Last updated: 27 January 2021

Differences between us

Aside from a slightly greater social mindset in my friend than myself, there are a number of other neurological differences between us outside the social mindset.

Almost all of them appear to be related to the synaptic development of the temporal-lobe region and are strong opposites between us. Their neurology appears to be directly inherited from our families; in my case, it is an accentuated version of my father’s.

The differences point to increased consolidation/decreased pruning in this region in myself and decreased consolidation/increased pruning in my friend.

They show that differences in synaptic development in the temporal-lobe region are not a necessary part of our condition but rather a consequence of other mechanisms or tendencies.

Music

Music is an area in which we strongly differ.

My friend was not born into a musical family. He does not play an instrument and considered himself musically anhedonic until roughly the age of 15. He was unable to engage in any forced music lesson and considered them a huge source of stress.

Since around age 15, he has enjoyed power metal music.

I was born into a musical paternal lineage. My father is a pianist; my grandmother was a pianist; my great-grandfather was a violinist; and my uncle is a pianist. I began playing piano at around age 3 and had acquired perfect pitch by around age 5. I was given piano lessons from around age 5, whose grades I achieved the highest level in (‘distinction’) until secondary school started. I was also known for having a heightened ability to play back musical pieces I’d heard on the piano.

Since my earliest memories, I have enjoyed electronic music and have been able to produce it digitally since age 12. I receive more enjoyment the more complex the melodic, harmonic and rhythmic arrangements are.

Synaesthesia

We also differ in synaesthesia.

I had acquired grapheme–colour synaesthesia by around age 5.

My friend, on the other hand, does not have synaesthesia.

Imprinted anxieties

We differ strongly in imprinted anxieties present from early childhood.

I acquired several intense specific phobias in early childhood, while my friend does not have any significant phobias dating from early childhood.

Inability to breathe

Prior to around age 5, I had acquired a significant anxiety for the inability to breathe. The instigating factor (besides hypercapnia in the locus coeruleus[1]) appears to have been bathing instances with my mother in which she would pour a bucket of water over my head, causing me to panic due to the inability to breathe.

Initially, the fear impacted forced swimming lessons. The first time this was carried out, at around age 6, I protested vehemently when I saw all the other children splashing in the pool, which was successful in having me excused from the lessons. The idea of me learning to swim continued to be pressured on me by parents and teachers throughout early childhood, but I never accepted it. On some holidays, I fell underwater at a pool and felt immediate panic at drowning, causing me to eventually avoid all pools on holidays. By age 9, this fear also quickly grew to encompass the trigger of vomiting. This led me to avoid any and all potential stimuli of vomiting that I could, including gastroenteric pathogens, rollercoasters, travel on planes or trains, particularly bad-tasting food or bad smells, etc.

Starting at around age 9 and continuing throughout education, I would have episodes of panic centred around nausea, which would be severe enough that I would regularly have to leave either the lesson or the school. These episodes also occurred outside school, such as at home or on holidays. They happened on average at least once a month. The phobia may have also resulted in an almost total inability to burp that I have had since mid-childhood. When gas rises in my oesophagus, it does not come out of my mouth but rather waits until it goes back down. This may have been a once-conscious defence mechanism that became unconscious.

At around the ages of 12–14, in secondary school, I was almost compressively asphyxiated a few times during intentional human-crush events in the school corridors. This, among other things, led me to consistently wait around 5 minutes for everyone to pass through the school before going to my next lesson as well as consistently taking the less-travelled routes.

Loud sounds

Prior to age 5, I had acquired a fear of loud sounds that were sudden and outside my control. The apparent source was therefore the acoustic startle reflex.

At around ages 3–4, I attended a childcare centre that would finish each day by getting all the children to sing/perform a rehearsed song that finished in a sudden loud scream. Every single time this happened, I ran away crying and looking for my mother. No other child present behaved this way.

At around ages 4–5, when I first started school, there would be assemblies in which the teachers had to adjust speakers and microphones to reach an appropriate volume without feedback. Every time there was loud feedback, I often had to leave the assembly then and there. Microphone feedback occurred in every school hereafter, and this caused me to have anxiety at the sight of the imminent use of a microphone on a stage or podium, such as at an assembly.

At around ages 5–8, I would be taken to certain theatres, cinemas or concerts. Almost every single one was too loud for me, and I would beg (successfully) to leave within minutes of the performance starting. At these same ages, my father would often encourage me to watch local air or firework shows, but I could never go outside during these.

At around ages 11–15 in secondary school, the teachers would often play videos on the projector for the class, or there would occasionally be an exam in the hall that involved audio playback. Half the time, the audio was too loud for me, and on at least one occasion, I left an exam in the middle of it because of this.

Maternal separation anxiety

The above phobias manifested with significant maternal separation anxiety, which had dissipated around the time of puberty.

Sexuality (imprints)

As regards sexuality besides sexual social-mindset associations, both of us have a degree of atypical sexual imprinting.

My friend is heterosexual and has the typical attraction to females and vaginal sex, however he has had one childhood homosexual encounter and at least one instance of feelings for a male.

I am heterosexual and have never had an instance of feelings for a male, only females. Despite this, the sight of a vagina has always generally caused me repulsion, and I have never been aroused by the thought of vaginal sex or vaginal stimulation of any kind. This has remained at the same level since earliest memories and does not appear to indicate the loss of a social-mindset association.

Despite this (the reason for heterosexual and not heteroromantic), I have had three partialisms that have been present to the same level since around age 5 (though two of them are weak). I have no impairment in arousal or masturbation to female media when using the main partialism.

Other differences in these regions

Migraines

Since early childhood, I have had migraines, though they usually only occur if I sleep for too long and only occur a few times a month or less. I also inherited them from my father, though his contain visual auras, while mine do not.

My friend does not have migraines.

Psychopathic traits

My friend has inherited mildly psychopathic traits from his family, all of whom display similar traits that have been heavily accentuated by their social mindset.

He has stated that his father has been ‘an alcoholic and smoker all his life’ who ‘has anger issues … goes to the casino … listens to rock and likes motorbikes.’ He has also stated, ‘They’ve produced a whole family of alcoholics on my dad’s sister’s side, whose children consist of alcoholics with varying amounts of tattoos.’

My friend’s inherited traits include a history of interest in gambling, stock markets, poker, metal detecting and online scams. He is quicker to anger than myself and has a slight sensitivity to rejection by romantic partners.

The lack of the social mindset has heavily muted these features in my friend compared to his family. He does not go out of his way to profit off manipulation and considers it a waste of time. He does not consume any recreational drug and will never get a tattoo.

At age 20, my friend stated:

‘I still get the good feelings and the kick out of it coming through, but I have the lack of the social mindset and that self-awareness that [my family] don’t have, so it allows me to overrule.

[What my father did is] exactly what I would be doing if I didn’t have the lack of the social mindset and the awareness that I do. I’d be smoking and drinking and having wild sex.’

On the other hand, my father does not have any such traits, and I have not inherited any.

My father has always been a calm personality, and I have not known him to get visibly drunk, smoke, gamble or partake in any behaviours similar to those aforementioned.

I have never pursued any of the aforementioned activities and have no interest in doing so. I also do not have any anger at rejection by romantic partners.

Neurology of these differences

The temporal lobe is located beneath the temporal bones in the sides of the skull and manages memorisation of and associations between inputs from the primary auditory and visual cortices (including semantic memory). It also contains the amygdala, the centre for consolidation of anxieties and visual sexual imprints.

Diagram showing the temporal lobe and the primary auditory and visual cortices

Several temporal lobe–regulated phenomena have a critical period in early childhood, during which visual and auditory exposure marks particular synapses for retention from a pool of overproduced synapses, while the remainder are pruned.[2]

These phenomena include visual sexual imprints,[3][4] early-childhood maternal separation anxiety,[5] early-childhood specific phobias,[6] grapheme–colour synaesthesia[7] and visual and auditory grammar.

The critical period ends at around age 5[2] (though another study indicates age 1 for visual and auditory grammar[8]). The critical period is well studied in birds, as manifested in visual sexual imprinting,[9] and it is especially prominent for auditory memorisation in mimicking birds.[10]

The dynamic synaptic processes for auditory memorisation are localised in the superior temporal gyrus in humans and area X of the striatum in mimicking birds and are controlled in both regions by the conserved transcription factor gene FOXP2,[11] whose periodic expression generally correlates with halting synaptic growth.[12]

Unlike in many other vertebrates, such as zebra finches[10] or rats,[5] in humans, there is a female bias in the prevalence, intensity or onset of these temporal-lobe critical-period phenomena, such as early-childhood specific phobias (2:1 female–male ratio for single, 4:1 for multiple[13]), grapheme–colour synaesthesia (6:1 female–male ratio[14]) and onset of language ability (earlier first words and sentences and larger vocabularies in females at the same age as boys[5]). For language, this correlates with greater or earlier expression of the conserved FOXP2 transcription factor in early childhood in females than males.[5]

In the male zebra finch, FOXP2 expression is highly reduced while practising song memorisation alone, an effect that can be increased by testosterone treatment, while FOXP2 expression is high when singing a memorised song to females during courtship, which can be increased by estrogen treatment.[10][15] Additionally, migraines are reported to have a 2.5:1 female–male ratio,[16] and their presence decreases with testosterone levels.[17]

Despite the male predominance in autism spectrum disorder, some of these ‘female temporal lobe’ features have been reported to be more common in autism spectrum disorder. Perfect pitch has been reported to be more common in those with subclinical autistic traits.[18][19] Synaesthesia is reported to be 3 times more common in those with autism spectrum disorder (18.9%, compared to the average 7.22% prevalence).[20] Specific phobias are reported to be around 4 times more common in those with autism spectrum disorder.[21]

Sexual imprinting

Facial/general

Studies have established positive sexual imprinting in sons on appearances similar to their mother in vertebrates from birds to humans, including hair and eye colour.[22][23][24]

Given a positive imprint on an appearance similar to the mother, there would need to be a negative imprint on the exact appearance of the mother to explain the prevalent avoidance of direct attraction to the mother (or other family members) across vertebrates; this is known as the Westermarck effect. A 2006 study on male zebra finches reported a sexual preference for those with a more extreme beak colour than that of their mother.[25]

When my friend and I compared our ideal anatomies, they both turned out to have characteristics that were opposed to those of our mothers in early childhood, especially in hair colour, hair length and eye colour.

Partialisms

Although partialisms have been attributed to sexual imprinting,[26] there have not been many studies and none (to my knowledge) detailing the resemblance of the partialism to the sources exposure in early childhood.

All three of my partialisms are for a form of the body part that least resembles that of myself or my family.

Many partialisms that are not cultural sexual social-mindset associations, such as breasts or buttocks, are for areas of the body that are ticklish. These include the feet, the armpits, the stomach and the neck.[27] This is despite the fact that, for example, the hands are far more sensitive to touch than the feet.[28]

Tickling involves the nerves responsible for pain in combination with those for touch.[29] The tickle response is diminished when pain nerves are severed,[30] and most ticklish areas are in the location of protective brainstem reflexes.[31]

Pain is received by the nerves and spinal cord and enters the amygdala to trigger brainstem responses. It is inhibited by the medial prefrontal cortex.[32]

Both laughter and crying are carried out by the brainstem and involve transmission through the amygdala to the hypothalamus to the dorsal pons of the brainstem.[33][34] The prefrontal cortex inhibits them, and they become context-based when they involve an incongruence in input from the anterior cingulate/prefrontal cortex.[34][35] Similarly, tickling requires this incongruence or unexpectedness, which explains the lack of ability to tickle the self.[28]

Despite instigating laughter, tickling is also considered unpleasant[36] and, when prolonged for a significant period of time, has been used as a form of torture.[37]

Tickling has thus been theorised to have evolved in certain mammals to facilitate rewarding combative play in childhood to bolster defensive skills.[28][31]

Conclusions

As described in above information, it appears that the early-childhood temporal-lobe synaptic-consolidation effect takes place in association with both anxiety and laughter.

It appears that when the stimulus is of anxiety (such as from pain or hypercapnia), a different form of the stimulus can later become a source of phobia, while when the stimulus is of laughter (such as the mother or a ticklish body part), a different form of the stimulus can later become a source of sexual arousal.

Across vertebrate species, in regions homologous to the medial temporal lobe in humans, young offspring form a visual imprint on their mother (or the first individual they’re significantly exposed to) that regulates a separation anxiety mechanism. When separated from the mother, they express their distress vocally, which facilitates retrieval by the parent. As mentioned earlier, this effect has a critical period and is regulated by the same FOXP2 transcription factor that regulates auditory memorisation in mimicking birds and humans.[5]

Visually imprinted partner preference therefore appears to be a result of the visually imprinted separation anxiety a child has with the parent that results in more laughter/smiling when the child can see the parent compared to when they cannot. Over time, this appears to manifest the laughter-induced imprint based on the parent. Some studies have reported more consistent imprinting in children who had a positive relationship with their opposite-sex parent.[38][39][40]

Visually imprinted anatomical partialisms, on the other hand, appear to be a result of the more intense and short-term laughter episodes facilitated by the mammalian-evolved tickling mechanism. When the body part in question is consistently observed in association with this intense laughter, it may form a strong visual imprint. The mechanism may also explain the predominance of the foot partialism over other partialisms for less visible or accessible ticklish regions such as the armpit, even if there were equal tickling attempts of these regions in early childhood.

Tickling itself is a fetish,[41] but I do not have this. The tickling fetish is a sexual social-mindset association that is attached to episodes of having a body part at the centre of a partialism stimulated, which will almost certainly lead to ticklishness, leading tickling itself to be attached as a situational trigger of arousal. The tickling fetish is common in BDSM scenarios,[41] which are also sexual social-mindset associations.

Instead, the mechanism described above suggests that, in early childhood, the tickling triggers laughter, which, over time, creates a visual imprint that triggers sexual arousal in the same way sexual arousal to the face is created due to smiling/laughter while seeing the parent.

Hypothesis for opposing nature of imprint

Given this evidence, a hypotheses arises as to how a sexual imprint for an opposing difference to the source of the imprint (parent, body part) is created without causing attraction to other things, sexes or species.

At birth, there is no temporal-lobe regulation over sexuality, as evidenced by Klüver–Bucy syndrome (caused by damage to or removal of the medial temporal lobe).[42][43][44] Most of what one sees becomes negatively imprinted.

According to the hypothesis, anything one sees while laughing/smiling is, according to the intensity of laughter and duration of exposure, marked as an active ‘reference negative imprint’ or ‘trunk’ of a synaptic tree. This is strongest for the parent (due to both parental care and imprinted separation anxiety) and ticklish body parts, in both cases due to the consistency/duration of exposure (often years) and, in the latter case, due to the intensity of laughter.

With these ‘reference negative imprints’ established by laughter/smiling, incrementally similar appearances that are seen are progressively marked as ‘branches’ of the ‘trunk’ in a tree fashion. At any given time, the ends of the synaptic tree (the ‘twigs’) are reserved as the future positive imprint, though they are also continually being transformed into branches as more incrementally similar appearances are seen.

This process finishes at the end of the critical period at around age 5, with the ‘twigs’ of the synaptic tree remaining as the positive imprint, while other synapses are pruned. The imprint can either potentially be very similar in appearance to the ‘trunk’ with little exposure to incrementally similar appearances or, alternatively, can be highly but clearly incrementally diverged from the ‘trunk’ with higher exposure to incrementally similar appearances. Regardless of how diverged, the final imprint should still represent something the child was able to see during early childhood. The final imprint will only be an ideal, permitting some attraction to appearances that are somewhat similar to it.

In theory, the effect of this process should be stronger for those with higher synaptic consolidation in the temporal lobe (evidenced by early-childhood specific phobias, grapheme–colour synaesthesia, musical ability, etc.) and weaker for those with lower synaptic consolidation in the temporal lobe (lacks of these features). This is reflected in my presence of imprinted partialisms vs. my friend’s lack of these and my strict heterosexuality vs. my friend’s mild bisexual tendencies.

Hypothesis for formation of early-childhood specific phobias

Given the above explanations also involving negative brainstem responses (pain/hypercapnia), it is probable that the imprinted phobia of spiders and insects (in those with high temporal-lobe synaptic consolidation) comes from instances in early childhood of feeling pain from the prick of a sharp object. The final, positively imprinted synaptic ‘twigs’ likely end up being insects and arachnids (things with multiple spines) also witnessed during early childhood.

There is also a compelling case to be made for phobias of snakes, slugs or worms to be related to aversion from the noxious stimuli of faeces in early childhood. Likewise, the final, positively imprinted synaptic ‘twigs’ likely end up being snakes, slugs or worms (irregular, roughly tortuous cylindrical things) also witnessed during early childhood. Cats are known to fear cucumbers placed behind them,[45] and monkeys are more reluctant to eat food placed on top of visual replicas of faeces.[46] Similarly, cows[47] and sheep[48] avoid grazing on patches of grass containing faeces.

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