1.Jonathan Lipman — Direct/Cross/Redirect/Recross

JONATHAN LIPMAN: My name is Jonathan Joseph Lipman, L-I-P-M-A-N.

JONATHAN LIPMAN: I'm a neuropharmacologist.

JONATHAN LIPMAN: A neuropharmacologist is a person who is trained in the expertise of dealing with the effects of drugs on nerve, brain and behavior. Some of us work in the industry developing and researching these new drugs, some of us work in academia and some of us consult clinically.

JONATHAN LIPMAN: Yes, sir. My educational background is originally British. So it differs in some ways from the American trajectory. My advanced level certificates of education came from Kitson College of Science in Leeds, England. I went on to do my professional degree at the Hatfield Polytechnic in Hertfordshire. It's known as Hertfordshire University. It changed its name. I did my externship at the National Hospital for Nervous Diseases in Queen Square, London and I obtained by State certification as a biomedical scientist, as well as my professional degree, in 1979. I went on then to do my doctoral work at the University of Wales Institute of Science and Technology obtaining a PHD in neuropharmacology. Excuse me. I just misspoke. It was my PHD that I graduated in 1979. Forgive me. And I then went to do a post-doctoral fellowship at the University of Tennessee Center for the Health Sciences in Memphis, Tennessee and over the ensuing years, continued to acquire additional education and board certifications as I moved through my academic and other professional positions.

JONATHAN LIPMAN: Well, I mentioned, of course, my biomedical science certification in England. I am certified, also, in England, by the Healthcare Professions Council, which is a national organization that controls healthcare professionals. Over the years that I was at the University of Tennessee Center for Health Sciences, and later Vanderbilt University where I held positions for 10 years in the departments of medicine and surgery, I obtained additional training and qualifications, becoming board certified as a -- by the American Board of Disability Analysts, the Medical Psychotherapists and Psychometricians, and the American College of Forensic Examiners. A number of different Boards. And the education still continues. It does not stop. I moved from Vanderbilt to join the industry after 10 years at Vanderbilt and worked in the pharmaceutical industry in the medical device development field for 10 years before rejoining academia at East Tennessee State University where I now am on the facility, clinical facility, and continue to consult with industry and the courts.

JONATHAN LIPMAN: Yes. Academia, though continuing to consult in neuropharmacology outside of the academic setting, in addition to academic work in research and development.

JONATHAN LIPMAN: I was Head of pharmacology for the first year of that time at a company that was spun off from Abbott Laboratories. It was called Medical -- Molecular Geriatrics. We were developing drugs that were based on anti-psychotic molecules for neurological purposes, and then transitioned to a medical device development track for Neuroscience Toolworks developing devices and methods for assessing subjective states of pain and suffering in humans by objective methods.

JONATHAN LIPMAN: At that point we would -- the devices and methods that we were using were to assess the effectiveness of drugs that we were then not developing. We were developing the methods of assessing them.

JONATHAN LIPMAN: Yes. One of the principle interests was pain medicines, which, of course, takes you into the area of addiction and dependence and withdrawal.

JONATHAN LIPMAN: I'm currently affiliated with East Tennessee State University, as I mentioned.

JONATHAN LIPMAN: I have a list of previous affiliations, no longer current.

JONATHAN LIPMAN: Well, I mentioned the first, which was the Institute of Neurology. Department of Neurosurgical Studies of National Hospital for Nervous Diseases in Queen Square, London. And then through my departments at University of Tennessee Center of Health Sciences, my affiliations were with the anesthesiology department, the biochemistry department and the Faculty Medical Practice Pain Clinic. At Vanderbilt I was affiliated with -- formally affiliated with the Department of Medicine and Surgery and maintained an adjunct position for some years after that. I'm not sure if it's still current. Possibly not after this time. With work that I was doing with the Department of Neurosurgery on pain assessment and pain treatment methods in chronic pain and intractable pain patients, and there developed several methods for objective measurement of pain, addiction, withdrawal. As I mentioned, I was group leader at Molecular Geriatrics Corporation, which was a spinoff of Abbott Labs. At the university now I hold a number of positions.

JONATHAN LIPMAN: Well, I'm on the Grand Rounds Committee for the Department of Psychiatry. I'm affiliated with the Department of Continuing Medical Education there, and I also am -- last year I was one of the coordinators for the forensics course in the psychiatry residency program, and also a lecturer on that program, and I am still a lecturer on that program. This is in the postgraduate training of psychiatrists.

JONATHAN LIPMAN: I'd have to look at my own CV. There are many.

JONATHAN LIPMAN: The Antidepressant Drug Pipeline was one that I gave a couple of years ago, Genetic Testing in Pain Management was a lecture I gave the previous year as part of a one day seminar for -- actually, it was not just East Tennessee. It was just held there. It was for people from all over. I gave a Grand Rounds that same year on pharmacogenetics. I have given a lecture entitled Update on Recent Trends in Drug -- Abused Drugs, and in 2014, New and Future Drugs of Abuse. One was given to the US Criminal Justice Administration called Drug Abuse Addiction in The Brain, Forensic Relevance. I could go on, but there are many.

JONATHAN LIPMAN: I do. I hold several, both in the U.S. and abroad, on pain assessment methods. International patents and, I believe, Canadian.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Well, throughout my time at Vanderbilt, I was the beneficiary of numerous grants assessing the effects of dementia and of drugs on the brain, and some of these came from the Division of Toxicology. It's called the Program in Toxicology. Some from the National Institutes of Health. One was with UCLA, Los Angeles VA, on dialysis dementia. Uremic encephalopathy funding that I was part of at Vanderbilt came from Dialysis Clinics Incorporated, a private organization that was funding my work on the brain in dementing patients. After leaving Vanderbilt, the work that I was doing in Chicago with Molecular Geriatrics and with Neuroscience Toolworks was funded through the National Institutes of Health. These were quite large grants. One -- a quarter million was one, $850,000 was another, to fund our work there on the development of methods for assessing the effects of drugs. I think that might have been my last NIH funded grant.

JONATHAN LIPMAN: Oh, yes.

JONATHAN LIPMAN: Yes, it is. These -- what's in my CV are just the peer reviewed ones, but there are more than this, some of which were not in peer reviewed journals.

JONATHAN LIPMAN: Yes. Toxicologists have their expertise in the measurement of drug effects in body fluids, body tissues, biological samples. The analytical methods. To some extent their training includes the poisoning effects of those drugs. The difference between a drug effect and the poison effect of that drug is one largely of dose. Now, pharmacologists have their expertise in the mechanism of action of drugs, therapeutic and adverse, how they work and how they interact. We are the people, for instance, that test drugs prior to marketing. We are the people that perform post-marketing surveillance of drug effects in the population being prescribed. And pharmacologists are also the people who research, develop and design these drugs. Now, in the process of that, some of our training is in the measurement of those drug effects. Sorry. Measurement of those drug concentrations in tissues, but that is not our principle focus. So there is a certain amount of toxicological training in a pharmacological career, but it isn't our main focus, whereas that is the main focus of a toxicologist. We rather deal with the effects of drugs, measuring the effects of drugs, assessing the effects of drugs and in the treatment of disease. We -- such as psychiatric disease. We assess the efficacy of the drug, the effectiveness of it, and of drug interactions.

JONATHAN LIPMAN: Drug effects are determined more than by dose. Drug effects have very individual determinates of drug action. In other words, it depends who is -- who the drug is acting upon as to what the effect will be. Drugs produce different effects in different people, and the effect of a drug is influenced then by factors such as their underlying medical condition, their underlying genetic predispositions, their underlying metabolic capabilities. Underlying disease states will completely change the effect of a drug. There are a number of other determinates, but also relevant to the examination of a drug at the time of inspection is the set and setting of drug use because that also determines the effect.

JONATHAN LIPMAN: The set and setting are -- set is what you bring to the drug experience and the setting is the experience -- is the milieu surrounding the effect of drug action. So just to give you an example of how setting can be relevant. Anti-psychotic drugs that are very helpful and therapeutic in a controlled milieu in a psychiatric ward may be completely useless in the chaos of everyday life with traffic and people and responsibilities and noise and family and intrusions. The milieu, the setting, has a lot to do with how effective of the drug will be, and the converse is also true. Not only may a therapeutic drug lose its benefits in the wrong milieu, but a drug that could be relatively innocuous, for instance, LSD, a psychotomimetic drug, can produce catastrophic effects if the milieu is threatening, frightening, uncontrolled, and that would be called a bad trip. The dose hasn't changed, the drug hasn't changed, but the setting has changed the effect of the drug. So set and setting are important determinates of how a drug expresses its effect on an individual.

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: Well, as I explained, the underlying medical, psychological, psychiatric, genetic, familial condition of the individual can determine, in large part, the effect of a drug.

JONATHAN LIPMAN: Correct. That -- as I said, medical. Yeah. For a drug that acts on the brain, it's very important to know how the brain is functioning to start with.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes, I have.

JONATHAN LIPMAN: For a number of reasons. One reason is that, depending on other factors, the effect of a drug at a certain time of interest, when we examine that time of interest may be related to the effect of the drug historically. In some cases, that may have an effect -- for instance, like tolerance in alcohol use. A person who using it regularly will develop some tolerance and will not be as intoxicated at a blood level that we measure at the time of interest because they are tolerant to it, unlike a person who has never had alcohol and who then achieves the same blood level and is unable to get up off the floor. So the history of drug use is relevant from that point of view. And it's also relevant because prior drug use can effect other things such as the development of the brain, the development of the liver, the development of a certain cognitive and other factors. And depending on the age at which it is used, it will have different effects. Therefore, the history of drug use is relevant to an examination of how a drug acts at a particular time.

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: Yes, I did review that.

JONATHAN LIPMAN: Marijuana contains cannabinoid drugs.

JONATHAN LIPMAN: I did. He was prescribed that at the time of this offense.

JONATHAN LIPMAN: I believe that his use of synthetic cannabinoid AB Pinaca more likely than not exacerbated his pre-existing and his continuing psychosis spectrum mental illness, which drove his irrational behavior.

JONATHAN LIPMAN: Cannabis --

JONATHAN LIPMAN: Cannabis contains a number of different drugs. It contains quite a few. Two of them we think of as the main ones. Future research may reveal more.

JONATHAN LIPMAN: Cannabidiol and delta-9-tetrahydrocannabinol.

JONATHAN LIPMAN: C-A-N-N-A-B-I-N-O-L. So it's delta-9-tetrahydrocannabinol. T-E-T-R-A-H-Y-D-R-O --

JONATHAN LIPMAN: T-E-T-R-A-H-Y-D-R-O-C-A-N-N-A-B-I-N-O-L

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes, it's usually called THC.

JONATHAN LIPMAN: Cannabidiol. C-A-N-N-A-B-I-D-I-O-L.

JONATHAN LIPMAN: That doesn't act on the same receptor as the THC and it exerts different effects. In fact, the effects are very, very different and are currently being evaluated for use as potentially anti-psychotic drugs. And yet, both of them are in the same plant, along with others that may have effects we haven't yet elucidated properly.

JONATHAN LIPMAN: To some extent. Some marijuana species more than others. Yes.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Let me explain that. There's a reason why cannabis acts on the brain. Can I start there?

JONATHAN LIPMAN: The brain has receptors for cannabis -- for cannabinoids. And the reason it has receptors is because the human physiology manufactures its own cannabinoids and they have very important purposes in brain function. These are -- we call them endocannabinoids. They are involved in the regulation of temperature, body temperature, blood pressure, they're involved in the regulation of perception, they're involved in memory, and they are neurotransmitters which our brain relies on to function, these endocannabinoids. The first to be identified and synthesized was one called anandamide. A-N?

JONATHAN LIPMAN: A-N-A-N-D-A-M-I-D-E. And, of course, it was tested for possible use in humans as a therapeutic drug. Be that as it may, the point is that our brain possesses receptors for endocannabinoids, and it is of those receptors that the cannabinoids in marijuana act. A receptor is a patch on a neuron which, when activated, produces a signal in that nerve. The receptor has a very specific shape and only things that will fit that shape will bind to the receptor.

JONATHAN LIPMAN: Yes. You might think of the receptor as being the lock and the chemical, either anandamide or THC or a synthetic, as being the key. When the combination occurs between the neurotransmitter and the receptor, it occurs with a certain vigor that is measurable by neuropharmacologists. A certain attraction. Think of it as the strength of a magnet maybe. And we call that attractiveness of the receptor for the neurotransmitter, we call that affinity. It's a measurable thing. Different drugs have different affinities for the receptor, and yet in order to evoke an effect, simply combining with the receptor is not enough. It must also provoke a response and --

JONATHAN LIPMAN: That is -- that response is also measurable, and that is called the efficacy of the neurotransmitter or the drug. So whether a drug produces an effect or not --

JONATHAN LIPMAN: Efficacy.

JONATHAN LIPMAN: Sorry.

JONATHAN LIPMAN: Yes. Affinity and efficacy, as we would say it in England, are measurable metrics in relation to the action of a drug or a neurotransmitter on a receptor in the brain. Now, when a drug produces a post-receptor action as a result of its binding, its affinity and its effect, its efficacy, we call that an agonist drug.

JONATHAN LIPMAN: Efficacy. Yes. Not all drugs produce such effects. And an example, for instance, of something that antagonizes an agonist, we call them antagonist drugs, is a drug that perhaps has high affinity to bind with the receptor will, perhaps, even displace the first drug from the receptor, but it has itself no efficacy. All it can do is bind.

JONATHAN LIPMAN: Naloxone, Narcan, is an example of an opiate drug that has high affinity, but no efficacy. Therefore, it competes with morphine for the opiate receptor, but it doesn't produce a morphine like effect itself, and this ends the morphine action by displacing it. So it has no efficacy, it has high affinity. Whereas, morphine itself has high affinity and high efficacy. It goes into the lock and it activates it.

JONATHAN LIPMAN: It has more affinity, but no efficacy. An example -- just to complete the metaphor -- or the example. Heroin has a higher affinity and a higher efficacy than morphine. If a person is under the influence of morphine, heroin can displace that and produce a greater effect because they're both agonists. They both have receptor binding capability and receptor activation capability. Narcan binds, but it has no effect, no efficacy. So it displaces.

JONATHAN LIPMAN: Yeah. Well, all of the receptors, and there are a number of receptors for the cannabinoids, are called the CB receptors. The one that THC acts on is the CB1 receptor. It's present in the hippocampus of the brain, it's present throughout the limbic system, and I mentioned earlier it has some very lower brain function areas that it is binding to, because that's where anandamide binds. The endogenous cannabinoid that we make ourselves.

JONATHAN LIPMAN: Yes, there is. The efficacy and the affinity may not be one-hundred percent. There are some drugs that will bind with great avidity to the receptor and you can't get them off. Some will bind gently and they can be bumped off by competing agents. Some will bind strongly and aggressively produce an effect. In a sense, when both affinity and efficacy are at maximum, we have what we call a full agonist drug.

JONATHAN LIPMAN: It is not. It is a partial agonist. It is weaker than a full agonist at binding to the receptor and producing post-receptor effects.

JONATHAN LIPMAN: Yes. Yes. It's a partial agonist. It's not a full agonist.

JONATHAN LIPMAN: They do. They do. Of course, they are not accompanied by the other compounds found in marijuana because they are synthetic. They are just modifications of the shape of the THC molecule made by neuropharmacologists and medicinal chemists for research purposes for exploring how the brain works and how therapeutic drugs may be developed.

JONATHAN LIPMAN: That's correct.

JONATHAN LIPMAN: The current generation are full agonists. Yes. There are some available that are partial agonists that have been made by medicinal chemists for research purposes. The reason why you would make them is because there's therapeutic potential in the endocannabinoid system.

JONATHAN LIPMAN: Well, anorexia, sexual dysfunctions, cachexia in cancer where people just starve themselves to death, insomnia in some cases. There are a number of psychiatric illnesses that cannabinoids have been purposed as potential treatment for, but we couldn't, of course, use THC. It's neither specific, nor potent enough, and marijuana contains too many compounds anyway.

JONATHAN LIPMAN: Yes, intentionally.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes. They're designed by medicinal chemists. So they are designer drugs.

JONATHAN LIPMAN: Yes. The first one was developed by J. W. Hoffman and the drug that -- well, a family of drugs are all called the J.W.H drugs because he named them. And J.W.H 017 and 018 were, I think, the first drugs that managed to escape from the lab, as it were, and find themselves in street use.

JONATHAN LIPMAN: It would have to be dozens. I -- about a year ago, I tracked how many new molecule entities are and each of them is really a different generation, and the number then was 150.

JONATHAN LIPMAN: That was a year ago. And they no longer really resemble THC at all either in their effect or in their pharmacology.

JONATHAN LIPMAN: Not entirely, but you're not getting legal weed. You will be getting a very selective effect due to a selective part of the marijuana experience. It would lack, for instance, the cannabidiol that marijuana contains.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: The oil presumably contains CBD. But there is no FDA control over that except in the case of one legal product, which is used in the treatment of a certain type of childhood epilepsy. That is FDA approved. I have no idea whether or if you will find true cannabidiol in CBD oil that you buy on the street. But yes, that's the intention.

JONATHAN LIPMAN: No, it does not affect it at all. No. It's actually an entirely different mechanism that really is not related to the intoxication effect of marijuana.

JONATHAN LIPMAN: There's no cannabidiol in synthetic marijuanas. They are all analogues. I shouldn't call it -- well, synthetic cannabinoids is best. They're all analogues, at least, built upon the structure of THC. Delta-9-THC.

JONATHAN LIPMAN: Yes. It is -- well, it is being evaluated as -- molecules derive from it. Excuse me. Not cannabidiol itself. But molecules designed by pharmacologists and medicinal chemists designed around the cannabidiol molecule are being evaluated for use and treatment of anxiety and psychosis.

JONATHAN LIPMAN: Well, it depends so much on the individual. Obviously, it produces euphoria in most people. It increases appetite, it has a range of potential adverse effects.

JONATHAN LIPMAN: Yeah. They will affect different people differently, and that relates to their underlying psychological integrity and history, but the -- obviously, the reason why a person would use marijuana or a synthetic is because they are looking for the euphoria. But even THC itself produces, in certain vulnerable people, states of high anxiety, irritability, fear, which can be irrational, which can be paranoid. It can also be grandiose. Paranoia is not always a fear. You may feel that you are a supernatural being with angelic powers. That is also a paranoia. Although, in the vernacular term, people use the word paranoid to mean only fear.

JONATHAN LIPMAN: Yes, it can. And in a large enough dose, even marijuana will do that.

JONATHAN LIPMAN: Yes. The drug has different effects on different people depending on what you might call how level the playing field is in their mind.

JONATHAN LIPMAN: I think most people have some loose bolts in their past, but -- or in their present or fears. But the adverse effects, even in a normal person, can resemble -- can involve panic and anxiety, and to some degree a psychosis like state that we call psychotomimetic, because it isn't true psychosis but it is like a psychosis, and it is transient. It isn't a permanent condition. Maybe --

JONATHAN LIPMAN: Yes. It's the adverse effects of the intoxication.

JONATHAN LIPMAN: No.

JONATHAN LIPMAN: P-S-Y-C-H.

JONATHAN LIPMAN: Yes. Psychotomimetic.

JONATHAN LIPMAN: It's mimetic of some psychiatric psychotic symptomatology, and it's an adverse effect of the drug. In the vernacular in the street, you will find some people say weed makes me paranoid. I start to hear police radios. I think people are following me. That is a psychotomimetic effect. And then, of course, after a few hours, it passes off.

JONATHAN LIPMAN: Yes. We'd call it an adverse effect. Some people would call it a side-effect. It depends on the individual as to how vulnerable they are to experiencing that. And that's the problem, you see. You're asking me what are the adverse effects in a normal individual. A normal individual is someone you don't know very well. There's a range of normality in normal.

JONATHAN LIPMAN: There are two factors that I have to explain in that regard.

JONATHAN LIPMAN: Psychosis does not usually emerge until quite later in development. Usually around age 20 plus. Prior to that, there may be a condition that we call prodromal psychosis. The person is not psychotic, but they are very unusual and magical in their thinking. Odd. They may be identifiably odd. That doesn't necessarily mean that they're going to turn out to be psychotic. The point being that psychosis is something that develops into adulthood. Now, we have found from a number of different studies, epidemiological and otherwise, that when cannabis, presumably due to its THC content, is used in early childhood, particularly prior to age 15, the odds of developing psychosis later on by age 26, according to one study, are considerably higher. They're, at least, threefold higher than normal, which means that, in part answer to your question of what is the relevance in psychosis, it can have a role in the development of psychosis in the first place.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: It can. And --

JONATHAN LIPMAN: There are multiple studies and -- because this is the reason why we should keep marijuana away from children because it could produce irreparable effects later on if they are vulnerable to it, but we won't know that they're vulnerable to it until they're in their very late teens.

JONATHAN LIPMAN: Yes, I do.

JONATHAN LIPMAN: Could you clarify your question?

JONATHAN LIPMAN: Oh, I see what you're asking. Yes. It's somewhat ironic in that we know that in schizophrenics, for instance, marijuana use makes their psychosis worse, and yet they claim that it relieves their dysphoric mood.

JONATHAN LIPMAN: Unhappiness. And I don't dispute that it may alleviate some of their dysphoric mood, but the problem that they're suffering from is not primarily a mood disorder. It is that they're out of contact with reality, and that is exacerbated by cannabis. So people with psychotic illnesses should not use THC or cannabis even though they may feel that it is helping their dysphoric mood, their unhappiness, because their underlying psychotic illness is exacerbated.

JONATHAN LIPMAN: It's gasoline on the fire of their illness.

JONATHAN LIPMAN: Okay. This is the point about psychosis. Psychotics don't think they are psychotic. Their view of reality is very, very different from ours, but it's their reality and they don't see themselves as mentally ill as a rule, unlike people who have a mood disorder who know that they're miserable and depressed and crying. That is identifiable. But when your thinking is so out of line with conventional norms of reality, that can be difficult to identify as an illness. You may think that you are particularly spiritual, for instance, or you may think that you are endowed with certain telepathic powers, or you may think that you are endowed with special functions that most humans don't have, but you do not think of yourself as ill.

JONATHAN LIPMAN: Yes, that's an example.

JONATHAN LIPMAN: Yes. Oftentimes -- let me point out that psychotic people of the schizophrenic variety are very often highly intelligent, but usually they are described as odd, idiosyncratic, a little weird, and their behavior may not be entirely congruent with what is typical, but maybe not enough to start the alarm bells running in peoples' minds. But an example that I could give you of a fellow that I evaluated who had this odd way of walking down stairs --

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Something labeled Scooby Snax, yes.

JONATHAN LIPMAN: It did, yes.

JONATHAN LIPMAN: Yes. I wanted not just confirmation of the AB Pinaca, but there was evidence coming across my desk that some of the synthetic cannabinoids containing AB Pinaca also contained other synthetic cannabinoids. And so, I asked that they be -- that the sample be examined to see if that was the case with this sample, also.

JONATHAN LIPMAN: Usually it's related to the medical -- the medicinal chemist who has developed the drug or the company that has developed the drug. In fact, AB Pinaca was developed by Pfizer Labs and patented by them in 2009.

JONATHAN LIPMAN: It is a pure agonist unlike THC and it has vastly greater potency as a combination of affinity and efficacy on the CB1 receptor. There are different ways of measuring that affinity and that efficacy, but it is of the order of possibly 20 times, and in some examples of research many more times more potent than THC itself. And it is not a partial agonist. It is a full agonist.

JONATHAN LIPMAN: It would actually displace naturally occurring THC from the brain.

JONATHAN LIPMAN: It doesn't have any other compounds. It's a pure THC agonist at the CB1 receptor.

JONATHAN LIPMAN: Typically -- the high typically lasts about 10 hours. We haven't got pharmacokinetic studies in humans of AB Pinaca. They haven't been published if they have been done. The --

JONATHAN LIPMAN: That means that no one has actually given it to normal volunteers, as far as I can tell, in the published literature, and measured their blood level and their effect over time. We've done that for the other compounds. The earlier ones. I mentioned the early synthetic J.W.H 017 and 018. That's being done ad nauseam. But as far as I know, no one has published -- they may have done the research, but they haven't published it, on measuring the blood level related to the mental effect. We know how it's metabolized, for instance, in the liver, but that doesn't tell us anything at all about its duration of action in the brain. Many drugs, for instance, disappear from blood not because they're being excreted, but because they're being deposited in the brain or other body tissues. So to see it disappearing in blood does not mean it has necessarily stopped acting on the brain.

JONATHAN LIPMAN: There are still effects. Yes.

JONATHAN LIPMAN: Well -- okay. Drugs are metabolized. An example, for instance, if I could just compare it to THC. THC from marijuana is metabolized ultimately to carboxy-THC. Now, carboxy-THC is inactive. It doesn't act on the brain, but it is deposited in fat, including -- presumably, including the myelin fat around the nerves, and it leeches out of body fat for a period of -- well, many days. In a person who is a regular user of marijuana who isn't using it anymore, from the time that they stop, their urine level, for instance, will go down about 15 milligram per ML per day for a month or more, and yet they're not high and the cannabidiol is leeching out of their body tissues into their urine, and thus being excreted. Now, that -- cannabidiol, as I said, is a metabolite of THC, but it is inactive. We do not have that situation with AB Pinaca. The metabolites of AB Pinaca are active. They are THC like, they are -- well, they're AB Pinaca like. And so, to show that the drug is converted to its metabolite does not, of course, mean that it is now inactivated in the case of AB Pinaca. Unlike the case of THC, that's likely an activation. The same is true of many therapeutic drugs. Prozac, Prozac is not an active drug. The metabolite of Prozac is the active drug. So to see it being converted by metabolism into its metabolite is to actually see the active drug being created.

JONATHAN LIPMAN: Let me just clarify what I wanted to say a moment ago. I was actually intending to use the word Risperdal -- Risperdal, because that's an anti-psychotic drug. Not Prozac. The therapeutic effect of it is therefore maintained by its metabolite. Here we have an intoxicating drug, AB Pinaca, and if metabolites are active -- now, it's not a therapeutic drug at the moment, but it's an example of how metabolism can actually continue the effect of the drug. So I think I answered your question that we don't know what the pharmacokinetics are. They're very complicated because the metabolites are active and they have not, as far as I know, by publication been measured in humans.

JONATHAN LIPMAN: It will make it very much worse, and because it's an underlying psychotic illness it is subject to becoming unstable and getting worse.

JONATHAN LIPMAN: Well, you might think of, say, an acrobat working on a high-wire. This would be, maybe, the psychotic in some state of balance, going to work and living a life with very unusual thoughts. If the drug then pushes them off the high-wire, their underlying illness in this metaphor is made vastly worse, and that exacerbation continues after the drug has left their system. The exacerbation is not simply a matter of intoxication on top of an illness. The illness is made worse by the intoxication. The underlying mental illness is made worse.

JONATHAN LIPMAN: Acute alcohol intoxication would not be appropriate, but there is actually an analogy in alcohol in that where we have populations of people who used to be alcoholics and some of the VA domiciliary units are filled with these people. Their alcohol intoxication has damaged their brain. They are no longer drinking, but they are no longer normal and they are demented, and their intoxication continues until death, but there is no alcohol there.

JONATHAN LIPMAN: Yes. It was legal. I did research that.

JONATHAN LIPMAN: The FDA published an announcement -- no. I'd have to look it up. But it was, I think, the following year. Maybe even later.

JONATHAN LIPMAN: Yes, I can.

JONATHAN LIPMAN: That's the trade name.

JONATHAN LIPMAN: Yeah.

JONATHAN LIPMAN: Chantix, the actual drug is called Varenicline. Oddly, it's also made by Pfizer Pharmaceuticals, the company that patented AB Pinaca. It is a synthetic drug, but it is based on a natural compound called cysteine that is found in the Scotch broom shrub, and cysteine has a nicotine like effect on the brain's receptors. In fact, during the Second World War, I believe, when tobacco imports from America were halted in Europe, Scotch broom was used as a smoking material for people who were dependent on nicotine. It does substitute. So, obviously, you can't patent a natural product. Therefore, the company made a modification of that molecule and called it Varenicline and trademarked it as Chantix.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes, indeed, there were.

JONATHAN LIPMAN: Well, they emerged in the pre-market approval. They were so serious with attempted suicides, depression, psychosis, hallucinations, that in applying for a license to market the drug to the Food and Drug Administration, the Food and Drug Administration insisted that they put what's called a black box warning. The black box warning -- I have it in front of me. Should I read it?

JONATHAN LIPMAN: Yes, I do.

JONATHAN LIPMAN: Yes, it is.

JONATHAN LIPMAN: Yes, it was.

JONATHAN LIPMAN: I would need a hand lens, but it looks the same.

JONATHAN LIPMAN: It's a requirement of the Food and Drug Administration and they are not common. In order to obtain marketing approval of a drug through the Food and Drug Administration, what the Food and Drug Administration actually controls is -- apart from the purity and quality of the drug itself, is what's called the label. The label is what most people would call the package insert, and this contains detailed instructions to the practitioner, to the patient, to the pharmacist regarding what the Food and Drug Administration believes, and the company has agreed the users and practitioners need to know. Most labels don't have a black box warning. A black box warning is potentially a reason to keep a drug off the market, unless it is black boxed, and that is -- therefore, there is complete disclosure that there is a problem with this drug and that is put on the black box in the labeling.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes, sir.

JONATHAN LIPMAN: Okay.

JONATHAN LIPMAN: There's only one way that I know, but that way involves several different doses. The patient is given what's called a starter pack and the starter pack, this has green coloration, contains 11 doses of .5 milligram, a half a milligram, to begin treatment and 42 tablets of one milligram tablets to be used in the continuing weeks after the initial week. And the process begins with taking one white pill, that's half a milligram, daily for days one through three, followed by one white half a milligram pill twice daily on days four through seven, and thereafter the patient takes continuation doses of one blue pill, that's a milligram, twice daily. Now, the subsequent doses are all of the latter type. They are all blue one milligram doses.

JONATHAN LIPMAN: That's a starter box. Yes.

JONATHAN LIPMAN: Yes. You would not be touching the blue box until you had finished the starter box or you'll become quite ill.

JONATHAN LIPMAN: It's a different kind of box now. We're talking about the box on the label.

JONATHAN LIPMAN: Yes. It was removed in December of 2016 following the representation by the company to the Food and Drug Administration that it had performed a study that they argued meant that the black box did not -- that the information could still be there, but not in a black box.

JONATHAN LIPMAN: Pfizer, the drug company.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: It is. Several publications came as a result of that. I've reviewed several of them. Not all of them.

JONATHAN LIPMAN: I did, but in order to explain it, I actually have to -- with tolerance of the Court, I have to read something from the black box or it won't -- my answer won't make any sense.

JONATHAN LIPMAN: Or let me do it from the monograph instead. "Patients should be observed for neuropsychiatric symptoms or worsening of pre-existing psychiatric illness, e.g., schizophrenia, depression --

JONATHAN LIPMAN: "Patients should be observed for neuropsychiatric symptoms or worsening of pre-existing psychiatric illness, e.g., schizophrenia, depression, bipolar disorder, during treatment with Varenicline due to some serious neuropsychiatric symptoms reported during use of the drug. Post-marketing reports have included mood or behavioral changes or a psychiatric event such as a psychosis, hallucinations, paranoia, delusions, homicidal ideation, hostility, agitation, anxiety, panic, mania, depression, suicidal ideation, suicide attempt and completed suicide in patients with or without a psychiatric history." Now, the EAGLE study was a study done by the company in psychotic patients. They were either schizoaffective or schizophrenic. They were selected for the study on that basis, and they were all under psychiatric treatment taking antipsychotic drugs. They were all stable, and if they'd had an episode, a return of psychosis or other mental illness in the previous months prior to the giving of them Varenicline, then they were excluded from the study.

JONATHAN LIPMAN: That's correct. And the company reported that unbalanced Varenicline was safe in those people who were actively under medicated antipsychotic control and mood control and monitored by therapists. However, even in that study, more patients in the Varenicline treated psychiatric cohort had serious neuropsychiatric events involving a psychiatric hospitalization than in patients receiving a placebo even in the EAGLE study, according to a review that I am reading, but the FDA agreed that the black box warning could be removed.

JONATHAN LIPMAN: Yes, I have. I don't have it in front of me, but I'm familiar with what he's been taking.

JONATHAN LIPMAN: It is.

JONATHAN LIPMAN: Pfizer, ironically.

JONATHAN LIPMAN: Yes, sir.

JONATHAN LIPMAN: Absolutely not or not to my knowledge. I can't imagine anyone wanting to.

JONATHAN LIPMAN: It is -- unless you're suffering from psychotic agitation, you would find the effect of Geodon suffocating. It would be oppressively tranquilizing, clouding of consciousness, blunting of mood, it blunts euphoria, which is why it's also useful in bipolar disorder and mania. It would be quite unpleasant as far as I'm aware.

JONATHAN LIPMAN: There is a risk with all of these drugs, less so with Geodon than some of the early ones, of producing brain damage. You can see the effects of it when the drug is still being given as a kind of tremor, extrapyramidal syndrome. The muscles may also be affecting the mouth and the tongue and the neck, which can effect voice. Speed of thought is clouded, slowed. Word-finding ability is impaired. There are neuropsychological impairments across the board. However, some of the effects on the striatum of the brain can be permanent, and tardive dyskinesia is the one that we worry about, which is a sort of parkinsonism syndrome. You do not use this drug unless the risks and benefits are carefully weighed and in a person who doesn't need it psychiatrically, there are no benefits. All there is, is risks. No physician would do that.

JONATHAN LIPMAN: That would be assault.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: It's quite short. Unlike some of the older more established antipsychotic drugs, the effect of the drug dissipates over about eight hours. So the drug is given regularly daily, and in some patients they clear it a little more quickly than others due to their metabolism, they are very, very ready for the next dose because their symptoms are already returning. This is quite different from some of the other longer acting older drugs. In some cases, they only need to be given once a day. In some cases, once every two weeks, but with Geodon, you cannot miss a dose. It is critical that you not miss a dose. You must carry the dose with you so that you do not miss the dose.

JONATHAN LIPMAN: There would be, yes. You would expect not only uncovering of the underlying illness, but because the underlying illness has been kept under control, suppressed by the drug therapeutically and benevolently, there is a risk of what we call rebound psychosis when the drug is discontinued for withdrawn, and rebound psychosis can be even worse than the underlying condition was before treatment began until it stabilizes.

JONATHAN LIPMAN: Yes, I do.

JONATHAN LIPMAN: It would have exacerbated his underlying psychiatric illness.

JONATHAN LIPMAN: I don't know.

JONATHAN LIPMAN: I don't remember. I'm sorry.

JONATHAN LIPMAN: It may or may not include Geodon. If you could refer me to what you're addressing, I will answer you.

JONATHAN LIPMAN: Yes. I think I referred to these side effects in my direct testimony. I said it would be slowing. It would be impairing. It would not be desirable.

JONATHAN LIPMAN: No. I can only -- I can only say that you represent it so. If I could have a few minutes with a computer --

JONATHAN LIPMAN: -- I could?

JONATHAN LIPMAN: I will need wireless.

JONATHAN LIPMAN: Yes. I testified in my direct about the side-effects that would be produced in a person who didn't need it. It would be quite unpleasant. They would be sedating, they would be disabling cognitively.

JONATHAN LIPMAN: I said all of the antipsychotic drugs. I didn't specifically say Geodon.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I would have to review my records.

JONATHAN LIPMAN: Yes, it was.

JONATHAN LIPMAN: Thank you. I have my notes. I don't actually have the record. But my notes say that he was admitted on the 13th of September, I believe, in safekeeping status without being on it. Let me double check that. Let me check that. And in the period 18 September to 25 September, he was getting Geodon 20 milligrams. And then on 25 September, the instructions were increase to one in the morning and two at night. That would be 60.

JONATHAN LIPMAN: On the milligrams that were being then dispensed, it would be 60 milligrams a day.

JONATHAN LIPMAN: No.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: In my notes, it says 18 September, 2014.

JONATHAN LIPMAN: But I don't have the actual notes in front of me.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: I am aware.

JONATHAN LIPMAN: On the 9th of October another drug was added. That was Prozac. And then -- which is relevant. And then on the 20th of November, his Prozac dose was increased to 60 milligrams a day.

JONATHAN LIPMAN: And then, although we don't have the dispensing record, we have a note here that he was, in fact, also being given Nortriptyline. That note being on the 10th of June, 2015.

JONATHAN LIPMAN: N-O-R-T-R-I-P-T-Y-L-I-N-E.

JONATHAN LIPMAN: That is a tricyclic antidepressant drug.

JONATHAN LIPMAN: One of the earlier tricyclics. Yes.

JONATHAN LIPMAN: And then, continuing to review my notes. Apparently, my notes do not continue beyond that. I am aware -- I have been told that his doses has been increased several times since then.

JONATHAN LIPMAN: I don't.

JONATHAN LIPMAN: Yes. Well, I don't have the Geodon literature in front of me, but I believe that to be true.

JONATHAN LIPMAN: There's no prohibition on using it above the maximum recommended dose. That is up to the discretion of the physician at their own risk.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes. Considering the risks and the benefits.

JONATHAN LIPMAN: I don't, but I -- well, if you could, perhaps, draw my attention to --

JONATHAN LIPMAN: Could I see the face page of what you're holding? I don't seem to have one with that date.

JONATHAN LIPMAN: Yes, I did. And thank you, I believe I found it. But there was more than one report, and due to some error, I do not have, in my file the one that you're holding.

JONATHAN LIPMAN: I do, but my point was, I have a report dated 2000 -- 13 November, 2017 that is different from the one that you are holding. It's a single page and it addresses the AB Pinaca found in blood and packaging.

JONATHAN LIPMAN: I recognize it, yes.

JONATHAN LIPMAN: Yes, ma'am.

JONATHAN LIPMAN: Correct. I did say that and I do believe that.

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: Well, I've been told so. I don't have any proof of it.

JONATHAN LIPMAN: The Defense attorney.

JONATHAN LIPMAN: He didn't mention any dosage. He just said it had been increased.

JONATHAN LIPMAN: It's possible that it had been decreased, and then increased back to 60. I don't know. I don't -- all I know is I was told it has been increased.

JONATHAN LIPMAN: I would like to have that information. It depends as to what question I'm being asked as to whether I need to rely on that.

JONATHAN LIPMAN: I haven't got recent prescription dispensing records for him. No.

JONATHAN LIPMAN: I don't have the -- I'm still reviewing. I don't have the -- the FDA package insert that I offered to print out when you asked me the previous question and I need it to answer this question.

JONATHAN LIPMAN: Because this doesn't say that he was getting 80 milligrams a day.

JONATHAN LIPMAN: Right. Without seeing the prescribing information, the FDA prescribing information that I offered to get on the previous question, I can't answer this question or the previous question or the one prior to that.

JONATHAN LIPMAN: Thank you.

JONATHAN LIPMAN: Yes. It doesn't actually describe the maximum dose on this page, but it does describe the typical dosing.

JONATHAN LIPMAN: Yes. Could I keep this here?

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: No. Not on this page. Oh, I'm sorry. Are you asking me to look elsewhere?

JONATHAN LIPMAN: Give me a moment, please. You've handed me two pages. The first page pertains to his administrations in April of 2016 and no other time. The second page, which relates to June of 2016 and at no other time, is not to be added to what he took in April. Am I misunderstanding your question? Could you clarify?

JONATHAN LIPMAN: Yes. In April, he was getting two dosages of 80 milligrams of Geodon a day, and in June he was getting two doses of Geodon a day in June.

JONATHAN LIPMAN: I fail to find your 360 milligrams.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: You have stapled together two pages. Maybe I could review this more closely. One of them pertains to a prescription on the 19th of November, 2015. The other pertains to a prescription on the 28th of April of 2016 beginning only on the 1st of the month. They are not -- I don't understand your question.

JONATHAN LIPMAN: It's just not --

JONATHAN LIPMAN: It's just not on these pages. I'm sorry.

JONATHAN LIPMAN: Regarding his neuropsychological testing only. Yes.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I still haven't seen that record, but --

JONATHAN LIPMAN: I'm happy to accept any stipulation.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes. As I wrote in 2016.

JONATHAN LIPMAN: Let me check my record. Again, I'm going from my notes rather than the actual record. I found in the 7 February 2014 record from Doctors Care, which was a clinic, John Saunders was the physician, that he was given a Chantix starter pack with two continuing months.

JONATHAN LIPMAN: The date I just spoke was 7/4 -- 7 February of 2014.

JONATHAN LIPMAN: Yes. That's what my note says.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Not with any certainty, no.

JONATHAN LIPMAN: No.

JONATHAN LIPMAN: That's correct.

JONATHAN LIPMAN: That's what he told his doctor. Yes.

JONATHAN LIPMAN: It does.

JONATHAN LIPMAN: I see that now. I have not seen them before.

JONATHAN LIPMAN: No.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct. You're also missing the starter pack, I think.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Apparently, yes.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: No.

JONATHAN LIPMAN: Let me answer that --

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: For some reason, I don't have that. It's possible I didn't. Let me --

JONATHAN LIPMAN: Let me look at my record of reviewed notes.

JONATHAN LIPMAN: Yes, I have that. Please name the last one that you --

JONATHAN LIPMAN: It's not in my list. I'm sorry.

JONATHAN LIPMAN: It appears not.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: That was his conclusion. Yes.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Yes. For its duration of use -- duration of action.

JONATHAN LIPMAN: That's correct, also.

JONATHAN LIPMAN: Well, psychosis is not one of them. That's the effect of the drug, not the withdrawal. Although, the effect on a person with an underlying psychosis can be very, very persistent.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: That is correct.

JONATHAN LIPMAN: That's correct, too.

JONATHAN LIPMAN: That is true. Yes.

JONATHAN LIPMAN: That's also true.

JONATHAN LIPMAN: Yes, that's right.

JONATHAN LIPMAN: On its own. Yes, I am.

JONATHAN LIPMAN: The only information I have is his self-report and the physical evidence that was attributed to his historic use. I don't have any blood from the time, for instance.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Yes, I do.

JONATHAN LIPMAN: I'm aware of that.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I think that was true, wasn't it?

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: I think I recall that, yes.

JONATHAN LIPMAN: That wasn't true, no.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I don't actually recall that.

JONATHAN LIPMAN: Yes, he was.

JONATHAN LIPMAN: He was able, yes.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: I actually don't recall that, but I accept that he did, yes.

JONATHAN LIPMAN: It wouldn't make any difference. His use on that day is not material. I wasn't suggesting that his intoxication at the time of the offense resulted in the misbehavior. My suggestion was that it exacerbated his underlying mental illness.

JONATHAN LIPMAN: That doesn't go --

JONATHAN LIPMAN: That doesn't go away when the drug goes away. That puts him -- that knocks him off the rails. And to that extent, he remains in need of antipsychotic medication.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: I have no doubt that Dr. Agharkar and Dr. Smith have diagnosed him as suffering from a psychosis spectrum mental illness.

JONATHAN LIPMAN: I rely on them for that diagnosis.

JONATHAN LIPMAN: He had -- I rely on him having told respondents that he had used it for two months prior to the killings and was continuing to use it after the killings.

JONATHAN LIPMAN: I'm not sure about that.

JONATHAN LIPMAN: My recollection is that he has said that he was using it for about two months prior. I think he told Dr. Frierson the same thing, and he's told the other psychological/psychiatric examiners the same thing.

JONATHAN LIPMAN: And I would add that his present condition is not being treated lightly. Whoever is prescribing him his medications right now is prescribing him because he has a psychotic mental illness.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I have not said that at all. What I said is -- what I continue to say is that he has told all of the examiners that he had been using it for about two months prior to the offense and continued to use it until his time of arrest following the offense. This is a drug that can exacerbate underlying psychosis spectrum mental illness. He continues to suffer very severely from psychosis spectrum illness. He is not now using AB Pinaca, we can assume, and yet his mental illness is profound enough for him to require antipsychotic medication.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Yeah. I haven't assessed his reliability. I really have no opinion about his reliability. My opinion is based on the assumptions that I have made, which I have described.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: I haven't assessed it.

JONATHAN LIPMAN: I do not.

JONATHAN LIPMAN: I charge for my time.

JONATHAN LIPMAN: I charge $275 an hour, time out of office, plus expenses, and $375 in court or deposition.

JONATHAN LIPMAN: I don't think I brought my invoices. It's not typically something I would be carrying. I'm sure it was a lot.

JONATHAN LIPMAN: I'm sure it was a lot.

JONATHAN LIPMAN: But --

JONATHAN LIPMAN: Possibly. Possibly.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: Correct.

JONATHAN LIPMAN: I drove here.

JONATHAN LIPMAN: I am. My assessment was that it would actually take longer to get here if I flew --

JONATHAN LIPMAN: -- coming from where I'm coming from.

JONATHAN LIPMAN: I'm being paid for my time.

JONATHAN LIPMAN: Correct. That was not my referral question.

JONATHAN LIPMAN: Apparently so.

JONATHAN LIPMAN: Apparently not.

JONATHAN LIPMAN: Yes, he is.

JONATHAN LIPMAN: I'm sorry. He is not. He's got to start it all over again.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yeah, or he'd be very sick.

JONATHAN LIPMAN: I did.

JONATHAN LIPMAN: Is that Schwartz-Watts?

JONATHAN LIPMAN: Yes, I did.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: It tells me that they are receiving a very large dose --

JONATHAN LIPMAN: Yes.

JONATHAN LIPMAN: It is what's -- it is what's done. And/or other medications are added, which are called adjunctive. I haven't seen his current prescribing information.

JONATHAN LIPMAN: Yes. 195 is two pages that are totally disconnected in time. It's rather misleading that they be stabled together like this. But I can answer the question.

JONATHAN LIPMAN: The first, which relates to the 1st of April, 2016 to the 30th of April, 2016, describes his daily administration record for Propranolol, which is a beta blocker drug. It lowers blood pressure, but also is used in the treatment of anxiety and PTSD. Ranitidine, which is something that's an antihistamine of the H2 class. Relevant to psychiatry is the fact that he's taking the Ziprasidone, that's the Geodon, and he's taking Prolixin 2.5 milligram, one tab in the morning and two tabs at bedtime, and Benadryl 50 milligrams. Now, Prolixin is one of the older antipsychotic medications. It's more stunning, more tranquilizing and it has a greater risk of producing both extrapyramidal syndrome and tardive dyskinesia. So he's taking two antipsychotic drugs. One is the Ziprasidone. The other is Prolixin. Prolixin, he's taking twice a day, Ziprasidone, twice a day, and the Benadryl he's taking twice a day. And although Benadryl is a common name and an over-the-counter drug, its use in this context is almost certainly in the treatment of the extrapyramidal syndrome because Benadryl, in addition to its antihistamine effects, is anticholinergic and it helps to control the Parkinsonian like twitching and shaking that is a side-effect of the antipsychotic drugs. You had asked me -- you had handed me the two pages together and the second one is of months later. It shows that he's still taking Ziprasidone twice a day. But in addition, he's also taking Fluoxetine 20 milligram, that's Prozac, and Mirtazapine 15 milligram at night. That is a sedative antidepressant drug. It's called Remeron. And he is taking -- that's interesting. I'm having difficulty reading some of this scribble. I'm sorry. And he is -- there may be another page, but it looks as though he's not taking the Benadryl. Oh, yes, he is. His Benadryl dose is now twice a day. 50 milligrams twice a day. So that is continuing. So that was in June. Therefore, there's been a change in the prescription of the drugs that are being given with the Geodon -- with the Ziprasidone, but he's still taking the Ziprasidone twice day 80 milligram. That's 160 milligram in April and in June of 2016.

JONATHAN LIPMAN: I guess, it does. Yes.

JONATHAN LIPMAN: Yes, apparently. Yeah. I haven't seen that -- those before.

JONATHAN LIPMAN: I have not actually researched that. That is certainly true, but the recommendation of the manufacturer is to discontinue if necessary.

JONATHAN LIPMAN: I believe that's correct.

JONATHAN LIPMAN: Well, he was diagnosed with a bipolar mood disorder.

JONATHAN LIPMAN: I believe that's correct. Yeah.

JONATHAN LIPMAN: Regarding the use of AB Pinaca and Scooby Snax and other cannabinoids for two months prior to and up to the time of arrest.

JONATHAN LIPMAN: No. Particularly from the prison, they're based on physicians, psychiatrists, nurse technician observations of him for months and months and months. He was not immediately put on antipsychotic medication after arrest. His condition had to be evaluated, and ultimately it was, and he is diagnosed as suffering from a psychosis spectrum mental disorder.

JONATHAN LIPMAN: Could you ask the question again?

JONATHAN LIPMAN: I may have misunderstood.

JONATHAN LIPMAN: I'm trying to refresh my memory.

JONATHAN LIPMAN: Well, I think there was also some neighbor witness interviews, but, essentially, yes.

JONATHAN LIPMAN: Could I look at my --

JONATHAN LIPMAN: Notes? I may be thinking of a different case.