Thinking of getting vaccinated?

[husaberg]

Will just leave this here.

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

With all due respect Dave i think steveo plus everyone in the KB conspiracy crew struggle to See how that Joel Rindelaub, Ph.D. and Research Fellow at the University of Auckland's medical experience could ever stack up against Taupo Steves B2 in School Cert English and Boyscout badge in First aid.
In all seriousness though what you need to remember is Taupo Steve gets a kick out of spreading false information and a hard-on that he might cause pain and suffering on a innocent child and their family.
While some might suggest the reason is, hes a sad little parasitic narcissistic troll stuck in a pathetic life who will never understand unconditional love. I wouldn't be that mean, i would just say hes an EGG

I would suggest suggest a far simpler way is to suggest to get Katman to stut up that in some instances where there is not a genetic reason for Autism research suggests there may be a tie in with Cannabis or some other chemical use or other substances from a pollutent may that have interfered with the receptors or their development.

[WALRUS]

Will just leave this here.

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

I'm assuming that has been posted in this thread at least 30 times from multiple sources but has been ignored as it does every other time its brought up

[Katman]

I'm assuming that has been posted in this thread at least 30 times from multiple sources but has been ignored as it does every other time its brought up

Wake me up if someone dies.

[Katman]

With all due respect Dave i think steveo plus everyone in the KB conspiracy crew struggle to See how that Joel Rindelaub, Ph.D. and Research Fellow at the University of Auckland's medical experience could ever stack up against Taupo Steves B2 in School Cert English and Boyscout badge in First aid.
In all seriousness though what you need to remember is Taupo Steve gets a kick out of spreading false information and a hard-on that he might cause pain and suffering on a innocent child and their family.
While some might suggest the reason is hes a sad little parasitic narcissistic troll stuck in a pathetic life who will never understand unconditional love. I wouldn't be that mean, i would just say hes an EGG

I would suggest suggest a far simpler way is to suggest to get Katman to stut up that in some instances where there is not a genetic reason for Autism research suggests there may be a tie in with Cannabis or some other chemical use or other substances from a pollutent may that have interfered with the receptors or their development.

Cool story bro moron.

[Katman]

Not as good a story aa how your fav herb that you think is harmless might be the "smoking gun" for Autism.

You should probably copy and paste that post again - in case anyone missed it the first six times.

[husaberg]

You should probably copy and paste that post again - in case anyone missed it the first six times.

I am pretty Sure anyone who bothered to follow thos thread has noticed you don't respond to real science, understand maths or comprehend reality.
Or it seems discuss the links between Your beloved herb and ASD.
Unless of course i got it all you are going to discuss it now?
ps Control V is all it takes to paste if you know anything about Computers
But our unwillingness to admit that there is a link is hilarious, your unwillingness to discuss it further proves you are not interested in Autism, You're 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.

Cannabis alters human DNA

A new study published by University of Leicester researchers has found "convincing evidence" that cannabis smoke damages DNA in ways that could potentially increase the risk of cancer development in humans.
Using a newly developed highly sensitive liquid chromatography-tandem mass spectrometry method, the University of Leicester scientists found clear indication that cannabis smoke damages DNA, under laboratory conditions.https://medicalxpress.com/news/2009-...human-dna.html

Genetic effects of marijuana.
Zimmerman S1, Zimmerman AM. ( not the same dude Katspam posted thats AW Zimmerman)
Marijuana and its constitutive cannabinoids--tetrahydrocannabinol (THC), cannabinol (CBN), and cannabidiol (CBD)--markedly affect mammalian cells. Cytogenetic studies have revealed that cannabinoids induce chromosome aberrations in both in vivo and in vitro studies. These aberrations include chromosomal breaks, deletions, translocations, errors in chromosomal segregation, and hypoploidy, and are due to the clastogenic action of cannabinoids or to cannabinoid-induced disruption of mitotic events or both. Conflicting reports of the cytogenetic effects of cannabinoids are partially explained by the different experimental protocols, cell types, and animals used by investigators. Cannabinoids also suppress macromolecular synthesis (DNA, RNA, and protein) as well as reduce the level of histone gene expression. In general these studies show that cannabinoids are detrimental to the health of an individual.https://www.ncbi.nlm.nih.gov/pubmed/2174024

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]

ps Control V is all it takes to paste if you know anything about Computers

You should post it again - just to be sure everyone's noticed you.

[husaberg]

You should post it again - just to be sure everyone's noticed i just wont discuss the cannabis autism link.

okay seeing you asked nicely
I am pretty Sure anyone who bothered to follow thos thread has noticed you don't respond to real science, understand maths or comprehend reality.
Or it seems discuss the links between Your beloved herb and ASD.
Unless of course i got it all you are going to discuss it now?
ps Control V is all it takes to paste if you know anything about Computers
But our unwillingness to admit that there is a link is hilarious, your unwillingness to discuss it further proves you are not interested in Autism, You're 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.

Cannabis alters human DNA

A new study published by University of Leicester researchers has found "convincing evidence" that cannabis smoke damages DNA in ways that could potentially increase the risk of cancer development in humans.
Using a newly developed highly sensitive liquid chromatography-tandem mass spectrometry method, the University of Leicester scientists found clear indication that cannabis smoke damages DNA, under laboratory conditions.https://medicalxpress.com/news/2009-...human-dna.html

Genetic effects of marijuana.
Zimmerman S1, Zimmerman AM. ( not the same dude Katspam posted thats AW Zimmerman)
Marijuana and its constitutive cannabinoids--tetrahydrocannabinol (THC), cannabinol (CBN), and cannabidiol (CBD)--markedly affect mammalian cells. Cytogenetic studies have revealed that cannabinoids induce chromosome aberrations in both in vivo and in vitro studies. These aberrations include chromosomal breaks, deletions, translocations, errors in chromosomal segregation, and hypoploidy, and are due to the clastogenic action of cannabinoids or to cannabinoid-induced disruption of mitotic events or both. Conflicting reports of the cytogenetic effects of cannabinoids are partially explained by the different experimental protocols, cell types, and animals used by investigators. Cannabinoids also suppress macromolecular synthesis (DNA, RNA, and protein) as well as reduce the level of histone gene expression. In general these studies show that cannabinoids are detrimental to the health of an individual.https://www.ncbi.nlm.nih.gov/pubmed/2174024

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/

[F5 Dave]

Time to unsubscribe again. See you in 6 months.

[TheDemonLord]

As much I'm loathe to cite it as a source:

http://www.msn.com/en-nz/news/world/...dg4K&ocid=iehp

This raises a very interesting possibility of a precedent - If an individually can be charged with knowingly infected people.

[Katman]

As much I'm loathe to cite it as a source:

http://www.msn.com/en-nz/news/world/...dg4K&ocid=iehp

This raises a very interesting possibility of a precedent - If an individually can be charged with knowingly infected people.

Well the answer's simple.

They should just mandate to vaccinate that whole tribe.

Those dirty savages could have passed any manner of germs onto that poor missionary.

[husaberg]

Well the answer's simple.

So what about the links between Cannabis use and Autism.
Are you ready to discuss that or are you burying your head in the sand of some dry riverbed in mexico

[TheDemonLord]

Well the answer's simple.

They should just mandate to vaccinate that whole tribe.

Those dirty savages could have passed any manner of germs onto that poor missionary.

actually - I'm more interested if this does go to court as to what legal precedents it may set.

[Katman]

actually - I'm more interested if this does go to court as to what legal precedents it may set.

Don't go getting your hopes too high.

[TheDemonLord]

Don't go getting your hopes too high.

Who said anything about Hopes? Eitherway (if it goes to court) a precedent of sorts will be set - and that will be interesting.