Nutrition in Bipolar Disorder (BD)
In recent years it has been increasingly indicated that diet/nutrition is important in the pathogenesis, course and effectiveness of treatment of various mental health disorders. It is therefore important to assess possible nutrient deficiencies as well as dietary habits in BD patients. This will most likely result in considering supplementation or dietary modifications (with obvious known benefits to mental health). Apart from nutrient deficiencies, making dietary changse can improve the effectiveness of BD treatment by increasing the sense of control and coping.
Diet (its composition and quality) may also cause/sustain biological disorders associated with the onset, development, and treatment of BD. These include:
- monoaminergic transmission
- inflammatory processes
- oxidative stress and mitochondrial dysfunction.
This assumes the importance of serotonergic, noradrenergic, and dopaminergic transmission disorders in the pathogenesis of affective disorders. Animal studies have shown that high-fat diets may directly affect monoaminoergic transmission. In humans, high-fat diets with high carbohydrate snacks reduced serotonergic transmission in the hypothalamus.
In recent years, attention has been paid to the importance of inflammatory processes in the pathogenesis of BD. Mediterranean diet and increased intake of fruits and vegetables are associated with decreased inflammation, whereas diets dominated by Western dietary patterns are considered “pro-inflammatory” diets associated with an increased concentration of inflammatory markers such as interleukin-6 and C-reactive protein (CRP). CRP should always be measured in BD patients.
Oxidative stress and mitochondrial dysfunction
Oxidative stress and mitochondrial dysfunction are also associated with BD pathogenesis. The brain is an organ whose function and structure is largely dependent on the energy supplied, and damage to the mitochondria (responsible for the neuron’s energy production) may lead to increased oxidative stress, further damaging mitochondria. Studies show that diets may significantly influence mitochondrial function by reducing oxidative stress and protecting mitochondrial DNA from oxidative damage. Mediterranean diet and increased fish intake are associated with decreased levels of oxidative stress markers in serum and urine. Animal studies indicate that a ketogenic diet can protect mitochondria from exposure to oxidative stress.
The mechanism of some Nutraceuticals
Polyunsaturated omega 3 (PUFA omega 3) (EPA, DHA) fatty acids are essential for brain development and function, including neuronal maturation, migration and synaptogenesis, plasticity, neurogenesis, and neurotransmission. It is thought that a dose of greater than 1,000mg per day of EPA and DHA is necessary for BP.
One of the major endogenous antioxidant compounds in the brain is glutathione. Oral supplementation of glutathione alone is not effective (it is mostly hydrolyzed and weakly penetrates the blood-brain barrier), but it has been found that N-acetylcysteine (NAC) should be given. NAC provides l-cysteine essential for the synthesis of glutathione, but it also exhibits antioxidant activity itself. In clinical trials, patients with BD have been given either 500 or 1000 mg of NAC twice daily for standard treatment for acute depressive episodes and during the maintenance therapy period, with a reported reduction in symptoms of depression and improved functioning and quality of life
Systematic reviews with meta-analysis have confirmed the association of low vitamin D levels with depression and have demonstrated the efficacy of vitamin D supplementation in reducing the symptoms of depression in patients with clinically more severe depression. Vitamin D supplementation largely relies on blood test results and may be around 2,000-5,000iu per day.
It is believed that folic acid and other folates can be important in the treatment of depression, which is explained by, among others, their contribution to the synthesis of neurotransmitters and the effect on DNA methylation. Many studies have reported that people with depression have lower plasma and erythrocyte folate concentrations compared to healthy individuals and patients with other mental disorders. Lower folate levels have been associated with a worse response to pharmacological antidepressant therapy (non responsive). It should be remembered that the effectiveness or ineffectiveness of folic acid can be attributed to the chemical form of this vitamin – since folic acid, unlike natural folate, must be converted into a metabolically active form to cross the blood-brain barrier and approximately 30% of the population has a genetically determined deficit of the enzyme necessary for this transformation. Variants in this gene (MTHFR) can be identified through simple genetic testing. It is safer to supplement with methylfolate (5MTHF) than folic acid.