High fructose corn syrup IS bad for you

Because I cannot leave controversial things well enough alone – at least not when I know there shouldn’t be any controversy – my ears caught up with my tongue yesterday when the latter sputtered: “There is strong evidence for eliminating sugar from commonly used food products like bread, cereal, cans, drinks, and so on, particularly against that awful high fructose corn syrup”. “Yeah? You “researched” that up, haven’t you? Google is your bosom friend, ain’t it?” was the swift reply. Well, if you get rid of the ultra-emphatic air-quotes flanking the word ‘researched’ and replace ‘Google’ with ‘Pubmed’, then, yes, I did researched it and yes, Pubmed is my bosom friend.

Initially, I wanted to just give you all a list with peer-reviewed papers that found causal and/or correlational links between high fructose corn syrup (HFCS) and weight gain, obesity, type 2 diabetes, cardiovascular disease, fatty liver disease, metabolic and endocrine anomalies and so on. But there are way too many of them; there are over 500 papers on the subject in Pubmed only. And most of them did find that HFCS does nasty stuff to you, look for yourselves here. Then I thought to feature a paper showing that HFCS is differently metabolized than the fructose from fruits, because I keep hearing that lie perpetrated by the sugar and corn industries that “sugar is sugar” (no, it’s not! Demonstrably so!), but I doubt my yesterday’s interlocutor would care about liver’s enzymatic activity and other chemical processes with lots of acronyms. So, finally, I decided to feature a straight forward, no-nonsense paper, published recently, done at a top tier university, with human subjects, so I won’t hear any squabbles.

Price et al. (2018) studied 49 healthy subjects aged age 18–40 yr, of normal and stable body weight, and free from confounding medications or drugs, whose physical activity and energy-balanced meals were closely monitored. During the study, the subjects’ food and drink intake as well as their timing were rigorously controlled. The researchers varied only the beverages between groups, in such a way that one group received a drink sweetened with HFCS-55 (55% fructose, 45% glucose, as the one used in commercially available drinks) with every controlled meal, whereas the other group received an identical drink in size (adjusted for their energy requirements in such a way that it provided the same 25% of it), but sweetened with aspartame. The study lasted two weeks. No other beverage was allowed, including fruit juice. Urine samples were collected daily and blood samples 4 times per day.

There was a body weight increase of 810 grams (1.8 lb) in subjects consuming HFCS-sweetened beverages for 2 weeks when compared with aspartame controls. The researches also found differences in the levels of a whole host of acronyms (ppTG, ApoCIII, ApoE, OEA, DHEA, DHG, if you must know) involved in a variety of nasty things, like obesity, fatty liver disease, atherosclerosis, cardiovascular disease, stroke, diabetes, even Alzheimer’s.

This study is the third part of a larger NIH-funded study which investigates the metabolic effects of consuming sugar-sweetened beverages in about 200 participants over 5 years, registered at clinicaltrials.gov as NCT01103921. The first part (Stanhope et al., 2009) reported that consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans” (title), and the second part (Stanhope et al., 2015) found that “consuming beverages containing 10%, 17.5%, or 25% of energy requirements from HFCS produced dose-dependent increases in circulating lipid/lipoprotein risk factors for cardiovascular disease and uric acid within 2 weeks” (Abstract). They also found a dose-dependant increase in body weight, but in those subjects the results were not statistically significant (p = 0.09) after correcting for multiple comparisons. But I’ll bet that if/when the authors will publish all the data in one paper at the end of clinical trials they will have more statistical power and the trend in weight gain more obvious, as in the present paper.  Besides, it looks like there may be more than three parts to this study anyway.

The adverse effects of a high sugar diet, particularly in HFCS, are known to so many researchers in the field that they have been actually compiled in a name: the “American Lifestyle-Induced Obesity Syndrome model, which included consumption of a high-fructose corn syrup in amounts relevant to that consumed by some Americans” (Basaranoglu et al., 2013). It doesn’t refer only to increases in body weight, but also type 2 diabetes, cardiovascular disease, hypertriglyceridemia, fatty liver disease, atherosclerosis, gout, etc.

The truly sad part is that avoiding added sugars in diets in USA is impossible unless you do all – and I mean all – your cooking home, including canning, jamming, bread-making, condiment-making and so on, not just “Oh, I’ll cook some chicken or ham tonight” because in that case you end up using canned tomato sauce (which has added sugar), bread crumbs (which have added sugar), or ham (which has added sugar), salad dressing (which has sugar) and so on. Go on, check your kitchen and see how many ingredients have sugar in them, including any meat products short of raw meat. If you never read the backs of the bottles, cans, or packages, oh my, are you in for a big surprise if you live in USA…

There are lot more studies out there on the subject, as I said, of various levels of reading difficulty. This paper is not easy to read for someone outside the field, that’s for sure. But the main gist of it is in the abstract, for all to see.

150 hfcs - Copy

P.S. 1. Please don’t get me wrong: I am not against sugar in desserts, let it be clear. Nobody makes a more mean sweetalicious chocolate cake or carbolicious blueberry muffin than me (both terms coined by me!), as I have been reassured many times. But I am against sugar in everything. You know I haven’t found in any store, including high-end and really high-end stores a single box of cereal of any kind without sugar? Just for fun, I’d like to be a daredevil and try it once. But there ain’t. Not in USA, anyway. I did find them in EU though. But I cannot keep flying over the Atlantic in the already crammed at premium luggage space unsweetened corn flakes from Europe which are probably made locally, incidentally and ironically, with good old American corn.

P.S. 2 I am not so naive, blind, or zealous to overlook the studies that did not find any deleterious effects of HFCS consumption. Actually, I was on the fence about HFCS until about 10 years ago when the majority of papers (now overwhelming majority) was showing that HFCS consumption not only increases weight gain, but it can also lead to more serious problems like the ones mentioned above. Or the few papers that say all added sugar is bad, but HFCS doesn’t stand out from the other sugars when it comes to disease or weight gain. But, like with most scientific things, the majority has it its way and I bow to it democratically until the new paradigm shift. Besides, the exposés of Kearns et al. (2016a, b, 2017) showing in detail and with serious documentation how the sugar industry paid prominent researchers for the past 50 years to hide the deleterious effects of added sugar (including cancer!) further cemented my opinion about added sugar in foods, particularly HFCS.


  1. Price CA, Argueta DA, Medici V, Bremer AA, Lee V, Nunez MV, Chen GX, Keim NL, Havel PJ, Stanhope KL, & DiPatrizio NV (1 Aug 2018, Epub 10 Apr 2018). Plasma fatty acid ethanolamides are associated with postprandial triglycerides, ApoCIII, and ApoE in humans consuming a high-fructose corn syrup-sweetened beverage. American Journal of Physiology. Endocrinology and Metabolism, 315(2): E141-E149. PMID: 29634315, PMCID: PMC6335011 [Available on 2019-08-01], DOI: 10.1152/ajpendo.00406.2017. ARTICLE | FREE FULTEXT PDF
  1. Stanhope KL1, Medici V2, Bremer AA2, Lee V2, Lam HD2, Nunez MV2, Chen GX2, Keim NL2, Havel PJ (Jun 2015, Epub 22 Apr 2015). A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. The American Journal of Clinical Nutrition, 101(6):1144-54. PMID: 25904601, PMCID: PMC4441807, DOI: 10.3945/ajcn.114.100461. ARTICLE | FREE FULTEXT PDF
  1. Stanhope KL1, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ (May 2009, Epub 20 Apr 2009). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of Clinical Investigation,119(5):1322-34. PMID: 19381015, PMCID: PMC2673878, DOI:10.1172/JCI37385. ARTICLE | FREE FULTEXT PDF

(Very) Selected Bibliography:

Bocarsly ME, Powell ES, Avena NM, Hoebel BG. (Nov 2010, Epub 26 Feb 2010). High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacology, Biochemistry, and Behavior, 97(1):101-6. PMID: 20219526, PMCID: PMC3522469, DOI: 10.1016/j.pbb.2010.02.012. ARTICLE | FREE FULLTEXT PDF

Kearns CE, Apollonio D, Glantz SA (21 Nov 2017). Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents. PLoS Biology, 15(11):e2003460. PMID: 29161267, PMCID: PMC5697802, DOI: 10.1371/journal.pbio.2003460. ARTICLE | FREE FULTEXT PDF

Kearns CE, Schmidt LA, Glantz SA (1 Nov 2016). Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Internal Medicine, 176(11):1680-1685. PMID: 27617709, PMCID: PMC5099084, DOI: 10.1001/jamainternmed.2016.5394. ARTICLE | FREE FULTEXT PDF

Mandrioli D, Kearns CE, Bero LA (8 Sep 2016). Relationship between Research Outcomes and Risk of Bias, Study Sponsorship, and Author Financial Conflicts of Interest in Reviews of the Effects of Artificially Sweetened Beverages on Weight Outcomes: A Systematic Review of Reviews. PLoS One, 11(9):e0162198.PMID: 27606602, PMCID: PMC5015869, DOI: 10.1371/journal.pone.0162198. ARTICLE | FREE FULTEXT PDF

By Neuronicus, 22 March 2019

Pic of the day: Total amount of DNA on Earth

139 DNA amount, better font - Copy

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).

138- Vogt - Copy.jpg

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.

138-alvarez - Copy

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.

138-chicxulub - Copy

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.

138-66 chixhulub - Copy

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).

138-timeline dinosaur - Copy

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.


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

No Link Between Mass Shootings & Mental Illness

On Valentine’s Day another horrifying school mass shooting happened in USA, leaving 17 people dead. Just like after the other mass shootings, a lot of people – from media to bystanders, from gun lovers to gun critics, from parents to grandparents, from police to politicians – talk about the link between mental illness and mass shootings. As one with advanced degrees in both psychology and neuroscience, I am tired to explain over and over again that there is no significant link between the two! Mass shootings happen because an angry person has had enough sorrow, stress, rejection and/or disappointment that leads to hating the ones they think are responsible for it and HAS ACCESS TO A MASS KILLING WEAPON. Yeah, I needed the caps. Sometimes scientists too need to shout to be heard.

So here is the abstract of a book chapter called straightforwardly “Mass Shootings and Mental Illness”. The entire text is available at the links in the reference below.

From Knoll & Annas (2015):

“Common Misperceptions

  • Mass shootings by people with serious mental illness represent the most significant relationship between gun violence and mental illness.
  • People with serious mental illness should be considered dangerous.
  • Gun laws focusing on people with mental illness or with a psychiatric diagnosis can effectively prevent mass shootings.
  • Gun laws focusing on people with mental illness or a psychiatric diagnosis are reasonable, even if they add to the stigma already associated with mental illness.

Evidence-Based Facts

  • Mass shootings by people with serious mental illness represent less than 1% of all yearly gun-related homicides. In contrast, deaths by suicide using firearms account for the majority of yearly gun-related deaths.
  • The overall contribution of people with serious mental illness to violent crimes is only about 3%. When these crimes are examined in detail, an even smaller percentage of them are found to involve firearms.
  • Laws intended to reduce gun violence that focus on a population representing less than 3% of all gun violence will be extremely low yield, ineffective, and wasteful of scarce resources. Perpetrators of mass shootings are unlikely to have a history of involuntary psychiatric hospitalization. Thus, databases intended to restrict access to guns and established by guns laws that broadly target people with mental illness will not capture this group of individuals.
  • Gun restriction laws focusing on people with mental illness perpetuate the myth that mental illness leads to violence, as well as the misperception that gun violence and mental illness are strongly linked. Stigma represents a major barrier to access and treatment of mental illness, which in turn increases the public health burden”.

REFERENCE: Knoll, James L. & Annas, George D. (2015). Mass Shootings and Mental Illness. In book: Gun Violence and Mental Illness, Edition: 1st, Chapter: 4, Publisher: American Psychiatric Publishing, Editors: Liza H. Gold, Robert I. Simon. ISBN-10: 1585624985, ISBN-13: 978-1585624980. FULLTEXT PDF via ResearchGate | FULLTEXT PDF via Psychiatry Online

The book chapter is not a peer-reviewed document, even if both authors are Professors of Psychiatry. To quiet putative voices raising concerns about that, here is a peer-reviewed paper with open access that says basically the same thing:

Swanson et al. (2015) looked at large scale (thousands to tens of thousands of individuals) data to see if there is any relationship between violence, gun violence, and mental illness. They concluded that “epidemiologic studies show that the large majority of people with serious mental illnesses are never violent. However, mental illness is strongly associated with increased risk of suicide, which accounts for over half of US firearms–related fatalities”. The last sentence is reminiscent of the finding that stricter gun control laws lower suicide rate.

REFERENCE: Swanson JW, McGinty EE, Fazel S, Mays VM (May 2015). Mental illness and reduction of gun violence and suicide: bringing epidemiologic research to policy. Annals of Epidemiology, 25(5): 366–376. doi: 10.1016/j.annepidem.2014.03.004, PMCID: PMC4211925. FULLTEXT | FULLTEXT PDF.

Further peer-reviewed bibliography (links to fulltext pdfs):

  1. Guns, anger, and mental disorders: Results from the National Comorbidity Survey Replication (NCS-R): “a large number of individuals in the United States have anger traits and also possess firearms at home (10.4%) or carry guns outside the home (1.6%).”
  2. News Media Framing of Serious Mental Illness and Gun Violence in the United States, 1997-2012: “most news coverage occurred in the wake of mass shootings, and “dangerous people” with serious mental illness were more likely than “dangerous weapons” to be mentioned as a cause of gun violence.”
  3. The Link Between Mental Illness and Firearm Violence: Implications for Social Policy and Clinical Practice: “Firearm violence is a significant and preventable public health crisis. Mental illness is a weak risk factor for violence despite popular misconceptions reflected in the media and policy”.
  4. Using Research Evidence to Reframe the Policy Debate Around Mental Illness and Guns: Process and Recommendations: “restricting firearm access on the basis of certain dangerous behaviors is supported by the evidence; restricting access on the basis of mental illness diagnoses is not”.
  5. Mental Illness, Mass Shootings, and the Politics of American Firearms: “notions of mental illness that emerge in relation to mass shootings frequently reflect larger cultural stereotypes and anxieties about matters such as race/ethnicity, social class, and politics. These issues become obscured when mass shootings come to stand in for all gun crime, and when “mentally ill” ceases to be a medical designation and becomes a sign of violent threat”.

131 gun - Copy

By Neuronicus, 25 February 2018

The oldest known anatomically modern humans in Europe

A couple of days ago, on December 1st, was the National Day of Romania, a small country in the South-East of Europe. In its honor, I dug out a paper that shows that some of the earliest known modern humans in Europe were also… dug out there.

Trinkaus et al. (2003) investigated the mandible of an individual found in 2002 by a Romanian speological expedition in Peștera cu Oase (the Cave with Bones), one of the caves in the SouthWest of the country, not far from where Danube meets the Carpathians.

First the authors did a lot of very fine measurement of various aspects of the jaw, including the five teeth, and then compared them with those found in other early humans and Neanderthals. The morphological features place the Oase 1 individual as an early modern human with some Neanderthal features. The accelerator mass spectrometry radiocarbon (14C) direct dating makes him the oldest early modern human discovered to that date in Europe; he’s 34,000–36,000 year old. I’m assuming is a he for no particular reason; the paper doesn’t specify anywhere whether they know the jaw owner’s gender and age. A later paper (Fu et al., 2015) says Oase 1 is even older: 37,000–42,000-year-old.

After this paper it seemed to be a race to see what country can boast to have the oldest human remains on its territory. Italy and UK successfully reassessed their own previous findings thusly: UK has a human maxilla that was incorrectly dated in 1989 but new dating makes it 44,200–39,000 year old, carefully titling their paper “The earliest evidence for anatomically modern humans in northwestern Europe” (Higham et al., 2011) while Italy’s remains that they thought for decades to be Neanderthal turned out to be 45,000-43,000 years old humans, making “the Cavallo human remains […] the oldest known European anatomically modern humans” (Benmazzi et al., 2011).

I wonder what prompted the sudden rush in reassessing the old untouched-for-decades fossils… Probably good old fashioned national pride. Fair enough. Surely it cannot have anything to do with the disdain publicly expressed by some Western Europe towards Eastern Europe, can it? Surely scientists are more open minded than some petty xenophobes, right?

Well, the above thought wouldn’t have even crossed my mind, nor would I have noticed that the Romanians’ discovery has been published in PNAS and the others in Nature, had it not been for the Fu et al. (2015) paper, also published in Nature. This paper does a genetic analysis of the Oase 1 individual and through some statistical inferences that I will not pretend to fully understand they arrive to two conclusions. First, Oase 1 had a “Neanderthal ancestor as recently as four to six generations back”. OK. Proof of interbreeding, nothing new here. But the second conclusion I will quote in full: “However, the Oase individual does not share more alleles with later Europeans than with East Asians, suggesting that the Oase population did not contribute substantially to later humans in Europe.”

Now you don’t need to know much about statistics or about basic logic either to know that from 1 (one) instance alone you cannot generalize to a whole population. That particular individual from the Oase population hasn’t contributed to later humans in Europe, NOT the entire population. Of course it is possible that that is the case, but you cannot scientifically draw that conclusion from one instance alone! This is in the abstract, so everybody can see this, but I got access to the whole paper, which I have read in the hopes against hope that maybe I’m missing something. Nope. The authors did not investigate any additional DNA and they reiterate that the Oase population did not contribute to modern-day Europeans. So it’s not a type-O. From the many questions that are crowding to get out like ‘How did it get past reviewers?’, ‘Why was it published in Nature (interesting paper, but not that interesting, we knew about interbreeding so what makes it so new and exciting)?’, the one that begs to be asked the most is: ‘Why would they say this, when stating the same thing about the Oase 1 individual instead about the Oase population wouldn’t have diminished their paper in any way?’ .

I must admit that I am getting a little paranoid in my older age. But with all the hate that seems to come out and about these days EVERYWHERE towards everything that is “not like me” and “I don’t want it to be like me”, one cannot but wonder… Who knows, maybe it is really just as simple as an overlooked mistake or some harmless national pride so all is good and life goes on, especially since the authors of all four papers discussed above are from various countries and institutions all across the Globe. Should that be the case, I offer my general apologies for suspecting darker motives behind these papers, but I’m not holding my breath.



1) Trinkaus E, Moldovan O, Milota S, Bîlgăr A, Sarcina L, Athreya S, Bailey SE, Rodrigo R, Mircea G, Higham T, Ramsey CB, & van der Plicht J. (30 Sep 2003, Epub 22 Sep 2003). An early modern human from the Peştera cu Oase, Romania. Proceedings of the National Academy of Sciences U S A,  100(20):11231-11236. PMID: 14504393, PMCID: PMC208740, DOI: 10.1073/pnas.2035108100. ARTICLE  | FREE FULLTEXT PDF

 2) Higham T, Compton T, Stringer C, Jacobi R, Shapiro B, Trinkaus E, Chandler B, Gröning F, Collins C, Hillson S, O’Higgins P, FitzGerald C, & Fagan M. (2 Nov 2011). The earliest evidence for anatomically modern humans in northwestern Europe. Nature. 479(7374):521-4. PMID: 22048314, DOI: 10.1038/nature10484. ARTICLE | FULLTEXT PDF via ResearchGate

3) Benazzi S, Douka K, Fornai C, Bauer CC, Kullmer O, Svoboda J, Pap I, Mallegni F, Bayle P, Coquerelle M, Condemi S, Ronchitelli A, Harvati K, & Weber GW. (2 Nov 2011). Early dispersal of modern humans in Europe and implications for Neanderthal behaviour. Nature, 479(7374):525-8. PMID: 22048311, DOI: 10.1038/nature10617. ARTICLE | FULLTEXT PDF via ResearchGate

4) Fu Q, Hajdinjak M, Moldovan OT, Constantin S, Mallick S, Skoglund P, Patterson N, Rohland N, Lazaridis I, Nickel B, Viola B, Prüfer K, Meyer M, Kelso J, Reich D, & Pääbo S. (13 Aug 2015, Epub 22 Jun 2015). An early modern human from Romania with a recent Neanderthal ancestor. Nature. 524(7564):216-9. PMID: 26098372, PMCID: PMC4537386, DOI:10.1038/nature14558. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 3 December 2016






A third way of neuronal communication

electrical fields - CopyEvery neuroscience or biology textbook will tell you that neurons communicate with one another in two ways: via chemical synapses (one neuron releases some substances that change the membrane potential of the receiving neuron) or via electrical synapses (neurons physically share some membrane proteins that allows the electrical impulse to go from one neuron to another). (Nota bene: for the taxonomic nitpickers, I decided that the other non-conventional forms of communication, like diffusion, fall in one or the other of the two categories above).

Now Qiu et al. (2015) have some evidence that there may be another way of neuronal chatting. Long ago (in 1924), Hans Berger observed that neurons have rhythmic and spontaneous electrical activity. The rhythmic activity of an entire population of neurons is called a wave and can be detected with rudimentary tools such as EEG. Qiu et al. reasoned that the speed of such a traveling wave is too slow to be explained by conventional neuronal communication (of which we know quite a lot).

So the researchers ran some computer simulations to test if diffuse electrical fields can explain the speed of a wave, instead of the conventional fast communications. In other words, can local, weak, slow endogenous fields sweep the brain by recruiting nearby neurons? The computer simulations said it is possible, with a very slow speed of 10 cm/s.

Then they recorded the electrical activity of mouse hippocampus isolated in a Petri dish. When the researchers blocked the electrical field there was a decrease in the speed of the wave, meaning the field is required for the wave speed observed.

To be fair, this is not a new idea; even in the early eighties these fields were suggested, because the wave persisted even when the other two ways of communicating have been blocked. And in the early noughts it was shown that a neural network is much more sensitive to electrical field manipulation than individual neurons. What makes this paper interesting is that the authors show that the endogenous electrical fields are not too weak to underlie the wave, as previously thought. The work has implications for the study of epilepsy, sleep, and memory.

Reference: Qiu C, Shivacharan RS, Zhang M, & Durand DM (2 December 2015). Can Neural Activity Propagate by Endogenous Electrical Field?, Journal of Neuroscience, 35(48): 15800-15811; doi: 10.1523/JNEUROSCI.1045-15.2015 Article | Full Text via Research Gate | ScienceAlert cover

By Neuronicus, 11 February 2016

Mechanisms of stress resilience

71 stress - CopyLast year a new peer-reviewed journal called Neurobiology of Stress made its debut. The journal is published by Elsevier, who, in an uncharacteristic move, has provided Open Access for its first three issues. So hurry up and download the papers.

The very first issue is centered around the idea of resilience. That is, exposed to the same stressors, some people are more likely to develop stress-induced diseases, whereas others seem to be immune to the serious effects of stress.

Much research has been carried out to uncover the effects of chronic stress or of an exposure to a single severe stressor, which vary from cardiovascular disorders, obesity, irritable bowel syndrome, immune system dysfunctions to posttraumatic stress disorder, generalized anxiety, specific phobias, or depression. By comparison, there is little, but significant data on resilience: the ability to NOT develop those nasty stress-induced disorders. Without doubt, one reason for this scarcity is the difficulty in finding such rare subjects in our extremely stressful society. Therefore most of the papers in this issue focus on animal models.

Nevertheless, there is enough data on resilience to lead to no less that twenty reviews on the subject. It was difficult to choose one as most are very interesting, tackling various aspects of resilience, from sex differences to prenatal exposure to stress, from epigenetic to neurochemical modifications, from social inequalities to neurogenesis and so on.

So I chose for today a more general review of Pfau & Russo (2015), entitled “Peripheral and central mechanisms of stress resilience”. After it introduces the reader to four animal models of resilience, the paper looks at the neruoendocrine responses to stress and identifies some possible chemical mediators of resilience (like certain hormones), then at the immune responses to stress (bad, bad cytokines), and finally at the brain responses to stress (surprisingly, not focusing on amygdala, hypothalamus or hippocampus, but on the dopamine system originating from ventral tegmental area).

I catalogue the review as a medium difficulty read because it requires a certain amount of knowledge of the stress field beforehand. But do check out the other ones in the issue, too!

Reference: Pfau ML & Russo SJ (1 Jan 2015). Peripheral and central mechanisms of stress resilience. Neurobiology of Stress, 1:66-79. PMID: 25506605, PMCID: PMC4260357, DOI: 10.1016/j.ynstr.2014.09.004. Article | FREE FULLTEXT PDF

By Neuronicus, 24 January 2016

Your blood is better than my blood

Siamese tomatoes. Taken from here.

Parabiosis is a surgical procedure that lets two animals to share the same blood; it’s a case of reverse conjoined twins restricted to the circulatory system.

The procedure is over 150 years old and is a useful technique in physiology, though rarely used, probably due to the perceived cruelty towards the animals, although today is performed under anesthesia and aseptic condition. It delivered good data; for example, it was a parabiosis experiment with rodents that showed is not the sugar in the blood that causes cavities but the sugar in the mouth. Similarly, parabiosis has been proven useful in cancer, diabetes, and ageing research.

Scudellari (2015) wrote a News piece for Nature describing some advancements in the ageing field using the parabiosis technique. Namely, by joining the circulatory systems of a young and an old mouse, researchers have observed that the old mouse is faster, smarter, with rejuvenated muscles and glossier fur. Now the race is to find out what in the blood does it. Researchers caution that the young blood is not effectively reversing ageing, but may have factors circulating in it that promote tissue repair. Already a muscle-rejuvenating protein has been identified.

I am not going through the original papers themselves as I usually do (they are provided as links in the Reference paper). Instead, I am featuring the news piece by Scudellari because in addition of looking at parabiosis and ageing result, it also provides a nice historical account of the use of parabiosis. Enjoy!

Reference: Scudellari, M. (22 Jan 2015). Ageing research: Blood to blood. Nature, 517: 426-429. Article | FREE Fulltext PDF

By Neuronicus, 4 January 2015

Yeast can make morphine

poppy - Copy

Opiates like morphine and heroin can be made at home by anybody with a home beer-brewing kit and the right strain of yeast. In 2015, two published papers and a Ph.D. dissertation described the relatively easy way to convince yeast to make morphine from sugar (the links are provided in the Reference paper). That is the bad news.

The good news is that scientists have been policing themselves (well, most of them, anyway) long before regulations are put in place to deal with technological advancements by, for example, limiting access to the laboratory, keeping things under lock and key, publishing incomplete data, and generally being very careful with what they’re doing.

Complementing this behavior, an article published by Oye et al. (2015) outlines other measures that can be put in place so that this new piece of knowledge doesn’t increase the accessibility to opiates, thereby increasing the number of addicts, which is estimated to more than 16 million people worldwide. For example, researchers can make the morphine-producing yeast dependent on unusual nutrients or engineer the existing strain to produce less-marketable varieties of opiates or prohibit the access to made-to-order DNA sequences for this type of yeast and so on.

You may very well ask “Why did the scientists made this kind of yeast anyway?”. Because some medicines are either very expensive or laborious to produce by the pharmaceutical companies, the researchers have sought a method to make these drugs more easily and cheaply by engineering bacteria, fungi, or plants to produce them for us. Insulin is a good example of an expensive and hard-to-get-by drug that we managed to engineer yeast strains to produce it for us. And opiates are still the best analgesics out there.

Reference: Oye KA, Lawson JC, & Bubela T (21 May 2015). Drugs: Regulate ‘home-brew’ opiates. Nature, 521(7552):281-3. doi: 10.1038/521281a. Article | FREE Fulltext PDF

By Neuronicus, 2 January 2016