Psychosis Urine Test

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Psychosis Urine Test

 

Journal of Orthomolecular Medicine: The Discovery of

Kryptopyrrole and its Importance. Vol. 10, No. 1, 1995

 

The Discovery of Kryptopyrrole and its Importance in

Diagnosis of Biochemical Imbalances in Schizophrenia

and in Criminal Behavior

 

by Abram Hoffer, M.D., Ph.D.

 

In this issue (JOM, Vol 10, No 1) Dr. Richard T. Kraus

describes a notorious serial killer who is serving a

250 year sentence for the murder of eleven women.

Unfortunately, serial killers are not a threatened

species. On the contrary, they threaten society more

and more, and with modern weapons of destruction seem

to be even more effective. This case report may be the

first in which four main factors which determine human

behaviour are discussed in detail. Dr. Kraus describes

“...a matrix of genetic, biochemical, neurological and

psychological deficits”. I am particularly interested

because the kryptopyrrole ( " kp " ) which was found in

this person’s urine was originally discovered in

Saskatchewan about 1960 when I was Director of

Psychiatric Research. The main biochemical research

was completed in Saskatchewan by Dr. D. Irvine,(1) and

in New Jersey by Dr. C. C. Pfeiffer (1) and his

research group of biochemists.

 

This report provides a model of how criminal behaviour

ought to be explored, with numerous references to the

medical literature for all of the four variables. I

will discuss mainly the biochemical findings and

provide a brief history of its discovery. The presence

of kp in urine is a valuable diagnostic aid especially

for determining more specific treatment. It is most

closely related to the schizophrenias but cuts across

all diagnostic categories. I think it could become an

important differential diagnostic test. It is simple

to do, any competent medical laboratory can do it. The

laboratory in Victoria has been

running them for me since 1976.

 

By 1960 the biochemical unit of the psychiatric

research program in Saskatchewan was gearing up to

investigate any possible relationships to the

schizophrenias. One of the studies involved examining

urine for several fractions and comparing the urine of

patients and controls. We were then treating many

alcoholics using psychedelic therapy. D-lysergic acid

diethylamide (LSD), the hallucinogen, was well studied

as a compound which could induce a model psychosis or

a psychotomimetic experience. It occurred to me that

inasmuch as LSD produced something very similar (but

not identical with) schizophrenia, perhaps it might

also generate in the body of a person (not

schizophrenic) the same type of biochemical

abnormality which we thought was present in the

patients. I asked Dr. N. Payza to examine the samples

of urine obtained from an alcoholic who had been given

LSD as part of his treatment.

 

The first morning specimen was obtained and another

one around noon, usually the height of the experience.

My idea was that if something appeared after LSD which

was not present before, this might give as a lead. We

were fortunate because the first patient we tested had

a large amount of a substance that was not present in

the morning specimen. We soon showed that it was not a

breakdown product from the LSD itself, which meant it

was created in the body by the impact of the

hallucinogenic drug upon one of the biochemical

systems. After we had improved the assay procedure we

began to test patients. One day I took into the

laboratory 12 specimens of urine. Six were obtained

from schizophrenic patients, five were obtained from

normal subjects and one was a blank. The code was kept

secret. I asked the biochemical team to analyze these

samples and to tell me which of the 12 were obtained

from the schizophrenic patients. They accurately

spotted all the schizophrenic samples. I concluded

that schizophrenic patients, not given LSD, had the

same substance in their urine as did some alcoholics

who had been given LSD, but that it was not present in

normal controls.

 

We needed large amounts of material for our chemical

studies. Fortunately for us a chronic schizophrenic

woman on the ward had huge quantities of this product.

For a moment we considered calling the compound the

Jensen factor. At first we called it the unknown

substance (US), and later the mauve factor because

when developed on the paper chromatogram it stained a

beautiful mauve. When it was identified we called it,

more accurately, kryptopyrrole. We named the disease

characterized by large amounts of mauve factor

“malvaria,” but Dr. Pfeiffer later gave it the more

appropriate term pyrolleuria.

 

I immediately started two lines of investigation: (1)

by Dr. Payza for short time, and then by Dr. D. Irvine

who continued the research first at the Research

Laboratory at the Saskatchewan Hospital in North

Battleford, and later at University Hospital in

Saskatoon. The objective was to determine the

structure of the substance and its source. (2) To

study its clinical correlates, i.e. could it be used

to assist in diagnosis, could it have therapeutic

significance, and could it be used to follow patients

both to determine if they were improving, and to

determine if they were getting worse.

 

Dr. Irvine showed that it was a pyrrole, later

identified as kryptopyrrole. We began to cooperate

with Dr. C. C. Pfeiffer at Princeton, New Jersey. Dr.

H. Osmond, my colleague in the earlier Saskatchewan

research, was then Director of Research for the state.

The two laboratories did the basic work. Dr. Pfeiffer

and his team discovered how to measure the amount of

this substance in the urine using a fairly simple

test, and they showed that this substance bound with

pyridoxine and zinc and when present in large amounts

produced a double deficiency of this vitamin and the

mineral. On the clinical side he described the

syndrome pyrolleuria, a form of schizophrenia with

clearly marked out symptoms and signs which could be

diagnosed by the present of kp in the urine.

 

Several years later we had examined thousands of

patients at three hospitals for the mauve factor.(2)

It was present mostly in schizophrenic patients but

was also present in one-quarter of other non

schizophrenic patients including depressions,

alcoholics, anxiety states, and in children with

learning and behavioral disorders. It was rarely

present in normal subjects, and was present in ten

percent of a non psychiatric stressed population drawn

from the surgical wards of the hospital. To my

surprise it was found in most cases of lung cancer.(3)

I found the following relationships:

 

1) Relationship to diagnosis - The mauve factor was

found in the following categories of patients:

 

Diagnosis; percent with the diagnosis mauve factor

 

Normal subjects 0

 

Physically ill

Adults 10

Children 10

Mood disorders 20

Alcoholics 20

 

Schizophrenics

Early, not treated 75

Recovered 0

Not recovered 50

 

Thus it was clear that although it was most closely

related to the schizophrenic

population, it could not be considered a test for

schizophrenia. Probably there will never be such a

test since the clinical diagnosis is subjective and

there is wide disagreement among clinicians about the

diagnosis. I therefore compared the results of testing

for this compound with the results obtained on the HOD

(Hoffer-Osmond Diagnostic) test.

 

2) Relationship to HOD Test.(4) This is a card sort

test similar in principle to the MMPI but containing

entirely different questions. Perceptual symptoms

including hallucinations and illusions are

specifically covered. The HOD test can be described as

a perceptual test. Patients sorted 145 cards into true

and false piles and these were recorded and scores

obtained. We standardized this test on thousands of

subjects and have reported the results widely. We

found that there was a better relationship between the

presence of high scores in the test and the presence

of kp in the urine than there was between kp and

clinical diagnosis. Schizophrenics had much higher

scores than did any other group of psychiatric

patients, with the exception of patients with delirium

tremens and normal subjects undergoing the LSD

experience. In one study in New York, the

investigating team found that the admission HOD test

results were more closely correlated to the final

discharge diagnosis than they were to the admitting

diagnosis, even though none of the clinicians were

able to see the results of the HOD test.

 

3) As an indicator for treatment. By 1960 we had

completed four double blind controlled prospective

studies on schizophrenic patients comparing niacin,

niacinamide and placebo.(5) Based upon these studies

and upon open clinical studies going back to 1951, I

had concluded that schizophrenic patients responded

better to any treatment when they were given adequate

doses of vitamin B3. Forty years later this is still

my conclusion, as it is of every physician who uses

the same treatment. The only physicians who disagree

are those who have never used the treatment and who

have even refused to examine earlier studies. There is

no patent on vitamin B3, and without a patent there is

no financial incentive for any company to promote this

treatment. Since schizophrenic patients, most of whom

had the factor in their urine, responded better when

treated with vitamin B3, I concluded that any

psychiatric disease, no matter what they were

diagnosed clinically, might also do better with this

vitamin. This was confirmed by a large series of open

clinical studies. I will not term these studies

anecdotal, which has become the politically correct

term for denigrating any studies that are not double

blind, since all clinical studies depend upon the

history or herstory of patients and how they respond,

i.e. upon anecdotes. The only difference is that in

double blind studies the anecdotes are collected by

physicians or others who are blinded by not knowing

what treatment is being given. At least this is the

theory of this type of procedure. In fact, the vast

majority of these studies are so imperfectly blinded

that few clinician or nurses have much difficulty

deciding whether the patient was on placebo or

something more active.

 

Worshippers of the double blind remind me of the

emperor whose nakedness was seen only by a child not

yet blinded by tradition. This report by Kraus is an

excellent example of the type of anecdotal history

which has contributed so much to medicine.

 

The presence of the mauve factor in urine became a

valuable indicator to use vitamin B3. Later, when Dr.

C. C. Pfeiffer showed that kp bound pyridoxine and

zinc and described the syndrome pyrolleuria, this

became another important indicator that vitamin B6 and

zinc must be used. It is especially valuable for

children, who are very difficult to diagnose because

they vary so much one from the other.

 

4) Response to treatment. Patients who responded to

treatment invariably became mauve factor or kp factor

negative. However, there were many patients who no

longer excreted this factor but who had not recovered.

I have not examined whether these patients might have

responded to longer treatment. In my recent report (6)

on chronic patients it is evident that many chronic

patients need five to seven years of treatment.

Perhaps some of the negative excretors after having

been positive might have fallen into this group.

Patients who were well and were kp free were followed

for months or years. If they became positive at any

time they also became clinically ill within a matter

of weeks or months.

 

Generally, the presence of kp is associated with

clinical conditions characterized by a high degree of

perceptual disorganization. These are chiefly the

schizophrenic patients, but also includes a

substantial proportion of other psychiatric diseases

also characterized by perceptual changes.

Unfortunately psychiatrists do not search their

patients’ mental state adequately and miss many of

these changes. They can be readily detected using

perceptual tests such as the HOD test. (7) In other

words, the presence of kp correlates strongly with

high scores on these perceptual tests. Perhaps Dr.

Kraus’s detailed report will arouse interest in this

test, sadly neglected for so many years.

 

In 1960 I examined a seven year old boy who had been

diagnosed retarded and preparations were being made to

send him to a special school. His parents were very

concerned and asked me whether I would examine him.

For over a year he had difficulty in school, could not

read, and avoided going to school as much as he could,

often staying away from home all day but not at

school. His mother, a teacher, had been spending a lot

of time giving him special instruction without

improvement. He was also developing behavioral

problems at home. I examined him early in 1960 and

could not locate any particular problem, perhaps

because I had not had much experience treating

children. I then had his urine analyzed for mauve

factor, kp, and to my surprise found a large amount. I

called his father, a friend of mine, and said in jest

“You are in luck, your son has schizophrenia.” He

answered, “Why does that make me so lucky?” I then

told him I was kidding him, and added seriously he was

certainly not schizophrenic, but since he had the same

biochemical factor in his urine we had found in

schizophrenics, and since they had responded well to

vitamin therapy, this suggested that his son might

respond in a similarly beneficial way.

 

I started him on niacinamide 1,000 milligrams after

each meal. In the fall his father asked me would I

like to know what had happened to his son. He then

told me that two months after his son had started on

the vitamin he had begun to read, that he had spent a

few months reading voraciously and that he was no

longer concerned about his behaviour. His son was

normal and remained well. He took his niacinamide

regularly until he was about 14. One day he asked his

mother why he was taking the pills. She brought him to

see me and I explained why I thought he should remain

on the vitamin until at least age 18 at which time he

could determine how well he could do without it. He is

still well, happily married with children, and is

fully employed in a responsible job.

 

This illustrates the use of the kp urine test for

pyrolleuria, and the use of niacinamide in large doses

to treat this condition successfully. I did not use

vitamin B6 nor zinc in 1960. Pyridoxine is essential

for the conversion of tryptophan to nicotinamide

adenine dinucleotide, the vitamin B3 coenzyme. With a

deficiency of pyridoxine, the synthesis of NAD in the

body is reduced. A pyridoxine deficiency will produce

a form of pellagra not distinguishable clinically from

the pellagra caused by a deficiency of vitamin B3.

 

References

Hoffer A: The Presence of Malvaria in Some Mentally

Retarded Children. Amer J Ment Def 67:730-732, 1963.

Hoffer A: Malvaria and the Law. Psychoso-matics,

7:303-310, 1966.

 

Hoffer A: A Program for the Treatment of Alcoholism:

LSD, Malvaria and Nicotinic Acid. In, The Use of LSD

in Psychotherapy and Alcoholism. Ed. HA

Abramson.Bobbs-Merril, New York, 343-402, 1967.

 

Hoffer A & Mahon M: The Presence of Unidentified

Substances in the Urine of Psychiatric Patients

2:331-362, 1961

 

Hoffer A & Osmond H: The Relationship Between an

Unknown Factor (US) in the Urine of Subjects and HOD

Test Results. J Neuropsychiatry 2:363-368, 1961.

 

Hoffer A & Osmond H: Malvaria: A New Psychiatric

Disease. Acta Psychiat Scand 39:335-366, 1963.

 

Hoffer A: The Psychophysiology of Cancer. J Asthma

Research 8:61-76, 1970.

 

Hoffer A & Osmond H: A Card Sorting Test Helpful in

Making Psychiatric Diagnosis. J Neuropsychiatry

2:306-330, 1961.

 

Hoffer A & Osmond H: A Card Sorting Test Helpful in

Establishing Prognosis. Am J Psychiatry 118:840-841,

1962.

 

Hoffer A & Osmond H: The Relationship Between an

Unknown Factor (US) in the Urine of Subjects and HOD

Test Results. J Neuropsychiatry 2:363-368, 1961.

 

Hoffer A & Osmond H: The Association Between

Schizophrenia and Two Objective Tests. Can Med Ass J

87:641-646, 1962.

 

Hoffer A, Kelm H & Osmond H: The Hoffer-Osmond

Diagnostic Test. RE Krieger Pub Co. Huntington, New

York, 1975.

 

Hoffer A, Osmond H, Callbeck MJ & Kahan I: Treatment

of Schizophrenia with Nicotinic Acid and Nicotinamide.

J Clin Exper Psychopathol 18:131-158, 1957.

 

Hoffer A: Niacin Therapy in Psychiatry. C.C.Thomas,

Springfield, IL, 1962.

 

Hoffer A & Osmond H: Treatment of Schizophrenia with

Nicotinic Acid - A Ten Year Follow-Up. Acta Psychiat

Scand 40:171-189, 1964.

 

Hoffer A: Treatment of Schizophrenia with a

Therapeutic Program Based Upon Nicotinic Acid as the

Main Variable. Molecular Basis of Some Aspects of

Mental Activity, Vol II. Ed. O Walaas, Academic Press,

New York, 1967.

 

Hoffer A: Megavitamin B-3 Therapy for Schizophrenia.

Can Psychiatric Assoc J 16:499-504, 1971.

 

Hoffer A: Treatment of Hyperkinetic Children with

Nicotinamide and Pyridoxine. Can Med Assoc J

107:111-112, 1972.

 

Hoffer A: Natural History and Treatment of Thirteen

Pairs of Identical Twins, Schizophrenic and

Schizophrenic-Spectrum Condi-tions. J Orthomolecular

Psychiatry 5:101-122, 1976.

 

Hoffer A: Orthomolecular Medicine for Physicians.

Keats Pub, New Canaan, CT, 1989.

 

Hoffer A: Orthomolecular Medicine. In, Molecules In

Natural Science and Medicine, An Encomium for Linus

Pauling. Ed Z.B. Maksic & M. Eckert-Maksic, Ellis

Horwood Ltd, Chichester, West Sussex, England, 1991.

 

Hoffer A: Vitamin B3 and Schizophrenia: Discovery,

Recovery, Controversy. Quarry Press, Kingston,

Ontario, 1994.

 

Hoffer A: Chronic Schizophrenic Patients Treated Ten

Years Or More. J. Orthomolecular Medicine, 9:7-37,

1994.

 

Hoffer A & Osmond H: How To Live With Schizophrenia.

University Books, New York, NY, 1966. Also published

by Johnson, London, 1966. New and Revised Ed. Citadel

Press, New York, N.Y. 1992

 

Hoffer A & Osmond H: The Hallucinogens. Academic

Press, New York, 1967.

 

Orthomolecular Psychiatry, Eds. D. Hawkins and Linus

Pauling. W.H. Freeman and Co., San Francisco, 1973.

 

(Also see References in Dr. Richard T. Kraus' paper.)

 

Reprinted with permission of the author.

 

A. Hoffer, M.D., Ph.D.

#3A - 2727 Quadra Street

Victoria, B.C. V8T 4E5