1602 lines
111 KiB
HTML
1602 lines
111 KiB
HTML
<html>
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<head><title>Thyroid, insomnia, and the insanities: Commonalities in disease</title></head>
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<body>
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<h1>
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Thyroid, insomnia, and the insanities: Commonalities in disease
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</h1>
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<p></p>
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<p><strong>SOME FACTORS IN STRESS, INSOMNIA AND THE BRAIN SYNDROMES:</strong></p>
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<p>
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Serotonin, an important mediator of stress, shock, and inflammation, is a vasoconstrictor that impairs
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circulation in a great variety of circumstances.
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</p>
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<p>
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Stress impairs metabolism, and serotonin suppresses mitochondrial energy production.
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</p>
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<p>
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Stress and shock tend to increase our absorption of bacterial endotoxin from the intestine, and endotoxin
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causes the release of serotonin from platelets in the blood.
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</p>
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<p>
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Schizophrenia is one outcome of stress, both cumulative and acute. Prenatal stress commonly predisposes a
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person to develop schizophrenia at a later age.
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</p>
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<p>
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Serotonin"s restriction of circulation to the uterus is a major factor in toxemia of pregnancy and related
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complications of pregnancy.
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</p>
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<p>
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Hypothyroidism increases serotonin activity in the body, as it increases estrogen dominance.
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</p>
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<p>
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Estrogen inhibits the enzyme monoamino oxidase (MAO), and is highly associated with increased serotonin
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activity. Progesterone has the opposite effect on MAO.
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</p>
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<p>
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The frontal lobes of the brain are hypometabolic in schizophrenia. Serotonin can cause vasoconstriction in
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the brain.
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</p>
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<p>Serotonin release causes lipid peroxidation.</p>
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<p>Schizophrenics have high levels of lipid peroxidation.</p>
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<p>
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Antioxidants, including uric acid, are deficient in schizophrenics.
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</p>
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<p>
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Therapies which improve mitochondrial respiration alleviate the symptoms of schizophrenia.
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</p>
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<p>
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Energy depletion leads to brain atrophy, but with normal stimulation and nutrition even adult brains can
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grow.
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</p>
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<p>
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Schizophrenics and depressed people have defective sleep.
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</p>
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<p>
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Increasing the body"s energy level and temperature improves the quality of sleep.
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</p>
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<p><span style="font-size: 14pt; font-weight: normal"><hr /></span></p>
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<p>
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Everyone is familiar with the problem of defining insanity, in the case of people who plead innocent by
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reason of insanity. The official definition of insanity in criminal law is "the inability to tell right from
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wrong." Obviously, that can"t be generalized to everyday life, because any sane person realizes that
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certainty is impossible, and that most situations, including elections, offer you at best the choice of "the
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lesser of two evils," or the opportunity to "do the right thing," and to "throw your vote away." People who
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persist in doing what they know is really right are "eccentric," in the sense that they don"t adapt to
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society"s norms. In a society that chooses to destroy ecosystems, rather than adapting to them, the question
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of sanity should be an everyday political issue.
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</p>
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<p>
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The use of medical terms tends to give authority to the people who are in charge of defining the terms, and
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it can give the impression of objectivity when there really isn"t any scientific validity behind the terms.
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In their historical senses, "crazy" (flawed) and "insane" (unsound) are probably more objective terms than
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the medically-invented terms, dementia praecox (premature idiocy) or schizophrenia (divided mind).
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</p>
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<p>
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"Odd Speech" is one of the dimensions used in the diagnosis of insanity. I am reminded of William
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Wordsworth"s dismissal of William Blake as insane after failing to understand some of Blake"s
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poems--Wordsworth was conventional enough to become England"s Poet Laureate, and to his limited perspective,
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Blake"s clear verses were incomprehensibly odd.
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</p>
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<p>
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Whenever a trusted government employee decides to blow the whistle on criminal activities, his agency
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invariably puts out the information that this now discharged employee is psychologically unbalanced.
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Dissent, in other words, is easy to dispose of by psychiatric tainting.
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</p>
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<p>
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If we are going to speak of mental impairment, then we should have objective measures of what we are talking
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about. Blake unquestionably could do anything better than Wordsworth, because he was neither stupid nor
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dishonest, and it"s almost a rule that ordinary employees are more competent than the administrators who
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evaluate their work. Objective standards of mental impairment would be more popular among patients than
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among diagnosticians, judges, and lawmakers.
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</p>
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<p>
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In a famous test of the objectivity of diagnosis, a filmed interview with a patient was shown to British and
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U.S. psychiatrists. 69% of the Americans diagnosed the patient as schizophrenic, but only 2% of the British
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psychiatrists did.
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</p>
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<p>
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The strictly medical/psychological definition of insanity is still, despite the existence of the
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International Classification of Diseases, and in the U.S. the Diagnostic and Statistical Manual, which
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enumerate a large number of "mental disorders," a crazily indefinite grouping of symptoms, and hasn"t made
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diagnosis more objective.. For example, in the last 30 years autism has been separated from childhood
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schizophrenia, but now the tendency is for both of them to be called developmental brain disorders. Both
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schizophrenia and autism are now often described in terms of a "spectrum of conditions," which hardly
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matters, since they are not understood in terms of cause, prevention, or cure.
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</p>
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<p>
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The problem is in the history of psychosis as a medical idea. About 100 years ago, attempts were made to
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classify psychoses by their symptoms, unifying a great variety of old diagnostic categories into two groups,
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manic-depressive mood disorders, and "dementia praecox," or schizophrenia, which (as indicated by its name,
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premature dementia) was considered to be progressive and incurable. Several kinds of mental disorder were
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found to have clear causes, including vitamin deficiencies and various poisons and infections, but the idea
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of a certain thing called schizophrenia still persists.
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</p>
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<p>
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The unitary concept of psychosis grew up in a culture in which "endogenous insanity" was a "hereditary
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taint," that for a time was "treated" by imprisonment, and that more recently has been treated with
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sterilization or euthanasia to eliminate the "insanity genes."
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</p>
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<p>
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The idea that the disease is "in the genes" now serves the drug industry well, since they offer chemicals
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that will correct the specific "chemical error."
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</p>
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<p>
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Not all psychiatrists and psychologists subscribed to the idea of a unitary psychosis, defined by a variety
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of symptoms. A positive contribution of Freudian psychoanalysis (and its congeners and competitors) was that
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it made people think in terms of causes and the possibility of cures, instead of hopelessness,
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stigmatization, isolation and eradication. Although Freud expressed the thought that biological causes and
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cures would eventually be found, the profession he founded was not sympathetic to the idea of physiological
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therapies.
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</p>
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<p>
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Looking for general physiological problems behind the various symptoms is very different from the practice
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of classifying the insanities according to their symptoms and the hypothetical "brain chemicals" that are
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believed to "cause the symptoms." The fact that some patients hallucinate caused many psychiatrists to
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believe that hallucinogenic chemicals, interfering with nerve transmitter substances such as dopamine or
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serotonin, were going to provide insight into psychotic states. The dopamine excess (or serotonin
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deficiency) theories developed at a time when only a few "transmitter substances" were known, and when they
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were thought to act as very specific on/off nerve switches, rather than as links in metabolic networks. The
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drug industry helps to keep those ideas alive.
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</p>
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<p>
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The idea that the brain is like a computer, and that the nerves are like wires and switches, is behind all
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of the theories about transmitter substances and synapses. If this metaphor about the nature of the brain
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and the organism is fundamentally wrong, then the theories of schizophrenia based on nerve transmitter
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substances can hardly be right. Another theory of schizophrenia based on the computer metaphor has to do
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with the idea that nerve cells" wire-like and switch-like functions depend on their membranes, and, in the
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most popular version, that these all-important membranes are made of fish oil. The supporting evidence is
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supposed to be that the fish-oil-like fatty acids are depleted from the tissues of schizophrenics. Just
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looking at that point, the "evidence" is more likely to be the result of stress, which depletes unsaturated
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fatty acids, especially of the specified type, in producing lipid peroxides and other toxic molecules.
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</p>
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<p>
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In one of its variations, the "essential fatty acid deficiency" doctrine suggests that a certain
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prostaglandin deficiency is the cause of schizophrenia, but experiments have shown that an <span
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style="font-style: italic"
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>excess</span>
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<span style="font-style: normal"> of that prostaglandin mimics the symptoms of psychosis.</span>
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</p>
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<p>
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<span style="font-style: normal">The drug industry"s effect on the way the organism is commonly understood
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has been pervasively pathological. For example, the dogma about "cell surface receptors" has sometimes
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explicitly led people to say that the "brain chemicals" are active
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</span>
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<span style="font-style: italic">only</span>
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<span style="font-style: normal"> at the surface of cells, and not inside the cells. </span>
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</p>
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<p>
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<span style="font-style: normal">The consequences of this mistake have been catastrophic. For example,
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serotonin"s precursor, tryptophan, and the drugs called "serotonin reuptake inhibitors," and other
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serotonergic drugs, and serotonin itself, are carcinogenic and/or tumor promoters. Excessive serotonin
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is a major factor in kidney and heart failure, liver and lung disease, stroke, pituitary abnormalities,
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inflammatory diseases, practically every kind of sickness, at the beginning, middle, and end of life. In
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the brain, serotonin regulates circulation and mitochondrial function, temperature, respiration and
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appetite, alertness and learning, secretion of prolactin, growth hormones and stress hormones, and
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participates in the most complex biochemical webs. But the pharmaceutical industry"s myth has led people
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to believe that serotonin is the chemical of happiness, and that tryptophan is its benign nutritional
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precursor, and that they are going to harmlessly influence the "receptors on nerve membranes."
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</span>
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</p>
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<p>
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<span style="font-style: normal"
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>A particular drug has many effects other than those that are commonly recognized as its "mechanism of
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action," but when an "antidepressant" or a "tranquilizer" or a "serotonin reuptake inhibitor" alleviates
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a particular condition, some people argue that the condition must have been caused by the "specific
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chemistry" that the drug is thought to affect. Because of the computer metaphor for the brain, these
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effects are commonly thought to be primarily in the synapses, the membranes, and the transmitter
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chemicals.</span>
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</p>
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<p>
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<span style="font-style: normal"
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>The argument for a "genetic" cause of schizophrenia relies heavily on twin studies in which the frequency
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of both twins being schizophrenic is contrasted to the normal incidence of schizophrenia in the
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population, which is usually about 1%. There is a concordance of 30% to 40% between monozygotic
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(identical) twins, and a 5% to 10% concordance between fraternal twins, and both of these rates are
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higher than that of other siblings in the same family. That argument neglects the closer similarity of
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the intrauterine conditions experienced by twins, for example the sharing of the same placenta, and
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experiencing more concordant biochemical interactions between fetus and mother.</span>
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</p>
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<p>
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<span style="font-style: normal"
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>Defects of the brain, head, face, and even hands and fingerprints are seen more frequently in the
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genetically identical twin who later develops schizophrenia than the twin who doesn"t develop
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schizophrenia. Of the twins, it is the baby with the lower birth weight and head size that is at a
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greater risk of developing schizophrenia.</span>
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</p>
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<p>
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<span style="font-style: normal">Oliver Gillie (in his book, </span>
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<span style="font-style: italic">Who Do You Think You Are?)</span>
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<span style="font-style: normal">
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discussed some of the fraud that has occurred in twin studies, but no additional fraud is needed when
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the non-genetic explanation is simply ignored and excluded from discussion. The editors of most medical
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and scientific journals are so convinced of the reality of genetic determination that they won"t allow
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their readers to see criticisms of it.</span>
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</p>
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<p>
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<span style="font-style: normal"
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>Prenatal malnutriton or hormonal stress or other stresses are known to damage the brain, and especially its
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most highly evolved and metabolically active frontal lobes, and to reduce its growth, relative to the
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rest of the body.</span>
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</p>
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<p>
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<span style="font-style: normal">The standard medical explanation for the association of pregnancy toxemia
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and eclampsia with birth defects has been, until recently, that both mother and child were genetically
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inferior, and that the defective child created the pregnancy sickness. The same "reasoning" has been
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invoked to explain the association of birth complications with later disease<span
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style="font-weight: bold"
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>:</span><span style="font-weight: normal">
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The defective baby was the
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</span></span>
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<span style="font-weight: normal; font-style: italic">cause</span>
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<span style="font-weight: normal; font-style: normal">
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of a difficult birth. That argument has recently been discredited (McNeil and Cantor-Graae, 1999).</span
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>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Schizophrenics are known to have had a higher rate of obstetrical complications, including oxygen
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deprivation and Cesarian deliveries, than normal people. Like people with Alzheimer"s disease, the
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circumference of their heads at birth was small, in proportion to their body weight and gestational
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age.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Animal studies show that perinatal brain problems tend to persist, influencing the brain"s metabolism and
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function in adulthood.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Like the other major brain diseases, shizophrenia involves a low metabolic rate in crucial parts of the
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brain. In schizophrenics, "hypofrontality," low metabolism of the frontal lobes, is characteristic,
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along with abnormal balance between the hemispheres, and other regional imbalances.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>A very important form of prenatal stress occurs in toxemia and preeclampsia, in which estrogen is dominant,
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and endotoxin and serotonin create a stress reaction with hypertension and impaired blood circulation to
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the uterus and placenta.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>The brain, just like any organ or tissue, is an energy-producing metabolic system, and its oxidative
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metabolism is extremely intense, and it is more dependent on oxygen for continuous normal functioning
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than any other organ. Without oxygen, its characteristic functioning (consciousness) stops instantly
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(when blood flow stops, blindness begins in about three seconds, and other responses stop after a few
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more seconds). The concentration of ATP, which is called the cellular energy molecule, doesn"t decrease
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immediately. Nothing detectable happens to the "neurotransmitters, synapses, or membrane structures" in
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this short period</span>
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<span style="font-weight: bold; font-style: normal">;</span>
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<span style="font-weight: normal; font-style: normal">
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consciousness is a metabolic process that, in the computer metaphor, would be the flow of electrons
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itself, under the influence of an electromotive force, a complex but continuous sort of electromagnetic
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field. The computer metaphor would seem to have little to offer for understanding the brain.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal">In this context, I think it"s necessary, for the
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present, to ignore the diagnostic details, the endless variety of qualifications of the idea of
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"schizophrenia," that fill the literature. Those diagnostic concepts seem to tempt people to look for
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"the precise cause of this particular subcategory" of schizophrenia, and to believe that a specific drug
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or combination of drugs will be found to treat it, while encouraging them to ignore the patient"s
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physiology and history.
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</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>If we use the standard medical terms at all, it should be with the recognition that they are, in their
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present and historical form, not scientifically meaningful.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>The idea that schizophrenia is a disease in itself tends to distract attention from the things it has in
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common with Alzheimer"s disease, autism, depression, mania, the manic-depressive syndrome, the
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hyperactivity-attention deficit syndrome, and many other physical and mental problems. When brain
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abnormalities are found in "schizophrenics" but not in their normal siblings, it could be tempting to
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see the abnormalities as the "cause of schizophrenia," unless we see similar abnormalities in a variety
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of sicknesses.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>For the present, it"s best to think first in the most general terms possible, such as a "brain stress
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syndrome," which will include brain aging, stroke, altitude sickness, seizures, malnutrition, poisoning,
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the despair brought on by inescapable stress, and insomnia, which are relatively free of culturally
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arbitrary definitions. Difficulty in learning, remembering, and analyzing are objective enough that it
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could be useful to see what they have to do with a "brain stress syndrome."</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Stress damages the energy producing systems of cells, especially the aerobic mitochondria, in many ways,
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and this damage can often be repaired. The insanities that are most often called schizophrenia tend to
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occur in late adolescence, or around menopause, or in old age, which are times of stress, especially
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hormonal stress. Post-partum psychosis often has features that resemble schizophrenia.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Although the prenatal factors that predispose a person toward the brain stress syndrome, and those that
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trigger specific symptoms later in life, might seem to be utterly different, the hormonal and
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biochemical reactions are probably closely related, involving the adaptive responses of various
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functional systems to the problem of insufficient adaptive ability and inadequate energy.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>By considering cellular energy production, local blood flow, and the systemic support system, we can get
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insight into some of the biochemical events that are involved in therapies that are sometimes
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successful. A unified concept of health and disease will help to understand both the origins and the
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appropriate treatments for a great variety of brain stress syndromes.</span>
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</p>
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<p></p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>The simple availability of oxygen, and the ability to use it, are regulated by carbon dioxide and
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serotonin, which act in opposite directions. Carbon dioxide inhibits the release of serotonin. Carbon
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dioxide and serotonin are regulated most importantly by thyroid function. Hypothyroidism is
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characterized by increased levels of both noradrenalin and serotonin, and of other stress-related
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hormones, including cortisol and estrogen. Estrogen shifts the balance of the "neurotransmitters" in the
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same direction, toward increased serotonin and adrenalin, for example by inhibiting enzymes that degrade
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the monoamine "neurotransmitters."</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal">When an animal such as a squirrel approaches
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hibernation and is producing less carbon dioxide, the decrease in carbon dioxide releases serotonin,
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which slows respiration, lowers temperature, suppresses appetite, and produces torpor.
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</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>But in energy-deprived humans, increases of adrenalin oppose the hibernation reaction, alter energy
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production and the ability to relax, and to sleep deeply and with restorative effect.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal">In several ways, torpor is the opposite of sleep.
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Rapid eye movement (REM), that occurs at intervals during sleep and in association with increased
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respiration, disappears when the brain of a hibernating animal falls below a certain temperature. But
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torpor isn"t like "non-REM" deep sleep, and in fact seems to be
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</span>
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<span style="font-weight: normal; font-style: italic">like wakefulness,</span>
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<span style="font-weight: normal; font-style: normal"> in the sense that a sleep-debt is incurred</span>
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<span style="font-weight: bold; font-style: normal">:</span>
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<span style="font-weight: normal; font-style: normal">
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Hibernating animals periodically come out of torpor so they can sleep, and in those periods, when their
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temperature rises sharply, they have a very high percentage of deep "slow wave sleep."</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Although it is common to speak of sleep and hibernation as variations on the theme of economizing on energy
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expenditure, I suspect that nocturnal sleep has the special function of minimizing the stress of
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darkness itself, and that it has subsidiary functions, including its now well confirmed role in the
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consolidation and organization of memory. This view of sleep is consistent with observations that
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disturbed sleep is associated with obesity, and that the torpor-hibernation chemical, serotonin,
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powerfully interferes with learning.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>Babies spend most of their time sleeping, and during life the amount of time spent sleeping decreases, with
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nightly sleeping time decreasing by about half an hour per decade after middle age. Babies have an
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extremely high metabolic rate and a stable temperature. With age the metabolic rate progressively
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declines, and as a result the ability to maintain an adequate body temperature tends to decrease with
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aging.</span>
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</p>
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<p>
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<span style="font-weight: normal; font-style: normal"
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>(The simple fact that body temperature regulates all organic functions, including brain waves, is
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habitually overlooked. The actions of a drug on brain waves, for example, may be mediated by its effects
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on body temperature, but this wouldn"t be very interesting to pharmacologists looking for
|
|
"transmitter-specific" drugs.)</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Torpor is the opposite of restful sleep, and with aging, depression, hypothyroidism, and a variety of brain
|
|
syndromes, sleep tends toward the hypothermic torpor.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>An individual cell behaves analogously to the whole person. A baby"s "high energy resting state" is
|
|
paralleled by the stable condition of a cell that is abundantly charged with energy</span>
|
|
<span style="font-weight: bold; font-style: normal">;</span>
|
|
<span style="font-weight: normal; font-style: normal">
|
|
ATP and carbon dioxide are at high levels in these cells. Progesterone"s effects on nerve cells include
|
|
favoring the high energy resting state, and this is closely involved in progesterone"s "thermogenic"
|
|
effect, in which it raises the temperature set-point.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>The basal metabolic rate, which is mainly governed by thyroid, roughly corresponds to the average body
|
|
temperature. However, in hypothyroidism, there is an adaptive increase in the activity of the
|
|
sympathetic nervous system, producing more adrenalin, which helps to maintain body temperature by
|
|
causing vasoconstriction in the skin. In aging, menopause, and various stressful conditions, the
|
|
increased adrenalin (and the increased cortisol production which is produced by excess adrenalin) causes
|
|
a tendency to wake more easily, and to have less restful sleep.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>While the early morning body temperature will sometimes be low in hypothyroidism, I have found many
|
|
exceptions to this. In protein deficiency, sodium deficiency, in menopause with flushing symptoms, and
|
|
in both phases of the manic depression cycle, and in some schizophrenics, the morning temperature is
|
|
high, corresponding to very high levels of adrenalin and cortisol. Taking the temperature before and
|
|
after breakfast will show a reduction of temperature, the opposite of what occurs in simple
|
|
hypothyroidism, because raising the blood sugar permits the adrenalin and cortisol to fall.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>The characteristic sleep pattern of hypothyroidism and old age is similar to the pattern seen in
|
|
schizophrenia and depression, a decrease of deep slow wave sleep. Serotonin, like torpor, produces a
|
|
similar effect. In other words, a torpor-like state can be seen in all of these brain-stress states.
|
|
Several studies have found that anti-serotonin drugs improve sleep, and also reduce symptoms of
|
|
schizophrenia and depression. It is common for the "neuroleptic" drugs to raise body temperature, even
|
|
pathologically as in the "neuroleptic malignant syndrome."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>In old people, who lose heat easily during the day, their extreme increase in the compensatory nervous and
|
|
hormonal adrenalin activity causes their night-time heat regulation (vasoconstriction in the
|
|
extremities) to rise to normal.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Increased body temperature improves sleep, especially the deep slow wave sleep. A hot bath, or even warming
|
|
the feet, has the same effect as thyroid in improving sleep. Salty and sugary foods taken at bedtime, or
|
|
during the night, help to improve the quality and duration of sleep. Both salt and sugar lower the
|
|
adrenalin level, and both tend to raise the body temperature.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Hypothyroidism tends to cause the blood and other body fluids to be deficient in both sodium and glucose.
|
|
Consuming salty carbohydrate foods momentarily makes up to some extent for the thyroid deficiency.</span
|
|
>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>In the peiodic table of the elements, lithium is immediately above sodium, meaning that it has the chemical
|
|
properties of sodium, but with a smaller atomic radius, which makes its electrical charge more intense.
|
|
Its physiological effects are so close to sodium"s that we can get clues to sodium"s actions by watching
|
|
what lithium does.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Chronic consumption of lithium blocks the release of adrenalin from the adrenal glands, and it also has
|
|
extensive antiserotonin effects, inhibiting its release from some sites, and blocking its actions at
|
|
others.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Lithium forms a complex with the ammonia molecule, and since the ammonia molecule mimics the effects of
|
|
serotonin, especially in fatigue, this could be involved in lithium"s antiserotonergic effects. Ammonia,
|
|
like serotonin, impairs mitochondrial energy production (at a minimum, it uses energy in being converted
|
|
to urea), so anti-ammonia, anti-serotonin agents make more energy available for adaptation. Lithium has
|
|
been demonstrated to restore the energy metabolism of mitochondria (Gulidova, 1977).</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal; font-style: normal"
|
|
>Therapies that have been successful in treating "schizophrenia" include penicillin, sleep therapy,
|
|
hyperbaric oxygen, carbon dioxide therapy, thyroid, acetazolamide, lithium and vitamins. These all make
|
|
fundamental contributions to the restoration of biological energy. Antibiotics, for example, lower
|
|
endotoxin formation in the intestine, protect against the induction by endotoxin of serotonin,
|
|
histamine, estrogen, and cortisol. Acetazolamide causes the tissues to retain carbon dioxide, and
|
|
increased carbon dioxide acidifies cells, preventing serotonin secretion.</span>
|
|
</p>
|
|
<p></p>
|
|
<p></p>
|
|
<p><span style="font-size: 10pt"> <span style="font-weight: bold"><h3>REFERENCES</h3></span></span></p>
|
|
<p></p>
|
|
<p>
|
|
<span style="font-weight: normal">Gen Pharmacol 1994 Oct;25(6):1257-1262.</span>
|
|
<span style="font-weight: bold">
|
|
Serotonin-induced decrease in brain ATP, stimulation of brain anaerobic glycolysis and elevation of
|
|
plasma hemoglobin; the protective action of calmodulin antagonists.</span>
|
|
<span style="font-weight: normal">
|
|
Koren-Schwartzer N, Chen-Zion M, Ben-Porat H, Beitner R Department of Life Sciences, Bar-Ilan
|
|
University, Ramat Gan, Israel.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>1. Injection of serotonin (5-hydroxytryptamine) to rats, induced a dramatic fall in brain ATP level,
|
|
accompanied by an increase in P(i). Concomitant to these changes, the activity of cytosolic
|
|
phosphofructokinase, the rate-limiting enzyme of glycolysis, was significantly enhanced. Stimulation of
|
|
anaerobic glycolysis was also reflected by a marked increase in lactate content in brain. 2. Brain
|
|
glucose</span>
|
|
<span style="font-weight: normal">
|
|
1,6-bisphosphate level was decreased, whereas fructose 2,6-bisphosphate was unaffected by serotonin. 3.
|
|
All these serotonin-induced changes in brain, which are characteristic for cerebral ischemia, were
|
|
prevented by treatment with the calmodulin (CaM) antagonists, trifluoperazine or thioridazine. 4</span>
|
|
<span style="font-weight: bold"
|
|
>. Injection of serotonin also induced a marked elevation of plasma hemoglobin, reflecting lysed
|
|
erythrocytes,</span>
|
|
<span style="font-weight: normal"> which was also prevented by treatment with the CaM antagonists. 5.</span>
|
|
<span style="font-weight: bold">
|
|
The present results suggest that CaM antagonists may be effective drugs in treatment of many
|
|
pathological conditions and diseases in which plasma serotonin levels are known to increase.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">WMJ 1990 Nov-Dec;62(6):93-7.</span>
|
|
<span style="font-weight: bold">
|
|
[Effect of inflammatory mediators on respiration in rat liver mitochondria].</span>
|
|
<span style="font-weight: normal"> Semenov VL.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: bold"
|
|
>Vopr Med Khim 1990 Sep-Oct;36(5):18-21 [Regulation by biogenic amines of energy functions of
|
|
mitochondria].</span>
|
|
<span style="font-weight: normal">
|
|
Medvedev A.E. Biogenic amines (phenylethylamine, tyramine, dopamine, tryptamine,
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>serotonin and spermine) decreased activities of the rotenone-insensitive NADH-cytochrome c reductase, the
|
|
succinate cytochrome c reductase and the succinate dehydrogenase</span>
|
|
<span style="font-weight: normal">.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Vopr Med Khim 1991 Sep-Oct;37(5):2-6.</span>
|
|
<span style="font-weight: bold">
|
|
[The role of monoamine oxidase in the regulation of mitochondrial energy functions].</span>
|
|
<span style="font-weight: normal"> Medvedev AE, Gorkin VZ.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Lik Sprava 1997 Jan-Feb;(1):61-5.</span>
|
|
<span style="font-weight: bold">
|
|
[Microhemodynamics and energy metabolism in schizophrenia patients].</span>
|
|
<span style="font-weight: normal"><hr /></span>
|
|
<span style="font-weight: bold">
|
|
showed lowering of ATP level and rise in the content of cathodic LDG4-LDG5 fractions, accumulation in
|
|
blood of lactic and pyruvic acids.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1996 Oct 18;22(1):41-7. </span>
|
|
<span style="font-weight: bold"
|
|
>Are reduced head circumference at birth and increased obstetric complications associated only with
|
|
schizophrenic psychosis? A comparison with schizo-affective and unspecified functional psychoses.</span>
|
|
<span style="font-weight: normal">
|
|
McNeil TF, Cantor-Graae E, Nordstrom LG, Rosenlund T.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1993 Jun;10(1):7-14. </span>
|
|
<span style="font-weight: bold">Puberty and the onset of psychosis.</span>
|
|
<span style="font-weight: normal">
|
|
Galdos PM, van Os JJ, Murray RM Department of Child and Adolescent Psychiatry, Bethlem Royal Hospital,
|
|
London, UK. According to the neurodevelopmental hypothesis of schizophrenia, maturational events in the
|
|
brain at puberty interact with congenital defects to produce psychotic symptoms. As girls reach puberty
|
|
at a younger age than boys, we predicted that (i) females would show earlier onset of psychotic illness
|
|
arising around puberty, and (ii)</span>
|
|
<span style="font-weight: bold">
|
|
onset of psychosis in females would be related to menarche.</span>
|
|
<span style="font-weight: normal">
|
|
Analysis of epidemiological data regarding admission to psychiatric units in (a) England over the period
|
|
1973-1986, (b) France over the period 1975`-1980, as well as examination of 97 psychotic adolescents
|
|
referred to an adolescent unit over a 14 year period, supported both these propositions.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Int J Psychophysiol 1999 Dec;34(3):237-47.</span>
|
|
<span style="font-weight: bold">
|
|
Timing of puberty and syndromes of schizotypy: a replication.</span>
|
|
<span style="font-weight: normal">
|
|
Kaiser J, Gruzelier JH. "Active syndrome findings were confined to the male subsample with late maturing
|
|
males showing higher scores on the
|
|
</span>
|
|
<span style="font-weight: bold">Cognitive Failures and Odd Speech </span>
|
|
<span style="font-weight: normal"
|
|
>subscales than early maturers. As in the previous study, there was no relationship between a global
|
|
psychosis proneness scale and maturational rate. These findings support a neurodevelopmental model of
|
|
psychosis-proneness and show the importance of adopting a syndromal view."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Am J Physiol 1978 Mar;234(3):H300-4. </span>
|
|
<span style="font-weight: bold"
|
|
>Potentiation of the cerebrovascular response to intra-arterial 5-hydroxytryptamine.</span>
|
|
<span style="font-weight: normal">
|
|
Eidelman BH, Mendelow AD, McCalden TA, Bloom DS. Infusion of 5-hydroxytryptamine (5HT) into the internal
|
|
carotid artery of normal baboons was not accompanied by alteration of gray matter cerebral blood flow.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>In animals pretreated with depot estrogen and progesterone (dosage equivalent to oral contraceptive
|
|
preparations), infusion of 5HT produced a marked decrease in gray matter blood flow.</span>
|
|
<span style="font-weight: normal">
|
|
A similar decrease in flow was obtained when the 5HT was infused with a concentrate of beta-lipoprotein.
|
|
Steroid substances appear to enhance the cerebrovascular constrictor responses to 5HT. A further series
|
|
of six experiments has shown that the monoamine oxidase inhibitor tranylcypromine similarly produced
|
|
constrictor responses to 5HT. It is possible that the steroids, the beta-lipoprotein, and the
|
|
tranylcypromine produced constrictor responses to 5HT by the same mechanism (inhibition of
|
|
cerebrovascular monoamine oxidase).</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">FASEB J 1989 Apr;3(6):1753-9. </span>
|
|
<span style="font-weight: bold"
|
|
>Steroid regulation of monoamine oxidase activity in the adrenal medulla.</span>
|
|
<span style="font-weight: normal">
|
|
Youdim MB, Banerjee DK, Kelner K, Offutt L, Pollard HB. "Administration of different steroid hormones in
|
|
vivo has distinct and specific effects on the MAO activity of the adrenal medulla." "As in the intact
|
|
animal, we found that</span>
|
|
<span style="font-weight: bold">
|
|
endothelial cell MAO activity was stimulated 1.5- 2.5-fold by 10 microM progesterone, hydrocortisone,
|
|
and dexamethasone, inhibited by ca. 50% by 17-alpha-estradiol,</span>
|
|
<span style="font-weight: normal">
|
|
but unaffected by testosterone." ". . . steroid-induced changes in total cell division ([14C]thymidine
|
|
incorporation) and total protein synthesis ([14C]leucine incorporation) were seen after changes in MAO
|
|
A."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Pharmacol Exp Ther 1984 Apr;229(1):244-9 </span>
|
|
<span style="font-weight: bold"
|
|
>Mechanisms of specific change by estradiol in sensitivity of rat uterus to serotonin.</span>
|
|
<span style="font-weight: normal"> Ichida S, Oda Y, Tokunaga H, Hayashi T, Murakami T, Kita T.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Neuroendocrinology 1983;36 (3): 235-41. </span>
|
|
<span style="font-weight: bold"
|
|
>Gonadal hormone regulation of MAO and other enzymes in hypothalamic areas.</span>
|
|
<span style="font-weight: normal">
|
|
Luine VN, Rhodes JC. "Activities of type A monoamine oxidase (MAO), acetylcholine esterase (AChE), and
|
|
glucose-6-phosphate dehydrogenase (G6PDH) were differentially altered in hormone-sensitive areas of the
|
|
preoptic-hypothalamic continuum after administration of estrogen and progesterone."
|
|
</span>
|
|
<span style="font-weight: bold">"Estrogen decreased activity of MAO in the PVE of the anterior hypothalamus,
|
|
pars lateralis of the ventromedial nucleus and in the Ar-ME. Acute administration of progesterone (1 h)
|
|
to estrogen-treated females did not further alter estrogen-dependent changes in AChE or G6PDH; however,
|
|
MAO activity in the ventromedial nucleus and Ar-ME was rapidly increased after progesterone."
|
|
</span>
|
|
<span style="font-weight: normal">"Administration of the protein synthesis inhibitor anisomycin prior to
|
|
progesterone
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>did not antagonize progesterone-dependent increases in MAO. Progesterone added in vitro to homogenates from
|
|
estrogen-treated but not from untreated females increased MAO activity."</span>
|
|
<span style="font-weight: normal"> </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neurochem 1981 Sep;37(3):640-8. </span>
|
|
<span style="font-weight: bold"
|
|
>Gonadal influences on the sexual differentiation of monoamine oxidase type A and B activities in the rat
|
|
brain.</span>
|
|
<span style="font-weight: normal">
|
|
Vaccari A, Caviglia A, Sparatore A, Biassoni R</span>
|
|
<span style="font-weight: bold">
|
|
"When masculinization was prevented by neonatal administration of estradiol (E)</span>
|
|
<span style="font-weight: normal">
|
|
to males, hypothalamic MAO-A and MAO-B activities increased in both control and MAO-inhibited rats." ".
|
|
. . single, high doses of steroids to adult, but not to newborn rats, did acutely affect the kinetics of
|
|
MAO-A.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>The activity of MAO-A was also decreased by high concentrations of E or TS in vitro. The imprinting for
|
|
patterns</span>
|
|
<span style="font-weight: normal">
|
|
of hypothalamic MAO-A and MAO-B in the two sexes results, probably, from genetic predetermination."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Gynecol Obstet Invest 2000;49(3):150-5.</span>
|
|
<span style="font-weight: bold">
|
|
Transport and metabolism of serotonin in the human placenta from normal and severely pre-eclamptic
|
|
pregnancies.</span>
|
|
<span style="font-weight: normal">
|
|
Carrasco G, Cruz MA, Gallardo V, Miguel P, Dominguez A, Gonzalez C. "These findings suggest that the
|
|
higher plasma-free serotonin levels observed in severe pre-eclampsia
|
|
</span>
|
|
<span style="font-weight: bold">are mainly due to a reduction in MAO-A activity</span>
|
|
<span style="font-weight: normal"> and not limited by the rate of serotonin uptake into the cells."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychiatry Res 1989 Jun;28(3):279-88.</span>
|
|
<span style="font-weight: bold">
|
|
Acetazolamide and thiamine: an ancillary therapy for chronic mental illness.</span>
|
|
<span style="font-weight: normal">
|
|
Sacks W, Esser AH, Feitel B, Abbott K Cerebral Metabolism Laboratory, Nathan S. Kline Institute for
|
|
Psychiatric Research, Orangeburg, NY 10962. Twenty-four chronic schizophrenic patients were treated
|
|
successfully with the addition of acetazolamide and thiamine (A + T) to their unchanged existing
|
|
therapies in a double-blind, placebo-controlled crossover study. Therapeutic effects were measured by
|
|
the Scale for the Assessment of Positive Symptoms and the Scale for the Assessment of Negative Symptoms.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>Overall, 50% of the patients showed improvement on all assessment scales.</span>
|
|
<span style="font-weight: normal">
|
|
No untoward effects occurred in these patients or in patients in previous studies who have been treated
|
|
continuously with A + T therapy for as long as 3 years.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neural Transm 1998;105(8-9):975-86. </span>
|
|
<span style="font-weight: bold"
|
|
>Role of tryptophan in the elevated serotonin-turnover in hepatic encephalopathy.</span>
|
|
<span style="font-weight: normal">
|
|
Herneth AM, Steindl P, Ferenci P, Roth E, Hortnagl H. "The increase of the brain levels of
|
|
5-hydroxyindoleacetic acid (5-HIAA) in hepatic encephalopathy (HE) suggests an increased turnover of
|
|
serotonin (5-HT)."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neurosci Res 1981;6(2):225-36 </span>
|
|
<span style="font-weight: bold"
|
|
>A difference in the in vivo cerebral production of [1-14C] lactate from D-[3-14C] glucose in chronic mental
|
|
patients.</span>
|
|
<span style="font-weight: normal">
|
|
Sacks W, Schechter DC, Sacks S. "Previously unpublished whole-blood lactate determinations in these
|
|
experiments indicated a cerebral production of much higher specific activity of [1-14C]-lactate from the
|
|
D-[3-14C] glucose by mental patients."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Ther Umsch 2000 Feb;57(2):76-80.</span>
|
|
<span style="font-weight: bold"> [Antidepressive therapy by modifying sleep].</span>
|
|
<span style="font-weight: normal"> Haug HJ, Fahndrich E.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1998 Jun 22;32(1):1-8. </span>
|
|
<span style="font-weight: bold">Reduced status of plasma total antioxidant capacity in schizophrenia.</span>
|
|
<span style="font-weight: normal"> Yao JK, Reddy R, McElhinny LG, van Kammen DP.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">FASEB J 1998 Dec;12(15):1777-83. </span>
|
|
<span style="font-weight: bold"
|
|
>Increased F2-isoprostanes in Alzheimer's disease: evidence for enhanced lipid peroxidation in vivo.</span>
|
|
<span style="font-weight: normal">
|
|
Pratico D, MY Lee V, Trojanowski JQ, Rokach J, Fitzgerald GA.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Dis Nerv Syst 1976 Feb;37(2):98-103. </span>
|
|
<span style="font-weight: bold">Glucose-insulin metabolism in chronic schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Brambilla F, Guastalla A, Guerrini A, Riggi F, Rovere C, Zanoboni A, Zanoboni-Muciaccia W.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychiatr Clin (Basel) 1975;8(6):304-13. </span>
|
|
<span style="font-weight: bold"
|
|
>Blood flow and oxidative metabolism of the brain in patients with schizophrenia.</span>
|
|
<span style="font-weight: normal"> Hoyer S, Oesterreich K.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Zh Nevropatol Psikhiatr Im S S Korsakova 1977;77(8):1179-86 </span>
|
|
<span style="font-weight: bold">[Effect of lithium on the energy metabolism of nervous tissue].</span>
|
|
<span style="font-weight: normal"> Gulidova GP, Khzardzhian VG, Mikhailova NM</span>
|
|
<span style="font-weight: bold">. </span>
|
|
<span style="font-weight: normal"
|
|
>"Lithium (0.5--4 mM) either significantly increase, either completely normalizers the intensity of the
|
|
oxidative and energy metabolism of the brain mitochondria, decreased by the influence of the blood serum
|
|
of patients with manic-depressive psychosis and attack like schizophrenia." "Processes of
|
|
phosphorilation become normalized in a joint action on the mitochondria by lithium and antioxidants."
|
|
"It is assumed that an increase in the intensity of the energy metabolism is one of the mechanisms of
|
|
therapeutical and prophylactic action of lithium."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Ateneo Parmense Acta Biomed 1975 Jan-Apr;46(1-2):5-19.</span>
|
|
<span style="font-weight: bold">
|
|
[Clinical significance of changes in tryptophan metabolism].</span>
|
|
<span style="font-weight: normal">
|
|
Ambanelli U, Manganelli P. "The oxidative pathway is most important of the metabolic pathway of the
|
|
amino acid; the degredation of tryptophan is</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">particularly influenced by steroid hormones and vitamins' want. The
|
|
metabolic anomalies are demonstrable both in malignant tumors (mostly in bladder cancer and Hodgkin's
|
|
disease), both during psychiatric diseases (such as depression and schizophrenia) and in the diseases of
|
|
connective tissue in addition to congenital errors of the degradation of tryptophan (such as Hartnup's
|
|
disease, tryptophanuria and 3-hydroxychinureninuria)."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Acta Neurol Scand Suppl 1977;64:534-5.</span>
|
|
<span style="font-weight: bold">
|
|
Blood flow and oxidative metabolism of the brain in the course of acute schizophrenia.</span>
|
|
<span style="font-weight: normal"> Hoyer S, Oesterreich K. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Med Hypotheses 1994 Dec;43(6):420-35</span>
|
|
<span style="font-weight: bold">
|
|
Schizophrenia is a diabetic brain state: an elucidation of impaired neurometabolism.</span>
|
|
<span style="font-weight: normal"> Holden RJ, Mooney PA.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Neuropsychobiology 1990-91;24(1):1-7. </span>
|
|
<span style="font-weight: bold"
|
|
>Frontality, laterality, and cortical-subcortical gradient of cerebral blood flow in schizophrenia:
|
|
relationship to symptoms and neuropsychological functions.</span>
|
|
<span style="font-weight: normal"> Sagawa K, Kawakatsu S, Komatani A, Totsuka S. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1989 Nov-Dec;2(6):439-48.</span>
|
|
<span style="font-weight: bold">
|
|
Effect of attention on frontal distribution of delta activity and cerebral metabolic rate in
|
|
schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Guich SM, Buchsbaum MS, Burgwald L, Wu J, Haier R, Asarnow R, Nuechterlein K, Potkin S. "Analysis
|
|
confirmed increased delta activity in the frontal region of patients with schizophrenia in comparison to
|
|
normal controls, and a significant correlation between increased frontal delta and relative reduction in
|
|
frontal</span>
|
|
<span style="font-weight: bold">
|
|
lobe metabolism among patients with schizophrenia. This finding of increased delta is consistent with
|
|
PET, blood flow and topographic EEG studies of schizophrenia, suggesting reduced frontal
|
|
activity."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Br J Psychiatry 1990 Feb;156:216-27.</span>
|
|
<span style="font-weight: bold">
|
|
Glucose metabolic rate in normals and schizophrenics during the Continuous Performance Test assessed by
|
|
positron emission tomography.</span>
|
|
<span style="font-weight: normal">
|
|
Buchsbaum MS, Nuechterlein KH, Haier RJ, Wu J, Sicotte N, Hazlett E, Asarnow R, Potkin S, Guich S "When
|
|
the group of schizophrenic patients was divided into deficit and nondeficit types, a preliminary
|
|
exploratory analysis suggested</span>
|
|
<span style="font-weight: bold">
|
|
thalamic, frontal, and parietal cortical hypometabolism in the deficit subgroup, with normal metabolism
|
|
in the nondeficit patient group in those areas; in contrast, hippocampal and anterior cingulate cortical
|
|
metabolism was reduced in both deficit and nondeficit subtypes. These results suggest that the limbic
|
|
system, especially the hippocampus, is functionally involved in schizophrenic psychosis and that
|
|
different manifestations of schizophrenia may involve different neuronal circuits."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychol Med 1994 Nov;24(4):947-55.</span>
|
|
<span style="font-weight: bold">
|
|
Patterns of cortical activity in schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Schroeder J, Buchsbaum MS, Siegel BV, Geider FJ, Haier RJ, Lohr J, Wu J, Potkin SG.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>"Schizophrenics were significantly more hypofrontal than the controls,</span>
|
|
<span style="font-weight: normal">
|
|
with higher values on the 'parietal cortex and motor strip' factor and a trend towards higher values in
|
|
the temporal cortex.
|
|
</span>
|
|
<span style="font-weight: bold">A canonical discriminant analysis confirmed that the 'hypofrontality' and
|
|
'parietal cortex and motor strip' factors accurately separated the schizophrenic group from the healthy
|
|
controls."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1996 Mar;19(1):41-53</span>
|
|
<span style="font-weight: bold"
|
|
>. Cerebral metabolic activity correlates of subsyndromes in chronic schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Schroder J, Buchsbaum MS, Siegel BV, Geider FJ, Lohr J, Tang C, Wu J, Potkin SG. "The delusional</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">cluster showed a significantly reduced hippocampal activity, while the
|
|
negative symptoms cluster presented with a prominent hypofrontality and significantly increased left
|
|
temporal cortex values."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychiatry Res 1997 Oct 31;75(3):131-44.</span>
|
|
<span style="font-weight: bold">
|
|
Cerebral glucose metabolism in childhood onset schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Jacobsen LK, Hamburger SD, Van Horn JD, Vaituzis AC, McKenna K, Frazier JA, Gordon CT, Lenane MC,
|
|
Rapoport JL, Zametkin AJ. "Decreased frontal cortical glucose metabolism has been demonstrated in adult
|
|
schizophrenics both at rest and while engaging in tasks that normally increase frontal metabolism, such
|
|
as the Continuous Performance Test (CPT).". "These findings suggest that childhood onset schizophrenia
|
|
may be associated with a similar, but not more severe, degree of hypofrontality relative to that seen in
|
|
adult onset schizophrenia."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Pharmacol Biochem Behav 1990 Apr; 35(4):955-62. </span>
|
|
<span style="font-weight: bold"
|
|
>The effects of ondansetron, a 5-HT3 receptor antagonist, on cognition in rodents and primates.</span>
|
|
<span style="font-weight: normal">
|
|
Barnes JM, Costall B, Coughlan J, Domeney AM, Gerrard PA, Kelly ME, Naylor RJ, Onaivi ES, Tomkins DM,
|
|
Tyers MB. "The selective 5-HT3 receptor antagonist, onansetron, has been assessed in three tests of
|
|
cognition in the mouse, rat and marmoset. In a habituation test in the mouse, ondansetron facilitated
|
|
performance in young adult and aged animals, and inhibited an impairment in habituation induced by
|
|
scopolamine, electrolesions or ibotenic acid lesions of the nucleus basalis magnocellularis." "In an
|
|
object discrimination and reversal learning task in the marmoset, assessed using a Wisconsin General
|
|
Test Apparatus, ondansetron improved performance in a reversal learning task. We</span>
|
|
<span style="font-weight: bold">
|
|
conclude that ondansetron potently improves basal performance in rodent and primate tests of cognition
|
|
and inhibits the impairments in performance caused by cholinergic deficits."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal"
|
|
>Pharmacol Biochem Behav 1992 May;42(1):75-83. Ondansetron and arecoline prevent scopolamine-induced
|
|
cognitive deficits in the marmoset.</span>
|
|
<span style="font-weight: bold">
|
|
Carey GJ, Costall B, Domeney AM, Gerrard PA, Jones DN, Naylor RJ, Tyers MB
|
|
</span>
|
|
<span style="font-weight: normal">School of Pharmacy, University of Bradford, UK. </span>
|
|
<span style="font-weight: bold">The cognitive-enhancing potential of the 5-hydroxytryptamine (5-HT)
|
|
selective 5-HT3 receptor antagonist, ondansetron, was investigated in a model of cognitive impairment
|
|
induced by the muscarinic receptor antagonist, scopolamine.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Comp Physiol Psychol 1977 Jun;91(3): 642-8. </span>
|
|
<span style="font-weight: bold"
|
|
>Tryptophan and tonic immobility in chickens: effects of dietary and systemic manipulations.</span>
|
|
<span style="font-weight: normal">
|
|
Gallup GG Jr, Wallnau LB, Boren JL, Gagliardi GJ, Maser JD, Edson PH.
|
|
</span>
|
|
<span style="font-weight: bold">"Systemic injections of tryptophan, the dietary precursor to serotonin, led
|
|
to a dose-dependent increase in immobility, with optimal effects being observed within 30 min after
|
|
injection. Dietary depletion of endogenous tryptophan served to attenuate the duration of immobility,
|
|
and a diet completely free of tryptophan, but supplemented with niacin, practically abolished the
|
|
reaction.
|
|
</span>
|
|
<span style="font-weight: normal">Dietary replacement served to reinstate the response." </span>
|
|
<span style="font-weight: bold"
|
|
>"The data are discussed in light of evidence showing serotonergic involvement in tonic immobility."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neurosci Res 1995 Feb 15;40(3):407-413. </span>
|
|
<span style="font-weight: bold"
|
|
>Endotoxin administration stimulates cerebral catecholamine release in freely moving rats as assessed by
|
|
microdialysis.</span>
|
|
<span style="font-weight: normal"> Lavicky J, Dunn AJ. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neurosci Res 1998 Feb 15;51(4):517-525. </span>
|
|
<span style="font-weight: bold">Lipopolysaccharide regulates both serotonin- and thrombin-induced
|
|
intracellular calcium mobilization in rat C6 glioma cells: possible involvement of nitric oxide
|
|
synthase-mediated pathway.
|
|
</span>
|
|
<span style="font-weight: normal">Tawara Y, Kagaya A, Uchitomi Y, Horiguchi J, Yamawaki S.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 9pt">Infect Immun 1996 Dec;64(12):5290-5294..<span
|
|
style="font-weight: bold"
|
|
>Biphasic, organ-specific, and strain-specific accumulation of platelets induced in mice by a
|
|
lipopolysaccharide from Escherichia coli and its possible involvement in shock.
|
|
</span><span style="font-weight: normal"
|
|
>Shibazaki M, Nakamura M, Endo Y. "Platelets contain a large amount of 5-hydroxytryptamine (5HT,
|
|
serotonin). Intravenous injection into BALB/c mice of a Boivin's preparation of lipopolysaccharide
|
|
(LPS) from Escherichia coli induced rapid 5HT accumulation in the lung (within 5 min) and slow 5HT
|
|
accumulation in the liver (2 to 5 h later)." "A shock, which was</span><span
|
|
style="font-weight: bold"
|
|
>
|
|
</span><span style="font-weight: normal">manifested by crawling, convulsion, or prostration, followed
|
|
shortly after the rapid accumulation of 5HT in the lung. On the other hand, the slow accumulation of
|
|
5HT in the liver could be induced by much lower doses of LPS (1 microg/kg or less), even when given
|
|
by intraperitoneal injection."
|
|
</span></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Life Sci 1997;61(18):1819-1827. </span>
|
|
<span style="font-weight: bold"
|
|
>Serotonin 5HT2A receptor activation inhibits inducible nitric oxide synthase activity in C6 glioma
|
|
cells.</span>
|
|
<span style="font-weight: normal"> Miller KJ, Mariano CL, Cruz WR.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Harefuah 2000 May 15;138(10):809-12, 910.</span>
|
|
<span style="font-weight: bold">
|
|
[Jet lag causing or exacerbating psychiatric disorders].</span>
|
|
<span style="font-weight: normal">
|
|
Katz G, Durst R, Zislin J, Knobler H, Knobler HY. We presume, relying on the literature and our
|
|
accumulated experience, that in predisposed individuals jet lag may play a role in triggering
|
|
exacerbation of, or de novo affective disorders, as well as, though less convincing, schizophreniform
|
|
psychosis or even schizophrenia. An illustrative case vignette exemplifies the possible relationship
|
|
between jet lag following eastbound flight and psychotic manifestations.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Life Sci 1987 May 18;40(20):2031-9.</span>
|
|
<span style="font-weight: bold">
|
|
Dysfunction in a prefrontal substrate of sustained attention in schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Cohen RM, Semple WE, Gross M, Nordahl TE, DeLisi LE, Holcomb HH, King AC, Morihisa JM, Pickar D.
|
|
Regional brain metabolism was measured in normal subjects and patients with schizophrenia while they
|
|
performed an auditory discrimination task designed to emphasize sustained attention. A direct
|
|
relationship was found in the normal</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal"
|
|
>subjects between metabolic rate in the middle prefrontal cortex and accuracy of performance. The metabolic
|
|
rate in the middle prefrontal cortex of patients with schizophrenia, even those who performed as well as
|
|
normals, was found to be significantly lower than normal and unrelated to performance. The findings
|
|
point to a role of the mid-prefrontal region in sustained attention and to dysfunction of this region in
|
|
schizophrenia.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Acta Psychiatr Scand 1987 Dec;76(6):628-41. </span>
|
|
<span style="font-weight: bold"
|
|
>Regional brain glucose metabolism in drug free schizophrenic patients and clinical correlates.</span>
|
|
<span style="font-weight: normal">
|
|
Wiesel FA, Wik G, Sjogren I, Blomqvist G, Greitz T, Stone-Elander S. "Thus, the lower the metabolic rate
|
|
was, the more autistic the patient. Metabolic rates were not correlated to atrophic changes of the
|
|
brain. No basis for a specific alteration in frontal cortical metabolism of schizophrenics was obtained.
|
|
Changes in regional metabolic rates in schizophrenia are suggested to reflect disturbances in more
|
|
general mechanisms which are of importance in neuronal function."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Chung Hua Shen Ching Ching Shen Ko Tsa Chih 1991 Oct;24(5):268-71, 316-7.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>[Developments observation of serum thyrohormone level in schizophrenics.</span>
|
|
<span style="font-weight: normal">
|
|
Wang X. "The authors reported that abnormal levels of T4, FT4I in 16 cases patients relate to disease
|
|
course and severe symptoms and suggested that the change of serum T4, FT4I in some cases was related to
|
|
the disease in itself."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 10pt">Biol Psychiatry 1991 Mar 1;29(5):457-66.<span style="font-weight: bold">
|
|
Multidimensional hormonal discrimination of paranoid schizophrenic from bipolar manic
|
|
patients.</span><span style="font-weight: normal"> Mason JW, Kosten TR, Giller EL. </span></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Zh Nevropatol Psikhiatr Im S S Korsakova 1991;91(1):122-3 </span>
|
|
<span style="font-weight: bold">[Status of the thyroid gland in patients with schizophrenia].</span>
|
|
<span style="font-weight: normal">
|
|
Turianitsa IM, Lavkai IIu, Mishanich II, Margitich VM, Razhov KF. "The rise of TTH concentration
|
|
represents one of the mechanisms of correction, aimed at the attainment of the physiological content of
|
|
T4 at the expense of its additional output for its level in the blood serum is appreciably
|
|
reduced."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Can J Psychiatry 1990 May;35(4):342-3. </span>
|
|
<span style="font-weight: bold">Increased detection of elevated TSH using immunoradiometric assay.</span>
|
|
<span style="font-weight: normal">
|
|
Little KY, Kearfott KS, Castellanos X, Rinker A, Whitley R. Using a highly sensitive immunoradiometric
|
|
assay, the authors detected an increased rate of elevated thyrotropin in 2,099 patients vs 1,789
|
|
patients examined with radioimmunoassay. Closer scrutiny of mood disorder patients with elevations found
|
|
confirmatory evidence of thyroid dysfunction in most.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Metabolism 1990 May;39(5):538-43.</span>
|
|
<span style="font-weight: bold">
|
|
Serum thyrotropin in hospitalized psychiatric patients: evidence for hyperthyrotropinemia as measured by
|
|
an ultrasensitive thyrotropin assay.</span>
|
|
<span style="font-weight: normal"> Chopra IJ, Solomon DH, Huang TS. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Nerv Ment Dis 1989 Jun;177(6):351-8.</span>
|
|
<span style="font-weight: bold">
|
|
Serum thyroxine levels in schizophrenic and affective disorder diagnostic subgroups.</span>
|
|
<span style="font-weight: normal"> Mason JW, Kennedy JL, Kosten TR, Giller EL Jr</span>
|
|
<span style="font-weight: bold"
|
|
>. "For TT4, 75% of the PS group showed a rise during recovery in contrast to 4% of the remaining groups;
|
|
for FT4, 50% of the PS group showed a rise compared with 14% of the other groups." "This study
|
|
emphasizes the importance of exploring more fully the psychiatric significance of thyroxine levels
|
|
within the endocrinological normal range and of doing longitudinal assessments of thyroxine and symptom
|
|
changes during clinical recovery in psychiatric disorders."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Biol Psychiatry 1989 Jan;25(1):67-74. </span>
|
|
<span style="font-weight: bold"
|
|
>Serum thyroxine change and clinical recovery in psychiatric inpatients.</span>
|
|
<span style="font-weight: normal">
|
|
Southwick S, Mason JW, Giller EL, Kosten TR. "A strong correlation between the range values for BPRS
|
|
[Brief Psychiatric Rating Scale] sum and for FT4 (p less than 0.005) and TT4 (p less than 0.001) levels
|
|
indicated that change in overall symptom severity was linked to change in thyroxine levels during
|
|
clinical recovery." "These findings suggest that a "normalizing" principle underlies the relationship
|
|
between clinical recovery and thyroxine levels and that both FT4 and TT4 levels within the normal range
|
|
appear to have clinical significance in either reflecting or contributing to the course of a variety of
|
|
psychiatric disorders and possibly having a role in pathogenesis."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Clin Psychiatry 1980 Sep;41(9):316-8. </span>
|
|
<span style="font-weight: bold">Myxedema psychosis--insanity defense in homicide.</span>
|
|
<span style="font-weight: normal"> Easson WM. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Int J Psychiatry Med 1988;18(3):263-70.</span>
|
|
<span style="font-weight: bold">
|
|
The diagnostic dilemma of myxedema and madness, axis I and axis II: a longitudinal case report.</span>
|
|
<span style="font-weight: normal">
|
|
Darko DF, Krull A, Dickinson M, Gillin JC, Risch SC. "A patient with presumed chronic paranoid
|
|
schizophrenia had chronic thyroiditis and Grade I hypothyroidism. Psychosis cleared following treatment
|
|
with thyroid replacement." "The differential diagnosis among hypothyroidism and primary axis I psychotic
|
|
and depressive psychopathology has always been problematic."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 10pt">P R Health Sci J 1993 Jun;12(2):85-7.<span style="font-weight: bold">
|
|
[Alzheimer's disease: the untold story].</span><span style="font-weight: normal">
|
|
Pico-Santiago G. After considering the potential relationship between amyloid deposits and
|
|
myxedematous infiltrations, the hypothesis is formulated that Alzheimer's disease may be due to
|
|
functional hypothyroidism and may thus respond to thyroid therapy.</span></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychiatry Res 1998 Jul 27;80(1):29-39.</span>
|
|
<span style="font-weight: bold">
|
|
Reduced level of plasma antioxidant uric acid in schizophrenia.</span>
|
|
<span style="font-weight: normal"><hr /></span>
|
|
<span style="font-weight: bold">
|
|
and inversely correlated with psychosis. There was a trend for lower uric acid levels in relapsed
|
|
patients relative to clinically stable patients. Smoking, which can modify plasma antioxidant capacity,
|
|
was not found to have prominent effects on uric acid levels. The present finding of a significant
|
|
decrease of a</span>
|
|
<span style="font-weight: normal">
|
|
selective antioxidant provides additional support to the hypothesis that oxidative stress in
|
|
schizophrenia may be due to a defect in the antioxidant defense system."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 9pt">Zh Nevropatol Psikhiatr Im S S Korsakova 1989; 89(5):108-10.<span
|
|
style="font-weight: bold"
|
|
>
|
|
[Lipid peroxidation processes in patients with schizophrenia].</span><span
|
|
style="font-weight: normal"
|
|
>
|
|
Kovaleva ES, Orlov ON, Tsutsu'lkovskaia MIa, Vladimirova TV, Beliaev BS.
|
|
</span></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Zh Nevropatol Psikhiatr Im S S Korsakova 1991;91(7):121-4. </span>
|
|
<span style="font-weight: bold"
|
|
>[Significance of disorders of the processes of lipid peroxidation in patients with persistent paranoid
|
|
schizophrenia resistant to the treatment].</span>
|
|
<span style="font-weight: normal">
|
|
Govorin NV, Govorin AV, Skazhutin SA.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Patol Fiziol Eksp Ter 1999 Jul-Sep;(3):19-22. </span>
|
|
<span style="font-weight: bold"
|
|
>[The biogenic amine content of rat tissues in the postresuscitation period following hemorrhagic shock and
|
|
the effect of the preparation semax].</span>
|
|
<span style="font-weight: normal">
|
|
Bastrikova NA, Shestakova SV, Antonova SV, Krushinskaia IaV, Goncharenko EN, Kudriashova NIu,
|
|
Novoderzhkina IS, Sokolova NA, Kozhura VL. "Early after resuscitation the trend was noted to higher LPO
|
|
products concentration in plasma and serotonin in the brain stem." "It is suggested that biogenic
|
|
amines, especially serotonin system, are involved in mechanisms of postresuscitation disorders, in
|
|
cerebral defects in particular, through prolongation of secondary hypoxia early after hemorrhagic shock
|
|
and activation of hypothalamo-hypophyso-adrenal system late after the shock."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Prostaglandins Leukot Essent Fatty Acids 1996 Aug;55(1-2):33-43.
|
|
</span>
|
|
<span style="font-weight: bold">Free radical pathology in schizophrenia: a review.</span>
|
|
<span style="font-weight: normal">
|
|
Reddy RD, Yao JK.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Res 1996 Mar;19(1):19-26. </span>
|
|
<span style="font-weight: bold">Impaired antioxidant defense at the onset of psychosis.</span>
|
|
<span style="font-weight: normal">
|
|
Mukerjee S, Mahadik SP, Scheffer R, Correnti EE, Kelkar H.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Biol Psychiatry 1998 May 1;43(9):674-9. </span>
|
|
<span style="font-weight: bold"
|
|
>Elevated plasma lipid peroxides at the onset of nonaffective psychosis.</span>
|
|
<span style="font-weight: normal">
|
|
Mahadik SP, Mukherjee S, Scheffer R, Correnti EE, Mahadik JS.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Brain Res 1999 Aug 21;839(1):74-84.</span>
|
|
<span style="font-weight: bold">
|
|
Psychological stress-induced enhancement of brain lipid peroxidation via nitric oxide systems and its
|
|
modulation by anxiolytic and anxiogenic drugs in mice.</span>
|
|
<span style="font-weight: normal">
|
|
Matsumoto K, Yobimoto K, Huong NT, Abdel-Fattah M, Van Hien T, Watanabe H. "The effects of diazepam and
|
|
FG7142 were abolished by the BZD receptor antagonist flumazenil (10 mg/kg, i.p.). These results indicate
|
|
that psychological stress causes oxidative damage to the brain lipid via enhancing constitutive
|
|
NOS-mediated production of NO, and that drugs with a BZD or 5-HT(1A) receptor agonist profile have a
|
|
protective effect on oxidative brain membrane damage induced by psychological stress."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Anesteziol Reanimatol 1998 Nov-Dec; (6):20-5. </span>
|
|
<span style="font-weight: bold"
|
|
>[Role of hyperbaric oxygenation in the treatment of posthypoxic encephalopathy of toxic etiology].</span>
|
|
<span style="font-weight: normal">
|
|
Ermolov AS, Epifanova NM, Romasenko MV, Luzhnikov EA, Ishmukhametov AI, Golikov PP, Khvatov VB, Kukshina
|
|
AA, Davydov BV, Kuksova NS, et al. Hyperbaric oxygenation (HBO) was used in the treatment of 475
|
|
patients with toxic encephalopathy (TE) developing as a result of exo- and endotoxicosis. HBO promoted
|
|
correction of all components of homeostasis,
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>decreased endotoxicosis, reduced psychopathological and neurological disorders, and promoted social
|
|
adaptation.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Neurochem 2000 Jan; 74(1): 114-24. </span>
|
|
<span style="font-weight: bold"
|
|
>Metabolic impairment elicits brain cell type-selective changes in oxidative stress and cell death in
|
|
culture.</span>
|
|
<span style="font-weight: normal">
|
|
Park LC, Calingasan NY, Uchida K, Zhang H, Gibson GE. "Abnormalities in oxidative metabolism and
|
|
inflammation accompany many neurodegenerative diseases. Thiamine deficiency (TD) is an animal model in
|
|
which chronic oxidative stress and inflammation lead to selective neuronal death, whereas other cell
|
|
types show an inflammatory response." "Among the cell types tested, only in neurons did TD induce
|
|
apoptosis and cause the accumulation of 4-hydroxy-2-nonenal, a lipid peroxidation product. On the other
|
|
hand, chronic lipopolysaccharide-induced inflammation significantly inhibited cellular dehydrogenase and
|
|
KGDHC activities in microglia and astrocytes but not in neurons or endothelial cells. The results
|
|
demonstrate that the selective cell changes during TD in vivo reflect inherent properties of the
|
|
different brain cell types."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychol Med 1976 Aug;6(3):359-69.</span>
|
|
<span style="font-weight: bold">
|
|
Possible association of schizophrenia with a disturbance in prostaglandin metabolism: a physiological
|
|
hypothesis.</span>
|
|
<span style="font-weight: normal">
|
|
Feldberg W. Schizophrenia may be associated with increased prostaglandin synthesis in certain parts of
|
|
the brain. This hypothesis is based on the following findings: (1) Catalepsy, which is the nearest
|
|
equivalent in animals to human catatonia,</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal"
|
|
>develops in cats when prostaglandin E1 is injected into the cerebral ventricles and when during endotoxin
|
|
or lipid A fever the prostaglandin E2 level in cisternal c.s.f. rises to high levels; however, when
|
|
fever and prostaglandin level are brought down by non-steroid anti-pyretics which inhibit prostaglandin
|
|
synthesis, catalepsy disappears as well. (2) Febrile episodes are a genuine syndrome of
|
|
schizophrenia.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Zh Nevropatol Psikhiatr Im S S Korsakova 1966;66(6):912-7. </span>
|
|
<span style="font-weight: bold"
|
|
>[Treatment of acute schizophrenia with antibiotics, gamma-globulin and vitamins].</span>
|
|
<span style="font-weight: normal">
|
|
Neikoya M.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Prostaglandins Med 1979 Jan;2(1):77-80. </span>
|
|
<span style="font-weight: bold">Penicillin and essential fatty acid supplementation in schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Vaddadi KS.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Psychiatr Dev 1989 Spring;7(1):19-47.</span>
|
|
<span style="font-weight: bold">
|
|
Positron emission tomography in psychiatry.</span>
|
|
<span style="font-weight: normal">
|
|
Wiesel FA. "Schizophrenia is the most extensively studied psychiatric disorder. Most studies have
|
|
demonstrated decreased metabolic rates in wide areas of the brain. It is proposed that the metabolic
|
|
changes observed in the brains of schizophrenic patients are due to a fundamental change in neuronal
|
|
function." "Bipolar depressed patients probably have a decreased brain metabolism." "Alcohol dependent
|
|
subjects with a long duration of abuse may have a decreased brain metabolism."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Arch Gen Psychiatry 1976 Nov;33(11):1377-81. </span>
|
|
<span style="font-weight: bold"
|
|
>Platelet monamine oxidase in chronic schizophrenia. Some enzyme characteristics relevant to reduced
|
|
activity.</span>
|
|
<span style="font-weight: normal">
|
|
Murphy DL, Donnelly CH, Miller L, Wyatt RJ. "These findings suggest that the reduced MAO activity found
|
|
in chronic schizophrenic patients is apparently not accounted for by nonspecific changes in platelets or
|
|
platelet mitochondria."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Exp Neurol 1997 May;145(1):118-29.</span>
|
|
<span style="font-weight: bold">
|
|
Long-term reciprocal changes in dopamine levels in prefrontal cortex versus nucleus accumbens in rats
|
|
born by Caesarean section compared to vaginal birth.</span>
|
|
<span style="font-weight: normal">
|
|
El-Khodor BF, Boksa P. "Epidemiological evidence indicates a higher incidence of pregnancy and birth
|
|
complications among individuals who later develop schizophrenia, a disorder linked to alterations in
|
|
mesolimbic dopamine (DA) function. Two birth</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal"
|
|
>complications usually included in these epidemiological studies, and still frequently encountered in the
|
|
general population, are birth by Caesarean section (C-section) and fetal asphyxia." "At 2 months of age,
|
|
in animals born by rapid C-section, steady state levels of DA were decreased by 53% in the prefrontal
|
|
cortex and increased by 40% in both the nucleus accumbens and striatum, in comparison to the vaginally
|
|
born</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal"
|
|
>group. DA turnover increased in the prefrontal cortex, decreased in the nucleus accumbens, and showed no
|
|
significant change in the striatum, in the C-section group. Thus, birth by a Caesarean procedure
|
|
produces long-term reciprocal changes in DA levels and metabolism in the nucleus accumbens and
|
|
prefrontal cortex." "Although appearing robust at birth on gross observation, more subtle measurements
|
|
revealed that rat pups born by C-section show altered respiratory rates and activity levels and
|
|
increased levels of whole brain lactate, suggestive of low grade brain hypoxia, during the first 24 h of
|
|
life, in comparison to vaginally born controls." "It is concluded that C-section birth is sufficient
|
|
perturbation to produce long-lasting effects on DA levels and metabolism</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">in the central nervous system of the rat."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Rehabilitation (Stuttg) 1983 May;22(2):81-5 </span>
|
|
<span style="font-weight: bold">[Physical capacity of schizophrenic patients]. </span>
|
|
<span style="font-weight: normal">Deimel H, Lohmann S.</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">"Reduced physical capacity in schizophrenic illness has been described in
|
|
medical literature, but so far not been substantiated empirically. The findings of progressive bicycle
|
|
ergometry confirm the assertion, with the following main results having been obtained: 1. As opposed to
|
|
a matched comparison group of untrained healthy clients, the schizophrenically ill patients demonstrated
|
|
significantly lower endurance levels
|
|
</span>
|
|
<span style="font-weight: bold">in respect of the aerobic-anaerobic threshold. </span>
|
|
<span style="font-weight: normal">2. Relative to the load maximum attainable highly significant differences
|
|
existed between the groups. Particularly noteworthy had been early exercise termination already at
|
|
submaximal loads by the schizophrenic patients. 3. The patients under study obtained values one third
|
|
below standard compared to the maximum load target for untrained persons, with age and weight being
|
|
taken into account."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Folia Psychiatr Neurol Jpn 1984;38(4):425-36 </span>
|
|
<span style="font-weight: bold"
|
|
>Antipsychotic and prophylactic effects of acetazolamide (Diamox) on atypical psychosis.</span>
|
|
<span style="font-weight: normal">
|
|
Inoue H, Hazama H, Hamazoe K, Ichikawa M, Omura F, Fukuma E, Inoue K, Umezawa Y We investigated the
|
|
antipsychotic and prophylactic effects of acetazolamide (Diamox) on atypical psychosis. Acetazolamide
|
|
was given to 30 patients: Type I, puberal periodic psychosis, a psychosis whose onset occurs during the
|
|
period of puberty and which appears repetitively with psychosis-like condition at about the same
|
|
interval as the menstrual cycle (6 cases); Type II, a) presenile atypical psychosis which initially
|
|
appears in patients in their 20s or 30s accompanied by manic-depressive cycles and shows acute
|
|
confusional and dreamy states in the presenile period, incurable cases (7), b) atypical psychosis, in
|
|
the narrow sense, cases which show acute hallucination, delusion, confusional and dreamy states
|
|
accompanied by affective symptoms (8 cases); Type III, repetitively the atypical manic and depressive
|
|
states, and atypical manic-depressive psychosis, and transient changes in consciousness, refractory
|
|
cases (2); Type IV, atypical schizophrenia, which is considered to be schizophrenia but shows the
|
|
abnormalities in electroencephalogram and emotional disorders (7 cases). Among these cases,</span>
|
|
<span style="font-weight: bold">
|
|
some extent of the therapeutic effects of acetazolamide (500-1,000 mg/day) was obtained in about 70%.
|
|
The high therapeutic effects were particularly observed in Types I, II and III. It was less effective
|
|
against atypical schizophrenia. Acetazolamide showed the effectiveness in 10 cases out of 13 cases to
|
|
which lithium carbonate and carbamazepine were ineffective.</span>
|
|
<span style="font-weight: normal">
|
|
The high therapeutic effects of acetazolamide were shown in the cases whose
|
|
</span>
|
|
<span style="font-weight: bold">symptoms were aggravated at the interval of the menstrual cycle.</span>
|
|
<span style="font-weight: normal">
|
|
No correlation was observed between the electroencephalographic abnormalities and the therapeutic
|
|
effects. In addition, the prophylactic effects of acetazolamide on the periodic crisis were observed in
|
|
9 cases. From these results, acetazolamide was considered to have the antipsychotic and prophylactic
|
|
effects on atypical psychosis.
|
|
</span>
|
|
<span style="font-weight: bold"
|
|
>Since side effects due to acetazolamide were rarely observed, the present drug was considered to have a
|
|
high safety margin.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Am J Psychiatry 1999 Apr;156(4):617-23 </span>
|
|
<span style="font-weight: bold"
|
|
>Minor physical anomalies, dermatoglyphic asymmetries, and cortisol levels in adolescents with schizotypal
|
|
personality disorder.</span>
|
|
<span style="font-weight: normal">
|
|
Weinstein DD, Diforio D, Schiffman J, Walker E, Bonsall R. "The schizotypal personality disorder group
|
|
showed more minor physical anomalies and dermatoglyphic asymmetries than the normal comparison group and
|
|
higher cortisol levels than both of the other groups."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Am J Psychiatry 1992 Jan;149(1):57-61 </span>
|
|
<span style="font-weight: bold"
|
|
>Congenital malformations and structural developmental anomalies in groups at high risk for psychosis.</span
|
|
>
|
|
<span style="font-weight: normal"> McNeil TF, Blennow G, Lundberg L. "The inferred genetic risk for</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal"
|
|
>psychosis does not appear to be associated with greater rates of early somatic developmental anomalies,
|
|
suggesting that early developmental anomalies do not represent an expression of genetic influence toward
|
|
psychosis."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Bull 1984;10(2):204-32.</span>
|
|
<span style="font-weight: bold">
|
|
Psychophysiological dysfunctions in the developmental course of schizophrenic disorders.</span>
|
|
<span style="font-weight: normal">
|
|
Dawson ME, Nuechterlein KH. "Two electrodermal anomalies are identified in different subgroups of
|
|
symptomatic</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">patients: (1) an abnormally high sympathetic arousal and (2) an abnormal
|
|
absence of skin conductance orienting responses to innocuous environmental stimuli."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Behav Brain Res 2000 Jan;107(1-2):71-83. </span>
|
|
<span style="font-weight: bold"
|
|
>Changes in adult brain and behavior caused by neonatal limbic damage: implications for the etiology of
|
|
schizophrenia.</span>
|
|
<span style="font-weight: normal">
|
|
Hanlon FM, Sutherland RJ. ."This study contributes to our understanding of the pathogenesis of
|
|
schizophrenia by showing that early damage to limbic structures produced behavioral, morphological, and
|
|
neuropharmacological abnormalities related to pathology in adult schizophrenics."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Neurochem Res 1996 Sep; 21(9):995-1004. </span>
|
|
<span style="font-weight: bold"
|
|
>Mitochondrial involvement in schizophrenia and other functional psychoses.</span>
|
|
<span style="font-weight: normal">
|
|
Whatley SA, Curti D, Marchbanks RM. "Gene expression has been studied in post-mortem frontal cortex
|
|
samples from patients who had suffered from schizophrenia and depressive illness." "We conclude that
|
|
changes in mitochondrial gene expression are involved in schizophrenia and probably other functional
|
|
psychoses."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 9pt">Eur J Pharmacol 1994 Aug 11;261(1-2):25-32.<span style="font-weight: bold">
|
|
The effect of alpha 2-adrenoceptor antagonists in isolated globally ischemic rat hearts.</span><span
|
|
style="font-weight: normal"
|
|
>
|
|
Sargent CA, Dzwonczyk S, Grover GJ. "The alpha 2-adrenoceptor antagonist, yohimbine, has been
|
|
reported to protect hypoxic myocardium. Yohimbine has
|
|
</span><span style="font-weight: bold"
|
|
>several other activities, including 5-HT receptor antagonism, at the concentrations at which protection
|
|
was found."</span><span style="font-weight: normal">
|
|
"The</span><span style="font-weight: bold">
|
|
cardioprotective effects of yohimbine were partially reversed by 30 microM 5-HT. These results
|
|
indicate that the mechanism for the cardioprotective activity of yohimbine may involve 5-HT receptor
|
|
antagonistic activity."
|
|
</span></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Cardiovasc Pharmacol 1993 Oct;22(4):664-672. </span>
|
|
<span style="font-weight: bold"
|
|
>Protective effect of serotonin (5-HT2) receptor antagonists in ischemic rat hearts.</span>
|
|
<span style="font-weight: normal">
|
|
Grover GJ, Sargent CA, Dzwonczyk S, Normandin DE, Antonaccio MJ.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Appl Physiol 1994 Jul;77(1):277-284.</span>
|
|
<span style="font-weight: bold">
|
|
Aerobic muscle contraction impaired by serotonin-mediated vasoconstriction.</span>
|
|
<span style="font-weight: normal">
|
|
Dora KA, Rattigan S, Colquhoun EQ, Clark MG.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">J Cereb Blood Flow Metab 1995 Jul;15(4):706-13. </span>
|
|
<span style="font-weight: bold"
|
|
>Enhanced cerebrovascular responsiveness to hypercapnia following depletion of central serotonergic
|
|
terminals.</span>
|
|
<span style="font-weight: normal">
|
|
Kelly PA, Ritchie IM, McBean DE, Sharkey J, Olverman HJ.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Arch Gen Psychiatry 1984 Mar;41(3): 293-300. </span>
|
|
<span style="font-weight: bold"
|
|
>Regional brain glucose metabolism in chronic schizophrenia. A positron emission transaxial tomographic
|
|
study.</span>
|
|
<span style="font-weight: normal">
|
|
Farkas T, Wolf AP, Jaeger J, Brodie JD, Christman DR, Fowler JS.
|
|
</span>
|
|
<span style="font-weight: bold">". . . schizophrenics had significantly lower activity in the frontal lobes,
|
|
relative to posterior regions."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Semin Nucl Med 1986 Jan;16(1):2-34. </span>
|
|
<span style="font-weight: bold"
|
|
>Positron emission tomography imaging of regional cerebral glucose metabolism.</span>
|
|
<span style="font-weight: normal">
|
|
Alavi A, Dann R, Chawluk J, Alavi J, Kushner M, Reivich M. "In patients with Alzheimer's disease . . .
|
|
parietal, temporal, and to some degree, frontal glucose metabolism is significantly diminished even in
|
|
the early stages of the disease. Patients with Huntington's disease and those at risk of developing this
|
|
disorder have a typical pattern of diminished CMRglu in the caudate nuclei and putamen. In patients with
|
|
stroke, PET images with FDG have demonstrated abnormal findings earlier than either XCT or MRI and with
|
|
a wider topographic distribution. FDG scans have revealed interictal zones of decreased LCMRglu in
|
|
approximately 70% of patients with partial epilepsy. The location of the area of hypometabolism
|
|
corresponds to the site of the epileptic focus as determined by electroencephalography and microscopic
|
|
examination of the resected tissue."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Schizophr Bull 1988; 14(2): 169-76.</span>
|
|
<span style="font-weight: bold">
|
|
From syndrome to illness: delineating the pathophysiology of schizophrenia with PET.</span>
|
|
<span style="font-weight: normal">
|
|
Cohen RM, Semple WE, Gross M, Nordahl TE. "In normal controls, the metabolic rate in the middle
|
|
prefrontal cortex, measured during the ongoing performance of auditory discrimination, is associated
|
|
with their accuracy of performance. In unmedicated patients with</span>
|
|
<span style="font-weight: bold"> </span>
|
|
<span style="font-weight: normal">schizophrenia, even those who performed as well as normals, the metabolic
|
|
rate in the mid-prefrontal cortex was found to be significantly lower than normal. Further, this
|
|
decreased metabolic rate was unrelated to performance." "The mid-prefrontal cortex and its dopamine
|
|
neurotransmitter pathway input are important biological determinants of sustained attention."
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Biol Psychiatry 1989 Apr 1;25(7):835-51. </span>
|
|
<span style="font-weight: bold"
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>Increased temporal lobe glucose use in chronic schizophrenic patients.</span>
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<span style="font-weight: normal">
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DeLisi LE, Buchsbaum MS, Holcomb HH, Langston KC, King AC, Kessler R, Pickar D, Carpenter WT Jr,
|
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Morihisa JM, Margolin R, et al. Temporal lobe glucose metabolic rate was assessed in 21 off-medication
|
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patients with schizophrenia and 19 normal controls by positron emission tomography with
|
|
18F-deoxyglucose. Patients with schizophrenia had significantly greater</span>
|
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<span style="font-weight: bold">
|
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metabolic activity in the left than the right anterior temporal lobe, and the extent of this
|
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lateralization was in proportion to the severity of</span>
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|
<span style="font-weight: normal"> psychopathology.</span>
|
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</p>
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<p>
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<span style="font-weight: normal">Am J Obstet Gynecol 1999 Dec;181(6):1479-84.</span>
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<span style="font-weight: bold">
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Stimulated nitric oxide release and nitric oxide sensitivity in forearm arterial vasculature during
|
|
normotensive and preeclamptic pregnancy.</span>
|
|
<span style="font-weight: normal">
|
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Anumba DO, Ford GA, Boys RJ, Robson SC. "Alterations in serotonin receptor coupling to nitric oxide
|
|
synthase, or a limitation of availability of the substrate for nitric oxide synthase (L-arginine) during
|
|
pregnancy, could account for the reduction in stimulated nitric oxide release."</span>
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</p>
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<p>
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<span style="font-weight: normal">J Hypertens 1999 Mar;17(3):389-96.</span>
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<span style="font-weight: bold">
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U46619-mediated vasoconstriction of the fetal placental vasculature in vitro in normal and hypertensive
|
|
pregnancies.</span>
|
|
<span style="font-weight: normal">
|
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Read MA, Leitch IM, Giles WB, Bisits AM, Boura AL, Walters WA.
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</span>
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</p>
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<p>
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<span style="font-weight: normal">Am J Obstet Gynecol 1999 Feb;180(2 Pt 1):371-7. </span>
|
|
<span style="font-weight: bold"
|
|
>Ketanserin versus dihydralazine in the management of severe early-onset preeclampsia: maternal
|
|
outcome.</span>
|
|
<span style="font-weight: normal">
|
|
Bolte AC, van Eyck J, Kanhai HH, Bruinse HW, van Geijn HP, Dekker GA. "Ketanserin [a selective serotonin
|
|
2 receptor blocker] is an attractive alternative in the management of severe early-onset
|
|
preeclampsia."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Am J Obstet Gynecol 1996 Dec;175(6):1543-50</span>
|
|
<span style="font-weight: bold"
|
|
>. Novel appearance of placental nuclear monoamine oxidase: biochemical and histochemical evidence for
|
|
hyperserotonomic state in preeclampsia-eclampsia.</span>
|
|
<span style="font-weight: normal">
|
|
Gujrati VR, Shanker K, Vrat S, Chandravati, Parmar SS. "Placental serotonin increases with severity
|
|
(rsystolic 0.84, rdiastolic 0.83) and monoamine oxidase decreases (rsystolic 0.86, rdiastolic 0.79).
|
|
Placental monoamine oxidase showed marked changes in preeclampsia-eclampsia." ."A severity-dependent
|
|
decrease was present in the nuclei of placentas with preeclampsia-eclampsia." "The study delineates an
|
|
impaired catabolism of placental serotonin in preeclampsia-eclampsia." "The novel appearance of
|
|
monoamine oxidase in nuclei in proximity to its normal site and low activity resulting in a
|
|
hyperserotonomic state may lead to preeclampsia-eclampsia."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Chung Hua Fu Chan Ko Tsa Chih 1996 Nov;31(11):670-2 </span>
|
|
<span style="font-weight: bold"
|
|
>[Changes of plasma levels of monoamines in normal pregnancy and pregnancy-induced hypertension women and
|
|
their significance].</span>
|
|
<span style="font-weight: normal">
|
|
Lin B, Zhu S, Shao B. "Compared with NP [normal pregnant], the contents of DA in moderate and severe PIH
|
|
[pregnancy-induced hypertension] were markedly and very markedly decreased respectively (P < 0.05 and
|
|
P < 0.01), while the levels of 5-HT in PIH increased significantly (P < 0.05)." "The changes of
|
|
monoamines may be one of the causes of small artery spasm in PIH."</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Lancet 1997 Nov 1;350(9087):1267-71. </span>
|
|
<span style="font-weight: bold"
|
|
>Randomised controlled trial of ketanserin and aspirin in prevention of pre-eclampsia.</span>
|
|
<span style="font-weight: normal"><hr /></span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Osaka City Med J 1989 Jun;35(1):1-11.</span>
|
|
<span style="font-weight: bold">
|
|
Serotonin and tryptamine metabolism in the acute hepatic failure model: changes in tryptophan and its
|
|
metabolites in the liver, brain and kidney.</span>
|
|
<span style="font-weight: normal">
|
|
Kodama C, Mizoguchi Y, Kawada N, Sakagami Y, Seki S, Kobayashi K, Morisawa S.
|
|
</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Br J Pharmacol 1984 Apr;81(4):645-650.</span>
|
|
<span style="font-weight: bold">
|
|
Induction of hypoglycaemia and accumulation of 5-hydroxytryptamine in the liver after the injection of
|
|
mitogenic substances into mice.
|
|
</span>
|
|
<span style="font-weight: normal">Endo Y</span>
|
|
<span style="font-weight: bold">.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Eur J Pharmacol 1983 Aug 5;91(4):493-499.</span>
|
|
<span style="font-weight: bold">
|
|
A lipopolysaccharide and concanavalin A induce variations of serotonin levels in mouse tissues.</span>
|
|
<span style="font-weight: normal"> Endo Y. </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Brain Res 1986 Jul 16;378(1):164-8 </span>
|
|
<span style="font-weight: bold">5-Hydroxytryptamine-2 antagonist increases human slow wave sleep.</span>
|
|
<span style="font-weight: normal">
|
|
Idzikowski C, Mills FJ, Glennard R Ritanserin, a specific 5-HT2 antagonist, was given to volunteers in a
|
|
double-blind placebo controlled sleep study. Slow wave sleep doubled in duration at the expense of stage
|
|
2. The finding that a serotonin antagonist changed the architecture of sleep without producing insomnia
|
|
is of fundamental importance and calls for a re-examination of traditional theories of sleep control
|
|
which assign a facilitatory role to serotonin.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Med Hypotheses 2000 Apr;54(4):645-7</span>
|
|
<span style="font-weight: bold">
|
|
Role of the pineal gland in hibernators: a concept proposed to clarify why hibernators have to leave
|
|
torpor and sleep.</span>
|
|
<span style="font-weight: normal"> Kocsard-Varo G</span>
|
|
<span style="font-weight: bold">.</span>
|
|
<span style="font-weight: normal"> </span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Chronobiol Int 2000 Mar;17(2):103-28.</span>
|
|
<span style="font-weight: bold">
|
|
The temporal organization of daily torpor and hibernation: circadian and circannual rhythms.</span>
|
|
<span style="font-weight: normal"> Kortner G, Geiser F.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-weight: normal">Neuroreport 2000 Mar 20;11(4):881-5 </span>
|
|
<span style="font-weight: bold"
|
|
>Slow waves in the sleep electroencephalogram after daily torpor are homeostatically regulated.</span>
|
|
<span style="font-weight: normal"> Deboer T, Tobler I.</span>
|
|
</p>
|
|
<p>
|
|
<span style="font-size: 10pt">Neuroendocrinology 1982 Jun; 34(6): 438-443.<span style="font-weight: bold">
|
|
Sleep organization in hypo- and hyperthyroid rats.
|
|
</span><span style="font-weight: normal">Carpenter AC, Timiras PS. "The results show an increased number
|
|
of awakenings during slow wave sleep (SWS) in hypothyroid animals, whereas total sleep time, levels
|
|
of SWS, paradoxical sleep, and diurnal organization were unaffected by thyroid status.
|
|
</span><span style="font-weight: bold"
|
|
>Our findings indicate that adequate levels of thyroid hormone are necessary to sustain extended periods
|
|
of SWS in the adult rat while hyperthyroid animals show no disruption of sleep organization.</span
|
|
><span style="font-weight: normal">
|
|
A corollary finding is that daily sleep quotas are independent of whole body metabolic rates."</span
|
|
></span>
|
|
</p>
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|
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© Ray Peat Ph.D. 2009. All Rights Reserved. www.RayPeat.com
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