Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature
We report the unexpected resolution of longstanding schizophrenic symptoms after starting a low-carbohydrate, ketogenic diet. After a review of the literature, possible reasons for this include the metabolic consequences from the elimination of gluten from the diet, and the modulation of the disease of schizophrenia at the cellular level.
C.D. is a 70 year-old Caucasian female with a diagnosis of schizophrenia since the age of seventeen. Her diagnosis was based on paranoia, disorganized speech, and hallucinations. She reported both auditory and visual hallucinations, including seeing skeletons and hearing voices that told her to hurt herself. According to her history, she has had these hallucinations on almost a daily basis since the age of seven. C.D. has also been hospitalized at least five times over the last six years for suicide attempts and increased psychotic symptoms.
C.D.'s other medical problems (and approximate year of diagnosis) included obesity (1950's), hypertension (1970's), depression (1940's), obstructive sleep apnea (2002), gastroesophageal reflux disease (2003), urinary incontinence (2002), glaucoma (1999), trochanteric bursitis (2004), peripheral neuropathy of unknown etiology (2006), and prior cholecystectomy (1978).
A typical day's diet consisted of the following: egg and cheese sandwich, diet soda, water, pimento cheese, barbequed pork, chicken salad, hamburger helper, macaroni and cheese, and potatoes. She rated her baseline fatigue as a "3" using a standardized questionnaire (0 = none, 4 = severe or frequent). Her body weight was 141.4 kilograms (BMI 52.6 kg/m2), sitting blood pressure (BP) was 130/72 mmHg, and pulse was 68 beats per minute. Physical examination showed an obese, mildly disheveled female with poor attention to hygiene, but was otherwise unremarkable. She was instructed how to follow a dietary regimen consisting of unlimited meats and eggs, 4 ounces of hard cheese, 2 cups of salad vegetables, and 1 cup of low-carbohydrate vegetables per day. This diet restricts carbohydrate intake to fewer than 20 grams per day
Over the course of 12 months, C.D. has continued the low-carbohydrate, ketogenic diet and has had no recurrence of her auditory or visual hallucinations. She has also continued to lose weight (body weight 131.4 kilograms) and experience improvements in her energy level. She acknowledged having 2–3 isolated episodes of dietary non-compliance that lasted several days, where she ate pasta, bread, and cakes around the winter holidays; however she had no recurrence of her hallucinations.
Niacin deficiency seems to be an important contributor in the development of the clinical picture of schizophrenia. Studies and sparse case reports indicate that niacin augmentation could help a subset of patients suffering from schizophrenia.
These patients could benefit from an early intervention of addition of therapeutic doses of schizophrenia in addition to ongoing treatment.
Niacin sensitivity and efficacy were reduced in schizophrenia. In the control group, there was significant correlation between AA levels and niacin sensitivity as well as a trend toward correlation between AA levels and niacin efficacy. In contrast, neither sensitivity nor efficacy of niacin correlated with AA levels in schizophrenia. An expected correlation between the levels of AA and its elongation product (adrenic acid) was absent in schizophrenia. Adrenic acid levels correlated with niacin efficacy in schizophrenia.
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