Possible Cause of Autism Symptoms(New Findings)

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I'm talking abo[quote]ut the stereotypical behaviors associated with aspergers. Obviously everyone is different and it seems hard to be put into a group when you are obviously different. I'm going by MY experience, which is pretty stereotypical at least in regards to my pursuit of only a few core interests. I'm trying to objectify only one part of the whole issue. We could get into low functioning mirror neurons or comorbid ADHD and the role of dopamine but I hate tangents. The other part of the endorphin model is that it has been shown that when given larger amounts of exorphins a rodent subject cares much less for affection and prefers to be left alone.

It is my understanding that these types of disorders, if you want to call them that, stem from multiple physical dysfunctions. That being said, I know where you're coming from but I am sure I'm on to something here.

I'm also in the process of trying to logically pin point some of the reasons for psychotic disorders. My one hypothesis involves an underproduction or use of interocular melatonin levels in schizophrenia causing abnormal sleep and the body's reaction to insufficient REM sleep.

So this is the theory you mentioned to me in another thread. I'm too stupid to actually understand it properly.

I'm dysphoric around things that aren't my interests. So much so that I need SSRIs to ameliorate this dysphoria. I've also been an on and off opiate addict, as well - though only with the milder opiates.

I've always been quite anhedonic. You might have hit upon the reason, but I don't know enough about neurochemistry to say.

And I just recently made another assumption. Mirror neurons do not fire properly in those who have autistic spectrum disorders. I am postulating that the increase in endorphin levels in autistic patients "shut down" the mirror neurons. It's like when you think about doing something and you get a rush, and when you do it it seems obsolete. I always wondered why when I thought of something and did it it felt the same but if you build up something for someone else their endorphins burn out when the mirror neurons kick in. But we have enough floating around to be utilized a second time when the actual event happens. Or we can be apathetic to both since we experience very similar reactions.

Sorry about that huge thought explosion. In summary, I now believe that over production(or over reuptake) of endorphins limits mirror neuron functioning in those with autistic spectrum disorders. I want to test this so bad! Maybe with treatment with a mild opiate agonist people could learn to reuse the mirror neurons and function in social situations like normal people!

I was looking through information about how Oxytocin causes many dysfunctions associated with the Autism spectrum and I found a link that gives more evidence to my hypothesis of overproduction endorphins and proportional Kappa to Mu receptor activity. The answer lies in this paradox. The brain produces too much endorphins, causing half of the issue, but these endorphins REDUCE oxytocin!! This may be the answer.

Here is a bit from a research paper that deduced that endo as well as exo opiates change the behavior of oxytocin:
OPIATES and THE OXYTOCIN SYSTEM : MULTIPLE STUDIES in HUMANS and ANIMALS: --- MORPHINE reduces OXYTOCIN in Breast-feeding Mothers 1. Studies report lower levels of lactation ability ( less OXT ) 2. Studies suggest Opiate use adversely affects Maternal- Newborn “Bonding” during Breast-feeding ( less OXT ) --- OPIATES reduce OXYTOCIN during Childbirth Labor: 1. Morphine (and other synthetic narcotics) can stop Uterine contractions in early Human Labor by reducing Maternal OXYTOCIN levels 2. Opiate use for Pain Management (epidural use included) prior to the Transitional Phase of Labor can result in the need for Pitocin (synthetic medical Oxytocin) Augmentation of Uterine Contractions because of reduced levels of Maternal OXYTOCIN 3. Beta-Endorphin levels increase during Uterine Contractions causing Maternal OXYTOCIN levels to decline …allowing for the “rest period” between Labor Contractions. As the Pain subsides, the Endorphin levels decline …leading to “ permission” for the OXYTOCIN to be produced again. Similar findings are seen in Pigs, Cows, Monkeys, and Rodents …Opiates interfere with Labor by reducing Maternal OXYTOCIN Related Animal Findings: --- Opiates reduce Milk Production in Milking Cows ( less OXT ) --- Morphine impairs Maternal-pup care-giving in rodents ( less OXT ) --- Opiates lead to rapid weaning of pups in rodents ( less OXT ) HIGH LEVELS of CIRCULATING OPIATES RESULT in REDUCED PRODUCTION of OXYTOCIN IN LABOR and during BREAST-FEEDING
--- OPIATES suppress the OXYTOCIN release of Orgasm in both males and females in study settings (when Opiates were given prior to masturbation) --- similar findings are seen in multiple Animal Models (rodents, sheep, monkeys, Higher Primates) OPIATES and THE OXYTOCIN SYSTEM : --- OPIATES injected into Brain Tissue (rodents, sheep, monkeys) cause a reduction in Brain OXYTOCIN levels 1. Opiates impair social interactions and social recognition behavior ( less OXT ) 2. Opiates increase social aggression and diminish social skills ( less OXT ) SO…at least in Animal Models, the ability of OPIATES to reduce OXYTOCIN LEVELS seems to have Ramifications during “SOCIAL BONDING” as well. DO OPIATES HAVE AN IMPACT on OXYTOCIN PRODUCTION / RELEASE DURING HUMAN SEXUAL ACTIVITY ?? IMPORTANT QUESTIONS: --- HOW DOES THIS OPIATE INDUCED SUPPRESSION of THE OXYTOCIN RESPONSE AFFECT SEXUALLY- RELATED “BONDING” BEHAVIOR ? (ANIMAL MODELS) --- DOES THE “TIMING” OF OPIATE EXPOSURE DURING SEXUAL ACTIVITY PLAY A ROLE IN ITS INFLUENCE ON THE OXYTOCIN SYSTEM ? (ANIMAL MODELS, INDIRECT OBSERVATION STUDY IN WOMEN) --- SINCE SEXUAL ACTIVITY RELEASES LARGE LEVELS of ENDORPHINS at ORGASM…WOULDN’T THESE OPIATES BE EXPECTED TO INTERFERE WITH OXYTOCIN’S RELEASE DURING SEX…AND THUS CREATE A DILEMMA WHEREBY “SEX INHIBITS OXYTOCIN-BASED BONDING” BY REDUCING THE AVAILABLE OXYTOCIN ?"

This is mindblowing! Now I'm almost sure that a mild opiate antagonist would solve so many problems for people. I just need a degree and a research team and I'm golden. lol

Subgroupings, something me thinks is more like seperate conditions on top of what we are. Moreover why is noone bringing up the deep interests bit? Aren't those frontline physicists we talk about not autistic but also have a deep interest in their field? If noone had deep interest in certain fields then they would never specialize. I really can't believe this deep interests thing because it is speculation on behaviour in stressful environments somehow being the norm.

But usually there interest field is not borderline obsessive. I think we have a tendency to go overboard because it's like an endoaddiction to our own endorphins and being deprived is like constant withdrawal to a minor degree. I believe the subset of those with special interests should be classed as having a dysfunction of endomorphine allotment as a physiological diagnosis. Spectrum diagnoses as a whole should be postulated based on the neuro dysfunctions which can be observable but not on the subjective. It would allow for a better assessment and treatment procedure.