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The Failures of American Medicine: Why Americans Have Become Chronically Ill, and What Can Be Done About It
by Richard Jensen
219 pages; quality trade paperback (softcover); catalogue #02-0206; ISBN 1-55369-393-0; US$19.95, C$29.95, EUR19.50, £13.50
The Failures of American Medicine: Why Americans Have Become Chronically Ill, and What Can Be Done About It describes the failures of both conventional and alternative medicine, while also suggesting which treatments from both medical fields can be trusted
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about the book - from the author about the author excerpts catalogue info
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About the Book - From the Author
During my transition from adolescent to adult, I developed blood sugar swings, eye problems, asthma, and anxiety. Shockingly, when I went to various doctors for treatment of these problems, the usual response was "I can't help you". Fed up with both conventional and alternative medicine, I decided to do my own research on medical subjects that affect me and tens of millions of other Americans. The result is a unique and highly informative book that will help many American patients and physicians to properly deal with chronic illness.
-Richard Jensen
About the Author
Richard Jensen was born in Utah to two Liberal-Arts majors who never expected their son to become a biologist. He moved to California in 1985, received a B.S. and M.S. in Biology from San Diego State University and has done research in diverse fields such as gene transcription, cancer, and HIV. He is currently working with scientists to help produce an HIV vaccine.
Excerpts
Table of Contents
FOREWORD
INTRODUCTION: WHY AMERICAN MEDICINE HAS FAILED SO MANYPART I: THE BATTLE OVER NUTRITIONAL SUPPLEMENTS
CHAPTER ONE:
THE THEORY BEHIND SUPPLEMENTATION
CHAPTER TWO:
THE MINIMAL SUPPLEMENTATION LIST
CHAPTER THREE:
PHARMACEUTICAL AND NATURAL DRUGS
PART II: CHRONIC PHYSICAL ILLNESSES
CHAPTER FOUR:
WHY AMERICANS HAVE CHRONIC DIET-RELATED DISEASES CHAPTER FIVE:
CANCER CHAPTER SIX:
ALLERGIES AND ASTHMA
PART III: CHRONIC MENTAL ILLNESSES
CHAPTER SEVEN:
ANXIETY AND DEPRESSION
CHAPTER EIGHT:
MECHANISMS OF ANTIDEPRESSANT ACTION
CHAPTER NINE:
ANTIDEPRESSANTS
CHAPTER TEN:
BENZODIAZEPINES
CHAPTER ELEVEN:
NATURAL PSYCHIATRIC SUPPLEMENTATION
REFERENCES
INDEX
Antidepressant Side Effect Lists
ANTIDEPRESSANTS,
POTENTIALLY LETHAL SIDE EFFECTSAmitriptyline (Amiril, Elvil, Emitrip, Endep, Enovil, Levate, Meravil, Novotriptyn): Bone marrow depression
Amoxapine (Asendin): Seizures with even small overdose
Bupropion (Wellbutrin, Zyban): Seizures
Clomipramine (Anafranil): Neuroleptic malignant syndrome, agranulocytosis
Desipramine (Norpramin, Pertofrane): Heart block, bone marrow depression, agranulocytosis
Doxepin (Adapin, Sinequan, Triadapin, Zonalon): Agranulocytosis
Fluvoxamine (Luvox): Stevens-Johnson syndrome, toxic epidermal necrosis
Furazolidone (Furoxone): Agranulocytosis
Imipramine (Novopramine, Impril, Janimine, Tofranil): Heart attack, agranulocytosis, angioedema
Isocarboxazid (Marplan) Hypertension
Nortriptyline (Aventyl, Pamelor): Agranulocytosis
Phenelzine (Nardil): Hypertensive crisis, coma, respiratory depression, circulatory collapse
Protriptyline (Triptyl, Vivactil): Edema
Tranylcypromine: (Parnate) Hypertensive crisis
ANTIDEPRESSANTS,
RELATIVELY SAFE SIDE EFFECTSCitalopram (Celexa): Tachycardia, hypotension, anorexia
Fluoxetine (Prozac): Palpitations, anorexia, hypersensitivity reactions, hyponatremia
Maprotiline (Ludiomil): Seizures, psychosis, hallucinations, hypertension, tachycardia
Mirtazapine (Remeron): Depression(!), hypertension, anorexia
Nefazodone (Serzone): None important (a few isolated reports of liver failure)
Paroxetine (Paxil): Hyponatremia in elderly
Sertraline (Zoloft): Palpitations, hypertension, hypotension, tachycardia, delusions, hallucinations, paranoia, suicidal ideation, anorexia, depersonalization, bronchospasm, hyponatremia in elderly
Trazodone (Desyrel): Hypotension, hypertension, shortness of breath, tachycardia, palpitations, bradycardia, anorexia, anemia
Trimipramine (Surmontil): Seizures, tachycardia, hypertension
Venlafaxine (Effexor): Hypertension, tachycardia, palpitations,
from Chapter 11: lists of natural anti-depressants
ANTIOXIDANTSAntioxidants by themselves cannot completely relieve depression or anxiety. But they can still help general psychiatric problems a lot. Neurotransmitters are easily oxidized, and oxidation of neurotransmitters can form neurotoxins that can damage the brain(12). The central nervous system is especially susceptible to oxidative damage from its relatively high oxygen comsumption, iron storage, and oxidizable hormones and lipids(13,14). Antioxidants, especially vitamins C, E, and beta-carotene, may help stabilize mood disorders, if combined with either the drugs discussed in previous chapters or the supplements mentioned below. Interestingly, in animals a deficiency of vitamin E can upregulate the serotonin 1 receptor(15). Upregulated inhibitory type 1 receptors may cause depression.
Vitamin C is very important in both the brain and the adrenal glands, since it is most concentrated in these two regions(16-18). In animal studies, vitamin C has antipsychotic activity, in that like some antipsychotics (ex. haloperidol) it can inhibit dopamine-stimulated adenylate cyclase, but does not inhibit basal levels of adenylate cyclase activity(19). This property of vitamin C is an exception to the rule of it generally increasing levels of cAMP. In animals, stress increases ascorbate synthesis(20), but remember, humans cannot synthesize ascorbate, so it would be only logical to increase vitamin C intake during times of stress. Vitamin C also helps form NA from dopamine, and can reduce excess histamine(19). Since there are no known drug interactions with vitamin C, it would make sense for all mentally ill people to take several grams a day of this amazing vitamin.INOSITOL
Inositol is an unofficial member of the B-vitamin group. You know, the vitamin group that all of the health food stores claim will boost your energy? Well, I don't think that a B-complex tablet by itself will do much, but inositol will, at least in patients that can respond to pharmaceutical antidepressants. Even better, unlike synthetic drugs, inositol is nothing to be scared of, since you eat an average of 1 gram a day of it in your food. Unfortunately, inositol does not cross the blood-brain barrier very well, and 1 gram a day will not do much. However, 6 to 12 grams a day can cut depressive symptoms by an average of 50%, with no detectible metabolic abnormalities(43). It is also effective in panic disorder(21). Since the above studies were clinical and double-blind, I highly recommend inositol for treatment of depression.
I mentioned the inositol system in Chapter 9. Inositol is directly downstream of the serotonin 2 receptor, and thus an excess of inositol here may very well increase the signal transduction of the receptor pathway, shunting over to the NA pathway, and ultimately helping repair stress-induced brain damage and depression. The serotonin 2 receptor blocker ritanserin abolished the antidepressant activity of injected inositol in animals, providing evidence that supplemental inositol activates the serotonin 2 receptor pathway (22). This raises an interesting question: is serotonin itself low in depression, or could it be some other chemical, such as inositol and/or its metabolites? Functionally, it may not matter, because even if serotonin is low, extra inositol may normalize the signal anyway. Central nervous system levels of inositol are low in depression(23). Adequate levels of inositol are crucial for normal serotonin pathway functioning; in one study even a small reduction in free inositol led to a large decline in energy utilization in nerve cells(24).
Therapeutic doses of inositol can safely be combined with antidepressants (25). There is probably an additive effect when combining inositol with antidepressants. In other words, if the therapeutic "minimum" for Zoloft is 50 mg/day, and you take 6 grams/day of inositol, it could produce the equivalent of 100 mg/day of Zoloft's effects in the brain. Six to twelve grams of inositol daily are needed to produce an antidepressant effect, but when combined with a pharmaceutical antidepressant, lower doses may suffice, and overstimulation/ mania could occur. Raise the dose of inositol slowly, perhaps by 500 mg every few days. Treatment-resistant depressives may benefit from inositol supplementation, since... "the existence of abnormalities in signal transduction pathways suggests that for patients refractory to conventional medications, improved therapeutics may be obtained only by direct targeting of postreceptor sites"(26). Evidence for a second-messanger (ex. inositol) abnormality is inferred by a study that found no correlation between the severity of depression with any serotonin- binding data result(27). Inositol is a very safe chemical that can be taken with benzodiazepines(28). Finally, bipolar disorder patients should not take inositol, since lithium interferes with the inositol system and oral inositol could negate lithium's effectiveness.CHROMIUM
As I mentioned in Chapters 2 and 4, chromium is a very important mineral that helps stabilize blood sugar and insulin levels. There is a lot of evidence that sugar metabolism is altered in the brain of depressed patients. 100 ug/day of chromium should benefit anyone, whether they are depressed or not. The two questions are what therapeutic amount above 100 ug/day a depressed person should take, and if this amount has any side effects, including drug-mineral interactions. The maximum amount you can safely take may be 1 mg/day(29), but some people are more sensitive than others. If you go above 100 ug/day, do it very slowly. When I personally tried to go from 125 ug/day to 225 ug/day, just to see what would happen, I experienced a mild hypoglycemic reaction the very same day, about 2 hrs after eating breakfast and taking the supplement. Be careful with chromium‹it is a powerful mineral, and diabetics have to consult their doctor before taking any amount of chromium.
Chromium can be especially effective for patients with treatment- resistant depression(30). Chromium increases tryptophan availability (for serotonin synthesis) and norepinephrine release(29). Since chromium enhances the peripheral effects of insulin, and insulin helps tryptophan enter the brain, chromium may indirectly increase serotonin synthesis also(31). Fortunately, chromium appears to be safe to take with pharmaceutical antidepressants(32); the same cannot be said with many other natural antidepressants. Chromium picolinate is the normal form of chromium that is found in stores, but chromium polynicotinate may be more helpful for some people as an antidepressant(32).S-ADENOSYL METHIONINE (SAMe) AND FOLATE
SAMe is a very interesting molecule, as it is a fusion of an amino acid (methionine) and a nucleic acid (adenosine, which is found in RNA). SAMe is involved in methylation reactions, which are very important in a wide variety of intracellular biochemical pathways, and SAMe is also biochemically related to folic acid (see below)(33). There is evidence of methylation disturbance in depression. SAMe mimics the functions of traditional antidepressants in many ways, including activation of PKA and the MAP-2 protein(34) (see Chapter 9). Also, SAMe increases synthesis of serotonin, NA, and dopamine(34), which makes it more similar to tricyclics and MAO inhibitors than to SSRI's. SAMe seems to act on serotonin and dopamine pathways more than the NA pathway(35). SAMe appears to act relatively quickly (4-7 days), and the maxiumum daily dose should be 1600 mg(35). Unlike folate, which will be discussed below, SAMe is usually not effective for treatment-resistant depression(36). As with any antidepressant, natural or synthetic, SAMe has the potential to cause anxiety and mania. SAMe should not be combined with any herbs, inositol, or any pharmaceutical antidepressant, because the risk of the serotonin syndrome is real (ex. serotonin syndrome with SAMe combined with a tricyclic(37)).
Depressed patients have low folate levels(38). Interestingly, patients with low folate levels were more likely to have severe (melancholic) depression that is unresponsive to Prozac treatment(39). This is why everyone should take a B-complex supplement. Antidepressant nonresponders may soon find that they do respond once they start supplementing with vitamins and minerals! As I mentioned in Chapter 2, more than 15 grams a day of folate has produced significant side effects. The recommended dose is 0.4 mg/day, so there is plenty of room to up the dose before reaching, say, 5-10 mg/day--do it slowly. Personally, I wouldn't take more than 1 mg/day, but if more than 1 mg/day works, then go with it. Do not megadose on folic acid and SAMe together.5-HYDROXYTRYPTOPHAN (5-HTP)
5-HTP is the immediate precursor to serotonin, and unlike tryptophan itself, it crosses the blood-brain barrier. So, in theory, 5-HTP should be the ideal chemical to restore normal serotonin levels. In reality, things are different. Many people do take 5-HTP, and some are helped by it, but unlike the three natural chemicals I mentioned above, I cannot recommend 5- HTP therapy, because of the side effects. 5-HTP injection can cause severe side effects(40). In a meta-analysis of uncontrolled studies, about 60% of people were helped by 5-HTP, with at least 18% having marked side effects(41). The side effects included hallucinations, convulsions, seizures, anxiety and panic, blurred vision, bradycardia (slow heartbeat), and psychosis. Doesn't sound very fun to me!
ST. JOHN'S WORT
The most common natural remedy for depression is St. John's Wort, followed by SAMe and 5-HTP. Hardly anyone takes inositol and/or chromium for depression, and yet these two substances may be the most effective and cause the least side effects of the five major natural treatments for depression. St. John's Wort does appear to be effective in mild or moderate depression. Although St. John's Wort is heavily advertised, and some people swear by it, like 5-HTP I also cannot recommend St. John's Wort. St. John's Wort by itself may cause the serotonin syndrome(42), although I have not read of anyone dying from it yet. Like 5-HTP, side effects are high, including serotonin syndrome and food-drug interactions(43). The serotonin syndrome it causes must be relatively mild, or else hundreds of people would have died by now. But that doesn't mean that you should ignore the side effects of St. John's Wort! As far as the food-drug interactions are concerned, this is probably due to St. John's Wort being implicated in MAO inhibition (see Chapter 9). In other words, if you take this supplement, avoid all "aged" foods, especially meats, cheeses, and wines.
endnotes
12. Vatassery, G., et. al. 1984. Vitamin E concentrations in the brains and some selected peripheral tissues of tissues of selenium-deficient and vitamin E-deficient mice. J Neurchem. 42: 554.
13. Halliwell, B., et. al. p. 188-276. Lipid peroxidation: a radical chain reaction. In: Free Radicals in Biology and Medicine. New York, NY: Oxford (Clarendon) Press, 1989.
14. Jesberger, J., et. al. 1991. Oxygen free radicals and brain dysfunction. Intern J Neurosci. 57: 1.
15. Castano, A., et. al. 1993. Turnover of monoamines in hippocampus of rats fed on vitamin E-deficient diet. Brain Res. 604: 154.
16. Damron, C., et. al. 1952. JBC. 195: 599.
17. Hughes, R., et. al. 1972. Br J Nutr. 26: 433.
18. Subramanian, N. 1977. Life Sci. 20: 1479.
19. Thomas, T., et. al. 1977. Inhibition of dopamine sensitive adenylate cyclase from rat brain striatal homogenates by ascorbic acid. J Neurochem. 28: 663.
20. Conney, A., et. al. 1961. Ann NY Acad Sci. 92: 115.
21. Benjamin, J., et. al. 1995. Double-blind placebo-controlled, crossover trial of inositol treatment for panic disorder. Am J Psychiatry. 152(7): 1084.
22. Einat, H., et. al. 2001. The antidepressant activity of inositol in the forced swim test involves 5-HT 2 receptors. Behav Brain Res. 118: 77.
23. Barkai, A., et. al. 1978. Reduced myo-inositol levels in cerebrospinal fluid from patient with affective disorder. Biol Psychiatry. 13: 65.
24. Simmons, D., et. al. 1982. Science. 217: 848.
25. Levine, J., et. al. 1999. Combination of inositol and serotonin reuptake inhibitors in the treatment of depression. Biol Psychiatry. 45: 270.
26. Chen, G., et. al. 1999. Signal transduction and psychotropic drugs. Psychosom Med. 61: 599.
27. Hrdina, P., et. al. 1997. Platelet serotonergic indices in major depression: up-regulation of 5-HT 2A receptors unchanged by antidepressant treatment. Psychiatry Res. 66: 73.
28. Levine, J., et. al. 1995. Double-blind, controlled trial of inositol treatment of depression. Am J Psychiatry. 152(5): 792.
29. Anderson, R., et. al. 1997. Lack of toxicity of chromium chloride and chromium picolinate in rats. J Am Coll Nutr. 16: 273.
30. McLeod, M., et. al. 2000. Chromium treatment of depression. Int J Neuropsychopharmacol. 3(4): 311.
31. Fernstrom, J. 1976. The effect of nutritional factors on brain amino acid levels and monoamine synthesis. Fed Proc. 35: 1151.
32. McLeod, M., et. al. 1999. Chromium potentiation of antidepressant pharmacotherapy for dysthymic disorder in 5 patients. J Clin Psychiatry. 60(4): 237.
33. Reynolds, E., et. al. 1984. Methylation and mood. Lancet. (July 28): 196.
34. Zanotti, S., et. al. 1998. Modifications in brain cAMP- and calcium/calmodulin-dependent protein kinases induced by treatment with S-adenosylmethionine. Neuropharmacol. 37: 1081.
35. Friedel, H., et. al. 1989. S-adenosyl-L-methionine. A review of its pharmacological properties and therapeutic potential in liver dysfunction and affective disorders in relation to its physiological role in cell metabolism. Drugs. 38(3): 389.
36. Rosenbaum, J., et. al. 1988. An open-label pilot study of oral S-adenosyl-L-methionine in major depression: interim results. Psychopharmacol Bull. 24: 189.
37. Iruela, L., et. al. 1993. Toxic interaction of S-adenosylmethionine and clomipramine. Am J Psychiatry.
150(3): 522.
38. Abou-Saleh, M., et. al. 1989. Serum and red blood cell folate in depression. Acta Psychiatr Scand. 80: 78.
39. Fava, M., et. al. 1997. Folate, vitamin B 12 , and homocysteine in major depressive disorder. Am J Psychiatry. 154(3): 426.
40. Den Boer, J., et. al. 1990. Behavioral, neuroendocrine, and biochemical effects of 5-hydroxytryptophan administration in panic disorder. Psychiatry Res. 31(3): 267.
41. Byerley, W., et. al. 1987. 5-hydroxytryptophan: a review of its antidepressant efficacy and adverse effects. J Clin Psychiatry. 7(3): 127.
42. Parker, V., et. al. 2001. Adverse reaction to St. John's Wort. Can J Psychiatry. 46(1): 77.
43. Beckman, S., et. al. 2000. Consumer use of St. John's Wort: a survey on effectiveness, safety, and tolerability. Pharmacotherapy. 20(5): 568.
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