Advanced Nutrition and Food Therapy - Advanced Nutrition for Bipolar Disorder

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taken not to promote a manic episode and research has cautioned against use of some antidepressants because of this purpose. Elevated levels of cytokines are known to be associated with both depression and mania.(Wadee, et al, 2002)

Treatment

Lithium is the specific psychotropic drug used as treatment for BPD, as it decreases manic episodes and helps control behaviour (Bryant & Knights, 2007). Cabamazeping, Lamotrigine and Valporate are also commonly prescribed. Anti-anxiety drugs (benzodiazepines) and antixeizure drugs may be used. Antidepressants are sometimes used in conjunction to other drugs to treat the depression. (MedlinePlus)

Morbidity

BPD can affect the patient’s ability to function in society, affecting personal relationships, work and finances. Alcohol and/or drug abuse is common amongst sufferers. Suicide is a very possible threat. (MedlinePlus). There is also co-morbidity with cardiovascular diseases and diabetes. (Kato & Kato, 2000)

Nutrients and Food Review

CoenzymeQ10

Recent research supports the theory of mitochondrial dysfunction in BPD, (Kato & Kato, 2000, Jou et al, 2009, Konradi et al, 2004, Fattal et al. 2006). Many factors support this theory including, co-morbidity of BPD with mitochondrial diseases such as cardiovascular disease and diabetes (Kato & Kato, 2000). CoQ10 has been found to offer some protection in these states (Braun, 2007, Schultz Johansen et al, 2005), and it has been proposed as a useful supplement in the treatment of BPD.

The evidence include: impaired energy metabolism in the brain detected using results of magnetic resonance spectroscopy, electron microscopy, co-morbidity with mitochondrial diseases, the effects of psychotropics on mitochondria, increased mitochondrial DNA (mtDNA) deletion in the brain, and association with mtDNA mutations/polymorphisms or nuclear-encoded mitochondrial genes. (Fattal, O, 2006).

A large study of gene arrays, found abnormalities in gene expression coding for mitochondrial proteins in BDP compared with normal samples, which would lead to decreased adenosine triphosphate (ATP) production. (Konradi, et al, 2004). In a review of evidence, Kato and Kato (2000), found studies showing BPD patients had low phosphocreatine and ATP.

Coenzyme q10 is concentrated on the inner membrane of the mitochondrion and is crucial in energy production. It is an essential co-factor, by accepting electrons in the electron transport chain which produces andenosine triphosphate (ATP) (Braune, 2007). Therefore, supplementation with coq10 to increase ATP is warranted in BPD patients who are depressed, it may help regulate ATP levels and prevent feedback mechanisms which may cause increase in ATP.

Clinical trials for the treatment of BPD with coenzyme q10 were being recruited for but have recently been withdrawn, with previous clinical evidence being limited to case studies. Shinkai et al. (2000), reported 30mg/day (increased to 70mg/day) of coenzyme q10 taken by a 48 year old woman experiencing psychiatric symptoms, showed an improvement after 3 months.

Coq10 is also an anti-oxidant and neuroprotective (Braun, 2007). Animal studies have found coq10 to have a neuroprotective action and have implicated its use for treating Parkinsons Disease, (Cleren et al. 2008). The powerful anti-oxidant action of Coq10 in the neuronal cells has also been observed in a study by Somayajulu et al. (2005), which found CoQ10 inhibited oxidative stress, reactive oxidative species and cell membrane collapse, in tissue samples.

Choline

Choline has been used as an adjunct to lithium treatment (Stoll et al. 1996). The theory of mitochondrial dysfunction in BPD, includes the fluctuations in ATP levels in neurons. In manic episodes, ATP has been found to be increased while in depression it’s reduced (Kato & Kato, 2000). Choline is theorised to be useful as is shown to increase brain phosphatidlycholine, an integral cell membrane phospholipid, which consumes 10-15% ATP in its production. If Choline can help balance the ATP/high energy phosphate levels in the cell, it is theorised to reduced the feedback mechanism which may be present in causing rapid-cycling bipolar, in which the patients episodes fluctuate.

In a small double blind trial done on 8 rapid-cycling bipolar patients, 4 received 50mg/kg/day of choline bitratrate in a tablet, while 4 took placebo, over 12 weeks. The study didn’t observe symptoms of the disorder, rather it measured brain purine levels which showed a decrease with choline administration, showing that choline administration may lead to consumption of ATP. This study helps explain the anti-manic effect of choline as an adjunct treatment as found in 6 case studies by Stoll et al. (1996). Stoll et al. (1996) administered from 2-4 g/day to 3-8 g/day to six rapid-cycling bipolar patients, each case self assessed their manic and depression rates and 5 of 6 were found to have clinically significant antimanic responses to choline. The effect on depressive states was variable and further studies are needed to determine if the anti-manic effect of choline also promotes depression.

Inositol

Deranieh and Greenberg (2009), present a summary of the biochemical pathways involving inositol, which provoke question to the theory that inositol depletion is the mechanism of action for effective BPD medications, and suggest rather, that there are negative cellular consequences of inositol depletion. Inositol has been found to be important in intracellular signalling molecules which affect phospholipid synthesis, the unfolded protein response and protein secretion). Phosphoinositides and inositol phosphates may be altered by inositol depletion, and this dysfunction has been implicated in disorders including neurodegeneration disorders. (Deranieh & Greenberg, 2009).

Considering the importance of beneficial inositol functions in the neuron, the clinical support