Applying Science to Senate Bill No. 269 in Texas | Medical Marijuana Bill 2017

Wording taken From: 85R1145 GCB-F

By:  Menéndez                                                                                                                                            S.B. No. 269

A BILL TO BE ENTITLED

AN ACT

(A)…..

Senate Bill 269 Menendez Texas 2017
Senate Bill 269 Menendez Texas 2017

(The following information cites at least 2 related Scientific or Medical journals as resources citing topics specifically related to the “qualifying” disease, syndrome, or disability. )

cancer,

Cannabis Interaction with Cancer
Cannabis Interaction with Cancer
  • Cannabinoids as therapeutic agents in cancer: current status and future implications

    “The pharmacological importance of cannabinoids has been in study for several years. Cannabinoids comprise of (a) the active compounds of the Cannabis sativa plant, (b) endogenous as well as (c) synthetic cannabinoids. Though cannabinoids are clinically used for anti-palliative effects, recent studies open a promising possibility as anti-cancer agents. They have been shown to possess anti-proliferative and anti-angiogenic effects in vitro as well as in vivo in different cancer models. Cannabinoids regulate key cell signaling pathways that are involved in cell survival, invasion, angiogenesis, metastasis, etc. There is more focus on CB1 and CB2, the two cannabinoid receptors which are activated by most of the cannabinoids. In this review article, we will focus on a broad range of cannabinoids, their receptor dependent and receptor independent functional roles against various cancer types with respect to growth, metastasis, energy metabolism, immune environment, stemness and future perspectives in exploring new possible therapeutic opportunities.”
    Cited by 45

  • [HTML] Behavioral analysis of marijuana effects on food intake in humans RW Foltin, JV Brady, MW Fischman – Pharmacology Biochemistry and …, 1986 – Elsevier… Keywords. Marijuana; THC; Cannabis; Food intake; Eating; Humans. References. 1. EL Abel; Effects of marihuana on the solution of anagrams, memory and appetite. … CT Tart; Marijuana intoxication: Common experiences. Nature, 226 (1970), pp. 701–704.
    Cited by 163
  • [HTML] Δ9‐Tetrahydrocannabinol induces apoptosis in human prostate PC‐3 cells via a receptor‐independent mechanismL Ruiz, A Miguel, I Dı́az-Laviada – FEBS letters, 1999 – Abstract. The effect of Δ 9-tetrahydrocannabinol (THC), the major psycho-active component of marijuana, in human prostate cancer cells PC-3 was investigated. THC caused apoptosis in a dose-dependent manner.
    Cited by 127
  • [PDF] Marijuana smoking and head and neck cancer M Hashibe, DE Ford, ZF Zhang – The Journal of Clinical …, 2002 – Wiley Online Library… It will be of interest to examine the association of THC levels and cancer in epidemiological … DarlingMR, Arendorf TM: Effects of cannabis smoking on oral soft tissues … Sidney S, Quesenberry CPJr, Friedman GD, Tekawa IS: Marijuana use and cancer incidence (California, United …
    Cited by 53

glaucoma,

positive status for human immunodeficiency virus,

acquired immune deficiency syndrome,

hepatitis C,

In conclusion, daily cannabis smoking is significantly associated with fibrosis progression during CHC. Patients with ongoing CHC should be advised to refrain from regular cannabis use. (HEPATOLOGY 2005;.) – Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C Authors Christophe Hézode, Françoise Roudot-Thoraval, Son Nguyen, Pascale Grenard, Boris Julien, Elie-Serge Zafrani, Jean-Michel Pawlostky, Daniel Dhumeaux, Sophie Lotersztajn, Ariane Mallat – First published: 12 May 2005 Full publication history Cited by: 120 articles

amyotrophic lateral sclerosis,

Crohn’s disease,

ulcerative colitis,

agitation of Alzheimer’s disease,

  • [HTML] A molecular link between the active component of marijuana and Alzheimer’s disease pathology

    LM Eubanks, CJ Rogers, AE Beuscher IV… – Molecular …, 2006 – ncbi.nlm.nih.gov
    Abstract Alzheimer’s disease is the leading cause of dementia among the elderly, and with
    the ever-increasing size of this population, cases of Alzheimer’s disease are expected to
    triple over the next 50 years. Consequently, the development of treatments that slow or halt
    Cited by 139
  • [HTML] Alzheimer’s disease; taking the edge off with cannabinoids?

    VA Campbell, A Gowran – British journal of pharmacology, 2007 – Wiley Online Library
    Cannabidiol (CBD) is the principal non-psychoactive component of Cannabis sativa, with Δ 9
    THC inhibits AChE, resulting in enhanced cholinergic transmission and reduced AD, Alzheimer
    disease; AChE, acetylcholinesterase; CB, cannabinoid; CBD, cannabinoid; Δ 9 –THC
    Cited by 106

post-traumatic stress disorder,

autism,

  • The in vitro GcMAF effects on endocannabinoid system transcriptionomics, receptor formation, and cell activity of autism-derived macrophagesDario Siniscalco Email author, JamesJ effrey Bradstreet, Alessandra Cirillo and Nicola Antonucci Journal of Neuroinflammation 2014
    Abstract – Background
    Immune system dysregulation is well-recognized in autism and thought to be part of the etiology of this disorder. The endocannabinoid system is a key regulator of the immune system via the cannabinoid receptor type 2 (CB2R) which is highly expressed on macrophages and microglial cells. We have previously published significant differences in peripheral blood mononuclear cell CB2R gene expression in the autism population. The use of the Gc protein-derived Macrophage Activating Factor (GcMAF), an endogenous glycosylated vitamin D binding protein responsible for macrophage cell activation has demonstrated positive effects in the treatment of autistic children. In this current study, we investigated the in vitro effects of GcMAF treatment on the endocannabinoid system gene expression, as well as cellular activation in blood monocyte-derived macrophages (BMDMs) from autistic patients compared to age-matched healthy developing controls.
  • Endocannabinoid signaling in autism

    B Chakrabarti, A Persico, N Battista, M Maccarrone – Neurotherapeutics, 2015 – Springer

    In the last 25 years a good deal of information has been accumulated on the main components of the “endocannabinoid (eCB) system”, a rather complex ensemble of lipid signals (“endocannabinoids”), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.
    Cited by 3

sickle cell anemia,

  • Identification and functional characterization of brainstem cannabinoid CB2 receptors

    MD Van Sickle, M Duncan, PJ Kingsley… – …, 2005 – science.sciencemag.org
    Abstract The presence and function of CB 2 receptors in central nervous system (CNS)
    neurons are controversial. We report the expression of CB 2 receptor messenger RNA and
    protein localization on brainstem neurons. These functional CB 2 receptors in the brainstem
    Cited by 1190
  • Understanding the causes of problematic pain management in sickle cell disease: evidence that pseudoaddiction plays a more important role than genuine analgesic dependence

    James Elander, PhD'Correspondence information about the author PhD James Elander
    , Joanne Lusher, MSc, David Bevan, FRCP, Paul Telfer, MRCP, Bernice Burton, BSc, RHV

    Department of Psychology (J.E., J.L.), London Metropolitan University; Department of Hematology (D.B.), St George’s Hospital Medical School; Department of Hematology, Oncology and Imaging (P.T.), St. Bart’s and the Royal London School of Medicine and Dentistry; and Sickle Cell and Thalassemia Center (B.B.), Plaistow Hospital, London, United Kingdom

    “All the positive responses involved using cannabis either to help manage pain, to relax, or as an alternative to prescribed analgesics:

    “I’ve used cannabis for about seven years, it helps me to avoid hospital and enables me to stay home during crises.” (Interview 2)

    “My boyfriend smokes a lot [cannabis] and I drink it in tea. It helps with the sickle cell pain, relaxes the muscles and joints.” (Interview 10)

    “Weed does help. If I run out of DF118s [dihydrocodeine], I ask a friend for some weed.” (Interview 23) ”
    Cited by 98

severe fibromyalgia,

spinal cord disease,

  • Treatment of Human Spasticity with Δ9‐Tetrahydrocannabinol

    DJ PETRO, C Ellenberger –

    Abstract: Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P < 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with “tonic spasms.” No benefit was noted in patients with cerebellar disease.
    Cited by 228

  • Activation of the CB 1 cannabinoid receptor protects cultured mouse spinal neurons against excitotoxicity

    ME Abood, G Rizvi, N Sallapudi, SD McAllister – Neuroscience letters, 2001 – Elsevier “We present for the first time evidence that the activation of the CB1 cannabinoid receptor effectively modulates kainate toxicity in primary neuronal cultures prepared from mouse spinal cord. Addition of Δ9-tetrahydrocannabinol to the culture medium attenuated the toxicity produced by kainate. The CB1 receptors were localized to spinal neurons and astrocytes. The neuroprotective effect was blocked with the CB1 receptor antagonist, SR141716A, indicating a receptor-mediated effect.”
    Cited by 121

spinal cord injury,

  • Cannabis effect on spasticity in spinal cord injury.

    J Malec, RF Harvey, JJ Cayner – Archives of Physical Medicine and …, 1982 -“A study was done to examine the perceived effects of cannabis on spasticity of spinal cord injured persons. Data compiled from 43 questionnaires of spinal cord injured persons suggested the following: 1) spinal cord injured persons reported decreased spasticity with marijuana use; 2) present use of marijuana correlated positively with past use; and 3) the person’s reference or peer group contributed significantly to current use. The study suggests the need to examine the relationship between measurable and reported changes in spasticity.”
    Cited by 74
  • A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms

    DT Wade, P Robson, H House, P Makela… – Clinical …, 2003 – Conclusions: Cannabis medicinal extracts can improve neurogenic symptoms unresponsive to standard treatments. Unwanted effects are predictable and generally well tolerated. Larger scale studies are warranted to confirm these findings.
    Cited by 323

traumatic brain injury or

  • Cannabinoids and brain injury: therapeutic implications

    R Mechoulam, D Panikashvili, E Shohami – Trends in molecular medicine, 2002 – Elsevier
    In most of their pharmacological activities, these body constituents parallel the effects
    of Δ 9 –THC, the active constituent of marijuana. The cannabis plant constituent, Δ 9 –THC,
    which is a cannabinoid receptor agonist, is also neuroprotective.
    Cited by 240
  • Endocannabinoids and traumatic brain injury

    R Mechoulam, E Shohami – Molecular neurobiology, 2007 – Springer
    “Moreover, the CB1, CB2, and TRVP1 receptors are expressed on microvascular endothelial cells, and their activation by 2-AG counteracts endothelin (ET-1)-induced cerebral microvascular responses (namely, Ca2+ mobilization and cytoskeleton rearrangement). This suggests that the functional interaction between 2-AG and ET-1 may provide a potential alternative pathway for abrogating ET-1-inducible vasoconstriction after brain injury and play a role in the neuroprotective effects exerted by 2-AG, as a potent vasodilator.”
    Cited by 86

post-concussion syndrome,

  • Mild traumatic brain injury

    GL Iverson, RT Lange – The little black book of neuropsychology, 2011 – Springer
    Non-acute (residual) neurocognitive effects of cannabis use: a meta-analytic study. in Iraq and
    Afghanistan: persistent postconcussive symptoms and posttraumatic stress disorder. Presence
    of postconcussion syndrome symptoms in patients with chronic pain vs mild traumatic
    Cited by 89
  • Long-term outcomes after uncomplicated mild traumatic brain injury: a comparison with trauma controls

    J Ponsford, P Cameron, M Fitzgerald… – Journal of …, 2011 – online.liebertpub.com
    history (excluding psychosis), prior mTBI, and reported alcohol and/or cannabis use were
    screening for 16 axis I DSM-IV disorders and one personality disorder. A controlled prospective
    inception cohort study on the postconcussion syndrome outside the medicolegal context.
    Cited by 131

chronic traumatic encephalopathy,

Parkinson’s disease,

  • Survey on cannabis use in Parkinson’s disease: subjective improvement of motor symptoms

    K Venderová, E Růžička, V Voříšek… – 2004 – An anonymous questionnaire sent to all patients attending the Prague Movement Disorder Centre revealed that 25% of 339 respondents had taken cannabis and 45.9% of these described some form of benefit. © 2004 Movement Disorder Society
    Cited by 75
  • Cannabidiol for the treatment of psychosis in Parkinson’s disease

    AW Zuardi, JAS Crippa, JEC Hallak… – Journal of …, 2009 – “The management of psychosis in Parkinson’s disease (PD) has been considered a great challenge for clinicians and there is a need for new pharmacological intervention. Previously an antipsychotic and neuroprotective effect of Cannabidiol (CBD) has been suggested. Therefore, the aim of the present study was to directly evaluate for the first time, the efficacy, tolerability and safety of CBD on PD patients with psychotic symptoms. This was an open-label pilot study. Six consecutive outpatients (four men and two women) with the diagnosis of PD and who had psychosis for at least 3 months were selected for the study. All patients received CBD in flexible dose (started with an oral dose of 150 mg/day) for 4 weeks, in addition to their usual therapy. The psychotic symptoms evaluated by the Brief Psychiatric Rating Scale and the Parkinson Psychosis Questionnaire showed a significant decrease under CBD treatment. CBD did not worsen the motor function and decreased the total scores of the Unified Parkinson’s Disease Rating Scale. No adverse effect was observed during the treatment. These preliminary data suggest that CBD may be effective, safe and well tolerated for the treatment of the psychosis in PD.
    Cited by 121
  • Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity in vivo and in vitro: relevance to Parkinson’s disease

    I Lastres-Becker, F Molina-Holgado, JA Ramos -2005 – “Cannabinoids have been reported to provide neuroprotection in acute and chronic neurodegeneration. In this study, we examined whether they are also effective against the toxicity caused by 6-hydroxydopamine, both in vivo and in vitro, which may be relevant to Parkinson’s disease (PD)”….”Daily administration of Δ9-tetrahydrocannabinol (Δ9-THC) during these 2 weeks produced a significant waning in the magnitude of these reductions, whereas it failed to affect dopaminergic parameters in the contralateral structures. This effect of Δ9-THC appeared to be irreversible since interruption of the daily administration of this cannabinoid after the 2-week period did not lead to the re-initiation of the 6-hydroxydopamine-induced neurodegeneration. In addition, the fact that the same neuroprotective effect was also produced by cannabidiol (CBD), another plant-derived cannabinoid with negligible affinity for cannabinoid CB1 receptors, suggests that the antioxidant properties of both compounds, which are cannabinoid receptor-independent, might be involved in these in vivo effects, although an alternative might be that the neuroprotection exerted by both compounds might be due to their anti-inflammatory potential. As a second objective, we examined whether cannabinoids also provide neuroprotection against the in vitro toxicity of 6-hydroxydopamine. We found that the non-selective cannabinoid agonist HU-210 increased cell survival in cultures of mouse cerebellar granule cells exposed to this toxin. However, this effect was significantly lesser when the cannabinoid was directly added to neuronal cultures than when these cultures were exposed to conditioned medium obtained from mixed glial cell cultures treated with HU-210, suggesting that the cannabinoid exerted its major protective effect by regulating glial influence to neurons. In summary, our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data indicated that these neuroprotective effects might be due, among others, to the antioxidant properties of certain plant-derived cannabinoids, or exerted through the capability of cannabinoid agonists to modulate glial function, or produced by a combination of both mechanisms.”
    Cited by 225
  • Δ9‐tetrahydrocannabinol (Δ9‐THC) exerts a direct neuroprotective effect in a human cell culture model of Parkinson’s disease

    CB Carroll, ML Zeissler, CO Hanemann… – Neuropathology and …, 2012 – Wiley Online Library
    Parkinson’s disease (PD) is a neurodegenerative condition characterized by loss of dopaminergic
    neurones in the substantia nigra pars compacta with resulting neurochemical imbalance throughout
    the basal ganglia [6]. Cannabinoids modulate neurotransmitter release within the basal ganglia
    Cited by 38

muscular dystrophy, or

Huntington’s disease;

  • Controlled clinical trial of cannabidiol in Huntington’s disease

    P Consroe, J Laguna, J Allender, S Snider… – Pharmacology …, 1991 – Elsevier
    G. Chesher, P. Consroe, R. Musty (Eds.), Marijuana: An international research report. Quantitative
    measurement of delta-9-THC and two major metabolites in physiological specimens kinetics of
    deuterium labelled delta-1-tetrahydrocannabinol in heavy and light cannabis users.
    Cited by 186
  • Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington’s disease

    C Blázquez, A Chiarlone, O Sagredo, T Aguado… – Brain, 2011 – Oxford Univ Press
    type 1 cannabinoid (CB 1 ) receptors, the same receptors targeted by Δ 9 -tetrahydrocannabinol
    (THC), the major active component of marijuana (Gaoni and and Robertson, 2000; Lastres-Becker
    et al., 2002; McCaw et al., 2004) of Huntington’s disease, a devastating
    Cited by 107

(B)  a chronic medical condition that produces, or the treatment of a chronic medical condition that produces:

(i)  cachexia or wasting syndrome;

  • Cancer cachexia and cannabinoids

    RW Gorter – Forschende Komplementärmedizin/Research in …, 1999 – “In 1986, delta-9-tetrahydrocannabinol (THC), the main effective constituent of cannabis, was licensed as an anti-emetic drug in cancer patients receiving chemotherapy. In addition, in clinical studies THC has shown significant stimulation of appetite and increase of body weight in HIV-positive and cancer patients. The appetite- stimulating effect of cannabis itself has also been well documented in many anecdotal cases. There are strong indications that cannabis is better tolerated than THC alone, because cannabis contains several additional cannabinoids, like cannabidiol (CBD), which antagonize the psychotropic actions of THC, but do not inhibit the appetite-stimulating effect. Therefore, we intend to compare the therapeutic effects of whole- plant extracts of cannabis to those of THC (dronabinol) alone in controlled studies.”
    Cited by 39
  • Comparison of Orally Administered Cannabis Extract and Delta-9-Tetrahydrocannabinol in Treating Patients With Cancer-Related Anorexia-Cachexia Syndrome: A Multicenter, Phase III, Randomized, Double-Blind, Placebo-Controlled Clinical Trial From the Cannabis-In-Cachexia-Study-Group

    “Of 289 patients screened, 243 were randomly assigned and 164 (CE, 66 of 95 patients; THC, 65 of 100 patients; and PL, 33 of 48 patients) completed treatment. At baseline, groups were comparable for age (mean, 61 years), sex (54% men), weight loss (32% ≥ 10%), PS (13% ECOG = 2), antineoplastic treatment (50%), appetite (mean VAS score, 31/100 mm), and QOL (mean score, 30/100). Intent-to-treat analysis showed no significant differences between the three arms for appetite, QOL, or cannabinoid-related toxicity. Increased appetite was reported by 73%, 58%, and 69% of patients receiving CE, THC, or PL, respectively. An independent data review board recommended termination of recruitment because of insufficient differences between study arms.

(ii)  severe pain;

(iii)  severe nausea;

(iv)  seizures, including those characteristic of epilepsy; or

  • Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy

    BE Porter, C Jacobson – Epilepsy & Behavior, 2013 – Elsevier
    The 2-year-old patient had experienced intractable seizures for 16 months before The dosages
    of THC contained within those samples were reported to range from 0 information, parents reported
    having their preparations tested at commercial medical cannabis testing facilities.
    Cited by 142
  • The endogenous cannabinoid system regulates seizure frequency and duration in a model of temporal lobe epilepsy

    MJ Wallace, RE Blair, KW Falenski, BR Martin… – … of Pharmacology and …, 2003 – ASPET
    “These data indicate not only anticonvulsant activity of exogenously applied cannabinoids but also suggest that endogenous cannabinoid tone modulates seizure termination and duration through activation of the CB1 receptor. Furthermore, Western blot and immunohistochemical analyses revealed that CB1 receptor protein expression was significantly increased throughout the CA regions of epileptic hippocampi. By demonstrating a role for the endogenous cannabinoid system in regulating seizure activity, these studies define a role for the endogenous cannabinoid system in modulating neuroexcitation and suggest that plasticity of the CB1 receptor occurs with epilepsy.”
    Cited by 252

(v)  severe and persistent muscle spasms, including those characteristic of multiple sclerosis; or

(C)  any other medical condition approved as a debilitating medical condition by department rule or any symptom caused by the treatment of a medical condition that is approved as a debilitating medical condition by department rule.

*Cite count for each article is according to Google Scholar, No information provided here should be considered as Medical Advice or insinuate that cannabis be solely substituted for any current medication. Please contact your physician for any questions concerning the above information.

Information listed above was compiled by Lee West, founder of Good Acts, who advocates for Whole Plant research for medical cannabis.
Contributions include GH Medical for their research on this plant and their public disclosure of research,
Nishi Whiteley who shows the average person how to find relief from chronic illness in her book, My Chronic Relief, and many other authors and researchers who take the time and show their sources.
Texas needs Compassionate relief in the form of Whole Plant Medicine.

 

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