Side effects

It is important to specify that where there are numerous evidences on the adverse effects of recreational use of cannabis, there is not much information in the medical use of cannabis. In both cases, in fact, dosages and routes of administration may be significantly different.

The most common side effects observed after the recreational use of cannabis are: alteration mood, insomnia and tachycardia, paranoid and anxiety crises, psychotic reactions, and finally, syndrome amotivational. The latter consists of apathy, lack of motivation, lethargy, worsening of the memory and concentration, and altered state of judgment.

The effects of cannabis on the central nervous system may not be predictable for new employers. Therefore, it is advisable to take the first dose of preparation in a quiet environment and above all, always in presence of another person who may experience a healthcare if necessary. For patients with severe pathologies Cardiac and kidney stones, it is recommended that the medication be taken under medical supervision in a healthcare environment hospital / outpatient.

Under no circumstances is it recommended to smoke the preparation, as it is the most common route of administration susceptible to the occurrence of undesirable effects.

The use of the plant substance can determine positivity to anti-doping tests (Law 376/2000), controls provided by the Road Code (Article 187 of the Road Code: Guidance in Psycho-Physical Condition for the use of narcotic drugs), or the procedures for health assessments established by the Stability Pact of 8 September 2008 on workers at risk. Cannabis is one of the most commonly used psychotropic substances. It can cause complex dependence, can cause cognitive damage to memory, mood changes and altered perceptions; Can promote psychosis.

Indeed, cannabis, in addition to possessing an anabolic effect, is capable of modulating, in the additive sense, the system brain of the gratification and reward of any individual.

These effects can be "evaluated" and lived by the subject in several ways: in some cases they do not important importance and do not cause any alteration of the psychic and behavioral equilibrium of the subject; In others, however, can be the basis for the start of improper use of cannabis and the progressive incorporation of a complex addiction state.

When using cannabis for medical use, the recommended therapeutic doses, usually lower than those for recreational use, and do not use sub-therapeutic doses, it reduces the risk of dependence complex. It is therefore considered appropriate for the prescribing physician to be carefully evaluated in each subject eligible for treatment, the dosage of the useful substance in the specific case, taking into account also the areas.

Interaction with other medicinal products and other forms of interaction due to the high first-passage effect, especially in the case of oral administration cannabis, pharmacokinetic interactions with drugs may occur, which are metabolised through the Isoenzymes of cytochrome P450 system. The simultaneous use of the enzyme inhibitors mentioned above may increase the bioavailability of delta-9-tetrahydrocannabinol and with this the potential for undesirable effects.

Synergy sedatives or additives are described as a result of the simultaneous intake of substances psychotropic as ethyl alcohol and drugs such as benzodiazepines, antidepressants, antiepileptics, barbiturates and opiates.
Δ9-THC is oxidized by the cytochrome P450 family (CYP) 2C9, 2C19, and 3A4. Therefore, substances that inhibit these CYP isoenzymes as some antidepressants (eg fluoxetine, fluvoxamine, and nefazodone), proton pump inhibitors (eg cimetidine and omeprazole), macrolides (ad Example, clarithromycin and erythromycin), antimycotics (eg itraconazole, fluconazole, Ketoconazole, miconazole), calcium antagonists (for example, diltiazem, verapamil), protease inhibitors HIV (eg ritonavir), amiodarone and isoniazid may potentially increase bioavailability Of Δ9-THC, as well as the potential for side effects associated with THC.

On the other hand, drugs that accelerate metabolism of Δ9-THC through isoenzymes 2C9 and 3A4 such as Rifampicin, carbamazepine, phenobarbital, phenytoin, primidone, rifabutin, troglitazone, and the herb of San
Giovanni (Hypericum, Hypericum perforatum L.) may, on the contrary, reduce the bioavailability of THC and therefore its effectiveness when used in a therapeutic context.

THC, cannabidiol (CBD) and cannabinoid (CBN) are known to inhibit CYP isoenzymes, such as CYP1A1, 1A2 and 1B1. Cannabis can therefore increase the bioavailability of drugs metabolised by these enzymes.

Such drugs include amitriptyline, phenacetin, theophylline, granisetron, dacarbazine, and flutamide.

THC, carbos-Δ9-THC, CBD and CBN in vitro stimulate, and in some cases inhibit, the activity of P-glycoprotein flow conveyor. This suggests a potential additional mechanism for it cannabinoids can affect the efficacy and toxicity of co-administered drugs. Physicians must, therefore, be aware of other medications that the patient is taking and closely monitoring the patients in treatment with other drugs when taking cannabis.

Therefore, it is recommended to always evaluate possible pharmacological interactions before prescribing cannabis-based preparations.