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Depression

Nutrition and Depression: Nutrition, Detoxification, and Depression, Part 4

Does liver detoxification influence your mood?

Nutrition, Detoxification, and Depression
An additional avenue through which nutrition can help mood disorders is via liver detoxification, which can influence mood via the modification of steroid hormone metabolism (e.g., DHEA, testosterone, estrogen, cortisol).

Detoxification occurs in two phases: In phase one the CYP 450 enzymes are supported by a variety of nutrients (B2, B3, B6, folic acid, B12,Glutathione, branched-chain amino acids, flavinoids, phospholipids). Once these CYP450 enzymes have acted on the lipid soluble molecule, (drug, hormones, toxins), by adding an oxygen, these activated intermediates, (if not further detoxified via phase two, due to nutritional deficiency) can increase oxidative stress, and via mitochondrial damage, reduce neuronal function. Phase two conjugation pathways require glutathione, glycine, taurine, glutamine, ornithine, arginine, N-acetylcysteine, cysteine, methionine, selenium. If phase two conjugation is functioning well, the substances are rendered water soluble and can pass out of the body via the kidney, or bile (where in the presence of dysbioisis they may be re-absorbed if cleaved in the intestine [soluble fiber helps to counter this]).

Failure to detoxify steroid hormones, such as estradiol, can alter the synaptic availability of neurotransmitters, thereby affecting mood disorders. Failure to detoxify endocrine disrupting chemicals (e.g., PCB's, BPA) will adversely affect mood disorders by altering normal endocrine function, which is necessary for normal brain function.

Nutritional Balance and Depression
Finally, we must look at the macronutrient aspect of the diet. Meals must be balanced in protein (1/3 of the meal volume) and complex carbohydrates (2/3 of the meal volume). This will keep blood sugar steady, eliminating the significant dysglycemic contribution to intra-day mood swings, irritability, and anxiety. Along these lines, it is important that the clinician manage insulin resistance and diabetes via diet, exercise, and supportive nutrients such as R-Lipoic Acid, chromium, vanadium. Van Praag (14) demonstrated that "50% of depressed patients had lower glucose utilization during a glucose tolerance test than did control subjects." Furthermore, Cassidy (15) demonstrated that manic-depressive patients with diabetes mellitus (n=357) have a more severe course of illness, as indicated by a greater number of psychiatric hospitalizations (p=<0.05).

Summary
Based on this quick overview, it should be clear that adequate and individualized nutritional assessment and intervention is a cornerstone of appropriate treatment of mood disorders. Failure to utilize this basic information accounts for a significant component of treatment resistant depression, medication failure, and polypharmacy.

References:

1)Rush, AJ. STAR-D: What have we learned? Am J Psychiatry. 2007;164-201
2) Pigott, et al. Efficacy and Effectiveness of Antidepressants: Current Status:Psychother Psychosom. 2010;79(5):267-79.
3)Bourre, JM: J. Nutrition, Health & Aging: Vol 10(5) 2006: 377-385. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain: Part 1: micronutrients.
4)Miller HL :et al.: Clinical and biochemical effects of catecholamine depletion on antidepressant-induced remission of depression. Arch Gen Psychiatry. Vol.53( 2):117-128.
5)Spillmann MK. Et.al.; Tryptophan depletion in SSRI recovered depressed outpatients. Psychopharmacology (Berl)2001, May;155 (2):123-127
6)Maes M.,et al.:Hypozincemia in depression. J Affective Disorders; 31(2):13Maes M.: "Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness" Biol Psychiatry: 42(5):349-358 (1997).
5-140 (1994)
7)Maes M.Et.al.: Lower serum zinc in major depression in relation to changes in serum acute phase proteins. J. Affect Disord 1999:56(2-3):189-194
8)Methylenetetrahydrofolate Reductase (MTHFR) Genetic Polymorphisms (C677T variant) and Psychiatric Disorders: A HuGE Review: Am J Epidemiol 2007;165:1-13
9)Coppen A, et al.: Enhancement of antidepressant action of fluoxetine by folic acid: a randomized, placebo controlled trial. J Affect Disord: 2000:60(Nov.):121-130
10)Rutten: Epigenetic Mediation of Environmental influences in Major Psychotic Disorders Schizophrenia Bulletin; 2009: Vol 35 (6):1045-1056
11)McGowan: the epigenetics of social adversity in early life: Implications for mental health outcomes. Neurobiology of Disease (2010): In Press
12)Hedelin, M. Dietary Intake of Fish, Omega 3's, Omega 6 PUFA's and Vitamin D and the pPrevalence of Psychotic Symptoms in a Cohort of 33,000 Women from the General Population. BMC Psychiatry 2010 (10): 38; 1-13
13)Wilkins CH., et al.: Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatric Psychiatry, 2006 Dec;14(12):1032-40
14)Van Praag: Depression, glucose tolerance, peripheral glucose uptake and their alterations under the influence of anti-depressive drugs of the hydrazine type. Psychopharmacologia (Berlin) 1965;8:67-78.)
15)Cassidy, F. et.al.: Elevated Frequency of Diabetes Mellitus in Hospitalized Manic-Depressive Patients. Am J Psychiatry 1999;156 1417-1420.
16)Weiss JH., et.al.: Zn(+2): a novel ionic mediator of neural injury in brain disease. Trends Pharmacol Sci 2001: 21(12):112-3
17)Lindenbaum J. et.al.: Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytois. N Engl J Med 1988;318:1720-1728.
18)Vogiatzoglou, A. Determinants of Methylmalonic Acid in a Large Population: Implications for Assessment of Vitamin B12 Status. Clinical Chemistry (55)12: 2198-2206 (2009)

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