In 2012 the United States Veteran Administration determined that every day 22 veterans complete suicide. Using the number of suicides in the U.S. in a given year (+/- 38,000).
38,000 suicides / 365 days = 104 104 per day x 22% = 22 veteran suicides a day.
The VA’s 2012 Suicide Data Report Analyzed death certificates from 21 states dating from 1999 to 2011. They did this by using death certificates from just 21 states, dating from 1999 to 2011. It is not the easiest thing to determine a suicide as well. Many suicides are considered accidental overdoses in which case their deaths are not included in the overall numbers.
We examined two major factors that contribute to this epidemic:
PTSD and Chronic Pain
PTSD is nothing new:
Accounts of psychological symptoms following military trauma date back to ancient times. Going back in history to 425 BC, Homer, in The Odyssey said “Must you carry the bloody horror of combat in your heart forever?”
The American Civil war is when we first see medical attempts to address PTSD. Civil war doctors called it hysteria, melancholia, and insanity. In WWI they called in shell-shock or neurosis. In World War II, the shell shock diagnosis was replaced by Combat Stress Reaction (CSR), also known as "battle fatigue." Said these veterans were ‘war weary’. PTSD is no longer an Anxiety Disorder. PTSD is sometimes associated with other mood states (for example, depression) and with angry or reckless behavior rather than anxiety. So, PTSD is now in a new category, Trauma- and Stressor-Related Disorders.
PTSD is a mental health problem that some people develop after experiencing or witnessing a life-threatening event such as:
Combat, natural disaster, a car accident, sexual assault and more.
It manifests itself in these ways:
1. You may have bad memories or nightmares. You even may feel like you're going through the event again. Also known as a flashback.
2. Avoidance - You’ll avoid situations or people that trigger memories of the traumatic event and avoid talking or thinking about the event.
3. The way you think about yourself and others may change because of the trauma. You may feel guilt or shame. Or, you may not be interested in activities you used to enjoy. The world is now a dangerous and you can't trust anyone. You might be numb, or find it hard to feel happy.
4. Feeling keyed up (also called hyperarousal). You may be jittery, or always alert and on the lookout for danger. Or, you may have trouble concentrating or sleeping. You might suddenly get angry or irritable, startle easily, or act in unhealthy ways (like smoking, using drugs and alcohol, or driving recklessly.
People with PTSD may also have other problems. These include: Feelings of hopelessness, shame, or despair, depression, anxiety, drinking or drug problems, physical symptoms or chronic pain, employment problems, relationship problems, including divorce and loss of parental rights, and ultimately in too many cases, suicide.
PTSD symptoms usually start soon after the traumatic event, but they may not appear until months or years later. They also may come and go over many years. If the symptoms last longer than four weeks, cause you great distress, or interfere with your work or home life, you might have PTSD.
There are two main types of treatment, psychotherapy (sometimes called counseling or talk therapy) and medication. They are sometimes combined.
Psychotherapy for PTSD -
Psychotherapy, involves meeting with a therapist. There are different types of psychotherapy:
Cognitive behavioral therapy (CBT) is the most effective treatment for PTSD.
There are different types of CBT. One type is Cognitive Processing Therapy (CPT) the other is Prolonged Exposure (PE)
There are only 2 recognized drug options available.
Paxil, Paxil CR, Pexeva: Paroxetine is an oral drug that is used for treating depression. (SSRI) Paxil - is an oral drug that is used for treating depression. It is in a class of drugs called selective serotonin reuptake inhibitors (SSRIs), a class that also contains (fluoxetine) Prozac, and (citalopram) Celexa.
Zoloft (sertraline) is an antidepressant in a group of drugs called selective serotonin reuptake inhibitors (SSRIs). Zoloft is used to treat depression, obsessive-compulsive disorder, panic disorder, anxiety disorders, post-traumatic stress disorder (PTSD), and premenstrual dysphoric disorder (PMDD).
Thought to be effective at relieving depression and anxiety symptoms because we have been told that they lower relapse rates of depression and anxiety disorders, including OCD, panic disorder, social anxiety disorder, and generalized anxiety disorder. It causes drowsiness, so it's good for people who have trouble sleeping. Can cause weight gain, which can be helpful if you've recently lost weight or have a low appetite.
You should not use Zoloft if you are allergic to sertraline, if you also take pimozide, or if you are being treated with methylene blue injection. Do not use Zoloft if you have taken an MAO inhibitor in the past 14 days. A dangerous drug interaction could occur. MAO inhibitors include isocarboxazid, linezolid, phenelzine, rasagiline, selegiline, and tranylcypromine. After you stop taking Zoloft, you must wait at least 14 days before you start taking an MAOI.
To make sure Zoloft is safe for you, tell your doctor if you have:
Liver or kidney disease; seizures or epilepsy; a bleeding or blood clotting disorder; bipolar disorder (manic depression); or a history of drug abuse or suicidal thoughts.
Ask your doctor before taking a nonsteroidal anti-inflammatory drug (NSAID) for pain, arthritis, fever, or swelling. This includes aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve), celecoxib (Celebrex), diclofenac, indomethacin, meloxicam, and others. Using an NSAID with Zoloft may cause you to bruise or bleed easily. Drinking alcohol can increase certain side effects of Zoloft. Do not take the liquid form of Zoloft if you are taking disulfiram (Antabuse). Liquid Zoloft may contain alcohol and you could have a severe reaction to the disulfiram. This medication may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert. Antidepressants have been linked to increases in suicidal ideation among children and young adults. Older adults have increased risks of stroke and death from all causes. Pregnant women using antidepressants are at increased risk of miscarriage, and if they don’t miscarry, their offspring are more likely to be born with autism, birth malformations, persistent pulmonary hypertension, and newborn behavioral syndrome.
Taking Zoloft with other drugs that make you sleepy or slow your breathing can increase these effects. Ask your doctor before taking Zoloft with a sleeping pill, narcotic pain medicine, muscle relaxer, or medicine for anxiety or seizures. Like any other antidepressant; cimetidine; phenytoin; St. John's wort; tolbutamide; tramadol; tryptophan (sometimes called L-tryptophan); a blood thinner - warfarin, Coumadin, Jantoven; Heart rhythm medicine - digoxin, flecainide, propafenone, and others; Medicine to treat anxiety, mood disorders, or mental illness such as schizophrenia - diazepam, lithium, valproate, and others; Migraine headache medicines - sumatriptan, zolmitriptan, and others.
Other drugs may interact with sertraline, including prescription and over-the-counter medicines, vitamins, and herbal products. *This list is not complete.
***The effectiveness of sertraline for longer than three months has not been systematically evaluated in controlled trials.***
Adverse effects that are reported most often to the FDA:
Approximately 20% of people attempted to quit taking antidepressants show withdrawal symptoms. Among the side effects of antidepressants are sexual dysfunction effects like low libido and an inability to orgasm (which affects 70–80% of patients on SSRIs). Before you were depressed, now your sexually dysfunctional too. Can harm an unborn child, so you can't take it if you're pregnant. Taking Paxil during the first trimester was linked to a 23 percent increase in risk for major congenital malformations and a 28 percent higher risk of heart defects
Like most antidepressants, it can cause a higher risk of suicidal thoughts and behavior for people younger than age 24. Likely to cause minor weight gain (1 to 5 pounds) or make you feel sick if you miss a dose long-term weight gain, insomnia, nausea, and diarrhea. Perhaps the most surprising health consequence of antidepressant use is one that affects people of all ages. Antidepressants increase the risk of relapse after one has recovered. People are more likely to become depressed again after treatment by antidepressants than after treatment by other means – including placebo treatment.
Antidepressants and the Placebo Effect :
September 28th, 2015 Irving Kirsch published an article ‘’Antidepressants and the Placebo Effect’’ Irving is Associate Director of the Program in Placebo Studies and lecturer in medicine at the Harvard Medical School. They performed meta data analysis on antidepressants. Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. But in reality all antidepressants are different, some increase serotonin levels, some decrease it, and some have no effect at all on serotonin?
Yet, they all show the same therapeutic benefit. How?
Well, analyses of the published data and the KEY WORD unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. How is it possible that medications with such weak efficacy data with were approved by the FDA? The answer lies in an understanding of the approval criteria used by the FDA. Meta-data means using all the results across all the tests conducted to get better overall picture.
The FDA requires two adequately conducted clinical trials showing a significant difference between drug and placebo. But there is a loophole: There is no limit to the number of trials that can be conducted in search of these two significant trials!
That means that even if 98 out of 100 studies show the drug to be ineffective or worse, 2 studies showing statistical significance is good enough.
Trials showing negative results simply do not count.
Do you think baseball players would like to count only their successful at bats? That’s what the drug companies are doing. Do you think that skews the results? We know it does. The failure to mention the unsuccessful trials was not merely an oversight; it reflects a carefully decided FDA policy dating back for decades. To my knowledge, there is only one antidepressant in which the FDA included information on the existence of negative trials. Furthermore, the clinical significance of the findings is not considered. All that matters is that the results are statistically significant.
It doesn’t have to be clinically significant; it just has to be statistically significant.
I should mention here the difference between statistical significance and clinical significance. Statistical significance concerns how reliable an effect is. Statistical significance does not tell you anything about the size of the effect. Clinical significance, on the other hand, deals with the size of an effect and whether it would make any difference in a person’s life. Imagine, for example, that a study of 500,000 people has shown that smiling increases life expectancy – by 5 min. With 500,000 subjects, I can virtually guarantee you that this difference will be statistically significant, but it is clinically meaningless.
So if the only two drugs approved for PTSD shouldn’t be, so what else can we give them?
Off Label anti-anxiety drugs prescribed for PTSD include:
Alprazolam (Xanax), Buspirone (Buspar), Chlordiazepoxide (Librium), Clonazepam (Klonopin), Diazepam (Valium), Estazolam (ProSom, Eurodin), Hydroxyzine (many names), Lorazepam (Ativan, Orfidal), Midazolam (Dormicum, Hypnovel, Versed), Oxazepam (Serax, many others), Temazepam (Restoril), Triazolam (Halcion, Trilam, others)
Off label mood stabilizing drugs prescribed for PTSD include the following anticonvulsants:
Carbamazepine (Tegretol, Carbatrol, others) Requires monitoring of white blood cell counts due to risk of agranulocytosis. Will self-induce its own metabolism and increase the metabolism of other medications including oral contraceptives
Divalproex sodium (Depakote) Requires monitoring of liver function tests due to risk of hepatotoxicity and platelet levels due to risk of thrombocytopenia. Target dosage is 10 times the patient's weight in pounds, Lamotrigine (Lamictal) Requires slow titration according to the package insert due to risk of serious rash., Oxcarbazepine (Trileptal), Valproic acid (Depakene, Valproate)
Off label antipsychotic drugs prescribed for PTSD:
• Aripiprazole (Abilify)
• Asenapine (Saphris)
• Fluphenazine (Prolixin, Modecate)
• Haloperidol (Haldol, others)
• Iloperidone (Fanapt)
• Loxapine (Loxapac, Loxitane)
• Lurasidone (Latuda)
• Olanzapine, sometimes in combination with fluoxetine
(Zyprexa, Zypadhera, or Symbyax)
• Perphenazine (Trilafon)
• Pimozide (Orap)
• Prochlorperazine (Compazine, Phenotil, more)
• Quetiapine (Seroquel)
• Risperidone (Risperdal)
• Thiothixene (Navane)
• Ziprasidone (Geodon, Zeldox, Zipwell)
Tricyclic Antidepressants (such as Imipramine)
Mirtazapine (Remeron) 7.5 mg to 45 mg daily
Venlafaxine (Effexor) 75 mg to 300 mg daily
Nefazodone (Serzone) 200 mg to 600 mg daily
Fluoxetine (Prozac) 20 mg to 60 mg daily
Monoamine Oxidase Inhibitors (MAOIs) (such as Phenelzine)
Topiramate (Topimax). Requires clinical monitoring for glaucoma, sedation, dizziness and ataxia.
Risperidone (Risperdal) is contraindicated for use as an adjunctive agent - potential harm (side effects) exceeds benefits.
Every single one of these medications have awful side effects and can be fatal if over ingested.
Veterans and Chronic Pain:
Thanks to advances in military medicine and personal protective gear, service members injured in combat during Operation Enduring Freedom, Iraqi Freedom, and New Dawn have the highest survival rate in modern history. Approximately 55,000 military personnel have been injured in these conflicts—as many as 16,000 of them so severely, they likely would not have survived had they sustained the same wounds in previous conflicts. Surviving the battlefield is often just the first step on the road to recovery and healing. The journey may be long because, in addition to the impact of their physical trauma, many of these wounded warriors also bear psychological scars that may manifest as depression or post-traumatic stress disorder (PTSD).
Veterans are returning home with comorbid mental and physical health problems. Somatic complaints, especially pain, have been strongly associated with mental health disorders, particularly PTSD, in prior-era veterans, and similarly, high rates of comorbid pain and PTSD diagnoses have been reported in veterans who have returned from Iraq and Afghanistan.
VA approved treatment options for pain:
Opioid therapy - Nationwide, the prescription of opioid analgesics has nearly doubled since 1994 because of a greater recognition of the importance of treating pain.
But at the same time, rates of prescription opioid misuse and overdose have increased sharply, and prescription opioids are now a leading cause of death in the United States!
The U.S. Department of Veterans Affairs acknowledges its role in creating a large population of opioid-addicted veterans by overprescribing painkillers for injuries and post-traumatic stress disorder. After the agency tightened prescribing practices in 2013, many veterans bought pain pills sold illicitly on the streets. When those became too expensive, they sought heroin and fentanyl, a potent synthetic narcotic.
A study in JAMA: the Journal of the American Medical Association, indicates soldiers returning from Iraq and Afghanistan who have mental health diagnoses, especially those with posttraumatic stress disorder (PTSD), are at an "increased risk of receiving opioids for pain, high-risk opioid use and adverse clinical outcomes.“
Veterans with mental health diagnoses (who were) prescribed opioids with PTSD, were more likely to have comorbid drug and alcohol use disorders; receive higher-dose opioid regimens; continue taking opioids longer; receive concurrent prescriptions for opioids, sedative hypnotics, or both; and obtain early opioid refills.
Substance abuse disorders are over 12% for veterans serving after 9/11, leaving more than 65 thousand veterans seeing the VHA for opioid use disorder!
Addicted veterans can be referred to one of the VA’s 43 inpatient rehab centers around the country, which combined have 906 beds, according to a 2014 VA audit.
Waits are usually longer than 30 days, though, which deters referrals, and beds often stay empty because of lack of staffing, the audit said. We have more than 65 thousand veterans seeing the VHA for opioid use disorder. 906 beds. The VA has done the best they can under the circumstances to address the problems based on what the government allows them to.
Psychological therapies -
Psychological therapies, exercise treatments, and multidisciplinary psychosocial rehabilitation have been found to be effective for reducing pain the VA says. These interventions are safe and have not been shown to increase morbidity or mortality. Faced with the option of drugs or talk for pain treatment, who would rather talk?
Combining these two issues has left us with an epidemic. It is just not good enough. How bad is the epidemic? Every 65 minutes another veteran completes suicide. 365 days x 22 = 8030 suicides every year x 17 years = 136,510 veterans since 9/11/01.
Historical medical uses of Cannabis:
Cannabis has been used for millennia for medical, recreational, and manufacturing purposes. Around 2900 BCE, the Chinese Emperor Fu Hsi characterized cannabis as having sacred yin (weak, passive forces) and yang (strong, active forces) features, suggesting that it could restore homeostasis to an unbalanced body. Physicians in ancient India, Egypt, Persia, Rome, Arabia, and Greece used cannabis for spiritual and medicinal purposes, including menstrual fatigue, gout, rheumatism, malaria, beriberi, constipation, pain, and absentmindedness . Early documented uses of cannabis to treat seizures include a Sumerian text from 2900 BCE and an Arabian document from the twelfth century.
The 1854, the US Dispensatory listed cannabis to treat neuralgia, depression, pain, muscle spasms, insomnia, tetanus, chorea, insanity, and other disorders . Cannabis was valued for its analgesic, anti-inflammatory, appetite-stimulating, and antibiotic properties. In the mid-1800s, the British surgeon William O’Shaughnessy reported cannabis therapy for the treatment of epilepsy, recounting an “alleviation of pain in most, a remarkable increase of appetite in all, unequivocal aphrodisia, and great mental cheerfulness” [14, 18].
Two of England’s most prominent mid-to-late nineteenth- century neurologists, J.R. Reynolds and W. Gowers, also noted the benefits of cannabis in epilepsy . Gowers reported a man who previously failed bromides whose seizures were controlled on 9.8 g of Cannabis indica, dosed 3 times daily for up to 6 months .
Cannabis was first regulated in the USA with the 1906 “Pure Food and Drug Act”. The follow-up 1937 Marijuana Tax Act was opposed by the American Medical Association, which considered the more severe restrictions an infringement on physician’s freedom to treat patients.
During the hearing Harry Anslinger testified that:
“Reefer makes darkies think they’re as good as white men”
“There are over 100,000 total marijuana smokers in the U.S. and most are Negros, Hispanics, Filipinos, and entertainers. Their satanic music, Jazz and Swing, result from marijuana use! This marijuana causes white women to seek sexual relations with Negros, entertainers, and any others!”
“Marijuana is the most violence-causing drug in the history of mankind; If you smoke a joint you’re likely to kill your brother!” and more.
The tax act was quickly and quietly passed.
Then in 1970, the US Comprehensive Drug Abuse Prevention and Control Act categorized marijuana as a Schedule I drug with high potential for abuse and no accepted medicinal use. This came after the Nixon administration had commissioned the Shafer Commission Report on Marijuana and Drugs, which today is known as “The Shafer Report” after its chair, Raymond P. Shafer, former Republican Governor of Pennsylvania. Gov. Shafer and eight other members of the Commission were appointed by President Richard Nixon. The other four members of the Commission were Senators and Members of Congress appointed by the Congressional leadership, for a total of 13 members. It employed a staff of 76. It commissioned numerous reports and technical papers, totaling over 3700 pages, published in four volumes of appendices.
The Shafer Commission’s Report was the most in depth political look the United States has ever done.
In 1972 the Shafer Commission returned with their official findings, findings that flew in the face of everything the prohibitionists and Government had been saying for sixty years.
The commission stated:
“[that the] possession of marijuana for personal use no longer be an offense, [and that the] casual distribution of small amounts of marihuana for no remuneration, or insignificant remuneration, no longer be an offense.”
The report was buried and it was a career ender for Gov. Shafer. Then in 2016 a decades old quote from President Nixon's administration was making front page news and being shared widely around the web. The quote from John Ehrlichman, who served as President Richard Nixon’s domestic policy chief gained new notoriety after appearing in a cover story in Harper’s Magazine by author Dan Baum.
“You want to know what this was really all about,” Ehrlichman, who died in 1999, said, referring to Nixon’s declaration of war on drugs. “The Nixon campaign in 1968, and the Nixon White House after that, had two enemies: the antiwar left and black people. You understand what I’m saying. We knew we couldn’t make it illegal to be either against the war or black, but by getting the public to associate the hippies with marijuana and blacks with heroin, and then criminalizing both heavily, we could disrupt those communities. We could arrest their leaders, raid their homes, break up their meetings, and vilify them night after night on the evening news. Did we know we were lying about the drugs? Of course we did.”
Despite this, over the last 50 years, the main chemical constituents of cannabis have been isolated and synthesized. Δ9-THC was isolated in 1964 and synthesized in 1971 [21, 22]. CBD was isolated in 1940 and synthesized in 1963 [23, 24]. The cannabinoid type 1 (CB1R) and type 2 (CB2R) receptors, which bind Δ9-THC, were cloned in the 1990s [25, 26], supporting an endogenous system for this principal cannabinoid’s pharmacological activity.
The Endocannabinoid System:
The discovery of the endocannabinoid system in the early 1990s revealed the neuronal mechanisms that underlie the psychoactive effects of Δ9-THC in cannabis. Initial studies demonstrated that brief postsynaptic depolarization reduced neurotransmitter release from excitatory terminals onto Purkinje cells in the cerebellum and inhibitory terminals onto pyramidal neurons in the hippocampus [27, 28].
This phenomenon was termed “depolarization-induced suppression of excitation/inhibition” (DSE and DSI, respectively). Postsynaptic depolarization was postulated to trigger the release of an undiscovered substance that transiently limited presynaptic neurotransmitter release. Along with the discovery of nitric oxide (NO), this paradigm-shifting view suggested the concept of retrograde signaling in contrast to a primarily anterograde view of synaptic signaling. Application of a CB1R agonist (or antagonist) enhanced (or prevented) DSE and DSI, suggesting that it was mediated by an endogenous cannabinoid ligand [29–31]. These endocannabinoids were identified as the hydrophobic ligands N-arachidonoyl ethanolamide (anandamide)  and 2-arachidonoyl glycerol (2-AG) [33, 34].
Anandamide and 2-AG are synthesized from postsynaptic membrane phospholipid precursors and released in an activity-dependent, “on-demand” manner, unlike traditional vesicular neurotransmitters (Fig. 1). Depolarization of the postsynaptic cell or direct activation of metabotropic glutamate receptors increases levels of intracellular calcium, which trigger second messenger cascades that promote endocannabinoid synthesis [35–39].
Anandamide is synthesized via phospholipase D-mediated hydrolysis of N-arachidonoyl-phosphatidylethanolamine, and degraded by the fatty acid amide hydrolase (FAAH) into arachidonic acid and ethanolamine [40–43]. 2-AG is synthesized via diacylglycerol (DAG) lipase (DAGL) α-mediated hydrolysis of DAG, and degraded by FAAH into arachidonic acid and glycerol, or by monoacylglycerol lipase [41–44]. Chronic hyperexcitability leads to dynamic changes in the endocannabinoid pathway (see “The Endocannabinoid System: CB1Rs”). Thus, the enzymes that regulate metabolism and cannabinoid receptors represent attractive targets to treat several neurological disorders . Accordingly, the selective CB1R blocker rimonabant was approved in >50 countries as an anorectic to treat obesity , and showed promise in helping smokers quit tobacco use , but its use was suspended when postmarketing surveillance revealed high rates of depression and suicidal ideation.
The widely touted theory that marijuana causes brain damage comes from the Heath-Tulane study of 1974. Dr. Heaths Research methodology involved strapping Rhesus monkeys into a chair and pumping them with equivalent of 63 Colombian strength joints in “five minutes, through gas masks,” losing no smoke. Playboy discovered that Heath had administered 63 joints in five minutes over just three months instead of administering 30 joints per day over a one-year period as he had first reported. Heath did this, it turned out, in order to avoid having to pay an assistant’s wages every day for a full year. The monkeys were suffocating! Three to five minutes of oxygen deprivation causes brain damage—“dead brain cells.” (Red Cross Lifesaving and Water Safety Manual) 1974
Cannabis and PTSD:
There is convincing evidence from multiple studies for reduced endocannabinoid availability in PTSD. Brain imaging studies show molecular adaptations with elevated cannabinoid type 1 (CB1) receptor availability in PTSD which is linked to abnormal threat processing and anxious arousal symptoms.
A few years ago, a growing body of evidence suggested that cannabis can alleviate the symptoms of PTSD, so researchers at NYU’s Medical Center took a look:
The results of the study were published in the Sept. 2013 issue of Molecular Psychiatry.
They irradiated (shot radiation into) the brains of a cohort of people, including veterans with PTSD so the parts that respond to cannabinoids (“CB 1 receptors”) would actually glow when activated.
The focus of this study was not plant-derived cannabinoids but endocannabinoids, our bodies’ own naturally occurring chemicals similar to the active ingredients in cannabis THC.
They discovered abnormally dense networks of CB1 receptors in the regions associated with fear and anxiety—which is just what you might expect in veterans suffering from PTSD.
What was not necessarily expected is that the brains of the PTSD sufferers differed not just from those of the general population but also from those who had experienced trauma but not PTSD.
While peering inside the now radioactive brains, the researchers also recorded lowered overall levels of one endocannabinoid, anandamide.
Do you know what anandamide is?
It was discovered by researching THC. Once isolated it was given a name. The name is taken from the Sanskrit word ananda, which means "joy, bliss, delight“.
It is what occurs chemically in your brain when you’re happy. When you see a loved one, or laugh with friends.
Why are we prescribing medications for ptsd? To make people who are not happy, happy again, right?
Anadamide is an endogenous cannabinoid and functions as a neurotransmitter because it sends chemical messages between nerve cells (neurons) throughout the nervous system. It affect brain areas that influence pleasure, memory, thinking, concentration, movement, coordination, and sensory and time perception.
The neural communication network that uses these cannabinoid neurotransmitters, known as the endocannabinoid system, plays a critical role in the nervous system’s normal functioning.
Furthermore, outside the brain, anandamide acts as a chemical messenger between the embryo and uterus during implantation of the embryo in the uterine wall. As such, it's one of the first communications that occurs between mother and child.
THC’s chemical structure is similar to the brain chemical anandamide. Because of this similarity, THC is able to attach to CB1 receptors on neurons in these brain areas and activate them, disrupting various mental and physical functions.
If we are defining what happens when ingesting THC, you’re not getting high, you’re getting delighted, blissed, or joyous. Cannabis is not a simple medicine. Do you understand how normal Western medications work? When a plant shows bioactivity in humans we must attribute that effect to a single, predominant compound in the plant. We label that the active principal, we isolate it, synthesize it and make a pharmaceutical out of it.
In summary, the research team may have just proved that PTSD is not merely an intense form of general anxiety but a dysfunction all its own because the brain is no longer producing the naturally occurring chemicals on its own and they may have uncovered its unique biological markers. An over abundance of CB1 receptors plus a very low amount of the very chemical that gives you joy!
What if we could test cannabis for ptsd? Wouldn’t that be cool???
PHOENIX, ARIZ. — As of March 15, 2017, five participants have received marijuana (cannabis) provided by the National Institute on Drug Abuse (NIDA) in an ongoing Phase 2 clinical trial sponsored by the non-profit Multidisciplinary Association for Psychedelic Studies (MAPS) at the Scottsdale Research Institute (SRI) in Phoenix, Ariz.
It is a Placebo-Controlled, Triple-Blind, Randomized Crossover Pilot Study of the Safety and Efficacy of Four Different Potencies of Smoked Marijuana in 76 Veterans with Chronic, Treatment-Resistant PTSD
How is the testing going?
All six batches of cannabis tested negative for harmful microbes, mycotoxins, pesticides, arsenic, cadmium, and mercury. Two batches tested negative for lead. Four batches tested positive for low levels of lead.
Based on exposure limits set by the World Health Organization (WHO) the amount of possible lead exposure from NIDA cannabis was found to be well within the guidelines provided, and thus was considered safe for use in this clinical trial. “It’s crucial that the public is aware that their taxpayer dollars are going to support a single government-enforced monopoly, the sole federally legal supply of cannabis for any and all cannabis controlled trials,” It’s unclear whether mold, lead or discrepancies in potency has been a problem in prior cannabis studies, because until now, it appears that no one looked. NIDA says this is the first time researchers have expressed concern about mold or potency testing. Neither the agency nor the University of Mississippi tests samples for mold before they’re shipped. There’s no telling how many subjects in past studies were exposed. How can we be sure that all the past studies were not contaminated?
On top of this, 2 days after alerting the public to these alarming findings, this happened:
Eighteen months after joining a study on using marijuana to treat post-traumatic stress disorder, Johns Hopkins University has pulled out without enrolling any veterans, the latest setback for the long-awaited research. They informed the public by leaving a recording on their VM line that veterans were using to contact them to enroll. Ryan Vandry and John Hopkins had received $600,000 in funding, many thousands of dollars of equipment as well as 3lbs. of cannabis from the University of Mississippi that the DEA will not allow to be shipped anywhere else. Even though its not great by any stretch of the imagination, it is still usable. The test center in Scottsdale, Arizona, has close to a dozen veterans enrolled out of a planned 76. Researchers at the University of Pennsylvania and the University of Colorado who had been signed up to help with the study are continuing their participation. So studies have started but it is still not enough.
Cannabis and Pain Management:
Cannabis sativa has been used to treat pain since the third millennium BC. An endogenous pain-processing system has been identified, mediated by endogenous cannabinoid ligands acting on specific cannabinoid receptors. These findings, coupled with anecdotal evidence of the analgesic effects of smoked cannabis, support a reconsideration of cannabinoid agents as analgesics.
Oral cannabinoids such as tetrahydrocannabinol, cannabidiol and nabilone have, alone and in combination, shown efficacy in central and peripheral neuropathic pain, rheumatoid arthritis and fibromyalgia.
For the study, researchers analyzed all deaths caused by opioid overdoses between 1999 and 2010 in the U.S. Then, they determined the association between medical cannabis laws and opioid analgesic-related deaths using linear time-series regression models. The various models helped the researchers determine that in every state that legalized medical marijuana between the aforementioned years (a total of 13 states), there was a 25% reduction in deaths related to the overdose of legally prescribed painkillers.
Cannabis has been known as medicine for millennia throughout the world. It is time to reverse public policy in Missouri, the United States, and worldwide. This plant provides a safe, non-toxic alternative to dangerous and often ineffective medications that are killing our veterans in droves.