Understanding the Biochemical and Biobehavioral Nexus of Depression

©Copyright 1997 by Patricia Kane, Ph.D., Millville, New Jersey, USA.
(Explore Issue: Volume 8, Number 1)

From within the depths of despair countless Americans are seeking help from their physicians only to be handed a prescription, an order for a drug that will make the pain go away either by Prozac or Zoloft, Elavil or Asendin, Norpramin or Adapin, Luvox or Tofranil, Serzone or Marplan, Ludiomil or Aventyl, Paxil or Nardil, Lithium or Vivactil, Parnate or Desyrel, Surmontil or Effexor or any other number of antidepressants, inhibitors of serotonin reuptake or monoamine oxidase. The unrestrained administration of medications such as Prozac for depression has become epidemic in this country and is an accepted practice in the most sophisticated circles of society to individuals of the simplest means. A retired gentleman who has recently lost his wife, a young woman whose menstrual cycles are irregular and a three year old child with autism are all hastily prescribed Prozac by their primary care physician, their gynecologist and their pediatrician. Most often, no laboratory tests are performed, no examination is made, no discussion is commenced. Our gross lack of awareness in regard to neurochemistry is shocking. Victims of depression often cannot resist such archaic approaches to their debilitating disorder and certainly after dutifully swallowing the prescribed antidepressant they never will. It is the perfect solution to silencing the patient.

Unbeknownst to the silent victim an imbalance in their blood chemistry and lipid metabolism impacted by the choices they make every day in regard to the food they consume or do not consume may hold the answers to their state of depression. Although it is well established that very high levels of cholesterol and certain lipoproteins are strongly associated with cardiovascular disease, it is equally well established that hypocholesterolemia is also a predictor of acute and chronic medical illness as well as mortality, however, this is not amplified to the public. Instead we are bombarded with advertising denouncing the use of fat and referring to cholesterol as "coronary glue, blood mud and blood sludge" which in turn makes us fearful of consuming fat. The fact is that hypocholesterolemia has been associated with depression, suicide and affective disorders. The connection between affective disorders and hypocholesterolemia may be associated most closely with alteration of cytokine mediators of inflammation produced by the brain which in turn, create changes in mood and behavior. As medicine flounders in controlling the right neurotransmitter or even the immune-endocrine-central nervous system link to affective disorders they have forgotten the very basis of control of these systems-the lipid metabolism. Rapidly accumulating evidence suggests that low or lowered cholesterol may be associated with increased non-illness related mortality (suicide, accidents) mediated by lipid-induced changes in brain chemistry by which impacting the lipid environment of the brain profoundly modulates neurotransmitter action and function of neuronal proteins. The tertiary and quaternary structures of neuronal proteins as receptors, ion channels and protein kinase depend upon the electrical and fluidity parameters determined by electrolytes and the lipid environment of the brain. Lipid and electrolyte abnormalities have a marked impact on neuronal disturbance and ultimately, mood and behavior.

RBC Fatty Acids and Plasmalogens CPT 82491 Submit Specimen in Lavender EDTA Tube Refrigerate tube, do not freeze, Freeze ice pak only, Ship overnight Linoleic acid, Gamma Linolenic, Eicosadienoic, Dihomogammalinolenic, Arachidonic Docosadienoic, Docosapentaenoic w6, Vaccenic, Alpha Linolenic, Eicosapentaenoic Docosapentaenoic, Docosahexaenoic, Myristoleic, Palmitoleic Oleic, 11-Eicosenoic Nervonic, Erucic, Capric, Lauric, Palmitelaidic, Elaidic, Myristic, Palmitic, Stearic Arachidic, Linolelaidic, Behenic, Lignoceric, Hexacosanoic, Pentadecanoic Heneicosanoic, Heptadecanoic, Nonadecanoic, Tricosanoic, Heptacosanoic Docosapentaenoic w3, Phytanic, Linolelaidic and dimethyl acetyls from plasmalogens 16DMA, 18:1DMA and 18DMA

The construct of a hypertryglyceridemia-driven metabolic cause of depression has also been demonstrated in controlled clinical trials by Glueck that triglyceride lowering alleviates the symptoms of depression. The connection of hypertriglyceridemia and depression involves insulin resistance as the ingestion of carbohydrate releases insulin which immobilizes the enzyme delta 6 desaturase negatively impacting the production of prostaglandins, cytokines, hormones, membrane traffic, brain chemistry

The biochemistry of depression is often characteristic in the blood chemistry as deep suppression of Cholesterol, Iron, Potassium, Albumin and Nitrogen markers as Blood Urea Nitrogen (BUN), Creatinine, Uric Acid and elevation of Triglycerides. Clinicians often fail to alleviate their patient's symptoms of depression if the basic needs for raw materials (micro and macro nutrients) are not met. Cholesterol is the substrate by which the cascade of all hormones are derived from and to add in DHEA, for example, without consideration of the fatty acid metabolism and coenzyme involvement as nitrogen retention, visceral proteins, potassium, iron, targeted lipids and overall mineral density there is a high risk of poor outcome by approaching this patient in such an allopathic fashion.

Boldly approaching disturbances in the neurochemistry of the brain is a new frontier in biological medicine as research and detailed management of laboratory data have isolated specific characteristic aberrations in comprehensive blood analysis. Blood chemistry has long been used as an overall general investigation into the systems of the body yet often critical markers and patterns are overlooked due to a lack of organized data available to the clinician. Clearly, there exists poor communication between the researcher, the laboratory chemist and the practitioner thus medical data often is not expeditiously introduced into clinical practice. Unique patterns related to individual patient need do appear in general blood chemistries in regard to disease processes, drug interactions and specific metabolic interactions and have been noted by clinical chemists for a decade. The medical literature is abound with data supporting the use of nutritional pharmacology but the difficulty has been the retrieval of that data. The use of medline is often frustrating to the researcher of biological medicine due to the awkward entry of keywords in the system itself. Case in point is the effect of ascorbic acid on the enzyme delta 6 desaturase (critical in prostaglandin metabolism). Entering "delta 6 desaturase and nutrients" as key words will not pull up ascorbic acid out of the medline, rather one must accidentally stumble upon it by entering glucagon and fatty acids as keywords into medline. The use of trans fats used in medical protocols grossly delayed the profound data on fatty acid metabolism that has finally started to emerge as individual fatty acids are isolated and researched.

Fatty Acid Report

Disturbances in fatty acid metabolism are now rapidly being linked to a myriad of mental and physical disorders. Examination of red cell membrane fatty acids profiling is reflective of long term insufficiencies and imbalances in fatty acid metabolism. Plasma fatty acids reflect dietary intake of a few days duration rather than metabolic conversion observed in fatty acids incorporated into red cell membranes. Exploration of fatty acid metabolism leads the clinician into a wide realm of metabolic strategies to influence the health of the patient. Lipids evolve into hormones, the bilipid layer of every cell in the body, prostaglandins, cytokines, immune components, and myelin. There is virtually no system of the body that does not require attenuation of specific fatty acid substrates and coenzymes to maintain health and repair of bodily tissues. Finite testing and analysis of blood chemistry and red cell membrane fatty acids is now available through BodyBio medical data management analysis. Examination of patients with affective disorders, depression, schizophrenia, anxiety, autism, seizure disorders, aggression, attention deficit disorder as well as physically oriented acute and chronic illness reveal characteristic patterns that may be addressed with lipid manipulation with targeted fatty acids through competitive inhibition but of equal critical importance is the stabilization of the electrolytes, nitrogen retention, dietary manipulation (removal of all trans fats and sharp increase in nutrient density) and coenzyme supplementation (K, Na, Cl, Ca, Mn, Zn, Cr, riboflavin, ascorbate, biotin, cobalamin, folate, alpha tocopherol, pyridoxine, thiamine, niacin, pantothenic acid). Attention must be focused on the modulation of the disturbed metabolism. Brain function depends on the organic metal constituents of the central nervous system as well as lipids but the convergence of these systems occurs in the case of depression of cholesterol, for example, as manganese must be administered to create the synthesis of cholesterol. Much may be gleaned from critical care medicine as acute and chronically ill patients often become severely depressed and lose their will to live when serum potassium levels drop to below the low end of the laboratory reference range. Macronutrients such as consumption of high quality proteins and the supplementation of creatine, ammonium chloride, urea, glutamine, and niacin as indicated in the patient's blood chemistry will attenuate nitrogen retention. Often the simplest understanding of basic chemistry leads us to understand intricate connections: the inhalation of nitrous oxide (laughing gas) may evoke the emotion of pleasure while exposure to high altitudes, atmospheric low pressure or a full moon where a downward nitrogen shift is created may evoke feelings of depression or exacerbate mood disorders. Nitrogen retention is dependent upon dietary consumption of nitrogen rich foods along with lipid consumption, electrolyte stability and mineral density and balance. Individuals with affective disorders have unique patterns in their blood chemistry that must be attenuated to their specific need. Unexpected patterns in red cell membrane fatty acids are often revealed as in depression of Arachadonic acid (found in butter) and Docosahexaenoic acid (found in marine oil) in schizophrenia as observed by Horrobin and derangement in very long chain fatty acids as primarily peroxisomal rather than mitochondrial disturbances as in elevation of the very long chain fatty acids Docosahexaenoic, Docosapentaenoic w3, Behenic, Lignoceric, and Nervonic as observed by Kane.

It is prudent to define the exact aberrations in individual patients through laboratory data rather than administer medication or a handful of "just try this". The exploration of the characteristic features of aberrant fatty acid metabolism and alteration of the blood chemistries of adults and children with neuropsychological disorders is a bold frontier that is merging traditional science with biological medicine -- Brave New Medicine.

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About the Author

Patricia Kane, PhD. Is a clinician in private practice specializing in traumatic brain injury, intractable seizure disorders, autistic spectrum disorders, pervasive developmental delay, and preterm neonatal care. Her approach to complex medical situations is unique in that she blends the sciences of chemistry and physics to resolve deep biochemical aberrations that are often labeled hopeless by standard medical care. Kane has a unique background of fifteen years of clinical research, practicums with individual leaders in metabolic intervention, and private practice in the field of nutritional biochemistry. She has served as the past Chief of Nutrition at the Carl C. Markwood Preventive Medicine and Clinical Allergy Center in Sacramento, CA, and presently serves as Director of Nutritional Biochemistry at the Kaplan Foundation in Orangevale, CA (since 1983), Director of Medical Research for the Carbon Based Corporation, in Incline Village, NV, and Director of The Body Bio Centre in Millville, NJ.

Kane is the author of Food Makes the Difference (Simon and Schuster, 1985) Mommy, I'm Hungry (Cougar Books, 1982), The Neurochemistry and Neurophysics of Autism (1996) and numerous articles on nutritional biochemistry published in Explore!, Explore More!, Alternative Medicine Digest and The Townsend Letter for Doctors. Kane focuses a great deal of her efforts towards clinical instruction of medical research in the application of metabolic pharmacology. She believes that boldly addressing metabolic irregularities can help to resolve complex medical problems and unique biochemical needs. Dr. Kane has heavily researched the literature on blood chemistry/metabolics and was part of a research team who developed an advanced computerized report, the Carbon Based Blood Chemistry analysis that is now available to the medical profession. This report has been the basis of her medical protocol for the metabolic mapping of profound neurochemical disturbances. Her innovative work has opened the doors of San Diego Children's Hospital, Kennedy Krieger Institute and John Hopkins Medical Hospital to nutritional pharmacology.

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