The Kallmann syndrome should be Maestre syndrome (or MSJJ)

Few of the Generation X people are unfamiliar with the super-hit/movie cult Twin Peaks. And from those, even fewer find the dwarf dancing in the Red Room not scary as hell. And yet even fewer know who the man singing “Sycamore Trees” in that room is. For memory refreshment, here is the clip.

The man with the unusual voice, to match all the rest of the… um… “unusualness”, is none other than Jimmy Scott, a phenomenal jazz singer. If you listen to him, particularly in the hit “I’m Afraid The Masquerade Is Over“, you’ll notice that, if you close your eyes, you might be confused on whether the voice belongs to an adult man or a very gifted prepubertal boy.

And that is because Jimmy Scott suffered his entire life from a rare and obscure disease, called the “Kallmann syndrome”. This is a genetic disorder that prevents a person to start or to fully complete puberty. And that is because they have low circulating sex hormones: testosterone in males and estrogen and progesterone in females. And that is because their hypothalamus does not produce enough or at the proper times gonadotropin-releasing hormone (GnRH). And that is because sometime during the first trimester of pregnancy, there was an abnormality in the development of the olfactory fibers. You might ask what does smell development has with sex hormones? Well, I’m glad you asked. The cells that will end up releasing GnRH during puberty need to migrate from where they are born (nasal epithelium) to hypothalamus. If something impedes said migration, like, say, a mass, then the cells cannot reach their destination and you get a person who cannot start or finish puberty, plus a few other symptoms (Teixeira et al., 2010).

As some of you might have already surmised, something else besides lack of puberty must happen to these people regarding their sense of smell. After all, their olfactory fibers got tangled during embryonic development, forming, probably, a benign tumor, a neuroma. Not surprisingly, the person ends up with severely diminished or absent sense of smell, information that can be clinically used for diagnosis (Yu et al., 2022).

The first one to notice that people with failure to start or fully complete puberty are also anosmic was Aureliano Maestre de San Juan, a Spanish scientist. Unfortunately, the syndrome he documented in 1856 was named not named after him, but after the German scientist Franz Joseph Kallmann who described it almost a century later, in 1944 (Martin et al., 2011). Kallmann not only he did not discover the syndrome himself, but he was a staunch supporter of “racial hygiene”, advocating for finding and sterilizing relatives of people with schizophrenia so to eradicate the disease from future generations. Ironically, he fled Germany in 1939 because he was of Jewish heritage into a country which enthusiastically embraced eugenics and performed their own sterilizations programs, the USA (Benbassat, 2016).

So, I hereby propose, in an obscure unvisited corner of the Internet, to rename the disease the Maestre syndrome or MSJJ, after the guy who actually noticed it the first time and published about it. Besides, it’s his birthday today, having been born on October 17, 1828.

REFERENCES (in order of appearance):

Yu B, Chen K, Mao J, Hou B, You H, Wang X, Nie M,Huang Q, Zhang R, Zhu Y, Sun B, Feng F, Zhou W, & Wu X (2022, Sep 22).The diagnostic value of the olfactory evaluation for congenital hypogonadotropic hypogonadism. Frontiers in Endocrinology (Lausanne). 2022; 13: 909623. doi: 10.3389/fendo.2022.909623, PMCID: PMC9523726, PMID: 36187095. ARTICLE | FREE FULLTEXT PDF

Teixeira L, Guimiot F, Dodé C, Fallet-Bianco C, Millar RP, Delezoide A-L, & Hardelin J-P (2010, Oct 1, Published online 2010 Sep 13). Defective migration of neuroendocrine GnRH cells in human arrhinencephalic conditions. Journal of Clinical Investigation, 120(10): 3668–3672. doi: 10.1172/JCI43699, PMCID: PMC2947242, PMID: 20940512. ARTICLE | FREE FULLTEXT PDF

Benbassat, CA (2016, Published online 2016 Apr 19). Kallmann Syndrome: Eugenics and the Man behind the Eponym. Rambam Maimonides Medical Journal, 7(2): e0015. doi: 10.5041/RMMJ.10242, PMCID: PMC4839542, PMID: 27101217. ARTICLE | FREE FULLTEXT ARTICLE

Martin C, Balasubramanian R, Dwyer AA, Au MG, Sidis Y, Kaiser UB, Seminara SB, Pitteloud N,  Zhou Q-Y, & Crowley, Jr WF (2011, Published online 2010 Oct 29). The Role of the Prokineticin 2 Pathway in Human Reproduction: Evidence from the Study of Human and Murine Gene Mutations. Endocrine Reviews, 32(2): 225–246. doi: 10.1210/er.2010-0007, PMCID: PMC3365793, PMID: 21037178. ARTICLE | FREE FULLTEXT PDF

Original references which I couldn’t find, as they appear in Martin et al. (2011):

Maestre de San Juan A. (1856). Teratologia: Falta total de los nervios olfactorios con anosmia en un individuo en quien existia una atrofia congénita de los testículos y miembro viril. Siglo Medico, 3:211–221 [Google Scholar]

Kallmann F, Schoenfeld W & Barrera S (1944). The genetic aspects of primary eunuchoidism. Am J Ment Defic, 48:203–236 [Google Scholar]

By Neuronicus, 17 October 2022

Masks work against COVID

I want to share an observation that’s been on my mind for a while. I was visiting a Zoo with my family before the vaccine was available for regular people, around early Spring 2021. A big Zoo. All the enclosures where animals were indoors (penguins, monkeys and so on) had a big sticker on the door asking to “Please wear a mask for our animals’ sake. They too can get COVID19”. An overwhelming majority were putting on their masks upon reading this sign. Really, close to 99% of people, adults and children alike. At the same zoo, the same people were entering maskless in the Gift Shop and other indoor facilities like toilets and so on. I eyeballed less than 10% were wearing masks in “human enclosures”. I spent a lot of time at this Zoo watching for this behavior instead of looking at the other animals to make sure I’m not imagining things.

My lesson: humans are not deemed worthy the masking trouble, but zoo animals are… Now please explain to me how no mask-wearing is about “freedom”, “COVID is a scam/flu/doesn’t exist”, “masks don’t work” and so on and not about a conscious moral choice to knowingly endanger other people and their kids?

By Neuronicus, 17 August 2021

EDIT: Mrs. Clinton’s first name is Hillary, not Hilary.

REFERENCES:

Howard J, Huang A, Li Z, Tufekci Z, Zdimal V, van der Westhuizen HM, von Delft A, Price A, Fridman L, Tang LH, Tang V, Watson GL, Bax CE, Shaikh R, Questier F, Hernandez D, Chu LF, Ramirez CM, Rimoin AW. (26 Jan 2021). An evidence review of face masks against COVID-19. Proceeding of the National Academy of Sciences of the USA, 118(4):e2014564118. doi: 10.1073/pnas.2014564118. PMID: 33431650. ARTICLE | FREE FULLTEXT PDF P.S. Since this paper was published, dozens of others have been published that say the same thing: wear a mask for all our sakes.

Kahane LH (5 Jan 2021). Politicizing the Mask: Political, Economic and Demographic Factors Affecting Mask Wearing Behavior in the USA. Eastern economic journal, 1-21. doi: 10.1057/s41302-020-00186-0, PMCID: PMC7783295, PMID: 33424048. ARTICLE | FREE FULLTEXT PDF

Air pollution and mortality

The authors used a chemical transport model called GEOS-Chem to estimate the global exposure levels to airborne particulate matter derived from fossil fuel combustion. It’s a worldwide used model for estimating dispersion, for example the simulation of surface pollination. The model has been validated, meaning its predictions were compared with the reality and they matched. Levels of fossil fuels emission were inputted from publicly available data “from multiple sectors (power generation, industry, ships, aircraft, ground transportation, backup generators, kerosene, oil/gas extraction), detailed oxidant-aerosol chemistry, and reanalysis meteorology from the NASA Global Modeling and Assimilation Office” (page 5 of the manuscript). The mortality due to air pollution was computed by starting with the classical risk assessment analysis from epidemiological research and then adjusting for other variables like in-door particulate exposure (smoking) and so on. It sounds straightforward enough but the math and stats involved are very complicated. You have to take into consideration concentration, exposure time, and other factors that affect the outcome.

In addition, the authors calculated the mortality caused by fossil-fuel air pollution in children between 0 and 4 years of age, which was 876 in North America, 747 in South America, and 605 in Europe, annually. Pollution data is from 2012, mortality from 2015. The authors are hopeful that aggressive regulation designed to curb emissions in the last few years may have already lowered these numbers. Policy-makers, take note!

REFERENCE: Vohra K, Vodonos A, Schwartz J, Marais EA, Sulprizio MP, & Mickley LJ (Apr 2021, Epub 9 Feb 2021). Global mortality from outdoor fine particle pollution generated by fossil fuel combustion: Results from GEOS-Chem. Environmental Research, Volume 195, 110754. PMID: 33577774, DOI: 10.1016/j.envres.2021.110754, ARTICLE.

By Neuronicus, 11 March 2021

Penis Size

For whoever needs to be reassured…

L is for length and W is for… circumference. I could have corrected the pic, but it generated far more interesting comments as it is on social media.

REFERENCE: Veale D, Miles S, Bramley S, Muir G., & Hodsoll J (Jun 2015).  Am I normal? A systematic review and construction of nomograms for flaccid and erect penis length and circumference in up to 15 521 men. British Journal of Urology International, 115(6):978-986. PMID: 25487360, DOI: 10.1111/bju.13010. ARTICLE | FREE FULLTEXT PDF | Editorial | Science cover

By Neuronicus, 11 November, 2020

People with mild COVID-19 symptoms can STILL develop serious and long lasting brain damage

Some meme is circulating around saying that for any 1 dead of COVID-19 there is an x amount of people who survive but experience vastly debilitating and sometimes life long lasting diseases. That x number is usually a subject of controversy based on little or confusing hearsay-type of information. The believers in the x number use it to argue that mask-wearing and healthier behaviors literally save lives of people, while the non-believers in the x number, well… they just don’t believe the x number exists at all and that’s that. Either you die of COVID-19 or you survive and make a full recovery. I prefer to think that this is the case instead of the unfortunately way more probable, callous, cruel and dehumanizing “x exists and so what, I’m ok with people dying, ‘cause people die all the time, as long as it’s not me”.

The x number exists all right. Paterson et al. (2020) just published a paper last week (July 8th) that puts some numbers in the place of x, at least when it concerns neurological disorders. Because I have heard all sorts of “excuses” like, yeah, but those people who had it bad were old, had previous medical conditions, were black or poor or [insert your favorite post-hoc rationalization here], I decided to comb through the paper’s supplementals and give you a bit more of the background of the people investigated in this article.

If you’re not interested, you can skip the following section and go directly to the conclusion as long as you get the take-home message: many people of all sorts of ages and races, with no previous medical conditions and with mild COVID-19 symptoms can still have life long seriously debilitating neurological conditions. How many, you ask? I’m eyeballing almost a half of the investigated patients in this paper were not “at risk” in any way.

So. We have 43 patients treated from April 9 to May 15, 2020, in UK, out of which:

• 29 were SARS-CoV-2 PCR positive and definite, meaning a PCR test.
• 8 were probable meaning “clinical and laboratory features highly suggestive of COVID-19—lymphopenia, raised D-dimer, suggestive chest radiology in the absence of PCR evidence” p. 6
• 6 were possible in whom “temporal or laboratory features indicate an association but another cause was also found” p. 6

Demographics: 24 males and 19 females with ages ranging from 16–85 years, 53% were non-white.

Symptoms were classified as:

• Mild (non-pneumonia or mild pneumonia)
• Severe (dyspnoea and hypoxia requiring supplementary oxygen)
• Critical (respiratory failure requiring assisted ventilation, septic shock, and/or multi-organ dysfunction)

Out of these patients:

10 had encephalopathies (delirium and psychosis).

• Survival: all 10 are alive
• Age: 39-72 years old
• Both females and males, both whites and non-whites
• Hospital admission reason: 6 neurological, 1 respiratory, 3 both
• Past medical history : 4 none, 3 hypertension, 2 cancer, 1 stroke, 2 diabetes, 1 asthma
• Days of onset of encephalopathies from onset of COVID-19 symptoms: -4 to 21
• Severity of COVID-19 symptoms: 6 mild, 2 severe, 2 critical
• Diagnosis: 8 definite, 2 probable COVID-19
• Recovery: 7 complete, 1 incomplete, 1 significant, 1 not recovered.
• Survival: all 10 are alive

Vignette A: As a note for people who think a bit of delirium is not a big deal, let’s peak at a case that the authors describe in the paper for representative reasons. A 55-year old White woman with no previous medical or psychiatric conditions was admitted to hospital with mild to severe COVID-19 symptoms and a positive SARS-CoV2 test. She stayed in the hospital for 3 days, requiring minimal oxygen. But after discharge, the woman started behaving oddly, confused, agitated, putting on and off her coat repeatedly, hallucinated lions and monkeys in the house, other auditory hallucinations, had persecutory delusion, Capgras delusion (husband replaced by impostor), and became aggressive and combative with family and hospital staff. This started 17 days after her fist COVID-19 symptoms which were fever, cough, aches and loss of smell and taste. Normal brain MRI and EEG.  She was put on serious antipsychotics with an on-off improvement result. She’s classified as significantly recovered.

12 patients had neuroinflammatory syndromes (encephalitis) post-COVID

• Age: 27-60  
• Hospital admission reason: 6 neurological, 1 respiratory, 3 both
• Both females and males, both whites and non-whites
• Days of onset of syndrome from onset of COVID-19 symptoms: -6 to 27
• Severity of COVID-19 symptoms: 6 mild, 2 severe, 2 critical
• Diagnosis: 8 definite, 3 probable, 1 possible
• Past medical history: 3 none, 3 diabetes, 2 asthma, 3 hypertension, 2 arthritis, 1 hypothyroidism, 1 treated breast cancer with high cholesterol and other diseases and this is the one who died.
• Severity of COVID-19 symptoms: 6 mild, 2 severe, 4 critical
• Recovery:  1 complete, 10 incomplete, 1 died
• Survival: 11 alive, 1 dead (which had mild symptoms)

Vignette B: A 65-year-old Black female with osteoarthritis and a 2-year history of cognitive decline was admitted for involuntary right hand and then widespread involuntary movements. Then she developed complex visual hallucinations (people in the house, objects flying in the room), vision impairments including double vision, speaking impairments, disorientation and confusion, shaking, remarkable twitching and hyper reflexes. “MRI brain, EEG and CSF examination were normal” p. 12. She had a positive SARS-CoV2 test and severe COVID-19 symptoms, meaning she required oxygen therapy. Given medicines for muscle spasms and oxygen for COVID-19. She’s classified as incomplete recovery.

Vignette C: A 52-year-old Asian male with asthma presented with 10 days of cough, difficulty breathing and muscle aches. The SARS-CoV2 test was positive. His oxygen supply was getting worse and he required intubation for 17 days, meaning now his symptoms are considered critical. He was slow to wake up from intubation. MRI showed significant lesions and cysts with white matter damage and haemorrhage. He has a severely impaired conscious level responding to pain only. He’s classified as incomplete recovery.

Vignette D: A 47 year old female of Other ethnicity with asthma as a previous medical condition presented neurological symptoms: left side numbness and weakness, with headache, vomiting and reduced conscious level. Prior to this, for a week she had cough, fever and shortness of breath. All other markers and symptoms (minus neurological) pointed to COVID-19 but no PCR test was administered. Because she had low conscious level she was incubated, thus her COVID-19 symptoms are catalogued as severe, even if the reason of intubation was not low oxygen. MRI showed severe brain and brain blood vessels swelling. Was aggressively treated for brain swelling. After 2 days of this treatment when she was not responding and when she developed fixed dilated right pupil, emergency surgery was performed to remove part of her skull to release intracranial pressure from all the swelling. After 4 more days of intubation she was de-intubated and “continues to improve clinically, and is able to weight bear with support” p. 10. She’s classified as incomplete recovery.

Vignette E: A 52 year-old White male with no past medical history presented with progressive limb weakness, headache, vomiting, and back pain that lasted for the past 3 days. MRI showed multiple lesions in the brain. Over 5 days, these lesions increased in size and there were multiple bleeding sites in the brain. He was positive for SARS-CoV2 and 3 days later developed fever and shortness of breath. About the same time his neurological symptoms increased in severity and number. A nerve conduction test supported a diagnosis of Guillain–Barré syndrome (a nasty autoimmune disease in which your immune system eats your nerves). He was intubated due to oxygen requirements. Three days after corticosteroid treatment he was able to open eyes and mouth words and after 2 weeks, he was able to talk and flex both arms. He’s classified as incomplete recovery. He’s still in the hospital.

8 patients had strokes post-COVID

• Age: 24 -85 
• Both females and males, both whites and non-whites.
• Days of onset of syndrome from onset of COVID-19 symptoms: -2 to 15.
• Severity of COVID-19 symptoms: 6 mild, 2 severe, 2 critical
• Diagnosis: 6 definite, 2 probable
• Reason for hospital admission: 5 neurological, 3 respiratory
• Past medical history: 2 none, 2 with hypertension, 1 with stroke, 1 obese, 2 heart disease (1 of them is the one who died) and others
• Severity of COVID-19 symptoms: 5 mild, 3 severe
• Recovery:  1 complete, 3 incomplete, 1 no improvement (3 still in the hospital)
• Survival: 7 alive, 1 dead (of the ones with severe symptoms)

Vignette F: A 58-year-old Black male with only arthritis of the spine as a pre-existing condition came to the hospital with difficulty in speaking and weakness on the right side after 2 days of coughing and being tired. He had a high-risk occupation for getting COVID-19 and all other COVID-19 signs and symptoms were there minus a COVID-19 test. So he is thought to be probably carrying it. Brain CT showed a stroke. Treated with heparin for a lung blood clot and other anti-blood clot medicines for the stroke. On day 8 he was discharged to the Rehabilitation unit of the hospital.  

7 patients developed Guillain–Barré syndrome (GBS) post-COVID

• Age: 20-63
• All males, both whites and non-whites.
• Days of onset of syndrome from onset of COVID-19 symptoms: -1 to 21.
• Severity of COVID-19 symptoms: 6 mild, 2 severe, 2 critical
• Diagnosis: 4 definite, 4 possible
• Reason for hospital admission: all neurological
• Past medical history: 4 none, 1 with stroke and myeloma, 1 with high cholesterol, and 1 with diabetes, headaches and arrhythmia
• Severity of COVID-19 symptoms: 7 mild, 1 severe
• After treatment with immunoglobulins: 1 requires assisted ventilation, 1 is bedridden, 5 able to walk 5m but incapable of manual work/running, and 1 unknown
• Survival: all

5 patients developed neurological symptoms difficult to characterize post-COVID

• Age: 16-40
• Both males and females, both whites and non-whites.
• Days of onset of syndrome from onset of COVID-19 symptoms: 6 to 26.
• Severity of COVID-19 symptoms: 2 mild, 1 severe, 2 critical
• Diagnosis: 3 definite, 1 probable, 1 possible
• Reason for hospital admission: 2 neurological, 2 respiratory, 1 other
• Past medical history: 1 none, 1 heavy periods, 1 with epilepsy, hypertension, congenital disorders and all sorts of other stuff, 1 with leukemia, and 1 with inflammation of the eyes and joints
• Severity of COVID-19 symptoms: 7 mild, 1 severe
• Recovery: 1 complete, 3 incomplete , and 1 no improvement (3 still in the hospital)
• Survival: 7 alive, 1 dead (of the ones with severe symptoms)

These patients’ symptoms ranged from the headaches to seizures, from weakness to low conscious level. Some also had hemorrhages, encephalopathy, brain abscess, diarrhea, cardiac stuff, all sorts. MRIs were all abnormal except for the one who was declared recovered and discharged.

CONCLUSIONS

To recapitulate, what I did was basically re-write the paper’s tables in lay terms because few of us are proficient in medical jargon, but, more importantly, even fewer – except the scientists and medical doctors – have the time and patience to comb through the supplemental to form the image I gave you. So here you go. Professionals don’t need my blog, they can go directly to the bottom of the post and read the source in original. The image I wanted to convey is that

By long lasting I mean “irreversible”, even if slowly improvable. Please note that the vast majority of these patients were admitted to the hospital not for COVID-19 respiratory symptoms, but for neurological symptoms.

There’s also something else of extraordinary interest in the paper. Eight of the patients had either brain biopsies or spinal tap tested for SARS-CoV2 and all these tests were negative, meaning the virus is not itself causing these neurological problems. In some patients, there was evidence of the cytokine storm, meaning the virus put the immune system in overdrive and this one, in turn, attacked the body, here the brain. So far, the autoimmune hypothesis seems to be the most plausible and parsimonious explanation.

As far the x number is concerned, the authors just gave us the data and let us interpret it. They do offer a hint of just how to interpret them though: the number of brain inflammation cases they saw in 5-weeks is normally seen in London only over a period of 5 months (p. 14). You do the math.

Also, some commentator on the Facebook post raised the question of asymptomatics. Which is a very good question. How do they fare? I don’t know and neither are you. But let me remind you that most of the people in this study were admitted to hospital for neurological reasons, not COVID-19 symptoms. So if they were never having the COVID-19 symptoms, i.e. were asymptomatics, nobody would have done a COVID-19 test on them… and so they’d be treated as regular neurological patients. To figure out what happens to the asymptomatics we need to wait probably a year when we can look at the general epidemiological incidence of heart attacks or GBS or strokes in the general population. And so we’ll probably attribute that increase to COVID-19.

REFERENCE: Paterson RW, Brown RL, Benjamin L, Nortley R, Wiethoff S, Bharucha T, Jayaseelan DL, Kumar G, Raftopoulos RE, Zambreanu L, Vivekanandam V, Khoo A, Geraldes R, Chinthapalli K, Boyd E, Tuzlali H, Price G, Christofi G, Morrow J, McNamara P, McLoughlin B, Lim ST, Mehta PR, Levee V, Keddie S, Yong W, Trip SA, Foulkes AJM, Hotton G, Miller TD, Everitt AD, Carswell C, Davies NWS, Yoong M, Attwell D, Sreedharan J, Silber E, Schott JM, Chandratheva A, Perry RJ, Simister R, Checkley A, Longley N, Farmer SF, Carletti F, Houlihan C, Thom M, Lunn MP, Spillane J, Howard R, Vincent A, Werring DJ, Hoskote C, Jäger HR, Manji H, Zandi MS; UCL Queen Square National Hospital for Neurology and Neurosurgery COVID-19 Study Group (8 Jul 2020). The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings, Brain, online ahead of print PMID: 32637987. DOI: 10.1093/brain/awaa240 ARTICLE | FREE FULLTEXT PDF | SUPPLEMENTALS | Deutsche Welle cover | University College London Press release 

How long does the Coronavirus last on surfaces?

REFERENCE: Moriarty LF, Plucinski MM, Marston BJ, et al. (ePub: 23 March 2020). Public Health Responses to COVID-19 Outbreaks on Cruise Ships — Worldwide, February–March 2020. MMWR Morbidity and Mortality Weekly Report. DOI: http://dx.doi.org/10.15585/mmwr.mm6912e3external icon. ARTICLE| FREE FULLTEXT PDF

By Neuronicus, 24 March 2020

Teach handwriting in schools!

I have begun this blogpost many times. I have erased it many times. That is because the subject of today – handwriting – is very sensitive for me. Most of what I wrote and subsequently erased was a rant: angry at rimes, full of profanity at other times. The rest were paragraphs that can be easily categorized as pleading, bargaining, imploring to teach handwriting in American schools. Or, if they already do, to do it less chaotically, more seriously, more consistently, with a LOT more practice and hopefully before the child hits puberty.

Because, contrary to most educators’ beliefs, handwriting is not the same as typing. Nor is printing / manuscript writing the same as cursive writing, but that’s another kettle.

Somehow, sometime, a huge disjointment happened between scholarly researchers and educators. In medicine, the findings of researchers tend to take 10-15 years until they start to be believed and implemented in medical practice. In education… it seems that even findings cemented by Nobel prizes 100 years ago are alien to the ranks of educators. It didn’t used to be like that. I don’t know when educators became distrustful of data and science. When exactly did they start to substitute evidence with “feels right” and “it’s our school’s philosophy”. When did they start using “research shows… ” every other sentence without being able to produce a single item, name, citation, paper, anything of said research. When did the educators become so… uneducated. I could write (and rant!) a lot about the subject of handwriting or about what exactly a Masters in Education teaches the educators. But I’m so tired of it before I even begun because I’m doing it for a while now and it’s exhausting. It takes an incredible amount of effort, at least for me, to bring the matter of writing so genteelly, tactfully, and non-threateningly to the attention of the fragile ego of the powers that be in charge of the education of the next generation. Yes, yes, there must be rarae aves among the educators who actually teach and do listen to or read papers on education from peer-reviewed journals; but I didn’t find them. I wonder who the research in education is for, if neither the educators nor policy makers have any clue about it…

Here is another piece of education research which will probably go unremarked by the ones it is intended for, i.e. educators and policy makers. Mueller & Oppenheimer (2014) took a closer look at the note-taking habits of 65 Princeton and 260 UCLA students. The students were instructed to take notes in their usual classroom style from 5 x >15 min long TED talks, which were “interesting but not common knowledge” (p. 1160). Afterwards, the subjects completed a hard working-memory task and answered factual and conceptual questions about the content of the “lectures”.

The students who took notes in writing (I’ll call them longhanders) performed significantly better at conceptual questions about the lecture content that the ones who typed on laptops (typers). The researchers noticed that the typers tend to write verbatim what it’s being said, whereas the longhanders don’t do that, which corresponds directly with their performance. In their words,

“laptop note takers’ tendency to transcribe lectures verbatim rather than processing information and reframing it in their own words is detrimental to learning.” (Abstract).

Because typing is faster than writing, the typers can afford to not think of what they type and be in a full scribe mode with the brain elsewhere and not listening to a single word of the lecture (believe me, I know, both as a student and as a University professor). Contrary to that, the longhanders cannot write verbatim and must process the information to extract what’s relevant. In the words of cognitive psychologists everywhere and present in every cognitive psychology textbook written over the last 70 years: depth of processing facilitates learning. Maybe that could be taught in a Masters of Education…

Pet peeves aside, the next step in the today’s paper was to see if you force the typers to forgo the verbatim note-taking and do some information processing might improve learning. It did not, presumably because “the instruction to not take verbatim notes was completely ineffective at reducing verbatim content (p = .97)” (p. 1163).

The laptop typers did take more notes though, by word count. So in the next study, the researchers asked the question “If allowed to study their notes, will the typers benefit from their more voluminous notes and show better performance?” This time the researchers made 4 x 7-min long lectures on bats, bread, vaccines, and respiration and tested them 1 week alter. The results? The longhanders who studied performed the best. The verbatim typers performed the worst, particularly on conceptual versus factual questions, despite having more notes.

For the sake of truth and in the spirit of the overall objectivity of this blog, I should note that the paper is not very well done. It has many errors, some of which were statistical and corrected in a Corrigendum, some of which are methodological and can be addressed by a bigger study with more carefully parsed out controls and more controlled conditions, or at least using the same stimuli across studies. Nevertheless, at least one finding is robust as it was replicated across all their studies:

“In three studies, we found that students who took notes on laptops performed worse on conceptual questions than students who took notes longhand” (Abstract)

Teachers, teach handwriting! No more “Of course we teach writing, just…, just not now, not today, not this year, not so soon, perhaps not until the child is a teenager, not this grade, not my responsibility, not required, not me…”.

REFERENCE: Mueller, PA & Oppenheimer, DM (2014). The Pen Is Mightier Than the Keyboard: Advantages of Longhand Over Laptop Note Taking. Psychological Science, 25(6): 1159–1168. DOI: 10.1177/0956797614524581. ARTICLE | FULLTEXT PDF | NPR cover

By Neuronicus, 1 Sept. 2019

P. S. Some of my followers pointed me to a new preregistered study that failed to replicate this paper (thanks, followers!). Urry et al. (2019) found that the typers have more words and take notes verbatim, just as Mueller & Oppenheimer (2014) found, but this did not benefit the typers, as there wasn’t any difference between conditions when it came to learning without study.

The authors did not address the notion that “depth of processing facilitates learning” though, a notion which is now theory because it has been replicated ad nauseam in hundreds of thousands of papers. Perhaps both papers can be reconciled if a third study were to parse out the attention component of the experiments by, perhaps, introspection questionnaires. What I mean is that the typers can do mindless transcription and there is no depth of processing, resulting in the Mueller & Oppenheimer (2014) observation or they can actually pay attention to what they type and then there is depth of processing, in which case we have Urry et al. (2019) findings. But the longhanders have no choice but to pay attention because they cannot write verbatim, so we’re back to square one, in my mind, that longhanders will do better overall. Handwriting your notes is the safer bet for retention then, because your attention component is not voluntary, but required for the task, as it were, at hand.

REFERENCE: Urry, H. L. (2019, February 9). Don’t Ditch the Laptop Just Yet: A Direct Replication of Mueller and Oppenheimer’s (2014) Study 1 Plus Mini-Meta-Analyses Across Similar Studies. PsyArXiv. doi:10.31234/osf.io/vqyw6. FREE FULLTEXT PDF

By Neuronicus, 2 Sept. 2019

Pic of the day: African dogs sneeze to vote

Excerpt from Walker et al. (2017), p. 5:

“We also find an interaction between total sneezes and initiator POA in rallies (table 1) indicating that the number of sneezes required to initiate a collective movement differed according to the dominance of individuals involved in the rally. Specifically, we found that the likelihood of rally success increases with the dominance of the initiator (i.e. for lower POA categories) with lower-ranking initiators requiring more sneezes in the rally for it to be successful (figure 2d). In fact, our raw data and the resultant model showed that rallies never failed when a dominant (POA1) individual initiated and there were at least three sneezes, whereas rallies initiated by lower ranking individuals required a minimum of 10 sneezes to achieve the same level of success. Together these data suggest that wild dogs use a specific vocalization (the sneeze) along with a variable quorum response mechanism in the decision-making process. […]. We found that sneezes, a previously undocumented unvoiced sound in the species, are positively correlated with the likelihood of rally success preceding group movements and may function as a voting mechanism to establish group consensus in an otherwise despotically driven social system.”

REFERENCE: Walker RH, King AJ, McNutt JW, & Jordan NR (6 Sept. 2017). Sneeze to leave: African wild dogs (Lycaon pictus) use variable quorum thresholds facilitated by sneezes in collective decisions. Proceedings of the Royal Society B. Biological Sciences, 284(1862). pii: 20170347. doi: 10.1098/rspb.2017.0347. PMID: 28878054, PMCID: PMC5597819, DOI: 10.1098/rspb.2017.0347 ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 1 August 2019

Gaming can improve cognitive flexibility

It occurred to me that my blog is becoming more sanctimonious than I’d like. I have many posts about stuff that’s bad for you: stress, high fructose corn syrup, snow, playing soccer, cats, pesticides, religion, climate change, even licorice. So I thought to balance it a bit with stuff that is good for you. To wit, computer games; albeit not all, of course.

An avid gamer myself, those who know me would hardly be surprised that I found a paper cheering StarCraft. A bit of an old game, but still a solid representative of the real-time strategy (RTS) genre.

About a decade ago, a series of papers emerged which showed that first-person shooters and action games in general improve various aspects of perceptual processing. It makes sense because in these games split second decisions and actions make the difference between win or lose, so the games act as training experience for increased sensitivity to cues that facilitate said decisions. But what about games where the overall strategy and micromanagement skills are a bit more important than the perceptual skills, a.k.a. RTS? Would these games improve the processes underlying strategical thinking in a changing environment?

Glass, Maddox, & Love (2013) sought to answer this question by asking a few dozen undergraduates with little gaming experience to play a slightly modified StarCraft game for 40 hours (1 hour per day). “StarCraft (published by Blizzard Entertainment, Inc. in 1998) (…) involves the creation, organization, and command of an army against an enemy army in a real-time map-based setting (…) while managing funds, resources, and information regarding the opponent ” (p. 2). The participants were all female because they couldn’t find enough male undergraduates that played computer games less than 2 hours per day. The control group had to play The Sims 2 for the same amount of time, a game where “participants controlled and developed a single ‘‘family household’’ in a virtual neighborhood” (p.3.). The researchers cleverly modified the StarCraft game in such a way that they replaced a perceptual component with a memory component (disabled some maps) and created two versions: one more complex (full-map, two friendly, two enemy bases) and one less so (half-map, one friendly, one enemy bases). The difficulty for all games was set at a win rate of 50%.

Before and after the game-playing, the subjects were asked to complete a huge battery of tests destined to test their memory and various other cognitive processes. By carefully parsing these out, the authors conclude that “forty hours of training within an RTS game that stresses rapid and simultaneous maintenance, assessment, and coordination between multiple information and action sources was sufficient” to improve cognitive flexibility. Moreover, authors point out that playing on a full-map with multiple allies and enemies is conducive to such improvement, whereas playing a less cognitive resources demanding game, despite similar difficulty levels, was not. Basically, the more stuff you have to juggle, the better your flexibility will be. Makes sense.

My favorite take from this paper though is not only that StarCraft is awesome, obviously, but that “cognitive flexibility is a trainable skill” (p. 5). Let me tell you why that is so grand.

Cognitive flexibility is an important concept in the neuroscience of executive functioning. The same year that this paper was published, Diamond was publishing an excellent review paper in which she neatly identified three core executive functions: inhibition/control (both behavioral and cognitive), working memory (the ability to temporarily hold information active), and cognitive flexibility (the ability to think about and switch between two different concepts simultaneously). From these three core executive functions, higher-order executive functions are built, such as reasoning (critical thinking), problem solving (decision-making) and planning.

Unlike some old views on the immutability of the inborn IQ, each one of the core and higher-order executive functions can be improved upon with training at any point in life and can suffer if something is not right in your life (stress, loneliness, sleep-deprived or sick). This paper adds to the growing body of evidence showing that executive functions can be trainable. Intelligence, however you want to define it, relies upon executive functions, at least some of them, and perhaps boosting cognitive flexibility might result in a slight increase in the IQ, methinks.

Bottom line: real-time strategy games with huge maps and tons of stuff to do are good for you. Here you go.

The StarCraft images, both foreground and background, are copyrighted to © 1998 Blizzard Entertainment.

REFERENCES:

1. Glass BD, Maddox WT, Love BC. (7 Aug 2013). Real-time strategy game training: emergence of a cognitive flexibility trait. PLoS One, 2;8(8):e70350. eCollection 2013. PMID: 23950921, PMCID: PMC3737212, DOI: 10.1371/journal.pone.0070350. ARTICLE | FREE FULLTEXT PDF
2. Diamond A (2013, Epub 27 Sept. 2012). Executive Functions. Annual Review of Psychology, 64:135-68. PMID: 23020641, PMCID: PMC4084861, DOI: 10.1146/annurev-psych-113011-143750. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 15 June 2019

Epigenetics of BDNF in depression

Depression is the leading cause of disability worldwide, says the World Health Organization. The. The. I knew it was bad, but… ‘the’? More than 300 million people suffer from it worldwide and in many places fewer than 10% of these receive treatment. Lack of treatment is due to many things, from lack of access to healthcare to lack of proper diagnosis; and not in the least due to social stigma.

To complicate matters, the etiology of depression is still not fully elucidated, despite hundreds of thousand of experimental articles published out-there. Perhaps millions. But, because hundreds of thousands of experimental articles perhaps millions have been published, we know a helluva a lot about it than, say, 50 years ago. The enormous puzzle is being painstakingly assembled as we speak by scientists all over the world. I daresay we have a lot of pieces already, if not all at least 3 out of 4 corners, so we managed to build a not so foggy view of the general picture on the box lid. Here is one of the hottest pieces of the puzzle, one of those central pieces that bring the rabbit into focus.

Before I get to the rabbit, let me tell you about the corners. In the fifties people thought that depression is due to having too little neurotransmitters from the monoamine class in the brain. This thought did not arise willy-nilly, but from the observation that drugs that increase monoamine levels in the brain alleviate depression symptoms, and, correspondingly, drugs which deplete monoamines induce depression symptoms. A bit later on, the monoamine most culpable was found to be serotonin. All well and good, plenty of evidence, observational, correlational, causational, and mechanistic supporting the monoamine hypothesis of depression. But two more pieces of evidence kept nagging the researchers. The first one was that the monoamine enhancing drugs take days to weeks to start working. So, if low on serotonin is the case, then a selective serotonin reuptake inhibitor (SSRI) should elevate serotonin levels within maximum an hour of ingestion and lower symptom severity, so how come it takes weeks? The second was even more eyebrow raising: these monoamine-enhancing drugs work in about 50 % of the cases. Why not all? Or, more pragmatically put, why not most of all if the underlying cause is the same?

It took decades to address these problems. The problem of having to wait weeks until some beneficial effects of antidepressants show up has been explained away, at least partly, by issues in the serotonin regulation in the brain (e.g. autoreceptors senzitization, serotonin transporter abnormalities). As for the second problem, the most parsimonious answer is that that archeological site called DSM (Diagnostic and Statistical Manual of Mental Disorders), which psychologists, psychiatrists, and scientists all over the world have to use to make a diagnosis is nothing but a garbage bag of last century relics with little to no resemblance of this century’s understanding of the brain and its disorders. In other words, what DSM calls major depressive disorder (MDD) may as well be more than one disorder and then no wonder the antidepressants work only in half of the people diagnosed with it. As Goldberg put it in 2011, “the DSM diagnosis of major depression is made when a patient has any 5 out of 9 symptoms, several of which are opposites [emphasis added]”! He was referring to DSM-4, not that the 5 is much different. I mean, paraphrasing Goldberg, you really don’t need much of a degree other than some basic intro class in the physiology of whatever, anything really, to suspect that someone who’s sleeping a lot, gains weight, has increased appetite, appears tired or slow to others, and feels worthless might have a different cause for these symptoms than someone who has daily insomnias, lost weight recently, has decreased appetite, is hyperagitated, irritable, and feels excessive guilt. Imagine how much more understanding we would have about depression if scientists didn’t use the DSM for research. No wonder that there’s a lot of head scratching when your hypothesis, which is logically correct, paradigmatically coherent, internally consistent, flawlessly tested, turns out to be true only sometimes because your ‘depressed’ subjects are as a homogeneous group as a pack of Trail Mix.

I got sidetracked again. This time ranting against DSM. No matter, I’m back on track. So. The good thing about the work done trying to figure out how antidepressants work and psychiatrists’ minds work (DSM is written overwhelmingly by psychiatrists), scientists uncovered other things about depression. Some of the findings became clumped under the name ‘the neurotrophic hypothesis of depression’ in the early naughts. It stems from the finding that some chemicals needed by neurons for their cellular happiness are in low amount in depression. Almost two decades later, the hypothesis became mainstream theory as it explains away some other findings in depression, and is not incompatible with the monoamines’ behavior. Another piece of the puzzle found.

One of these neurotrophins is called brain-derived neurotrophic factor (BDNF), which promotes cell survival and growth. Crucially, it also regulates synaptic plasticity, without which there would be no learning and no memory. The idea is that exposure to adverse events generates stress. Stress is differently managed by different people, largely due to genetic factors. In those not so lucky at the genetic lottery (how hard they take a stressor, how they deal with it), and in those lucky enough at genetics but not so lucky in life (intense and/or many stressors hit the organism hard regardless how well you take it or how good you are at it), stress kills a lot of neurons, literally, prevents new ones from being born, and prevents the remaining ones from learning well. Including learning on how to deal with the stressors, present and future, so the next time an adverse event happens, even if it is a minor stressor, the person is way more drastically affected. in other words, stress makes you more vulnerable to stressors. One of the ways stress is doing all these is by suppressing BDNF synthesis. Without BDNF, the individual exposed to stress that is exacerbated either by genes or environment ends up unable to self-regulate mood successfully. The more that mood is not regulated, the worse the brain becomes at self-regulating because the elements required for self-regulation, which include learning from experience, are busted. And so the vicious circle continues.

Maintaining this vicious circle is the ability of stressors to change the patterns of DNA expression and, not surprisingly, one of the most common findings is that the BDNF gene is hypermethylated in depression. Hypermethylation is an epigenetic change (a change around the DNA, not in the DNA itself), meaning that the gene in question is less expressed. This means lower amounts of BDNF are produced in depression.

After this long introduction, the today’s paper is a systematic review of one of epigenetic changes in depression: methylation. The 67 articles that investigated the role of methylation in depression were too heterogeneous to make a meta-analysis out of them, so Li et al. (2019) made a systematic review.

The main finding was that, overall, depression is associated with DNA methylation modifications. Two genes stood out as being hypermethylated: our friend BDNF and SLC6A4, a gene involved in the serotonin cycle. Now the question is who causes who: is stress methylating your DNA or does your methylated DNA make you more vulnerable to stress? There’s evidence both ways. Vicious circle, as I said. I doubt that for the sufferer it matters who started it first, but for the researchers it does.

A little disclaimer: the picture I painted above offers a non-exclusive view on the causes of depression(s). There’s more. There’s always more. Gut microbes are in the picture too. And circulatory problems. And more. But the picture is more than half done, I daresay. Continuing my puzzle metaphor, we got the rabbit by the ears. Now what to do with it…

Well, one thing we can do with it, even with only half-rabbit done, is shout loud and clear that depression is a physical disease. And those who claim it can be cured by a positive attitude and blame the sufferers for not ‘trying hard enough’ or not ‘smiling more’ or not ‘being more positive’ can bloody well shut up and crawl back in the medieval cave they came from.

REFERENCES:

1. Li M, D’Arcy C, Li X, Zhang T, Joober R, & Meng X (4 Feb 2019). What do DNA methylation studies tell us about depression? A systematic review. Translational Psychiatry, 9(1):68. PMID: 30718449, PMCID: PMC6362194, DOI: 10.1038/s41398-019-0412-y. ARTICLE | FREE FULLTEXT PDF

2. Goldberg D (Oct 2011). The heterogeneity of “major depression”. World Psychiatry, 10(3):226-8. PMID: 21991283, PMCID: PMC3188778. ARTICLE | FREE FULLTEXT PDF

3. World Health Organization Depression Fact Sheet

By Neuronicus, 23 April 2019

Milk-producing spider

In biology, organizing living things in categories is called taxonomy. Such categories are established based on shared characteristics of the members. These characteristics were usually visual attributes. For example, a red-footed booby (it’s a bird, silly!) is obviously different than a blue-footed booby, so we put them in different categories, which Aristotle called in Greek something like species.

Biological taxonomy is very useful, not only to provide countless hours of fight (both verbal and physical!) for biologists, but to inform us of all sorts of unexpected relationships between living things. These relationships, in turn, can give us insights into our own evolution, but also the evolution of things inimical to us, like diseases, and, perhaps, their cure. Also extremely important, it allows scientists from all over the world to have a common language, thus maximizing information sharing and minimizing misunderstandings.

All well and good. And it was all well and good since Carl Linnaeus introduced his famous taxonomy system in the 18^th Century, the one we still use today with species, genus, family, order, and kingdom. Then we figured out how to map the DNAs of things around us and this information threw out the window a lot of Linnean classifications. Because it turns out that some things that look similar are not genetically similar; likewise, some living things that we thought are very different from one another, turned out that, genetically speaking, they are not so different.

You will say, then, alright, out with visual taxonomy, in with phylogenetic taxonomy. This would be absolutely peachy for a minority of organisms of the planet, like animals and plants, but a nightmare in the more promiscuous organisms who have no problem swapping bits of DNA back and forth, like some bacteria, so you don’t know anymore who’s who. And don’t even get me started on the viruses which we are still trying to figure out whether or not they are alive in the first place.

When I grew up there were 5 regna or kingdoms in our tree of life – Monera, Protista, Fungi, Plantae, Animalia – each with very distinctive characteristics. Likewise, the class Mammalia from the Animal Kingdom was characterized by the females feeding their offspring with milk from mammary glands. Period. No confusion. But now I have no idea – nor do many other biologists, rest assured – how many domains or kingdoms or empires we have, nor even what the definition of a species is anymore!

As if that’s not enough, even those Linnean characteristics that we thought set in stone are amenable to change. Which is good, shows the progress of science. But I didn’t think that something like the definition of mammal would change. Mammals are organisms whose females feed their offspring with milk from mammary glands, as I vouchsafed above. Pretty straightforward. And not spiders. Let me be clear on this: spiders did not feature in my – or anyone’s! – definition of mammals.

Until Chen et al. (2018) published their weird article a couple of weeks ago. The abstract is free for all to see and states that the females of a jumping spider species feed their young with milk secreted by their body until the age of subadulthood. Mothers continue to offer parental care past the maturity threshold. The milk is necessary for the spiderlings because without it they die. That’s all.

I read the whole paper since it was only 4 pages of it and here are some more details about their discovery. The species of spider they looked at is Toxeus magnus, a jumping spider that looks like an ant. The mother produces milk from her epigastric furrow and deposits it on the nest floor and walls from where the spiderlings ingest it (0-7 days). After the first week of this, the spiderlings suck the milk direct from the mother’s body and continue to do so for the next two weeks (7-20 days) when they start leaving the nest and forage for themselves. But they return and for the next period (20-40 days) they get their food both from the mother’s milk and from independent foraging. Spiderlings get weaned by day 40, but they still come home to sleep at night. At day 52 they are officially considered adults. Interestingly, “although the mother apparently treated all juveniles the same, only daughters were allowed to return to the breeding nest after sexual maturity. Adult sons were attacked if they tried to return. This may reduce inbreeding depression, which is considered to be a major selective agent for the evolution of mating systems (p. 1053).”

During all this time, including during the emergence into adulthood of the offsprings, the mother also supplied house maintenance, carrying out her children’s exuviae (shed exoskeletons) and repairing the nest.

The authors then did a series of experiments to see what role does the nursing and other maternal care at different stages play in the fitness and survival of the offsprings. Blocking the mother’s milk production with correction fluid immediately after hatching killed all the spiderlings, showing that they are completely dependent on the mother’s milk. Removing the mother after the spiderlings start foraging (day 20) drastically reduces survivorship and body size, showing that mother’s care is essential for her offsprings’ success. Moreover, the mother taking care of the nest and keeping it clean reduced the occurrence of parasite infections on the juveniles.

The authors analyzed the milk and it’s highly nutritious: “spider milk total sugar content was 2.0 mg/ml, total fat 5.3 mg/ml, and total protein 123.9 mg/ml, with the protein content around four times that of cow’s milk (p. 1053)”.

Speechless I am. Good for the spider, I guess. Spider milk will have exorbitant costs (Apparently, a slight finger pressure on the milk-secreting region makes the mother spider secret the milk, not at all unlike the human mother). Spiderlings die without the mother’s milk. Responsible farming? Spider milker qualifications? I’m gonna lay down, I got a headache.

REFERENCE: Chen Z, Corlett RT, Jiao X, Liu SJ, Charles-Dominique T, Zhang S, Li H, Lai R, Long C, & Quan RC (30 Nov. 2018). Prolonged milk provisioning in a jumping spider. Science, 362(6418):1052-1055. PMID: 30498127, DOI: 10.1126/science.aat3692. ARTICLE | Supplemental info (check out the videos)

By Neuronicus, 13 December 2018

Pic of the day: Dopamine from a non-dopamine place

Reference: Beas BS, Wright BJ, Skirzewski M, Leng Y, Hyun JH, Koita O, Ringelberg N, Kwon HB, Buonanno A, & Penzo MA (Jul 2018, Epub 18 Jun 2018). The locus coeruleus drives disinhibition in the midline thalamus via a dopaminergic mechanism. Nature Neuroscience,21(7):963-973. PMID: 29915192, PMCID: PMC6035776 [Available on 2018-12-18], DOI:10.1038/s41593-018-0167-4. ARTICLE

Pooping Legos

Yeah, alright… uhm… how exactly should I approach this paper? I’d better just dive into it (oh boy! I shouldn’t have said that).

The authors of this paper were adult health-care professionals in the pediatric field. These three males and three females were also the participants in the study. They kept a poop-diary noting the frequency and volume of bowel movements (Did they poop directly on a scale or did they have to scoop it out in a bag?). The researchers/subjects developed a Stool Hardness and Transit (SHAT) metric to… um.. “standardize bowel habit between participants” (p. 1). In other words, to put the participants’ bowel movements on the same level (please, no need to visualize, I am still stuck at the poop-on-a-scale phase), the authors looked – quite literally – at the consistency of the poop and gave it a rating. I wonder if they checked for inter-rater reliability… meaning did they check each other’s poops?…

Then the researchers/subjects ingested a Lego figurine head, on purpose, somewhere between 7 and 9 a.m. Then they timed how much time it took to exit. The FART score (Found and Retrieved Time) was 1.71 days. “There was some evidence that females may be more accomplished at searching through their stools than males, but this could not be statistically validated” due to the small sample size, if not the poops’. It took 1 to 3 stools for the object to be found, although poor subject B had to search through his 13 stools over a period of 2 weeks to no avail. I suppose that’s what you get if you miss the target, even if you have a PhD.

The pre-SHAT and SHAT score of the participants did not differ, suggesting that the Lego head did not alter the poop consistency (I got nothin’ here; the authors’ acronyms are sufficient scatological allusion). From a statistical standpoint, the one who couldn’t find his head in his poop (!) should not have been included in the pre-SHAT score group. Serves him right.

I wonder how they searched through the poop… A knife? A sieve? A squashing spatula? Gloved hands? Were they floaters or did the poop sink at the base of the toilet? Then how was it retrieved? Did the researchers have to poop in a bucket so no loss of data should occur? Upon direct experimentation 1 minute ago, I vouchsafe that a Lego head is completely buoyant. Would that affect the floatability of the stool in question? That’s what I’d like to know. Although, to be fair, no, that’s not what I want to know; what I desire the most is a far larger sample size so some serious stats can be conducted. With different Lego parts. So they can poop bricks. Or, as suggested by the authors, “one study arm including swallowing a Lego figurine holding a coin” (p. 3) so one can draw parallels between Lego ingestion and coin ingestion research, the latter being, apparently, far more prevalent. So many questions that still need to be answered! More research is needed, if only grants would be so… regular as the raw data.

The paper, albeit short and to the point, fills a gap in our scatological knowledge database (Oh dear Lord, stop me!). The aim of the paper was to show that ingested objects by children tend to pass without a problem. Also of value, the paper asks pediatricians to counsel the parents to not search for the object in the faeces to prove object retrieval because “if an experienced clinician with a PhD is unable to adequately find objects in their own stool, it seems clear that we should not be expecting parents to do so” (p. 3). Seems fair.

REFERENCE: Tagg, A., Roland, D., Leo, G. S., Knight, K., Goldstein, H., Davis, T. and Don’t Forget The Bubbles (22 November 2018). Everything is awesome: Don’t forget the Lego. Journal of Paediatrics and Child Health, doi: 10.1111/jpc.14309. ARTICLE

By Neuronicus, 27 November 2017

Raising a child costs 13 million calories

That’s right. Somebody actually did the math on that. Kaplan in 1994, to be exact.

The anthropologist and his colleague, Kate Kopischke, looked at how three semi-isolated populations from South America live. Between September 1988 and May 1989, the researchers analyzed several variables meant to shed light mainly on fertility rate and wealth flow. They measured the amount of time spent taking care of children. They estimated the best time to have a second child. They weighed the food of these communities. And then they estimated the caloric intake and expenditure per day per individual.

Human children are unable to provision for themselves until about the age of 18. So most of their caloric intake requirements are provided by their parents. Long story (39 pages) short, Kaplan (1994) concluded that a child relies on 13 million calories provided by the adults. Granted, these are mostly hunter-gatherer communities, so the number may be a bit off from your average American child. The question is: which way? Do American kids “cost” more or less?

P.S. I was reading a paper, Kohl (2018), in the last week’s issue of Science that quoted this number, 13 million. When I went to the cited source, Hrdy (2016), that one was citing yet another one, the above-mentioned Kaplan (1994) paper. Luckily for Kohl, Hrdy cited Kaplan correctly. But I must tell you from my own experience, half of the time when people cite other people citing other people citing original research, they are wrong. Meaning that somewhere in the chain somebody got it wrong or twisted the original research finding for their purposes. Half of the time, I tell you. People don’t go for the original material because it can be a hassle to dig it out, or it’s hard to read, or because citing a more recent paper looks better in the review process. But that comes to the risk of being flat wrong. The moral: always, always, go for the source material.

P.P.S. To be clear, I’m not accusing Kohl of not reading Kaplan because accusing an academic of citing without reading or being unfamiliar with seminal research in their field (that is, seminal in somebody else’s opinion) is a tremendous insult not be wielded lightly by bystanders but to be viciously used only for in-house fights on a regular basis. No. I’m saying that Kohl got that number second-hand and that’s frowned upon. The moral: always, always, go for the source material. I can’t emphasize this enough.

P.P.P..S. Ah, forget it. P.S. 3. Upon reading my blog, my significant other’s first question was: “Well, how much is that in potatoes?” I had to do the math on a Post-It and the answer is: 50,288 large skinless potatoes, boiled without salt. That’s 15,116 Kg of potatoes, more than 15 metric tones. Here you go. Happy now? Why are we talking about potatoes?! No, I don’t know how many potatoes would fit into a house. Jeez!

REFERENCE: Kaplan, H. (Dec. 1994). Evolutionary and Wealth Flows Theories of Fertility: Empirical Tests and New Models. Population and Development Review, Vol. 20, No. 4, pp. 753-791. DOI: 10.2307/2137661. ARTICLE

By Neuronicus, 22 October 2018

Locus Coeruleus in mania

From all the mental disorders, bipolar disorder, a.k.a. manic-depressive disorder, has the highest risk for suicide attempt and completion. If the thought of suicide crosses your mind, stop reading this, it’s not that important; what’s important is for you to call the toll-free National Suicide Prevention Lifeline at 1-800-273-TALK (8255).

The bipolar disorder is defined by alternating manic episodes of elevated mood, activity, excitation, and energy with episodes of depression characterized by feelings of deep sadness, hopelessness, worthlessness, low energy, and decreased activity. It is also a more common disease than people usually expect, affecting about 1% or more of the world population. That means almost 80 million people! Therefore, it’s imperative to find out what’s causing it so we can treat it.

Unfortunately, the disease is very complex, with many brain parts, brain chemicals, and genes involved in its pathology. We don’t even fully comprehend how the best medication we have to lower the risk of suicide, lithium, works. The good news is the neuroscientists haven’t given up, they are grinding at it, and with every study we get closer to subduing this monster.

One such study freshly published last month, Cao et al. (2018), looked at a semi-obscure membrane protein, ErbB4. The protein is a tyrosine kinase receptor, which is a bit unfortunate because this means is involved in ubiquitous cellular signaling, making it harder to find its exact role in a specific disorder. Indeed, ErbB4 has been found to play a role in neural development, schizophrenia, epilepsy, even ALS (Lou Gehrig’s disease).

Given that ErbB4 is found in some neurons that are involved in bipolar and mutations in its gene are also found in some people with bipolar, Cao et al. (2018) sought to find out more about it.

First, they produced mice that lacked the gene coding for ErbB4 in neurons from locus coeruleus, the part of the brain that produces norepinephrine out of dopamine, better known for the European audience as nor-adrenaline. The mutant mice had a lot more norepinephrine and dopamine in their brains, which correlated with mania-like behaviors. You might have noticed that the term used was ‘manic-like’ and not ‘manic’ because we don’t know for sure how the mice feel; instead, we can see how they behave and from that infer how they feel. So the researchers put the mice thorough a battery of behavioral tests and observed that the mutant mice were hyperactive, showed less anxious and depressed behaviors, and they liked their sugary drink more than their normal counterparts, which, taken together, are indices of mania.

Next, through a series of electrophysiological experiments, the scientists found that the mechanism through which the absence of ErbB4 leads to mania is making another receptor, called NMDA, in that brain region more active. When this receptor is hyperactive, it causes neurons to fire, releasing their norepinephrine. But if given lithium, the mutant mice behaved like normal mice. Correspondingly, they also had a normal-behaving NMDA receptor, which led to normal firing of the noradrenergic neurons.

So the mechanism looks like this (Jargon alert!):

No ErbB4 –> ↑ NR2B NMDAR subunit –> hyperactive NMDAR –> ↑ neuron firing –> ↑ catecholamines –> mania.

In conclusion, another piece of the bipolar puzzle has been uncovered. The next obvious step will be for the researchers to figure out a medicine that targets ErbB4 and see if it could treat bipolar disorder. Good paper!

P.S. If you’re not familiar with the journal eLife, go and check it out. The journal offers for every study a half-page summary of the findings destined for the lay audience, called eLife digest. I’ve seen this practice in other journals, but this one is generally very well written and truly for the lay audience and the non-specialist. Something of what I try to do here, minus the personal remarks and in parenthesis metacognitions that you’ll find in most of my posts. In short, the eLife digest is masterly done. As my continuous struggles on this blog show, it is tremendously difficult for a scientist to write concisely, precisely, and jargonless at the same time. But eLife is doing it. Check it out. Plus, if you care to take a look on how science is done and published, eLife publishes all the editor’s rejection notes, all the reviewers’ comments, and all the author responses for a particular paper. Reading those is truly a teaching moment.

REFERENCE: Cao SX, Zhang Y, Hu XY, Hong B, Sun P, He HY, Geng HY, Bao AM, Duan SM, Yang JM, Gao TM, Lian H, Li XM (4 Sept 2018). ErbB4 deletion in noradrenergic neurons in the locus coeruleus induces mania-like behavior via elevated catecholamines. Elife, 7. pii: e39907. doi: 10.7554/eLife.39907. PMID: 30179154 ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 14 October 2018

The Global Warming IPCC 2018 Report

The Special Report on Global Warming of 1.5ºC (SR15) was published two days ago, on October 8^th, 2018. The Report was written by The Intergovernmental Panel on Climate Change (IPCC), “which is the UN body for assessing the science related to climate change. It was established by the United Nations Environment Programme (UN Environment) and the World Meteorological Organization (WMO) in 1988 to provide policymakers with regular scientific assessments concerning climate change, its implications and potential future risks, as well as to put forward adaptation and mitigation strategies.” (IPCC Special Report on Global Warming of 1.5ºC, Press Release).

The Report’s findings are very bad. Its Summary for Policymakers starts with:

“Human activities are estimated to have caused approximately 1.0°C of global warming above pre-industrial levels, with a likely range of 0.8°C to 1.2°C. Global warming is likely to reach 1.5°C between 2030 and 2052 if it continues to increase at the current rate.”

That’s 12 years from now.

Extract from the IPCC (2018), Global Warming of 1.5 ºC, Summary for Policymakers. “Observed monthly global mean surface temperature (GMST) change grey line up to 2017, from the HadCRUT4, GISTEMP, Cowtan – Way, and NOAA datasets) and estimated anthropogenic global warming (solid orange line up to 2017, with orange shading indicating assessed likely range). Orange dashed arrow and horizontal orange error bar show respectively central estimate and likely range of the time at which 1.5°C is reached if the current rate of warming continues. The grey plume on the right of  shows the likely range of warming responses, computed with a simple climate model, to a stylized pathway (hypothetical future) in which net CO2 emissions  decline in a straight line from 2020 to reach net zero in 2055 and net non – CO2 radiative forcing increases to 2030 and then declines. “

Which means that we warmed up the world by 1.0°C (1.8°F) since 1850-1900. Continuing the way we have been doing, we will add another 0.5°C (0.9°F) to the world temperature sometime between 2030 and 2052, making the total human-made global warming to 1.5°C (2.7°F).

That’s 12 years from now.

Half a degree Celsius doesn’t sound so bad until you look at the highly confident model prediction saying that gaining that extra 0.5°C (0.9°F) will result in terrible unseen before superstorms and precipitation in some regions while others will suffer prolonged droughts, along with extreme heat waves and sea level rises due to the melting of Antarctica. From a biota point of view, if we reach the 1.5°C (2.7°F) threshold, most of the coral reefs will become extinct, as well as thousands of other species (6% of insects, 8% of plants, and 4% of vertebrates).

That’s 12 years from now.

All these will end up increasing famine, homelessness, disease, inequality, poverty, and refugee numbers to unprecedented levels. Huge spending of money on infrastructure, rebuilding, help efforts, irrigation, water supplies, and so on, for those inclined to be more concerned by finances. To put it bluntly, a 1.5°C (2.7°F) increase in global warming costs us about $54 trillion.

That’s 12 years from now.

These effects will persist for centuries to millennia. To stay at the 1.5°C (2.7°F)  limit we need to reduce the carbon emissions by 50% by 2030 and achieve 0 emissions by 2050.

That’s 12 years from now.

The Report emphasizes that a 1.5°C (2.7°F)  increase is not as bad as a 2°C (3.6°F), where we will loose double of the biota, the storms will be worse, the droughts longer, and altogether a more catastrophic scenario.

Technically, we ARE ABLE to limit the warming at 1.5°C (2.7°F), If, by 2050, we rely on renewable energy, like solar and wind, to supply 70-85% of energy, we will be able to stay at the 1.5°C (2.7°F). Lower the coal use as energy source to single digits percentages. Expanding forests and implementing large CO₂ capture programs would help tremendously. Drastically reduce carbon emissions by, for example, hitting polluters with crippling fines. But all this requires rapid implementation of heavy laws and regulation, which will come from a concentrated effort of our leaders.

Therefore, politically, we ARE UNABLE to limit the warming at 1.5°C (2.7°F). Instead, it’s very likely that we will warm the planet by 2°C (3.6°F) in the next decades. If we do nothing, by the end of the century the world will be even hotter, being warmed up by 3°C (5.4°F) and there are no happy scenarios then as the climate change will be beyond our control. That is, our children’s control.

There are conspiracy theorists out there claiming that there are nefarious or hidden reasons behind this report, or that its conclusions are not credible, or that it’s not legit, or it’s bad science, or that it represents the view of a fringe group of scientists and does not reflect a scientific consensus. I would argue that people who claim such absurdities are either the ones with a hidden agenda or are plain idiots. Not ignorants, because ignorance is curable and whoever seeks to learn new things is to be admired. Not honest questioning either, because that is as necessary to science as the water to the fish. Willful ignorance, on the other hand, I call idiocy and is remarkably resistant to presentation of facts. FYI, the Report was conducted by a Panel commissioned by an organization comprising 195 countries, is authored by 91 scientists, has an additional 133 contributing authors, all these spanning 40 countries, analyzing over 6000 scientific studies. They can’t all be “in it”. Oh, and the Panel received the 2007 Nobel Peace Prize. I daresay it looks legit. The next full climate assessment will be released in 2021.

REFERENCES:

1. The Intergovernmental Panel on Climate Change (IPCC) (2018). Global Warming of 1.5 ºC, an IPCC Special report on the impacts of global warming of 1.5 ºC above pre-industrial levels and related global greenhouse gas emission pathways, in the context of strengthening the global response to the threat of climate change, sustainable development, and efforts to eradicate poverty. Retrieved 10 October 2018. Website  | Covers: New York Times | Nature  | The Washington Post | The Guardian | The Economist | ABC News | Deutsche Welle | CNN | HuffPost Canada| Los Angeles Times | BBC | Time .
2. The IPCC Summary for Policymakers PDF
3. The IPCC Press Release PDF
4. The 2007 Nobel Peace Prize.

By Neuronicus, 10 October 2018

Pic of the day: Total amount of DNA on Earth

Approximately… give or take…

REFERENCE: Landenmark HKE, Forgan DH, & Cockell CS (11 Jun 2915). An Estimate of the Total DNA in the Biosphere. PLoS Biology, 13(6): e1002168. PMCID: PMC4466264, PMID: 26066900, DOI: 10.1371/journal.pbio.1002168. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 1 September 2018

The FIRSTS: The cause(s) of dinosaur extinction

A few days ago, a follower of mine gave me an interesting read from The Atlantic regarding the dinosaur extinction. Like many of my generation, I was taught in school that dinosaurs died because an asteroid hit the Earth. That led to a nuclear winter (or a few years of ‘nuclear winters’) which killed the photosynthetic organisms, and then the herbivores didn’t have anything to eat so they died and then the carnivores didn’t have anything to eat and so they died. Or, as my 4-year-old puts it, “[in a solemn voice] after the asteroid hit, big dusty clouds blocked the sun; [in an ominous voice] each day was colder than the previous one and so, without sunlight to keep them alive [sad face, head cocked sideways], the poor dinosaurs could no longer survive [hands spread sideways, hung head] “. Yes, I am a proud parent. Now I have to do a sit-down with the child and explain that… What, exactly?

Well, The Atlantic article showcases the struggles of a scientist – paleontologist and geologist Gerta Keller – who doesn’t believe the mainstream asteroid hypothesis; rather she thinks there is enough evidence to point out that extreme volcano eruptions, like really extreme, thousands of times more powerful than anything we know in the recorded history, put out so much poison (soot, dust, hydrofluoric acid, sulfur, carbon dioxide, mercury, lead, and so on) in the atmosphere that, combined with the consequent dramatic climate change, killed the dinosaurs. The volcanoes were located in India and they erupted for hundreds of thousands of years, but most violent eruptions, Keller thinks, were in the last 40,000 years before the extinction. This hypothesis is called the Deccan volcanism from the region in India where these nasty volcanoes are located, first proposed by Vogt (1972) and Courtillot et al. (1986).

So which is true? Or, rather, because this is science we’re talking about, which hypothesis is more supported by the facts: the volcanism or the impact?

The impact hypothesis was put forward in 1980 when Walter Alvarez, a geologist, noticed a thin layer of clay in rocks that were about 65 million years old, which coincided with the time when the dinosaurs disappeared. This layer is on the KT boundary (sometimes called K-T, K-Pg, or KPB, looks like the biologists are not the only ones with acronym problems) and marks the boundary between the Cretaceous and Paleogenic geological periods (T is for Triassic, yeah, I know). Walter asked his father, the famous Nobel Prize physicist Louis Alvarez, to take a look at it and see what it is. Alvarez Sr. analyzed it and decided that the clay contains a lot of iridium, dozens of times more than expected. After gathering more samples from Europe and New Zealand, they published a paper (Alvarez et al., 1980) in which the scientists reasoned that because Earth’s iridium is deeply buried in its bowels and not in its crust, this iridium at the K-Pg boundary is of extraterrestrial origin, which could be brought here only by an asteroid/comet. This is also the paper in which it was put forth for the first time the conjecture that the asteroid impact killed the dinosaurs, based on the uncanny coincidence of timing.

The discovery of the Chicxulub crater in Mexico followed a more sinuous path because the geophysicists who first discovered it in the ’70s were working for an oil company, looking for places to drill. Once the dinosaur-died-due-to-asteroid-impact hypothesis gained popularity outside academia, the geologists and the physicists put two-and-two together, acquired more data, and published a paper (Hildebrand et al., 1991) where the Chicxulub crater was for the first time linked with the dinosaur extinction. Although the crater was not radiologically dated yet, they had enough geophysical, stratigraphic, and petrologic evidence to believe it was as old as the iridium layer and the dinosaur die-out.

But, devil is in the details, as they say. Keller published a paper in 2007 saying the Chicxulub event predates the extinction by some 300,000 years (Keller et al., 2007). She looked at geological samples from Texas and found the glass granule layer (indicator of the Chicxhulub impact) way below the K-Pg boundary. So what’s up with the iridium then? Keller (2014) believes that is not of extraterrestrial origin and it might well have been spewed up by a particularly nasty eruption or the sediments got shifted. Schulte et al. (2010), on the other hand, found high levels of iridium in 85 samples from all over the world in the KPG layer. Keller says that some other 260 samples don’t have iridium anomalies. As a response, Esmeray-Senlet et al. (2017) used some fancy Mass Spectrometry to show that the iridium profiles could have come only from Chicxulub, at least in North America. They argue that the variability in iridium profiles around the world is due to regional geochemical processes. And so on, and so on, the controversy continues.

Actual radioisotope dating was done a bit later in 2013: date of K-Pg is 66.043 ± 0.043 MA (millions of years ago), date of the Chicxulub crater is 66.038 ±.025/0.049 MA. Which means that the researchers “established synchrony between the Cretaceous-Paleogene boundary and associated mass extinctions with the Chicxulub bolide impact to within 32,000 years” (Renne et al., 2013), which is a blink of an eye in geological times.

Now I want you to understand that often in science, though by far not always, matters are not so simple as she is wrong, he is right. In geology, what matters most is the sample. If the sample is corrupted, so will be your conclusions. Maybe Keller’s or Renne’s samples were affected by a myriad possible variables, some as simple as shifting the dirt from here to there by who knows what event. After all, it’s been 66 million years since. Also, methods used are just as important and dating something that happened so long ago is extremely difficult due to intrinsic physical methodological limitations. Keller (2014), for example, claims that Renne couldn’t have possibly gotten such an exact estimation because he used Argon isotopes when only U-Pb isotope dilution–thermal ionization mass spectrometry (ID-TIMS) zircon geochronology could be so accurate. But yet again, it looks like he did use both, so… I dunno. As the over-used always-trite but nevertheless extremely important saying goes: more data is needed.

Even if the dating puts Chicxulub at the KPB, the volcanologists say that the asteroid, by itself, couldn’t have produced a mass extinction because there are other impacts of its size and they did not have such dire effects, but were barely noticeable at the biota scale. Besides, most of the other mass extinctions on the planet have been already associated with extreme volcanism (Archibald et al., 2010). On the other hand, the circumstances of this particular asteroid could have made it deadly: it landed in the hydrocarbon-rich areas that occupied only 13% of the Earth’s surface at the time which resulted in a lot of “stratospheric soot and sulfate aerosols and causing extreme global cooling and drought” (Kaiho & Oshima, 2017). Food for thought: this means that the chances of us, humans, to be here today are 13%!…

I hope that you do notice that these are very recent papers, so the issue is hotly debated as we speak.

It is possible, nay probable, that the Deccan volcanism, which was going on long before and after the extinction, was exacerbated by the impact. This is exactly what Renne’s team postulated in 2015 after dating the lava plains in the Deccan Traps: the eruptions intensified about 50,000 years before the KT boundary, from “high-frequency, low-volume eruptions to low-frequency, high-volume eruptions”, which is about when the asteroid hit. Also, the Deccan eruptions continued for about half a million years after KPB, “which is comparable with the time lag between the KPB and the initial stage of ecological recovery in marine ecosystems” (Renne et al., 2016, p. 78).

Since we cannot get much more accurate dating than we already have, perhaps the fossils can tell us whether the dinosaurs died abruptly or slowly. Because if they got extinct in a few years instead of over 50,000 years, that would point to a cataclysmic event. Yes, but which one, big asteroid or violent volcano? Aaaand, we’re back to square one.

Actually, the last papers on the matter points to two extinctions: the Deccan extinction and the Chicxulub extinction. Petersen et al., (2016) went all the way to Antarctica to find pristine samples. They noticed a sharp increase in global temperatures by about 7.8 ºC at the onset of Deccan volcanism. This climate change would surely lead to some extinctions, and this is exactly what they found: out of 24 species of marine animals investigated, 10 died-out at the onset of Deccan volcanism and the remaining 14 died-out when Chicxulub hit.

In conclusion, because this post is already verrrry long and is becoming a proper college review, to me, a not-a-geologist/paleontologist/physicist-but-still-a-scientist, things happened thusly: first Deccan traps erupted and that lead to a dramatic global warming coupled with spewing poison in the atmosphere. Which resulted in a massive die-out (about 200,000 years before the bolide impact, says a corroborating paper, Tobin, 2017). The surviving species (maybe half or more of the biota?) continued the best they could for the next few hundred thousand years in the hostile environment. Then the Chicxulub meteorite hit and the resulting megatsunami, the cloud of super-heated dust and soot, colossal wildfires and earthquakes, acid rain and climate cooling, not to mention the intensification of the Deccan traps eruptions, finished off the surviving species. It took Earth 300,000 to 500,000 years to recover its ecosystem. “This sequence of events may have combined into a ‘one-two punch’ that produced one of the largest mass extinctions in Earth history” (Petersen et al., 2016, p. 6).

By Neuronicus, 25 August 2018

P. S. You, high school and college students who will use this for some class assignment or other, give credit thusly: Neuronicus (Aug. 26, 2018). The FIRSTS: The cause(s) of dinosaur extinction. Retrieved from https://scientiaportal.wordpress.com/2018/08/26/the-firsts-the-causes-of-dinosaur-extinction/ on [date]. AND READ THE ORIGINAL PAPERS. Ask me for .pdfs if you don’t have access, although with sci-hub and all… not that I endorse any illegal and fraudulent use of the above mentioned server for the purpose of self-education and enlightenment in the quest for knowledge that all academics and scientists praise everywhere around the Globe!

EDIT March 29, 2019. Astounding one-of-a-kind discovery is being brought to print soon. It’s about a site in North Dakota that, reportedly, has preserved the day of the Chicxhulub impact in amazing detail, with tons of fossils of all kinds (flora, mammals, dinosaurs, fish) which seems to put the entire extinction of dinosaurs in one day, thus favoring the asteroid impact hypothesis. The data is not out yet. Can’t wait til it is! Actually, I’ll have to wait some more after it’s out for the experts to examine it and then I’ll find out. Until then, check the story of the discovery here and here.

REFERENCES:

1. Alvarez LW, Alvarez W, Asaro F, & Michel HV (6 Jun 1980). Extraterrestrial cause for the cretaceous-tertiary extinction. PMID: 17783054. DOI: 10.1126/science.208.4448.1095 Science, 208(4448):1095-1108. ABSTRACT | FULLTEXT PDF

2. Archibald JD, Clemens WA, Padian K, Rowe T, Macleod N, Barrett PM, Gale A, Holroyd P, Sues HD, Arens NC, Horner JR, Wilson GP, Goodwin MB, Brochu CA, Lofgren DL, Hurlbert SH, Hartman JH, Eberth DA, Wignall PB, Currie PJ, Weil A, Prasad GV, Dingus L, Courtillot V, Milner A, Milner A, Bajpai S, Ward DJ, Sahni A. (21 May 2010) Cretaceous extinctions: multiple causes. Science,328(5981):973; author reply 975-6. PMID: 20489004, DOI: 10.1126/science.328.5981.973-aScience. FULL REPLY

3. Courtillot V, Besse J, Vandamme D, Montigny R, Jaeger J-J, & Cappetta H (1986). Deccan flood basalts at the Cretaceous/Tertiary boundary? Earth and Planetary Science Letters, 80(3-4), 361–374. doi: 10.1016/0012-821x(86)90118-4. ABSTRACT

4. Esmeray-Senlet, S., Miller, K. G., Sherrell, R. M., Senlet, T., Vellekoop, J., & Brinkhuis, H. (2017). Iridium profiles and delivery across the Cretaceous/Paleogene boundary. Earth and Planetary Science Letters, 457, 117–126. doi:10.1016/j.epsl.2016.10.010. ABSTRACT

5. Hildebrand AR, Penfield GT, Kring DA, Pilkington M, Camargo AZ, Jacobsen SB, & Boynton WV (1 Sept. 1991). Chicxulub Crater: A possible Cretaceous/Tertiary boundary impact crater on the Yucatán Peninsula, Mexico. Geology, 19 (9): 867-871. DOI: https://doi.org/10.1130/0091-7613(1991)019<0867:CCAPCT>2.3.CO;2. ABSTRACT

6. Kaiho K & Oshima N (9 Nov 2017). Site of asteroid impact changed the history of life on Earth: the low probability of mass extinction. Scientific Reports,7(1):14855. PMID: 29123110, PMCID: PMC5680197, DOI:10.1038/s41598-017-14199-x. . ARTICLE | FREE FULLTEXT PDF

7. Keller G, Adatte T, Berner Z, Harting M, Baum G, Prauss M, Tantawy A, Stueben D (30 Mar 2007). Chicxulub impact predates K–T boundary: New evidence from Brazos, Texas, Earth and Planetary Science Letters, 255(3–4): 339-356. DOI: 10.1016/j.epsl.2006.12.026. ABSTRACT

8. Keller, G. (2014). Deccan volcanism, the Chicxulub impact, and the end-Cretaceous mass extinction: Coincidence? Cause and effect? Geological Society of America Special Papers, 505:57–89. doi:10.1130/2014.2505(03) ABSTRACT

9. Petersen SV, Dutton A, & Lohmann KC. (5 Jul 2016). End-Cretaceous extinction in Antarctica linked to both Deccan volcanism and meteorite impact via climate change. Nature Communications, 7:12079. doi: 10.1038/ncomms12079. PMID: 27377632, PMCID: PMC4935969, DOI: 10.1038/ncomms12079. ARTICLE | FREE FULLTEXT PDF 

10. Renne PR, Deino AL, Hilgen FJ, Kuiper KF, Mark DF, Mitchell WS 3rd, Morgan LE, Mundil R, & Smit J (8 Feb 2013). Time scales of critical events around the Cretaceous-Paleogene boundary. Science, 8;339(6120):684-687. doi: 10.1126/science.1230492. PMID: 23393261, DOI: 10.1126/science.1230492 ABSTRACT 

11. Renne PR, Sprain CJ, Richards MA, Self S, Vanderkluysen L, Pande K. (2 Oct 2015). State shift in Deccan volcanism at the Cretaceous-Paleogene boundary, possibly induced by impact. Science, 350(6256):76-8. PMID: 26430116. DOI: 10.1126/science.aac7549 ABSTRACT

12. Schoene B, Samperton KM, Eddy MP, Keller G, Adatte T, Bowring SA, Khadri SFR, & Gertsch B (2014). U-Pb geochronology of the Deccan Traps and relation to the end-Cretaceous mass extinction. Science, 347(6218), 182–184. doi:10.1126/science.aaa0118. ARTICLE

13. Schulte P, Alegret L, Arenillas I, Arz JA, Barton PJ, Bown PR, Bralower TJ, Christeson GL, Claeys P, Cockell CS, Collins GS, Deutsch A, Goldin TJ, Goto K, Grajales-Nishimura JM, Grieve RA, Gulick SP, Johnson KR, Kiessling W, Koeberl C, Kring DA, MacLeod KG, Matsui T, Melosh J, Montanari A, Morgan JV, Neal CR, Nichols DJ, Norris RD, Pierazzo E,Ravizza G, Rebolledo-Vieyra M, Reimold WU, Robin E, Salge T, Speijer RP, Sweet AR, Urrutia-Fucugauchi J, Vajda V, Whalen MT, Willumsen PS.(5 Mar 2010). The Chicxulub asteroid impact and mass extinction at the Cretaceous-Paleogene boundary. Science, 327(5970):1214-8. PMID: 20203042, DOI: 10.1126/science.1177265. ABSTRACT

14. Tobin TS (24 Nov 2017). Recognition of a likely two phased extinction at the K-Pg boundary in Antarctica. Scientific Reports, 7(1):16317. PMID: 29176556, PMCID: PMC5701184, DOI: 10.1038/s41598-017-16515-x. ARTICLE | FREE FULLTEXT PDF 

15. Vogt, PR (8 Dec 1972). Evidence for Global Synchronism in Mantle Plume Convection and Possible Significance for Geology. Nature, 240(5380), 338–342. doi:10.1038/240338a0 ABSTRACT

How to wash SOME pesticides off produce

While EU is moving on with legislation to curtail harmful chemicals from our food, water, and air, USA is taking a few steps backwards. The most recent de-regulation concerns chlorphyrifos (CFP), a horrible pesticide banned in EU in 2008 (and in most of the world. China also prohibited its use on produce in 2016). CFP is associated with serious neurodevelopmental defects in humans and is highly toxic to the wildlife, particularly bees.

The paper that I’m covering today wanted to see if there is anything the consumer can do about pesticides in their produce. Unfortunately, they did not look at CFP. And why would they? At the time this study was conducted they probably thought, like the rest of us, that CFP is over and done with [breathe, slowly, inhale, exhale, repeat, focus].

Yang et al. (2017) bought organic Gala apples and then exposed them to two common pesticides: thiabendazole and phosmet (an organophosphate) at doses commonly used by farmers (125 ng/cm²). Then they washed the apples in three solutions: sodium bicarbonate (baking soda, NaHCO₃, with the concentration of 10 mg/mL), Clorox (germicidal bleach with the concentration of 25 mg/L available chlorine) and tap water.

Before and after the washes the researchers used surface-enhanced Raman spectroscopy (which is, basically, a special way of doing microscopy) to take a closer look at the apples.

They found out that:

1) “Surface pesticide residues were most effectively removed by sodium bicarbonate (baking soda, NaHCO3) solution when compared to either tap water or Clorox bleach” (abstract).

2) The more you wash the more pesticide you remove. If you immerse apples in backing soda for 12 minutes for thiabendazole and 15 minutes for phosmet and then rinse with water there will be no detectable residue of these pesticides on the surface.

3) “20% of applied thiabendazole and 4.4% of applied phosmet penetrated into apples” (p. 9751) which cannot be removed by washing. Thiabendazole penetrates into the apple up to 80μ, which is four times more than phosmet (which goes up top 20 μm).

4) “the standard postharvest washing method with Clorox bleach solution for 2 min did not effectively remove surface thiabendazole” (p. 9748).

5) Phosmet is completely degraded by baking soda, whereas thiabenzole appears to be only partially so.

True to my nitpicking nature, I wish that the authors washed the apples in tap water for 8 minutes, not 2, like they did for Clorox and baking soda in the internal pesticide residue removal experiment. Nevertheless, the results stand as they are robust and their detection method is ultrasensitive being able to detect thiabendazole as low as 2μg/L and phosmet as low as 10 μg/L.

Thiabendazole is a pesticide that works by interfering with a basic enzymatic reaction in anaerobic respiration. I’m an aerobe so I shouldn’t worry about this pesticide too much unless I get a huge dose of it and then it is poisonous and carcinogenic, like most things in high doses. Phosmet, on the other hand, is an acetylcholinesterase (AChE) inhibitor (AChEI), meaning its effects in humans are akin to cholinergic poisoning. Normally, acetylcholine (ACh) binds to its muscarinic and nicotinic receptors in your muscles and brain for proper functioning of same. AChE breaks down ACh when is not needed any more by said muscles and brain. Therefore, an AChEI stops AChE from breaking down ACh resulting in overall more ACh than it’s good for you. Meaning it can kill you. Phosmet’s effects, in addition to, well…, death from acute poisoning, include trouble breathing, muscle weakness or tension, convulsions, anxiety, paralysis, quite possible memory, attention, and thinking impairments. Needles to say, it’s not so great for child development either. Think nerve gas, which is also an AChEI, and you’ll get a pretty good picture. Oh, it’s also a hormone mimicker.

I guess I’m back buying organic again. Long ago I have been duped for a short while into buying organic produce for my family believing, like many others, that it is pesticide-free. And, like many others, I was wrong. Just a bit of PubMed search told me that some of the “organic” pesticides are quite unpleasant. But I’ll take copper sulfate over chlorphyrifos any day. The choice is not from healthy to unhealthy but from bad to worse. I know, I know, the paper is not about CFP. I have a lot of pet peeves, alright?

Meanwhile, I gotta go make a huge batch of baking soda solution. Thanks, Yang et al. (2017)!

REFERENCE: Yang T, Doherty J, Zhao B, Kinchla AJ, Clark JM, & He L (8 Nov 2017, Epub 25 Oct 2017). Effectiveness of Commercial and Homemade Washing Agents in Removing Pesticide Residues on and in Apples. Journal of Agricultural and Food Chemistry, 65(44):9744-9752. PMID: 29067814, doi: 10.1021/acs.jafc.7b03118. ARTICLE

By Neuronicus, 19 May 2018

NASA, not media, is to blame for the Twin Study 7% DNA change misunderstanding

In case the title threw you out of the loop, let me pull you back in. In 2015, NASA sent Scott Kelly to the International Space Station while his twin brother, Mark, stayed on the ground. When Scott came back, NASA ran a bunch of tests on them to see how space affects human body. Some of the findings were published a few weeks ago. Among the findings, one caught the eyes of media who ran stories like:  Astronaut Scott Kelly now has different DNA to his identical twin brother after spending just a year in space (Daily Mail), Astronaut’s DNA no longer matches identical twin’s after time in space, NASA finds (Channel 3), Astronaut Scott Kelly’s genes show long-term changes after a year in space (NBC), Astronaut Scott Kelly is no longer an identical twin: How a year in space altered his DNA (Fox News), Scott Kelly Spent a Year in Space and Now His DNA Is Different From His Identical Twin’s (Time),  Nasa astronaut twins Scott and Mark Kelly no longer genetically identical after space trip (Telegraph), Astronaut’s DNA changes after spending year in space when compared to identical twin bother (The Independent), Astronaut Scott Kelly’s DNA No Longer Matches Identical Twin’s After a Year in Space (People), NASA study: Astronaut’s DNA no longer identical to his identical twin’s after year in space (The Hill), NASA astronaut who spent a year in space now has different DNA from his twin (Yahoo News), Scott Kelly: NASA Twins Study Confirms Astronaut’s DNA Actually Changed in Space (Newsweek), If you go into space for a long time, you come back a genetically different person (Quartz), Space can change your DNA, we just learned (Salon), NASA Confirms Scott Kelly’s Genes Have Been Altered By Space Travel (Tech Times), even ScienceAlert 😦 ran Scott Kelly’s DNA Is No Longer Identical to His Twin’s After a Year in Space.  And dozens and dozens more….

Even the astronauts themselves said their DNA is different and they are no longer twins:

Alas, dear Scott & Mark Kelly, rest assured that despite these titles and their afferent stories, you two share the same DNA, still & forever. You are still identical twins until one of you changes species. Because that is what 7% alteration in human DNA means: you’re not human anymore.

So what gives?

Here is the root of all this misunderstanding:

“Another interesting finding concerned what some call the “space gene”, which was alluded to in 2017. Researchers now know that 93% of Scott’s genes returned to normal after landing. However, the remaining 7% point to possible longer term changes in genes related to his immune system, DNA repair, bone formation networks, hypoxia, and hypercapnia” (excerpt from NASA’s press release on the Twin Study on Jan 31, 2018, see reference).

If I wouldn’t know any better I too would think that yes, the genes were the ones who have changed, such is NASA’s verbiage. As a matter of actual fact, it is the gene expression which changed. Remember that DNA makes RNA and RNA makes protein? That’s the central dogma of molecular biology. A sequence of DNA that codes for a protein is called a gene. Those sequences do not change. But when to make a protein, how much protein, in what way, where to make this protein, which subtly different kinds of protein to make (alternative splicing), when not to make that protein, etc. is called the expression of that gene. And any of these aspects of gene expression are controlled or influenced by a whole variety of factors, some of these factors being environmental and as drastic as going to space or as insignificant as going to bed.

Some more scientifically inclined writers understood that the word “expression” was conspicuously missing from the above-mentioned paragraph and either ran clarification titles like After A Year In Space, NASA Astronaut’s Gene Expression Has Changed. Possibly Forever. (Huffington Post) or up-front rebukes like No, space did not permanently alter 7 percent of Scott Kelly’s DNA (The Verge) or No, Scott Kelly’s Year in Space Didn’t Mutate His DNA (National Geographic).

Now, I’d love, LOVE, I tell you, to jump to the throat of the media on this one so I can smugly show how superior my meager blog is when it comes to accuracy. But, I have to admit, this time is NASA’s fault. Although it is not NASA’s job to teach the central dogma of molecular biology to the media, they are, nonetheless, responsible for their own press releases. In this case, Monica Edwards and Laurie Abadie from NASA Human Research Strategic Communications did a booboo, in the words of the Sit-Com character Sheldon Cooper. Luckily for these two employees, the editor Timothy Gushanas published this little treat yesterday, right at the top of the press release:

“Editor’s note: NASA issued the following statement updating this article on March 15, 2018:

Mark and Scott Kelly are still identical twins; Scott’s DNA did not fundamentally change. What researchers did observe are changes in gene expression, which is how your body reacts to your environment. This likely is within the range for humans under stress, such as mountain climbing or SCUBA diving.

The change related to only 7 percent of the gene expression that changed during spaceflight that had not returned to preflight after six months on Earth. This change of gene expression is very minimal.  We are at the beginning of our understanding of how spaceflight affects the molecular level of the human body. NASA and the other researchers collaborating on these studies expect to announce more comprehensive results on the twins studies this summer.”

Good for you for rectifying your mistake, NASA! And good for you too the few media outlets that corrected their story like CNN who changed their title from Astronaut’s DNA no longer same as his identical twin, NASA finds to Astronaut’s gene expression no longer same as his identical twin, NASA finds.

But, seriously, NASA, what’s up with you guys keep screwing up molecular biology stuff?! Remember the arsenic-loving bacteria debacle? That paper is still not retracted  and that press release is still up on your website! Ntz, ntz, for shame… NASA, you need better understanding of basic science and/or better #Scicomm in your press releases. Hiring? I’m offering!

REFERENCE: NASA. Edwards, M.  & Abadie, L. (Jan. 31, 2018). NASA Twins Study Confirms Preliminary Findings, Ed. Timothy Gushanas, retrieved on March 14,15, & 16, 2018. Address: https://www.nasa.gov/feature/nasa-twins-study-confirms-preliminary-findings

By Neuronicus, 16 March 2018

P.S. Sometimes is a pain to be obsessed with accuracy (cue in smallest violins). For example, I cannot stop myself from adding something just to be scrupulously correct. Since the day they were conceived, identical twins’ DNAs are starting to diverge. There are all sorts of things that do change the actual sequence of DNA. DNA can be damaged by radiation (which you can get a lot of in space) or exposure to some chemicals. Other changes are simply due to random mutations. So no twins are exactly identical, but the changes are so minuscule, nowhere near 1%, let alone 7%, that it is safe to say that their DNA is identical.

P.P.S. With all this hullabaloo about the 7% DNA change everybody glossed over and even I forgot to mention the one finding that is truly weird: the elongation of telomeres for Scott, the one that was in space. Telomeres are interesting things, they are repetitive sequences of DNA (TTAGGG/AATCCC) at the end of the chromosomes that are repeated thousands of times. The telomere’s job is to protect the end of the chromosomes. You see, every time a cell divides the DNA copying machinery cannot copy the last bits of the chromosome (blame it on physics or chemistry, one of them things) and so some of it is lost. So evolution came up with a solution: telomeres, which are bits of unusable DNA that can be safely ignored and left behind. Or so we think at the moment. The length of telomeres has been implicated in some curious things, like cancer and life-span (immortality thoughts, anyone?). The most common finding is the shortening of telomeres associated with stress, but Scott’s were elongated, so that’s the first weird thing. I didn’t even know the telomeres can get elongated in living healthy adult humans. But wait, there is more: NASA said that “the majority of those telomeres shortened within two days of Scott’s return to Earth”. Now that is the second oddest thing! If I would be NASA that’s where I would put my money on, not on the gene expression patterns. And I would really, really like to see which types of cells show those longer telomeres, because I have a hunch is some type of dermal cell, which may be ontogenetically related to a neuronal cell.