What Experts Are Saying About Drug Addictions


In this article, we will focus on heroin addiction, how heroin is metabolised in the body and short and long-term effects of drug addictions. We will also look at the effects it has on the developing brain.

Heroin Metabolism

There are two main ways that heroin is metabolised; one of the ways is through the Hepatic First Pass when it is taken orally through the removal of an acetyl group. The other way is through injections; Heroin that is administered this way does not go through the Hepatic first pass but instead will very fast cross the blood-brain barrier. This is because of the presence of an acetyl group that makes it more soluble in fat, once, in the brain, the acetyl group is removed, and heroin is reduced to 3-monoacetylmorphine and 6-monoacetylmorphine.

These compounds are then reduced to morphine that then binds to opioid receptors that are found in the brain. Opioid receptors are important for autonomic processes of the body such as breathing, blood pressure, pain and arousal. Heroin binds to these receptors reduces pain, users of the drug also report a feeling of euphoria, dry mouth and a flush of the skin accompanied with heavy extremities (Chetna J. Mistry, 2014). An individual can also develop tolerance to the drug, meaning more quantity of the drug may be needed to achieve the desired effect.

Research indicates that the presence of 6- MAM molecules in the blood after heroin has been reduced could account for its high metabolism. There is also a noticeable difference in alleles among different ethnic groups. The study that was done on SNPs showed the variant Single nucleotide polymorphism A118G did not show altered binding affinities to most opioid receptors and alkaloids, however the variant receptor A118G binds beta-endorphin and endogenous opioids that activate the Mu opioid receptors more tightly than the most common receptor (CHERIE BOND, JIANHUA GONG, & MARY JEANNE KREEK, 1998).

Also, beta-endorphins are more potent at the A118G variant than at the most common allelic forms; this is in the agonist-induced activation of the G proteins that have Potassium on their channels (Ying Zhang, 2005). The study concluded that the SNPs in the Mu receptor could alter the binding and signal transduction in the receptors (Chetna J. Mistry, 2014). This may affect the normal physiology of the body and may affect the treatment of an individual; this can also play a part in how an individual deals with disease.

Studies have also found that there is a common reward pathway for drug addiction and that these addictions usually occur in individuals that are vulnerable to both neurologically and genetically. This pathway is in the primitive limbic system; opiates drugs can affect this pathway by; increasing the postsynaptic sensitivity dopamine or by increasing the release of dopamine by the neurons (CHERIE BOND et al., 1998).

Heroin is a very addictive drug that, if injected or taken orally can mimic the body’s endorphin pathway of the CNS, normally the endorphins activate the bodies opioid receptors. These receptors are found at the surface of the cell membrane, in the Limbic system (controls pain, smell and hunger) where there are numerous. The receptors that heroin binds to influences whether the ion channels will open and in some cases influence the excitability of the neuron.

In addition to this Heroin also affect the GABA inhibitory receptors of the ventral tegmental area, when Heroin binds to these receptors the amounts of GABA is reduced. In normal physiology, GABA reduces the amount of dopamine that is produced in the brain. Prolonged use of the drug will cause the reduction in cAMP. Cyclic AMP is one of the molecules that determine the ability of the neuron to produce electrical impulses; it has been found that the increase in these molecules is what causes cravings in heroin users (Guitart, Thompson, Mirante, Greenberg, & Nestler, 1992).

Effects on Adolescents

Studies have shown that prolonged use of the drug may cause structural changes to the brain by shrinking or enlarging some parts of the brain. For example, structural MRI has shown that prolonged use of the drug can cause changes to the prefrontal cortex of the brain. The images revealed that the prefrontal cortex showed a lower proportion of the white matter, this is also seen in the brains of individuals with psychiatric abnormalities (Fowler, Volkow, Kassed, & Chang, 2007). These findings were correlated with the fact that individuals with these changes in the brain structure had a lower score in Wisconsin’s test. This is the area of the brain that controls logical thinking, goal setting and planning; this explains why heroin user usually teenagers that are addicted to the drug have risky behaviours, are withdrawn from society and are aggressive.

Other signs of teenage drug addictions are; cognitive difficulties, short-term memory, a reduction in attention span, poor information processing and poor problem-solving skills compared to non-heroin or drug users. Some of the warning signs that a teenager is using drugs are; withdrew, low self-esteem, a sudden drop in the grads at school and when they suddenly start having older friends (Lambie, 2007).

Heroin and Pregnancy

Heroin is a lipophilic drug, hence the usage of the drug through pregnancy can cause a wide range of effects, and one of them is Neonatal abstinence syndrome. NAS is syndrome where the foetus together with the mother becomes dependent on the drug; the symptoms are; low birth weight, excessive crying, seizures, and irritability. Children that addicted to the drug also show reduced motor and behaviour development and hepatitis if the mother was sharing needles during pregnancy. Current treatment of heroin addiction during pregnancy is the use of methadone (Fajemirokun-Odudeyi et al., 2006). According to the Australian government of health and warfare, NAS is most likely to be found in young Australian women, unmarried and indigenous (AIHW, 2006).

Teenage Drug use in society

There a lot of factors that play a part in drug addiction, recent studies have found that children from single-parent homes and teens that come from poor families are more likely to use drugs. Also, teens with poor relationships and with a family history of drug addictions are more likely to use drugs. You also find addiction in families that have no interest in education and if there is a history of any abuse or if the person suffers from depression and anxiety.

This is a men’s recovery centre that is located in the Perth Western Australia.


AIHW. (2006). Statistics on drug use in Australia 2006. from http://www.aihw.gov.au/publication-detail/?id=6442467962


gene alters b-endorphin binding and activity: Possible

implications for opiate addiction. from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC21386/pdf/pq009608.pdf

Chetna J. Mistry, M. B., Dipika Desai, David C. Marsh, Zainab Samaan,. (2014). Genetics of Opioid Dependence: A Review of the Genetic Contribution to

Opioid Dependence. Current Psychiatry Reviews.

Fajemirokun-Odudeyi, O., Sinha, C., Tutty, S., Pairaudeau, P., Armstrong, D., Phillips, T., & Lindow, S. W. (2006). Pregnancy outcome in women who use opiates. European Journal of Obstetrics & Gynecology and Reproductive Biology, 126(2), 170-175. doi: http://dx.doi.org/10.1016/j.ejogrb.2005.08.010

Fowler, J. S., Volkow, N. D., Kassed, C. A., & Chang, L. (2007). Imaging the addicted human brain. Sci Pract Perspect, 3(2), 4-16.

Guitart, X., Thompson, M. A., Mirante, C. K., Greenberg, M. E., & Nestler, E. J. (1992). Regulation of Cyclic AMP Response Element-Binding Protein (CREB) Phosphorylation by Acute and Chronic Morphine in the Rat Locus Coeruleus. Journal of Neurochemistry, 58(3), 1168-1171. doi: 10.1111/j.1471-4159.1992.tb09377.x

Lambie, G. W., & Davis, K. M.,. (2007). Adolescent Heroin Abuse: Implications for the Consulting Professional School Counselor. Journal of Professional Counseling, Practice, Theory, & Research.

Megan Wood. (2004). Illicit drug use in australia from http://www.studnets.adelaisehs.sa.edu.au/subjects/issues/illictdrugs.pdf

Ying Zhang, D. W., Andrew D. Johnson, Audrey C. Papp and Wolfgang Sadée. (2005). Allelic Expression Imbalance of Human mu Opioid Receptor (OPRM1) Caused by Variant A118G*. Journal of biological chemistry.



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