Nutritional Interventions in the Treatment of Schizophrenia: A Case Report

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FOR IMMEDIATE RELEASE
Orthomolecular Medicine News Service, February 20, 2025

by Aarti Midha, M.D.

Abstract

Schizophrenia is a psychiatric disorder for which conventional medicine uses antipsychotic medications. This is a case report of a 28-year-old male who arrived at my clinic in 2018 with symptoms of muttering, fearfulness, and withdrawn behavior and was taking antipsychotics and benzodiazepines for many years. We investigated him for metabolic causes, and the investigations revealed raised serum aluminum and high HSCRP. We started with the nutrients N-acetylcysteine, alpha-lipoic acid, and antioxidants to reduce oxidative stress and enhance phase 2 detoxification support, along with other nutrients. He also started an antioxidant-rich, gluten-free diet with probiotics. He started improving after three months. We monitored serum aluminum levels in this process. We started reducing psychotropic medications thereafter and continued antioxidant support to reduce inflammation and oxidative stress. He has been symptom-free for the last four years. He is on a low-dose mood stabilizer along with antioxidant support. He has not taken any antipsychotics in the last four years. Based on the positive outcome, we propose the role of nutritional intervention in reducing inflammation in psychiatric disorders.

Keywords: case report, schizophrenia, heavy metal toxins, aluminum

Introduction

Schizophrenia is characterized by a variety of symptoms, such as hallucinations, delusions, disordered thinking, and poor social functioning. Research indicates that a variety of genetic, environmental, and neurological factors may play a role in the development of schizophrenia, even though its precise etiology is still unknown.

The probable involvement of environmental toxins, in particular heavy metals, in the development of schizophrenia has attracted increasing attention in recent years. These days, the environment is heavily contaminated with heavy metals like lead, cadmium, mercury, aluminum and arsenic. Toxic levels of all of these heavy metals can be found in the air, water, soil, and food, often in locations near industrial and trash disposal sites.

Chronic exposure to these heavy metals impairs numerous normal biological functions and results in a series of health problems1, such as aberrant immunological responses and neuropathological conditions2,3. Moreover, it has been reported that toxic heavy metals can cause oxidative stress and subsequently DNA damage, lipid peroxidation, and protein modification, all of which play a role in the pathogenesis of numerous diseases because of chronic inflammation, including cancer, diabetes, and neurological disorders4. Toxic heavy metals are an important risk factor for psychiatric diseases since they cause neurobehavioral alterations and disrupt dopamine receptors5.

Numerous studies have studied the link between exposure to heavy metals and the likelihood of developing schizophrenia6.

A 28-year-old male who arrived at my clinic in 2018 with symptoms of muttering, fearfulness and withdrawn behavior, with a medication history of many antipsychotics and benzodiazepines over many years with no relief in symptoms.

This longitudinal case study is of a medication-resistant schizophrenia patient who had a history of heavy metal exposure and got improved with nutritional interventions and is now asymptomatic for last 4 years. This case study seeks to further explore the potential connection between heavy metal toxicity, chronic inflammation and schizophrenia.

This case study makes a significant contribution to the field by highlighting the significance of taking environmental factors into account when managing and treating this crippling disease and by shedding light on the involvement of heavy metal toxins in the etiology and development of schizophrenia.

Timeline

2018-09-27
The patient was investigated for routine investigations along with blood and urine levels of heavy metal toxins. His serum aluminum level was 63.59 μg/mL. His HSCRP was 4.78 mg/l.
2018-09-28
We started antioxidants and phase 2 detoxification nutrients support: N-acetylcysteine 1200 mg, alpha-lipoic acid 300 mg, taurine 1000 mg, and phosphatidylcholine 1 g along with Vitamin C, magnesium, and Vit D3, and started a gluten-free diet. We observed mild improvement in clinical symptoms.
2018-10-22
He was complaining of low-grade fever and body aches. He was referred to a physician for workup. There was nothing significant from the physician's side. We started minocycline 50 mg in the morning and evening.
2018-10-23
His symptoms started improving. We increased the minocycline dose to 100 mg BD for 2 weeks along with probiotics. He had improvement in psychotic symptoms also.
2018-12-28
We started observing clinical improvement.
2019-04-03
His serum aluminum test was repeated. It was 24.16 ug/ml. There was clinical improvement His family started adding gluten to his diet. After starting gluten, his aggression has increased. So, family members stopped giving gluten. We presumed gluten intolerance and a hyperpermeable gut. He used to improve after a few weeks of stopping gluten.
2020-01-29
He was symptom-free. He was not taking any antipsychotics. He was on oxcarbamazepine 300 mg , pregablin 75 mg along with antioxidants.
2021-05-22
He was stable on oxcarbazepine 300 mg OD and antioxidants. His family is enjoying gluten in their diet on and off.
2024- 12-07
Not only asymptomatic, he is also planning to start a new business in Jaipur.

Discussion

This longitudinal case study of the patient leaves us concerned that people diagnosed with schizophrenia may be covert sufferers of undiagnosed environmental toxin exposure, inflammation, hyperpermeable gut, and oxidative stress.

The patient has been in follow-up with the treating doctor for the last six years, and both the patient and their family are satisfied with the progress made. The patient continues to follow an anti-inflammatory diet, take antioxidants, and regularly use a low-dose mood stabilizer, oxcabamazeipine 300 mg, with antioxidants such as vitamin C and n-acetylcysteine, and vitamin D and magnesium. These interventions have contributed to the patient's improvement. During this 6 year follow-up period there has been no relapse in schizophrenic symptoms.

Recent studies have suggested metabolic syndrome as a risk factor for schizophrenia, attributed to poor dietary habits, unhealthy lifestyles, and physical inactivity of the patient7 and side effects of second-generation antipsychotics8. On the other hand, heavy metal toxins such as As9 and Pb10 were found to be associated with metabolic diseases, suggesting a role of abnormal metabolism in linking toxic heavy metal exposure and schizophrenia.

The gluten intolerance hypothesis is based on mechanisms linking gluten intake, immune reactions and inflammation with the development of schizophrenia. In this model, it is proposed that within the subgroup of people with schizophrenia and related psychosis with inflammation, consumption of gluten can drive an immune response and is implicated in the pathophysiology of the illness. Elevated anti-gliadin antibodies (AGA) are more frequent in people with schizophrenia than in people without, and AGA has been positively associated with peripheral inflammatory markers11.

Family Perspective

We admitted our brother multiple times to a psychiatric hospital but did not get results with standard medications. We have always been keen to investigate any alternative therapies that could provide relief and enhance the quality of life for our brother as we watch him suffer from incapacitating symptoms.

Initially we were unaware of nutritional interventions for treatment of schizophrenia. The idea of adding particular foods and supplements to our loved one's diet felt strange to us because we had mainly relied on conventional medical treatments.

Patience, empathy, and a willingness to make big dietary modifications for our family were necessary to support our loved one during this journey. Together, we discovered the significance of including anti-inflammatory and antioxidant-rich foods in our diets, as well as the need to stay away from items that contain aluminum. This required alterations to our grocery shopping, meal preparation, and cooking techniques. Even if it wasn't always simple, seeing how these treatments might improve the mental health of our brother made it all worthwhile.

We eventually began to see improvements in our brother's health. The symptoms lessened in intensity and frequency, enabling him to participate more actively in their everyday lives and interpersonal interactions. His mood, cognitive capacity, and behavior all improved. These developments offered us reason for optimism and strengthened our faith in the effectiveness of dietary therapies as an additional strategy for treating schizophrenia.

In conclusion, we have seen firsthand as family members how nutritional therapies can significantly reduce inflammation brought on by aluminum in the treatment of schizophrenia. We urge other families to learn more about these therapies, educate themselves on the possible advantages, and work cooperatively with medical professionals to include them in the care of their loved ones.

Conclusion

Treatment of schizophrenia with medication is limited and often comes with severe side effects. This case report explores potential mechanisms and nutritional interventions for improving the condition. Nutritional interventions that aim to reduce oxidative stress and inflammation can be a safe and effective addition to treatment.

Author contact: Dr Aarti Midha, gawriaarti@yahoo.com

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