Love and the immune system

Valentine’s day is a day when we celebrate romantic love (well, some of us tend to) long before the famous greeting card company Hallmark was established. Fittingly, I found the perfect paper to cover for this occasion.

In the past couple of decades it became clear to scientists that there is no such thing as a mental experience that doesn’t have corresponding physical changes. Why should falling in love be any different? Several groups have already found that levels of some chemicals (oxytocin, cortisol, testosterone, nerve growth factor, etc.) change when we fall in love. There might be other changes as well. So Murray et al. (2019) decided to dive right into it and check how the immune system responds to love, if at all.

For two years, the researchers looked at certain markers in the immune system of 47 women aged 20 or so. They drew blood when the women reported to be “not in love (but in a new romantic relationship), newly in love, and out-of-love” (p. 6). Then they sent their samples to their university’s Core to toil over microarrays. Microarray techniques can be quickly summarized thusly: get a bunch of molecules of interest, in this case bits of single-stranded DNA, and stick them on a silicon plate or a glass slide in a specific order. Then you run your sample over it and what sticks, sticks, what not, not. Remember that DNA loves to be double stranded, so any single strand will stick to their counterpart, called complementary DNA. You put some fluorescent dye on your genes of interest and voilà, here you have an array of genes expressed in a certain type of tissue in a certain condition.

Talking about microarrays got me a bit on memory lane. When fMRI started to be a “must” in neuroscience, there followed a period when the science “market” was flooded by “salad” papers. We called them that because there were so many parts of the brain reported as “lit up” in a certain task that it made a veritable “salad of brain parts” out of which it was very difficult to figure out what’s going on. I swear that now that the fMRI field matured a bit and learned how to correct for multiple comparisons as well as to use some other fancy stats, the place of honor in the vegetable mix analogy has been relinquished to the ‘-omics’ studies. In other words, a big portion of the whole-genome or transcriptome studies became “salad” studies: too many things show up as statistically significant to make head or tail of it.

However, Murray et al. (2019) made a valiant – and successful – effort to figure out what those up- or down- regulated 61 gene transcripts in the immune system cells of 17 women falling in love actually mean. There’s quite a bit I am leaving out but, in a nutshell, love upregulated (that is “increased”) the expressions of genes involved in the innate immunity to viruses, presumably to facilitate sexual reproduction, the authors say.

The paper is well written and the authors graciously remind us that there are some limitations to the study. Nevertheless, this is another fine addition to the unbelievably fast growing body of knowledge regarding human body and behavior.

Shame that this research was done only with women. I would have loved to see how men’s immune systems respond to falling in love.

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REFERENCE: Murray DR, Haselton MG, Fales M, & Cole SW. (Feb 2019, Epub 2 Oct 2018). Falling in love is associated with immune system gene regulation. Psychoneuroendocrinology, Vol. 100, Pg. 120-126. doi: 10.1016/j.psyneuen.2018.09.043. PMID: 30299259, PMCID: PMC6333523 [Available on 2020-02-01], DOI: 10.1016/j.psyneuen.2018.09.043 ARTICLE

FYI: PMC6333523 [Available on 2020-02-01] means that the fulltext will be available for free to the public one year after the publication on the US governmental website PubMed (https://www.ncbi.nlm.nih.gov/pubmed/), no matter how much Elsevier will charge for it. Always, always, check the PMC library (https://www.ncbi.nlm.nih.gov/pmc/) on PubMed to see if a paper you saw in Nature or Elsevier is for free there because more often than you’d think it is.

PubMed = the U.S. National Institutes of Health’s National Library of Medicine (NIH/NLM), comprising of “more than 29 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites” .

PMC = “PubMed Central® (PMC) is a free fulltext archive of biomedical and life sciences journal literature at the U.S. National Institutes of Health’s National Library of Medicine (NIH/NLM)” with a whooping fulltext library of over 5 million papers and growing rapidly. Love PubMed!

By Neuronicus, 14 February 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.

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All well and good. And it was all well and good since Carl Linnaeus introduced his famous taxonomy system in the 18th 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.

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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

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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.

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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

Apathy

Le Heron et al. (2018) defines apathy as a marked reduction in goal-directed behavior. But in order to move, one must be motivated to do so. Therefore, a generalized form of impaired motivation also hallmarks apathy.

The authors compiled for us a nice mini-review combing through the literature of motivation in order to identify, if possible, the neurobiological mechanism(s) of apathy. First, they go very succinctly though the neuroscience of motivated behavior. Very succinctly, because there are literally hundreds of thousands of worthwhile pages out there on this subject. Although there are several other models proposed out-there, the authors’ new model on motivation includes the usual suspects (dopamine, striatum, prefrontal cortex, anterior cingulate cortex) and you can see it in the Fig. 1.

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Fig. 1 from Le Heron et al. (2018). The red underlining is mine because I really liked how well and succinctly the authors put a universal truth about the brain: “A single brain region likely contributes to more than one process, but with specialisation”. © Author(s) (or their employer(s)) 2018.

After this intro, the authors go on to showcasing findings from the effort-based decision-making field, which suggest that the dopamine-producing neurons from ventral tegmental area (VTA) are fundamental in choosing an action that requires high-effort for high-reward versus a low-effort for low-reward. Contrary to what Wikipedia tells you, a reduction, not an increase, in mesolimbic dopamine is associated with apathy, i.e. preferring a low-effort for low-reward activity.

Next, the authors focus on why are the apathetic… apathetic? Basically, they asked the question: “For the apathetic, is the reward too little or is the effort too high?” By looking at some cleverly designed experiments destined to parse out sensitivity to reward versus sensitivity to effort costs, the authors conclude that the apathetics are indeed sensitive to the reward, meaning they don’t find the rewards good enough for them to move.  Therefore, the answer is the reward is too little.

In a nutshell, apathetic people think “It’s not worth it, so I’m not willing to put in the effort to get it”. But if somehow they are made to judge the reward as good enough, to think “it’s worth it”, they are willing to work their darndest to get it, like everybody else.

The application of this is that in order to get people off the couch and do stuff you have to present them a reward that they consider worth moving for, in other words to motivate them. To which any practicing psychologist or counselor would say: “Duh! We’ve been saying that for ages. Glad that neuroscience finally caught up”.  Because it’s easy to say people need to get motivated, but much much harder to figure out how.

This was a difficult write for me and even I recognize the quality of this blogpost as crappy. That’s because, more or less, this paper is within my narrow specialization field. There are points where I disagree with the authors (some definitions of terms), there are points where things are way more nuanced than presented (dopamine findings in reward), and finally there are personal preferences (the interpretation of data from Parkinson’s disease studies). Plus, Salamone (the second-to-last author) is a big name in dopamine research, meaning I’m familiar with his past 20 years or so worth of publications, so I can infer certain salient implications (one dopamine hypothesis is about saliency, get it?).

It’s an interesting paper, but it’s definitely written for the specialist. Hurray (or boo, whatever would be your preference) for another model of dopamine function(s).

REFERENCE: Le Heron C, Holroyd CB, Salamone J, & Husain M (26 Oct 2018, Epub ahead of print). Brain mechanisms underlying apathy. Journal of Neurology, Neurosurgery & Psychiatry. pii: jnnp-2018-318265. doi: 10.1136/jnnp-2018-318265. PMID: 30366958 ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 24 November 2018

No licorice for you

I never liked licorice. And that turns out to be a good thing. Given that Halloween just happened yesterday and licorice candy is still sold in USA, I remembered the FDA’s warning against consumption of licorice from a year ago.

So I dug out the data supporting this recommendation. It’s a review paper published 6 years ago by Omar et al. (2012) meant to raise awareness of the risks of licorice consumption and to urge FDA to take regulatory steps.

The active ingredient in licorice is glycyrrhizic acid. This is hydrolyzed to glycyrrhetic acid by intestinal bacteria possessing a specialized ß-glucuronidase. Glycyrrhetic acid, in turn, inhibits 11-ß-hydroxysteroid dehydrogenase (11-ß-HSD) which results in cortisol activity increase, which binds to the mineralcorticoid receptors in the kidneys, leading to low potassium levels (called hypokalemia). Additionally, licorice components can also bind directly to the mineralcorticoid receptors.

Eating 2 ounces of black licorice a day for at least two weeks (which is roughly equivalent to 2 mg/kg/day of pure glycyrrhizinic acid) is enough to produce disturbances in the following systems:

  • cardiovascular (hypertension, arrhythmias, heart failure, edemas)
  • neurological (stroke, myoclonia, ocular deficits, Carpal tunnel, muscle weakness)
  • renal (low potassium, myoglobinuria, alkalosis)
  • and others

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Although everybody is affected by licorice consumption, the most vulnerable populations are those over 40 years old, those who don’t poop every day, or are hypertensive, anorexic or of the female persuasion.

Unfortunately, even if one doesn’t enjoy licorice candy, they still can consume it as it is used as a sweetener or flavoring agent in many foods, like sodas and snacks. It is also used in naturopathic crap, herbal remedies, and other dangerous scams of that ilk. So beware of licorice and read the label, assuming the makers label it.

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Licorice products (Images: PD, Collage: Neuronicus)

REFERENCE: Omar HR, Komarova I, El-Ghonemi M, Fathy A, Rashad R, Abdelmalak HD, Yerramadha MR, Ali Y, Helal E, & Camporesi EM. (Aug 2012). Licorice abuse: time to send a warning message. Therapeutic Advances in Endocrinology and Metabolism, 3(4):125-38. PMID: 23185686, PMCID: PMC3498851, DOI: 10.1177/2042018812454322. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 1 November 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!

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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 Mom Brain

Recently, I read an opinion titled When I Became A Mother, Feminism Let Me Down. The gist of it was that some feminists, while empowering women and girls to be anything they want to be and to do anything a man or a boy does, they fail in uplifting the motherhood aspect of a woman’s life, should she choose to become a mother. In other words, even (or especially, in some cases) feminists look down on the women who chose to switch from a paid job and professional career to an unpaid stay-at-home mom career, as if being a mother is somehow beneath what a woman can be and can achieve. As if raising the next generation of humans to be rational, informed, well-behaved social actors instead of ignorant brutal egomaniacs is a trifling matter, not to be compared with the responsibilities and struggles of a CEO position.

Patriarchy notwithstanding, a woman can do anything a man can. And more. The ‘more’ refers to, naturally, motherhood. Evidently, fatherhood is also a thing. But the changes that happen in a mother’s brain and body during pregnancy, breastfeeding, and postpartum periods are significantly more profound than whatever happens to the most loving and caring and involved father.

Kim (2016) bundled some of these changes in a nice review, showing how these drastic and dramatic alterations actually have an adaptive function, preparing the mother for parenting. Equally important, some of the brain plasticity is permanent. The body might spring back into shape if the mother is young or puts into it a devilishly large amount of effort, but some brain changes are there to stay. Not all, though.

One of the most pervasive findings in motherhood studies is that hormones whose production is increased during pregnancy and postpartum, like oxytocin and dopamine, sensitize the fear circuit in the brain. During the second trimester of pregnancy and particularly during the third, expectant mothers start to be hypervigilent and hypersensitive to threats and to angry faces. A higher anxiety state is characterized, among other things, by preferentially scanning for threats and other bad stuff. Threats mean anything from the improbable tiger to the 1 in a million chance for the baby to be dropped by grandma to the slightly warmer forehead or the weirdly colored poopy diaper. The sensitization of the fear circuit, out of which the amygdala is an essential part, is adaptive because it makes the mother more likely to not miss or ignore her baby’s cry, thus attending to his or her needs. Also, attention to potential threats is conducive to a better protection of the helpless infant from real dangers. This hypersensitivity usually lasts 6 to 12 months after childbirth, but it can last lifetime in females already predisposed to anxiety or exposed to more stressful events than average.

Many new mothers worry if they will be able to love their child as they don’t feel this all-consuming love other women rave about pre- or during pregnancy. Rest assured ladies, nature has your back. And your baby’s. Because as soon as you give birth, dopamine and oxytocin flood the body and the brain and in so doing they modify the reward motivational circuit, making new mothers literally obsessed with their newborn. The method of giving birth is inconsequential, as no differences in attachment have been noted (this is from a different study). Do not mess with mother’s love! It’s hardwired.

Another change happens to the brain structures underlying social information processing, like the insula or fusiform gyrus, making mothers more adept at self-motoring, reflection, and empathy. Which is a rapid transformation, without which a mother may be less accurate in understanding the needs, mental state, and social cues of the very undeveloped ball of snot and barf that is the human infant (I said that affectionately, I promise).

In order to deal with all these internal changes and the external pressures of being a new mom the brain has to put up some coping mechanisms. (Did you know, non-parents, that for the first months of their newborn lives, the mothers who breastfeed must do so at least every 4 hours? Can you imagine how berserk with sleep deprivation you would be after 4 months without a single night of full sleep but only catnaps?). Some would be surprised to find out – not mothers, though, I’m sure – that “new mothers exhibit enhanced neural activation in the emotion regulation circuit including the anterior cingulate cortex, and the medial and lateral prefrontal cortex” (p. 50). Which means that new moms are actually better at controlling their emotions, particularly at regulating negative emotional reactions. Shocking, eh?

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Finally, it appears that very few parts of the brain are spared from this overhaul as the entire brain of the mother is first reduced in size and then it grows back, reorganized. Yeah, isn’t that weird? During pregnancy the brain shrinks, being at its lowest during childbirth and then starts to grow again, reaching its pre-pregnancy size 6 months after childbirth! And when it’s back, it’s different. The brain parts heavily involved in parenting, like the amygdala involved in the anxiety, the insula and superior temporal gyrus involved in social information processing and the anterior cingulate gyrus involved in emotional regulation, all these show increased gray matter volume. And many other brain structures that I didn’t list. One brain structure is rarely involved only in one thing so the question is (well, one of them) what else is changed about the mothers, in addition to their increased ability to parent?

I need to add a note here: the changes that Kim (2016) talks about are averaged. That means some women get changed more, some less. There is variability in plasticity, which should be a pleonasm. There is also variability in the human population, as any mother attending a school parents’ night-out can attest. Some mothers are paranoid with fear and overprotective, others are more laissez faire when it comes to eating from the floor.

But SOME changes do occur in all mothers’ brains and bodies. For example, all new mothers exhibit a heightened attention to threats and subsequent raised levels of anxiety. But when does heightened attention to threats become debilitating anxiety? Thanks to more understanding and tolerance about these changes, more and more women feel more comfortable reporting negative feelings after childbirth so that now we know that postpartum depression, which happens to 60 – 80% of mothers, is a serious matter. A serious matter that needs serious attention from both professionals and the immediate social circle of the mother, both for her sake as well as her infant’s. Don’t get me wrong, we – both males and females – still have a long way ahead of us to scientifically understand and to socially accept the mother brain, but these studies are a great start. They acknowledge what all mothers know: that they are different after childbirth than the way they were before. Now we have to figure out how are they different and what can we do to make everyone’s lives better.

Kim (2016) is an OK review, a real easy read, I recommend it to the non-specialists wholeheartedly; you just have to skip the name of the brain parts and the rest is pretty clear. It is also a very short review, which will help with reader fatigue. The caveat of that is that it doesn’t include a whole lotta studies, nor does it go in detail on the implications of what the handful cited have found, but you’ll get the gist of it. There is a vastly more thorough literature if one would include animal studies that the author, curiously, did not include. I know that a mouse is not a chimp is not a human, but all three of us are mammals, and social mammals at that. Surely, there is enough biological overlap so extrapolations are warranted, even if partially. Nevertheless, it’s a good start for those who want to know a bit about the changes motherhood does to the brain, behavior, thoughts, and feelings.

Corroborated with what I already know about the neuroscience of maternity, my favourite takeaway is this: new moms are not crazy. They can’t help most of these changes. It’s biology, you see. So go easy on new moms. Moms, also go easy on yourselves and know that, whether they want to share or not, the other moms probably go through the same stuff. You’re not alone. And if that overactive threat circuit gives you problems, i.e. you feel overwhelmed, it’s OK to ask for help. And if you don’t get it, ask for it again and again until you do. That takes courage, that’s empowerment.

P. S. The paper doesn’t look like it’s peer-reviewed. Yes, I know the peer-reviewing publication system is flawed, I’ve been on the receiving end of it myself, but it’s been drilled into my skull that it’s important, flawed as it is, so I thought to mention it.

REFERENCE: Kim, P. (Sept. 2016). Human Maternal Brain Plasticity: Adaptation to Parenting, New Directions for Child and Adolescent Development, (153): 47–58. PMCID: PMC5667351, doi: 10.1002/cad.20168. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 28 September 2018

The Benefits of Vacation

My prolonged Internet absence from the last month or so was due to a prolonged vacation. In Europe. Which I loved. Both the vacation and the Europe. Y’all, people, young and old, listen to me: do not neglect vacations for they strengthen the body, nourish the soul, and embolden the spirit.

More pragmatically, vacations lower the stress level. Yes, even the stressful vacations lower the stress level, because the acute stress effects of “My room is not ready yet”/”Jimmy puked in the car”/”Airline lost my luggage” are temporary and physiologically different from the chronic stress effects of “I’ll lose my job if I don’t meet these deadlines”/”I don’t know if I can keep my health insurance with this job”/”I’m worried for my child’s safety”/”My kids will suffer if I get a divorce”/”I can’t make the rent this month”.

Chronic stress results in a whole slew of real nasties, like cognitive, learning, and memory impairments, behavioral changes, issues with impulse control, immune system problems, weight gain, cardiovascular disease and so on and so on and so on. Even death. As I told my students countless of times, chronic stress to the body is as real and physical as a punch in the stomach but far more dangerous. So take a vacation as often as you can. Even a few days of total disconnect help tremendously.

There are literally thousands of peer-reviewed papers out there that describe the ways in which stress produces all those bad things, but not so many papers about the effects of vacations. I suspect this is due to the inherent difficulty in accounting for the countless environmental variables that can influence one’s vacation and its outcomes, whereas identifying and characterizing stressors is much easier. In other words, lack of experimental control leads to paucity of good data. Nevertheless, from this paucity, Chen & Petrick (2013) carefully selected 98 papers from both academic and nonacademic publications about the benefits of travel vacations.

These are my take-home bullet-points:

  • vacation effects last no more than a month
  • vacations reduce both the subjective perception of stress and the objective measurement of it (salivary cortisol)
  • people feel happier after taking a vacation
  • there are some people who do not relax in a vacation, presumably because they cannot ‘detach’ themselves from the stressors in their everyday life (long story here why some people can’t let go of problems)
  • vacations lower the occurrence of cardiovascular disease
  • vacations decrease work-related stress, work absenteeism, & work burnout
  • vacations increase job performance
  • the more you do on a vacation the better you feel, particularly if you’re older
  • you benefit more if you do new things or go to new places instead of just staying home
  • vacations increase overall life satisfaction

Happy vacationing!

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REFERENCE: Chen, C-C & Petrick, JF (Nov. 2013, Epub 17 Jul. 2013). Health and Wellness Benefits of Travel Experiences: A Literature Review, Journal of Travel Research, 52(6):709-719. doi: 10.1177/0047287513496477. ARTICLE | FULLTEXT PDF via ResearchGate.

By Neuronicus, 20 July 2018

Is piracy the same as stealing?

Exactly 317 year ago, Captain William Kidd was tried and executed for piracy. Whether or not he was a pirate is debatable but what is not under dispute is that people do like to pirate. Throughout the human history, whenever there was opportunity, there was also theft. Wait…, is theft the same as piracy?

If we talk about Captain “Arrr… me mateys” sailing the high seas under the “Jolly Roger” flag, there is no legal or ethical dispute that piracy is equivalent with theft. But what about today’s digital piracy? Despite what the grieved parties may vociferously advocate, digital piracy is not theft because what is being stolen is a copy of the goodie, not the goodie itself therefore it is an infringement and not an actual theft. That’s from a legal standpoint. Ethically though…

For Eres et al. (2016), theft is theft, whether the object of thievery is tangible or not. So why are people who have no problem pirating information from the internet squeamish when it comes to shoplifting the same item?

First, is it true that people are more likely to steal intangible things than physical objects? A questionnaire involving 127 young adults revealed that yes, people of both genders are more likely to steal intangible items, regardless if they (the items) are cheap or expensive or the company that owned the item is big or small. Older people were less likely to pirate and those who already pirated were more likely to do so in the future.

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In a different experiment, Eres et al. (2016) stuck 35 people in the fMRI and asked them to imagine the tangibility (e.g., CD, Book) or intangibility (e.g., .pdf, .avi) of some items (e.g., book, music, movie, software). Then they asked the participants how they would feel after they would steal or purchase these items.

People were inclined to feel more guilty if the item was illegally obtained, particularly if the object was tangible, proving that, at least from an emotional point of view, stealing and infringement are two different things. An increase in the activation the left lateral orbitofrontal cortex (OFC) was seen when the illegally obtained item was tangible. Lateral OFC is a brain area known for its involvement in evaluating the nature of punishment and displeasurable information. The more sensitive to punishment a person is, the more likely it is to be morally sensitive as well.

Or, as the authors put it, it is more difficult to imagine intangible things vs. physical objects and that “difficulty in representing intangible items leads to less moral sensitivity when stealing these items” (p. 374). Physical items are, well…, more physical, hence, possibly, demanding a more immediate attention, at least evolutionarily speaking.

(Divergent thought. Some studies found that religious people are less socially moral than non-religious. Could that be because for the religious the punishment for a social transgression is non-existent if they repent enough whereas for the non-religious the punishment is immediate and factual?)

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Like most social neuroscience imaging studies, this one lacks ecological validity (i.e., people imagined stealing, they did not actually steal), a lacuna that the authors are gracious enough to admit. Another drawback of imaging studies is the small sample size, which is to blame, the authors believe, for failing to see a correlation between the guilt score and brain activation, which other studies apparently have shown.

A simple, interesting paper providing food for thought not only for the psychologists, but for the law makers and philosophers as well. I do not believe that stealing and infringement are the same. Legally they are not, now we know that emotionally they are not either, so shouldn’t they also be separated morally?

And if so, should we punish people more or less for stealing intangible things? Intuitively, because I too have a left OFC that’s less active when talking about transgressing social norms involving intangible things, I think that punishment for copyright infringement should be less than that for stealing physical objects of equivalent value.

But value…, well, that’s where it gets complicated, isn’t it? Because just as intangible as an .mp3 is the dignity of a fellow human, par example. What price should we put on that? What punishment should we deliver to those robbing human dignity with impunity?

Ah, intangibility… it gets you coming and going.

I got on this thieving intangibles dilemma because I’m re-re-re-re-re-reading Feet of Clay, a Discworld novel by Terry Pratchett and this quote from it stuck in my mind:

“Vimes reached behind the desk and picked up a faded copy of Twurp’s Peerage or, as he personally thought of it, the guide to the criminal classes. You wouldn’t find slum dwellers in these pages, but you would find their landlords. And, while it was regarded as pretty good evidence of criminality to be living in a slum, for some reason owning a whole street of them merely got you invited to the very best social occasions.”

REFERENCE: Eres R, Louis WR, & Molenberghs P (Epub 8 May 2016, Pub Aug 2017). Why do people pirate? A neuroimaging investigation. Social Neuroscience, 12(4):366-378. PMID: 27156807, DOI: 10.1080/17470919.2016.1179671. ARTICLE 

By Neuronicus, 23 May 2018