Texas MMJ: Treating Neurodegenerative Diseases with Medical Marijuana

Treating Neurodegenerative Diseases With Medical Marijuana

  • Medical marijuana be used to treat neurodegenerative diseases in Texas

  • Cannabis effective at relieving the symptoms of neurodegenerative diseases

  • Incurable neurodegenerative conditions causes and treatments

  • How Texans with conditions such as ALS, Alzheimer’s, Parkinson’s, and Huntington’s can get cannabis medicine

Incurable neurodegenerative diseases are now among the list of qualifying conditions to get a Texas medical marijuana card, or more of a TX MMJ doctors certification in the form of a prescription. Dealing with neurodegenerative conditions is hard enough without the serious side effects that come with traditional drugs. However, the good news is that patients in Texas are finding a measure of relief with medical marijuana.

So, what are neurodegenerative diseases? And how does cannabis work to reduce the neurodegenerative disease symptom? Let’s look at this more closely.

What Qualifies As A Neurodegenerative Disease Under Texas Medical Marijuana Rules?

Neurodegenerative diseases are diverse in their complexity. Nature.com tells us that these conditions are “characterized by the progressive degeneration of the structure and function of the central nervous system or peripheral nervous system.”  Neurodegeneration results from the breaking down and eventual death of neurons, causing a progressive loss of function. Neurodegeneration can affect the entire neuronal circuitry system on a molecular and/or a systemic level and cause any of the following symptoms:
  • Seizures

  • Paralysis

  • Muscle weakness

  • Pain

  • Loss of sensation

Neurodegenerative Diseases

Neurodegenerative diseases that qualify Texas residents for a medical marijuana card include Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, ALS, and Batten disease.  There are no known cures for these horrendous conditions at this time. Neurodegenerative conditions are often also accompanied by psychological symptoms such as: 
  • Memory loss

  • Apathy

  • Anxiety

  • Depression

  • Agitation

  • Loss of inhibition

  • Mood swings

  • Difficulty reading and writing

  • Decreased alertness

  • Poor cognitive abilities

Thus far, studies have failed to yield a specific reason for these conditions, as the causes may vary. Genetic anomalies, congenital defects, infections, malnutrition, environmental health issues, brain, spinal cord and nerve injury, environmental sensitivities, and gluten intolerance are believed to be some of the causes hastening the onset of neurological diseases. There are numerous similarities between the myriad neurodegenerative conditions such as atypical protein assemblies.

Alzheimer's disease

The brain of an Alzheimer’s patient is considerably smaller than the brain of a healthy individual. In fact, the brain shrinks down to as little as one-third its normal size as the disease progresses. In Alzheimer’s patients, beta-amyloids designed to encourage neuron growth, survival, and repair are fragmented by enzymes that can re-assemble into senile and amyloid plaque deposits. These deposits kill brain cells causing severe dementia, memory loss, and agitation, ultimately resulting in death. 

More on Medical Marijuana for Alzheimer’s Disease in Texas

Parkinson's disease

The second most prevalent neurodegenerative disease is Parkinson’s. The symptoms manifested are generally postural instability, tremors, and rigidity. There is no known cause for what appears to be the death of neurons in the midbrain. Defects in protein transport mechanisms may play a significant role in the onset of Parkinson’s. Genetic mutations may play a role in the development of Parkinson’s disease, however the highest risk factor is old age.

Huntington's disease

Huntington’s disease is a neurodegenerative condition caused by mutations in the Huntington gene. The condition is characterized by a loss of particular sets of neurons. This degeneration causes a weakening of signals that modulate and initiate motion resulting in dramatically impaired motor function 

ALS

Amyotrophic lateral sclerosis is characterized by the degeneration of selectively targeted motor neurons. Studies have indicated that some patients have a chemical imbalance and high levels of glutamate (a chemical messenger) near the motor neurons thought to be toxic to nerve cells in high concentrations. Another possible cause is a disorganized immune response, causing the death of nerve cells. 

Batten disease

Batten disease is a genetic condition that appears to manifest mainly in small children. It affects the function of lysosomes, which are the cell’s recycling bin. They break down proteins, waste, and lipids (fatty compounds) into smaller components that can be recycled or discarded in the cell. The disease is triggered when the mutated genes stop producing the correct amount of proteins needed for lysosomal function. These proteins are imperative for neurons and other cells to function normally. Over time, patients will lose the ability to communicate and lose all cognitive functions.

TX CBD Retailers

Treating neurodegenerative disorders with medical marijuana

The Compassionate Use Program (CUP), an expansion of the state’s medical cannabis program, was approved in June 2019 by the Texas Legislature. Prior to the expansion, only intractable epilepsy was considered a viable condition for entry into the program. 

Under the new guidelines of HB 3703, patients with all forms of seizure disorders, multiple sclerosis, spasticity, autism, terminal cancer, amyotrophic lateral sclerosis, and all incurable neurodegenerative diseases now qualify patients for medical cannabis treatment.

Doctors may use their discretion when neurodegenerative diseases are not listed and may submit a request for the addition of the disorder.

Readers can find a full list of the newly added conditions here

The human endocannabinoid system (ECS) naturally protects the body against stressors, toxins, and unhealthy lifestyles whilst maintaining homeostasis. If the ECS is compromised, the chances of developing a neurodegenerative disease are much greater.  

The phytocannabinoids found in cannabis have the ability to mimic our own naturally produced endocannabinoids to some extent and could be used to activate the ECS. This, in turn, might prevent neurological disorders or reduce their progression.

THC and Cannabidiol CBD, two of the main components of cannabis, are being thoroughly researched for their potential efficacy and safety in the treatment of neurodegenerative diseases. THC interacts with CB1 receptors found in the brain and nervous system while CBD interacts with CB2 receptors found in the immune system and major organs.

A common issue with neurological disorders is the chronic inflammation of neurons. Both THC and CBD have been shown to produce strong anti-inflammatory responses that may trigger the onset of neurological diseases.

Furthermore, THC and CBD have antioxidant properties and are known to protect against the degeneration of neurons and nerve cells in the brain.

Studies On Medical Marijuana or Cannabidol For Treating Neurodegenerative Diseases

There is much speculation as to the efficacy of cannabis in treating, arresting, or reversing neurodegenerative diseases. But there is also a growing body of anecdotal, lab, and clinical evidence to support the use of medical marijuana for treating neurodegenerative conditions.

More human trials are needed, says Juan Sanchez-Ramos, MD, PhD, a professor of molecular pharmacology and physiology at the University of South Florida, but due to the federal government’s stance on the legality of cannabis, progression has been impeded by regulations and obstacles for almost 50 years. 

Studies that have been undertaken on this issue

Here are just a few examples of the studies that have been undertaken on this issue. Links to these and other studies can be found at the end of this article.
  • An early study by Dr. Sanchez-Ramos indicated that cannabinoids facilitate neuroprotective and anti-oxidative actions. The report states that cannabinoids can potentially “slow the onset and progression of neurodegenerative conditions.” 

  • In 2012, Dr. Andras Bilkei-Gorzo said in a research review: “At first sight, it is striking that cannabinoid agonists, substances known to impair cognitive functions, could be beneficial in neurodegenerative cognitive disorders. However, cannabinoid receptor activation could reduce oxidative stress and excitotoxicity, suppress neuroinflammatory processes and thus alleviate the symptoms of neurodegenerative motor and cognitive diseases.”

  • In March 2014, The British Journal of Pharmacology concluded in a review that “modulating the endogenous cannabinoid system is emerging as a potentially viable option in the treatment of neurodegeneration.”

  • In August 2015, in an evidence-based systematic review, the American Academy of Neurology reported the efficacy or probable efficacy of cannabinoids for the treatment of neurological disorders. This review was based on randomized, controlled trials in which cannabis demonstrated the ability to alleviate painful spasms, spasticity, and central pain associated with multiple sclerosis. 

Marijuana strains and delivery methods available in Texas for treating neurodegenerative diseases 

Under Texas medical marijuana regulations, all medical cannabis products are required to contain less than one-half of one percent THC. While that is not a lot it is quite a bit higher than the 0.03 percent THC limit for so-called industrial hemp strains. Furthermore, products must contain a minimum of 10 percent CBD.

These high-CBD, low-THC strains do have their benefits and are often more effective than THC-free hemp CBD oil. In addition to cannabinoids, compounds known as terpenes also contribute to the overall effects of a strain. The combined effect of cannabinoids and terpenes found in a medical marijuana strain is commonly known as the entourage effect.

To find the ideal strain for their condition patients should discuss their needs with their physicians as well as the experts at their local medical marijuana dispensary

Various types of preparations are made from low-THC strains. These include:

  • Inhalation – smoking and vaporizing dried flower or concentrated cannabis extracts

  • Edibles – cannabis-infused candy, baked foods, etc. (diabetics, be aware of sugar content)

  • Tinctures/drops – cannabis-infused oils and drops

  • Capsules/pills – cannabis-infused gelcaps, softgels, and tablets

  • Topicals – cannabis-infused pain relief creams

How To Get Cannabidiol For Neurodegenerative Diseases In Texas

The first step for patients suffering from a neurodegenerative disease would be to visit a Texas-certified medical marijuana doctor. A quick phone call can usually help to determine if a patient qualifies for a Texas High CBD cannabis medicine and set up an appointment for an in-person or online evaluation using medcard telemedicine.

Once an application has been approved, the physician will enter the patient’s name into the state’s patient registry. The patient will immediately be eligible to purchase medical marijuana from a Texas dispensary or via home delivery.

Texas Med Marijuana Certifications

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Neurodegenerative Diseases Expanded Upon

Neurodegenerative diseases expand the playing field significantly. A qualifying physician under Texas Occupations Code, Chapter 169, may prescribe low-THC cannabis to a patient with a documented diagnosis of one or more of the following incurable neurodegenerative diseases:

  • (1) Incurable Neurodegenerative Diseases with Adult Onset:
    • (A) Motor Neuron Disease:
      • (i) Amyotrophic lateral sclerosis;
      • (ii) Spinal-bulbar muscular atrophy; and
      • (iii) Spinal Muscular Atrophy.
    • (B) Muscular Dystrophies:
      • (i) Duchenne Muscular Dystrophy;
      • (ii) Central Core; and
      • (iii) Facioscapulohumeral Muscular Dystrophy.
    • (C) Freidreich’s Ataxia.
    • (D) Vascular dementia.
    • (E) Charcot Marie Tooth and related hereditary neuropathies.
    • (F) Spinocerebellar ataxia.
    • (G) Familial Spastic Paraplegia.
    • (H) Progressive dystonias DYT genes 1 through 20.
    • (I) Progressive Choreas: Huntington’s Disease.
    • (J) Amyloidoses:
      • (i) Alzheimer’s Disease;
      • (ii) Prion Diseases:
        • (I) Creutzfeldt-Jakob Disease;
        • (II) Gerstmann-Straussler-Scheinker Disease;
        • (III) Familial or Sporadic Fatal Insomnia; and
        • (IV) Kuru.
    • (K) Tauopathies.
      • (i) Chronic Traumatic Encephalopathy:
      • (ii) Pick Disease;
      • (iii) Globular Glial Tauopathy;
      • (iv) Corticobasal Degeneration;
      • (v) Progressive Supranuclear Palsy;
      • (vi) Argyrophilic Grain Disease;
      • (vii) Neurofibrillary Tangle dementia, also known as Primary Age-related Tauopathy; and
      • (viii) Frontotemporal dementia and parkinsonism linked to chromosome 17 caused by mutations in MAPT gene.
    • (L) Synucleinopathies:
      • (i) Lewy Body Disorders:
        • (I) Dementia with Lewy Bodies; and
        • (II) Parkinson’s Disease; and
      • (ii) Multiple System Atrophy.
    • (M) Transactive response DNA-binding protein-43 (TDP-43) Proteinopathies:
      • (i) Frontotemporal Lobar Degeneration;
      • (ii) Primary Lateral Sclerosis; and
      • (iii) Progressive Muscular Atrophy.
  • (2) Incurable Neurodegenerative Diseases with Pediatric Onset:
    • (A) Mitochondrial Conditions:
      • (i) Kearn Sayers Syndrome;
      • (ii) Mitochondrial Encephalopathy Ragged Red Fiber;
      • (iii) Mitochondrial Encephalopathy Lactic Acidosis Stroke;
      • (iv) Neuropathy, Ataxia, and Retinitis Pigmentosa;
      • (v) Mitochondrial neurogastrointestinal encephalopathy;
      • (vi) Polymerase G Related Disorders:
        • (I) Alpers-Huttenlocher syndrome;
        • (II) Childhood Myocerebrohepatopathy spectrum;
        • (III) Myoclonic epilepsy myopathy sensory ataxia; and
        • (IV) Ataxia neuropathy spectrum;
        • (vii) Subacute necrotizing encephalopathy, also known as Leigh syndrome;
        • (viii) Respiratory chain disorders complex 1 through 4 defects: Co Q biosynthesis defects;
        • (ix) Thymidine Kinase;
        • (x) Mitochondrial Depletion syndromes types 1 through 14:
          • (I) Deoxyguanisine kinase deficiency;
          • (II) SUCLG1-related mitochondrial DNA depletion syndrome, encephalomyopathic form with methylmalonic aciduria; and
          • (III) RRM2B-related mitochondrial disease.
    • (B) Creatine Disorders:
      • (i) Guanidinoacetate methytransferase deficiency;
      • (ii) L-Arginine/glycine amidinotransferase deficiency; and
      • (iii) Creatine Transporter Defect, also known as SLC 6A8.
    • (C) Neurotransmitter defects:
      • (i) Segawa Diease, also known as Dopamine Responsive Dystonia;
      • (ii) Guanosine triphosphate cyclohydrolase deficiency;
      • (iii) Aromatic L-amino acid decarboxylase deficiency;
      • (iv) Monoamine oxidase deficiency;
      • (v) Biopterin Defects:
        • (I) Pyruvoyl-tetahydropterin synthase;
        • (II) Sepiapterin reductase;
        • (III) Dihydropteridine reductase; and
        • (IV) Pterin-4-carbinolamine dehydratase.
    • (D) Congenital Disorders of Glycosylation.
    • (E) Lysosomal Storage Diseases:
      • (i) Mucopolysaccaridosis:
        • (I) Mucopolysaccharidosis Type I, also known as Hurler Syndrome or Scheie Syndrome;
        • (II) Mucopolysaccharidosis Type II, also known as Hunter Syndrome;
        • (III) Mucopolysaccharidosis Type III, also known as Sanfilippo A and B;
        • (IV) Mucopolysaccharidosis Type IV, also known as Maroteaux-Lamy; and
        • (V) Mucopolysaccharidosis Type VII, also known as Sly.
      • (ii) Oligosaccharidoses:
        • (I) Mannosidosis;
        • (II) Alpha-fucosidosis;
        • (III) Galactosialidosis;
        • (IV) Asparylglucosaminuria;
        • (V) Schindler; and
        • (VI) Sialidosis;
      • (iii) Mucolipidoses:
        • (I) Mucolipidoses Type II, also known as Inclusion Cell disease; and
        • (II) Mucolipidoses Type III, also known as pseudo-Hurler polydystrophy;
      • (iv) Sphingolipidoses:
        • (I) Gaucher Type 2 and Type 3;
        • (II) Neimann Pick Type A and B;
        • (III) Neimann Pick Type C;
        • (IV) Krabbe;
        • (V) GM1 gangliosidosis;
        • (VI) GM2 gangliosidosis also known as Tay-sachs and Sandhoff Disease;
        • (VII) Metachromatic leukodystrophy;
        • (VIII) Neuronal ceroid lipofuscinosis types 1-10 including Batten Disease; and
        • (IX) Farber Disease; and
      • (v) Glycogen Storage-Lysosomal: Pompe Disease.
    • (F) Peroxisomal Disorders:
      • (i) X-linked adrenoleukodystrophy;
      • (ii) Peroxisomal biosynthesis defects:
        • (I) Zellweger syndrome:
        • (II) Neonatal Adrenoleukodystrophy; and
      • (iii) D Bidirectional enzyme deficiency.
    • (G) Leukodystrophy:
      • (i) Canavan disease;
      • (ii) Pelizaeus-Merzbacher disease;
      • (iii) Alexander disease;
      • (iv) Multiple Sulfatase deficiency;
      • (v) Polyol disorders;
      • (vi) Glycine encephalopathy, also known as non-ketotic hyperglycinemia;
      • (vii) Maple Syrup Urine Disease;
      • (viii) Homocysteine re-methylation defects;
      • (ix) Methylenetetrahydrofolate reductase deficiency severe variant;
      • (x) L-2-hydroxyglutaric aciduria;
      • (xi) Glutaric acidemia type 1;
      • (xii) 3-hydroxy-3-methylglutaryl-CoA lyase deficiency;
      • (xiii) Galactosemia;
      • (xiv) Manosidosis alpha and beta;
      • (xv) Salidosis;
      • (xvi) Peripheral neuropathy types 1 through 4;
      • (xvii) Pyruvate Dehydrogenase Deficiency;
      • (xviii) Pyruvate Carboxylase Deficiency;
      • (xix) Refsum Disease; and
      • (xx) Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy.
    • (H) Fatty Acid Oxidation:
      • (i) Trifunctional protein deficiency; and
      • (ii) Long-chain L-3 hydroxyacyl-CoA dehydrogenase deficiency.
    • (I) Metal Metabolism:
      • (i) Wilson Disease;
      • (ii) Pantothenate Kinase Associated Neurodegeneration; and
      • (iii) Neurodegeneration with brain iron accumulation.
    • (J) Purine and Pyrimidine Defects:
      • (i) Adenylosuccinate synthase Deficiency;
      • (ii) 5-aminoimidazole-4-carboxamide ribonucleotide transformylase deficiency;
      • (iii) Hypoxanthine-guanine phosophoribosyltransferase Deficiency also known as Lesch-Nyhan disease;
      • (iv) Dihydropyrimidine dehydrogenase Deficiency; and
      • (v) Dihydropirimidinase Deficiency.

As the TX Medical Marijuana Program evolves, more qualifying conditions may be added.

Sources and additional reading

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