Posted by Larry Hoover on April 2, 2003, at 12:21:29
In reply to Ok- now who takes vitamins/what kind(s)/how many?, posted by Janelle on April 1, 2003, at 21:58:06
> I got some good and helpful answers about how many MEDS some people out there are on; and I'm in the middle range - some take less, others take more, so I feel *reassured*!!
>
> However, several people mentioned taking supplements like vitamins and minerals - gosh, I don't take that - well, just a multivitamin - I used to take more supplements. Think I'll ask pdoc next time, although he probably won't have a clue about that kind of stuff.I was really hoping somebody else would jump in here.....I could go on and on and on....
Most Western doctors are taught a philosophy which places vitamins in a peculiar role in nutrition, i.e. they are useful solely to avoid deficiency diseases. There is no perception that intake above the preventative dose may have some optimization of effects, quite apart from the absence of the particular deficiency syndrome.
If you have a few minutes, you may want to read an essay which discusses the different paradigms of vitamin supplementation:
http://www.internetwks.com/pauling/hoffer.html
One recent study, which ought to have received far greater publicity than it did, found a massive correlation between sugar consumption and the incidence of major depression. We know that correlation does not imply causation, but the obvious implication is that diet can have a major impact on mood. It may not be sugar that is the culprit, as dietary sugar can also be a measure of food processing taken as a whole. Why doesn't this issue get media attention, rather than e.g. comparisons of side-effect profiles of psychotropic drugs?
Depress Anxiety 2002;16(3):118-20
A cross-national relationship between sugar consumption and major depression?
Westover AN, Marangell LB.
Mood Disorders Center (MDOC), Department of Psychiatry, Baylor College of Medicine, Houston, Texas, USA. anwestover@yahoo.com
We have preliminarily investigated the hypothesis that sugar consumption may impact the prevalence of major depression by correlating per capita consumption of sugar with the prevalence of major depression. Major depression prevalence data (annual rate/100) was obtained from the Cross-National Epidemiology of Major Depression and Bipolar Disorder study [Weissman et al., 1996]. Sugar consumption data from 1991 was obtained from the Food and Agricultural Organization of the United Nations. For the primary analysis, sugar consumption rates (cal/cap/day) were correlated with the annual rate of major depression, using the Pearson correlation coefficient. For the six countries with available data for the primary analysis, there was a highly significant correlation between sugar consumption and the annual rate of depression (Pearson correlation 0.948, P=0.004). Naturally, a correlation does not necessarily imply etiology. Caveats such as the limited number of countries with available data must be considered. Although speculative, there are some mechanistic reasons to consider that sugar consumption may directly impact the prevalence of major depression. Possible relationships between sugar consumption, beta-endorphins, and oxidative stress are discussed. Copyright 2002 Wiley-Liss, Inc.
Now, you may have caught the closing statement, which implicates oxidative stress. What is oxidative stress? Broadly, it is a destructive process which degrades the structural and functional integrity of all cells in the body. Many alternative therapies for depression (e.g. SAMe, inositol, fish oil, B-vitamins, minerals such as magnesium, zinc, and selenium) directly address the physiological consequences of oxidative stress. Honestly, I think that ought to be the central theme of any supplement strategy with respect to mood disorders.
You suggested that your pdoc may neither be aware of, nor supportive of, nutritional strategies. I assure you that the information has been available in mainstream journals for some time. Here are a few abstracts which deal with one B-vitamin, folate, and its interaction with another, B-12, in the context of oxidative stress (blood homocysteine is a marker), and neurological dysfunction:
Nutr Rev 1996 Dec;54(12):382-90
Folate, vitamin B12, and neuropsychiatric disorders.
Bottiglieri T.
Kimberly H. Courtwright and Joseph W. Summers Institute of Metabolic Disease, Baylor University Medical Center, Dallas, Texas, USA.
Folate and vitamin B12 are required both in the methylation of homocysteine to methionine and in the synthesis of S-adenosylmethionine. S-adenosylmethionine is involved in numerous methylation reactions involving proteins, phospholipids, DNA, and neurotransmitter metabolism. Both folate and vitamin B12 deficiency may cause similar neurologic and psychiatric disturbances including depression, dementia, and a demyelinating myelopathy. A current theory proposes that a defect in methylation processes is central to the biochemical basis of the neuropsychiatry of these vitamin deficiencies. Folate deficiency may specifically affect central monoamine metabolism and aggravate depressive disorders. In addition, the neurotoxic effects of homocysteine may also play a role in the neurologic and psychiatric disturbances that are associated with folate and vitamin B12 deficiency.
Am J Psychiatry 1997 Mar;154(3):426-8
Folate, vitamin B12, and homocysteine in major depressive disorder.Fava M, Borus JS, Alpert JE, Nierenberg AA, Rosenbaum JF, Bottiglieri T.
Depression Clinical and Research Program, Clinical Psychopharmacology Unit, Massachusetts General Hospital, Boston 02114, USA. favam@A1.mgh.harvard.edu
OBJECTIVE: The authors examined the relationships between levels of three metabolites (folate, vitamin B12, and homocysteine) and both depressive subtype and response to fluoxetine treatment in depressed patients. METHOD: Fluoxetine, 20 mg/day for 8 weeks, was given to 213 outpatients with major depressive disorder. At baseline, depressive subtypes were assessed, and a blood sample was collected from each patient. Serum metabolite levels were assayed. Response to treatment was determined by percentage change in score on the 17-item Hamilton Depression Rating Scale. RESULTS: Subjects with low folate levels were more likely to have melancholic depression and were significantly less likely to respond to fluoxetine. Homocysteine and B12 levels were not associated with depressive subtype or treatment response. CONCLUSIONS: Overall, the results are consistent with findings linking low folate levels to poorer response to antidepressant treatment. Folate levels might be considered in the evaluation of depressed patients who do not respond to antidepressant treatment.
Acta Neurol Scand Suppl 1994;154:27-31
Effects of the disruption of transmethylation in the central nervous system: an animal model.
Scott JM, Molloy AM, Kennedy DG, Kennedy S, Weir DG.
Department of Biochemistry, Trinity College, Dublin, Ireland.
INTRODUCTION--Central nervous system (CNS) methyltransferases methylate a wide range of substrates including proteins, lipids, nucleic acids and hormones. In every instance the methyl donor is S-adenosylmethionine (SAMe) and the demethylated product is S-adenosylhomocysteine (SAH). Methylation can be disrupted when there is an inadequate supply of methionine synthase (following vitamin B12 deficiency or folate deficiency), SAMe synthetase (due to ethanol), or SAH hydrolase (for unknown reasons). MATERIAL AND METHODS--5-week-old pigs were maintained in an environment of either air or nitrous oxide, which inhibits methionine synthase, and were fed either a methionine-unsupplemented or methionine-enriched diet. After 3 to 10 weeks, pigs were killed by pentobarbitone injection and the levels of methionine and SAMe in the pigs' brain, spinal cord, plasma, liver, and kidney assessed. RESULTS--Pigs maintained in nitrous oxide displayed a dramatic fall in methionine levels in plasma and brain tissues but maintained relatively normal SAMe levels in these tissues. Brain and spinal cord cystathionine levels were markedly elevated, especially in those animals receiving oral methionine, as in the absence of methionine synthase homocysteine can be metabolized only through the catabolic pathway to cystathionine and cysteine. CONCLUSION--Disorders such as vitamin B12 deficiency or folate deficiency inhibit methylation by limiting the availability of SAMe or by elevating levels of the inhibitor SAH. In either case, the disruption of a wide range of methylation reactions can cause clinical sequelae ranging from structural abnormalities such as myelopathy to functional abnormalities such as depression.
And here's one on the testable deficiency in B-12:
Blood 1990 Sep 1;76(5):871-81
Comment in:
Blood. 1991 Apr 15;77(8):1853-4.
Blood. 1991 Jan 1;77(1):206-7.Clinical spectrum and diagnosis of cobalamin deficiency.
Stabler SP, Allen RH, Savage DG, Lindenbaum J.
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262.
To better estimate how frequently patients with low serum cobalamin (Cbl) levels in current clinical practice are truly deficient in Cbl and to determine the incidence of atypical or nonclassic presentations of Cbl deficiency, we prospectively studied 300 unselected consecutive patients with serum Cbl concentrations less than 200 pg/mL seen at two medical centers over a 2-year period. Baseline hematologic, neuropsychiatric, and biochemical measurements were obtained, followed by a course of parenteral Cbl therapy and reassessment. A response to Cbl therapy was defined as one or more of the following: (1) an increase in hematocrit of 0.05 or more; (2) a decrease in mean cell volume of 5 fL or more; (3) a clearing of hypersegmented neutrophilis and macroovalocytes from the peripheral blood smear; and (4) an unequivocal and prompt improvement of neuropsychiatric abnormalities. Of the 300 patients with serum Cbl levels less than 200 pg/mL, 86 had one or more responses to Cbl therapy and 59 had no response. In 155, insufficient data was available. In the Cbl-responsive patients, normal values were found for the following tests: hematocrit, 44%; mean cell volume less than or equal to 100 fL, 36%; white blood cell count, 84%; platelet count, 79%; serum lactic dehydrogenase, 43%; and serum bilirubin, 83%. Peripheral blood smears were nondiagnostic in 6% when reviewed by the investigators, but 33% as reported by routine laboratories. Serum Cbl levels in the 100 to 199 pg/mL range were present in 38%. Neuropsychiatric abnormalities were noted in 28%, often in the absence of anemia, macrocytosis, or both. Serum levels of methylmalonic acid and/or total homocysteine were elevated greater than 3 SDs above the mean for normal subjects in 94% of the Cbl-responsive patients. We conclude that Cbl deficiency should be considered and investigated in patients with unexplained hematologic or neuropsychiatric abnormalities of the kind seen in Cbl deficiency, even if anemia, an elevated mean cell volume, a marked depression of the serum Cbl, or other classic hematologic or biochemical abnormalities are lacking. Levels of serum methylmalonic acid and total homocysteine are useful as ancillary diagnostic tests in the diagnostis of Cbl deficiency.
For this first-level reply to your question, I just wanted to lay the foundation for any detailed answer. The physiological need for nutrients is very likely enhanced in the case of psychiatric disorders, may be made worse by psychotropic medication, and is confounded by a general decline in the nutrient quality of our food supply (and downwards adjustments in the RDI (Reference Daily Intake) of many nutrients, corresponding to the decline in their availability). Add to that the pervasive attitude that most people obtain adequate nutrition from a typical diet (wrong!), and you've got a recipe for treatment-resistance.How much detail do you want?
Lar
poster:Larry Hoover
thread:215282
URL: http://www.dr-bob.org/babble/20030402/msgs/215420.html