The Drug Addiction and Clonidine

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Table of Contents

Executive summary
Pharmacodynamics
Pharmacokinetics
General discussion and conclusion
Reference List

Executive summary

Originally, clonidine was employed in cases where blood pressure was to be reduced. Basically, clonidine works on the central nervous system resulting in a significant reduction in the number of withdrawal symptoms that are associated with different addictive habits like smoking (Gourlay, Stead, & Benowitz 2004). Researchers have recently begun an investigation on the addictive nature of clonidine. Recent results reveal that clonidine is currently being abused, but in a combination with other drugs, that is, it is being abused due to a lack of other opiate maintenance drugs like methadone, which are deemed difficult to acquire (Melnikova 2012). By definition, addiction refers to a case where one is physically or psychologically enslaved to a given practice, or to any kind of habit-forming substance to an extent that the cessation of such habit leads to great trauma to such an individual (Angres & Bettinardi 2008). The addict’s body tends to adjust so as to incorporate the substance in its normal functioning, a condition where one becomes psychologically dependent on the drug (Rogge & Taft 2009). On the other hand, clonidine is a sympatholytic drug that is employed in the treatment of disorders such as anxiety, ADHD and high blood pressure, usually categorized as a₂adrenergic agonist (Volkow et al. 2005). Another point worth noting is that clonidine does not have any addictive effects on its own, although its combination with other potent substances has proved to be abusive (Guha 2012).

Turning to addiction interventions, the addict’s body may simply react towards abstaining from the substances that are addictive (withdrawal) (Crommelin, Sindelar & Meibohm 2008). However, this process might result in undesired body reactions. For instance, there is a high possibility of occurrence of hormonal and/or chemical imbalance due to failure to re-introduce former substances (Williams 2012). Lastly, significant psychological stress could occur if the substances that the body was used to are not available (Golan et al. 2011).

There are a number of therapeutic methods of curbing addiction, one of them being methadone maintenance (Golan et al. 2011). With this approach, a drug is administered in a clinical locale where there is full supervision (Golan et al. 2011). This process leads to a slow but steady increase in levels of brain opiate whereas the high feeling is not produced at all. The drug then remains in the system for a reasonably long time so as to prevent the addicts from re-using the addictive substance (American Society for Addiction Medicine, 2012).

Pharmacodynamics

According to Gourlay, Stead, & Benowitz (2004), clonidine is seen to have high specificity for a₂ receptors that are presynaptic, located in the vasomotor center in the stem of the brain. As soon as it gets to the brain, it reacts by binding on the a₂ receptors, a process that leads to a reduction in the levels of presynaptic calcium (American Society for Addiction Medicine 2012). This as well hinders norepinephrine release and thus achieves a general reduction in sympathetic tone. More still, clonidine produces antihypertensive impacts as a result of agonism on the imidazoline receptors. This action tends to facilitate actions such as sympathy-inhibitory so as to lower the levels of blood pressure (Marstrand et al. 2010).

As a treatment model of ADHD, clonidine directly raises the PFC’s noradrenergic tone by binding to postsynaptic receptors (the kind of receptors known as adrenergic a_2A), whereas, indirectly, the locus coeruleus’ norepinephrine input is raised (Rossi 2013).

Rossi also suggests that clonidine, which is an imidazoline-offshoot and hypotensive agent, tends to cross the barrier on the blood-brain towards the hypothalamus and prompts a significant reduction in the addict’s or patient’s blood pressure (American Society for Addiction Medicine 2012). The process occurs as this drug is able to arouse alpha-adrenoceptors (otherwise known as a₂ receptors) in the stem of the patient’s brain. As a result, the existing sympathetic outflow is completely minimized from the central nervous system. As an adjunct treatment of severe pain caused by cancer, clonidine is administered in form of an epidural infusion (Rossi 2013). This is a case where the present opiate analgesic is unable to completely suppress such pain. Thus, since clonidine helps to reduce the sympathetic tones, it is an appropriate drug that can help withdraw most addicts from several substances, although it is associated with several side effects (Golan et al. 2011).

Another alternative, as per the American Society for Addiction Medicine, is one that deeply stimulates the addicts’ brains. In this approach, the DBS procedure is made to target a number of brain parts, PFC being the major one. In a similar manner, clonidine is seen to work this way. It targets most receptors like a₂ and a_2A of such brain parts, binds on them and inhibits the release of norepinephrine and thus a general reduction in sympathetic tone is achieved (Angres & Bettinardi 2008).

Pharmacokinetics

Starting with addiction, most of the addicts’ bodies usually find recreational value in the abused drugs. According to a report by WHO on nicotine addiction, most of the physiological functions of their bodies adapt to such substances and thus cause them to be completely dependent on such substances to do any kind of activity.

With clonidine, its overdose may lead to a patient experiencing difficulties in breathing, feeling dizzy, cold, extreme/unusual tiredness and pinpoint eye pupils (Marstrand et al. 2010). Patients may also experience potassium loss, an incident that is portrayed through increased thirst, mental changes, dryness of the mouth, nausea, pain of the muscles and weak pulse. With excessive sodium loss, patients may react by exhibiting confusion, muscle cramps, seizures and irritability (Williams 2012).

General discussion and conclusion

As substantiated above, clonidine indeed lacks any recreational value, unless it is combined with other potent drugs (Angres & Bettinardi 2008). Thus, this is the best method that could be used to withdraw most of the substance addicts from the drugs they are abusing. In most cases, clinical trials are taken as indicators of the appropriateness of a given drug. Unfortunately, continuous use of the same approved drug over a long period of time will reveal that it has some effects, some of which could be very harmful. Although the medical industry contends that clonidine has no recreational value, most addicts are combining it with the potent substances after they fail to acquire the appropriate drugs to suppress their high feelings (Crommelin, Sindelar & Meibohm 2008).

Furthermore, there are a number of side effects that accompany clonidine treatment. Some of these include drowsiness (or low blood pressure), dizziness and dry mouth. Also, withdrawal from the usage of clonidine is likely to result in a risk of rebound high blood pressure. This occurs after a swift rise in diastolic BPs, a process that causes insomnia, nervousness, anxiety, palpitation, pain, agitation, and tremor, increased heart rate, nausea and increased muscle pain.

Moreover, there is fairy tangible evidence that when individuals are exposed to a given treatment, they respond differently. Individuals’ response to given drugs is generally affected by factors like the environment.

Therefore, despite the fact that clonidine can be employed in the treatment of several addictive effects like those of alcohol, it can be addictive when combined with other potent drugs. Thus, any kind of drug is likely to have an addictive effect if the users will misuse it (Marstrand et al. 2010).

Reference List

Angres, DH & Bettinardi, K 2008, “The Disease of addiction: origins, treatment and recovery”, Dis Mon, vol.54, no.10, pp. 696-721.

Crommelin, D J, Sindelar, R D & Meibohm, B 2008. Pharmaceutical Biotechnology: Fundamentals and Applications, 3rd edn, Informa Healthcare New York, US.

Golan, D, Tashjian, A. H., Armstrong, E J & Armstrong, 2011, Principles of pharmacology: the pathophysiologic basis of drug therapy, 3rd edn, Lippincott Williams & Wilkins, Philadelphia.

Gourlay, SG, Stead, LF & Benowitz, N 2004, “Clonidine for Smoking Cessation”, Cochrane Database of Systematic Reviews, vol.1, no. 3, p.58.

Guha, M 2012, “Hedgehog Inhibitor Gets Landmark Skin Cancer Approval, But Questions Remain for Wider Potential,” Nature Reviews Drug Discovery, vol.11, no.4, pp. 257-258.

Marstrand, T T, Borup, R, Willer, A, Borregaard, N, Sandelin, A, & Porse, B T, Theilgaard-Melnikova, I 2012, “From the analyst’s couch: Rare diseases and orphan drugs”, Nature Reviews DrugDiscovery, vol.11, no. 1, pp. 267-268.

Rogge, M. C. & Taft, DR 2009, Preclinical Drug Development, 2nd edn, Informa Healthcare, New York.

Rossi, S 2013, Australian Medicines Handbook, The Australian Medicines Handbook Unit Trust, Adelaide.

Williams, DA 2012, Foye’s Principles of Medicinal Chemistry, 7th edn, Lippincott Williams & Wilkins, Philadelphia.

American Society for Addiction Medicine. (2012). Definition of addiction. Web.

Volkow, ND, Wang, GJ, Ma, Y, Fowler, JS, Wong, C, Ding, YS, Hitzemann, R, Swanson, JM & Kalivas, P 2005, “Activation of orbital and medial prefrontal cortex by methylphenidate in cocaine addicted-subjects but not in controls: relevance to addiction”, Journal of Neuroscience, vol. 25, no. 15, pp. 3932-3939.

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