Tag Archives: Brook Harris

What Dr. Kurtzman Knew

March 27, 2013

I apologize for not posting this on the date promised, real life got in the way.


In her blog Toni Ingram has consistently criticized Dr. Robert Kurtzman for conclusions he reached in the autopsy of Morgan Ingram.  Toni has claimed on more than one occasion that retired medical examiners, two forensic pathologists, doctors, specialists, and a pharmaceutical scientist have all contacted her to let her know that Dr. Kurtzman should have known right away that the level of amitriptyline found in Morgan’s blood was lethal.   Apparently Toni expects readers to believe members of the medical community would criticize one of their own for not jumping to an immediate conclusion and exercising too much caution.  Although I don’t believe Toni I was curious why Dr. Kurtzman did not rule Morgan’s death a suicide from the very beginning.  Did Dr. Kurtzman know something we don’t?  Could death by amitriptyline intoxication be more complex than Toni Ingram would like her readers to believe?  The answers required research.

As I began researching Amitriptyline it became evident to me that information from the Morgan’s Stalking blog contradicted my research.  I will note these contradictions as they occur.

So what exactly is amitriptyline?

Amitriptyline is a disturbingly effective killer; a chemical perfect storm for the suicidal.  It is an extremely complex medication originally approved by the U.S. Food and Drug Administration to treat various forms of depression.  It also has several off-label uses (off-label means not FDA approved) such as treatment of neuropathic pain, and migraine prophylaxis.  Amitriptyline is a tricyclic, antidepressant, so-called because of its three-ring chemical structure.  It is the most frequently abused/misused of the tricyclic antidepressants.  In a review of 165 persons with tricyclic poisonings admitted to one hospital in a two year period, 62% involved amitriptyline.

Amitriptyline is readily absorbed from the gastro-intestinal tract, with peak plasma concentrations occurring within a few hours of oral administration (contradicts MS blog, “She would have to have been given this stuff between noon and nine pm-ish for that high of a levelSeptember 15, 2012  http://morganingram.com/wordpress/?p=1207 )

It is highly lipid soluble meaning it is stored by fat cells and not released until the body exhausts the rest of the dose.Peak drug concentrations occur early and this is the reason why most deaths from poisoning occur outside the hospital.

Amitriptyline undergoes extensive first-pass metabolism and is demethylated in the liver to its primary active metabolite, nortriptyline. Amitriptyline is widely distributed throughout the body and is extensively bound to plasma and tissue protein.

AMI is a mild antiemetic (prevents vomiting) and in fact is used successfully to treat a condition called Cyclic Vomiting Syndrome. (contradicts MS “did not regurgitate any of them back up, as is most common with Amitriptyline” and ”A research scientist and doctor who works at a pharmaceutical company has assured us there is no way Morgan could ingest enough Amitriptyline to produce that level without vomiting it up. It can’t happen” March 12, 2013 http://morganingram.com/wordpress/?p=3198).

Amitriptyline is anticholinergic and therefore will inhibit parasympathetic nerve impulses by blocking acetylcholine. Acetylcholine is a vital neurotransmitter that is released at the ends of nerve fibers in the somatic and parasympathetic nervous systems and transmits nerve impulses across a synapse.  The nerve fibers of the parasympathetic system are responsible for the involuntary movements of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, etc.  This is why Morgan developed pulmonary edema, not because  her heart stopped for only a few seconds, then her lungs would have automatically filled up with fluid and this would have been enough to kill her,”  March 26, 2013  http://morganingram.com/wordpress/?p=3386

The anticholinergic effect is exponential to the amount of the drug consumed. To put it plainly, amitriptyline slows down vital body functions, including significant reduction in gastrointestinal mobility.This results in a prolonged period of absorption.

If all this was not enough, amitriptyline and its active metabolite nortriptyline are subject to enterohepatic recirculation.  This means it is secreted into bile which is held by the gall bladder and dumped back into the small intestine creating an efficient deadly cycle.

Amitriptyline has a narrow therapeutic index, meaning there is a fine line between a therapeutic and toxic dose.  A lethal dose can be as low as 5mg/kg.  Morgan Ingram weighed 115 lbs. or 52.1 kg., so theoretically a fatal dose could have been as low as 260.5 mg or approx. 10 25 mg pills.  The fact that such a small amount could be fatal is another unique characteristic of amitriptyline (contradicts MS “18 – 25mg pills is 450 mg., simple math 18 X 25 = 450.  And it is not a lethal dose, yes you read that right, 450 mg. is not a lethal dose.  Once again I welcome you to find a qualified expert who will testify that 450 mg. of Amitriptyline is a lethal dose” March 15, 2013  http://morganingram.com/wordpress/?p=3272

Any “qualified expert” could tell Toni Ingram the most frightening fact about amitriptyline is scientists do not know how it will behave from one patient to the next due to a high degree of genetic variability in the specific liver enzymes that process the drug.  A lethal amount for one person might have little effect on another.  Depending on the genetic variant, the liver enzyme that processes amitriptyline, known as CYP2D6, will metabolize in one of the following ways:

Poor metabolizer–these subjects have little or no CYP2D6 function

Intermediate metabolizers–these subjects metabolize drugs at a rate somewhere between the poor and extensive metabolizers,

Extensive metabolizer–these subjects have normal CYP2D6 function

Ultra rapid metabolizer–these subjects have multiple copies of the CYP2D6 gene expressed, and therefore greater-than-normal CYP2D6 function

The only way to know which variant a patient will express, other than trial and error, is to run a plasma concentration assay.


In light of this drug’s many complexities, I hope it’s obvious to readers why Dr. Kurtzman didn’t immediately and carelessly blame amitriptyline for Morgan’s death.  Given Toni Ingram’s previous track record for omitting facts that undermine her version of the “truth,” I don’t think I’m off base suggesting we don’t have the entire story.  I strongly suspect Dr. Kurtzman told the Ingrams he was issuing a tentative death certificate per legality, but cause and manner could change as pending reviews and results became available.

By gaining a greater understanding of amitriptyline I unintentionally gained a greater understanding of Toni Ingram.  I believe the numerous unnamed medical experts and their opinions of Dr Kurtzman are fabrications born out of desperation.   In my opinion this woman is so arrogant, so convinced of her superiority she didn’t even bother to research how amitriptyline is processed.  I don’t think it occurred to her that anyone would question what she says.

Toni knows Keenan Vanginkel and Brooke Harris will never be charged with murder.  The alleged evidence consists of hearsay and lies and the visions of psychics and pet communicators.  There is no chain of custody for the alleged physical evidence.

There is no cover-up being perpetrated by the police or the forensic pathologist. Why would they risk their careers to protect Keenan?  He’s a kid who works at a grocery store.  He doesn’t have any connections or know anyone with political clout.

Toni Ingram knows this but she will never accept it.


Toni Ingram, full credit for italicized quotes, 2012-2013 Morgan’s Stalking, http://morganingram.com/wordpress/

Gergov, Merja, et al. “CYP2D6 and CYP2C19 genotypes and amitriptyline metabolite ratios in a series of medicolegal autopsies.” Forensic Science International 10 May 2006: 177+. Academic OneFile. Web. 15 Mar. 2013.

Bachofer, Julia, et al. “Amitriptyline or not, that is the question: pharmacogenetic testing of CYP2D6 and CYP2C19 identifies patients with low or high risk for side effects in amitriptyline therapy.” Clinical Chemistry 51.2 (2005): 376+.

Academic OneFile. Web. 15 Mar. 2013

/CASE REPORTS/ In a case of acute overdosage (225 mg) a patient in light coma had temporary complete oculomotor paresis, unresponsive to caloric stimulation or doll’s head maneuvers.

[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 85] **PEER REVIEWED**

/CASE REPORTS/ A 34-yr-old man … suffered from severe adverse effects during treatment with amitriptyline, 50 mg/day. It was subsequently shown that the patient was a slow metabolizer of amitriptyline. However, he tolerated a dose of 200 mg of imipramine/day, which was necessary in order to reach a therapeutic level of about 900 nM for imipramine plus desipramine.

[Broson K et al; Ther Drug Monit 13 (2): 177-82 (1991)] **PEER REVIEWED** PubMed Abstract



     March 29, 2013 2:54 P.M.- Grammar

     April  2, 2013  3:16 P.M – Added and corrected attributions.

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