Thinking of getting vaccinated?

[TheDemonLord]

I don't think you would.

In fact, I think your fear of being proven wrong is greater than your fear of measles or unvaccinated people.

In numerous debates (such as Monsantano and Glycol etc.) I've always advocated for proper science to be done.

What you've got at the moment isn't anything even approaching proper science.

You've got a population wide scenario that refutes your underlying premise (MMR > Autism). A point which you steadfastly refuse to accept or address - funny that.

You've got a theory which firstly needs far more research done - because they can't seem to decide whether the rate of this condition amongst people with ASD is ~7% or ~80% (bit of a difference).

Then you've got to factor in that IF this is a causal factor, then ANY pathogen can aggravate the underlying pre-existing condition, not just attenuated vaccines - which makes the whole exercise a moot point, since children at that age WILL encounter pathogens.

When that is factored in, IF this research is accurate (a single 'possible', 'maybe', 'could' case mind) then it doesn't actually provide any reason not to vaccinate. Since any pathogen can trigger it, and exposure to pathogen is a 1 in 1 chance, may as well vaccinate and be protected from serious injury and death than not vaccinate.

Remembering - that was the conclusion of the Dr you cited - funny how you ignore that part and the parts where he ridiculed Wakefield and Greer - would you like some cream with all those Cherries you are picking?

As for Fear of Measles or Unvaccinated people - it's not Fear, it's pointing out the realities of a highly virulent, potentially fatal disease that with a proper vaccination schedule can have the fatality rate reduced to 0 and stay at 0 for over a Decade. When people stop vaccinating, children start dying - it's as simple as that.

[Katman]

As for Fear of Measles or Unvaccinated people - it's not Fear, it's pointing out the realities of a highly virulent, potentially fatal disease that with a proper vaccination schedule can have the fatality rate reduced to 0 and stay at 0 for over a Decade. When people stop vaccinating, children start dying - it's as simple as that.

And just to further rot your socks, have you noticed the thread view count?

I found myself wondering whether it was just you, me and the Berk throwing shit at each other so I took note of the number.

The thread has had over 3000 views in just under a week.

So while we don't know the actual opinion of those shy guests that appear at the bottom of the page it certainly appears that the importance of the topic has a far greater scope than just us three.

[Katman]

Maybe?

That doesn't sound very scientific or factual...

I've never claimed to be a geneticist.

I'm just exercising my brain.

You should try it some time.

[TheDemonLord]

And just to further rot your socks, have you noticed the thread view count?

I found myself wondering whether it was just you, me and the Berk throwing shit at each other so I took note of the number.

The thread has had over 3000 views in just under a week.

So while we don't know the actual opinion of those shy guests that appear at the bottom of the page it certainly appears that the importance of the topic has a far greater scope than just us three.

I've never noticed the thread view count - I'm not the kind of person that needs that sort of psychological validation...

[Katman]

I've never noticed the thread view count - I'm not the kind of person that needs that sort of psychological validation...

You should probably start with a psychological evaluation.

Wait, that's right - you've been there already, haven't you?

[TheDemonLord]

You should probably start with a psychological evaluation.

Wait, that's right - you've been there already, haven't you?

Nope.

Any more unfounded bullshit about me you'd like to sling out?

[Katman]

Nope.

Really? Did you diagnose your 'condition' yourself, did you?

[husaberg]

I've never claimed to be a geneticist.

I'm just exercising my brain.
.

You often claim to know more than scientists doctors and medical researchers, that not exercise, That's your narcissism completely overstepping your complete lack of ability.
But seeing as you claimed to be interested in Autism and you mention it practically every page, plus your keen interest in cannabis It's rather odd that you don't want to talk about how cannabis might have a role in causing Autism.
Its like you keep trying to change the subject away from it.

Maybe you could also post why it is if the mum smokes Dope and cigarettes during pregnancy she is twice as likely to have an autistic child. than if she just smoke cigarettes.
Also why The Royal College of Psychiatrists (RCP) say there is “growing evidence” that people with serious mental illnesses, like depression and psychosis, are more likely to use cannabis.
In addition they say using the drug regularly appears to double the risk of developing a psychotic episode or long-term schizophrenia.
The RCP also maintains that there is a “clear link” to cannabis use and later mental health issues where someone has a genetic vulnerability.
But wait theres more
Over the course of two years, Dr. Lucy Troup studied the long-term effects of 70 participants who either smoked cannabis, smoked casually, or smoked chronically, according to self-reported data. The study took place in three parts: an implicit emotion test, an explicit emotion text, and an empathy test, where volunteers were asked to view a facial emotion—positive, neutral, or negative—and were rated on their ability to empathize. One of the most surprising results was that cannabis users generally had lower empathy ratings than the control group.
This result has opened up questions around weed and autism, though this current study has not looked directly at the link between the two. "I've been approached by a number of researchers who are very interested in the use of cannabis to treat autism and if the two are related or causal," Dr. Troup says. "We found that when you ask a cannabis user to think about other people's emotions and relate to them, it's harder for them. That inability to empathize would be a parallel to autistic-like behaviors.
Additionally, Dr. Troup also asked participants to undergo an implicit emotional task. Both the control group of non-smokers and the cannabis users were hooked up to an electroencephalogram (EEG) while they were shown faces with positive, neutral, and negative facial expressions, but asked to focus on the sex of the face displayed. Later they were asked to recall the emotions they were shown, and the cannabis users faired much worse with this task than non-cannabis users. From these results, Dr. Troup infers that weed inhibits a person's ability to intuitively identify emotions when they're not explicitly focusing on them.
Increased use of tetrahydrocannabinol (THC) during childbearing years

In utero exposure to drugs that interact with neural pathways has been implicated as an important risk factor for ASD. Cannabis/ tetrahydrocannabinol (THC) is the most widely used psychotropic drug; its use has increased substantially over the past 20 years; moreover, more recent formulations of the drug display enhanced potency due to changes in preparation methods [17]. Currently, cannabis use during pregnancy is estimated at 10%. Recent studies by Passey et al. [18] and Shabani et al. [19] have shown that neural deficits can result from in utero cannabis exposure. Moreover, Siniscalco et al. [20] have suggested that the endocannabinoid (EC) system may play an important role in the integrated IS/CNS developmental pathway that is dysregulated in autism. Their research has shown that the cannabinoid receptor type 2(CBR2) signal pathway is upregulated in peripheral blood mononuclear cells (PBMCs) from children with ASD. This finding raises the possibility that the endocannabinoid (EC) system may be associated with ASD. In addition, the authors found reduced levels of bone marrow differentiated macrophages (BMDCs) in children with ASD that may be linked to altered CBR-2 levels.

Endogenous cannabinoids bind to type-1 cannabinoid receptors in the central nervous system (CNS) to guide neural pattern formation and network connectivity in the developing brain. Research by Cutando et al. provides evidence that THC binding of EC-1 receptors as a consequence of subchronic cannabis exposure may affect these signal pathways, at least in part, by activating microglial cells important to neural function [21]. Similar patterns of cerebellar microglial activation have been documented in the brains of autistic children, suggesting similar pathways may be involved. Tortoriello et al. [22] have recently determined that THC affects EC-1 receptor signaling in the developing fetal brain by altering fetal cortical circuitry, further implicating THC as a potential cause of autism.
Researchers from Georgetown University Medical Center combed through papers studying cannabinoids and their effect on human embryos, using mostly animal models published between 1975 and 2015. They found that Tetrahydrocannabinol or THC, the active ingredient in marijuana, can cross the placenta thus exposing the fetus to the chemical.

“We know from limited human studies that use of marijuana in early pregnancy is associated with many of the same risks as tobacco, including miscarriage, birth defects, developmental delays and learning disabilities, but animal research suggests the potential for many more developmental issues linked with the drug
Cannabinoids can affect the use of folic acid, which is important for normal growth and development of the placenta and the embryo. A deficiency in folic acid can cause low birth weight, increase the risk of spontaneous abortion and neural tube defects like spina bifida.

Researchers also found that THC levels in marijuana that is smoked has increased 25-fold since 1970. The studies, however, did not analyze the harmful effects of smoking marijuana in the animals.
https://www.medicaldaily.com/marijua...sorders-399684
https://broadly.vice.com/en_us/artic...-like-behavior
https://www.omicsonline.org/open-acc....php?aid=68552

[Katman]

Its like you keep trying to change the subject away from it.

Go back and read post #4627 again - carefully this time.

(Sound out the words if it helps).

[husaberg]

Go back and read post #4627 again - carefully this time.

(Sound out the words if it helps).

If drug use by a pregnant mother is a factor it usually manifests in a child who shows compromised health and retarded development from birth.

It doesn't explain the incidence of children who are developing normally but show almost immediate regression following vaccination.

It sounds like another one of your bullshit 'girls receive far more vaccines than boys' claims.

(And your 'pregnant mothers receive flu vaccines' observation does nothing to discount the possibility that the flu vaccine could adversely affect the unborn child).

Lets see i did answer all of what you said but seeing as you think you know better here is a doctors opinion
But first children with ASD are not crack babies or premature babbies they suffer a complex not well understood neuological issue that doent allow them to disseminate complex feelings or emotions or display or interact with others in a socially acceptable manner.
None of these are going to be easy to diagnoses as a two year old if you had children you would understand that.

At present, autism can’t be reliably diagnosed until around 2 years of age. However, parents often notice symptoms before then. In fact, analysis of videotapes from children’s first-birthday parties shows that signs of autism are already present for many children at that age, even when parents don’t become concerned until months or years later.
Is it possible that autism starts even earlier? Research tells us “yes.”
In most medical conditions, the underlying processes are triggered before their signs and symptoms become obvious. Consider arthritis. The joints are breaking down and inflammation is setting in years before the aches and pains appear. In dyslexia (reading disability), the symptoms aren’t obvious until a child starts learning how to read. But the symptoms are rooted in brain differences that are present much earlier in development.

A similar chain of events occurs in autism. We know that toxic exposures during pregnancy and complications associated with delivery can disrupt brain processes before birth and shortly afterwards. Mutations in the genes associated with autism can affect how the brain develops and functions, starting well before birth.
Even though the outward symptoms of autism may not be apparent immediately after birth, the underlying brain differences are accumulating. Sometimes the brain can compensate to make up for the disrupted processes. Eventually though, if the disruption was sufficiently severe, the compensatory processes are no longer enough, and symptoms emerge.
This may likewise explain many cases of autistic regression, in which a young child seems to be developing normally, only to lose abilities, or regress, into autism. Perhaps the initial disruption in brain development continued worsening. Or perhaps the compensatory processes couldn’t keep up.
Given how complex the brain is, it can be very difficult to correct differences in brain development and function that start so early in life. This is why treatment for autism needs to be so intensive, and why early diagnosis and treatment are so important.
developmental-behavioral pediatrician Paul Wang, Senior vice president for medical research.

Understand the Changeable First Year
As for autism, studies demonstrate that behavioral signs can begin to emerge as early as 6 to 12 months. However, most professionals who specialize in diagnosing the disorder won’t attempt to make a definite diagnosis until 18 months. This is because autism symptoms can continue to emerge – or fade away – until around 24 months. At that time, we say that an autism diagnosis tends to become “stable.”

To illustrate what I mean, consider the example of a toddler who is meeting all his or her developmental milestones at 18 months, but then begins to lose skills, or “regress.” In other words, autism can’t be ruled out at 18 months. Conversely some babies show early signs and delays, but than catch up with their peers by 24 months.

Recognize the Range
That said, some children can be diagnosed earlier than 24 months. I once saw a 14-month-old boy who wasn’t babbling, making eye contact or engaging in social games. He played only in a highly repetitive fashion. By the time he was 18 months old, his autism diagnosis was very clear, and he responded well to early intervention.

It’s also important to remember that many high-functioning children with autism aren’t diagnosed until they enter school and start struggling socially.

https://www.autismspeaks.org/expert-...m-be-diagnosed
Lauren Elder, PhD, Autism Speaks former assistant director of dissemination science

Autism represents an unusual pattern of development beginning in infancy or the toddler years and defined by deficits in 3 areas: reciprocal social interaction, communication, and restricted and repetitive behaviors.1,2 While parents typically report concerns in the first year of life,3 many children do not receive diagnoses until much later. Several studies have suggested that diagnoses of autism made at age 2 years are stable through age 3 years,4-7 and diagnoses made by age 5 years are stable up to late adolescence.8 A recent study reported relatively good diagnostic stability but limited continuity in symptom severity to age 7 years for children given autism diagnoses at age 2 years.9

Several intervention projects reported diagnostic changes and extraordinary levels of improvement in a substantial minority of young children with autism.10,11 Other reports found little diagnostic change and fewer marked improvements.12,13 Possible explanations for these conflicting results are diagnostic instability or the lack of age-appropriate diagnostic criteria for very young children. In addition, epidemiological,14 genetic,15 and diagnostic studies16 have extended the conceptualization of autism to include a broader spectrum of disorders that range from autism to potentially milder forms of social deficits, including pervasive developmental disorder not otherwise specified (PDD-NOS),17,18 atypical autism, and Asperger syndrome.19,20 Recently, investigators have begun to ask about the stability for the broader autism spectrum disorder (ASD) as well as for more narrowly defined autism.21

High stability has been found for clinical diagnoses between ages 2 and 3 years when health care professionals interpreted standard criteria for autism.
Catherine Lord, PhD; Susan Risi, PhD; Pamela S. DiLavore, PhD; et al
https://jamanetwork.com/journals/jam...article/209669

Cannabis is strongly linked to autism whether you like it or not.
Your unwillingness to admit that is hilarious, your unwillingness to discuss it further proves you are not interested in Autism, Youre only interests revolve around trolling about vaccines.

So why does the Royal College of Psychiatrists (RCP) say there is “growing evidence” that people with serious mental illnesses, like depression and psychosis, are more likely to use cannabis.
In addition they say using the drug regularly appears to double the risk of developing a psychotic episode or long-term schizophrenia.
The RCP also maintains that there is a “clear link” to cannabis use and later mental health issues where someone has a genetic vulnerability.
But wait theres more
Over the course of two years, Dr. Lucy Troup studied the long-term effects of 70 participants who either smoked cannabis, smoked casually, or smoked chronically, according to self-reported data. The study took place in three parts: an implicit emotion test, an explicit emotion text, and an empathy test, where volunteers were asked to view a facial emotion—positive, neutral, or negative—and were rated on their ability to empathize. One of the most surprising results was that cannabis users generally had lower empathy ratings than the control group.
This result has opened up questions around weed and autism, though this current study has not looked directly at the link between the two. "I've been approached by a number of researchers who are very interested in the use of cannabis to treat autism and if the two are related or causal," Dr. Troup says. "We found that when you ask a cannabis user to think about other people's emotions and relate to them, it's harder for them. That inability to empathize would be a parallel to autistic-like behaviors.
Additionally, Dr. Troup also asked participants to undergo an implicit emotional task. Both the control group of non-smokers and the cannabis users were hooked up to an electroencephalogram (EEG) while they were shown faces with positive, neutral, and negative facial expressions, but asked to focus on the sex of the face displayed. Later they were asked to recall the emotions they were shown, and the cannabis users faired much worse with this task than non-cannabis users. From these results, Dr. Troup infers that weed inhibits a person's ability to intuitively identify emotions when they're not explicitly focusing on them.
Increased use of tetrahydrocannabinol (THC) during childbearing years

In utero exposure to drugs that interact with neural pathways has been implicated as an important risk factor for ASD. Cannabis/ tetrahydrocannabinol (THC) is the most widely used psychotropic drug; its use has increased substantially over the past 20 years; moreover, more recent formulations of the drug display enhanced potency due to changes in preparation methods [17]. Currently, cannabis use during pregnancy is estimated at 10%. Recent studies by Passey et al. [18] and Shabani et al. [19] have shown that neural deficits can result from in utero cannabis exposure. Moreover, Siniscalco et al. [20] have suggested that the endocannabinoid (EC) system may play an important role in the integrated IS/CNS developmental pathway that is dysregulated in autism. Their research has shown that the cannabinoid receptor type 2(CBR2) signal pathway is upregulated in peripheral blood mononuclear cells (PBMCs) from children with ASD. This finding raises the possibility that the endocannabinoid (EC) system may be associated with ASD. In addition, the authors found reduced levels of bone marrow differentiated macrophages (BMDCs) in children with ASD that may be linked to altered CBR-2 levels.

Endogenous cannabinoids bind to type-1 cannabinoid receptors in the central nervous system (CNS) to guide neural pattern formation and network connectivity in the developing brain. Research by Cutando et al. provides evidence that THC binding of EC-1 receptors as a consequence of subchronic cannabis exposure may affect these signal pathways, at least in part, by activating microglial cells important to neural function [21]. Similar patterns of cerebellar microglial activation have been documented in the brains of autistic children, suggesting similar pathways may be involved. Tortoriello et al. [22] have recently determined that THC affects EC-1 receptor signaling in the developing fetal brain by altering fetal cortical circuitry, further implicating THC as a potential cause of autism.
Researchers from Georgetown University Medical Center combed through papers studying cannabinoids and their effect on human embryos, using mostly animal models published between 1975 and 2015. They found that Tetrahydrocannabinol or THC, the active ingredient in marijuana, can cross the placenta thus exposing the fetus to the chemical.

“We know from limited human studies that use of marijuana in early pregnancy is associated with many of the same risks as tobacco, including miscarriage, birth defects, developmental delays and learning disabilities, but animal research suggests the potential for many more developmental issues linked with the drug
Cannabinoids can affect the use of folic acid, which is important for normal growth and development of the placenta and the embryo. A deficiency in folic acid can cause low birth weight, increase the risk of spontaneous abortion and neural tube defects like spina bifida.

Autistic disorders (ADs) are heterogeneous neurodevelopmental disorders arised by the interaction of genes and environmental factors. Dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and non-verbal behaviours are common features of ADs. There are no defined mechanisms of pathogenesis, rendering curative therapy very difficult. Indeed, the treatments for autism presently available can be divided into behavioural, nutritional and medical approaches, although no defined standard approach exists. Autistic children display immune system dysregulation and show an altered immune response of peripheral blood mononuclear cells (PBMCs). In this study, we investigated the involvement of cannabinoid system in PBMCs from autistic children compared to age-matched normal healthy developing controls (age ranging 3-9 years; mean age: 6.06 ± 1.52 vs. 6.14 ± 1.39 in autistic children and healthy subjects, respectively). The mRNA level for cannabinoid receptor type 2 (CB2) was significantly increased in AD-PBMCs as compared to healthy subjects (mean ± SE of arbitrary units: 0.34 ± 0.03 vs. 0.23 ± 0.02 in autistic children and healthy subjects, respectively), whereas CB1 and fatty acid amide hydrolase mRNA levels were unchanged. mRNA levels of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D gene were slightly decreased. Protein levels of CB-2 were also significantly increased in autistic children (mean ± SE of arbitrary units: 33.5 ± 1.32 vs. 6.70 ± 1.25 in autistic children and healthy subjects, respectively). Our data indicate CB2 receptor as potential therapeutic target for the pharmacological management of the autism care.

Children exposed in utero to cannabis present permanent neurobehavioral and cognitive impairments. Psychoactive constituents from Cannabis spp., particularly Δ(9)-tetrahydrocannabinol (THC), bind to cannabinoid receptors in the fetal brain. However, it is unknown whether THC can trigger a cannabinoid receptor-driven molecular cascade to disrupt neuronal specification. Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry. By interrogating the THC-sensitive neuronal proteome we identify Superior Cervical Ganglion 10 (SCG10)/stathmin-2, a microtubule-binding protein in axons, as a substrate of altered neuronal connectivity. We find SCG10 mRNA and protein reduced in the hippocampus of midgestational human cannabis-exposed fetuses, defining SCG10 as the first cannabis-driven molecular effector in the developing cerebrum. CB1 cannabinoid receptor activation recruits c-Jun N-terminal kinases to phosphorylate SCG10, promoting its rapid degradation in situ in motile axons and microtubule stabilization. Thus, THC enables ectopic formation of filopodia and alters axon morphology. These data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis, whose imbalance can limit the computational power of neuronal circuitries in affected offspring.

Researchers also found that THC levels in marijuana that is smoked has increased 25-fold since 1970. The studies, however, did not analyze the harmful effects of smoking marijuana in the animals.

Chronic cannabis exposure can lead to cerebellar dysfunction in humans, but the neurobiological mechanisms involved remain incompletely understood. Here, we found that in mice, subchronic administration of the psychoactive component of cannabis, delta9-tetrahydrocannabinol (THC), activated cerebellar microglia and increased the expression of neuroinflammatory markers, including IL-1β. This neuroinflammatory phenotype correlated with deficits in cerebellar conditioned learning and fine motor coordination. The neuroinflammatory phenotype was readily detectable in the cerebellum of mice with global loss of the CB1 cannabinoid receptor (CB1R, Cb1(-/-) mice) and in mice lacking CB1R in the cerebellar parallel fibers, suggesting that CB1R downregulation in the cerebellar molecular layer plays a key role in THC-induced cerebellar deficits. Expression of CB2 cannabinoid receptor (CB2R) and Il1b mRNA was increased under neuroinflammatory conditions in activated CD11b-positive microglial cells. Furthermore, administration of the immunosuppressant minocycline or an inhibitor of IL-1β receptor signaling prevented the deficits in cerebellar function in Cb1(-/-) and THC-withdrawn mice. Our results suggest that cerebellar microglial activation plays a crucial role in the cerebellar deficits induced by repeated cannabis exposure.

https://www.omicsonline.org/open-acc....php?aid=68552
https://www.ncbi.nlm.nih.gov/pubmed/23934130
https://www.omicsonline.org/open-acc....php?aid=68552
https://www.ncbi.nlm.nih.gov/books/NBK333029/

[Katman]

Your unwillingness to admit that is hilarious, your unwillingness to discuss it further proves you are not interested in Autism, Youre only interests revolve around trolling about vaccines.

And you have the gall to accuse me of changing the subject?

[husaberg]

And you have the gall to accuse me of changing the subject?

You are trying to again.

Go back and read post #4627 again - carefully this time.

(Sound out the words if it helps).

If drug use by a pregnant mother is a factor it usually manifests in a child who shows compromised health and retarded development from birth.

It doesn't explain the incidence of children who are developing normally but show almost immediate regression following vaccination.

It sounds like another one of your bullshit 'girls receive far more vaccines than boys' claims.

(And your 'pregnant mothers receive flu vaccines' observation does nothing to discount the possibility that the flu vaccine could adversely affect the unborn child).

Lets see i did answer all of what you said but seeing as you think you know better here is a doctors opinion
But first children with ASD are not crack babies or premature babbies they suffer a complex not well understood neuological issue that doent allow them to disseminate complex feelings or emotions or display or interact with others in a socially acceptable manner.
None of these are going to be easy to diagnoses as a two year old if you had children you would understand that.

At present, autism can’t be reliably diagnosed until around 2 years of age. However, parents often notice symptoms before then. In fact, analysis of videotapes from children’s first-birthday parties shows that signs of autism are already present for many children at that age, even when parents don’t become concerned until months or years later.
Is it possible that autism starts even earlier? Research tells us “yes.”
In most medical conditions, the underlying processes are triggered before their signs and symptoms become obvious. Consider arthritis. The joints are breaking down and inflammation is setting in years before the aches and pains appear. In dyslexia (reading disability), the symptoms aren’t obvious until a child starts learning how to read. But the symptoms are rooted in brain differences that are present much earlier in development.

A similar chain of events occurs in autism. We know that toxic exposures during pregnancy and complications associated with delivery can disrupt brain processes before birth and shortly afterwards. Mutations in the genes associated with autism can affect how the brain develops and functions, starting well before birth.
Even though the outward symptoms of autism may not be apparent immediately after birth, the underlying brain differences are accumulating. Sometimes the brain can compensate to make up for the disrupted processes. Eventually though, if the disruption was sufficiently severe, the compensatory processes are no longer enough, and symptoms emerge.
This may likewise explain many cases of autistic regression, in which a young child seems to be developing normally, only to lose abilities, or regress, into autism. Perhaps the initial disruption in brain development continued worsening. Or perhaps the compensatory processes couldn’t keep up.
Given how complex the brain is, it can be very difficult to correct differences in brain development and function that start so early in life. This is why treatment for autism needs to be so intensive, and why early diagnosis and treatment are so important.
developmental-behavioral pediatrician Paul Wang, Senior vice president for medical research.

Understand the Changeable First Year
As for autism, studies demonstrate that behavioral signs can begin to emerge as early as 6 to 12 months. However, most professionals who specialize in diagnosing the disorder won’t attempt to make a definite diagnosis until 18 months. This is because autism symptoms can continue to emerge – or fade away – until around 24 months. At that time, we say that an autism diagnosis tends to become “stable.”

To illustrate what I mean, consider the example of a toddler who is meeting all his or her developmental milestones at 18 months, but then begins to lose skills, or “regress.” In other words, autism can’t be ruled out at 18 months. Conversely some babies show early signs and delays, but than catch up with their peers by 24 months.

Recognize the Range
That said, some children can be diagnosed earlier than 24 months. I once saw a 14-month-old boy who wasn’t babbling, making eye contact or engaging in social games. He played only in a highly repetitive fashion. By the time he was 18 months old, his autism diagnosis was very clear, and he responded well to early intervention.

It’s also important to remember that many high-functioning children with autism aren’t diagnosed until they enter school and start struggling socially.

https://www.autismspeaks.org/expert-...m-be-diagnosed
Lauren Elder, PhD, Autism Speaks former assistant director of dissemination science

Autism represents an unusual pattern of development beginning in infancy or the toddler years and defined by deficits in 3 areas: reciprocal social interaction, communication, and restricted and repetitive behaviors.1,2 While parents typically report concerns in the first year of life,3 many children do not receive diagnoses until much later. Several studies have suggested that diagnoses of autism made at age 2 years are stable through age 3 years,4-7 and diagnoses made by age 5 years are stable up to late adolescence.8 A recent study reported relatively good diagnostic stability but limited continuity in symptom severity to age 7 years for children given autism diagnoses at age 2 years.9

Several intervention projects reported diagnostic changes and extraordinary levels of improvement in a substantial minority of young children with autism.10,11 Other reports found little diagnostic change and fewer marked improvements.12,13 Possible explanations for these conflicting results are diagnostic instability or the lack of age-appropriate diagnostic criteria for very young children. In addition, epidemiological,14 genetic,15 and diagnostic studies16 have extended the conceptualization of autism to include a broader spectrum of disorders that range from autism to potentially milder forms of social deficits, including pervasive developmental disorder not otherwise specified (PDD-NOS),17,18 atypical autism, and Asperger syndrome.19,20 Recently, investigators have begun to ask about the stability for the broader autism spectrum disorder (ASD) as well as for more narrowly defined autism.21

High stability has been found for clinical diagnoses between ages 2 and 3 years when health care professionals interpreted standard criteria for autism.
Catherine Lord, PhD; Susan Risi, PhD; Pamela S. DiLavore, PhD; et al
https://jamanetwork.com/journals/jam...article/209669

Cannabis is strongly linked to autism whether you like it or not.
Your unwillingness to admit that is hilarious, your unwillingness to discuss it further proves you are not interested in Autism, Youre only interests revolve around trolling about vaccines.

So why does the Royal College of Psychiatrists (RCP) say there is “growing evidence” that people with serious mental illnesses, like depression and psychosis, are more likely to use cannabis.
In addition they say using the drug regularly appears to double the risk of developing a psychotic episode or long-term schizophrenia.
The RCP also maintains that there is a “clear link” to cannabis use and later mental health issues where someone has a genetic vulnerability.
But wait theres more
Over the course of two years, Dr. Lucy Troup studied the long-term effects of 70 participants who either smoked cannabis, smoked casually, or smoked chronically, according to self-reported data. The study took place in three parts: an implicit emotion test, an explicit emotion text, and an empathy test, where volunteers were asked to view a facial emotion—positive, neutral, or negative—and were rated on their ability to empathize. One of the most surprising results was that cannabis users generally had lower empathy ratings than the control group.
This result has opened up questions around weed and autism, though this current study has not looked directly at the link between the two. "I've been approached by a number of researchers who are very interested in the use of cannabis to treat autism and if the two are related or causal," Dr. Troup says. "We found that when you ask a cannabis user to think about other people's emotions and relate to them, it's harder for them. That inability to empathize would be a parallel to autistic-like behaviors.
Additionally, Dr. Troup also asked participants to undergo an implicit emotional task. Both the control group of non-smokers and the cannabis users were hooked up to an electroencephalogram (EEG) while they were shown faces with positive, neutral, and negative facial expressions, but asked to focus on the sex of the face displayed. Later they were asked to recall the emotions they were shown, and the cannabis users faired much worse with this task than non-cannabis users. From these results, Dr. Troup infers that weed inhibits a person's ability to intuitively identify emotions when they're not explicitly focusing on them.
Increased use of tetrahydrocannabinol (THC) during childbearing years

In utero exposure to drugs that interact with neural pathways has been implicated as an important risk factor for ASD. Cannabis/ tetrahydrocannabinol (THC) is the most widely used psychotropic drug; its use has increased substantially over the past 20 years; moreover, more recent formulations of the drug display enhanced potency due to changes in preparation methods [17]. Currently, cannabis use during pregnancy is estimated at 10%. Recent studies by Passey et al. [18] and Shabani et al. [19] have shown that neural deficits can result from in utero cannabis exposure. Moreover, Siniscalco et al. [20] have suggested that the endocannabinoid (EC) system may play an important role in the integrated IS/CNS developmental pathway that is dysregulated in autism. Their research has shown that the cannabinoid receptor type 2(CBR2) signal pathway is upregulated in peripheral blood mononuclear cells (PBMCs) from children with ASD. This finding raises the possibility that the endocannabinoid (EC) system may be associated with ASD. In addition, the authors found reduced levels of bone marrow differentiated macrophages (BMDCs) in children with ASD that may be linked to altered CBR-2 levels.

Endogenous cannabinoids bind to type-1 cannabinoid receptors in the central nervous system (CNS) to guide neural pattern formation and network connectivity in the developing brain. Research by Cutando et al. provides evidence that THC binding of EC-1 receptors as a consequence of subchronic cannabis exposure may affect these signal pathways, at least in part, by activating microglial cells important to neural function [21]. Similar patterns of cerebellar microglial activation have been documented in the brains of autistic children, suggesting similar pathways may be involved. Tortoriello et al. [22] have recently determined that THC affects EC-1 receptor signaling in the developing fetal brain by altering fetal cortical circuitry, further implicating THC as a potential cause of autism.
Researchers from Georgetown University Medical Center combed through papers studying cannabinoids and their effect on human embryos, using mostly animal models published between 1975 and 2015. They found that Tetrahydrocannabinol or THC, the active ingredient in marijuana, can cross the placenta thus exposing the fetus to the chemical.

“We know from limited human studies that use of marijuana in early pregnancy is associated with many of the same risks as tobacco, including miscarriage, birth defects, developmental delays and learning disabilities, but animal research suggests the potential for many more developmental issues linked with the drug
Cannabinoids can affect the use of folic acid, which is important for normal growth and development of the placenta and the embryo. A deficiency in folic acid can cause low birth weight, increase the risk of spontaneous abortion and neural tube defects like spina bifida.

Autistic disorders (ADs) are heterogeneous neurodevelopmental disorders arised by the interaction of genes and environmental factors. Dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and non-verbal behaviours are common features of ADs. There are no defined mechanisms of pathogenesis, rendering curative therapy very difficult. Indeed, the treatments for autism presently available can be divided into behavioural, nutritional and medical approaches, although no defined standard approach exists. Autistic children display immune system dysregulation and show an altered immune response of peripheral blood mononuclear cells (PBMCs). In this study, we investigated the involvement of cannabinoid system in PBMCs from autistic children compared to age-matched normal healthy developing controls (age ranging 3-9 years; mean age: 6.06 ± 1.52 vs. 6.14 ± 1.39 in autistic children and healthy subjects, respectively). The mRNA level for cannabinoid receptor type 2 (CB2) was significantly increased in AD-PBMCs as compared to healthy subjects (mean ± SE of arbitrary units: 0.34 ± 0.03 vs. 0.23 ± 0.02 in autistic children and healthy subjects, respectively), whereas CB1 and fatty acid amide hydrolase mRNA levels were unchanged. mRNA levels of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D gene were slightly decreased. Protein levels of CB-2 were also significantly increased in autistic children (mean ± SE of arbitrary units: 33.5 ± 1.32 vs. 6.70 ± 1.25 in autistic children and healthy subjects, respectively). Our data indicate CB2 receptor as potential therapeutic target for the pharmacological management of the autism care.

Children exposed in utero to cannabis present permanent neurobehavioral and cognitive impairments. Psychoactive constituents from Cannabis spp., particularly Δ(9)-tetrahydrocannabinol (THC), bind to cannabinoid receptors in the fetal brain. However, it is unknown whether THC can trigger a cannabinoid receptor-driven molecular cascade to disrupt neuronal specification. Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry. By interrogating the THC-sensitive neuronal proteome we identify Superior Cervical Ganglion 10 (SCG10)/stathmin-2, a microtubule-binding protein in axons, as a substrate of altered neuronal connectivity. We find SCG10 mRNA and protein reduced in the hippocampus of midgestational human cannabis-exposed fetuses, defining SCG10 as the first cannabis-driven molecular effector in the developing cerebrum. CB1 cannabinoid receptor activation recruits c-Jun N-terminal kinases to phosphorylate SCG10, promoting its rapid degradation in situ in motile axons and microtubule stabilization. Thus, THC enables ectopic formation of filopodia and alters axon morphology. These data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis, whose imbalance can limit the computational power of neuronal circuitries in affected offspring.

Researchers also found that THC levels in marijuana that is smoked has increased 25-fold since 1970. The studies, however, did not analyze the harmful effects of smoking marijuana in the animals.

Chronic cannabis exposure can lead to cerebellar dysfunction in humans, but the neurobiological mechanisms involved remain incompletely understood. Here, we found that in mice, subchronic administration of the psychoactive component of cannabis, delta9-tetrahydrocannabinol (THC), activated cerebellar microglia and increased the expression of neuroinflammatory markers, including IL-1β. This neuroinflammatory phenotype correlated with deficits in cerebellar conditioned learning and fine motor coordination. The neuroinflammatory phenotype was readily detectable in the cerebellum of mice with global loss of the CB1 cannabinoid receptor (CB1R, Cb1(-/-) mice) and in mice lacking CB1R in the cerebellar parallel fibers, suggesting that CB1R downregulation in the cerebellar molecular layer plays a key role in THC-induced cerebellar deficits. Expression of CB2 cannabinoid receptor (CB2R) and Il1b mRNA was increased under neuroinflammatory conditions in activated CD11b-positive microglial cells. Furthermore, administration of the immunosuppressant minocycline or an inhibitor of IL-1β receptor signaling prevented the deficits in cerebellar function in Cb1(-/-) and THC-withdrawn mice. Our results suggest that cerebellar microglial activation plays a crucial role in the cerebellar deficits induced by repeated cannabis exposure.

https://www.omicsonline.org/open-acc....php?aid=68552
https://www.ncbi.nlm.nih.gov/pubmed/23934130
https://www.omicsonline.org/open-acc....php?aid=68552
https://www.ncbi.nlm.nih.gov/books/NBK333029/

[TheDemonLord]

Really? Did you diagnose your 'condition' yourself, did you?

The condition I do have, is not and was not diagnosed by a psychologist. Nor by a psychological Evaluation.

So keep it up Katman, it's so nice to see you reveling in your habit of posting innacurate, disproved BS about things you've demonstrably got no clue about.

[F5 Dave]

Will just leave this here.

https://www.stuff.co.nz/national/hea...ill-believe-it

[Katman]

Will just leave this here.

https://www.stuff.co.nz/national/hea...ill-believe-it

6 reported cases in Waikato and 2 in the Bay of Plenty.

Oh my god, the sky's falling.

Chicken fucking little.