Brian Deer: Wakefield ‘MMR mother’ fabricated injury story

cannabisforautism:

An interesting development in the UK. Many have been wondering how some parents are able to get away with inflicting ineffective and often harmful ‘Biomedical’ procedures? It seems they are not able to get away with it, and it’s only a matter of time before these parents are deal with by the courts of law.

However, while cannabis remains illegal, our legal system is a joke. I can’t feel good about this ruling. I know it will galvanise the anti-vaccine contingent. I know it will be their ‘proof’ that even the UK courts are in on the vaccine conspiracy. Oh, and me too. #shillarmy

Originally posted on Left Brain Right Brain:

Brian Deer, the reporter who broke the story on Andrew Wakefield’s conflicts of interests, has a new story on his website:

Wakefield ‘MMR mother’ fabricated injury story
In a newly-released judgment from England’s Court of Protection, a prominent anti-vaccine campaigner is branded a manipulative liar. Brian Deer reports

The story is quite sad. And while it presents an extreme case, there are themes here which have been seen elsewhere.

A British “mother warrior”, who claimed that the combined measles, mumps and rubella vaccine is responsible for autism, fabricated accounts of injury to her son and persistently lied about his health, a London court has ruled.

The mother, “E”, who cannot be named so as to protect her son’s identity, concocted a story about how he reacted to an MMR shot in January 1991. She said that he became distressed with fever and then lost speech, eye contact and play immediately…

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Hammering Spilled Milk

From Hammering Spilled Milk.

To understand why we must change prohibition, and how we must change it, we must first know why that needs to happen. The answer is quite simple, it is in the numbers. Drug prohibition on a global scale is an exercise in Einstein’s definition of insanity. It is repeating the same procedure over and over while expecting to produce different results. If it didn’t work for the first century then it isn’t likely to start.

Prohibition is not unlike cleaning up spilled milk with a hammer, or putting out a grease fire with a garden hose. Regardless of the amount of effort you invest you will never accomplish those tasks with the stated tools. Continued hammering will only break up your kitchen tiles while milk is distributed farther and wider. Water on a grease fire will only spread it around, increase the surface area of the fuel and make a bigger fire. How long would you hammer spilled milk before you reached for a paper towel? Would you burn your whole house down rather than admitting you were wrong and putting a lid on the pan?

That sounds a bit tongue-in-cheek, but that is precisely what policy makers have been doing for the better part of eight decades, and continues to reinvest further effort and resources in despite past failures. It’s like destroying your own home to avoid the pain of admitting failure. You don’t have to capitulate to the essentially racist and classist motivations of prohibition when initially implemented to agree to the fact that whatever the reasons for it, drug prohibition doesn’t make anything better for anyone.

With military interventions in dozens of nations, drug enforcement in every member nation of the U.N. and millions of people in prison the world around there is no less drug abuse now than there was before prohibition was implemented. There is so much cocaine use in some nations it is measurable in the drinking water supply. After eight decades of open warfare a plant that only grows in a small part of South America it is still present in the water supply of the United Kingdom on the other side of the planet; it makes you think long and hard about just how realistic the goal of drug eradication actually is.

There is a certain point past which a society cannot consume any more drugs, and modern western civilization is at about that threshold. We’re arguably at that stage now, where drug abuse is so common in our society, quite often with the stamp of approval from medical professionals, that the repeal of prohibition laws wouldn’t really have a measurable impact. Are you going to go out tomorrow and take up smoking crack if criminal penalties for possession and distribution were removed? It doesn’t seem likely.

Even assuming we don’t reduce drug dependence by ending prohibition, we still accomplish the goal of harm reduction. Hard drug users are no longer forced to seek their supply from organized crime. Quality and dosage could be controlled, preventing overdoses and other health concerns associated with contaminants in drugs. Revenue could be taken from criminal enterprises and redirected to legitimate and regulated industry which is easier to hold to account. There are two potential options here, both of them result in people using drugs, but only one route gives us measures of control on that situation.

The trouble is that prohibition does not function as prohibition; rather it has become a de facto deregulation of dangerous drugs. The marketplace has not been eliminated, demand has not been measurably curbed, and so we have a multibillion dollar marketplace world-wide which we have absolutely no control over. The idea of unregulated milk on store shelves is unthinkable, that stuff can go bad and make people sick. The idea of unregulated drugs on our streets is a daily reality, and we just accept that without question, continually given empty assurances by our leaders that they are doing something to solve the problem.

They’ve had eight decades now to “do something” about this problem, and thus far all we have is an ocean of blood and a bigger prison population than any point in human history. They’ve done a terrible job! Why do we keep letting them do this crap?

There are risks, and we are right to be cautious about those risks. With every other market we have developed we mitigate those risks by regulating. The old saying “if you outlaw guns then only outlaws will have guns” holds true as much for drugs as it does for firearms. It’s actually easier to make drugs than it is a gun, that’s why there are more rogue meth cooks than rogue gunsmiths. In many cases the same group of people who decry the notion of banning guns are quick to say we must ban certain drugs – how do those thoughts fit in the same head?

This concept is hopelessly broken and not fit for any purpose, and so we have to start to formulate sensible schemes of production and regulation. Drugs are here to stay, they’ve been here since before the point when we had words to label them, and animals will probably get high long after we are dust. We can’t kill the big beast called “drugs”, so what are we going to do with it?

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RE: Would some cannabinoids ameliorate symptoms of autism?

Some (but not all) cannabinoids may partially (but not fully) and reversibly (but not permanently) reduce some (but not all) symptoms of autism for some (but not all) people with some (but probably not all) autism spectrum conditions.

In response to Bou Khalil RWould some cannabinoids ameliorate symptoms of autism,
Eur Child Adolesc Psychiatry. 2012 Apr;21(4):237-8. doi: 10.1007/s00787-012-0255-z. Epub 2012 Feb 17.

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Use of dronabinol (delta-9-THC) in autism


A prospective single-case-study with an early infantile autistic child.

René Kurz, Kurt Blaas. 21 Nov 2010

Abstract

Objective: To evaluate the effectiveness of dronabinol (delta-9-THC) as supplementary therapy in a child with autistic disorder.

Methods: A child who met the DSM-IV (Diagnostic and Statistical Manual of Mental Disorders) criteria for a diagnosis of autistic disorder and who took no other medication during the observation time was included in an open and uncontrolled study. Symptom assessment was performed using the Aberrant Behavior Checklist (ABC) before and after six months of medical treatment.

Result: Compared to baseline, significant improvements were observed for hyperactivity, lethargy, irritability, stereotypy and inappropriate speech at follow-up (p=0.043).

Conclusion: This study showed that the use of dronabinol may be able to reduce the symptoms of autism.

Keywords: early infantile autism, autistic disorder, dronabinol, cannabinoid

Download here: www.cannabis-med.org/data/pdf/en_2010_04_1.pdf

Or read an article about it here.

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Michigan Medical Cannabis for Autism Campaign Update. Call for expert and patient testimony.

Autism Campaign Update

So far three parents that are willing to provide testimony have come forward. Each is utilizing botanical extracts from cannabis successfully in the treatment of their autistic children. Additionally, seven experts from around the country have agreed to provide testimony ranging from specific case reports of their patients to the relative safety of cannabis. This is going to be very difficult for the review panel to deny once we get a new vote. We continue to seek adults suffering from autism that utilize cannabis, as well as those that would like to explore cannabis as a treatment option if they were granted protection under MI law.

Please contact Joe Stone – cannabinoidbasedtherapeutics@gmail.com for information on how to get involved. You can also contact Joe on Facebook.

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The Endocannabinoid System as it Relates to Autism – Joe Stone; Christian Bogner, M.D.

The Endocannabinoid System as it Relates to Autism.

Joe Stone; Christian Bogner, M.D.

The importance of the discovery and continued elucidation of the crucial role that the endocannabinoid system (ECS) plays in human health and disease cannot be understated. Cannabinoid receptors are the most highly expressed of any GPCR. They’re the only ones to play a direct role in virtually every aspect of the human body (CNS and immune systems, throughout the periphery, presynaptic, and postsynaptic). (Alger 2013)

The growing body of data in regards to this aspect of physiology continues to lead to the further elucidation of the physiological basis in a growing number of diseases (including psychiatric) (Pacher 2006). One reason that this is important is because one such pathogenesis is for that of autism (ASD). There are a number of direct correlations between ASD and the ECS. Some will be outlined in this paper.

NL3 Mutations Inhibit Tonic Endocannabinoid Secretions

“Rare mutations in neuroligins and nerexins predispose to autism” (Földy 2013). Neuroligin-3 is the only known protein required for tonic secretion of endocannabinoids that include AEA and 2-AG (Földy 2013). Neuroligin-3 mutations have been shown to inhibit tonic endocannabinoid secretion (Földy 2013). These alterations in endocannabinoid signaling may contribute to autism pathophysiology (Földy 2013, Krueger 2013, Onaivi 2011, Siniscalco 2013). These finding have in part prompted researchers to apply to conduct research with nonhuman primates in order to further elucidate this link (Malcher-Lopes 2013).

Endocannabinoid system deficiencies are suggested to be involved in the pathophysiology of a growing number of diseases (Marco 2012, Russo 2003). Pacher and Pertwee both cover the endocannabinoid system in detail (Pacher 2006, Pertwee 2010). The number of functions that endocannabinoid signaling regulate in the human body is extensive and beyond the scope of this paper (Pertwee 2010). For sake of brevity only a few potentially relevant aspects will be listed:

• “Endocannabinoids are key modulators of synaptic function” (Castillo 2012).

• Tonic secretions of endocannabinoids regulate GI functions (including metabolism) (Di Marzo 2011, Li 2011).

• Endocannabinoids (and exogenous cannabinoids) suppress proliferation and cytokine release (Cencioni 2010).

• Endocannabinoids regulate stress responses, in part via the modulation of the 5-HT system (Haj-Dahmane 2011).

• CB2 is expressed in Purkinje cells (Gong 2006). “In the cerebellar cortex, CB1Rs regulate several forms of synaptic plasticity at synapses onto Purkinje cells, including presynaptically expressed short-term plasticity and, somewhat paradoxically, a postsynaptic form of long-term depression (LTD) (Carey 2011).”

• “CB1 variations modulate the striatal function that underlies the perception of signals of social reward, such as happy faces. This suggests that CB1 is a key element in the molecular architecture of perception of certain basic emotions. This may have implications for understanding neurodevelopmental conditions marked by atypical eye contact and facial emotion processing, such as ASC” (Chakrabarti 2011).

• Additional targets of endocannabinoids (and exogenous cannabinoids), PPARα, PPARγ, and GPR55 expression levels have shown reductions in a valproic acid model of autism in rats (Kerr 2013).

• Endocannabinoids and CB1 agonists increase cerebrocortical blood flow (Iring 2013).

• Endocannabinoids (and exogenous cannabinoids) modulate of “GABA efflux from hippocampal nerve terminals” via CB1 and CB2 receptors (Andó 2012).

• “The expression patterns in malformations of cortical development highlight the role of cannabinoid receptors as mediators of the endocannabinoid signaling and as potential pharmacological targets to modulate neuronal and glial cell function in epileptogenic developmental pathologies” (Zurolo 2010).

• The endocannabinoid signalosome is “a molecular substrate for fragile X syndrome, which might be targeted by therapy” (Jung 2012).

Exogenous cannabinoids from cannabis display similar pharmacological characteristics to that of endogenous cannabinoids (Pertwee 2010). The potential therapeutic value of systemic administration of phytocannabinoids has been suggested in the treatment of a number of diseases with suspected underlying endocannabinoid deficiencies (Russo 2003). Documentation of their safety and clinical efficacy in a variety of treatments continues to grow (Hazekamp 2013). Some similar characteristics include:

• Neurogenesis (Galve-Roperh 2007, Jiang 2005, Avraham 2014, Campos 2013)
• Neuroprotection (Hampson 2003, Lara-Celador 2013, Sanchez 2012)
• Antioxidants (Borges 2013, Pertwee 2010, Hampson 1998, Hampson 2003)
• Neuromodulation (Davis 2007, Lara-Celador 2013, Pertwee 2010, Youssef 2012)
• Anti-inflammatory (Pertwee 2010, Izzo 2009, Nagarkatti 2009, Klein 2005)

Based on their relative safety, the similar pharmacological characteristics to endocannabinoids that are inhibited in ASD, and the significant role those endogenous cannabinoids play in human health, it’s possible that cannabinoids from cannabis could prove therapeutic value in treatments.

Increased Expression of CB2 Receptors Associated with ASD

The second direct link, of possibly equal or greater relevance for treatment, is the upregulation of CB2 receptors in the brains of those with ASD (Siniscalco 2013). This is believed to be part of an endogenous neuroprotective role of the endocannabinoid system:

• “CB2 receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up-regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB2 receptor up-regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB2 receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB2 receptors may represent promising therapeutic agents” (Fernández 2011).

• “CB2 expression is increased by inflammatory stimuli suggests that they may be involved in the pathogenesis and/or in the endogenous response to injury… receptors may be part of the general neuroprotective action of the ECS by decreasing glial reactivity. Neuropathological findings in human brains suggest that the upregulation of CB2 receptors is a common pattern of response against different types of chronic injury of the human CNS. In addition, their selective presence in microglial cells is highly suggestive of an important role in disease-associated neuroinflammatory processes. The antiinflammatory effects triggered by the activation of the CB2 receptor make it an attractive target for the development of novel anti-inflammatory therapies” (Benito 2008).

Given that CB2 is upregulated, and that it’s believed to play a neuroprotective role in the human brain, CB2 activation is believed to be a potential target for treatment of ASD (Siniscalco 2013). Endocannabinoids (AEA, 2-AG) and the most prominent cannabinoids in cannabis (including THC) are CB2 agonists (Izzo 2009).

Elevated Cytokine Levels Associated with ASD

Elevated cytokine levels are associated with ASD (Napolioni 2013). Whether this is a direct result of inhibited tonic secretion of endocannabinoids remains uncertain. However, endocannabinoids (AEA, 2-AG) have been shown to play key roles inhibiting cytokines via CB2 activation (Cencioni 2010, Panikashvili 2006). “Both THC and CBD have been shown to decrease cytokine production” via CB1/CB2 dependent and independent mechanisms (Juknat 2012, Kozela 2010). The majority of cannabinoids are PPAR gamma agonists (Izzo 2009), which have been shown to inhibit cytokine production (Jiang 1998).

Clinically Diagnosing ASD?

A team of researchers recently discovered and patented a process that claims that it’s possible to clinically diagnose ASD, and susceptibility to it, via observation of the degree of modulation that acetaminophen has on endocannabinoid levels (Schultz 2012). However, based of a series of deductions made within their published literature, it appears possible that their work may be somewhat premature.

Botanical Extracts > Dronabinol

Of equal relevance to this issue is the substantial data, including clinical studies, suggesting that the combined administration of CBD along with THC (and possibly other cannabinoids/terpenes present in cannabis) exhibit additive and synergistic effects resulting in greater clinical efficacies when compared to either cannabinoid alone (McPartland 2001, Izzo 2009, Russo 2011). The second most prominent cannabinoid in cannabis is CBD (Gertch 2010). CBD has been shown to inhibit intoxication, sedation, and tachycardia associated with THC (Russo 2006). It’s been shown to increase the clinical efficacy of THC, while adding therapeutic value in its own right (Russo 2006).

The added benefit of additional cannabinoids (and more control via case specifically tailoring ratios) is an important component that sets botanical extracts from cannabis apart from THC (Dronabinol) alone. How can CBD add value to THC treatments?:

• “CBD is demonstrated to antagonize some undesirable effects of THC including intoxication, sedation and tachycardia, while contributing analgesic, anti-emetic, and anti-carcinogenic properties in its own right. In modern clinical trials, this has permitted the administration of higher doses of THC, providing evidence for clinical efficacy and safety for cannabis based extracts in treatment of spasticity, central pain and lower urinary tract symptoms in multiple sclerosis, as well as sleep disturbances, peripheral neuropathic pain, brachial plexus avulsion symptoms, rheumatoid arthritis and intractable cancer pain. Prospects for future application of whole cannabis extracts in neuroprotection, drug dependency, and neoplastic disorders are further examined. The hypothesis that the combination of THC and CBD increases clinical efficacy while reducing adverse events is supported” (Russo 2006).

• “Several studies suggest that CBD is non-toxic in non-transformed cells and does not induce changes on food intake, does not induce catalepsy, does not affect physiological parameters (heart rate, blood pressure and body temperature), does not affect gastrointestinal transit and does not alter psychomotor or psychological functions. Also, chronic use and high doses up to 1,500 mg/day of CBD are reportedly well tolerated in humans” (Machado 2011).

An argument could be made that botanical extracts with CBD present offer safer options for patients, with greater clinical efficacy, when compared to THC (Dronabinol) alone (Russo 2006). CBD offers more than simply increasing the safety and efficacy of THC (Izzo 2009).

• “CBD has been shown to have an inhibitory effect on the inactivation of endocannabinoids (i.e. inhibition of FAAH enzyme), thereby enhancing the action of these endogenous molecules on cannabinoid receptors, which is also noted in certain pathological conditions. CBD acts not only through the endocannabinoid system, but also causes direct or indirect activation of metabotropic receptors for serotonin or adenosine, and can target nuclear receptors of the PPAR family and also ion channels” (Campos 2012).

Here are some of the demonstrated pharmacological characteristics of CBD that may be relevant:

• CB1/CB2 agonist blocker (can inhibit overstimulation of CB1 by THC)
• FAAH inhibition increases endocannabinoid levels (including AEA, 2-AG)
• AEA reuptake inhibitor
• 5-HT1a agonist
• Suppressor of tryptophan degradation
• PPAR alpha and gamma agonist Positive allosteric modulator at glycine receptors
• TRPV1 and TRPV2 agonist
• Adenosine uptake competitive inhibitor
• Antagonist at abnormal-CBD receptor
• Regulator of intracellular Ca 2+ T-type Ca 2+ channel inhibitor (Izzo 2009)

If we accept that tonic secretions of AEA and 2-AG are inhibited via NL3 mutations in ASD (both of which being CB1 and CB2 agonists), then it might be possible to suppose the potential benefits of low doses of THC in treatments as well. This seems especially true when the striking pharmacological similarities between THC and AEA are reviewed (Pertwee 2010). The majority of the research conducted thus far with ASD and cannabinoids has been with THC alone. Dronobinal has indicated potential in a single adolescent case study of autism (Kurz 2010). Does that mean THC along with CBD might offer increased clinical efficacy similar to the way they have been demonstrated to with other conditions (Russo 2006)? It’s possible to review the pharmacological characteristics of THC, but it seems appropriate to leave that for a later date. What might be more beneficial is to review how botanical extracts with specifically tailored ratios of CBD along with THC are currently being utilized by families in MI, and across the country.

Practical Use of Botanical Extracts

How can combinations of cannabinoids be put into practical use by individual families? For our purposes let’s review the anecdotal reports of cannabinoid based treatments currently being utilized in MI (and around the world) for pediatric epilepsy. I think this is a good comparison due to the range and complexity of both conditions. CBD continues to prove its effectiveness in treating many types of epilepsy, but not all (Porter 2013). Anecdotal reports provided in online groups with families that share dosing and other related information to cannabinoid based pediatric epilepsy treatments reveal that in many cases parents (and physicians) find that an increased ratio of THC is required to increase the efficacy of treatment. The range seems to vary significantly from 24:1 to 1:1 (CBD:THC). Some partial explanations for this might include the ability of THC to increase GABAergic transmissions via CB1 activation, its modulation of ion channels, and that it’s a PPAR gamma agonist which is neuroprotective in epilepsy (Stone 2014).

Due to the range of ASD it seems possible that, similar to cannabinoid based epilepsy treatments, varying ratios of cannabinoids (specifically CBD:THC) will prove to have a greater efficacy overall when compared to individual cannabinoid based treatments (like Dronobinal). This concept has been further supported by the research and clinical use of Sativex, a 1:1 (CBD:THC) botanical extract marketed for use in a range of treatments throughout the world (Hazekamp 2013, Russo 2006). The ability to specifically tailor cannabinoid ratios in botanical extracts from cannabis in a case specific manner may prove an even greater efficacy.

In pediatric epilepsy treatments, a first line of action might be a particularly high CBD ratio, at which point an increased ratio of THC is introduced if desired. An individually based case specific approach may also prove beneficial in ASD. Families and physicians should have the legal right to explore these options on an individual basis without fear of prosecution.

Treating Symptoms Associated with ASD

A considerably greater body of data can be gathered in regards to aspects of the involvement (and targeting for treatment) of the endocannabinoid system in a number of the symptoms, and diseases, associated with ASD (in comparison to the pathophysiology of ASD itself):

• G.I. Disorders (Camilleri 2013, Di Sabatino 2011, Wright 2008,)
• Repetitive Behaviors (Casarotto 2010, Deiana 2012, Gomes 2011)
• Seizures (Jones 2012, Porter 2013, van Rijn 2011)
• Sleep Dysfunction (Murillo-Rodriguez 2011, Ware 2010)
• Self Injurious Behavior and Tantrums (Müller-Vahl 2004, Onaivi 2011, Passie 2012)
• Tuberous Sclerosis (Krueger 2013, Shu, Hai-Feng 2013, Zurolo 2010)
• Cerebral Ischemia (Schmidt 2012, Choi 2013, Murikinati 2010, Garcia-Bonilla 2014)
• Depression/Anxiety (Hill 2009, Almeida 2013, Campos 2013, Schier 2012)
• Cachexia (Engeli 2012, Gamage 2012, Marco 2012)

Given the known role of the endocannabinoid system in ASD it seems entirely possible, if not likely, that cannabinoid rich botanical extracts from cannabis can be utilized as useful agents targeting the pathophysiology of ASD, as well as the many debilitating symptoms and conditions associated with it. The wealth of options that cannabis has to offer those that suffer from ASD in MI is not currently legally permitted. We believe that needs to change. But what about the known negative effects associated with THC?

Cannabis – the Lesser of Two Evils?

Acute and chronic administration of THC has been demonstrated to cause mild cognitive deficits related to memory and learning via CB1 activation in healthy brains (Sarne 2011). While this characteristic is not to be downplayed or overlooked, it should be pointed out that low doses of THC also activate preconditioning and postconditioning mechanisms that protect the brain from more sever insults (Sarne 2011). Which has more potential for damage, THC or the slew of other environmental toxicity, oxidative stress, and neuronal insult factors that autistic brains are suggested to be more vulnerable to (Kern 2006)? That answer seems dependent on the severity of the condition, and it’s important to note that we’re only referring to truly debilitating forms of ASD. Equally relevant is that the cognitive deficits are inhibited by CB1 antagonists like CBD (Sarne 2011).

Given the available data if a child has a form of autism that is truly debilitating, and is unresponsive to available treatments, should their family and physician be legally permitted to make the decision as to whether botanical extracts from cannabis may be a viable option for treatment, and the lesser of two evils? We believe that families and physicians should have the legal right to explore these options on an individual basis without fear of prosecution.

Please visit the original document on Scribd for the full citation list.

Available for contact and case specific research: cannabinoidbasedtherapeutics@gmail.com

 

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Mothers Advocating Medical Marijuana for Autism to begin work in next Texas legislative session

Originally posted on Texas Cannabis Report:

A conservative group says it will begin pushing hard for the legalization of marijuana for medical use in Texas, 1200 WOAI’s Berit Mason reports.

Mothers Advocating Medical Marijuana for Autism, or MAMMA, says the group will be urging lawmakers in the sessions that begins in January to push for revisions in state law to allow marijuana to be used as a treatment, especially for sick children who suffer from the seizures associated with autism. Read more

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