Failure in the Utilization of Carbohydrates in Mental Disease

Lingjaerde, Ottar

doi:10.1111/j.1600-0447.1956.tb04759.x

Cited by 3 publications

(2 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Goldner and Ricketts (73) have seriously challenged the concept of an anti-insulin factor, specifically in schizophrenic blood, for they were unable to confirm the work of Meduna et al Nevertheless, insulin resistance in schizophrenics has also been described by Freeman et al (55), Freeman (53), and Harris (76). However, abnormal insulin reactions are not characteristic of all schizophrenics and are frequently found in other forms of mental disease (115). Lingjaerde (115) has also shown that many patients with mental disorders require an excessive intake of carbohydrates in order to maintain normal concentrations of urobilin in their urine.…”

Section: Carbohydrate Metabolismmentioning

confidence: 99%

“…However, abnormal insulin reactions are not characteristic of all schizophrenics and are frequently found in other forms of mental disease (115). Lingjaerde (115) has also shown that many patients with mental disorders require an excessive intake of carbohydrates in order to maintain normal concentrations of urobilin in their urine. A decreased carbohydrate intake in such patients resulted in an abnormally high urobilin content and ketonuria.…”

Section: Carbohydrate Metabolismmentioning

confidence: 99%

See 1 more Smart Citation

Biochemical and Physiological Changes Associated with Schizophrenia.

Domino¹

1959

Psychopharmacology: Problems in Evaluation.

View full text Add to dashboard Cite

As our knowledge and clinical experience with phrenotropic drugs increases it is evident that agents such as reserpine, chlorpromazine, promazine, proclorperazine, perphenazine, and others make the disturbed psychotic more manageable but still leave him psychotic (48,130). The incidence of remissions following drug therapy appears no better than that following the myriad of more drastice somatic shock therapies. These results are not necessarily disappointing, for the widespread use of phrenotropic drugs as therapeutic adjuncts in psychiatry has strengthened the view that functions of the mind are the end result of an actively metabolizing brain. By giving fresh impetus to the search for possible physiochemical abnormalities in mental disease, the present nonspecific symptomatic drug therapies have already accomplished a great deal.Since the design of more specific drug treatments is dependent upon discrete knowledge of possible biochemical and physiological aberrations associated with mental disease, it is pertinent to the objectives of this conference to review critically the available evidence for such alterations. Both primary and secondary biochemical and physiological changes are of interest. Obviously it may be extremely difficult to distinguish between cause and effect. If one assumes that most mental disease has purely psychic etiological factors, it still follows that they will probably produce secondary physiological abnormalities; the psychosomatic literature provides many examples (40). The reverse is equally true; somatopsychic phenomena are well known. Physiological and biochemical alterations profoundly influence mental functions, as evidenced by the effects of hypoxia, hypoglycemia, and hypercapnia, and by such drugs as the hallucinogens LSD-25 and mescaline. Drug therapy, if rational, need not affect only primary physiochemical alterations, but may give symptomatic relief by modifying secondary disturbances. For example, an agent like amphetamine does not correct the primary psychopathology involving neurotic obesity but does curb the secondary increase in appetite.All physiological and biochemical changes in psychoses, if real, are of interest to the pharmacologist, for drugs might be designed that can affect either primary or secondary metabolic or physiologic disturbances. Presumably our present tranquilizers act to reduce secondary physiologic disturbances in the overreactive, vociferous, and hallucinating patient but do not affect his primary psychopathology.In 1895, Maudsley (132) wrote on insanity with excitement that: "The many diligent and elaborate chemical analyses of the urine which have been made by different inquirers in different countries, notwithstanding that the tabular exposition of them might fill a large volume, have failed to yield definite and constant results or to warrant any positive inference." This statement is equally true today for all types of insanity, but perhaps it should be qualified. Thus, in 1957, we can paraphrase Maudsley's remarks of 62 years ago and say t...

show abstract

Section: Carbohydrate Metabolismmentioning

confidence: 99%

Section: Carbohydrate Metabolismmentioning

confidence: 99%

Biochemical and Physiological Changes Associated with Schizophrenia.

Domino¹

1959

Psychopharmacology: Problems in Evaluation.

View full text Add to dashboard Cite

show abstract

A re-evaluation of glucose tolerance in schizophrenia

Brown

Quarrington

Stancer

1969

Journal of Psychiatric Research

View full text Add to dashboard Cite

Glucose Tolerance in Depression

Herzberg

Coppen

1968

Br J Psychiatry

View full text Add to dashboard Cite

There have been many reports which suggest that there may be abnormal glucose metabolism in severe depression. Glycosuria was first reported nearly 60 years ago (Allers, 1914). In 1919, using an oral glucose tolerance test, Kooy observed decreased tolerance in a heterogeneous group of mentally ill patients which included melancholics. Since then many investigators have reported decreased glucose tolerance in depressive illness, and the extensive literature is reviewed by McFarland and Goldstein (1939) and Altschule (1953). Oral glucose tolerance tests have usually shown high or delayed peaks and a slow return to fasting levels, although the latter are usually reported normal. Intravenous glucose tolerance tests have also shown results nearer those obtained in diabetic patients than in normal subjects. Pryce (1958) reported decreased glucose tolerance with intravenous tests in a sample of 20 depressed patients, and he also found that glucose tolerance did not alter significantly after clinical recovery. Glucose supplements were added to the diet of six patients prior to testing, but he concluded that these supplements did not appear to alter glucose tolerance.

show abstract

Failure in the Utilization of Carbohydrates in Mental Disease

Cited by 3 publications

References 2 publications

Biochemical and Physiological Changes Associated with Schizophrenia.

Biochemical and Physiological Changes Associated with Schizophrenia.

A re-evaluation of glucose tolerance in schizophrenia

Glucose Tolerance in Depression

Contact Info

Product

Resources

About