PTSD / Trauma Is Contagious, Can Be Transmitted Via Odor/pheromones

haidut

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This is an amazing study, which goes a long way in confirming what has been anecdotally known for centuries - bad experiences affect not only the individual experiencing them but everybody else this traumatized individual is in closed contact with. With one exception - psychopaths - who are largely immune to the induction of both first-hand and second-hand traumatic memories. In addition, the study shows that the trauma can be transmitted more than one individual away - i.e. the second-hand traumatized individual can traumatize a third or even further away removed individual. I don't know how far this "virulence" of trauma extends but the study makes it sound like there is no real limit to distance of propagation. This reminds of the older studies done in the 60s and 70s, which showed that medical staff working long shifts in hospitals with specific patients tend to acquire and even die of the same condition as their patients. This seems to be especially true of cancer and psychiatric conditions, but I suspect is present in all disease as the alarm signal does not discriminate among diseases.
The study also shows that the activation of the brain region responsible for releasing CRH is needed for both the induction of PTSD in the subject and the release of the "trauma" pheromone. While the study does not mention what that "trauma" pheromone might be, I suspect that it is a mix of oxytocin/estrogen/cortisol. Besides the obvious involvement of CRH (which stimulates cortisol release), in the studied mice the trauma signal was mostly released from the neck/genital area where oxytocin and estrogen are most likely to accumulate. In addition, humans exposed to oxytocin respond respond with elevated oxytocin levels themselves and activation of HPTA (cortisol). The good news is that pregnenolone should be able to block some of that pathway (CRH), as shown in another study I posted some time ago.
Pregnenolone Is The Most Potent Inhibitor Of The Stress Signal (CRH)
If oxytocin/estrogen/cortisol are involved in that "trauma" virulence signal then progesterone (or androgens) may also help limit the infectiousness of the traumatic experience and protect the larger populace as progesterone is known to block the oxytocin/estrogen/cortisol triad.


Social transmission and buffering of synaptic changes after stress
"...We found that stress primed glutamate synapses on PVN CRH neurons. This synaptic load was transmitted to naive individuals from the stressed subject. In addition, in females, but not males, the partner buffered the synaptic load in stressed individuals. Activation of PVN CRH neurons in the stressed subject seemed to be necessary to release a putative alarm pheromone. In the naive partner, PVN CRH neuron activation was required for investigative behavior and synaptic priming. Finally, the synaptic load could be transferred by the partner to a third member of the group (Supplementary Fig. 16). Priming of glutamate synapses in response to either authentic or transmitted stress unmasked associative STP. This STP, which lasted for at least a day after the stress, but might persist for several days [6] , requires the availability of CRHR1; this is consistent with earlier descriptions of STP in rats following immobilization or predator odor stress6 . The CRHR1-dependent downregulation of NMDA receptors allows for multi-vesicular glutamate release immediately following tetanization6 . Photostimulation of PVN CRH neurons, even in the absence of stress, was sufficient to unmask STP, whereas photoinhibition during stress prevented STP. These observations demonstrate that activation of PVN CRH neurons is both necessary and sufficient for the induction of STP. Combined with the finding that CRHR1 is required for STP, we conclude that locally released CRH binds to CRHR1, creating a synaptic environment that is permissive for STP. Abnormalities in the CRH system are evident in post-traumatic stress disorder (PTSD) and other stress-related affective disorders, such as anxiety and depression28, and recent work has implicated PVN CRH neurons as drivers of anxiety-like behaviors26,29. Although STP is a reliable consequence of acute stress, the endocrine response is not an accurate predictor of STP. More specifically, elevated CORT levels do not predict the occurrence of STP. CORT levels were elevated in both male and female subjects following exposure to either FS or NE; only female subjects, however, showed STP following NE exposure. This suggests that the consequence of stress on synapses is both graded and sex dependent and is consistent with our previous findings that relatively mild stressors have profound consequences for CRH neurons in females 2 . Although we have not explored the mechanisms responsible for this differential sensitivity, they may result from previously described sex differences in CRHR1 signaling30. Synaptic priming in both male and female mice is transmissible. Once synapses in a subject are loaded, regardless of the stress (FS or NE), transmission of the synaptic load to a partner occurs reliably following social interaction with the stressed subject. Thus, not only is stress transmitted from a stressed subject to partners, as previously reported in rodents9,11,13 and humans31, but the enduring synaptic consequence of stress, or the synaptic load, is also transmitted from subject to partners. These findings suggest that, in addition to consoling the stressed individual, affiliative behaviors in humans7 , primates8 and rodents9–11 may serve a strategic purpose by communicating information about a stressful event. Social interaction also modifies synaptic load in female subjects. Specifically, STP was reduced in stressed female subjects returned to a partner in the homecage, suggesting that the presence of a partner buffers the lingering effects of acute stress in females. This is consistent with previous work suggesting that females, through a ‘tend and befriend’ strategy, may buffer the effects of stress more effectively than males32. Given that STP is induced even if no time elapses between FS and slice preparation, CRH neurons must encode the biochemical signals of stress very rapidly. This also means that the 30-min interaction between females is not buffering the induction of the stress-associated biochemical changes necessary for STP, but instead is likely reducing the changes that have already occurred. The mechanisms through which this occurs are not known, although a recent report showing that oxytocin—a hormone that has been implicated in pro-social33, attachment34 and consolation behaviors11—decreases spontaneous glutamatergic drive to CRH neurons35, providing an interesting avenue for future studies. We observed that the partner acquires information from a stressed subject via olfaction. Partners engaged in sniffing behavior that was directed predominantly toward the anogenital region of the stressed subject, but also directed sniffing behavior toward the head/torso region, likely detecting pheromones from perianal glands and whisker pads, respectively22. This directional sniffing behavior toward a stressed conspecific has been reported previously13,20. Notably, exposing a single mouse to alarm pheromone while restricting its behavior in a NE results in avoidance behavior toward the alarm pheromone36. By contrast, mice housed in groups of three and exposed to alarm pheromone in their homecage show increased activity and seek out, rather than avoid, the source of the odor36. This suggests that social context and environment influence behaviors of mice toward alarm pheromones. Alarm pheromones released from the anal glands induce a stress response in recipients and are hypothesized to be critical for communicating stress 21,22,37. Our findings support this hypothesis, as partners of FS mice discriminated between anogenital sniffing and head/torso sniffing, spending more time anogenital sniffing; partners of NE subjects did not. Furthermore, mice that were exposed to a swab from the anogenital region of a stressed subject showed reliable STP, similar to stressed individuals; this STP was greater than that of mice exposed to a swab from the head/torso region of a stressed subject. Thus, although we cannot dismiss the involvement of other modes of communication, such as ultrasonic vocalizations38,39, our findings strongly support alarm pheromone, specifically from the anogenital region, as the predominant method of communication of stress and STP from subject to partner. The volatile chemicals released by mice under alarm conditions share common features with predator scents (kairomones)24. Both are detected by the vomeronasal organ40,41 and Grueneberg ganglion cells42 in mice, and may recruit parallel pathways43 that converge in the ventromedial hypothalamus44. Alarm pheromones activate key stress nuclei, including the bed nucleus of the stria terminalis, amygdala, dorsomedial hypothalamus and the PVN23. Although the pathway through which mouse alarm pheromone specifically activates PVN CRH neurons is not known, work using predator odors implicates a pathway from the olfactory bulb to the amygdalo-piriform transition area, which projects directly to PVN CRH neurons23,25. Our data indicate that the activity of PVN CRH neurons and recruitment of CRHR1 in the partner is required for anogenital sniffing to occur. This may be important in the initial arousal of the partner following the return of the subject to the homecage; in the absence of this arousal, the partner fails to approach or investigate the subject. When CRHR1 was inhibited in the stressed subject during and following stress, partner mice still exhibited anogenital sniffing. Similarly, photo-inhibition of PVN CRH neurons in the stressed subject during and following stress had no effect on sniffing by the partner. In both experiments, the initial arousal of the partner following the return of the subject to the homecage likely triggered this investigative behavior. In both experiments, however, STP in the partner was significantly reduced, as if the signal antecedent to the synaptic changes was not fully transmitted from subject to partner. It is plausible that, although partner mice engaged in anogenital sniffing behavior, the signal required to activate and prime PVN CRH neurons was not released by the subject. In support of this hypothesis are findings that photoactivation of PVN CRH neurons in a subject mouse in the absence of stress triggered anogenital sniffing behavior by the partner and resulted in STP in the partner. Here, activation of PVN CRH neurons in the subject initiated a currently unknown signaling cascade that culminated in the release of an alarm pheromone. PVN CRH neurons are therefore upstream of the alarm pheromone production in stressed subjects and are essential for generating the specific behaviors required for seeking out and detecting alarm pheromones in partners. These observations position PVN CRH neurons as central controllers in communication via alarm signals. From an ethological perspective, the ability to buffer the effects of stress11 while simultaneously extracting experiential information from the distressed individual has clear adaptive benefits. This information may promote coalition formation during times of stress45 while editing neural circuits to prepare for subsequent challenges without subjecting all group members to danger directly. In humans, buffering or consolation behavior is nearly universal32, yet our findings suggest that the partner, or consoling individual, may experience long-term synaptic consequences similar to those of the distressed individual. This may, for example, offer a potential explanation for why individuals who have themselves not experienced a trauma develop PTSD symptoms after learning of the trauma of others."
 

lvysaur

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Amazing find. Just goes to show the inadequacy of the mantra that everyone seems to go by: equating absence of evidence to evidence of absence.
 

Tarmander

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I wonder if it also works the same in reverse...positive, life giving hormones cause the same around you...there is however that saying that misery loves company, and not a really a corollary.
 

lampofred

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Damn. The people that need the most support are the ones that nature targets to repel others. Winners keep winning and losers keep losing.
 

Fractality

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Wow, just think about the media and how it sets off a "viral" contagion of PTSD. Everyone except psychopaths and monks isolated from civilization are traumatized. Someone who knows about somatic experiencing as a therapy should join in this thread. We need as many therapeutic options as possible.
 
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lollipop

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Just WoW. Thank you for posting @haidut.

I have experienced this and seen it in action. I never imagined it would be the subject of a study. Very very important finding.

@Tarmander - I would agree with the reverse as well. Have seen it in action and had direct experience of it.
 

DaveFoster

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Wow, just think about the media and how it sets off a "viral" contagion of PTSD. Everyone except psychopaths and monks isolated from civilization are traumatized. Someone who knows about somatic experiencing as a therapy should join in this thread. We need as many therapeutic options as possible.
Seldom listen to news. Paint or cook instead.

Literature such as War and Peace offer a meaningful medium for learning. Yet, we should engage with reality.
 

Ulysses

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Damn. The people that need the most support are the ones that nature targets to repel others. Winners keep winning and losers keep losing.
In a "state of nature," the people who need support might find it from a cohesive group, rather than a disparate collection of individuals. For example, certain African tribes have collective rituals in which a mentally ill or traumatized person is reintegrated into the community, by the whole community acting in concert. Theoretically, we might expect this to diffuse the "synaptic load," so that the total load borne by any given community member is tolerably low. Thus, it is modern atomization that creates the tragedy. Michel Houellebecq wrote a brilliant novel about it called "The Elementary Particles."
 

Travis

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➞ Abram Hoffer and Humphry Osmond. "The hallucinogens." Academic Press (1967)

All catecholamines can lose two electrons and condense into indoles. Adrenochrome, leuco-adrenochrome, and dopachrome are all indoles; serotonin and melatonin are also indoles, but unlike the catecholamine-derived indoles they derive from dietary tryptophan. Shown below is the condensation of dihydroxyphenylalanine (DOPA) into dopachrome and leucochrome (colorless):

ijms-17-01576-g027-550.jpg


Andrenaline (epinephrine) can do likewise, as can nor-epinephrine. When adrenaline condenses into an indole the resulting product is adrenochrome. As an indole, you would expect this to be psychedelic or nearly so. This molecule is small enough to be volatilized and inhaled, and is has actually been reported to induce psychosis—as seen below. Here are some quotes from Hoffer & Osmond:

'Since adrenaline is a standard treatment for asthma, it is possible that asthmatics who take large quantities of adrenaline may develop schizophrenic states (Hoffer, 1957c), as has occurred after inhalation of discolored adrenaline (Osmond and Hoffer, 1958).' ―Hoffer & Osmond

'The original observation that discolored adrenaline was psychologically active was made by a person who was forced to inhale large quantities of adrenaline for his asthma (Hoffer et al., 1954). He described the changes as if he had taken mescaline. We have since observed that these changes are not infrequent and, in fact, have been observed by many internists who have insisted that their patients not be given discolored adrenaline. ['discolored' here necessarily means that it had become adrenochrome, which is red] Mr. Kovish (Hoffer and Osmond, 1958) became psychotic a few hours after he began to inhale a port wine-colored adrenaline solution and remained so for one month while he continued to inhale it. Vencovsky and Peterova (1963) reported that a 57-year-old woman with asthma was made psychotic by inhalation of adrenaline. When the patient was admitted and given no more adrenaline she recovered but when, as a test, more adrenaline was given she once more became psychotic. The authors suggested the anoxia in asthma had something to do with an abnormal conversion of adrenaline to adrenochrome. It could then quickly be swept into the brain from the left side of the heart.' ―Hoffer & Osmond

And here are the citations below. The 1958 article is called The Case of Mr. Kovish yet appears impossible to read for free, and I've tried nearly everything; the Vencovsky study appears to have been written in czechoslovakian and near-impossible to find. Perhaps someone knows a few more tricks that I do.. .

Hoffer, A. (1954). A.M.A. Arch. Neurol. Psychiat. 71:80.
Hoffer, A., and Osmond, H. (1958). J. Mental Sci. 104:302.
Vencovsky, E., and Peterova, E. (1963). Comprehensive Psychiat. 59:217.
But from what I've read about adrenochrome, I would nominate this as the primary suspect. Although adrenaline may not be psychedelic, oxidized adrenaline (adrenochrome) certainly is. Adrenochrome is also more volatile due to the protection of adrenaline's polar methyl-amino group upon condensation (it would have less affinity for skin, water, or sweat drops as adrenochrome).
 
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Travis

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Indole derivatives are volatile enough to be used in perfumery:

➞ Ghostwriter. "The Chemistry of Death and Desire." deathscent·com... (2016)

'Indole, dirty, sexy, carnal Indole. You have smelled it thousands of times without knowing its name, but if you are smelling something a little bit overripe, heavy, and with a strange sweetness, it is most likely Indole.' ―Ghostwriter

'It wasn’t until the rebellious Flappers of the 20’s, and their racy new fragrances like Chanel No.5, that those smutty indolic florals were redefined.' ―Ghostwriter

➞ Gaudin, Jean-Marc. "Indole amides as perfuming ingredients." U.S. Patent Application (2010)

'Concentrations lower than these, such as in the order of 0.001% to 5% by weight, can be used when these compounds are incorporated into perfumed articles, percentage being relative to the weight of the article.' ―Gaudin
Gaudin's perfume indoles are similar to adrenochrome, yet all have an acetylated nitrogen. I think to be a schizophrenic indole it would need to be methylated. Nonetheless, his patent shows that small concentrations of N-acetylindoles can be detected—adrenochrome would be expected to be even more volatile that that (it is less polar and has a smaller molecular mass).
 
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dookie

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@haidut

The theory is really nice, but too bad the practical recommendations don't work. Progesterone and pregnenolone seem to cause "PTSD" in people like myself, probably because it is possible for them to change into stress hormones like estrogen/cortisol, despite common beliefs
 

LeeLemonoil

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In the Phero-scene, Preg as a phero never really made it into the most used and widely liked molecules.
Curiously, some report it gives of a happy, shiny vibe and also provides self-effects in line with that, but many also have experienced that preg used as a Phero is drastically Status and respect reducing for the wearer, so many shy away from its use.

Perfumes are Mighty mood and neuromodulators, never doubt that. Most aromchemicals are neuroactive, some are probably very estrogenic, others androgenic but many different Signalling pathways steht involved. Most lower Cortisol though acutely but might have more detrimental other impacts
 
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Jem Oz

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This study resonates. When I was 4 years old I was attacked in my bed by a burglar. It dramatically altered the course of my life. Over the years I've wondered if people could literally smell the trauma on me.

Aside from the unfortunate subject matter, this is an exciting area for research.
 

denise

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Wow, just think about the media and how it sets off a "viral" contagion of PTSD. Everyone except psychopaths and monks isolated from civilization are traumatized. Someone who knows about somatic experiencing as a therapy should join in this thread. We need as many therapeutic options as possible.
+1000 for somatic experiencing

I started doing SE last fall and also did a 12-week course about trauma healing that has been life changing. The understanding that trauma is primarily physiological, and then working on it from that angle, makes all the difference. I'm part of a FB group for people doing SE, and just yesterday I posted about how difficult and potentially dangerous it is to try to heal from trauma in isolation, or with only one person close to you, because it's just too much to ask one person to bear. Not only (as haidut is suggesting) can that person absorb your own trauma, but their response to this can help perpetuate your own (once they start withdrawing or shutting down, or even leaving you because they just can't handle it anymore, through no fault of their own). On the other hand, like @Ulysses was suggesting, if you have a community that is largely regulated, the burden can be shared and the healing can happen much more quickly.

And once you regulate your own nervous system, it really does radiate to those around you. Many people in the course I took have children and have found that their kids settle down and are better able to navigate their own emotional states once the parents are regulated. Babies aren't born knowing this stuff.

One thing I'd add is that although the measurable physiological effects are hormonal (cortisol, etc.), I don't think managing those hormones exogenously is a sustainable solution. If (with SE or whatever else) you can help your nervous system settle and come out of that chronic fight/flight/freeze response, your hormonal state will naturally balance itself out. Your system is stuck in that state for a reason, and trying to manhandle it with tons of supplements isn't going to fix it. (I'm not saying they can't or shouldn't be used for support--I just don't think it's the ultimate solution.)

By the way, you may all know this, but the freeze response looks exactly like hypothyroidism. I wonder how many people around here with crappy thyroids are just stuck in the shutdown phase of trauma? I know I am. It's getting better, but it's S L O W going. No quick fixes here, alas!
 
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haidut

haidut

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I wonder if it also works the same in reverse...positive, life giving hormones cause the same around you...there is however that saying that misery loves company, and not a really a corollary.

Yes, it does. Older people who work with young, healthy people tend to dramatically outlive their peers. There is a reason for the recent creepy craze about drinking and transfusing blood from your people to keep old/rich slabs of meat functional.
 
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haidut

haidut

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Does it take trauma

I would say yes. And usually a few traumas (estrogen/cortisol) in succession trigger puberty (to accelerate reproduction). It is well known that children of traumatized parents or children who have been traumatized themselves start puberty much earlier than their peers.
 
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haidut

haidut

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@haidut

The theory is really nice, but too bad the practical recommendations don't work. Progesterone and pregnenolone seem to cause "PTSD" in people like myself, probably because it is possible for them to change into stress hormones like estrogen/cortisol, despite common beliefs

What are those symptoms of "PTSD" they caused in you?
 

mangoes

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+1000 for somatic experiencing

I started doing SE last fall and also did a 12-week course about trauma healing that has been life changing.

And once you regulate your own nervous system, it really does radiate to those around you. Many people in the course I took have children and have found that their kids settle down and are better able to navigate their own emotional states once the parents are regulated. Babies aren't born knowing this stuff.

By the way, you may all know this, but the freeze response looks exactly like hypothyroidism. I wonder how many people around here with crappy thyroids are just stuck in the shutdown phase of trauma? I know I am. It's getting better, but it's S L O W going. No quick fixes here, alas!

Wow, I never thought about the freeze response > hypo correlation. What kind of exercises did the course get you to do to regulate the nervous system? Is it like somatic experiencing, which my knowledge goes as far as the "felt sense' and a shaking exercise to, expel tensions/trauma (?)

Also, I wonder if the course is international/online, I can only be put on a waiting list.
 
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denise

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Wow, I never thought about the freeze response > hypo correlation. What kind of exercises did the course get you to do to regulate the nervous system? Is it like somatic experiencing, which my knowledge goes as far as the "felt sense' and a shaking exercise to, expel tensions/trauma (?)

Also, I wonder if the course is international/online, I can only be put on a waiting list.
The exercises borrow a lot from SE and also Feldenkrais. The two main goals are to create more capacity (safety) in your system and then to release some of the stored trauma. The shaking exercise you're thinking of is TRE (Tension and Trauma Release Exercises) and isn't something she teaches, because if your system is super sensitive, you can easily overdo it and make things worse. Slow and gentle is the name of the game.

She runs the course online twice a year. I think the next class starts in April. It's expensive—$1500—but you get access to it forever, and the FB group for the class is hands down the most supportive community I've ever been a part of. I think the price is totally worth it. She also has an email course (for about $200) that you can sign up for at any time, and if you decide to do the full course, the $200 is deducted from that.

If you want to try out some of the basics, she has a lot of free resources—exercises and YouTube videos. Here are a few good ones to start with:
How to De-Stress in 7 Steps
4 Surprisingly Simple Steps to Calm Overwhelm & Out of Control Emotions
 
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