Is N.J. Going to Pot? Part One

New Jersey Sen. Nicholas Scutari (D-Union) has introduced a bill into the Senate to legalize marijuana and make it taxable.


According to the Bergen Record, “The measure would legalize marijuana possession and use for those who are at least 21 years old. If it does become law – and there is strong opposition to it from Gov. Christie – New Jersey would be the first state on the East Coast and third in the country to legalize the substance.”


Liberals, Libertarians, and Potheads should find out a few facts about pot beyond the commonly-held propaganda facts before cheering on this legislation. The following information comes from The National Institute on Drug Abuse’s website.


“Marijuana refers to the dried leaves, flowers, stems, and seeds from the hemp plant Cannabis sativa, which contains the psychoactive (mind-altering) chemical delta-9-tetrahydrocannabinol (THC), as well as other related compounds. This plant material can also be concentrated in a resin called hashish or a sticky black liquid called hash oil.


“Marijuana is the most common illicit drug used in the United States. After a period of decline in the last decade, its use has been increasing among young people since 2007, corresponding to a diminishing perception of the drug’s risks that may be associated with increased public debate over the drug’s legal status. Although the federal government considers marijuana a Schedule I substance (having no medicinal uses and high risk for abuse), two states have legalized marijuana for adult recreational use, and 20 states have passed laws allowing its use as a treatment for certain medical conditions.


“When marijuana is smoked, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to the brain and other organs throughout the body. It is absorbed more slowly when ingested in food or drink.


“However it is ingested, THC acts on specific molecular targets on brain cells, called cannabinoid receptors. These receptors are ordinarily activated by chemicals similar to THC that naturally occur in the body (such as anandamide) and are part of a neural communication network called the endocannabinoid system. This system plays an important role in normal brain development and function.


“The highest density of cannabinoid receptors is found in parts of the brain that influence pleasure, memory, thinking, concentration, sensory and time perception, and coordinated movement. Marijuana overactivates the endocannabinoid system, causing the “high” and other effects that users experience. These effects include altered perceptions and mood, impaired coordination, difficulty with thinking and problem solving, and disrupted learning and memory.


“Marijuana also affects brain development, and when it is used heavily by young people, its effects on thinking and memory may last a long time or even be permanent. A recent study of marijuana users who began using in adolescence revealed substantially reduced connectivity among brain areas responsible for learning and memory. And a large long-term study in New Zealand showed that people who began smoking marijuana heavily in their teens lost an average of 8 points in IQ between age 13 and age 38. Importantly, the lost cognitive abilities were not fully restored in those who quit smoking marijuana as adults. Those who started smoking marijuana in adulthood did not show significant IQ declines.


“A number of studies have linked chronic marijuana use and mental illness. High doses of marijuana can produce a temporary psychotic reaction (involving hallucinations and paranoia) in some users, and using marijuana can worsen the course of illness in patients with schizophrenia.


“A series of large studies following users across time also showed a link between marijuana use and later development of psychosis. This relationship was influenced by genetic variables as well as the amount of drug used, drug potency, and the age at which it was first taken—those who start young are at increased risk for later problems.


“Associations have also been found between marijuana use and other mental health problems, such as depression, anxiety, suicidal thoughts among adolescents, and personality disturbances, including a lack of motivation to engage in typically rewarding activities. More research is still needed to confirm and better understand these linkages.


“Additionally, because it seriously impairs judgment and motor coordination, marijuana contributes to risk of injury or death while driving a car. A recent analysis of data from several studies found that marijuana use more than doubles a driver’s risk of being in an accident. The combination of marijuana and alcohol is worse than either substance alone with respect to driving impairment.

For centuries, hashish and marijuana from the Indian hemp Cannabis sativa L., (“domesticated hemp”) have been grown in equatorial regions and used for medicinal and recreational purposes. In 1840, Schlesinger S. was apparently the first investigator to obtain an active extract from the leaves and flowers of hemp. A few years later, in 1848, Decourtive E. described the preparation of an ethanol extract that on evaporation of the solvent gave a dark resin, which he named “cannabin”. In 1964, the main active constituent of C. sativa L., Δ9-tetrahydrocannabinol (THC), was isolated and synthesized by Mechoulam’s laboratory. Two types of cannbinoid receptors, CB1 and CB2, responsible for the effects of THC, were discovered and cloned in the early 1990s.

Once cannabinoid receptors had been discovered, it became important to establish whether their agonists (a chemical that binds to a receptor cell and activates the receptor to produce a biological response. Whereas an agonist causes an action, an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist) occur naturally in the body. This search led to the discovery of the first endogenous cannabinoid (endocannabinoid), anandamide (arachidonoyl ethanolamide). Later on other endocannabinoids were found, for example 2-AG (2-arachidonoyl glycerol).


Anadaminde, also known as N-arachidonolyethanolomine or AEA, is an endogenous cannabinoid neurotransmitter. The name is taken from the Sanskrit word ananda, which means “bliss, delight” and a chemical compound called “amide.” The simplest amides are derivatives of ammonia. It is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which converts anandamide into ethanolomine (an organic chemical compound that is both a primary amine and a primary alcohol and arachidonic (fatty) acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.

These findings raised further questions about the pharmacological and physiological role of the cannabinoid system. This revived the research on cannabinoid receptor antagonists which were expected to help answer these questions. The use of the cannabinoid agonist, THC, in its many preparations to enhance appetite is a well-known fact. This fact led to the conclusion that blocking of the cannabinoid receptors might be useful in decreasing appetite and food intake. It was then discovered that the blockage of the CB1 receptor represented a new pharmacological target. The first specific CB1 receptor antagnoist/inverse agonist was rimonanbant, discovered in 1994.

The endogenous cannabinoid system includes cannabinoid receptors, their endogenous ligands (endocannabinoids) and enzymes for their synthesis and degradation.

There are two main receptor types associated with the endocannabinoid signaling system; cannabinoid recepter 1 (CB1) and 2 (CB2). Both receptors are 7-transmembrane G-protein coupled receptors (GPCRs) which inhibit the accumulation of cyclic adenosine monophosphate (a second messenger important in many biological processes) within cells. CB1 receptors are present in highest concentration in the brain but can also be found in the periphery. CB2 receptors are mostly located in the immune and haemtopoietic (blood formation) systems.

Endocannabinoids are eicosanoids (signaling molecules made by oxidation of 20-carbon fatty acids), which exert complex control over many bodily systems, mainly in inflamation or immunity, and as messengers in the central nervous system. The network of controls that depend upon eicosanoids are among the most complex in the human body. acting as agonists for cannabinoid receptors. They occur naturally in the body. Cannabinoid receptor-related processes are for example involved in cognition, memory, anxiety, control of appetite, emesis (you don’t want to know, unless you’re on chemotherapy), motor behavior, sensory, autonomic, and neuroendocrine responses, immune responses and inflammatory effects. There are two well-characterized endocannabinoids located in the brain and periphery. The first identified was anadamine (arachidonoyl ethanolamide) and the second was 2-AG (2-arachidonoyl glycerol). Additional endocannabinoids include virorhamine (O-arachidonoyl ethanolamine), noladin ether (2-arachidonoyl glyceryl ether) and NADA (N-arachidonoyl dopamine).


You can look up those long, Greek medical definitions yourself; they all pertain to sedation.


Where the scientists refer to “degradation,” it means the molecules are small enough to pass through the brain-blood barrier. The problem with pot appears to be its effect on myelin, the white matter that surrounds the axons, or transmission wires, in the brain that connect the synapses.

When the synapses fire, memories can either be restored or filed, or sent to other parts of the brain for storage. When the myelin fails or is destroyed, the synapses experience a power failure. The information is lost.


By age 23, at the very end of adolescence, the formation of myelin is completed. However, that process can be interrupted by disease, chemical reactions, and failure to absorb choline, the main component in myelin. Myelin is reinforced by constant, repetitious transmission and recall of information sent along the axon.


The Oxford English Dictionary records the earliest usages of cannabis meaning the plant “common hemp, Cannabis sativa” in 1548 and meaning parts of the plant “smoked, chewed, or drunk for their intoxicating or hallucinogenic properties” in 1848. The OED traces the etymology to the New Latin botanical term cannabis – proposed in 1728 and standardized in Caolus Linnaeus’s (1753) Species Plantarum – from an earlier Latin cannabis, coming from Greek kánnabis.

The Ancient Greek kánnabis transcribed a Scythian (Persian/Iranian horsemen) term in the earliest (ca. 440 BCE) reference to recreational cannabis usage. Herodotus recorded cannabis steam baths in The Histories.”

“The Scythians, as I said, take some of this hemp-seed [presumably, flowers], and, creeping under the felt coverings, throw it upon the red-hot stones; immediately it smokes, and gives out such a vapour as no Grecian vapour-bath can exceed; the Scyths, delighted, shout for joy.”

The historian and linguist Douglas Harper gives an etymology of English cannabis from Greek kannabis, from a Scythian or Thracian word, which is also the source for English “canvas” (viz., hempen fabric) and possibly hemp, a plant widely used to produce such common items as paper and rope.

The ancient Scythes didn’t know – and didn’t care – how kannabis affected their brains. It was enough that it made them “shout for joy.” Today’s pot-heads claim that marijuana is no different from alcohol. They’re right, in part. The chemistry of cannabis, the plant, contains an alcoholic element.


Where alcohol requires some time and varying amounts of consumption to have an effect, pot’s is instantaneous because its molecules are small enough to pass through the brain-blood barriers very tight net and more potent because the molecules have not been degraded. Rather like termites, they enter in a sort of stream, producing what’s known as the pothead’s “high.”


Totally harmless, Liberals and Libertarians would say. Or is it?


Published in: on March 26, 2014 at 11:19 am  Leave a Comment  

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