What is an endogenous cue

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2012.02.08 18:38 turlockmike Anti Memes - Upvote some of the things!

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2017.01.26 14:56 AlcoholicUnclePete Accidental Camouflage

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2024.03.28 02:30 darthemofan Hacking YAP/TAZ mechanosensor against skin aging (in the future)

Paper and links

This is a review of "YAP/TAZ activity in stromal cells prevents ageing by controlling cGAS-STING" in Nature. 2022 Jul 1; 607(7920): 790–798.
medline: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7613988/
pdf: on https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7613988/pdf/EMS158105.pdf

YAP/TAZ our old friend for scarless healing

I love to talk about verteporfin and its potential for scarless healing: understanding how verteporfin scarless healing works under the hood was very instructive.
YAP/TAZ is a mechanosensor for the cells: it detects tearing and shearing.
In mammals, this detection causes the activation of a pathway that creates a scar - but we still have "under the hood" in our cells the same ability for scarless regeneration as seen in other species, so if you put something that blocks YAP/TAZ mechanosensor (such as verteporfin), then there's no scar, and the tissues heals perfectly - with hair follicule and everything!
Personally, I can't wait to buy some verteporfin to test on myself! (2 small problems: I don't have any surgery planned that should leave a large scar, and there's a worldwide shortage, but a good friend told me it's available in China, so I'll see what I can do)
But this begs the questions: wtf is YAP/TAZ doing when you don't have a gaping wound?
In the human body, most things are multipurpose, so it should play some other kind of role the rest of the time. This is the principle of "no free lunch": blindly putting verteporfin anywhere like some kind of holy water should be bad - and if we don't know just "how bad", it means we don't know nothing.

TLDR: YAP/TAZ other job: limit aging

We now about the scar stuff, but YAP/TAZ is mostly involved in preventing senescence, by sensing the force applied to the cell (it's a mechanosensor) and respond to them by maintaining the ECM (extra cellular matrix)
Think about cells as being surrounded by a bunch of stuff: the stuff is the ECM (made of collagen elastin etc). When cells detect mechanical forces, the feedback loop is they make a little more ECM, to limit the tearing/shearing.
Compared to scarless healing, that means YAP/TAZ works the other way around: a knockout (removing the normal function) should give you a animal with scarless healing (unfortunately, something they didnt check) yet it would come at a price: faster ageing!
Here I'm jumping a big ahead, but let's look at how the paper came to these conclusions

YAP/TAZ knockout gives a faster aging mouse

"To experimentally mimic the decline of YAP/TAZ activity during physiological ageing, we carried out YAP/TAZ inactivation in stromal cells of young adult mice (...) YAP/TAZ were genetically deleted by Tamoxifen administration at 2.5 months of age, and mice were analyzed after 5-8 weeks (see Methods). Histopathological assessment of the skin of young Col-YAP/TAZ cKO mice showed a decreased number of fibroblasts (Fig. 2a, b and Extended Data Fig. 2b), upregulation of Cdkn1a mRNA (Fig. 2c and Extended Data Fig. 2c), and aberrant collagen deposition (Extended Data Fig. 2d, e), all established phenotypes of the ageing dermis11,14. YAP/TAZ ablation in dermal fibroblasts also led to non-cell-autonomous effects, such as reduction of subcutaneous fat and reduced density of hair follicles (Fig. 2d), well-known traits of the ageing skin15. In addition, the phenotype of Col-YAP/TAZ cKO mice overlaps with that of old mice"

After being captivated by the introduction and this detail (and it's just the beginning of the paper!), I thought, we're not so interested in artificially aging mices, but keeping them young and healthy.

Inducing YAP/TAZ prevent this

Well, doing "pulses" of YAP/TAZ activity with doxycyclin-inducible transgenes helps keep these faster aging mice in good health:

"In light of the above results on YAP/TAZ cKO mice, and given that declining YAP/TAZ activity accompanies physiological ageing, we next asked whether the converse experiment - experimentally sustaining YAP/TAZ activity - could delay or suppress features of ageing. For this, we used mice carrying a doxycycline-inducible transgene encoding active YAP (TetO-YAPS127A;R26-rtTAM2)16; starting from 3 months of age, mice were kept under a pulsating regimen of YAP expression (as measured by western blot on tail tip fibroblasts, Extended Data Fig. 2g) by administering low doses of doxycycline twice a week until they reached more than 21 months of age. We found that sustaining YAP function prevented several features of ageing, rescuing fibroblast density (..) and hair follicle density (Fig. 2d), all to levels comparable to those of younger mice."

So not only the mice didn't loose their hairs, but they also had good arteries:

"We next extended these conclusions to a second example of declining YAP/TAZ mechanosignalling during ageing, that is the aortic wall" (..) Thus, YAP/TAZ mechanotransduction in aortic SMCs is an essential signal integral to the youthful homeostasis of the aortic wall, and its attenuation drives pathological features typically associated with natural ageing.

YAP/TAZ mechanosensor needs a working ECM

After reading that, my first thought was: "could YAP/TAZ involvement in skin aging simply be a reduced signal sensibility due to the ECM degradation?
They indirectly tested the ECM idea by looking at mutations of Fibrillin-1: it does to the aorta the same changes as seem in aging, but again pulsing YAP/TAZ stopped progression of aorta elastic aging:

"If YAP/TAZ mechanotransduction is relevant for controlling the ageing process, then attenuating mechanotransduction through direct manipulation of the ECM should also favor the emerge of ageing phenotypes, and in a manner driven by YAP/TAZ inhibition. An ideal playground to test this hypothesis is represented by mutations in Fbn1, which encodes Fibrillin-1 - an adhesive protein associated with the elastic fibers." (..) As visualized by immunofluorescence for YAP/TAZ, p-MLC2 and by western blot for p-FAK, we found that Fbn1 mutation recapitulates, in a few months, the mechanosensing decline that normally occurs over a lifetime (Fig. 3c, d and Extended Data Fig. 3d-f).

They didn't directly test the ECM idea, but it's a good enough proxy!

YAP/TAZ shows all the signs of actual aging

It's the real aging stuff: take old cells and put them in a culture: they're still old

"old fibroblasts, analyzed shortly after explantation, retain the same cytoplasmic YAP/TAZ bias they display in vivo"

The cells also shows a SASP (senescence associated secretion profile) and beta-galactosidase, 2 well known hallmarks of aging, so it's likely YAP/TAZ causes both scarred healing (upon injury) and anti aging functions (upon normal condition):

"Loss of YAP/TAZ in cultured fibroblasts also activates senescence-associated β-Galactosidase (SA-β-Gal), a classic marker of senescence (Extended Data Fig. 4f), consistent with prior in vitro findings. (..) experimentally sustaining YAP/TAZ activity rejuvenated these cells, suppressing SASP and SA-β-Gal expression (Fig. 4b, Extended Data Fig. 4g,h). SASP suppression was also attained by sustaining endogenous mechanotransduction and YAP/TAZ nuclear levels, through treatment with the integrin agonist pyrintegrin22"

And it goes both ways:

"Conversely, senescence was readily induced in young fibroblasts by experimental attenuation of YAP/TAZ mechanotransduction through inhibition of Rho-GTPases (Extended Data Fig 4k, l), one of the key upstream inputs that, by modulating the actin cytoskeleton, positively controls YAP/TAZ activity6. Thus, induction of senescence in old fibroblasts functionally associates to declining YAP/TAZ function."

Finding ways to hack YAP/TAZ

YAP/TAZ mechanosensing is needed to limit senescence and if it's prevented for working by making a super rigid ECM, things like those seen in aging happen:

"Next, we investigated the role of mechanical cues in the regulation of the YAP/TAZ-cGAS axis. For this, we inhibited YAP/TAZ activity by plating fibroblasts on compliant ECM-hydrogels, as such reducing the pulling forces from the ECM6. Mechanical inhibition of YAP/TAZ led to activation of cGAS, which was indeed rescued by adding back YAP (Extended Data Fig. 6a,b). Similarly, in another model of low tensional state (cellular confinement onto small adhesive areas6), mechanical inhibition of endogenous YAP/TAZ also triggered activation of cGAS (Extended Data Fig. 6c); under these conditions, cells are forced to adopt a more rounded morphology, a phenomenon that has also been observed in human dermal fibroblast during ageing"

The most interesting is how it works under the hood, and how it can be avoided even if the ECM "rigidity" couldn't be fixed, by using drugs: then all the bad things can be avoided by inactivating STING!

"in the skin of YAP/TAZ cKO; STINGGt/Gt mice, STING inactivation prevented loss of fibroblasts and preserved youthful ECM organization, subcutaneous fat layer and hair follicle density" (..) Taken together, these data indicate that YAP/TAZ restrain cGAS-STING signalling during adult tissue homeostasis in vivo, preventing emergence of senescent cells, of a proinflammatory microenvironment and age-related tissue dysfunction"

That's a super long and detailed paper, each of the experiment would by themselves be worthy of a standalone paper. The coherent whole is worthy of nature!

Putting it all together

Let's look at the discussion:

"Here we identified a molecular mechanism regulating in vivo cell senescence and ageing centered on the YAP/TAZ-cGAS-STING signalling conduit (..) we show that physiological ageing of multiple tissues parallels declining mechanotransduction, as visualized by attenuated YAP/TAZ activity and reduced cellular mechanosignalling. Future work will be required to further dissect the intimate causes underlying changes in mechanotransduction during ageing; these may be due, for example, to alterations in the physical properties of the ECM, in the viscoelastic properties of the whole tissue, in integrin-ECM association, or linked to more cell intrinsic alterations, such as defective contractility, or other changes."

So they aren't fully certain the ECM degradation,

"The findings break new ground on the nature of the signals and mechanisms inducing senescence in vivo. Depletion of senescent cells by senolytics has been shown to ameliorate ageing traits as such connecting accumulation of senescent cells to ageing1,2. Yet, the upstream molecular events that induce senescence in living tissues have so far remained unclear"

But now we know at least 1 cause of senescence!

"The identity of the cell types initiating senescence in living tissues remains poorly investigated. Here we found that waning levels of YAP/TAZ mechanotransduction is not a generalized feature of all cell types but occurs primarily in stromal and contractile cells. It is in these same cell types that we validated the YAP/TAZ-cGAS-STING connection to senescence and ageing-related tissue dysfunctions; it is thus tempting to propose that ageing may primarily initiate in tissues providing the structural framework and mechanical support to mammalian organs"

And it's at least as important as scarless healing:

"Irrespectively, the endogenous function of YAP/TAZ as regulator of senescence in adult tissues in vivo, and in specific cell types, remained unexplored, let alone the role of YAP/TAZ in ageing. The present results establish YAP/TAZ as factors playing physiological functions in youthful tissue homeostasis. This represents a departure from the current view of YAP/TAZ as relevant for cancer and tissue regeneration but irrelevant for normal adult homeostasis, as inferred by the inconsequentiality of YAP/TAZ genetic ablation in many epithelial tissues49"

And it can be used to limit aging, at least in vitro

"Our work contributes to fill this gap by showing that STING inhibition in vivo is sufficient to prevent accrual of senescent cells and, in so doing, the later emergence of accelerated ageing traits"

And why:

"YAP/TAZ activity is in turn instrumental to preserve the mechanical resilience of the nuclear envelope. This raises the possibility of mechanically regulated feedback loops between YAP/TAZ and the physical attributes of the nucleus and the cytoskeleton to be explored in future work, and particularly in the context of ageing biology."

And how:

"STING inhibition may represent a valid alternative to current senolytics approaches, aiming to preserve tissue integrity by preventing senescence rather than eliminating cells"

My conclusions

It's an absolutely incredible groundbreaking work that'll certainly lead to major advances in healthcare ... and skincare!
If you activate YAP/TAZ mechanosensor or inhibit STING, it should stop the tissue aging, as is shown in their aorta examples, and maybe even rejuvenate them if the process is enough to restores the ECM (so make elastin, collagen etc), as the cells could then "sense" again the forces, and maintain their ECM.
Eventually, it should make it possible to "undo" the UV damage (80% of facial skin aging), so that the facial skin is like sun-protected skin (which responds well to E2 or E3!)
The only thing we need is something that:

either does the opposite of verteporfin and instead of "disabling" the mechanosensor (like, disconnecting the sensors: an antagonist) pushes the trigger (an agonist)
or disables STING (like they did in the paper)

Given what we keep learning about YAP/TAZ, I have no doubt that we'll get eventually drugs like that in a few years.
In the meantime, scarless healing is already a very cool thing, and verteporfin is an FDA approved drug. The shortages suck though!

Neboglamine subunit interactions

While Neboglamine enhances NR2 subunits and their functions, it increases the inhibitory effects of NR3, most likely removing most of the cognitive enhancement derived from NR2.
This makes it an undedirable compound for selective cognitive enhancement, and selective NMDA subunit modulators are much better targets for enhancing brain function. The unselectivity of NR2/NR3 makes it unreliable at best and imparing at worst.

Subjective effects replicating predictions

In some reports of trials of Neboglamine, it has been described as "enhancing flow state". This may seem desirable, however during flow, the PFC typically switches into a "transient hypofrontality" state, with the DLPFC being less active [9].
The use of subjective effects are limited, but there is a lack of efficacy being proven for spatial cognition and working memory for Neboglamine.
At the end of the day, depending on the individual, the benefits may outweigh the potential downsides of Neboglamine usage. But in general, it is not an ideal compound, pharmacokinetically and mechanically.
What is better?
NMDA subunit selective (or "undisclosed site"-selective) modulation (such as with a PAM or NAM) is likely a much better approach for enhancing high-level cognition. This has been shown with multiple preclinical compounds which I will discuss in another post.
Thanks for reading.

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2024.01.15 18:41 LinguisticsTurtle There's a 2017 paper that puts forward a hypothesis that ADHD has to do with "bottom-up" signals. But what post-2017 papers shed light on how likely this hypothesis is to be accurate?

The 2017 paper was 6 years ago. I wonder what's happened research-wise since that 2017 paper came out. To be clear, it's just a hypothesis; it's not like I (or any of the researchers who think it's a good hypothesis) assert that it's true. Evidence is still being collected. The data will reveal whether this hypothesis should be abandoned or whether it makes sense. See below an excerpt from the 2017 paper:
https://www.sciencedirect.com/science/article/abs/pii/S0306987717312306

Meta-analysis of adoption and twin-studies has suggested that genetics may explain as much as 71% and 73% of the variance in ADHD core symptoms inattentiveness and/or hyperactivity-impulsivity, with larger dominant genetic effects on inattention and larger additive effects on hyperactivity (7). There is though strong evidence that these symptoms are extremes of continuously varying population traits (8, 9), and not categorical in character. Intriguing epigenetic research is also beginning to nuance the picture of ADHD as being mainly a genetic condition (10-13). Despite this development GxE models and integrative approaches in studies addressing ADHD pathophysiology seem spare, and focus of research interest appears skewed towards CNS and behavioral outcomes. Given the neurobiological conceptualization above these outcomes can though be expected to interact with peripheral nervous system function; i.e. bottom-up processing. Although substantial evidence indicates tonic dysregulation (14-16) or altered autonomic reactivity (14, 17) in ADHD, the roots and consequences of autonomic imbalance on symptomatology of the disorder remains largely unproblematized in literature, and few studies to date have addressed the role of the third autonomic branch, the enteric nervous system (ENS). While the microbiome-gut-brain axis in ADHD is so far mainly unexplored, a paradigm transition in GxE psychopathology research and Neuroscience is expected (6, 18), that hold potential of altering the conceptualization of controlling mechanisms for the disorder.

And here are more excerpts:
https://www.sciencedirect.com/science/article/abs/pii/S0306987717312306

The enteric nervous system is connected to the sympathetic as well as the parasympathetic nervous system (83), and mainly communicates with the brain through the vagus nerve (cranial nerve X) and spinal cord pathways (84). Also, 75% of the parasympathetic nervous system consists of the vagus nerve (85), with a ratio of 9:1 for afferent versus efferent vagal fibres in peripheral nerve bundles (86). An autonomic dysregulation model of ADHD that involves enteric imbalance thus implies vagus nerve dysregulation. Several studies have reported altered activity and/or reactivity of the parasympathetic nervous system in ADHD (15-17, 87, 88), but findings are inconsistent (see overview in (15)). It is also unclear how cortical activation and peripheral arousal in ADHD are related, although preliminary data has suggested a possible inverse correlation (89).
Afferent vagus nerve stimulation may have effects comparable to elevated afferent vagal activity caused by enhanced enteric signaling, and can therefore be used as a model for evaluation of presumptive physiological CNS consequences. Afferent vagus nerve signaling stimulates the HPA-axis releasing glucocorticoid hormones (90). Also, animal studies have indicated that stimulation of vagal afferents inhibits parasympathetic efferent signaling to the heart, and thus reduces cardiac vagal tone (91, 92). In rodent studies, vagus nerve stimulation towards the nucleus of the solitary tract (i.e. afferent vagal activation), increased the firing rate of norepinephrine releasing neurons of the locus coeruleus and subsequent serotonin releasing neurons of the dorsal raphe nucleus (93). This indicates that vagus nerve stimulation support the excitatory pathway to the locus coeruleus more than the parallel inhibitory GABAergic pathway (93). A rodent study has also shown that chronic peripheral vagus nerve impairment caused by unilateral microchip low-frequency vagus stimulation lead to dopamine system inhibition in different brain structures (especially mesolimbic and mesocortical systems) (94). Additionally, electrical stimulation of the peripheral vagus nerve has resulted in significant alterations of physiologically important nutritional macro- and trace elements in dopamine related brain structures (substantia nigra and corpus striatum) of rodents (95). This indicates that enhanced afferent enteric signaling, as hypothesized here, may compromise metabolic homeostasis in vagus nerve related CNS regions. Metabolic alterations linked to vagus nerve activity have been found also in a clinical cohort study, showing that vagus nerve stimulation significantly increased energy expenditure (96), which has been reported elevated in ADHD subjects (28, 29). It is worth noticing that experimental overstimulation of a nerve is known to result in reduced transmission of stimuli due to lack of neurotransmitter substance (94). This can be relevant to severe ADHD symptoms, if viewed as continuous traits, and entail paradoxical effects that may cause equivocal findings. Neuro-immune modulatory interactions are often non-linear. It therefore seems reasonable to assume that vagus nerve dysregulation due to reduced but also enhanced enteric signaling may compromize homeostasis of immune system function and inflammatory regulation, and increase tryptophan metabolism along the kynurenine pathway. Vagus nerve stimulation in conditions with vagal underactivity (97- 99) may thus show positive efficacy outcomes that seem contradictory to our hypothesis if they are interpreted as linear interactions. It may equally be important whether efferent or afferent vagal stimulation is applied (90). Several studies have indicated altered immunological markers and tryptophan metabolism in ADHD (46, 75, 76, 100), which support our hypothesis of enteric dysregulation.

...

Inattention, with difficulty organizing and sustaining in activities or tasks, distractibility and frequent failure to attend details etc. are core symptoms in ADHD diagnostic criteria. These attention deficits have been suggested to reflect a low arousal level that secondary impair executive and endogenous (but not exogenous) attention orienting (101). Also, an integrative theoretical model has suggested that dysregulation between tonic and phasic activity of the locus coeruelus norepinephrine arousal system compromises attentional performance in ADHD and predispose to impulsive behaviors (102). Can ADHD attention symptoms be secondary to increased vagal afferent signaling that bias information processing towards bottom-up exogenous attention orienting?
Afferent vagus nerve fibers project sensory information to the locus coeruleus via the nucleus of the solitary tract (93). Evidence has indicated that activation of the locus coeruleus is triggered by environmental sensory cues that provoke interruption of ongoing behavior in order to reorientate and facilitate an adaptive behavior response (103). Norepinephrine from the locus coeruleus neurons is the only known source of this neurotransmitter for a majority of the forebrain (103). Like dopamine, norepinephrine has a U-shaped influence on prefrontal cortex cognitive abilities and physiology (104). This means that both too high levels (as in acute uncontrollable stress) and too low levels (as in fatigue and plausibly hypoarousal) impairs prefrontal cortex function (104). Low tonic arousal in normal subjects has been associated with asymmetric visuo-spatial attention, favoring stimuli from the right side (105). In the opposite direction, an experimental human study has shown that chronic psychosocial stress (i.e. elevated sympathetic activation) increased couplings between dorsolateral prefrontal cortex and temporal lobe areas that are involved in visual processing, which may have the short-term benefits of favoring a single, salient stimulus (106). Also, lower resting heart rate variability has been linked to a more exogenous attention orienting, which may impede effective emotion regulation (107). An ERP-study (scalp-recorded Event-Related brain Potential) has shown reduced automatic attention to salient sound stimuli in young adults (age 18-23) with ADHD (n=21) versus controls (n=18) (108). The results indicated that the attention problem in ADHD originates at a lower processing level, where inhibition is irrelevant. Authors suggested the locus coeruleus as the most likely site of deficit, due to its role in arousal and in regulating amplification of incoming (i.e. bottom-up) information (108). These results are supported by EEG recordings of evoked Gamma-Band Response (GBR) activity, which indicated increased distractibility in ADHD at an early level of perception (109). Importantly, no deviation was found during working memory encoding and retrieval, suggesting that the attention deficit in ADHD is specific to interference susceptibility (109).

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2023.10.30 07:59 yooooooUCD UPDATE: Karel Knize Seeds From 1983! (Experiment, Background, Discussion)

Tldr: I have not gotten any seeds to germinate so far, and that outcome is consistent with the current research on cactus seed viability.
Big shout out to u/FairDinkumSeeds for sending me gibberellic acid, and creating the guidelines for this test run!
First, let's go over the background and purpose of this experiment. I diverted these seeds from going into the trash at the UC Davis Botanical Conservatory. I find these to be a uniquely valuable resource to learn about cactus seed viability, because they have collection data and accompanying documentation. Unfortunately they were not stored in any sort of temperature or humidity control for 40 years.
Background: GA3 (gibberellic acid) is a well studied plant hormone that is used across the horticultural and agricultural industries. As with most (if not all) plant hormones, it does a lot of different things in different contexts. For our purposes, we will be focusing on its role in seed germination.
In this context, GA3 works as a hormone signal that induces the transcription of genes necessary to activate enzymes within the seed. These enzymes work to break down the energy stores within the seed and mobilize these nutrients to a developing embryo. This is an integral step in the natural germination process, a part of a biochemical cascade that is triggered by several environmental cues (which I will discuss later). Scientists have shown that seeds known to be deficient in GA3 will germinate at far higher rates if they are treated with an exogenous application of GA3. You can read more about this process here:
Jinrong Peng, Nicholas P Harberd, The role of GA-mediated signalling in the control of seed germination, Current Opinion in Plant Biology, Volume 5, Issue 5, 2002, Pages 376-381, ISSN 1369-5266, https://doi.org/10.1016/S1369-5266(02)00279-0. (https://www.sciencedirect.com/science/article/pii/S1369526602002790)
What is seed dormancy vs seed viability? How does GA3 tie into all this?
Before we get into the real nitty gritty, I just wanted to lay down some fundamentals of seed science. Almost all seeds must experience some degree of dormancy before they germinate. This is typically a stage of desiccation, after the seed has matured and the fruit is ‘ripe’. This lack of moisture is a great way to halt most biochemical processes and prevent pathogens from penetrating into the seed. If this didn’t occur, seeds could germinate in the fruit before being dispersed, or during the wrong time of year. Dormancy is broadly characterized as a state of stasis, where the seed is not ‘doing’ anything. However, the seed does have a number of sensors that are constantly monitoring the environment. These include phytochromes (light and temperature sensing proteins), as well as moisture actuated enzymes within cell membranes. These sensors are all calibrated to activate under specific conditions, often reflecting the particular environment to which a plant has become adapted. Note: some authors have a more stringent definition of seed dormancy, which requires a minimum amount of time to pass (3 months) between seed collection and germination, but I am using a broad definition here. If a seed is deficient in GA3, or the sensors which would set off the production of GA3 are not functioning, or if there is an excess of inhibitors (an endogenous chemical that interferes with the effects of GA3) within the seed, it will likely not germinate. Horticulturalists have successfully used GA3 treatments to break dormancy when these issues are present. Issues with breaking seed dormancy are inherently different from issues with seed viability. A non-viable seed may look exactly like a dormant seed, but it does not have the necessary faculties to carry out germination. This is sometimes caused by issues during seed maturation, or as a result of genetically incompatible parents, but oftentimes it is a result of degradation of the seed. The culprit is usually oxidation. When energy storing tissue and/ or enzymes become oxidized, the embryo no longer has access to the energy for germination. The embryo itself may be non-viable due to oxidation as well. In other terms, the seed no longer has the energy to germinate nor intact molecular mechanisms to carry out the process of germination. Since the penetration of oxygen into the seed is dependent on the seed coat quality as well as the surface area to volume ratio of the seed, it isn’t hard to imagine that cactus seeds are particularly vulnerable to oxidation damage. Their small form with a relatively thin coat likely lend themselves to rapid oxidation.
Read more about this topic here: A. M. Mayer (1986) HOW DO SEEDS SENSE THEIR ENVIRONMENT? SOME BIOCHEMICAL ASPECTS OF THE SENSING OF WATER POTENTIAL, LIGHT AND TEMPERATURE, Israel Journal of Botany, 35:1, 3-16, DOI: 10.1080/0021213X.1986.10677033
Maarten Koornneef, Leónie Bentsink, Henk Hilhorst, Seed dormancy and germination, Current Opinion in Plant Biology, Volume 5, Issue 1, 2002, Pages 33-36, ISSN 1369-5266, https://doi.org/10.1016/S1369-5266(01)00219-9. (https://www.sciencedirect.com/science/article/pii/S1369526601002199)
Wiebach J, Nagel M, Börner A, Altmann T, Riewe D. Age-dependent loss of seed viability is associated with increased lipid oxidation and hydrolysis. Plant Cell Environ. 2020 Feb;43(2):303-314. doi: 10.1111/pce.13651. Epub 2019 Sep 10. PMID: 31472094.
The Experiment:
u/FairDinkumSeeds (Website: fairdinkumseeds.com ) agreed to send three packets of plant hormone GA3 to me (u/yooooooUCD) for the purpose of attempting to germinate Karel Knize cactus seeds from 1983. With this package, u/FairDinkumSeeds sent the following instructions, “...buy 3x 1lt bottles of water. Add one pack GA3 to one bottle, that's the 500ppm group. Empty half out of the next bottle (and put aside to use as untreated control water) so now you have 500ml in the bottle, that's the 1000ppm group. Last bottle tip out all water except 250ml. Add a pack GA3 and that's the most often fatal 2000ppm group. Make 4 rows cups and divide seeds up. 0, 500, 1000, 2000. Add a couple drips appropriate solution to appropriate cup. Soak over night, plant the next day, firmly cross your fingers!”
I purchased three, one liter bottles of Crystal Geyser Alpine Spring Water. The dilution instructions followed exactly. Seeds were not sterilized before treatment. For the first run, I decided to test KK933 Echinopsis pereziensis, KK1033 Echinopsis ayopayana, KK1270 Echinopsis cerdana, and KK795 Echinopsis seminuda. Each set of seeds were placed in 2 inch diameter plastic petri dishes lined with aeropress unbleached coffee filters. Ten drops of GA3 solution were administered to each lot of seeds, with a control for each set given ten drops of pure bottled water. The filter paper readily absorbed and distributed the solution to the seeds in each dish. After 24 hours of treatment, I transferred each set of seeds into three inch diameter, clear plastic containers with sterilized potting mix. The seeds were placed on the surface of the potting mix, and then sprayed with a solution of 5x dilute 20-20-20 water soluble fertilizer (brand: Grow More). The planting matrix was then placed on heat mats, under a full spectrum grow light set to a canopy light intensity of 450 µmol/m^2/s.
I readily crossed my fingers (per instructions)
No germination observed within 4 weeks of planting. At 4 weeks, some seeds were consumed by a white filamentous fungus, though many were fully intact. Experiment ongoing as of 10/28/2023.
Discussion:
During this experiment I collected information on any recorded attempts to encourage cactus seed germination, whether through chemical/hormone treatments, testing viability over time, or controlling the germination environment. If you read no further than this just know that the current best known method to germinate any viable seed, regardless of age, is all basically the same. There doesn’t seem to be any strong evidence that a chemical treatment, besides fertilizer and water, increases cactus seed germination in general. Though, I recommend reading through the papers cited under this section to check for any germination treatments that may be beneficial in certain species tested. For example, a high altitude, cold weather cactus will more likely germinate at lower temperatures than a low elevation equatorial cactus. Nearly all cactus species (especially those in the Trichocereus genus) have a strong photoblastic response to white and red light. For growers, that means you should expose your seeds to light during germination.
General Germination Conditions For Trichocereus Cacti: Temperature: 20-30 deg. C (25 C seems to be best) Humidity: 100% (Water potential -0.2 to 0.0) Light: Full spectrum white light (far red light is the least effective treatment, red is second best, and white yields the greatest germination rate)
Some other cactus species benefit from various specific treatments, like a hydration-dehydration cycle. Some benefit from slightly cooler or warmer temperatures, and some others have been shown to respond positively to fungal inoculation. I wish I could’ve uncovered some secret trick to germinate Trichocereus seeds, but it seems like regular old light, water, and heat is the best way to break dormancy of viable seed. As for very old (probably non-viable) seeds, I haven’t found any solid research. I’ve heard some good things about soaking them in sugar water, making a tea with the enzymes and hormones associated with germination, and KNO3 treatments, though I couldn’t find any studies specifically testing these methods on old cactus seeds. In fact, the oldest cactus seed to be germinated that I could find was 10 years of age. I believe it is a strong possibility that cactus seeds general oxidize far too quickly to germinate (if stored at room temperature in normal atmosphere) after just a few years.
More reading:
Barrios, D., Sánchez, J. A., Flores, J., & Jurado, E. (2020). Seed traits and germination in the Cactaceae family: A review across Americas. Botanical Sciences, 98(3), 417-440. https://doi.org/10.17129/botsci.2501 (https://www.botanicalsciences.com.mx/index.php/botanicalSciences/article/view/2501)
J. Flores, E. Jurado, L. Chapa-Vargas, A. Ceroni-Stuva, P. Dávila-Aranda, G. Galíndez, D. Gurvich, P. León-Lobos, C. Ordóñez, P. Ortega-Baes, N. Ramírez-Bullón, A. Sandoval, C.E. Seal, T. Ullian, H.W. Pritchard, Seeds photoblastism and its relationship with some plant traits in 136 cacti taxa, Environmental and Experimental Botany, Volume 71, Issue 1, 2011, Pages 79-88, ISSN 0098-8472, https://doi.org/10.1016/j.envexpbot.2010.10.025. (https://www.sciencedirect.com/science/article/pii/S0098847210002236)
Mariana Rojas-Aréchiga, Alma Orozco-Segovia, Carlos Vázquez-Yanes, Effect of light on germination of seven species of cacti from the Zapotitlán Valley in Puebla, México, Journal of Arid Environments, Volume 36, Issue 4, 1997, Pages 571-578, ISSN 0140-1963, https://doi.org/10.1006/jare.1996.0218. (https://www.sciencedirect.com/science/article/pii/S0140196396902189)
Rojas-Aréchiga, Mariana & Vázquez-Yanes, Carlos. (2000). Cactus seed germination: A review. Journal of Arid Environments. 44. 85-104. 10.1006/jare.1999.0582. https://www.researchgate.net/publication/222679202_Cactus_seed_germination_A_review

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2023.10.01 22:19 normanboyster Gossip in Evolutionary Perspective

Based on Dunbar's Gossip paper (from the Module Two readings)
This is the reading below you have read whole and analyse it and on the baisis on this you have to answer the above question

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Gossip in Evolutionary Perspective R. I. M. Dunbar University of Liverpool Conversation is a uniquely human phenomenon. Analyses of freely forming conversations indicate that approximately two thirds of conversation time is devoted to social topics, most of which can be given the generic label gossip. This article first explores the origins of gossip as a mechanism for bonding social groups, tracing these origins back to social grooming among primates. It then asks why social gossip in this sense should form so important a component of human interaction and presents evidence to suggest that, aside from servicing social networks, a key function may be related explicitly to controlling free riders. Finally, the author reviews briefly the role of social cognition in facilitating conversations of this kind. For reasons that are not entirely clear, gossip has acquired a decidedly shady reputation.
It is seen as malicious, destructive, and largely reprehensible. Describing a person as an “old gossip” implies someone with more time on their hands than they know what to do with, too much hanging over the garden gate waiting for some passerby to pause for idle chat. To engage in gossip is to speak ill of one’s fellows, to interfere with the smooth running of the social relationships within which we are all embedded: in a word, to undermine the very fabric of society. Yet, the term gossip itself did not originally have that meaning. It meant simply the activity that one engaged in with one’s “godsibs,” one’s peer group equivalent of godparents: in other words, those with whom one was especially close. Whether it is in fact the case that tale-telling and tittle-tattle are all that we do with our nearest and dearest is, perhaps, a moot point. I want, instead, to focus on the broader nature of this activity and argue that gossiping (though perhaps not gossip in its contemporary malicious form) is the core of human social relationships, indeed of society itself.
Without gossip, there would be no society. In short, gossip is what makes human society as we know it possible. To be able to make this claim, I need first to step back in evolutionary time to what we might see as the ancestral state from which modern humans sprang. This is the nature of social relationships that pertain among our primate cousins. I then argue that language evolved as a mechanism for bonding large social groups, and that it does so precisely because it allows us to exchange information about the state of our social networks. In this context, the problem of free riders (those who take the benefits of sociality without paying the costs) is a central issue for which gossip provides a particularly powerful mechanism of control. Origins Humans are members of the order primates, a large and diverse group of mammals of very ancient lineage. We belong to that subgroup of primates known as the catarrhines, the Old World monkeys and apes. We share with these monkeys and apes a deep sociality that is predicated on relatively (by comparison with other mammals and birds) advanced forms of social cognition. This is represented in humans by such phenomena as theory of mind (Astington, 1993; Whiten, 1991; Wimmer & Perner, 1983) and more advanced forms of the intentional stance (Kinderman, Dunbar, & Bentall, 1998), which appear to be unique to humans (Call & Tomasello, 1999; Tomasello & Call, 1998).
(The “intentional stance” is the phenomenon of interpreting behavior in terms of the belief states of the mind that is behind the behavior, something that seems to be especially characCorrespondence concerning this article should be addressed to R. I. M. Dunbar, Economic and Social Science Research Council Research Centre in Economic Learning and Social Evolution, School of Biological Sciences, University of Liverpool, Crown Street, Liverpool L69 7ZB, England. E-mail: rimd@liv.ac.uk Review of General Psychology Copyright 2004 by the Educational Publishing Foundation 2004, Vol. 8, No. 2, 100–110 1089-2680/04/$12.00 DOI: 10.1037/1089-2680.8.2.100 100 teristic of humans [Dennett, 1983].)
Social cognition in these respects is based on the reflexively hierarchical phenomenon of mind-reading, the ability reflected in the claim that I suppose that you believe that I want you to think that X is the case. The extent to which other monkeys and apes share these particular capacities is not germane to the thesis of this article. The issue is more that Old World monkey and ape social relationships seem to be underpinned by relatively sophisticated forms of social cognition that find their fullest expression in the reflexive multilevel hierarchy of intentionality that we find in living humans. I return to this particular issue in the final section;
first, I simply want to establish why it is that the capacity to exchange information (i.e., language) evolved at all in humans. Anthropoid primate societies (and especially those of the Old World monkeys and apes) are characterized by an intensity of sociality that is not as conspicuous in other species. These species are deeply social; they are social in a sense that is all too readily apparent to anyone who has ever taken the trouble to spend any time observing their behavior. This intensity of sociality depends on two key phenomena. One is the ability to understand something of the workings of another’s mind. By this, I do not mean to suggest that monkeys and apes understand that other individuals have minds in the way that we humans take this for granted. Theirs is more the ethologist’s skill at reading behavior (Cheney & Seyfarth, 1990).
In effect, they are good at understanding correlations in behavior: that individuals behave in certain consistent ways that can vary widely from one individual to another, that others’ behavior can be deliberately manipulated to one’s own advantage. The second feature underpinning primate sociality is the use of trust and (in a weak sense) obligation to ensure that relationships work effectively and do the job they are intended to do. For monkeys and apes, predators are the single most important factor influencing group size: As a species’ ecological habits expose it to increased risk of attack by predators, so its group size must be proportionately larger to protect its members (for reviews, see Dunbar, 1988, 1996a).
Although protection against predators can be seen as clearly advantageous for primates, it is important not to lose sight of the fact that sociality has costs as well as benefits. Living together exposes animals to a number of stresses that include disturbances to feeding when one animal displaces another from a feeding site, harassment by more dominant individuals, and the generally disruptive effects that arise from the fact that animals in social groups are obliged to coordinate their behavior in ways that are not always ideal for each individual. Because the consequences of predation are so final for the individual, the costs of sociality must be held in check to minimize their impact; otherwise, the centrifugal forces of individuals’ selfish demands will rapidly and inevitably result in the dispersal of the group. Sociality, in short, demands compromise on one’s personal, short-term objectives so that one gains in the longer term through a greatly reduced risk of falling victim to a predator. The primate solution to this problem (essentially the need to balance short-term interests against the longer term gains to be had through group living) is the formation of alliances.
Often, these alliances are deeply rooted in matrilineal relationships (mothers and daughters, sisters). These relationships work (and are crucial in the life histories of the animals themselves) because they involve a strong element of trust and commitment. An alliance member can be relied on to come to one’s aid at the crucial moment when one is under attack. That sense of obligation is created through social grooming. We do not really understand how grooming makes this possible, though we do know that grooming is extremely effective at releasing endorphins (endogenous opiates produced naturally by the brain as part of the body’s pain control system; Keverne, Martensz, & Tuite, 1989). The flood of opiates triggered by being groomed (and perhaps even by the act of grooming itself) generates a sense of relaxation (grooming lowers heart rate, reduces signs of nervousness such as scratching, and can so relax the groomee that it may even fall asleep; Goosen, 1981).
We are ourselves familiar with these effects, because we show a striking preference for resorting to old-fashioned primate grooming in our more intimate relationships; here language is an inadequate means for communicating deep inner feelings (and especially emotions), and we often resort to physical contact forms of communication (rubbing, stroking, patting, and petting) that are extremely effective at triggering SPECIAL ISSUE: GOSSIP IN EVOLUTIONARY PERSPECTIVE 101 the release of endorphins. As the endorphins triggered by these behaviors begin to flood the body, we experience a rising sense of warmth, a feeling of peace with the world, of well-being toward those with whom we share such experiences of intimacy. The effect is instantaneous and direct: The physical stimulation of touch tells us more about the inner feelings of the “groomer,” and in a more direct way, than any words could possibly do. The key issue at this point is that the amount of grooming that primates do is directly related to the size of the groups they live in, apparently because the effectiveness with which an alliance works is a simple function of the amount of time devoted to grooming by its members.
Although, within a species, alliance size does not vary greatly as group size increases, the effectiveness with which the alliance must work does correlate with group size. As group size increases, individuals are subjected to increasing levels of ecological competition (local food sources are exhausted more quickly, forcing animals to search more widely for food) and reproductive stress (harassment by others is sufficient to destabilize a female’s menstrual hormone cycles, leading to anovulatory or infertile cycles; for a review, see Dunbar, 1988). The more stress imposed on the individual, the more effective its alliances must be to buffer it against these stresses. Because there must be an upper limit on the amount of time that can be devoted to social grooming, there will inevitably be an upper limit on the size of the group that can be bonded by this mechanism (Dunbar, 1998a). In actuality, of course, grooming time is constrained by the fact that animals have to forage for food. In practice, it seems that there is an upper limit on the amount of time that any given group of primates devote to grooming, and this is about 20% of the total waking time in each day.
Given the nature of the activity, this is, of course, a very substantial amount of time: Roughly one fifth of the day is being devoted to social investment. More important, however, this figure is equivalent to a group size of about 80 animals (Dunbar, 1992, 1998a). (Note that these values correspond to the mean group sizes for individual species, not the maximum possible group sizes that we might observe.) The problem for modern humans is that we have a natural group size of about 150 individuals (roughly equivalent to the number of individuals one knows personally; Dunbar, 1993; Hill & Dunbar, in press). At some point in our evolutionary history, hominid groups began to push against the ceiling on group size.

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The only way they could have broken through this ceiling so as to live in groups larger than about 80 individuals was to find an alternative mechanism for bonding in which the available social time was used more efficiently. Language appears to serve that function perfectly, precisely because it allows a significant increase in the size of the interaction group (Dunbar, 1993, 1996b). Grooming is very much a one-on-one activity (it still is, even for us), whereas conversation group sizes typically contain up to four individuals (invariably one speaker and three listeners; Dunbar, Duncan, & Nettle, 1995). In addition, speaking is something that we can do simultaneously with most other activities. As a result, we can “time share” more effectively to cram more into what limited time we do have available. Significantly perhaps, it turns out, from a sample of people’s time budgets drawn from a wide range of cultures around the world, that the average percentage of time humans spend in social interaction (mainly conversation, of course) is 20% (Dunbar, 1998b).
In other words, our social time allocation is at the upper limit of that seen in primates; we simply use the time more efficiently because language allows us to do so. Note that neither of these benefits requires more than speech; content is not explicitly required, because all that is necessary is to convey a message of social commitment (“I consider it more important standing here talking to you than being over there with [. . . anyone else]”). However, one further key feature of language is particularly important to the bonding of our unusually large social groups, namely the fact that language allows us to exchange information. That, after all, is what language itself is basically designed to do. Its role in social bonding is that it allows us to keep track of what is going on within our social networks, as well as using it to service those relationships. As important as the latter function is, it is in many ways the first that is especially important.
Lacking language, monkeys and apes are constrained in what they can know about their networks. They know only what they see. We are similarly limited when it comes to first-hand knowledge. 102 DUNBAR But language allows us to seek out what has been going on behind our backs. Indeed, we can even be proactive about it and tell our friends and relations what we have seen when we think it might be in their interests to know. Let me summarize the argument thus far. Primates live in groups to protect themselves against predation, and group size increases as predation risk increases. But group living comes at a cost in terms of the stresses it imposes on the individual. Monkeys and apes solve this problem by forming alliances that buffer them against these costs, thus facilitating the cohesion of large social groups.
These alliances are bonded through social grooming (a process that is mediated pharmacologically through the release of endorphins), but the cohesion of large social groups also depends on a unique form of cognitive engagement that allows animals to understand and exploit the mental states of other individuals. Sociality in primates is thus dependent on a two-pronged process. One involves heavy cognitive demands, in which any specieslevel increases in group size that are required to allow animals to exploit more predator-risky habitats are necessarily predicated on corresponding increases in brain size (and explicitly frontal lobe size) to handle the social cognitive demands of managing proportionately more relationships.
The other is a more ancient process based on the exploitation of grooming-based pharmacological mechanisms that facilitate bonding so as to allow the processes of mutual support on which group cohesion ultimately depends to work effectively. The evolutionary sequence here is this: Exploitation of more predator-risky habitats requires an increase in group size; to make this possible, it is necessary both to evolve the cognitive machinery to underpin the management of the social relationships involved (essentially a larger neocortex) and to invest more time in the necessary bonding processes. Humans represent the most extreme point in this sequence within the primates because hominid evolution has been characterized by the exploitation of increasingly open terrestrial habitats, both of these features being associated with increased predation risk. It may be that in the later stages of hominid (human?) evolution, the risk of predation by other humans became more important than the risks of predation by more conventional predators (Johnson & Earle, 1987), but this does not obviate the fundamental issue that risk of death from predators (of whatever kind) is the principal factor favoring increases in group size.
Language became part of this story because, at some point in hominid evolutionary history, the group size required exceeded that which could be bonded through social grooming alone; the constraint in this context was the fact that the time investment required by grooming is ultimately limited by the demands of foraging. Language enabled hominids to break through that particular glass ceiling because it allows time to be used more effectively than is possible with grooming: Speech allows us both to interact with a number of individuals simultaneously (grooming is a strictly one-on-one activity) and to exchange information about the state of our social network (lacking language, monkeys and apes are limited in their knowledge of their network by what they themselves see).
In the next section, I elaborate on this theme by arguing that the exchange of social information (i.e., gossip) has been crucial to our ability as a species to evolve large social groups. The Functions of Gossip A strong case can, then, be made for the suggestion that language evolved to facilitate the bonding of large social groups. It achieves this mainly because it allows us to increase the size of our broadcast network (the number of people with whom we can communicate directly and indirectly) and because it allows us to exchange information about changes that occur within our social networks. We can catch up on news of Uncle Joe and Aunt Jane, discover that Susan and Bill have parted company (and so avoid an embarrassing faux pas that might otherwise have upset what had once been a good relationship), and learn about new additions to the family. But language allows us to do much more than this. We can use language in at least four other ways (there may be others too, of course, but these will at least serve to illustrate the point I want to make here).
One is to seek advice or to discuss hypothetical situations: “How would you behave if . . . ?” A second is to provide us with a kind of policing function to control those who fail to abide by the formal and informal agreements that underpin society. (I have more to say about this particular issue in the next SPECIAL ISSUE: GOSSIP IN EVOLUTIONARY PERSPECTIVE 103 section.) The third possibility is that we can use language to advertise ourselves: Look at all my wonderful qualities as a potential mate or ally. Finally, in a variant on the last, we can use language to deceive: to tell others what we think it would help us for them to know, as when Iago poisoned Othello’s mind against Desdemona. It is perhaps important to appreciate that, although we can use language in all of these ways and possibly more, all of them are really derivative of the fact that language evolved to allow us to bond large social groups.
None of these additional functions would really be relevant (or so intrusive) if we did not first live in large groups. In contrast, without language as a means of exchanging information about the social network, large groups could not be kept together as viable, coherent social entities. So although we may use language to deceive or police, the possibility of being able to use it in this way would not exist without there being large groups in the first place. However, we should first ask what evidence there is that language is used in these various ways. In part, this really concerns the distinction between social and technical uses of language. Language is concerned with the exchange of information; that, after all, is what it (or, at least, grammar) is mainly designed to do. However, linguists and those in most other disciplines interested in language have traditionally assumed that the information to be exchanged is factual knowledge about the world; in other words, language evolved to allow our ancestors to exchange information about aspects of the physical world in which they lived. “This is how you make a good spear. . . . If you throw your spear this way, you are more likely to kill the prey. . . . I just saw some bison down by the lake as I was passing, so let’s go hunt them....
Never swim in the river because crocodiles [or dangerous spirits] live there and will grab you!” Of course, we can do amazing technical things only because we have language: Without language, Pythagoras would not have been able to explain his theorem, Newton would never have been able to expound on the nature of gravity, and probably none of their fellow men and women would have been the slightest bit interested in their rather exotic theories because they would not have seen the relevance of them. Who cares if the square on the hypotenuse is equal to the sum of the squares on the other two sides? Should I care why apples fall to earth so long as I can pick them up? It is enough that we know that they do!
The reality, however, is that language allows us to stand, as Newton so memorably put it, on the shoulders of the giants who went before us; language, and nothing else, has made the spectactular growth of knowledge in the last few centuries possible. This technological or economic view of what language is used for has so deeply colored our perception of the function of language that it has led us to see any other uses of language as trivial and largely driven by the boredom of idleness. Thus has gossip acquired its ill repute, for it is seen as mere time wasting when we could be doing something really useful with our time such as talking about jet engines or the technical details of how to earn more money by making our businesses more efficient. The real issue here, then, is which of these two broad uses of language is the chicken, and which is the egg?
In other words, did language evolve to facilitate the exchange of technological information (with gossip as an idle by-product), or did it evolve to facilitate the exchange of social information (with the exchange of technological information as a useful by-product)? The issue here is a purely empirical one: How do we use language? What do we actually talk about? My colleagues and I have carried out a number of observational studies of the content of conversations. All of these studies have been undertaken in public places, and we simply note the topic under discussion in free-running conversations at 30-s intervals. To ease the process of classification for the observer and avoid problems of unnecessary intrusion, we use only broadly defined categories (e.g., social, politics, sports, music and culture, and technical). The “social” category covers anything that has to do with explicitly social activities, personal relationships, and personal likes or dislikes.
Our aim here is to try to gain a basic description of how people use language in relaxed everyday situations. It is worth pointing out that almost all of the work carried out hitherto on conversations has been subject to one or both of two key distortions, namely the use of artificially convened groups or a focus on workplace environments. These circumstances introduce distortions because the situations are unnatural (despite the length of time we might be said to spend in our 104 DUNBAR places of work). Such distortions have not really been an issue in previous studies, because these investigations have focused on aspects of conversational behavior other than topic of conversation (e.g., the mechanics of conversation, how conversations are paced, and the cues used in signaling switching of roles; Beattie, 1983; Coates, 1993).

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However, these artificialities introduce serious distortions when our concern is to assess whether or not conversations are used to service existing relationships, because most such situations either do not involve individuals who have relationships or focus on contexts in which relationships are of a very specific and short-term nature (e.g., workplace relationships). It would be futile (and bizarre) to try to study how (or, worse still, whether) language is used to service social relationships by ensuring that there were no relationships to be serviced. In our design, participants can talk about relationships if they feel them to be important, but not if they do not wish to do so. The results we have obtained from a series of studies in different locations have been very consistent: Social topics (what I here define broadly as “gossip”) account for approximately 65% of speaking time, with only limited variation due to age or gender (Dunbar, Duncan, & Marriott, 1997; Seepersand, 1999).

Conclusion I have argued that gossip, in the broad sense of conversation about social and personal topics, is a fundamental prerequisite of the human condition. Were we not able to engage in discussions of these issues, we would not be able to sustain the kinds of societies that we do. Gossip in this broad sense plays a number of different roles in the maintenance of socially functional groups through time; although simple social bonding is perhaps the single most important of these roles (and was perhaps the original impetus to the evolution of language), language permits other social functions. Of these, the exchange of information on free riders has undoubtedly become important in the large dispersed societies of modern humans. In some respects, its development may be seen as a natural outgrowth of our social brain, because it exploits the intense interest that we naturally have in the doings of others. That it can be carried to extremes may be a matter for regret, but this should not distract us from the central issue that gossip (in its broadest sense) is the central plank on which human sociality is founded. In reality, the cognitive demands of gossip are the very reason why such large brains evolved in the human lineage.

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2022.12.19 12:42 FamilyFirstTherapy Developing Attachments Through Play

By Lorie Walton, M.Ed., Certified Theraplay® Therapist Trainer Supervisor Certified Child Psychotherapist Play Therapist Supervisor
A Theraplay® therapist is holding a disorganized, anxious child in her lap, checking out what a wonderful boy he is. The boy cries until, all of a sudden, the therapist honks the child‟s nose. The child stops, looks at the therapist and smiles. During another session, the child stops resisting all engaging attempts and is taken by surprise when the therapist blows a bubble which lands on the little boys hand and his little finger pops it. The therapist matches the child‟s amazement and asks in delight “What happened?” The child, who has forgotten to resist, begins to pop the bubbles as the therapist and parent match his delight. During the next session, the little boy is suddenly still when in his mother‟s arms, he becomes absorbed by the eyes of his mom, who attunes to every gesture and vocalization of her little boy. As she plays peek-a-boo with his little feet, she rhymes the child‟s “mama” into a little tune. Never before in his 4 years, has the child been in prolonged eye contact with his mother, or with anyone else for that matter. He reaches over to grasp his mother‟s finger as he giggles and looks intently at his mother saying “More Mama, more.” This mother says her son was „born to her‟ at that moment. (reframed from J. Makela, 2003)
Children with a history of failed attachments usually have developed a variety of problems. 65% to 82% of children who have been in foster care have attachment issues and are missing some key developmental skills necessary to develop secure attachments (Hughes, 1999). Anger, aggression, withdrawal, depression, refusal to follow family rules, and the need to be in control at all times are symptoms which not only worry parents, but cause detriments to healthy social and emotional development.
Children with these issues are difficult to parent. Theraplay® is an exciting therapy which helps to treat many issues children experience today; however it is especially helpful for children with attachment related problems. It is a well-established modality designed to enhance relationships, raise self-esteem, improve trust in others and create joyful interactions between parent and child.
The focus of Theraplay® is based on five essential qualities: Structure, Challenge, Engagement, Nurture and Playfulness (Jernberg & Booth, 1999). These qualities mirror early parent-child relationships which are easily adapted to suit any aged child. Its philosophy is based on the idea of “What would we do for an infant who is behaving this way?” Children with attachment disorders missed out on healthy early parent-child experiences and because of this their emotional development is often hindered and delayed. An attachment disordered 8 year-old could emotionally present as a 3-4 year old child: cries easily, hard to reason with, clingy, demanding. Theraplay helps to address this emotional delay by providing the child with new experiences that often replicate what he would have required as a baby but never had the good fortune to get. Often during Theraplay treatment, the parent is reminded to ask herself “If my child were 4, what response would I expect him to give?” or “If my child were still only 2, would I expect him to be able to calm himself if he were upset?” The answer is often “No‟. Thus, Theraplay® encourages parents to use techniques that they would have used with an infant or young child.
Working closely with parents, the therapist uses attachment-building techniques which help to provide corrective attachment experiences. Using playful methods which focus on Structure and Challenge help to provide the child with experiences and opportunities for success while remaining safe and supported. The fact that the adult is in charge is reassuring to the child. Challenging activities are fun and require a partnership, not done alone. They help the child take a mild, age appropriate risk and promote feelings of competence and confidence. A simple challenging activity like Balloon Between Two Bodies (see description of activities at end of article) can help the child feel competent and confident by encouraging the child to take a slight risk and to accomplish the activity with adult help. Simple structured activities such as the Bean Bag Game or Cotton Ball Hockey help to relieve the child of the burden of maintaining control of interactions. The adult sets limits, defines body boundaries, keeps the child safe and helps to complete sequences of activities.
Engaging and Nurturing methods provide experiences which accept and love the child unconditionally. Engagement interactions focus on the child in an intensive and personal way in order to make an attuned connection. The goal is that the child feels “seen” and “felt.” In addition to this crucial connection, engaging activities, such as Body Check-ups, Piggy Back Ride and Hand Clapping Games offer pleasant stimulation, variety and a fresh view of life, allowing the child to understand that surprises can be fun and new experiences enjoyable.
Soothing, calming, quieting, caretaking activities that make the world feel safe, predictable, warm and secure and reassure the child that the adult provides comfort and stability are what Nurturing tasks involve. The goal of activities such as Cotton Ball Touch and the Twinkle Song is to meet the child‟s unfulfilled younger needs by reinforcing the message that the child is worthy of care and that the adults will provide care without the child having to ask for it. Through nurturance the child is helped to relax and to be taken care of. The child‟s inner representation begins to build and he begins to believe that he is lovable and valued. Children learn what it feels like as interactions are regulated while they experience the joy of having a positive connection with another person.
There is a growing body of research which outlines the positive impact of healthy physical contact on people of all ages. Barnard & Brazelton (1990) and Field (1993) found that loving touch produces oxytocin and releases endogenous opioids, which are known to solidify infant-mother bonds. Many studies have found that withholding touch can be as damaging as inappropriate touch, as was seen in Romanian orphans. It is important that children, especially those with attachment-related issues experience gentle, kind, loving and safe touch. Thus, Theraplay®‟s treatment includes many opportunities for healthy touch – whereby the therapist deliberately plans to have the child touched because: ♥ Touch is an important modality for creating relationships ♥ Touch communicates safety, acceptance, playfulness and empathy ♥ Touch helps regulate a child‟s out of sync emotions (The Theraplay® Institute) The therapist helps the parents learn how to become more attuned to the child‟s reactions and to find ways to make touch acceptable.
One of the strongest and most effective components of Theraplay® is its ability to include the parents as a primary component of treatment. Parents are the crucial players because they are with the child 24/7 and because the child needs to learn how to trust and form a healthy relationship with them in order to be able to grow and form future healthy adult relationships. Parents learn how to become Theraplay® experts to their own children through modeling, guiding, discussions, feedback, role-playing and guided practice.
All children need consistent daily doses of warmth, nurturance, acceptance, structure, challenge and playfulness. Enlightened interventions such as Theraplay® can help counteract negative emotions, re-channel past or missing early childhood attachment experiences into more positive ones and give a child the chance of creating a trusting healthy attachment, possibly for the first time in his life (The Theraplay Institute).
The activities listed below are just a few of the simple games which are used during Theraplay® treatment and are not only effective because they are playful, fun and engaging. These and other Theraplay® activities allow for the child to experience special “first moments‟ between child and parent. Moments where the child realizes he‟s not only being “seen‟ but also thought about, living and having an effect in another‟s mind (Makela, 2003) and where the parent is supported in helping the the child to „let go‟ enough to accept his parents love. These special firsts are what help child and parent begin to build a trusting and enjoyable attachment.
Sample Theraplay® Activities (referenced from Jernberg & Booth, 1999 & Theraplay Institute)
Bean Bag Game: Place a beanbag or small beany baby toy on your child‟s head, give a signal (“when my eye blinks”) or a magic word (“when I say the word “bubbles‟”) to cue the child to drop the beanbag into your hands (child tilts his head toward you so you can catch the bean bag in your hands). Take turns.
Cotton Ball Hockey: Lie on the floor on your stomach (or sit with a pillow between you holding the pillow up to eye level). Blow cotton balls back and forth trying to get the cotton ball past the child’s nose and past your nose. You can increase the complexity by saying how many blows can be used to get the cotton ball across the pillow, or by both trying to blow at the same time to keep the cotton ball in the middle. You can increase the structure of this game by using magic or cue words to signal when to start or stop. Remember to keep control of the game and don’t allow the child to control it…keep it structured, but successful, fun and positive. Balloon Between Two Bodies: Hold a balloon between you and the child (such as between foreheads, stomachs, shoulders, elbows) and move across the mat without dropping or popping the balloon. See if you can do this without using hands, but use this opportunity to touch your child in a fun and playful way (ie: wrap your arms around each other to hold on to the balloon between your stomachs). Body Check-up: Check child’s body parts, such as nose, chin, ears, cheeks, fingers, toes, knees to see if they are warm/cold, hard/soft, wiggly/quiet and so on. Count freckles, toes, fingers and knuckles. Piggy Back Ride: Help the child get onto your back. Jog around the room with the child on your back. Child can give signals for turning, stopping, changing directions, “Whoa!” and “Giddy-up!” Hand Clapping Games: Older children enjoy these games very much. They can be simple (Patty Cake) or complex (elaborate rhythmic clapping patterns) and can have a variety of chants, for example, Miss Mary Mack or the Sailor Went to Sea. Cotton Ball Touch: Have the child close his eyes. Touch your child gently with a cotton ball. Have the child open his eyes and indicate where he was touched. Twinkle Song: Adapt the words of “Twinkle, Twinkle Little Star” to the special characteristics of the child. “What a special boy you are, Dark brown hair and soft soft cheeks, Bright brown eyes from which you peek, twinkle, twinkle little star, what a special boy you are.” Hold the child in your arms and touch the parts you refer to as you sing and rock him gently.
A bit about the author: Lorie Walton, M.Ed., is a private Child Psychotherapist Play Therapist Supervisor and Theraplay® Therapist Trainer Supervisor. She is the owner and lead therapist of Family First Play Therapy Center, in Bradford Ontario Canada where she helps children and families with attachment issues and emotional trauma. She is also the President of the Canadian Association for Child and Play Therapy (CACPT). She will be happy to answer any of your questions regarding Theraplay® or other questions you may have about your child‟s emotional development at familyfirstlw@bellnet.ca or by calling 905-775-1620.
References Barnard, K.E., & Brazelton, T.B (Eds.) Touch: The foundation of experience. Madison, CT: International Universities Press Inc., 1990.
Field, T. The therapeutic effect of touch. In G. Branningan & M. Merrens (Eds.). The undaunted psychologists: Adventures in research (pp. 3-12). New York: McGraw Hill, Inc., 1993 Jernberg, A & Booth, P. (1999). Theraplay. Helping Parents and Children Build Better Relationships Through Attachment Based Play. 2nd Edition. San Francisco,: Jossey-Bass. Harlow, H.F. The nature of love. American Psychologist, 1958, 13, 673-685. Hughes, D. (1997) Facilitating Developmental Attachment. Northvale, NJ: Jason Aronson, Inc.
J. Makela. What Makes Theraplay Effective: Insights from Developmental Sciences. Originally published in the Theraplay Institute Newsletter Fall / Winter, 2003.
The Theraplay Institute, Chicago. www.theraplay.org

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2022.12.17 10:44 FamilyFirstTherapy Theraplay® – A First Step to Managing Emotional Regulation

When children experience any type of challenge (emotional, developmental, educational, medical, familial) their emotional regulation systems experience a stress response. Ongoing stress reactions can impact the child’s ability to maintain emotional regulation. Stress hormones such as cortisol and adrenaline, surge thru the child’s body during stressful times. These hormones are negative and can impact the child’s developing regulating system in inhibitive ways. The heart rate increases to power the human body during ‘flight’ or ‘fight’ responses, and it must maintain its rhythmic pulse despite the varying demands placed on it. Thus, regulating heart rate during stress and controlling stress hormones are two critical tasks that require the brain to keep proper time (Perry, 2000).
Because children’s emotional systems are still in the early stages of development (along with their brain and body systems), they require help in being soothed as they are often unable to soothe themselves without an attentive adult’s help. If left unsoothed, the child’s overall emotional development may be negatively impacted long term thus potentially predisposing the child to anxiety and future mental health issues. Disturbances of the brain’s rhythm-keeping regions are often causes of depression and other psychiatric disorders (Perry, 2000). Therefore, if a young child’s primary regulating system doesn’t function well, not only will his hormonal and emotional reactions to stress be difficult to modulate, but other systems like sleeping and eating, learning motor functions, and responding to others in positive ways will be volatile as well.
Most often, children with dysregulated emotional systems require first an intervention which helps their body unconsciously experience soothing and calming from an external source BEFORE they can consciously begin to master their fight, flight, freeze responses in a controlled and motivated way. The regulation of emotions is equal to helping a child securely attach. Attachment researcher has demonstrated that attuned, engaging interactions between a baby and mother leads to secure attachment, positive internal working models of self and world and the capacity to regulate emotions and actions (Sroufe 2005).
When considering which therapeutic modality to use, it is best to consider two important aspects of the child’s presentation: 1. Does the child’s emotional system appear younger than his chronological age? And 2. Does the child have a significant attachment caregiver who can learn how to attune to the child’s internal dysregulated states and provide soothing and nurturing experiences to effectively help the child’s brain and body systems begin to ‘balance’?
Theraplay®(1) is an evidenced-based intervention which helps children experience emotional regulation by participating in playful, attuned experiences with a parent or caregiver. One of its many assets is its ability to assist a caregiver use attuned nurturing and soothing responses to help the emotionally dysregulated child’s body internalize new responses to stress. Below is a brief account on how Theraplay was used to help an anxious child. 7 year old Sara, was referred for Theraplay in order to help reduce the highly anxious behaviours she was presenting with. Sara’s parents spoke honestly of their own anxiety in regard to parenting Sara. They reported her behaviours as very challenging at times especially pertaining to separation when going to school. They also reported her as fearful, nervous and aggressive especially with family members.
Sara participated in 12 Theraplay sessions with her mother and father. The Marschak Interaction Method Assessment was done prior to Theraplay sessions in order to assess attachment and relationship strengths and needs. During this assessment, Sara was observed as hyper-vigilant, controlling, aggressive and rejecting and very anxious about being left alone. This behaviour substantiated reports from home, and strongly indicated Sara’s dysregulated emotional state. Thus, goals for Theraplay treatment were set to decrease her anxiety and hypervigilance, increase Sara’s self-confidence to master challenges and assist Sara in strengthening the bonds of attachment with her parents. Goals were also set to help Sara’s parents feel more confident about their ability to parent Sara.
The Theraplay sessions were structured so that Sara could interact with her father as much as with her mother. Nurturing and engaging techniques were introduced to assist in strengthening Sara’s trust with her parents. Through activities such as measuring, or cotton ball soothe, the parents were encouraged to point out special qualities about Sara to help her feel noticed and to encourage body awareness. Initially, Sara appeared somewhat uncomfortable when receiving positive comments about herself. She would not make eye contact and would often become fidgety and try to change the subject. At times, during more active games she would be rough towards her mom, but once encouraged to use Feather High-5’s(2) she was able to demonstrate her ability to be gentler and more controlled.
During initial Theraplay sessions, Sara sometimes appeared unable to keep up with the pace of activities and she often seemed anxious when too many directions were given at once. She appeared challenged when more than one person was speaking to her or when information was given at a pace which was difficult for her to process. Thus, the following modifications and suggestions were made to address these issues: • Modeling techniques were used to provide Sara with the opportunity to observe new tasks before it was her turn. • The parents were encouraged to have only one person speak to Sara at a time, so that she could process information more easily. • When providing Sara with directions, the parents were encouraged to give no more than 2 step directions at a time, to relieve some of the anxiety for Sara in completing the task. • Calming and relaxation techniques were modeled for Sara (i.e.: blowing on her fingers) to help Sara, learn how to reduce some of her anxious feelings. • The parents were encouraged to practice these techniques at home to assist Sara in using them when she most needed to.
During each session, the parents were invited to keep a physical connection with Sara. Sara would be placed on Dad’s knee facing Mom so that Mom could massage lotion into Sara’s hands and arms. Stick-together(3) games were incorporated to help the parents remain ‘physically’ connected to their daughter as much as possible. Nurturing activities such as Magic Carpet Ride(4) and snuggling Sara in a blanket while in mom’s arms were some of Sara’s favourites. It was observed during these nurturing moments that Sara seemed less anxious and much more settled. During one session, after being rocked in a blanket and then put into mom’s arms, Sara almost fell asleep.
After each Theraplay session, a co-therapist would take Sara into another room to play in order to allow the parents and therapist to review weekly progress and challenges. During these discussions, Sara’s parents were comfortable in expressing their anxiety around parenting Sara when she exhibited impulsivity and controlling and aggressive behaviors. Parenting strategies were suggested, and the parents were encouraged to attune to Sarah’s younger emotional needs. Over time, the parents reported that they had begun to proactively incorporate Theraplay strategies which included attunement, nurture, and structure as much as possible in order to help Sara feel less anxious and more secure.
The playful interactions within the Theraplay experience creates the opportunity to share one’s bodily reality and ones emotional reality in expanded, dyadic states of preverbal consciousness (Makela, 2003). Theraplay is tailored to give corrective experiences in physical coregulation through its extensive use of touch, eye contact and the calming and stimulating way of speaking throughout the playful interactions which include Structure, Engagement, Nurture and Challenge. At the same time, it creates a resonant hum of emotions through attunement – the noticing of the minutest emotional cues of the child and responding to them (Makela, 2003). Being’ noticed’ makes all the difference to an anxious child’s predisposition of insecurity.
There is a growing body of research which outlines the positive impact of healthy physical contact on people of all ages. Barnard & Brazelton (1990) and Field (1993) found that loving touch produces oxytocin and releases endogenous opioids, which are known to solidify infant-mother bonds. During Theraplay, touch is used in playful, nurturing, and structured ways to help connect the child’s unconscious brain and body systems to those of their parent’s calmer ones. Incorporating touch within the Theraplay session helps to reduce the child’s internal emotional stress responses. Oxytocin, opioids and endorphins counter-act the cortisol responses within the child’s body and allow the child to experience pleasure and internal calm. As the child begins to enjoy playful interactions with her parent, the child’s internal blueprint eventually becomes ‘rewritten’ to include a calmer internal response to external stressors. As the parent becomes the co-regulator of the child, the child begins to feel internal regulation which leads to security within oneself and then eventually with others in her world.
Theraplay helps children to experience the internal capacity of ‘calm’ from their coregulating caregivers at a pre-verbal level, which is lower on the hierarchy of cognitive development than other more cognitively sophisticated interventions. Once a child has cognitively and emotionally matured, more sophisticated interventions, such as CBPT, can then be considered to help anxious children begin to consciously master their internal stress reactions. Thus, Theraplay can be considered a ‘first-step’ in the intervention protocol to help a predisposed anxious child begin to master control over their emotional triggers.
By the end of the 12 sessions, Sara had begun to demonstrate her ability to respond with eagerness instead of with a ‘fight’ response such as aggression. Her parents also reported that Sara appeared less anxious, less controlling at home and appeared more confident in going to school. During a follow-up session, Sara’s parents reported that she seemed calmer and more affectionate with them. Her dad said it best when he stated “Now she wakes up singing in the morning!”
Lorie Walton, M.Ed., RP; is a Certified Play Therapist Supervisor and Theraplay® Therapist Trainer Supervisor. She is the owner of Family First Play Therapy Center Inc., in Bradford Ontario where children and families who are experiencing attachment issues and emotional trauma receive therapeutic support. She is also the Executive Director of Theraplay Canada, was Past-President of the Canadian Association for Child and Play Therapy (CACPT) and continues to be an active member within the Theraplay and Play Therapy community. She received the 2009 Monica Herbert Award from CACPT in recognition of her commitment to Child Psychotherapy Play Therapy growth and support across Canada.
(1) Theraplay®- www.theraplay.org (2) Feather High-5 – a wiggle of one persons fingers to another persons wiggling fingers instead of a hand-slap (3) Stick-Together Games are Theraplay games which incorporate the parent and child to keep a physical connection with one another at all times(such as linked elbows or a hand on the child’s shoulder, or nose to nose) while participating in Challenges (ie: stick together with nose to nose while getting balloon across the room as a team) Blowing feathers from one pillow to another as a team is also a fun game which promotes togetherness and helps to exercise deep breath exhales.(4) Magic Carpet Ride – spread a blanket on the floor and have child lay down on it. Parents and Therapist lift the child up in the blanket and move them around the room as if giving the child a magic carpet ride. Move slowly and swing softly so that the child feels a rhythm to the swinging and movement. (take them ‘across the ocean’ ‘over the treetops’ ‘over the mountains’ etc)
(First Published in The Canadian Association for Child and Play Therapy’s National Magazine – Playground, April 2011)
Lorie Walton, M.Ed, CPT/S, RP Certified Theraplay® Therapist Trainer Supervisor Owner of Family First Play Therapy Centre Inc www.familyfirstplaytherapy.net Executive Director of Theraplay Canada www.theraplaycanada.ca
References Barnard, K.E., & Brazelton, T.B (Eds.) ( 1990). Touch: The foundation of experience. Madison, CT: International Universities Press Inc. Field, T. (1993). The therapeutic effect of touch. In G. Branningan & M. Merrens (Eds.). The undaunted psychologists: Adventures in research (pp. 3-12). New York: McGraw Hill, Inc. Makela, J. (2003). What Makes Theraplay Effective: Insights From Developmental Sciences. Originally Published in the newsletter of The Theraplay Institute Fall/Winter. Perry, B.D. (2000) Traumatized children: How childhood trauma influences brain development. In: The Journal of the California Alliance for the Mentally Ill 11:1, 48-51. Sroufe, L. A. (2005). Attachment and development: A prospective, longitudinal study from birth to adulthood. Attachment & Human Development, 7, 349-367.

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2022.06.14 14:37 atmasabr (Gobstoppers would be so triggered by this)

Backlashes are interesting things. So this is apparently a week old article over a two-week old item, Ohio House just passed one of those stop Lia Thomas bills at the beginning of this month. (The Ohio Senate won't be considering it until it resumes session in November.)
https://www.dispatch.com/story/news/2022/06/07/bill-transgender-athletes-could-require-genital-checks-girls/7529718001/
As soon as House Republicans passed a bill to block transgender girls from playing on female sports teams in K-12 or college, opponents started questioning how physicians would verify a minor's biology.
They claim girls of all ages could be required to undergo full pelvic exams if an opposing team's coach, player or parent questioned their sex.
They're right.
Bill could require an internal exam
House Bill 151, also called the "Save Women's Sports Act," says if a participant's sex is disputed, she must verify her sex with a physician in "only" the following ways.

An exam of her internal and external reproductive anatomy.
Her normal "endogenously produced levels of testosterone."
An analysis of her genetic makeup.

It's not clear whether student-athletes could pick one of these options or would have to provide all three.
It's "not clear"? Oh, dear, she's right. These bills usually say "and" or "or" in them. This one doesn't.
Cue all kinds of tooth-nashing and garment rending and overall snowflake whining about how intrusive and unnecessary such exams are. I wish people had more room for such compassion when the LTs' many enablers were breaking social order barriers left and right. These weren't nothingburgers.
I can't imagine that these kind of exams would be intrusive to anyone who has a well-kept medical history... which means that the stronger weight of this kind of bill will be disproportionate based on class, national origin, and probably race.
Got more interesting stuff in that bill.
https://preview.redd.it/0owsrtqfzk591.png?width=570&format=png&auto=webp&s=6103d061a732f52b9c3ed1356172b914b89b6ea7
https://preview.redd.it/3bb0v21wzk591.png?width=600&format=png&auto=webp&s=2697d30236a1742832106f2d53877b2f78f6a559
Isn't Ohio supposed to be some kind of purple bellweather state? Or am I just showing my age?
It seems to me that the people of the United States are not impressed at being lectured by the media or social media about what is socially or politically correct or incorrect on behalf of women, and have determined that they can enact legislative change to maintain their priorities.
Anyway it's an interesting June this year. It's an interesting June.

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2022.05.23 18:18 sirsadalot Tropisetron is one of the best nootropics - V2

Welcome to my newest project. Now satisfied with my dopamine research, I'm taking on other challenges such as increasing human IQ. So I was very much excited reading this study, where GTS-21 improved working memory, episodic memory and attention. Not only was this conducted in healthy people, but these domains of cognition are important to IQ, consciousness and executive function, respectively.
GTS-21 is a failure, and I'll explain why. But it's a selective α7 nicotinic receptor partial agonist, so we can learn a lot from it. This led me to discover Tropisetron, a superior α7 nicotinic receptor partial agonist and also 5-HT3 antagonist.

The α7 nicotinic receptor and nicotine

Before progressing, I would like to outline the discrepancies between nicotine and α7 nicotinic receptors.
Addiction: This is people's first thought when they hear "nicotinic". But nicotine is not a selective α7 agonist, and in fact it has more bias towards α4. This is what causes dopamine release, and therefore euphoria and addiction.^\6])^\10])
Cognition: Unsurprisingly, short-term cognitive benefits of nicotine are likely mediated by α7 nicotinic receptors. This is bolstered by Wellbutrin (Bupropion) not impairing cognition in healthy people.^\11]) Compared to other nicotinic receptors, its affinity for α7 is the lowest.^\12])
Tolerance & Withdrawal: Tolerance at the nicotinic receptors is atypical and occurs through multiple mechanisms. In nicotine's case, α4 upregulation on inhibitory GABAergic neurons contributes to this, as well as the reduced dopamine release during withdrawal.^\10]) But with α7s, it would appear it a structural issue of ligands themselves, with some remaining bound long beyond their half life and "trapping" the receptor in a desensitized state.^\7]) This, along with nausea is what caused GTS-21 to fail.^\4]) But this doesn't appear to be the case with Tropisetron, which could be due structural dissimilarity, or perhaps it acting as a co-agonist and "priming" the receptor for activation, which is why increasing acetylcholine enhances its nootropic effects.^\2]) Aside from the fact that Tropisetron is quite literally an anti-nausea medicine with a long history of prescription use.
Other: α7 nicotinic receptor partial agonists appear to be better anti-inflammatory agents than nicotine.^\9])

Tropisetron, α7 nicotinic receptor partial agonist and 5-HT3 antagonist

In the medical world, treating illness is priority. As such, studies in the healthy are uncommon. However, Tropisetron has improved cognition in conditions characterized by learning disorders, such as Schizophrenia.^\3]) Nootropic effects are also shown in primates^\2]) correlating with the results found in healthy people given GTS-21.
Multifunctional: It is a very broadly applicable drug, showing promise for OCD,^\23]) and Fibromyalgia. Also anxiety, but only mildly.^\16]) It reports strong antidepressant effects in rodent models,^\15]) which correlates with other 5-HT3 antagonists.^\21]) 5-HT3 antagonism is a desirable target, as it isn't associated with side effects or tolerance^\13]) and appears neuroprotective^\20]) and pro-cognitive^\17])^\18])^\19]) potentially due to enhancing acetylcholine release. An atypical SSRI and 5-HT3 antagonist, Vortioxetine^\14]) was also shown to improve cognition in the majorly depressed, an unexpected outcome for most antidepressants.
Alzheimer's and excitotoxicity: α7 nicotinic receptor overactivation can cause excitotoxicity. But a partial agonist is neuroprotective, dampening excitotoxic potential while stimulating calcium influx in a way that promotes cognition. But Tropisetron is also valuable for Alzheimer's (AD), binding to beta amyloids and improving memory better than current AD treatments such as Donepezil and Memantine.^\25]) It is a 5-HT3 antagonist, but this doesn't appear responsible for all of its neuroprotective effects. Improved blood flow from α7 partial agonism appears to play a role.^\26])
Other: Tropisetron shows promise for lifespan extension and healthy aging with antioxidant and anti-inflammatory effects,^\22]) has data to suggest it benefits fatty liver disease^\24]) and although it was GTS-21 to be trialed, potentially ADHD. Tropisetron is mildly dopaminergic at low doses (<10mg), and antidopaminergic at high doses (>10mg).^\8])
Tropisetron stacks? Similarly to Piracetam, it would appear increased acetylcholine improves its memory enhancement. ALCAR, an endogenous and potent cholinergic seems logical here. Tropisetron's antidepressant effects are potentiated by increased cAMP, so Bromantane or PDEIs such as caffeine would make sense.
ROA, dose, half life and shelf life: Tropisetron is best used orally at 5-10mg. It has a half life of 6 hours but effects that may persist for much longer. Shelf life is around 3 years.

Summary

Tropisetron fits every criteria required to earn the title "nootropic". Furthermore, it may be one of the most effective in existence due to its selective actions at α7 nicotinic receptors and 5-HT3. Tropisetron encompasses a wide range of potential benefits, from improving cognitive function to generalized benefits to mental health.
Route of administration: Oral. Effective at 5-10mg, and a solution with 20mg/mL is available. The pipet is labeled, so the concentration is accurate every time.
Read the comments to see where to buy Tropisetron.
References:

GTS-21's nootropic effect in healthy men: https://www.nature.com/articles/1300028
Tropisetron's nootropic effect in primates: https://sci-hub.se/https://doi.org/10.1016/j.neuropharm.2017.02.025
Tropisetron's nootropic effect in Schizophrenics: https://www.nature.com/articles/s41386-020-0685-0
GTS-21's (DMXB-A) failure to treat Schizophrenia: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746983/
Tropisetron side effect profile and duration: https://pubmed.ncbi.nlm.nih.gov/7507039/
α7 nicotinic receptors and nicotine cue: https://europepmc.org/article/med/10515327
α7 desensitization by GTS-21: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672872/
Effect of Tropisetron on hormones and neurotransmitters: https://www.tandfonline.com/doi/abs/10.1080/030097400446634
Effect of GTS-21 on inflammation versus nicotine: https://hal.archives-ouvertes.fhal-00509509/document
Nicotine tolerance and withdrawal: https://www.jneurosci.org/content/27/31/8202
Wellbutrin's effect on cognition in healthy people: https://sci-hub.se/https://link.springer.com/article/10.1007/s00213-005-0128-y
Wellbutrin not selective to α7: https://pubmed.ncbi.nlm.nih.gov/10991997/
5-HT3 antagonists and anxiety: https://pubmed.ncbi.nlm.nih.gov/10706989/
Vortioxetine and cognition: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851880/
Tropisetron's potential antidepressant effects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084677/
Tropisetron when tested for anxiety: https://pubmed.ncbi.nlm.nih.gov/7871001/
5-HT3 antagonists and cognition 1: https://pubmed.ncbi.nlm.nih.gov/8983029/
5-HT3 antagonists and cognition 2: https://pubmed.ncbi.nlm.nih.gov/2140610/
5-HT3 antagonists and cognition 3: https://pubmed.ncbi.nlm.nih.gov/12622180/
Broad potential of 5-HT3 antagonists: https://pubmed.ncbi.nlm.nih.gov/31243157/
5-HT3 antagonists and depression: https://pubmed.ncbi.nlm.nih.gov/20123937/
Tropisetron activates SIRT1: https://pubmed.ncbi.nlm.nih.gov/32088214/
Tropisetron and OCD: https://pubmed.ncbi.nlm.nih.gov/31575326/
Tropisetron and mice with fatty liver: https://pubmed.ncbi.nlm.nih.gov/21903748/
Tropisetron and Alzheimer's: https://www.reddit.com/NooTopics/comments/uvtp29/tropisetron_and_its_targets_in_alzheimers_disease/
Tropisetron vs other 5-HT3 antagonist: https://www.reddit.com/NooTopics/comments/uvtnal/tropisetron_but_not_granisetron_ameliorates/

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2020.09.21 07:47 omega_constant [Theory] Why is reality so... weird? Here's why!

Let's start with the simulation hypothesis (SH). SH is often invoked in the course of explaining ME. After all, most of us who have played regular computer games are familiar with, say, changing skins in the game to completely alter the superficial appearance of objects and scenes in the game while leaving the underlying physics, characters and maps unchanged. ME is a lot like this. One or a small subset of things are "tweaked" (often superficial things, but not always) while everything else remains (apparently) the same.
Most of us are relatively familiar with the basic idea of an electronic digital computer. It has an internal state that can be represented as a bitmap of billions of 1's and 0's and these bits are all "flipping" according to rules at an enormous frequency ... billions of cycles per second in most computers.
Most of us are less familiar with quantum computers and even experts in the field do not give us much comfort. Quotes like "If you think you understand quantum mechanics, you don't understand quantum mechanics." (Richard P. Feynman) can leave one feeling adrift in an ocean of hopelessness. But quantum computers are a welcome restriction of the domain of quantum theory to a much more manageable abstraction (the qubit and quantum circuits involving qubits). While quantum computers are not easy to understand, they are not harder to understand than complex numbers and matrix multiplication. Because that's really what a quantum computer is ... a very fast complex matrix multiplier -- vastly faster on large matrices than any classical computer could ever be. And it turns out that complex matrix multiplication is completely general -- you can describe any quantum system (not just qubits) with it. For that matter, you can describe the evolution of any classical system (with sufficient attention to detail). You can describe any classical logic circuit. The quantum computer is not necessarily efficient for all these applications but the point remains that the QC is capable, in principle, of simulating all of these systems.
Seth Lloyd -- MIT professor who jokingly refers to himself as a "quantum mechanic" -- has said the following: "the universe is observationally indistinguishable from a quantum computer." In short, if you want to know what it is like to be inside of a quantum computer, just look around you. The stronger version of Lloyd's statement is as follows: you cannot describe any experiment that would rule out the possibility that you are inside a quantum computer. This statement does not hold for classical computers. As we already know, classical computers are very inefficient at simulating our physical universe which strongly suggests that our universe is not a simulation running on a classical computer.
But even the QC simulation theory is missing one crucial component -- choice and consciousness itself. There is some concept of "quantum choice" but it's not really about choice in the ordinary sense. And quantum theory strictly applies to the waking world... a purely quantum world is a dreamless world. So, the fact that we experience dreams and we make choices (assuming we make choices) means that there is more to reality than quantum theory alone can explain.
But is that it? Do we just throw our hands up? Wait for the theoretical physicists to make one superstring theory to rule them all? Well, there is one more model of computation that is not often discussed but which is every bit as powerful as a Turing machine or a quantum computer -- this is the actor model of computation. And unlike with Turing machines or quantum computers, the actor model of computation can be interpreted in an entirely endogenous way. That is, I do not have to think of an actor as some "other thing" that is "outside of myself" and is "simulating" me or my world. Rather, I AM an actor, that is, I am an agent! I receive and send messages. I make decisions. And I can even create more agents (reproduction or, via invention, mechanical agents). So I fulfill all the criteria of being an agent in an actor model of computation. And so do you.
Now, in the theory of computation, there are provably unsolvable problems. These are problems that nobody -- not even God himself -- could solve. They just sit there and mock the very concept of solution. In addition, there are problems that we can prove are efficiently solvable under some sufficiently loose definition of "efficient". Some of these problems we haven't solved, but we know there exists some solution to them, and it is efficient. But between the unsolvable problems and the efficiently solvable problems is a very large and important class of problems that are theoretically solvable but for which no efficient solution is known to exist (or, in some cases, no efficient solution can exist). In fact, most of the computational problems we most urgently need to solve in science and mathematics are problems of this form. And while quantum computers can push us further into solving problems in the "efficiently solvable" space, it actually cannot help us solve problems for which there is no efficient solution (or no known efficient solution). However, that doesn't mean that all of these problems are unsolvable with the means available to us. For example, it is always possible to get lucky and stumble onto a solution by accident.
Which brings us to the evolutionary algorithm. In a way, the evolutionary algorithm is the "null algorithm." It's the algorithm you run when you don't have any more clever way to solve a problem. It is better than random search on problems which have a structured solution space. That is because, if there is a structured solution, the evolutionary algorithm will tend to bump into parts and pieces of that solution early on. And using simple "greedy hill-climbing", in combination with massively parallel search, it can combine those precursor solutions into better and better solutions by extracting more and more structure from the problem space. So, an evolutionary algorithm is exactly the kind of algorithm that we (or an alien species or a sentient hyper-intelligence or fill-in-the-blank superior-thingy) would run when tackling a theoretically solvable problem for which no efficient solution exists, or is known to exist. And, by golly-gee, guess what... we live on a planet teeming with evolving creatures. Surprise!
To stimulate your imagination, take a look at this list of Nature-inspired meta-heuristics. These meta-heuristics have already been successfully applied to solving problems in that space of problems that are "theoretically solvable but no efficient method of solution is known". So, we're not speculating -- this actually works.
But I want you to notice that a computation running on the actor model could implement any of these algorithms, and many more besides. In fact, it is perfectly reasonable to map all living species on this planet to an actor-model simulation being played out for some unknown objective. And it would be a mistake to stop at natural evolution -- social evolution and even artificial evolution (humans running artificial evolutionary simulations) are also part of one, cohesive model. So your sentient awareness and the choices that it makes are just a part of one, gigantic simulation. You are the qubit; the qubit is not something "out there" simulating you. You are the hardware. And the software that is running on you are the instincts, desires, social cues and every other layer of evolutionary programming that is active and operative in your awake consciousness. And, using the actor model, we do not have to make any distinction between your waking life and your dreams. So you are in a reality that is in a dream, that is in a reality, and so on -- quantum simulations running inside of quantum simulations, ad nauseum.
Our mistake was thinking that this entropic ball of scat was ever "real" in the sense of being compelled to follow some deterministic set of rules. Quite the opposite, the software is completely unrestricted. For the evolutionary algorithm itself, the genes are just bits that can be flipped at practically no cost. But you are the hardware. You were birthed into this plane at great cost and you are constrained by countless tiny threads of control that determine how your inner state will evolve in response to the states of everything within your local environment.
YOU ARE THE QUBIT... and that's a lot weirder than the weirdest Mandela Effect.

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2019.11.20 10:35 lupinepublisher-NBD Lupine Publishers Addiction and Evolutionary Process, Common Aspects in Physio-Pathologic Pathways Useful in PharmacoToxicological Approach

Lupine Publishers Addiction and Evolutionary Process, Common Aspects in Physio-Pathologic Pathways Useful in PharmacoToxicological Approach

Lupine Publishers Journal off Neurology and Brain Disorders- Addiction and Evolutionary Process, Common Aspects in Physio-Pathologic Pathways Useful in PharmacoToxicological Approach

Abstract

Observing vertebrates evolutionary in mammalian are present characteristic pathways involved in progeny take care in first period after birth. In this behavior and instinct, learning neuronal circuits are evolved and reward mechanism the same. In addiction is possible to observe that definite neuronal circuits plays a crucial role. In this work are showed this similarity to better understand the addiction condition. Reward mechanism (primary, intrinsic or extrinsic) are involved in food, reproductive- sexual activity but also in other human condition. Conditioning, reinforce, reward, learning behavior, depression status, level of motivations is common concept involved also in addiction.
Keywords: Addiction; Toxicology; Physiology; Anatomy; Mammalians; Vertebrates

Introduction

Starting from the evolutionary of vertebrates is possible to verify that mammalians vs reptile in example show a great characteristic in cooperative behavior, maternal instinct, high mother depending of progeny and other relevant aspects. So is clear that this kind of vertebrates show a great depending relationship between mother-progeny and we can say that this kind of “animals species” are under a high constraint under an (behavioral, instinct, psychology, neurological aspect). (Anatomically are involved cortex, basal ganglia and thalamus but also other system like amygdala) Dopaminergic- Mesolimbic pathway in example Dopamine is involved in many physiological functions like emotion, pleasure, movement (extrapyramidal), Breast feeding, involved in depression or schizophrenia, prolactin regulation, nausea and vomiting and other. Other molecules involved in “happiness”: dopamine, serotonin, endorfin and oxytocin. (oxytocin: role in mother-infant relations, attachment, and bonding in humans). Neuronal circuits of rewards, dopaminergic, glutaminergic, gabaergic (circuits play a relevant role in this mechanism. Breastfeed imply a prolactin and dopaminergic involvement as well as oxytocin and is an evolutionary advantages towards other vertebrates. Viviparous, Parental care of progeny, breast feed, communication abilities between individuals, associative learning, emotional control are common properties of mammalians like emotional, social behavior. (hierarchy, communication to other member of the group of danger and so on).

Material and Methods

Using an observational approach from biomedical and scientific literature in PUB MED is possible to verify the Neuro pharmacolgical pathways involved in some mammalian behavior and istinct and in addiction condition.
The bibliography reported is chosed related the keywords and related the aim of this work.

Results

According Biomedical Literature is Possible to Verify that: Archeology science not to be consider only related human product and manufacts but also an inside disciple to verify archeological process related to mind- set kinetics and to other system or organs. Brain, mind, immunologic system and other relevant physiological functions are deeply influenced by a primitive structure and to deeply understand the meaning of this complex system inside us make possible to better explain today Human behavior and physiology and other process [1].
Marco Diana [2]: “Dopamine (DA) transmission is deeply affected by drugs of abuse, and alterations in DA function are involved in the various phases of drug- addiction and potentially exploitable therapeutically. studies have documented a reduction in the electrophysiological activity of DA neurons in alcohol, opiate, cannabinoid, and other drug-dependent rats. DA release in the Nucleus accumbent is decreased in virtually all drug-dependent rodents. these research studies are supported by increments in intracranial self-stimulation (ICSS) thresholds during withdrawal from alcohol, nicotine, opiates, and other drugs of abuse, thereby suggesting a hypofunction of the neural substrate of ICSS. morphological evaluations fed into realistic computational analysis of the medium spiny neuron of the Nacc, post-synaptic counterpart of DA terminals, show profound changes in structure and function of the entire mesolimbic system.
Human imaging studies have shown a reduction of dopamine receptors accompanied by a lesser release of endogenous DA in the ventral striatum of cocaine, heroin, and alcohol-dependent subjects, thereby offering visual proof of the “dopamine-impoverished” addicted human brain. The lasting reduction in physiological activity of the DA system leads to the idea that an increment in its activity, to restore pre-drug levels, may yield significant clinical improvements (reduction of craving, relapse, and drug-seeking/ taking). In theory, it may be achieved pharmacologically and/or with novel interventions such as transcranial magnetic stimulation. Its anatomo-physiological rationale as a possible therapeutic aid in alcoholics and other addicts will be described and proposed as a theoretical framework to be subjected to experimental testing in human addicts [2].
Andrew B Barron et al. [3]: Motile animals actively seek out and gather resources they find rewarding, and this is an extremely powerful organizer and motivator of the animal behavior. Mammalian research studies have revealed interconnected neurobiological systems for reward learning, reward assessment, reinforcement and reward-seeking; all involving the biogenic amine dopamine. The neuro-biology of reward-seeking behavioral systems is less well understood in the invertebrates, but in many diverse invertebrate groups, reward learning and responses to food rewards also involve dopamine. The obvious exceptions are the arthropods in which the chemically related biogenic amine octopamine has a greater effect on reward learning and reinforcement than dopamine. We review the functions of these biogenic amines in behavioral responses to rewards in different animal groups and discuss these findings in an evolutionary contex [3].
Tonse NK Raju [4]: “Sometimes, even the most obvious facts need to be reiterated. An infant suckling at his or her mother’s breast is not simply receiving a meal, but is intensely engaged in a dynamic, bidirectional, biological dialogue. It is a process in which physical, biochemical, hormonal, and psychosocial exchange takes place, designed for the transfer of much needed nutrients, for building a lasting psychosocial bond between the mother and her infant. Among mammals, breastfeeding has evolved over millions of years as a multitiered interaction to meet the biological and psychosocial needs of the progeny, enhancing its well-being and survival chances, as well as complementing the nurturing role of the mother. this unique, dynamic process benefits both the mother and her infant. Breastfeeding needs to be considered quintessentially as a continuation of the more intense, intrauterine dialogue, mediated through the placenta and the umbilical cord between the mother and her fetus.
Whether feeding at the breast is complementary to the nutritional value of human milk, which might explain the diverse range of benefits to the mother and her infant, remains to be studied. innovative methods from different scientific disciplines, such as behavioral, cognitive, and developmental neurosciences, and social anthropology may be useful to study this unexplored territory. Among the many benefits from breastfeeding during the first year of an infant’s life, the effects on long-term cognitive development and IQ have been most controversial. Some researcher contend that breastfeeding should be considered the social norm, and lower cognitive scores in infants fed formula should be considered abnormal. Sullivan asked, “Is it possible that some property in the infant formula may not be conducive to full cognitive development?” It is an interesting question that needs to be elucidated in future studies. Be that as it may, the above arguments require one to critically consider the cause-and-effect relationships between breast-feeding and cognitive outcomes. 2 recent publications answer the concerns about the causal relationships.
In a longitudinal study of neurodevelopmental evaluation Jedrychowski et al. assessed 468 infants of non-smoking women at 1, 2, 3, 6, and 7 years of age. Infants who were exclusively breastfed consistently demonstrated between 2.1 and 3.8 higher IQ points at each measurement session compared with those who received mixed feeding (human milk plus infant formula). The longer the duration of exclusivity of breastfeeding, the higher was the IQ benefit. In this and and similar studies,1-4 the overall IQ advantage from breastfeeding appear to be small, but the effect size is highly significant from a public health perspective. Improvements of even a few IQ points, especially at the lower end of the IQ distribution, will reduce the number of children who might otherwise need special education [4].
“We have seen in last 2 centuries different way to have a brain map using various strategies. Since from the BROADMAN theories we have seen the introducing of technologies to support this working method. (Old and new) as EEG, TC, PET, FMRI, MEG, NIRS ant other with the scope to differentiates brain area in order to show their specific activity. This has made possible to produce anatomic images and map about the different brain area to be related with some different functions / disfuncions. But what we can think is to create a new ANATOMIC brain map using the drugs and substances that show high Activity level in neurology field. a new pharmacology brain map can be obtained using different molecules or physiopathological conditions: BDZ GABA receptor, Barbiturate, Opioids, Neuroleptics, antiepileptic’s, Anti depressive and ipnotics. Anti-migraine, Amphetamine, Anti Parkinson, Ant dementia, Antimuscarinics, Anticholinergic Analgesics, General anesthetics, Antistaminics, Poisons and toxins, Antipyretics, antihypertensive Addiction substanties, Ethanol, Nicotine, New smart drugs, Heavy metals. Vegetal substances, Cannabinoids, Oxygen and Co2, Toxic substances (as cyanide), insulin Food (involved in lepton metabolisms), carbohydrates level, metabolic toxic subst, MABS and many other drugs and substanties or phisiophatological conditions [5].
Howard D Weiss et al. [6]: Impulse control disorders and compulsive behaviors associated with dopaminergic therapies in Parkinson disease” and “Impulse control disorders (ICD) (most commonly pathologic gambling, hypersexuality, and uncontrollable spending) and compulsive behaviors can be triggered by dopaminergic therapies in Parkinson disease (PD) [6].
Swapnil Gupta et al. [7]: Drug dependence is a major cause of morbidity and loss of productivity. Various theories ranging from economic to psychological have been invoked in an attempt to explain this condition. With the advent of research at the cellular and subcellular levels, perspectives on the etiology of drug dependence have also changed. Perhaps the greatest advance has been in the identification of specific receptors for each of the drugs, their target neurotransmitter systems and the intracellular changes produced by them. These receptors also provide potential targets for treatment strategies of drug dependence. This study attempts to present the mechanisms in the development of dependence and the newer treatment strategies for the major drugs of abuse like alcohol, opioids, cannabis, nicotine cocaine. Human addictions are chronically relapsing disorders characterized by compulsive drug use, inability to limit the intake of drugs, the emergence of a withdrawal syndrome during cessation of the drug use. Dependence has been defined as a cluster of behavioral, cognitive and physiological phenomena that develop after repeated substance use. It includes a strong desire to take the drug, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to drug use than to other activities and obligations, increased tolerance and sometimes a physical withdrawal state (International Classification of Diseases (ICD).
Drug addiction has been conceptualized as a complex and chronic disease process occurring in the brain, which is modulated by genetic, developmental and environmental factors. The most consistent and reproducible finding in drug addiction is that abused substances activate the mesolimbic dopamine system, which reinforces both pharmacological and natural rewards. The mesolimbic -system consists of dopaminergic neurons in the ventral tegmental area (VTA) and their axonal projections to terminal fields in the nucleus accumbens (NAc) and the prefrontal cortex. Opioids, alcohol, nicotine, cannabinoids and psychostimulants all act on this system to increase synaptic levels of dopamine (DA). All these substances have specific receptors in the brain and the increase in dopamine levels in the mesolimbic system is the final effect that they produce. Receptor-mediated activity is the principal mechanism by which any chemical messenger acts. Chemical messengers are regulatory macromolecules, usually proteins. Receptors have two major functions of recognition and transduction., each receptor has two domains, i.e., a ligand-binding and an effector domain. The ligand-binding domain has a hydrophilic and lipophilic region and is usually hetero-polymeric. The binding of the ligand causes a change in the quaternary structure of the receptor. Receptors have various effector mechanisms, which are broadly of four types:
a) G protein-coupled receptors (Gs, Gi, Gq and G13)
b) Receptors with intrinsic ion channels
c) Enzymatic receptors
d) Receptors regulating gene expression
One of the most dramatic advances in drug- abuse research has been the identification of the target of every major drug abuse substantia. This advance occurred with the advent of radioligandbinding techniques, the biochemical characterization of drug binding sites and ultimately, with the application of molecular biology to clone and isolate these structures. Drugs can upregulate or downregulate their receptors and their effector mechanisms. These changes are effected through genetic mechanisms and are implicated in the development of tolerance and withdrawal. Earlier biochemical data supported that the site of action of drugs was homogeneous. It is now known that there is great diversity in drug-receptor interactions. nicotine was thought to have a homogeneous class of binding sites in the brain. It is now known that there are many different oligomeric receptors that bind and are activated by nicotine. the diversity of the receptor types, the cross-modality of drug-receptor interactions are becoming more and more significant. It was earlier thought that drug use caused changes in the specific binding sites, inactivation mechanisms or levels of endogenous ligand. The diversity of drug receptors now forces a consideration of changes in the actual structure of the receptor molecule or changes in the distribution of these molecules on surface of the neuron. Drugs of abuse also have long-term effects resulting from the expression of genes activated as a consequence of the action of the drug.” [7].
Nestler Ej [8]: Regulation of gene expression is considered a plausible mechanism of drug addiction, given the stability of behavioral abnormalities that define an addicted state. Among many transcription factors known to influence the addiction process phenomena, one of the best characterized is DeltaFosB, which is induced in the brain’s reward regions by chronic exposure to virtually all drugs of abuse and mediates sensitized responses to drug exposure. Since DeltaFosB is a highly stable protein, it represents a mechanism by which drugs produce lasting changes in gene expression long after the cessation of drug use. Studies are underway to explore the detailed molecular mechanisms by which DeltaFosB regulates target genes and produces its behavioural effects. We are approaching this phenomenon using DNA expression arrays coupled with the analysis of chromatin remodeling--changes in the post-translational modifications of histones at drug-regulated gene promoters--to identify genes that are regulated by drugs of abuse via the induction of DeltaFosB and to gain insight into the detailed molecular mechanisms involved. Our research findings establish chromatin remodeling as an important regulatory mechanism underlying drug-induced behavioural plasticity, promise to reveal fundamentally new insight into how DeltaFosB contributes to addiction by regulating the expression of specific target genes in brain reward- pathways [8].
Kovács GL et al. [9]: Neuropeptides affect adaptive central nervous system CNS processes related to opiate ethanol and cocaine addiction. Oxytocin (OXT), a neurohypophyseal neuropeptide synthesized in the brain and released at the posterior pituitary, also is released in the central nervous system (CNS). OXT acts within the CNS and has been shown to inhibit the development of tolerance to morphine, and to attenuate various symptoms of morphine withdrawal in mice. In rats, IV self-administration of heroin was potently decreased by OXT treatment. In relation to cocaine abuse, OXT dose-dependently decreased cocaine-induced hyperlocomotion and stereotyped grooming behavior. Following a chronic cocaine treatment, the behavioral tolerance to the sniffinginducing effect of cocaine was markedly inhibited by OXT. Behavioral sensitization to cocaine, on the other hand, was facilitated by OXT. OXT receptors in the CNS--mainly those located in limbic and basal forebrain structures--are responsible for mediating various effects of OXT in the opiate- and cocaine-addicted organism. Dopaminergic DA neurotransmission-primarily in basal forebrain structures--is another important biochemical mediator of the central nervous system effects of OXT. Tolerance to ethanol ( hypothermia-inducing effect of ethanol) also was inhibited by the OXT [9].
Tammy Saah [10]: Addiction from an evolutionary perspective, we may understand its underlying significance and evaluate its three-fold nature: biology, psychology, and social influences. In this investigation research it is important to delve into the co-evolution of mammalian brains and ancient psychotropic plants. Gaining an understanding of the implications of ancient psychotropic substance use in altering mammalian brains will assist in assessing the causes - effects of addiction in a modern-day context. By exploring addiction in this manner, we may move towards more effective treatment early prevention, treating the root of the issue rather than the symptoms.
As we find ourselves in the beginning of a new millennium periods, we are faced with challenges to our survival as a human population. Some of the greatest threats to our survival are sweeping epidemics that affect millions of individuals worldwide. Drug addiction, although often regarded as a personality disorder, may also be seen as a worldwide epidemic with evolutionary genetic, physiological, and environmental influences controlling this behavior. the use of drugs has reached all-time highs. On average, drug popularity differs from nation to nation. The United Nations Office on Drugs and Crime identified major problem drugs on each continent by analyzing treatment demand. From the 1998 to 2002, Asia, Europe, and Australia showed major problems with the opiate addiction, South America predominantly was affected by cocaine addiction, Africans were treated most often for the addiction to cannabis.
Only in North America was drug addiction distributed relatively evenly between the use of opiates, cannabis, cocaine, amphetamines, and the other narcotics. all types of drugs are consumed throughout each continent.
Among the different approaches for diagnosis, prevention, treatment of drug addiction, exploring the evolutionary basis of addiction would provide us with better understanding since evolution, personality, behavior and drug abuse are tightly interlinked. It is our duty as scientists to explore the evolutionary basis and origins of drug addiction so as to uncover the underlying causes rather than continuing to solely focus on the physiological signs and global activity of this epidemic phenomena. Too often the treatment of addiction simply works to alleviate the symptoms of addiction, dealing with overcoming the physiological dependence and working through withdrawal symptoms as the body readjusts to a non-dependent state of homeostasis. we must not only concentrate on this aspect of addiction when considering the global treatments and preventative programs. We must take into consideration that it is not purely the physiology of addiction we are battling.
Drug addiction is thought of as an adjunctive behavior, or a subordinate behavior catalyzed by deeper, more significant psychological and biological stimuli. It is not just a pharmacological reaction to a chemical but a mode of compensation for a decrease in Darwinian fitness. There are three main components involved in substance addiction: developmental attachment, pharmacological mechanism, and social phylogeny including social inequality, dominance, and social dependence. Developmental attachment created by environmental influences, such as parental care or lack thereof, may influence children’s vulnerability to drug addiction. Evolutionarily speaking, children that receive care that is more erratic may focus more so on short-term risks that may have proved to be an adaptive quality for survival in ancient environments. Compounding that attachment, the pharmacological mechanism describes the concept of biological adaptation of the mesolimbic dopamine system to endogenous substance intake.
These factors combined with the influence of social phylogeny create a position for predisposition to drug addiction. They attribute to the common belief that many substances of abuse have great powers to heal and is often the driving motivation for overuse and addiction. Evolutionary perspective shows an intermediate and fleeting expected gain associated with drug addiction correlated with the conservation in most mammals of archaic neural circuitry, most often being a falsified sense of increased fitness and viability related to the three components of drug abuse. The chemical changes associated with fitness and viability are perceived by mammals as emotions, driving human behavior. Human behavior is mediated primarily by dopaminergic and serotonergic systems, both of ancient origins probably evolving before the phylogenetic splits of vertebrates and invertebrates. 5-HT (serotonin), stimulated by a small range of drugs, mediates arousal. It is believed to be inhibited by hallucinogens and also helps control wanting for ethanol and cocaine consumption.
The cortico-mesolimbic dopaminergic system, on the other hand, is believed to be the target of a wide range of drugs, including marijuana and cocaine, increasing the transmission of dopamine to the nucleus accumbens. This system mediates emotion and controls reinforcement, and is the primary pathway acted on by antipsychotic drugs such as chlorprothixene and thioridazine. Problematic use of drugs develops into addiction as the brain becomes dependent on the chemical neural homeostatic circuitry altered by the drug. No matter the theory of drug addiction, there remains one constant: withdrawal is inevitable. As a drug is administered continuously and an individual becomes addicted, the brain becomes dependent on the presence of the drug. With an absence of the drug, withdrawal symptoms are experienced as the brain attempts to deal with the chemical changes. There are believed to be evolutionary origins of drug addiction, which will be discussed further, as well as a link between physiological addiction and the evolution of emotion [10].
Zimmerberg B et al. [11]: Some of the behavioral deficits caused by prenatal or postnatal alcohol exposure have been demonstrated to be ameliorated by environmental manipulations such as handling or environmental enrichment. This experiment, in contrast, investigated whether behavioral deficits due to prenatal alcohol exposure could be exacerbated by a stressful experience, early weaning. Pregnant dams were given either a liquid diet with 35% of the calories derived from alcohol, a liquid diet without alcohol to control for any effects of the liquid diet administration, or ad libitum food and water. Half of each litter were weaned at 15 days of age (early weaning) and half were weaned at 21 days of age (normally weaned). Offspring were weighed, tested for activity in an open field at 18 days of age, and trained to find a hidden platform in the Morris water maze at 22-24 days of age. Alcohol-exposed subjects who were weaned early were more impaired in spatial navigation ability than any other group. the combination of early weaning and prenatal alcohol exposure caused the slowest growth. All subjects exposed to alcohol, regardless of weaning condition, had greater latencies to find the platform than those from the two control groups. There was no synergistic effect of alcohol and stress on activity levels, but all early-weaned females were more active than normally weaned females; males did not show this effect. Thus, environmental stressors such as early weaning can compound detrimental symptoms of prenatal alcohol exposure. These results have implications for the understanding of the effects of the environment on neuronal plasticity [11].
Tim Clutton Brock [12]: Traditional interpretations of the evolution of animal societies have suggested that their structure is a consequence of attempts by individuals to maximize their inclusive fitness within constraints imposed by their social and physical environments. In contrast, some recent re-interpretations have argued that many aspects of social organization should be interpreted as group-level adaptations maintained by selection operating between groups or populations. I review our current understanding of the evolution of mammalian societies, focusing, in particular on the evolution of reproductive strategies in societies where one dominant female monopolizes reproduction in each group and her offspring are reared by other group members. studies of the life histories of females in these species show that dispersing females often have little chance of establishing new breeding groups and so are likely to maximize their inclusive fitness by helping related dominants to rear their offspring. As in eusocial insects, increasing group size can lead to a progressive divergence in the selection pressures operating on breeders and helpers and to increasing specialization in their behaviour and life histories. there is little need to invoke group-level adaptations in order to account for the behaviour of individuals or the structure of mammalian groups [12].

Neural Pathways in Drug Addiction

Dopamine DA is considered the primary neural pathway underlying the neural causations of excitement, curiosity, and exploration. Several studies in the past have challenged a unitary role of the pathway in “pleasure.” The common neural pathways surrounding mesolimbic dopaminergic neurons are commonly thought to mediate subjective reward and maintain reinforcement processes via hedonic affect. Dopamine alters behavior via incentive salience in which motivational components are applied to stimuli that have shown to be rewarding in the past. Mesolimbic and neostriatal dopamine systems exhibit residual reward capacity even after depletion of dopamine, which demonstrates a value in learning that is independent of hedonia and strict reward-based learning. The concept of “wanting” has been defined from the idea of reward-related stimuli conferring a motivational value to an organism, which is distinct from hedonia. The “wanting” mechanism may be modulated by dopamine systems via perceived attractiveness, rather than the traditional view of receiving pleasure, or “liking” a stimulus.
The distinction between “wanting” and “liking” is important as it appears that drug-mediated dopamine responses progress by “wanting” something more but “liking” it less; Drugs can be associated with certain contextual cues, such as a novel environment. In example, when an organism is conditioned to receive a psychoactive drug paired with a sensory cue, associated neural functions are activated in response to the environmental cue. In the absence of the drug itself, the effect goes so far to reactivate and sustain drug seeking behavior.
The dopaminergic pathways are responsible for feelings of desire and reward in humans through their influence on the ventral tegmental region, medial forebrain bundle and the nucleus accumbens, and can modulate compulsive behavior characteristic of drug addiction in several mammalian models. Dopamine is also implicated in a more direct learning process, in which mesolimbic dopamine neurons fire unconditionally in affiliation with natural rewards often associated with survival. this dopaminergic activity will shift from firing in response to the reward itself to firing in response to the cue that is predictive of the novel reward Although reward can be grouped into a few separate processes; an object’s incentive value, the connective learning process of predictive cues and the object of attraction including the object’s ability to produce hedonism are distinct in their own way and they each relate to a dopaminergic response that reinforces reward; It is seemingly paradoxical, that humans and animals are susceptible to addictive effects of cocaine, a neurotoxic chemical that has been shown to be evolutionarily adapted to protect the coca plant from insect herbivory by interfering with motor control in the organisms that consume coca plant. The dopaminergic system should be affected by cues that provide reward, not a plant neurotoxin that is designed to thwart predation. Many theories have been proposed that attempt to provide an evolutionary explanation for this phenomenon, ranging from co-evolution of herbivores and plants, to simple fundamental differences in response to the chemical by mammals compared to arthropods.
The introduction of invertebrate model in evolutionarily relevant studies of drug-induced reinforcement, compulsion, withdrawal, reinstatement, and addiction has greatly broadened this field of research. These systems have shown to be powerful tools in the understanding of the neuroanatomical and behavioral processes underlying the addictive process. Benefits of invertebrates, aside from being more cost effective, offering reduced moral concerns, and behaviors patterned by experimentally accessible neural structures, are shared homologies with mammals in the key neurochemical aspects of reward, including receptor elements, neuropharmacology, mechanisms of action, deactivation, and association with similar behavioral contexts. Monoamine systems developed during the transition to metazoan life, where they were used to adapt functions of individual cells to disturbances within their environment. dopamine and serotonin receptors predate the chordate lineage, and divergence has given rise to considerable diversity in specific subtypes within different lineages, along with some unique differences in receptor subunits and pharmacological properties in both vertebrates and invertebrates.
As a result of the divergence during evolution, mammals utilize oxidation and methylation while flies use N-acetylation and β-alanylation for dopamine (DA) metabolism. Indeed, flies lack the genes required to synthesize norepinephrine and epinephrine, and these are two major catecholamines derived from DA that function in neuromodulation signaling in mammals. A cloned dopamine receptor from D. melanogaster has similar structural - functional properties with vertebrate D1-type receptors, but the pharmacological properties are very different. The characterization of the sensitivity of D. melanogaster to cocaine in an in-situ hybridization study demonstrates that dopamine transporter (dDAT) lacks all the structural components that are found in the mammalian catecholamine transporters. Cocaine displayed a lower affinity for dDAT when compared with serotonin transporter. This study provides evidence that the structural and pharmacological profiles of dDAT is different from the DAT of vertebrate species. it indicates that injected cocaine, methamphetamine or morphine agonists or antagonists may function differently in vertebrate and invertebrate models of addiction. Despite the differences that exist between vertebrates and invertebrates, crayfish, D. melanonogaster and the other invertebrate model systems will continue to provide new insights into the regulatory mechanisms of DA signaling drug addiction research.

Results

Mammalians and their related instinct - behavior is a clear and an real evolutionary advantages. Various neurological systems are involved (circuits and neurotransmitters or hormone like dopamine, oxytocin, prolactin and also other related neuronal pathways). The rewards liking circuits, compulsive behavior, craving, wanting and some other neuronal circuits are deeply involved in addictions reported in biomedical literature.

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2019.08.21 05:04 Clara_mtg Public Policy expert finds that rich people are more likely to live in expensive neighborhoods, blames Foreigners

Before I start this R1 I just want to note that someone else wrote a critique here. Unfortunately that critique is a bit crap and rather misses the forest for the trees. Data critiques are rather pointless in the face of fundamental methodological and statistical failures. Also I hate anthing that ever criticizes something as a fallacy. It drives me absolutely nuts.
I had intended for this R1 to be longer but I gave up trying to find data to actually analyze the situation. If anyone knows of/has data and wants to let me have at it I’d love to. I’m trying to get some stats projects in my portfolio and the more of them that are relevant to people other than nerds the better.
This is version two of this R1. My first versions was much much less tactful and probably not appropriate for this sub. Unfortunately much of structure has been lost so I apologize for the incredibly poor organization. I'm not very good at putting thoughts together in an organized manner even during the best of times.
The thrust of this paper is that the weirdness in the relationship between prices and income in Vancouver is due to the amount of foreign ownership. In particular underreporting of income that leads to higher price to income ratios.
The housing market is an incredibly complicated market. It exhibits almost every difficulty you could come up with: Spatial autocorrelation, normal autocorrelation, really complicated causal relationships, lots of causal interplay among various factors, clustering effects and probably lots more I didn’t think of.
Attempting to analyze the housing market with single point in time estimates is a fool’s errand. Doubly so if you don’t understand basic economics. Tripely so if you don’t understand how regressions work.
Let’s get the really obvious critique out of the way. Regressions with n=6, 14 or 23 don’t count especially when said data points are not independent of each other.

It is important, then, to step back and grasp which factors could not account for this pattern, or are very unlikely to do so. Consider a few factors that have been offered up in the housing debate to account for Vancouver’s affordability woes: development charges and other “supply constraints”, lax mortgage lending, and low interest rates. None of these causal factors could plausibly explain the divergence in ratios between municipalities.

Let’s take a look at the author’s justification for this:

If lax mortgage lending or interest rate differences were driving the divergence, then we would expect that mortgage lending policy and interest rates varied sharply across municipalities. But the idea that Burnaby has a different mortgage lending regime than Surrey, say, or has much lower interest rates, is implausible and not supported by any available evidence.

Why should we expect variances in mortgage lending practices be uniform across the income distribution? It seems a pretty reasonable assumption to me that a banks willingness to lend to someone depends on their income and the distribution of incomes across municipalities is not constant.

The idea that development charges or restrictions (e.g., permit times) could account for the pattern is similarly implausible. Development charges do not typically apply to building (or rebuilding) a detached house, which is the most that could be at play given that almost none of the municipalities can build any net new detached houses (due to the Agricultural Land Reserve). Thus it’s hard to see how development charges could have a substantial effect on detached house prices.

Housing prices do not exist in a vacuum. Condos, apartments and other types of housing are substitute goods and their prices can (and do) affect the prices of single detached homes.

Differing permit times are also unlikely to have any substantial effect: buyers are not going to pay massively more if the permit time for a new build is 6 months instead of 3. In fact, it is unlikely to be a significant factor at all.

sigh Those extra three months to get a permit cost money. If it costs more to build a house then the price of said house will likely increase. In addition the distribution of permit times is right skewed with things like apartment complexes taking longer to get approved which affects a larger amount of housing than a permit for a single family unit or condo.

What might account for the divergence then? If substantial amounts of foreign money were used to purchase housing, then that might generate such a pattern, since the declared Canadian incomes of this international elite might have little relationship to buyers’ purchasing power.

It is worth remembering that wealth has a large effect on people’s ability to purchase housing. This doesn’t really undermine the author’s point though.

The relationship between foreign ownership and de-coupling is depicted in Figure 3 for 2016. The correlation is 0.96. (1 is a perfect correlation, 0 is the absence of any correlation.)

There is nothing wrong with this I just want to put it out here so y’all can get a sense of the kind of paper we’re working with.

This is a remarkably strong relationship: the vast majority of the variation in price to income ratios can be accounted for by foreign ownership.

If you have an R² = .93 when analyzing a population that we know to have pretty significant variation this should raise red flags. If one factor explains this much you're probably regressing left shoe on right shoe. Which is almost assuredly what is happening here. P/I ratio depends a lot on the types of housing. Foreign owners buy more expensive housing on average which tends to be concentrated in specific areas. This concentration raises the prices of single family detached homes without an increase in the median income of the same magnitude for two reasons. First because the relationship between housing prices and income is not linear and second because single family detached homes and other types of housing are imperfect substitutes so changes in one will not induce the same change in the other.

A common rejoinder is that “correlation is not causation”, but that is unlikely to be a valid critique here

No. No no no. 2SLS exists for a reason. Determining causation is very difficult especially in a market as complicated as a housing market. Attempting to do so with a point in time sample is insane. There could be all kinds of unidentified cofounders, reality is complicated and we’re not omniscient.

We have a good causal theory for the relationship to exist, and there does not seem to be any other plausible contending factors that might account for the pattern, as noted above.

Ignoring the fact this is false, saying that there are no other plausible confounding factors does not make it true. It certainly would make statistics dramatically easier if we could just think of all of the possible causal links and control for them. Especially if we just prax away all endogeneity.

the face of all this evidence, a skeptic might reply: “Well sure, you’ve found the relationship in Vancouver, but it might be spurious – maybe there’s something else driving that relationship.”

And here we come so close to enlightenment. But no such luck.

As explained above, this is highly unlikely, given the strength of the relationship and the absence of any plausible alternative factors.
The relationship is somewhat weaker (r = 0.76) than in Vancouver, likely due to the weaker relative influence of foreign ownership in Toronto, but the connection remains strong and unmistakable.

This doesn’t make any sense. Less foreign influence should result in different data. I don’t see why it should result in a different slope or a worse correlation. Why should we expect foreign ownership to effect Toronto differently than Vancouver? As far as I can tell they have similar laws.

The City of Toronto is also an outlier.14 If the City of Toronto is removed from the scatterplot, the correlation increases to r = 0.88.

No.
NO NO NO NO
Dropping 👏 Outliers 👏 without 👏 good 👏 reason 👏 is 👏 not 👏 acceptable.
It makes my regression worse is not a good reason. It is pure hackery.
You should never drop an outlier without discussion. This doesn’t mean it’s never appropriate to perform an analysis after having dropped an outlier but reality isn’t pretty and outliers do exist.

This may reflect amalgamation, which has the effect of pooling many lower income renters (who typically live in apartments) with higher income detached homeowners, thus boosting the price to income ratio.

Why is this the only point in the paper when the author considers the distribution of types of housing in the sample districts? The types of housing people live in is obviously not constant across municipalities and clearly affects the prices of housing yet it is completely ignored in the rest of the paper.

We should be thankful for his [Richard Wonzy] candor and insight, we need more of that today.

Oof. I certainly agree that we need more insight although not exactly in the manner that the author means.
There are quite a few issues with this paper that I didn’t address primarily data issues but I found it very difficult to write a good criticism of a statistical analysis that is so poor as to be incoherent. The assuredly are many issues I did not cover but the statistical rigor on display is so poor that I cannot tell exactly what is meant, how the data is gathered or even what the data is. To be entirely honest I’m not entirely clear on what this paper is saying. It seems to cycle through a number of different ideas around foreign ownership and housing prices but never quite settles on one thought.
As with many things, this paper would benefit significantly from being precise in the question it is trying to answer. Too often questions may sound similar but in actuality be very different and a failure to be precise enough in your questions can easily lead to poor statistical analysis.
I apologize that the above R1 is a bit disjointed and poorly organized. I wanted to just do the analysis correctly but I was unable to find adequate data.
I would like to finish this off by discussing some actual results on this issue by people that know what they’re on about.
Suher 2016.pdf) finds that non resident owners have a significant impact on housing prices but with very little spillover. This is very important because the study presumes significant spillover effects from foreign buyers. Without significant spillover we should expect the price changes to be localized to locations that are desirable to non residential owners. These are high price areas and as such will not change the median home price. Thus any analysis that is conducted about the effects of non residential ownership needs to be conducted at a lower level than the municipal level because heterogeneity in housing will make municipal level data rather useless.
As a partial counterpoint to the above Fisher Füss and Stehle find spillover effects from regular housing transactions on the neighborhood level although these effects are diminished in booming housing markets like the one that Vancouver is currently experiencing. Again this shows the importance of being careful when analysing the situation because heterogeneity in housing will destroy your data if you don’t look closely.
This report talks about the difficulties of talking about housing affordability. In particular “Caution, however, should be used in using this measure assess affordability challenges among different income levels or household types as variations in the cost of other necessities would suggest the need for corresponding variations in the payment standard used” is important. We see a pattern emerging. Housing is rather heterogeneous and clumping different types of housing together can often lead to misleading or nonsensical results.
This AEI presentation covers limitations of the price to income metric of affordability and presents an alternative metric that takes into account other affordability constraints on housing beyond the literal cost of housing.
This paper by Dragana Cvijanovic and Christophe Spaenjers is an excellent example of how to go about answering questions like those posed in the report. It finds results more or less in line with what you’d expect. Foreign non resident owners cause price increases in attractive (luxury) areas.
When I first read this paper I dismissed as a combination of incompetence and hackery but going back through this and learning more about the context of this discussion this paper makes me mad. Not just because it's crap, if I got mad at every crap paper I wouldn't have enough time to sleep. It makes me mad because of how it legitimizes many xenophobic viewpoints. It sticks everything on foreigners. It ignores all other posibilities prefering instead to focuse on the evil other. Xenophobic writing like this is a more insideous kind of xenophobia. The blatently xenophobic is easy to dismiss. But stuff like this, hiding behind a veil of science, is much harder to dismiss. How do you explain to a lay audience the complications of statistics? This particular paper is bad enough that you probably could explain it but stuff like this happens all the time and often in much more sophisticated ways.
I would like to talk about outliers for a second. This isn't really relevant to the R1 but they came up a bit and I want to clear some stuff up.
An outlier that happens because of sampling error, measurement error, etc is not an outlier. These are just not valid data points and no analysis should be performed with those data points.
In general outliers should not be ignored. Their existence does matter. Often it suggests that there is something that you did not consider in your model. Sometimes outliers can cause significance where none would otherwise exist. Others may not cause or remove significance but change it. There is no magical formula for what to do about outliers. It depends on the context of your analysis. Sometimes it is appropriate to drop them for a variety of reasons but this should not be done without reason.
If you don’t want to read this incredibly poorly organized mess here’s a TL;DR:
2SLS exists for a reason and no matter how hard you prax you can’t prax an entire ~~flowchart~~ DAG out of thin air.

submitted by Clara_mtg to badeconomics [link] [comments]

2013.10.06 16:56 tabledresser [Table] IAmA: I am Douglas T. Kenrick, evolutionary psychologist, TEDx presenter, and author of “The Rational Animal” and “Sex, Murder, and the Meaning of Life” AMA!

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Date: 2013-10-05
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Questions	Answers
I've heard that evolutionary psychology is just a bunch of "just so stories" how do you know that the things that you talk about in your book are actually evolutionarily derived? What's an example of a senseless decision that is evolutionarily evolved?	Good question. The term "just-so stories" was used by Stephen Jay Gould to suggest that evolutionary ideas about behavior were simply untestable ruminations, like many myths about the origin of the universe. It is true that is easy to spin a yarn about the possible adaptive significance of any behavior (or any physical trait, such as a giraffe's long neck). In fact, all scientists, whether evolutionary theorists or otherwise, begin scientific investigation by spinning a plausible account. What distinguishes science from mythmaking is that scientists go out and test their account with empirical data, and preferably compare their account to an alternative. For example, my colleague Rich Keefe and I hypothesized that the attraction of older men to relatively younger women was not linked to the "norms of American society" as previously argued by social scientists, but instead to the fact that women were relatively fertile in their teens and twenties. If that were true, then the pattern should be universal, not limited to American society. We found across many societies that it is. Second, one should find that very young men (early teens) should be attracted to slightly older women (since younger girls are less fertile). This was also the case. I'll answer the question about a senseless decision in a separate line.
What about cougars? I know that typically we think about women being attracted to older men with lots of money but what about the women who are past their reproductive years that go after young men?	Kenrick, D.T., Nieuweboer, S., & Buunk, A.P. (2010). Universal mechanisms and cultural diversity: Replacing the blank slate with a coloring book. Pp. 257-271 in M. Schaller, A. Norenzayan, S. Heine, T. Yamagishi, & T. Kameda (eds.) Evolution, culture, and the human mind. New York: Psychology Press.
What do you think about the way humans see reproduction in the animal kindgom as largely 'rape-like' or non-consensual?	I love UBC, and visit there every summer.
How can we understand the natural process of mating without the human centric perspective?	In response to 1, I don't agree that most of us see animal reproduction as non-consensual. But even if some people do, they have it wrong, biologists point out that "female choice" is a more powerful influence on mating than is male choice. The reason for this is that females have more to lose from a bad mating decision (in humans and other mammals, they carry the young and nurse them afterwards). This leads to a general tendency for males to compete to be chosen.
What do you think about the resurgence of mind-altering substances in the context of legitimate basic and applied research?	Kenrick, D.T., & Gomez-Jacinto, L. (2013). Economics, sex, and the emergence of society: A dynamic life history model of cultural variation. 78-115 in M. Gelfand, C.Y. Chiu, and Y.Y. Hong (Eds.) Advances in Culture and Psychology, Volume 3, New York: Oxford University Press
Why do you think these substances do what they do to the human experience in an evolutionary context?	Nesse, R. M., & Berridge, K. C. (1997). Psychoactive drug use in evolutionary perspective. Science, 278(5335), 63-66.
Did humans at some point in their evolution develop sensitivity to these chemicals, was it merely an incredible coincidence, or convergent/divergent evolution (endogenous NTs just aren't chemically unique and it's actually not unlikely that other organic molecules are similar enough to be psychoactive) that lead us to have an intense neurological response to such substances?	Keep trying to volunteer in a lab. There are a number of great cognitive and social cognitive psychologists at UBC. You don't need specifically to work on a particular kind of research at this point, any experience will get you a letter of recommendation for grad school.
What is your advice for an undergrad getting involved in research and starting a career in biopsych academia?	For movies, I liked An Education, also classics: Metropolitan, Dersu Ursala, and Sheltering Sky.
Do you have any advice on places I should be looking into for grad school/supervising profs?	Music, I love most of Ry Cooder's collaborations, esp. the one with Ali Farka Toure "Talking Timbuktu"
Edit: Bonus question - What's your preferred genre of entertainment?	Books, John Alcock's Triumph of Sociobiology, and of course "The Rational Animal" by Kenrick and Griskevicius!
Any suggestions for books, tv, music, etc.?	Link to www.amazon.com
Why do women so often wear makeup?	Why do men value physical attractiveness? Other research suggests that is due to the fact that attractiveness is linked to health and fertility cues. Because male humans invest heavily in the offspring, they are more selective than males in other species where males invest nothing beyond sperm. Nevertheless, male selectivity is different from female selectivity - focusing not on resources and status, but on cues that suggest that this individual will be able to bear children. Women focus on resources because our female ancestors who chose males who could help provide for the care and feeding of the offspring did better than those who did not.
Are lifted trucks a type of peacocks tail?	On lifted trucks and peacock's tails: My colleagues and I have conducted some research on male conspicuous displays and their relationship to mating. I describe this work at length in my new book "The Rational Animal"
Are all men wired to pursue multiple mates?	Are all men wired to pursue multiple mates? Most evolutionary theorists are interactionists, and presume that a person's mating strategy is a function of environmental inputs -- which ancestrally would have triggered alternative investment strategies. Because human females are selective, and one selection criterion is faithfulness, men who were inclined to be faithful would do well. Of course, there is a trade-off for the male, who would in theory do well with multiple mates (males can in theory have hundreds of offspring, and some have), but only if he can still attract females, and if attempts to attract other females will not lose him his only shot at a partner. Hence, males who get feedback that many women find them attractive, perhaps because they have "good genes" (i.e., look healthy and robust) or have plenty of resources (e.g. the maharajah) may be inclined to play an alternative strategy. But for many men, that is not an option, and their developmental experiences, as well as continuing lack of opportunities from interested females, will incline them not to waste resources trying to pursue multiple mates.
Has politics (e.g. feminism) impacted your research in any way? If so, how? Or alternatively, how's the relationship between feminism an EP research like?	It depends on how you define "feminism." Many of the leading figures in the study of human behavior in evolutionary perspective are women: Leda Cosmides, Margo Wilson, Jane Lancaster, and Sarah Hrdy, for example, as well as a strong younger generation, including Martie Haselton, Deb Lieberman, Sarah Hill, Kristina Durante, and recent students from lab such as Jill Sundie, Jessica Li, and Becca Neel.
	And probably the emphasis on "female choice" came out of thinking about human behavior through the eyes of women, such as Barb Smuts.
	Old school gender feminists, who have a political commitment that differences between men and women MUST only be explained as products of a male dominated social conspiracy, have had a hard time with data emerging from numerous cultures and studies comparing species, that suggest this pure constructivist view cannot be correct. This politics-first, science-second perspective has more sway in other departments, is decreasing in influence in psychology, where empirical data gets a lot of emphasis (even though most psychologists, including evolutionary psychologists, are liberal in their politics, we are able to separate dogma from science, and try not to be climate-change deniers)
Would you rather fight 100 duck sized horses or 1 horse sized duck?	Ancestral logic would suggest that I should try my luck with the 100 duck sized horses, because the horse-sized duck could down me in one bite!
	Oh, Von Hippel has research on teenage skateboarders that suggests if I were a young male, and there was an attractive female around, I might instead choose to take on that giant carnivorous duck!
Finally, I just wanted to say thanks for doing this AMA! I'm a grad student in the field, and it's nice to see someone engaging with reddit.	Kenrick, D.T. (2013). Men and women are only as different as they look! Psychological Inquiry, 24, 202–206.
I read you have two sons. Which one is your favorite? You can justify it with a evolutionary reason if you like.	From an evolutionary perspective, the 35 year old has already passed on my genes, but the 9 year old has more of those cute little kitten-like support-triggering mechanisms. And they both share 50% of my genes!
Where are the best places to study things like evolutionary psychology?	Traditionally, students interested in evolutionary psychology have applied to UCSB to work with Tooby, Cosmides, Roney, and other great people in biology and anthropology, to University of Texas to work with David Buss, to University of New Mexico to work with Steve Gangestad and Geoffrey Miller, now to Harvard to work with Pinker, Sidanius, and others. ASU has me, Steve Neuberg, Adam Cohen, Lani Shiota, and great people in anthropology and biology. UBC to work with Mark Schaller, Joe Henrich, and Jess Tracy is another great option. But there are lots of former students of these programs now running great places: Vlad Griskevicius and Jeff Simpson at University of Minnesota, Jon Maner at Florida State, Josh Ackerman is at MIT business, Jessica Li at University of Kansas, Becca Neel at Iowa, Jill Sundie and Kristina Durante at UTSA, Deb Lieberman and Mike McCullough at Miami, Martie Haselton and Kerri Johnson at UCLA, and lots of other good options these days. I know I missed some, but needed to stop some time, please add comments, or ask follow-ups if you know folks I missed (like Rob Kurzban at Penn!)
To your mind, what is the most fascinating experiment you've ever run?	Link to www.youtube.com
Can you tell me more about those homicidal fantasies? What are some of yours?	Asexuality: There are distributions on every trait, including sex drive. Some of the variations may be linked to life experiences, to phase in life history, or other cues that can alter developmental trajectories. Homicidal fantasies. I did indeed begin studying homicidal fantasies because I had an argument with a colleague who suggested that it was bizarre to have a homicidal fantasy when I mentioned that I figured they were normal. So we asked a large sample of students, and I was not surprised to find that the majority of males had had at least one fantasy. I WAS surprised to find that almost as high a percentage of females also had at least one. The females fantasies were less detailed, shorter, and less violent, also less recent. Which may explain why males commit 90 percent of homicides in virtually every society ever studied throughout history.
Your field sounds really interesting since it covers so many things!	And thanks. The field, like real life, is interesting enough to keep a researcher fascinated for a lifetime!
Humor me with a scifi type question. How do you see humans evolving over the next few hundred (thousand/million) years? (Behaviorally.) I know it's speculation, just want to hear it coming from someone with some evolutionary insight.	I did an essay for Edge called "Is Idiocracy Looming" in which I speculated that because traditional religions encourage reproduction, and there is a (slight) negative correlation between religiosity and intelligence, that the future could look like it does in the movie Idiocracy (rather silly, but with a fun premise, that less intelligent will increasingly outnumber intellectuals in the future, to the point where everyone is rather intellectually challenged). That said, the Flynn Effect seems to suggest a trend in the opposite direction: of increasing IQ.
Basically, are any movies that take place in the future right about human behavior in your opinion? What did they miss?	Link to www.edge.org
What is your view on the Simmons, Nelson, Simonsohn 2011 paper -link- that suggests researchers are being too flexible in their data analysis, which can lead to a high rate of false positive findings? Have any of your data analysis methods changed since the recent controversy surrounding "p-hacking"?	Most of my published papers have several internal replications, which makes for a lot of revision, and a long time coming for most papers, but leaves me less worried about false positives in our stuff. My coauthor and occasional journal editor Steve Neuberg is more concerned about lots of interesting findings that do not get published because of the phobia of false positives, and a lack of concern about false negatives.
Can you offer any insight into the debate about group selection that's been going on lately?	To be honest, I find the issue like a Necker cube (one of those images that flips around from front to back as you look at it). There was a meeting of much greater minds than mine here at ASU in which Bert Holldoebler (who cowrote the Ants and Superorganism with E.O. Wilson) and Kim Hill (who did the classic anthropological study of the Ache) talked about why most evolutionary biologists don't love the idea. It is not that animals (like humans) are not selected for traits that promote group cooperation, it is just that those traits also typically serve the individual (if you don't cooperate, you will be excluded, and that's not good for your individual genes). There is some support for what is called "multi-level selection" - in the same way that the genes in your body need to operate in a way that keeps the body running, rather than crippling it by "self" interest, likewise, organisms must act in ways that keep them in a group, and groups that have more cooperaters will do better than those that do not overall. But again, I'm not an expert on this topic at all.
Hey Doc,	Nesse, R. M. (1994). Fear and fitness: An evolutionary analysis of anxiety disorders. Ethology and Sociobiology, 15(5), 247-261.
How do reconcile many of the more ludicrous ideas that have gotten traction in EP, for example the Lamarckian idea that people have evolved specific fears of spiders?	Öhman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: toward an evolved module of fear and fear learning. Psychological review, 108(3), 483.
Doug,	Kenrick, D.T., & Keefe, R.C. (1992). Age preferences in mates reflect sex differences in mating strategies. Behavioral & Brain Sciences, 15, 75- 91.
Which of your own studies are you most proud of and why?	At the time we published this, social psychologists tended to explain behaviors in terms of socialization. Several researchers had reported a 2 or 3 year spread in what men and women say they want in mates, and those researchers reliably said it was linked to something about American culture, with norms specifying that men should be older than their mates. But we found that, as you moved further from American society, the age differences got larger. This was impossible to explain in terms of norms of American society. As I mentioned in response to another question, we also published a paper in Developmental Psychology that showed that teenage boys (who are especially tuned in to "macho" norms) are NOT interested in younger females, but in older women, despite a full awareness that they had no shot at those older women. Again, suggested something other than social norms at work.
I'm afraid I am unfamiliar with your work personally, but I am fascinated by the field. I was just wondering where we are as far as a moleculaepigenetic level understanding of this subject. Where is the crossover that links the social behaviors to the hard-wiring?	That's the next frontier. There is an emerging field of social neuroscience that looks at the underlying mechanisms, and increasing interest in connecting genes, hormones, and psychological mechanisms. I just saw a chapter by Joan Chiao and colleagues in Advances in Culture and Psychology that is worth checking out ("Cultural neuroscience") Also, a lot of research looks at links with hormones such as testosterone, see Jim Roney's work, as well as studies by Jon Maner, Martie Haselton, Steve Gangestad, Dario Mastripieri, and others here.
Do you have several favorite intellectual mentors from a particular period in time, or do you draw your inspiration mainly from your own research? Also, what topic would you like to pursue for a future TED presentation? Love your work!	My main mentor in grad school was Robert Cialdini.
	I was turned on to evolutionary psychology by reading a book called Primate Behavior and the Emergence of Human Culture. A young faculty member named Ed Sadalla was at the same time reading Wilson's Sociobiology, and he had an idea for what became my first paper on this topic (Sadalla, Kenrick, & Vershure, 1987). Another young faculty member at ASU named Julian Edney was also beginning to think along these lines, but he left the field.
	After leaving grad school, I was influenced by reading David Barash's Sociobiology and Behavior, and Martin Daly & Margo Wilson's Sex, Evolution, and Behavior.
	And John Alcock's "Animal Behavior: An evolutionary perspective" was also an important influence on my thinking.
	And my colleague Rich Keefe has had a great influence on my thinking.
How has your selfishness made who you are right now, at this very second?	I actually argue in both "Sex, Murder, and the Meaning of Life" and in the "Rational Animal" that people are not really designed to be selfish (you need to distinguish between selfish genes and selfish organisms, the latter does not follow from the former). A lot of my time throughout later adulthood has been consumed with concern about my children. Again, that is selfish from the gene's perspective, but not from the organism's [or the psychological self's] perspective.
	Link to www.douglaskenrick.com
	Link to rationalanimalbook.com
Do you think a time will come when the majority of people do not believe in a god?	That is an interesting question. I am right now reading Ara Norenzayan's new book "Big Gods" he argues that over time, gods have gotten more powerful and religions have gotten larger. Hunter gatherer and horticulturalists had much less intrusive and all-powerful gods. Norenzayan argues that it was cultural co-evolution: as we moved into multi-tribal societies, those who also had big overseeing gods were able to control the cooperative behaviors of people who were not linked by genes or reciprocal relationships. On that view, the future would involve more religious. However, Norenzayan also points to societies like Sweden, where religion plays little role now, but did in the past. He believes that modern large states with police forces and centralized governments play the same role as overseeing gods (I may be distorting parts of his case). But he uses a metaphor of using religion to climb up to modern large states, and then kicking it away. We will see.
Suppose that i am tempted to cheat on my girlfriend, and i justify it to myself by taking an evolutionary perspective on the issue, would you say that that is (a) rational and laudable, (b) fooling myself, or (c) something else?	A lot of misconceptions about evolutionary psychology are linked to what is called the "naturalistic fallacy" - or the mistaken conclusion that because something is "natural" it is therefore "good." It is easy to see the problems with such an equation if you look at male homicide. Men commit most of the homicides - in American society, and in all other societies throughout history (Daly & Wilson have an excellent 1988 book titled "Homicide" that is well worth a read). From the perspective of evolutionary biology, this is likely linked to two broad principles - differential parental investment and sexual selection. In any species in which one sex contributes more to the offspring (usually, but not always, the female), that sex will be more careful about mating decisions. The other less-investing sex will need to compete amongst themselves to be chosen. Hence, competition and aggression throughout the animal kingdom is typically higher among males (there are exceptions, but they tend to prove the rule, occurring in species where the males make very high parental investment, such as phalaropes). Hence, the high levels of human male intrasexual competition (and consequent higher homicide rates) can be seen as "natural." But that doesn't make them laudable, and at a societal level, we would like to do whatever we can to remove the triggers to male violence (for example, Martin Daly has good evidence that fairer economic distributions are associated with lower homicide rates). Likewise for infidelity; males have less to lose by infidelity, and numerous studies show that they are more inclined to be unfaithful. But does this make it justifiable? Not at all. Other people also have a "natural" moral reaction to infidelity - your girlfriend, for example, and it may lead her to leave you. Or her kin, who may want to punish you in some way. Or your neighbors, who often take steps to reduce infidelity, because it can disrupt the stability of monogamous families. Furthermore, it carries other costs at a personal level, such as the danger that a man with children will fall in love with the woman with whom he has an affair, and be led to reduce his investment in any children he has. So, anything but "rational and laudable," I am afraid.
What is your take on Ted curbing their talks to avoid issues such as GMO's and healthy food habits? Do you think they caved to a company such as Monsanto?	First I've heard of it, though there's unfair influence everywhere you look. I'd hope for better, since TED's general approach is admirable: to try to spread information.
Have you worked with Steven J. C. Gaulin who used to research/teach at U. Pitt? He was a great professor and his Evo. Psych course really got me interested in the topic... even 10 years later.	Gaulin does some great research, and has been editor of the main journal in evolutionary psychology, called "Human Behavior and Evolution"
	He did some research on homosexual preferences, which I have also studied. Punchline of that work is that sexual attraction does not seem to be controlled by a single mechanism: Homosexual men continue to find young attractive partners desirable, and not to care about status, so their preferences do not at all map onto what women want in men.
	Bailey, J. M., Gaulin, S., Agyei, Y., & Gladue, B. A. (1994). Effects of gender and sexual orientation on evolutionarily relevant aspects of human mating psychology. Journal of Personality and Social Psychology, 66(6), 1081.
	Kenrick, D. T., Keefe, R. C., Bryan, A., Barr, A., & Brown, S. (1995). Age preferences and mate choice among homosexuals and heterosexuals: A case for modular psychological mechanisms. Journal of Personality and Social Psychology, 69(6), 1166.
As an up-and-coming social psychologist, I have encountered a fair bit of push-back about pursuing EP directed studies, even at the PhD (student) level. I study ostracism, so it's not a huge jump to consider an evolutionary perspective. What is your advice for the ascent through graduate school? Did you have any struggles with faculty or peers on your way up, and how did you handle it?	When I was in grad school, psychologists had mostly not even heard the term "sociobiology" (Wilson's book was published toward the end), but were open to ethology (no official evolutionary psych yet, either, though William James used the term in 1890). I assume you know Neuberg and Kurzban's work, and I know they have gotten resistance from those who think it is not "nice" to think about any ancestral predispositions toward prejudice, stereotyping, and ostracism. More and more of your generation have taken at least a biology class, or been exposed to the "naturalistic fallacy" as a misconception, but it often helps to point out that you are not saying natural=good. The more you can present data, and try to avoid self-righteousness, the better it will go (though there are still those for whom affective associations trump information, that is part of how humans work). More specifically, I recommend that my students not identify as militant adaptationists, try to be careful in how you communicate, say "functional" instead of "evolved," don't overclaim, and stay connected to the mainstream, try to publish in JPSP, and save EHB for after you get tenure. The good news is that in the world of science, data talks (it doesn't always win the argument right away, of course, so we collect more data, and try to address the alternative possibilities)
Hello Douglas, great to have you doing an AMA! I want to ask you a question in relation to Hamiltons theory of Kinship and Trivers theory of Reciprocal Altruism. Recently I carried out research for my undergrad that investigated the role of genetic relatedness and Moral Judgment making and I found that participants engaged in a moral evolutionary conflict. With one half conforming to Kinship theory and the other half adhering to Reciprocal Altruism. My question is, do you believe that both theories can be somewhat unified to create a conflict system (specifically in moral decision making)?	I may need to know more about your research, but I certainly think both theories apply to all of us some of the time: Many those who are more into reciprocal altruism spend more time around non-relatives, those into kin altruism spend more time around relatives?
What do you think about masterbation ?	I went to Catholic school till I was a teenager, so try not to think about it.
	It does raise interesting questions, though: why waste energy on nonreproductive sex? I am not familiar with the literature, but I would imagine people have considered several possibilities: a) a byproduct of sex drive, low enough in costs not to be selected against, b) for males, who do it a lot more, a way to reduce feelings of deprivation and testosterone buildup when alternatives not sufficient, etc. I recall hearing that it is a way of discharging older sperm cells, which are replenished.
	But evolutionary models can be applied to more than sex and aggression, and my group has been studying various social behaviors, including conformity, consumption decisions, creative displays, and so on. In my recent book "the Rational Animal" Marketing prof Vlad Griskevicius and I consider economic decision making in diverse forms. And in my book "Sex, Murder, and the Meaning of Life" I discuss research on many topics beyond sex and murder. There is also great work on family life, as in books by Sarah Hrdy "Mother Nature" and the collection of papers edited by Todd Shackelford and Catherine Salmon.
From my psychology grad student girlfriend: As an EP, what is your opinion on cunnilingus as infidelity detection (Pham & Shackelford, 2013)?	I hadn't heard about it, but before looking, I would guess that a way to test this would be to determine if the practice is more common when a man has reason to believe his partner has been unfaithful, and is less likely to do so when she has been around him, and not around other men recently. In a quick look at their abstract, they say they tested the idea with 231 men, and found that men at greater risk of sperm competition expressed greater interest in, and spent more time performing, oral sex on their partner. They say this relationship existed even after controlling for relationship length, relationship satisfaction, and sexual intercourse duration. That still leaves room for other possible confounds, but at least they subjected the idea to empirical test. Shackelford has done other research on "sperm competition" which although hardly a g-rated topic, is a fascinating, and surprising, phenomenon. I am afraid I encourage my students to try to study topics unrelated to explicit sex, such as economic decisions and conformity! An evolutionary perspective can inform us about everyday concerns far removed from sex and aggression (even though differential reproduction is always ultimately involved in any animal's behavior, including Homo sapiens). See for example our recent book on economic decision-making: "The Rational Animal: How evolution made us smarter than we think"
	Link to www.amazon.com
Can you recommend any reading in particular?	Salmon, C., & Shackelford, T. K. (Eds.). (2011). The Oxford handbook of evolutionary family psychology. Oxford University Press.
I'd also like to ask you if you're aware of any job prospecs for someone in this field besides academia?	And I just asked Catherine Salmon if she can make more specific recommendations.
Is there [in this field besides academia]such a thing as applied evolutionary psychology?	Griskevicius, V., & Kenrick, D.T. (2013). Fundamental Motives for Why We Buy: How Evolutionary Needs Influence Consumer Behavior. Journal of Consumer Psychology, 23. 372-386.
What is your response to people who say gender is a social construct.	I am running out, but have a lot to say about that, which I will get back to later.
	Briefly, there is the problem that many human "social roles" look a lot what is seen in other animals (male competitiveness, female selectiveness, etc.) plus they are widely shared across human societies. Preference for bell-bottoms is a social construct, sex differences are constructs that are wrapped around a hard core of biological reality.
	Kenrick, D.T., Trost, M.R., & Sundie, J.M. (2004). Sex-roles as adaptations: An evolutionary perspective on gender differences and similarities. . Pp. 65-91 in A. H. Eagly, A. Beall, & R. Sternberg (Eds.), Psychology of Gender. New York: Guilford.

Last updated: 2013-10-10 08:57 UTC
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