. Indeed, I seem to remember that the previous study by this group [2] courted similar publicity, with some familiar headlines...Not lecturing... @ Wikipedia The latest offering from Naviaux et al is not so dissimilar from their previous work on that mouse model of autism, this time testing "the hypothesis that the behavioral manifestations of the MIA [maternal immune activation] model are a consequence of pathological persistence of the evolutionarily conserved CDR [cell danger response]... and that the CDR is maintained by dysregulated purine metabolism and secondary abnormalities in purinergic signaling". The press release about the study can be viewed here.What this all translates into is that a state of immune arousal above and beyond what would be typically expected during pregnancy is somehow impacting on offspring development pertinent to an elevated risk of conditions like autism or schizophrenia. There is quite a bit of literature on this topic from the autism perspective (see here) and based on animal models other than just rodents (see here). The cell danger response (CDR) described by Naviaux (Robert that is) [3] represents "the evolutionarily conserved metabolic response that protects cells and hosts from harm". Indeed that last reference [3] contains just about every biological link known to autism science at the current time... including mitochondria. The idea is that triggering immune activation activates "a conserved cellular response to stress" called the CDR and the proposed master regulator of the CDR is purinergic signalling [4] - "purine nucleotides and nucleosides as extracellular messengers". ATP (adenosine triphosphate) as well as being quite an important molecular fuel source, is suggested to be one of the nucleotides which "can bind to cell surface receptors and act as signaling molecules and neuromodulators that are important in inflammation.. neurotransmission.. and many other biological processes".A few basic points about the Naviaux study:Mice were the lucky volunteers for this study, and again the 'good breeder' that is the C57BL/6J variety. As per their previous trial, pregnant female mice were given something to artificially stimulate their immune system and "initiate the MIA model" or a saline control and then their offspring were the study focus.Suramin or saline (as a control) was then administered to 6-month old offspring mice and thereafter "behaviors were evaluated". Suramin levels were also examined, as were a broad range of metabolites as part of some metabolomic analysis based on the use of triple quad mass spectrometry.Results: "MIA animals showed social deficits from an early age". Nothing too novel there bearing in mind previous observations in this area of research. But... "Single-dose APT [antipurinergic therapy] with suramin completely reversed the social abnormalities in 6.5-month-old adults". Social behaviour by the way, was quantified as "time spent interacting with a novel ("stranger") mouse".The benefit of suramin also lasted for quite a while: "a small residual benefit to social behavior was still detectable" even after 5 weeks following the intervention. There is some discussion by the authors about this effect; noted to be potentially "due to the development of metabolic memory and/or somatic epigenetic DNA changes that lasted longer than the physical presence of the drug".Then the biochemistry. Suramin seemed to by-pass that very important gateway, the blood-brain barrier (BBB) and end up in the brainstem following some analysis of sacrificed offspring mice: "consistent with the notion that nuclei in brainstem, or their projection targets in distant sites of the brain, may mediate the dramatic behavioral effects of acute and chronic APT in this model".And more: "Comprehensive metabolomic analysis revealed disturbances in several other metabolic pathways relevant to children with ASDs. These included disturbances in microbiome, phospholipid, cholesterol/sterol, sphingolipid, glycolytic and bile salt metabolism". This bearing in mind that only "male animals that had been behaviorally evaluated were tested". Purine metabolism and the gut microbiome seemed to be quite important to the author's results. At this point I'll refer you back to the work by Elaine Hsiao and colleagues... Moreover: "The top, non-microbiome-associated metabolite was quinolinic acid... which was decreased in the MIA model". Quinolinic acid implies the involvement of one of those aromatic amino acids, tryptophan, which is an autism research favourite [5]. More than that is the literature on the intersecting kynurenine pathway and how that might relate to a condition like schizophrenia (see here).The authors caution that their results are (a) mouse based and (b) "suramin is a poor drug choice for chronic use because of potentially toxic side effects that can occur with prolonged treatment". That being said, they do suggest that "new drugs might be given only once, or intermittently, during sensitive windows to unblock metabolism, restore more normal neural network function, improve resilience and plasticity, and permit improved development in response to behavioral and interdisciplinary therapies, and to natural play". Just in case you'd like an alternative reading of this study, have a look at this write-up too.I do apologise for all the quotes taken from the Naviaux paper and used in this post, but when the authors say it better than I could, why would I try and complicate things any further? Indeed, the more I read the paper by Naviaux and colleagues, the more I see what a potential gem it actually is. I say this based on the pretty comprehensive way that the authors went about looking at the MIA model and the effec... Read more »

  • June 19, 2014
  • 12:30 AM

Join The Thrill, Lift The FIFA World Cup Together !

by Shyamali Sharma in Workout Trends

A spoiled weekend… My friend asked me to come over to her place last weekend and texted me, “ I am all alone and bored to death, please come over!” It was already half past eight in the evening but I decided to go. On my way to her place, my idea of chilling was […]
The post Join The Thrill, Lift The FIFA World Cup Together ! appeared first on .
... Read more »

  • June 18, 2014
  • 11:22 PM

Cancer Vaccine

by Viputheshwar Sitaraman in Draw Science

Finally, a possible vaccine for cancer.... Read more »

Yukai He,, Yuan Hong,, Yibing Peng,, Lisa Butterfield,, Sheng Guo,, David Bartlett,, David Munn1,, Jose Guevara-Patino,, Junfeng Pang,, & Nahid Mivechi,. (2014) Engineering AFP and GPC3 to create highly immunogenic gene vaccines to prevent carcinogen-induced murine autochthonous hepatocellular carcinoma. The Journal of Immunology, 192(1). info:/

  • June 18, 2014
  • 01:00 PM

New and Exciting discoveries about Autism

by Gabriel in Lunatic Laboratories

Vaccines don’t cause autism. One more time, all together now, vaccines do not cause autism. Thankfully science understands that and is moving in on the actual cause for it. A combination […]... Read more »

  • June 18, 2014
  • 09:38 AM

Video Tip of the Week: e-PathGen, Using Genomics to Support Public Health

by Mary in OpenHelix

Recently I saw the Director of Public Health Genomics for the CDC tweet about a resource that was new to me, ePathGen, Pathogen Genomics for Epidemiology. This is an area that I’m glad to see getting attention. My undergrad degree was in microbiology, and certainly the most memorable class I had in college was about pathogenic […]... Read more »

  • June 18, 2014
  • 06:03 AM

Anti-Aging With Oxygen Instead Of Antioxidants

by Gunnar de Winter in United Academics

There have been previous hints that metformin slows down the aging process. The main players, it seems, are oxygen particles. But wait, what about the whole fuss about antioxidants?... Read more »

De Haes W, Frooninckx L, Van Assche R, Smolders A, Depuydt G, Billen J, Braeckman BP, Schoofs L, & Temmerman L. (2014) Metformin promotes lifespan through mitohormesis via the peroxiredoxin PRDX-2. Proceedings of the National Academy of Sciences of the United States of America. PMID: 24889636  

  • June 18, 2014
  • 04:37 AM

The developmental regression rate and autism

by Paul Whiteley in Questioning Answers

I have already made mention of the paper by Robin Goin-Kochel and colleagues [1] in a previous post on the topic of developmental regression and autism (see here). On that occasion it was to substantiate that approximately 40% of children diagnosed as being on the autism spectrum were reported to have shown some kind of developmental regression as part and parcel of their presentation. Given however the assertion in the Goin-Kochel paper about using "the largest, most comprehensively phenotyped sample to date" reflecting their participant numbers (N=2105) derived from the Simons Simpex Collection (SSC), I thought it worthwhile to include a separate blog entry for this important paper.I'm pretty sure that the topic of developmental regression and autism needs no further introduction. Suffice to say that as the name suggests, it's all about a loss of previously acquired skills and how this might map on to some of those 'autisms' that I seem to talk about quite a lot. After a bit of a laboured start (see here) there is now a general acceptance that regression can occur in cases of autism and sometimes pretty rapidly (see here) although I hasten to add, not seemingly present for everyone with autism.I have to thank Natasa for passing me a full-text copy of the Goin-Kochel paper, and without further ado, here are a few of the main points:The SSC was the source for participants, which meant that diagnoses of autism or autism spectrum disorder (ASD) were about as reliable as one could hope for. Interestingly, the authors do make mention of the whole DSM-IV to DSM-5 transition and what that might mean for databases such as the SSC but that's perhaps fodder for another day."Regression was operationalized using the skill-loss items from both the ADI-R and a supplemental interview that captured information about additional and more subtle skill losses". I've talked before about how ADI-R was a really important contributor to raising the profile of regression and autism as a function of it including items about 'loss of language/other skills'. In this case, researchers defined various types of 'loss' to include codings such as 'full losses' and 'subthreshold losses'. They also analysed data according to "skill loss at/before 36 months and those who experienced skill loss after 36 months".Results: "Overall, 36.9% of children had some type of regression". Such regression included a regression in language and/or other skills and included those with full losses and those with subthreshold losses. Another quote: "When combined, 585 (27.8%) children experienced some degree of language loss and 568 (27.0%) experienced some degree of other loss".The authors focused quite a lot on the pre-36 months loss side of things as a function of quite a lot of discussion on age of first parental concern being rooted in that critical period. So: "those with any degree of language loss (full or subthreshold) at/before 36 months scored significantly lower than those with no language loss" when looking at how regression might affect "cognitive and adaptive-functioning outcomes". Finally, a couple of other important details to mention: (a) "subthreshold losses of other skills occurred later than any type of language regression and later than full losses of other skills", and (b) duration of loss of skills is also discussed: "most children regained their skills by 3.5-5 years of age". They conclude that their study: "lends support to the argument that children whose parents report regression represent a distinct ASD subtype that may be associated with lower cognitive functioning".The participant group size and the use of the SSC are important features which make these results something to shout about. Alongside the meta-analysis by Barger and colleagues [2] autism research is beginning to build up quite a good picture on the rate of regression being reported in the autism research literature and some details on presentation and even outcome.That being said, there is still an awful lot more to do in this area. The Goin-Kochel did not set out to look at "etiological mechanisms" but the next stage in this research should surely be further study which looks at possible correlates to such regressive accounts. I wouldn't necessarily agree with the sentiments of the authors when they say: "An acknowledged limitation of this study is its reliance on parent-report data" especially when it comes to parent report and other issues such as gastrointestinal (GI) problems (see here) and the conclusions reached by Phillip Gorrindo and colleagues [3] (open-access here). Recall may well be affected by things like telescoping effects (see here) but in these days of home movies [4] and the rise of social media, many infants see the end of camera lens very, very early following their entry into the big wide world. Where regression occurs, I'm sure many parents would have their own ideas about the hows and whys which could be investigated including some slightly more biological / genetic based investigations [5].I've two more points to make on this study and research area and that's all. First is an issue which the authors touch upon in their discussion of their results: "... the SSC is largely comprised of Caucasian families". The recent abstract from Adiaha Spinks-Franklin and colleagues (which, at the time of writing, I don't yet think is published in a peer-reviewed form) hints at some racial differences in the occurrence of regression in autism. The question is whether this might also translate into a different pattern of regressive symptoms and indeed, any different effects on longer term outcome?Second is that issue of long-term outcome. As we're starting to see with the optimal outcome work (see here), longitudinal studies looking at outcome from all those developmental trajectories which make up the autisms is starting to yield some interesting results. The next question would be whether similar studies looking at regressive vs. non-regressive presentation (even different types of regression [6]) would similarly provide important data on the extent to which regression might affect future development and presentation and ways these could be positively affected. I'd also add that looking at any effects from regression on comorbidity outside of the core dyad of symptoms might also be included in any future work knowing what we (think we) know about this important issue.To close, Katy Perry and Last Friday Night (a song my brood are really enjoying at the moment).----------[1] Goin-Kochel RP. et al. Developmental regression among ... Read more »

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