Amphetamine dependence means psychological dependence caused by repeated use of amphetamine, dextroamphetamine, methamphetamine etc (members of the amphetamine family of drugs) that can cause a persecutory complex. Persecutory delusions and auditory hallucinations are the most consistent symptoms of meth-associated psychosis (MAP), and any clinical test can easily prove that in the case of frequent use of any of the above-mentioned, bodily functions and capacities are significantly suppressed. The main ways of using amphetamines illicitly include oral, intravenous, nasal or smoking (more immediate and longer-lasting effect than cocaine).
Members of the amphetamine family of drugs are easily manufactured and readily available. In the United States (US) in 2008, approximately 13,000,000 or 5% of persons aged 12 and older reported having used in their lifetime. Significant sub-groups remain particularly vulnerable to what mainstream, western and other schools of medicine deem as ‘meth use disorders’ (MUD). For example, rural persons in the US are more likely to use the drug than persons in either small or large metropolitan areas; an analysis of the US National Survey on Drug Use and Health noted meth use increased as the setting became more rural. The same has proven so in Australia, also, with rural areas highly represented in recent meth-use statistics.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5, the fifth edition, released in May 2013) did away with the separate ‘dependence’ and ‘abuse’ diagnoses and combined them into ‘Substance Use Disorder‘. This single disorder is measured on a continuum from mild to severe. Each specific substance is diagnosed based on the same over-arching criteria. Whereas a diagnosis of substance abuse previously required one symptom, mild substance use disorder in DSM-5 requires two to three symptoms from a list of eleven. Drug craving was added to the list and problems with law enforcement was eliminated because of cultural considerations that made the criteria difficult to apply internationally.
Amphetamines are known to enhance performance. While the heart beats faster and blood pressure rises, feelings of fatigue and appetite decrease. Amphetamines, like any other drugs used illicitly can lead to intoxication, making the individual lose appetite and not rest for long periods of time. Along with the ever-present risk of overdosing. After using amphetamines for a long time, the side-effects begin to mount and a list of ‘conditions’ can develop, including; insomnia, headaches, restlessness, hyperactivity and tremors.
Amphetamine overdose leads to exhaustion and constant fatigue. It is well documented that Cannabis successfully treats insomnia, makes an individual more relaxed and eliminates tremors. Cannabinoid receptors that populate the human body bind to natural compounds in Cannabis, know as phytocannabinoids. The phytocannabinoids in Cannabis work with the human Endocannabinoid (Endogenous [meaning ‘within the body’] Cannabinoid) System (ECS). They work to relax muscles affected by spasms (anti-spasmodic) and get rid of tremors; decreasing tension and providing deep, restful sleep. Cannabis is also well-know for “the munchies” effect; increasing appetite and making food more palatable.
Chronic dependence on amphetamine can cause not only medical problems, but also legal and social problems; across the world millions of people have been turned into social pariahs, labelled as ‘addicts‘ when they are generally truly suffering, in one way or another. Needing help, not castigation, discrimination, persecution and prosecution (aka, the failed ‘drug war’ approach) as British journalist and author Johann Hari says, it’s time to end the 100-year-old war on drugs and instead fight addiction with love and compassion.
Cannabis can complement other accepted treatments of amphetamine dependence and is successfully used to treat other syndromes such as; depression and schizophrenia etc. Cannabis is an alternative option for those who are addicted to alcohol, drugs and many types of pills, and Cannabis is one of the 50 ‘Fundamental Herbs‘ in traditional Chinese medicine (from 2737 BC).
Research suggests certain Cannabis compounds may be able to protect the brain from damage brought on by methamphetamine use. Italian researchers from the University of Cagliari published a study, 9-Tetrahydrocannabinol Prevents Methamphetamine-Induced Neurotoxicity, which indicates Cannabis, specifically the psychoactive compound Δ(9)-tetrahydrocannabinol (THC), is able to prevent brain damage sustained from the consumption of methamphetamine.
“In the study, we showed that THC, the principal constituent of Cannabis, attenuates the neurotoxic effect of meth by reducing two markers of neuronal damage”, according to the study authors. To formulate these results, researchers injected over a hundred rats with a steady regimen of methamphetamine, followed by doses of THC, which researchers say showed significant promise in offering protection to the brain.
This phenomenon is due to the way THC pathways, called CB2 receptors, react with immune cells and prevent inflammation. “A neuroprotective effect of cannabinoid was likely mediated, at least in part, by their anti-inflammatory properties”. The authors of the study conclude their findings provide the first scientific evidence that THC has the ability to reduce brain damage induced as the result of frequent meth binges, which, as researchers point out, provides additional fuel to the argument for the re-legalisation of Cannabis (worldwide).
Several studies have provided compelling evidence for the neuroprotective effects of cannabinoid CB1 receptor in several models of neuronal injury. Extensive in-vitro and in-vivo studies have shown that natural cannabinoids, e.g. THC and cannabinol (CBN), and synthetic CB1 receptor agonists, can attenuate experimentally-induced neurotoxicity in multiple pathological conditions, such as glutamate excitoxicity, hypoxia, ischaemic stroke, brain trauma and oxidative stress.
The neuroprotective effects of natural and synthetic cannabinoids have also been shown in animal models of Alzheimer’s, Parkinson’s and Huntington’s diseases and Multiple Sclerosis (MS). Indeed, a local and temporary increase of 2-arachidonoylglycerol (2-AG) level in response to traumatic brain injury has also been established.
The Abstract of the study, Prior stimulation of the Endocannabinoid System prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors, published in the journal, Neuropharmacology, in December 2014;
“Methamphetamine toxicity is associated with cell death and loss of dopamine neuron terminals in the striatum similar to what is found in some neurodegenerative diseases. Conversely, the Endocannabinoid System (ECS) has been suggested to be neuroprotective in the brain, and new pharmacological tools have been developed to increase their endogenous tone. In this study, we evaluated whether ECS stimulation could reduce the neurotoxicity of high doses of methamphetamine on the dopamine system. We found that methamphetamine alters the levels of the major endocannabinoids, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) in the striatum, suggesting that the ECS participates in the brain responses to methamphetamine. Δ(9)-tetrahydrocannabinol (THC), a Cannabis-derived agonist of both CB1 and CB2 cannabinoid receptors, or inhibitors of the main enzymes responsible for the degradation of AEA and 2-AG (URB597 and JZL184, respectively), blunted the decrease in striatal protein levels of tyrosine hydroxylase induced by methamphetamine. In addition, antagonists of CB2, but not of CB1, blocked the preventive effects of URB597 and JZL184, suggesting that only the former receptor subtype is engaged in neuroprotection exerted by ECS stimulation. Finally, we found that methamphetamine increases striatal levels of the cytokine tumor necrosis factor alpha, an effect that was blocked by ECS stimulation. Altogether, our results indicate that stimulation of ECS prior to the administration of an overdose of methamphetamine considerably reduces the neurotoxicity of the drug through CB2 receptor activation and highlight a protective function for the ECS against the toxicity induced by drugs and other external insults to the brain …”
Adapted from How Can Medical Marijuana Help With Amphetamine Dependence, with Substance Use Disorder Fact Sheet, The Diagnostic Criteria for Substance Use Disorders, Methamphetamine Psychosis, Granny Storm Crow’s List 2015, Prior stimulation of the Endocannabinoid System prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors, Amphetamines – past and present.