Gabor Mate: On Cannabis use, Addictions and Healing with Psychedelics

Understanding cannabis use, it’s effects, addiction and trauma.

Gabor answers questions regarding the use of Marijuana (Cannabis). He discusses addictions to some drugs, and how these are relative to the effects of legalized narcotics like tobacco, alcohol and prescription drugs.

Important point he made is on the effects of drugs on developing brains of young children and adolescents, putting a spotlight on prescription of drugs to children.

As a therapist, I fully appreciate his emphasis on psychological trauma as the root cause of addictive behavior. He tells us that the medical profession should be more aware of trauma.

Nicotine Addiction: the bio-psycho-social viewpoint of the smoking habit

This article is a reflection on the lecture series on the topic of addiction. The focus here is that of nicotine addiction.

Why Smoking?

Nicotine addiction seems less serious to law enforcers than addiction to other “hard substances” like opioids, for example. However, for the many persons who need to quit the cigarette for health reasons, addiction is an important issue. This short paper addresses some of the different aspects of nicotine addiction that warrant attention. Through this overview, we can appreciate how one “habit” transcends over many fields of science, and how psychotherapy, within these fields that can support cessation.

The Social Norms of Smoking Initiation

The habit of cigarette smoking is observed to be most often developed during adolescence. Qualitative studies were thus conducted by Peters, et al. (2005) involving high school students who are smokers, regarding the latter’s beliefs in smoking initiation and nicotine addiction.

Questions posed to the subjects were like, “who was with you the first time you smoked?”, to which the answers were largely peers and family members of the same age-group like cousins. Smokers from both genders regard “curiosity” and “peer pressure” as motivation for starting the habit, while for boys, the added motivation is for “cool / image”.

Other means of modelling and encouragement given to teenagers as motivation for initiation of smoking are:

  • Self medication and coping: “My parents were arguing so I went in her car and saw her cigarettes there, I wanted it to calm me down” and “Because I was having problems at my house and my friend told me if you want to feel better you should start doing it.”
  • Peer Pressure: “Because someone asked me if I have ever done it”, “because he (boyfriend) kept telling me try it, try it” and “because everybody was smoking one at the bus stop.”
  • Curiosity: “We were just curious”, “something to try” or “I was curious to see if it was an effect.”
  • Other Modeling Recurrence: “Because I saw my friends doing it”, and “Because everybody else was doing it, so I wanted one.”

The majority of the subjects revealed that the next time they smoked after the initiation is within 48 hours of the first smoke. This recurrence of smoking crystallizes the behavior into an addiction:

  • Craving/Withdrawal: “I was craving it and I wanted to be with my friends”, “I had to have another cigarette”, “When they are shaking.”

When asked “how long does someone have to smoke before they are hooked?” The first 3 times emerged as the most frequent response from the subjects. Most subjects also say that one pack or less is all it took for them to get hooked on the smoking habit.  This is also the topic of question for Birge, et al. (2017),  “What proportion of people who try one cigarette become daily smokers?”.

At the mention of “being hooked on the habit” or eventually “becoming daily smokers”, it is interesting to also note that it may not necessarily mean that the subjects were actually spontaneous addicted to the substance, nicotine, per se.  This would have only been clearer had the subjects who were just initiated, were induced to try to “quit” after the 2nd, 3rd (and so on) smoke after initiation.

Smoking Regularity and Nicotine Addiction in Adolescence

Selya et al. (2013) worked on the little-known time-varying effects of smoking quantity and nicotine dependence on the regularity of adolescent smoking behavior. The findings indicated that, in adults, smoking quantity and extent of nicotine dependence is significantly related to regularity of smoking during adolescence. Nicotine dependence is found to increase over time as the effects from regularity of smoking decreased with time. This indicates implicitly also that the initial phases of smoking have more significance in causing nicotine addiction.

A Brief Neurobiology of Nicotine Addiction

From the above studies alone, one gets the impression that, for adolescents at least, smoking is an addictive habit from the beginning. What is not so clear is to what extent, and which time frame does the biological effects of nicotine take over the psychological need to light up a cigarette. The students cite mainly psychological factors (e.g. image and peer pressure), rather than physical factors (e.g. pain management) in getting initiated to smoking.

Nicotine molecules target neuronal nicotinic acetylcholine receptor (AChRs) of cells, in particular neurons. Activation of these receptors is involved in a chain reaction that regulates the system related to dopamine (the dopaminergic system). Consuming of Nicotine regularly causes an “up-regulation” of these receptors. This means that the cells are genetically stimulated to produce more or more effective AChRs receptors. This change in biological structure in neuronal cells changes the normal homeostasis of the intercellular environment of the brain. This process of up-regulation is known to be responsible for the initiation of nicotine dependence (Ortells & Arias, 2010).

The motivation for smoking, like other drugs and addictive behaviors, relies on neurons in the brain’s reward system, based in a brain region called the ventral tegmental area (VTA). Obtaining a reward leads to excitation of these neurons and the release of a neurotransmitter, dopamine. Dopamine transmission from the VTA is critical for controlling both rewarding and aversive behaviors.  The degree to which the reward system can be activated is normally tightly controlled by a neurotransmitter called GABA which inhibits excitatory signaling in neurons and keeps the system in balance. Figure one pictorially represents how the main neurotransmitters are held in homeostasis in living cells (in particularly the brain). When a substance like nicotine affects the effects of a neurotransmitter— in this case, Acetycholine— the system would adjust itself to regain balance. Chronic exposure to nicotine leads to the cells adjusting permanently to the imbalances. Such changes are adaptations that occur at a genetic level (since it involves receptors, which are proteins). When the addictive substance is no longer in the system, the imbalance caused by the adaptation would be felt.

Figure 1: (Tretter, 2018)

 

Researchers have also discovered enzymes that disinhibits dopamine neuron action with chronic nicotine exposure (Buczynski, et al., 2016). Pointing further to the biochemical action of nicotine that leads to the addictive phenomenon.

Nicotine Effect on Metabolism

The negative side-effect of smoking caused by tar and “smoke pollution” (figure 2) that causes lung damage is well known and quite easily grasped. However, the effects of nicotine in itself on the biological system – especially on the metabolic system— is relatively not well understood by the general public.  This has likely given rise to the misconception that chewing nicotine or smoking nicotine vapors are the answer to countering the negative health effects of smoking.  In fact consuming nicotine only adds to the metabolic issues in the body.

 

Figure 2 (Ambrose & Barua, 2004)

The effects of cigarette smoking on metabolism is illustrated through a recent Japanese study by Kang, et al. (2009). Fasting blood insulin, glucose and lipid levels were measured in 2 groups of women. One group consisted of regular smokers and the other non-smokers.  Fasting levels of these substances are indicative of the efficiency of the metabolic system. During fasting, insulin levels and glucose levels in the blood should ideally be low. Since there is no food entering the body during fasting, one would expect that glucose that had entered the blood from the previous meal to is already removed from the blood stream. The hormone, Insulin, is produced by the Islets of Langerhan cells of the pancreas immediately during food consumption to signal to the other cells in the body that glucose released into the blood from digested food needs to be quickly removed from the blood.  High levels of glucose concentration in the blood is toxic to the body, and this process of insulin release is a form of homeostasis. During insulin release, fat cells convert glucose to fat, muscle cells convert glucose to glycogen, and cells stop releasing glucose (gluconeogenesis) into the blood stream. After a period of time, the blood glucose level is supposed to be lowered, and Insulin levels in the blood will drop to safe levels (Eckel, Grundy, & Zimmet, 2005).

 

As with the above study by Kang et al., when comparing the blood profiles of the group of cigarette smokers with the group of non-smokers, the results showed significantly higher mean Insulin and blood glucose levels while lower mean high-density lipoprotein (fats molecules) in smokers as compared with non-smokers.  This indicates that nicotine affects the functionality of Insulin by making this hormone inefficient in reducing the glucose levels in the blood. With nicotine, fat cells do not respond as effectively to insulin by storing fat, muscle cells do not respond as effectively to storing glycogen, and cells do not respond to Insulin as effectively to inhibit gluconeogenesis.  So blood glucose after meals take longer time to return to safe levels, causing more Insulin to be pumped into the blood. This conditions mimics that of type 2 diabetes or metabolic disorder.

 

There are many papers that have highlighted the link between smoking and cardiovascular-related illnesses. The above study is an example that explains to us that nicotine affects blood glucose regulation and the function of insulin.  Impaired blood- glucose regulation is related to a pre-diabetic condition also known as insulin resistance.

 

Weight Gain and Smoking Cessation

 

A better-known cause of insulin resistance is not smoking, but high carbohydrates and/or alcohol in the diet coupled with sedentary lifestyle. However, cessation of smoking leads to a “similar” phenomenon of gaining weight. This phenomenon is unpleasant, and it is a signal that nicotine consumption messes up the function of insulin in glucose metabolism.

 

Figure 3 is an illustration from a paper by Nogueiras et al. (2015) that examines the biochemical link between insulin resistance and nicotine use.  If more attention is paid to educating the general public (and doctors) on metabolism, the medical field can perhaps help people with smoking cessation.

 

During cessation, nicotine is suddenly “deprived” in the system, fat cells no longer become insulin resistant (which is a good thing). Fat cells start to “hear” the insulin signals, and mop up the glucose from the blood (also a good thing). Since there is excess insulin in the blood, blood sugar levels become very low and fat cells begin to hold on to the fat (which causes one to put on weight).

 

It could be, that one possible way out of this situation is to maintain a very controlled diet that does not cause more insulin to be released in blood. Since Insulin is mainly triggered when sugars enter the blood stream, it might just be that a very low intake of carbohydrates may be the answer. With time, the body would cope by producing less insulin. Less insulin means that the fat cells do not absorb more sugars but actually start to burn off the fat.  This is how the biochemical aspect of metabolism becomes paradoxical and really interesting, but this is a big subject in itself.

 

Figure 3 (Nogueiras, Diéguez, & López, 2015)

Conclusion

Smoking addiction begins with the initiation at mainly adolescence, which opens up a whole potential field of education, and psycho-social influences. There is also biochemistry. Biochemistry is many-factorial and complex. There is the harmful effects of tar and other chemicals other than nicotine.

 

Nicotine, being known as the addictive substance is significant to the field of neurochemistry and pharmacology.  What is interesting and important is nicotine on metabolism.   This could be relevant in psychotherapy, since it involves lifestyle and effects of hyperinsulinemia or a diabetic-like situation. Hyperinsulinemia is incidentally linked to as well to depression (Löwe, Hochlehnert, & Nikendei, 2006) (Vogelzangs & Penninx, 2007).

 

For psychotherapists, this is a common addiction of functioning (and also paying) clients. Knowledge of the different aspects of this addiction lends itself to a multifaceted way of providing therapeutic support.

 

 

Bibliography

Ambrose, J. A., & Barua, R. S. (2004). The pathophysiology of cigarette smoking and cardiovascular disease: an update. . Journal of the American college of cardiology., 43(10), 1731-1737.

Birge, M.,  Duffy, S., Miler, J. A., &  Hajek, P. (2017). What Proportion of People Who Try One Cigarette Become Daily Smokers? A Meta-Analysis of Representative Surveys, . Nicotine & Tobacco Research.

Buczynski, M. W., Herman, M. A., Hsu, K. L., Natividad, L. A., Irimia, C., Polis, I. Y., & Roberto, M. (2016). Diacylglycerol lipase disinhibits VTA dopamine neurons during chronic nicotine exposure. Proceedings of the National Academy of Sciences, 113, pp. 1086-1091.

Eckel, R. H., Grundy, S. M., & Zimmet, P. Z. (2005). The metabolic syndrome. . The lancet, 365, (9468), pp. 1415-1428.

Kang, Y., Imamura, H., Masuda, R., & Noda, Y. (2009). Cigarette Smoking and Blood Insulin, Glucose, and Lipids in Young Japanese Women. . Journal of health science, 55(2), 294-299.

Löwe, B., Hochlehnert, A., & Nikendei, C. (2006). Metabolic syndrome and depression. . Therapeutische Umschau. Revue therapeutique, 63(8), pp. 521-527.

Nogueiras, R., Diéguez, C., & López, M. (2015). Come to where insulin resistance is, come to AMPK country. . Cell metabolism, 21(5), 663-665.

Ortells, M. O., & Arias, H. R. (2010). Molecular mechanisms of nicotine dependence. Journal of Pediatric Biochemistry, 1(2), 75-89.

Peters, R. J., Kelder, S. H., Prokhorov, A. V., Meshack, A., Agurcia, C., Yacoubian, G., & Griffith, J. (2005). Beliefs and social norms about smoking onset and addictions among urban adolescent cigarette smokers. . Journal of psychoactive drugs, 37(4), 449-453.

Selya, A. S., Dierker, L. C., Rose, J. S., Hedeker, D., Tan, X., Li, R., & Mermelstein, R. (2013). Time-varying effects of smoking quantity and nicotine dependence on adolescent smoking regularity. Drug and Alcohol Dependence, 128(3).

Tretter, F. (2018, Feburary). Neuroscience and Genetics. Private lecture at the Sigmund Freud University. Vienna, Austria.

Vogelzangs, N., & Penninx, B. W. (2007). Cortisol and insulin in depression and metabolic syndrome. Psychoneuroendocrinology, 32(7), p. 856.