Drugs and the Brain

With Prof David Presti

Overprescription of Benzodiazepines in the Autism Population

Overprescription of Benzodiazepines in the Autism Population

Hari Srinivasan

Psych C19 Drugs and The Brain, UC Berkeley, Prof David Presti. Nov 2017

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Abstract

Benzodiazepines belong to the powerful sedative-hypnotic family and are some of the most widely prescribed class of drugs today.  There is, however, a serious overprescription of benzodiazepines in the developmentally disabled populations like Autism Spectrum Disorder without regard to the long-term health consequences.  Studies have shown that adult autistics have significantly fewer GABAA receptors and that benzodiazepines work by binding to the GABAA receptors, thereby potentiating the GABA neurotransmitter and producing its anxiolytic effects. Benzodiazepines are very effective in the short term so there is resistance to reducing medication as there is often a reversal of symptoms or other side effects.  Long-term usage even at moderate doses can impair cognition and memory and bring about tolerance and dependence. As the growing autism population ages, they may also be subject to the reported effects of benzodiazepines on the elderly, such as increased risk of hip fracture, Alzheimer’s, and dementia. In addition, studies have suggested that benzodiazepines themselves may contribute to behavioral symptoms which could be mistaken for other psychiatric behaviors which need to be further treated. This is ironic as benzodiazepines are given to mitigate these very symptoms. This paper suggests that more research is needed into understanding the underlying physiological underpinnings rather than just medicating based on observable symptoms or observable side effects. For instance, further investigation is needed into better and reliable ways to measure neurotransmitter levels so that dosages can be tailored more specifically for the individual and monitored, thus minimizing long-term effects.

Keywords: Benzodiazepine, Autism, GABA, Neurotransmitters, benzodiazepine side effects

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Overprescription of Benzodiazepines in the Autism Population

The use of medications like benzodiazepines is a growing problem in the developmentally disabled such as Autism Spectrum Disorder, who practically speaking often have less say on what medications are administered to them. From a young age, there is often pressure to medicate such individuals from schools, teachers, support staff, and therapists who often have to manage multiple students simultaneously.  Medication is often seen as a quick fix to mitigate disruptive or maladaptive social behaviors. Families too turn to medication in the hopes that it will improve the quality of life for the affected family member.

Benzodiazepines have been around since the 1960s with the introduction of chlordiazepoxide (Librium) in 1960, diazepam (Valium) in 1964 and a slew of other benzodiazepines since. Though they belong to the powerful sedative-hypnotic family, they are one of the most widely prescribed classes of drugs today. Prescriptions have, for instance, increased from 4.1% in 1996 to 5.6% in 2013 (Bachhuber, Hennessy, Cunningham, & Starrels, 2016). There is a serious overprescription of benzodiazepines in the vulnerable population of the intellectually disabled like Autism Spectrum Disorder, without regard to the long-term health consequences for these individuals.

Neural Mechanism of Benzodiazepines

Benzodiazepines are believed to work by potentiating GABA receptors at the chemical synapses in the brain. The neurotransmitter GABA inhibits the action of neurons by binding to GABAA receptors, thus producing its calming, sedating, anxiolytic, anticonvulsant, and vasodilation effects.  Benzodiazepines are not GABA agonists, rather they act as positive allosteric modulators (PAMs) since they can only act when GABA is bound at the receptor. Benzodiazepines actually bind to a subset of the GABAA receptor complex called BzR (benzodiazepine receptors). This serves to increase the inflow of chlorine ions at the ion channel, hyperpolarize the membrane potential of the neuron and reduce the chances of action potential. In effect, it makes the GABA receptor less sensitive. Since there are benzodiazepine receptors all over the brain connected to different neural circuits, there is bound to be variation in individual physiological responses to the drug.  Besides GABA, benzodiazepines also potentiate other neurotransmitters. For instance, clonazepam also acts as a serotonin agonist. In addition, benzodiazepines also stimulate the peripheral nervous system (PNS) as benzodiazepine receptors are found in the PNS tissues and glial cells. This could well account for its muscle relaxant effects (Griffin, Kaye, Bueno & Kaye, 2013).

Benzodiazepines are classified according to their elimination half-life action in the body. Shorter-acting ones (less than 12 hours) include midazolam (just 10 minutes duration of action) and alprazolam. Intermediate-acting ones (12-40 hours) include clonazepam and lorazepam, and longer-acting ones (40-250 hours) include diazepam. Benzodiazepines are further metabolized which extends their duration of action. For instance, diazepam metabolizes into nordiazepam, oxazepam, and temazepam. The speed of onset also differs for each. Midazolam (Versed) takes just 5 minutes to work while clonazepam (Klonopin) takes a few hours, though the latter also stays longer in the body (Griffin et al., 2013).

What makes benzodiazepines attractive to use is their relatively high therapeutic index when compared to barbiturates. This is believed to be due to the fact that benzodiazepines can open chloride ion channels only in the presence of GABA, unlike Barbiturates or propofol which can open the chloride ion channel independently.  When barbiturates are combined with alcohol it can cause respiratory depression to a degree that a person can stop breathing. The therapeutic index runs in the 100’s for benzodiazepines with diazepam at exactly 100. A high therapeutic index implies that it is difficult to overdose on benzodiazepines.  The rare cases of overdoses are treated with Flumazenil, which acts as an antagonist at the benzodiazepine binding sites (Tulane University School of Medicine, 2017).

It is not surprising therefore that benzodiazepines are often used to address symptoms associated with learning disabilities like Autism Spectrum Disorder.  In fact, a study by Oblack, Gibbs and Blatt (2009) found that the adult autistics had significantly fewer GABAA receptors and benzodiazepine sites when compared to the neuro-typical adults. Tomography results (Mendez et al., 2013) further indicate that there are reduced levels of GABA (specifically GABAA α5 subtype) in the nucleus accumbens and amygdala. There is a delicate balance in the brain between neuron excitation and neuron inhibition and their outputs to different regions of the brain. This balance, in turn, requires just the right amount of energy to the nerves. Disturbances in this mechanism could well be the underpinnings of the socio-emotional behaviors seen in Autism.

Effects of Benzodiazepines

Indeed, benzodiazepines are very effective in the short term. They are so effective that their use is continued to prolong the feel-good effects, especially on mood and anxiety.  In the meantime, tolerance builds up as does dependence. It is like being caught between Scylla and Charybdis, can’t live with them, can’t do without them either as other medications are less effective. It is ironic indeed that benzodiazepines are powerful enough to be classified as Schedule II drugs (“high potential for abuse”), yet are classified as Schedule IV (“low potential for abuse”) due to their prevalent use (Donaldson, Gizzarelli & Chanpong, 2007).

The study by Oswald and Sonenklar (2007) draws attention to the fact that almost 70% of children over age 8, with the Autism Spectrum diagnosis, were prescribed some form of psychoactive medication including benzodiazepines. Benzodiazepines are often given to this population for co-morbid conditions such as bipolar disorder, severe anxiety, obsessive compulsive behaviors and mood swings that can cause disruptive, aggressive or even self-injurious behaviors.

What is even more troubling is a study by Kalachnik, Hanzel, Sevenich and Harder (2002) which suggests that many of these behavioral symptoms could be caused by the benzodiazepines themselves and then be mistaken for other psychiatric behaviors which need to be further treated. Another study by Albrecht et al. (2014) had suggested a link between benzodiazepines and aggression, especially diazepam and alprazolam (Xanax). The effect is to synergistically disinhibit, especially if the diazepam were combined with other medications or substances such as alcohol, causing any bottled-up anger to come out. The irony is that benzodiazepines are often given to this population in the first place to mitigate these very behavioral symptoms.

This population is often also highly susceptible to dependence and addiction. There is resistance to stopping or reducing medication as there could be a resurgence of symptoms which are hard for the individual, their families or support staff in their social settings to cope with.  Withdrawal symptoms can include increased panic and anxiety, sweating, headache, palpitations and muscle stiffness (Pétursson, 1994). Withdrawal from higher doses could even result in seizures and psychosis. As a result, low to therapeutic doses are often continued long term to alleviate withdrawal symptoms which increases the risk of physical dependence (Busto & Sellers, 1991).  Inevitably, powerful drugs are also often accompanied by side effects and the benzodiazepines are no exception.  The toxicology list by the Tulane University’s School of Medicine include some worrying effects such as, “drowsiness, confusion, ataxia (loss of voluntary body movement), nystagmus (uncontrolled eye movements), slurring of speech, amnesia, hypotension and respiratory depression,” (2017). In addition, long term usage has shown to have negative effects on memory and cognition.

One in eighty-eight children are diagnosed with autism spectrum disorder today and the number just continues to increase (Center for Disease Control, 2016). Much of the current therapeutic interventions and research focus on the early years to take advantage of the neuroplasticity of a young brain. However, not every child benefits from the current array of therapies. This means that the main recourse for most adult autistics who did not benefit from early therapy is medication to control symptoms.  Recent research has however shown that neuroplasticity continues well into the adult years (Garrett, 2013). What is often overlooked is that all these growing thousands of young children with autism will age into adults with autism and then eventually the elderly with autism. Aging will bring about its own set of health issues with decreased immunity and reduced disease fighting ability. Wang, Bohn, Glynn, and Robert (2001) report that the use of even modest doses of benzodiazepines for over a month increased the risk of hip fracture by 50% in the elderly. Other studies have found links between continued use of benzodiazepines and increased risk of Alzheimer's and dementia (deGage et al., 2014). All this does not bode well for the Autism population who are already prone to a myriad of health issues, often due to a compromised immune system, such as seizures, allergies, respiratory issues, endocrine issues, digestive problems, sleep disorders, sensory dysregulation and bacterial or viral infections.

Conclusions and Future Study

There is clearly an overuse of medications such as benzodiazepines in the Autism population, without regard to consequences of long-term health effects. This is especially significant in light of the fact that the line between benzodiazepines alleviating symptoms and causing additional symptoms seem to be blurred in the Autism population. Currently, medication is based on observable outward behavioral symptoms and observable side effects. It is a shot in the dark as to whether they work or not, so various permutations, combinations, and substitutions are tried by medical specialists in an effort to mitigate maladaptive symptoms. The need of the hour is more research into understanding the underlying physiological underpinnings rather than just symptom-based medication. For instance, further investigation is needed into better and reliable ways to measure neurotransmitter levels so that dosages can be tailored more specifically for the individual and monitored, thus minimizing long-term effects.

References

Albrecht, B., Staiger, P. K., Hall, K., Miller, P., Best, D., & Lubman, D. I. (2014). Benzodiazepine use and aggressive behaviour: A systematic review. Australian & New Zealand Journal Of Psychiatry, 48(12), 1096. doi:10.1177/0004867414548902

Bachhuber, M. A., Hennessy, S., Cunningham, C. O., & Starrels, J. L., (2016). Increasing benzodiazepine prescriptions and overdose mortality in the United States, 1996–2013. AJPH. 106(4), 686-688. doi:10.2105/AJPH.2016.303061

Busto, U., & Sellers, E. M. (1991). Pharmacologic aspects of benzodiazepine tolerance and dependence. Pubmed. Retrieved November 10, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/1675689

Centers for Disease Control. (2016). Autism spectrum disorder (ASD). Retrieved November 10, 2017, from https://www.cdc.gov/ncbddd/autism/data.html

de Gage S.B., Moride, Y., Ducruet, T., Kurth, T., Veroux, H., Tournier, M., Pariente, A., & Begaud, B. (2014). Benzodiazepine use and risk of alzheimer’s disease: case-control study. British Medical Journal. 349:5205 https://doi.org/10.1136/bmj.g5205

Donaldson, M., Gizzarelli, G., & Chanpong, B. (2007). Oral sedation: A Primer on anxiolysis for the adult patient. Retrieved November 07, 2017, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993866/

Garrett, M. (2013, April 27). Brain plasticity in older adults. Psychology Today. Retrieved November 10, 2017, from https://www.psychologytoday.com/blog/iage/201304/brain-plasticity-in-older-adults

Griffin, C. E., Kaye, A. M., Bueno, F. R., & Kaye, A. D. (2013). Benzodiazepine Pharmacology and central nervous system–mediated effects. Retrieved November 07, 2017, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684331/

Kalachnik, J. E., Hanzel, T. E., Sevenich, R. & Harder H. R., (2003)  Brief Report: Clonazepam Behavioral Side Effects with an Individual with Mental Retardation. Development of Autism and Developmental Disorders. 33(3), 349-354 https://doi.org/10.1023/A:1024466819989

Mendez, M. A., Horder, J., Myers, J., Coghlan, S., Stokes, P., Erritzoe, D., Howes, O., … Nutt, D. (2013). The brain GABA-benzodiazepine receptor alpha-5 subtype in autism spectrum disorder: A pilot [11C]Ro15-4513 positron emission tomography study.  Neuropharmacology,  68, 195-201. https://doi.org/10.1016/j.neuropharm.2012.04.008

Oblak, A., Gibbs, T. T., & Blatt, G.J. (2009), Decreased GABAA receptors and benzodiazepine binding sites in the anterior cingulate cortex in autism. Autism Res, 2: 205–219. doi:10.1002/aur.88

Oswald, D. P., & Sonenklar, Neil. A.. (2007). Medication use among children with autism spectrum disorders. Journal of Child and Adolescent Psychopharmacology, V 17(3), 348-355. https://doi.org/10.1089/cap.2006.17303

Owen, R.T. & Tyrer, P. (1983). Benzodiazepine dependence. Drugs 25 (4): 385-398. https://doi.org/10.2165/00003495-1983

Pétursson, H. (1994). The benzodiazepine withdrawal syndrome. Pubmed. Retrieved November 10, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/7841856

Tulane University School of Medicine. (2017). Benzodiazepine Toxicology. Retrieved November 06, 2017, from http://tmedweb.tulane.edu/pharmwiki/doku.php/benzodiazepine_toxicology

Wang, P. S., Bohn, R. L., & Glynn. Robert. J. (2001). Hazardous benzodiazepine regimens in the elderly: effects of half-life, dosage, and duration on risk of hip fracture, The American Journal of Psychiatry, V 158 (6),892-898. https://doi.org/10.1176/appi.ajp.158.6.892

Coffee Beans

I tasted coffee beans for the first time in my life today. All in the name of learning about how caffeine affects our brain. Professor David Presti, who teaches “Drugs and the Brain,” at Cal, brought a whole bag of Peet’s Dark Roast Coffee Beans and passed them around for the class to taste. I’ve never tasted coffee before, let alone coffee beans, so this was a new experience. It was crunchy, kind of over burnt and somewhat bitter to the tongue. But I ate another bean anyway. I can see why folks love it so much. The effect was pretty immediate. I was more awake or maybe the immediate effect was due to the the bitterness.

The aroma, I’m familiar with, with my grandparents and most relatives all habitual coffee drinkers. My parents managed to kick the caffeine habit only recently after suffering the withdrawal symptoms of headache and fatigue. The coffee aroma is one I associate most with my grandparents. My Srinivasan grandpa who lives in Chennai, gets up before everyone else, receives the milk from the milkman, boils the milk and then brews a fresh batch of coffee decoction in a manual coffee filter. I’ve rarely seen grandpa in the kitchen otherwise, he really wants his coffee made the right way I guess. While in Chennai, I  wake up to the smell of coffee (and other things being prepared in the kitchen).  South Indian coffee looks different from the coffee ones sees in the coffee makers in the offices and restaurants here. It’s thicker as it has some chicory as well. Whenever my grandparents have visited the US, they’ve  brought coffee powder with them, as they did not prefer the local US brands. My other late Raghavan grandpa was also a coffee aficionado. He liked his coffee black without any sugar even and it had to be brewed just right. The coffee was not be be put on the stove or microwave directly to warm, rather the decoction had to warmed up in a hot water bath, else the taste would be spoiled.  During one of his visits to the US, he had one of the specialty coffee shop guys give him sample tastes of almost 2 dozen types of coffee beans before he found he kind of liked. My grandma would say that on a train journey, my  grandpa would keep stopping the coffee vendor who walked up and down almost every hour or so and ask for refills. At weddings, the coffee tray makes a regular appearance throughout the day.

Chemically, caffeine is one of the methylated xanthines. It’s an antagonist for the inhibitory neurotransmitter Adenosine. Inhibitory means slowing down of neural activity (or firing them up) while an antagonist is a molecule that blocks the action of the neurotransmitter at the receptor.. When Adenosine binds at the receptors it causes you to be calmer (helps sleep)  in addition to vasodilation or opening up of blood vessels (which allows for more oxygen flow). By blocking adenosine, caffeine causes the stimulating effects that is associated with coffee such as alertness, increased heart rate and increased BP.

One cup of 7 oz coffee or tea contains almost 100 mg of caffeine. But the giant sized drinks sold these days are almost 12oz, so extrapolate the caffeine. Apparently the so called decaf still has 3mg of caffeine. Energy drinks like Rockstar and RedBull have 120mg of caffeine and the tiny 5 Hour Energy Drink has a whopping 200mg.  Students have gone to the ER after a few of those high powered drinks - increased heart rate.  

A side note of interest was the Peet (of Peet’s Coffee) is from Berkeley and started his company in the 1960s. (Peet’s is now owned by a German Company.) Peet even showed the Starbucks guys how to make coffee.

Being Halloween, Prof Presti opened with a picture of a giant pumpkin stuck on top of the spire of the Campanile (Sather Clock Tower) in 2000 as part a Halloween Prank. The pumpkin had a giant “Live” carved into it. Wonder how they managed to get it up there. Apparently it was quite the spectacle till maintenance managed to get it down.

Plant Rituals

Plant Rituals - Brahmi Thailam and Neem

(Assignment about 2 Plant Rituals for Prof David Presti's, Drugs and the Brain Class at Cal)

My family has been vegetarian for generations and so are deeply rooted in plant traditions.  I was hard pressed as to which ones to pick. I focus on two of these - Brahmi Thailam and Neem.

Many a  weekend, I’m given a hair oil massage with Brahmi Thailam. Thailam means oil in Ayurveda lingo. A head massage with Brahmi Thailam is a most relaxing experience.

Fingers massage oil into the scalp.

Transdermal absorption of Brahmi

Neurotransmitters observe as they flow

Neural Communication, dendrites grow

Brahmi Thailam is a widely used  Ayurveda Oil to improve the functioning of the brain and nervous system. The main ingredients of Brahmi Thailam are Bacopa monnieri and Emblica officinalis (Amla). Bacopa monnieri is a nootropic herb and is thought to directly impact cognition and memory while reducing anxiety. In addition to being an antioxidant it is also thought to promote  dendrite growth and thus neural connections.  It can’t really be ingested orally as it can cause nausea. The other ingredient Alma, is a widely used plant and is used in many forms. I found the fruit is sour and tart to taste. It is widely used in cooking (dried or pickled) and common in most  hair oil preparations sold in India. Amla  is high in Vitamin C and is believed to help in longevity and promoting hair growth as well as neural function.

Ayurveda doshas, underlying physiological energies

Vata  brain, nervous system

Pitha  bile, digestive system and more

Kapha wind, respiratory and circulatory

Balance of doshas is the goal.

I’ve had a personal love affair with Ayurveda oils after my few summers of Ayurveda treatment in in Kerala, South India. Most of my knowledge and love of Ayurveda comes from what I learnt during that time. The Shirodhara (warm Ayurveda oil is slowly dribbled on the forehead for a full hour) and Kizhi (warm bundles of oil soaked herbs are applied on the body) treatments were deeply relaxing for the body, and for that duration at least the mind and thoughts would be in tranquility. That is saying something, for my mind seems to be ever in an excitatory state with my hyperactivity and other autism challenges. I long for the calm meditative state that an Ayurveda treatment brings. Alas, the effect is but temporary for me. The days of intense Ayurveda treatments in the land of coconut trees and elephants maybe in the past but the ritual that has continued on is the hair oil massages. The strong tang of the ayurveda oil wafts all over the room and I feel I am back in Kerala again. I soak in the oil anywhere from 10 mins to half an hour before taking a shower.

Kerala,

Swaying Coconut trees, Elephants, Houseboats

Gentle backwaters meet the Arabian Sea

Ayurveda Central, deemed Danvantri

A specific set of herbs is boiled with either Sesame Oil or Coconut Oil as a base to make Ayurveda oils. The Ayurveda hospital in Kerala where I’d received treatment had its own manufacturing wing. There was one oil there which took 100 days to prepare over a slow wood fire. They believed in  old style preparation- wood instead of gas fires as the latter could destroy the property of the concoction. Coconut oil is thought to be a more effective base by many of the Ayurveda doctors. But Coconut Oil becomes rancid within a few months while Sesame Oil can have a shelf life of upto 10 years so is preferred. Kerala is kind of like the Ayurveda central of India as there is where Ayurveda originated and is most practised, even amongst regular families with the knowledge passed down from generation to generation.

As winter approaches here, my oil massages become less frequent as they cool the body and that is asking to catch a cold in cold weather. I just look forward to them when the weather warms up again.

Another interesting tradition is the use of Neem. (Azadirachta indica, Margosa or Indian Lilac).  It is supposedly the ultimate anti-bacterial. I brush my teeth every night with Neem powder. Actually, I sprinkle a little bit of Neem powder on top of the toothpaste. It tastes slightly bitter but one gets used to the taste. In the olden days, folks did not have toothbrushes or toothpaste so they chewed away at a twig of the neem tree each morning, which basically cleaned their teeth. My grandma mentioned that it has now made a comeback in modern India with local vegetable vendors selling fresh neem twigs. My grandma even got me some but I found it sensorily hard to sustain chewing the twig - it literally is like chewing on the end of a pencil - a woody taste. However, the twigs have to be fresh when they are still soft, which makes bringing them into the US difficult as they dry out. So the substitute  has been a sprinkle of Neem.

Neem Neem, the village Pharmacy

Central gathering place, shade and cool air

Treetop to root, how I use thee

The neem tree was often called the village pharmacy as it had so many beneficial qualities and can be used from treetop to root. The Neem tree was usually found in the central village square. My other grandma (who has a large Neem tree in her front yard) tells me that neem leaves are used to treat chickenpox even today. Neem has been found to have many medicinal  properties -  anti-inflammation, anti-ulcer, anti-fungal, antioxidant, anti-bacterial, anti-mutagenic, anti-viral, anti-carcinogen and a powerful immunomodulator. It is thought to be a powerful medicine for the GI tract. I was on Neem supplements a few years back to help with GI inflammation. At my home,  the dried Neem inflorescence is often toasted in sesame oil and sprinkled on food items like our digestive drink called Rasam, which I’ve learnt to make. It lends a lovely flavor though it can be a little bitter.

I could go on about other plant rituals, but alas this assignment only calls for two.

Poison Plant Unmasked

Hari Srinivasan

Prof David Presti / GSI Carson McNeil

Psych C19 Drugs and the Brain

Commentary on Page 56, Pharmako Poeia by Dale Pendell

Poison Plant Unmasked

That plants have power is without a doubt. All are plant people in the end by fact and form, whether they be the modern science-backed western medicine or Ayurveda or the African Traditional Medicine. At times the poison of plants itself is the remedy. For instance, Foxglove is toxic yet has been used to develop treatments for congestive heart failure.

My sensory experience with plants has been largely influenced by the Ayurveda treatment I received in India over 5 summers in the coconut tree filled state of Kerala in South India. I have vivid memories of the scent of Ayurveda meds freshly concocted onsite from locally grown herbs in the nearby fields. The coconut and sesame oils boiled with Ayurveda powders made for sheer tranquility during the Shirodhara and Kizhi massages. The mind would be at peace and the soul in balance for that duration at least. The breeze from the nearby Bharatapuzha river would waft the scent through the cabin even as the cows on campus would wander up to receive a treat in the evenings. Even the very effective Ayurveda mosquito repellent smoke spread in the cabins in the evenings would carry the herbal tang in the air. But in all this euphoria, our eyes are blinded to the fundamental duality in life. For opposites coexist in all planes of life.

I am the power plant. I am the poison plant

… I build, I destroy

Fundamental Duality of Life

… Knowledge interlaced with ignorance

Debate: Plain Packaging on Tobacco Products

Hari Srinivasan

Prof David Presti / GSI Carson McNeil

Psych C19 Drugs and the Brain

First Debate at Cal for Prof David Presti's  Drugs and the Brain class

My task - Opening Statement 

Debate Topic: A plain-packaging requirement for tobacco products should NOT be implemented in the USA.

Our group supports the negative motion, that plain packaging for tobacco products should not be implemented.

It is ironic that in an age where more states are legalizing marijuana, which to a large extent is smoked, there is yet another move to suppress tobacco smoking through plain packaging. Tobacco has been around from ancient times. As we learnt in our last lecture, it was the primary shamanic plant of the Americas. It was used to bind friendships and seal covenants by Native Americans. The Hookah of the east has been around since the era of Akbar the Great in India. Why should Tobacco alone be demonized, targeted and penalized? After all it is but one of the many poison plants that we are surrounded by.

We argue that plain packaging is not evidence based, infringes on our intellectual property rights, curtails freedom of speech and  increases illicit trade.