Amino Acids: The Evidence

The Closest Things to Pharmaceuticals
One Can Find at the Health Food Store

Protein makes up about three quarters of the dry weight of most of the body's cells. Neurotransmitters, hormones, enzymes, the immune system - all are constructed from specialized mixes of protein. Just about everything interesting the body does it does by making specialized proteins.

Amino acids are the building blocks from which the body makes protein. If all essential cofactors are in place and enough metabolic pathways are open for business we can potentially steer a wide range of body processes simply by giving the body more of the amino acids it needs to make the proteins it needs to do the things we want it to do. My favorite work on this subject is The Healing Nutrients Within, by Eric Braverman, M.D.1 Much of this material on amino acids is condensed from his work.

We'll be looking at the mental health applications of:

Using individual amino acids is the closest "natural" medicine comes to pharmaceutical medicine. Many drugs work by mimicking or interfering with amino acids or the peptides and proteins the body makes from amino acids. And even though amino acids are the building blocks of protein, we buy them in the health food stores and think of them as "natural", most of them are actually made by genetically re-engineering bacteria to pump them out reliably and inexpensively.

For best results it's important to follow all necessary precautions. These are listed throughout this article in this BOLDFACED type.

If you're taking amino acids for a medical purpose it's important to take them on an empty stomach at least twenty minutes before eating a meal. Amino acids compete for transport into the body. Proteins in food break down into amino acids and will block some of your supplemental aminos from working. It's also important to be taking well-designed Basic Nutrients.

If you're already taking medication, have compromised liver or kidney function, need or are already under medical care please see your doctor before attempting use of the amino acids listed here. If you haven't had a physical lately get one, make sure your liver and kidneys are doing fine and talk to the doctor about what you want to do. If you have an undiagnosed medical condition and do a bad job of it with amino acids you can hurt yourself. If you need medical or psychological care please see a qualified professional.


The brain uses l-tryptophan to make serotonin - a relaxed, calming neurotransmitter.2 Serotonin helps us sleep and calms anxiety.3,4 Serotonin helps remodel our brain to better reflect the lessons we learn from life.5

Serotonin's been found helpful in endogneous6 major7 and bipolar depression.8 Lack of enough dietary tryptophan can make us hostile.9 When we're stressed or inflammed serotonin breaks down.10,11,12 This describes many people, particularly as they age. Aging digestive systems can weaken allowing undigested proteins to be absorbed into the blood, triggering chronic inflammation.

l-Tryptophan was banned for a time beginning in 1989 because a contaminated batch caused by a new manufacturing process from a Japanese company killed twenty-seven people. There's nothing wrong with tryptophan itself - it's abundant in many common foods like bananas. Tryptophan is essential to life. Since it's now difficult to get in supplement form, many people take 5-HTP instead when they want to boost their serotonin levels. 5-HTP is an intermediate step in the conversion of tryptophan to serotonin.

Besides getting better sleep and lifting depression, many people boost their serotonin to control their appetites. Carb binging boosts brain serotonin by triggering insulin secretion. Amino acids compete with each other for transport into the brain; insulin clears most aminos from the blood but spares tryptophan. This means that insulin surges can give us serotonin surges, at least in the short run.13,14 Boosting serotonin levels with 5-HTP is a more conscious and healthy way of giving the brain its serotonin payoff than carb binging.15

Typical American meals boost insulin and serotonin levels much more when they're based around carbohydrates than when they're meat-centered. Many Americans give themselves a strong sedative every morning just eating breakfast.16

But the picture isn't a simple one. The same serotonin doses that help some people focus their attention make it harder for others.17 In brains with overactive immune systems (ie: chronic allergic reactions) tryptophan is converted into an anti-serotonin substance - kynurenine, instead. Autistics have high levels of kynurenine.18 Asperger's syndrome (moderate to extreme social incompetence) is thought by some to be a high-functioning form of autism. It's possible that in some shy folks taking too much tryptophan could make them more withdrawn (others will lighten up and become more outgoing.)

Bipolar,19 anorectic20 and schizophrenics can have atypical responses to tryptophan and serotonin.21 MDMA (ecstacy) use significantly changes the way the brain responds to serotonin by releasing prolactin. Prolactin, released at orgasm, is sometimes called the "bonding" neurotransmitter. It also stimulates milk production in nursing mothers. MDMA users show a reduced prolactin response to serotonin.22

But again, these are atypical responses. Most anxious, over-focused, and many depressed people do better when using cool, calming serotonin-generators to loosen up. It helps most of us cope better with stress23 and deepens sleep leaving us more refreshed and alert in the morning.24


l-Tyrosine has a history of use in complementary medicine as an antidepressant25 and metabolism enhancer although attempts by researchers to model these results have been mixed.26,27,28,29 Eric Braverman, M.D., works extensively with amino acids in combination with other nutrients and pharmaceuticals. He reports tyrosine is most appropriate for cases of mild depression, known as dysthymia.30

Tyrosine is a key amino acid necessary for the formation of thyroid hormones as well as neurotransmitters like dopamine and norepinephrine. Many people are depressed because their thyroids aren't working hard enough or because of neurotransmitter or HPA axis irregularities. For years I used tyrosine with depressed patients and it seemed to work reasonably well for a number of them. I remember clearly one patient who didn't respond until he stopped drinking numerous cups of coffee every morning.

Large numbers of people are deficient in magnesium and zinc,31,32,33 essential co-factors in the production of the mood-elevating neurotransmitters tyrosine builds.34 Simply supplementing tyrosine without also supplying these critical trace minerals in a bio-available form may not work.35,36,37,38 Since caffeine consumption is so common and since caffeine is said to block tyrosine's mood elevating effects it may be that any beneficial effect of tyrosine would be masked in test groups drawn from the general population.

It may also be the case that tyrosine isn't as good at restoring low levels of mood-elevating neurotransmitters as it is in preventing us from losing our ability to make them in the first place. Because it supplies raw material used to make stress hormones l-tyrosine is used to help people cope with high stress levels. Tyrosine increases stress neurotransmitters,39,40 and builds stamina under stress.41

L-tyrosine metabolizes rapidly. Biopterin, niacin, folic acid, copper and vitamin C are all required in optimal amounts for its utilization. L-tyrosine should not be taken along with MAO inhibitors, one class of drugs commonly prescribed to treat high blood pressure and depression. Doing so can produce dangerous elevations of excitatory neurotransmitters and require hospitalization.


dl-Phenylalanine (DLPA) and tyrosine are both metabolic activators and human bodies can change them back and forth into each other. Phenylalanine is found in large amounts in the human brain. There it supplies the raw material for the brain's production of a wide range of neuroactive molecules. Fibroblasts, special cells involved in the growth of new tissue and damage repair, use large amounts of phenylalanine.

Phenylalanine enters the brain easily.42 The body can turn it into tyrosine and turn that into the neurotransmitters that wake us up, keep us focused and motivate us - adrenaline, noradrenaline and dopamine.43,44,45) Like tyrosine, people who have high blood pressure should avoid phenylalanine as should people on MAO (monoamine oxidase) inhibitors. Phenylalanine is an amino acid "pick-me-up," so it's not good for presentations with anxiety. These need to be calmed instead. Children with ADHD have elevated phenylalanine and so may do better with tryptophan instead.46,47,48

Phenylalanine is more versatile than tyrosine. Phenylalanine, in the form DPA, can block pain49,50 and enhances the pain-relieving effect of acupuncture.51 It does this by blocking the enzymes that break down the body's natural self-generated opiates (endorphins and enkephalins.)52,53

Some people get migraines when taking l-phenylalanine.54 About one person in sixty lacks one of the genes necessary to turn phenylalanine into tyrosine. Many of these people are not aware that they carry the gene.55,56,57 Since elevated phenylalanine levels are associated with mental retardation there are concerns both about aspartame, the artificial sweetener that is made up in part of phenylalanine, and phenylalanine supplements.58 That's why some people prefer to take tyrosine instead, sidestepping this potential problem.

Phenylalanine can increase assertiveness.59 Braverman reports that "children with attention deficit disorder and hyperactivity (ADHD) have been found to have elevated levels of plasma phenylalanine. These children respond to l-typtophan therapy, which lowers the phenylalanine level and improves their ability to concentrate."

While neither tyrosine nor phenylalanine are carcinogenic (they don't start cancers), melanomas love them. Watch those moles and birthmarks; any changes means consult a dermatologist. It's best to use both these aminos only when needed, avoiding prolonged supplementation (over 2 months) without professional advice. As with tyrosine, check for high blood pressure before starting l-phenylalanine.

l-Cysteine, NAC & Glutathione

Free radicals are electrically unbalanced little molecular thieves. They steal electrons right out of our body's big, tempting molecules and intiate oxdation. Oxidation spoils the fats in our cell walls like it spoils the surface of a piece of cheese forgotten on the counter overnight. Oxidation is often also a self-sustaining chain reaction - when free radicals pull electrons out of a relatively huge protein or fat molecule the imbalanced molecules that result become new free radicals themselves. These then go searching for their own electrons-to-steal. Biologists call this condition of heightened free radical activity oxidative stress.

Chronic stress increases oxidative stress.60 Oxidative stress has been suggested as an underlying condition contributing to chronic fatigue,61 depression,62 autism,63 schizophrenia,64 cognitive declines such as the vascular dementia65 and Alzheimer's66,67 resulting from cerebral aging.68,69

Anti-oxidants (AOs) keep this from happening, usually by being more electrochemically attractive to the free radicals than our body's tissues are. l-Cysteine is a very powerful antioxidant, more powerful even than Vitamin C. It converts to glutathione in the liver, one of the most powerful antioxidants known. Glutathione and l-cysteine detoxify us, protecting us from an increasingly poisonous world. Many toxins do their work by oxidizing us, so antioxidant sulphur-containing amino acids like l-cysteine or NAC offer a degree of protection. Many people prefer N-acetyl cysteine (NAC) to l-cysteine, but unless you're HIV positive they're functionally the same.

Glutathione is thought to be one of the earliest organic molecules formed. It appears spontaneously when watery models of earth's early seas are jolted with electric sparks; other organic molecules would probably not have survived long in earth's toxic early environment without its protection.

L-Cysteine pulls heavy metals out of our bodies70,71 such as mercury72 and copper. Copper plumbing carries water into many homes. Copper poisoning has been associated with schizophrenia.73 L-cysteine converted into glutathione also disarms organophosphates and chlorinated hydrocarbons.74 Many water systems chlorinate their water to keep bacterial growth down. When chlorine encounters organic matter in water mains and tanks, chlorinated hydrocarbons are formed. These toxic gases are then released into the air in our homes through our showers, dishwashers, lawn sprinklers.75,76 They also attack the fats in our brains.77 Dry cleaning residues in our clothes and closets are famously toxic. L-cysteine can offer a degree of protection against these and other assaults on our health.78,79

Not only does glutathione work with vitamin C as an antioxidant - soaking up free radicals that would otherwise be corroding our cells and tissues - l-cysteine protects us from environmental toxins.

When our body's immune system goes to work, the bacteria and viruses it destroys are oxidized by free radicals. Vitamin C and glutathione soak up these free radicals too before they can oxidize our fats. The brain is a very fatty organ. So is the liver. So when we're fighting off infections it's a good idea to stay saturated in antioxidants like glutathione and its l-cysteine or NAC precursors.

L-cysteine is also a good idea if we have addictive allergic eating habits. Because of certain neuroendocrine payoffs it's easy for the brain to rewire itself to crave whatever our favorite immune-stimulating allergens happen to be. When we indulge these cravings our bodies produce nitric oxide (NO). NO makes our blood vessel walls more permeable, which is why we swell up and get clogged when we have allergic reaction. NO can become peroxynitrate, a biologically essential oxidant that's also the most dangerous free radical in the body.80

The body's own cellular metabolism creates free radicals. We absorb free radicals from air pollution and the smoke in our environment and from rancid fats and oils in our diets. When was the last time your favorite fast food restaurant changed its oils?

Methionine & SAMe

Methionine is an amino acid available over the counter at most health food stores. It's also one of the oldest organic molecules. Bacteria were the first life forms and it appears methionine was central to their success. Methionine donates methyl groups at numerous critical junctures in bacterial metabolism. As one of its other roles methionine triggers the translation of DNA instructions into protein. So it's a good bet methionine is as old as life itself.

Methionine makes SAMe when it donates a methyl group to SAMe's precursor molecule. An abundant literature documents SAMe's utility in depression81,82,83,84 in part because it boosts serotonin levels.85,84 It augments the effects of common antidepressant medications (the SSRIs)87 helping patients achieve desired outcomes with smaller doses. SAMe is itself a methyl donor, and is even more easily available at health food stores. Methionine does much the same job and sometimes it's cheaper.

Humans can't make methionine. Bacteria in our guts donate some but stress damages digestion so even if we're successfully absorbing what the bacteria generate it may not be enough. It's probably even less if we've taken courses of antibiotics and those helpful bacteria aren't there anymore. So it can be a good idea to try methionine if fall's leaving one a little blue or overly aggressive.

Methlyation can be overdone - excessive methylation produces the hallucinogenic symptoms of schizophrenia and psychosis. Adequate pyridoxine (B6), cyanocobalamin (B12) and folic acid are required for methionine and SAMe's metabolism. Since serotonin function is so variable a subset of about 5% of the population may be comprised of vulnerable individuals may experience manic states when taking methionine or SAMe.88

l-Glutamine, Glutamic Acid, GABA

l-Glutamine is the most common amino acid found in the blood. It is 10-15 times more concentrated in brain fluid than in the blood.89 It changes into glutamic acid (GA), an excitatory neurotransmitter, as well as into GABA, an inhibitory neurotransmitter. These three substances together fuel the brain while turning the volume up (GA) and down (GABA) on brain activity.

Glutamic acid also soaks up excess ammonia and by doing so buffers the citric acid cycle, the energy-generating chemical reaction chain that drives the cells' engines, the mitochondria. Without enough glutamic acid we can get an excess ammonia-driven brain fog. Glutamic acid is plentiful in foods, but it has to be changed into l-glutamine before it can pass through the blood-brain barrier and into the brain itself. l-Glutamine is not plentiful in food.90 Manganese is critical for GA's conversion to the other forms.

GABA is a calming, sedative neurotransmitter available OTC in any health food store. Its role is discussed in more depth here.

L-glutamine has been used for behavioral disorders in children,91 and alcoholism.92,93,94 There have been reports of it being useful in curing sweet tooths. I decided to try it on my own, it worked, and now I've seen it work for hundreds of patients.95 The GA l-glutamine forms after it passes through the brain blood barrier can also be used as brain fuel. As needed and as cofactor supplies allow it becomes GABA, the calming neurotransmitter. Together these appear to shut off cravings for both sugar and alcohol.

It takes some people about eight weeks to get this effect; others less time. 2-3,000 mg/day will usually do it. As with all aminos, take them on an empty stomach with no solid food for at least twenty minutes. Some aminos can be mixed with each other, others interfere with each other. It's best to take them one at a time.

It's very important to calendar yourself to stop taking l-glutamine 8 weeks after starting. It's a bad idea to continue taking l-glutamine indefinitely. It's an excitatory neurotransmitter; continued in large doses indefinitely this can cause trouble. L-glutamine is not cancer-causing, but brain tumors that have already formed thrive on l-glutamine.


1. Braverman, Eric. The Healing Nutrients Within. 2003, 1987. North Bergen, N.J.: Basic Health Publications. Much of the material in this section is condensed from this work, and many of the research citations are drawn from it as well. The page numbers listed in the book citations listed below are from the 1987 edition unless otherwise noted.

2. Fuller, R.W. The involvement of serotonin in regulation of pituitary adrenal cortical function. 1992. Frontiers of Neuroendocrinology. 13:250-270.

3. Amen, Daniel. 1998. Change Your Brain Change Your Life. New York: Times Books. 47,53,93.

4. You, J.S., et al. 2005. Serotonin transporter and tryptophan hydroxylase gene polymorphisms in Chinese patients with generalized anxiety disorder. Psychiatric Genetics. 15(1):7-11.

5. Sodhi, M.S., Sanders-Bush, E. 2004. Serotonin and brain development International Review of Neurobiology. 59:111-174.

6. Quintana, J., et al. 1992. Platelet serotonin and plasma tryptophan decreases in endogenous depression. Clinical, therapeutic and biological correlations. Journal of Affective Disorders. 24(2):55-62.

7. Mann, J.J., et al. 1996. Demonstration in vivo of reduced serotonin responsivity in the brain of untreated depressed patients. American Journal of Psychiatry. 153(2):174-182.

8. Farkas, T. 1976. L-tryptophan in depression. Biological Psychiatry. 11(3):295-302

9. Young, S.N. 1988. The effect of altered tryptophan levels on mood and behavior in normal human males. Clinical Neuropharmacology. 11 Suppl. 1:S207-215.

10. Myint, A.M., Kim, Y.K. 2003. Cytokine-serotonin interaction through IDO: a neurodegeneration hypothesis of depression. Medical Hypotheses. 61(5-6):519-525..

11. Russo, S., et al. 2003. Tryptophan as a link between psychopathology and somatic states. Psychosomatic Medicine. 65(4):665-671.

12. Wichers, M.C., et al. 2005. IDO and interferon-alpha-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity. Molecular Psychiatry. 10(6):538-544.

13. Fernstrom, J.D. 1985. Dietary effects on brain serotonin synthesis: relationship to appetite regulation. American Journal of Clinical Nutrition. 42(5 Suppl.):1072-1082.

14. Leathwood, P.D., Fernstrom, J.D. 1990. Effect of an oral tryptophan/carbohydrate load on tryptophan, large neutral amino acid, and serotonin and 5-hydroxyindoleacetic acid levels in monkey brain. Journal of Neural Transmission. General Section. 79(1-2):25-34.

15. L-glutamine, used judiciously, can also help.

16. Wurtman, R.J., Wurtman, J.J. 2003. Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios. American Journal of Clinical Nutrition. 77(1):128-132.

17. Riedel, W.J., Sobczak, S., Schmitt, J.A. 2003. Tryptophan modulation and cognition. Advances in Experimental Medicine and Biology. 527:207-213.

18. Germano, Carl and Lombard, J. 2000. The Brain Wellness Plan. New York: Kensington Books. 260-261.

19. Henry, C., Demotes-Mainard J. 2003. Avoiding drug-induced switching in patients with bipolar depression. Drug Safety. 26(5):337-351.

20. Kaye, W.H., et al. 2003. Anxiolytic effects of acute tryptophan depletion in anorexia nervosa. International Journal of Eating Disorders.33(3):257-267

21. Cowen, M.A. 1976. An electrophysiological study on the effects of tryptophan and cortisol on schizophrenic and other mentally ill patient groups and on normal subjects. Biological Psychiatry. 11(4):389-401.

22. Gerra, G., et al. 2000. Long-lasting effects of (+/-)3,4-methylenedioxymethamphetamine (ecstasy) on serotonin system function in humans. Biological Psychiatry. 47(2):127-136.

23. Richell, R.A., et al. 2005. Effect of acute tryptophan depletion on the response to controllable and uncontrollable noise stress. Biological Psychiatry. 57(3):295-300.

24. Markus, C.R., et al. 2005. Evening intake of alpha-lactalbumin increases plasma tryptophan availability and improves morning alertness and brain measures of attention. American Journal of Clinical Nutrition. 81(5):1026-1033.

25. Goldberg, J.K. 1980. L-tyrosine in depression. Lancet. 2(8190):364-365.

26. Gelenberg A.J. and Gibson C.J. Tyrosine for the treatment of depression. 1984. Nutrition and Health. 3(3):163-173.

27. Harmer, C.J. et al, Tyrosine depletion attenuates dopamine function in healthy volunteers. 2001. Psychopharmacology (Berl). 154(1):105-11.

28. Meyers, S. Use of neurotransmitter precursors for treatment of depression. 2000. Alternative Medicine Review. 5(1):64-7.

29. Gelenberg, A.J. et al. Tyrosine for depression: a double-blind trial. 1990. Journal of Affective Disorders. 19(2):125-32.

30. Braverman, Ibid. 39-40.

31. Briefel, R.R. et al, Zinc intake of the U.S. population: findings from the third National Health and Nutrition Examination Survey, 1988-1994. 2000. Journal of Nutrition. 130(5S Suppl):1367S-73S.

32. Firoz M., Graber M. Bioavailability of US commercial magnesium preparations. 2001. Magnesium Research. 14(4):257-62.

33. Marier, J.R. Magnesium content of the food supply in the modern-day world. 1986. Magnesium. 5(1):1-8.

34. Thony, Beat et al, Tetrahydrobiopterin biosynthesis, regeneration and function. 2000. Biochemical Journal. 347:1-16.

35. Gelenberg A.J. and Gibson C.J. Tyrosine for the treatment of depression. 1984. Nutrition and Health. 3(3):163-173.

36. Harmer, C.J. et al, Tyrosine depletion attenuates dopamine function in healthy volunteers. 2001. Psychopharmacology (Berl). 154(1):105-11.

37. Meyers, S. Use of neurotransmitter precursors for treatment of depression. 2000. Alternative Medicine Review. 5(1):64-71.

38. Gelenberg, A.J. et al. Tyrosine for depression: a double-blind trial. 1990. Journal of Affective Disorders. 19(2):125-32.

39. Quirce, C.M., Odio, M, Maickel, R.P. 1984. Modification of the effects of repetitive restraint stress on brain biogenic amines by L-tyrosine. Zhongguo Yao Li Xue Bao. (4):226-8.

40. Reinstein, D.K., et al. 1984. Tyrosine prevents behavioral and neurochemical correlates of an acute stress in rats. Life Sciences. 34(23):2225-2231.

41. Gibson, C.J., et al. 1982. Behavioural and biochemical effects of tryptophan, tyrosine and phenylalanine in mice. Psychopharmacology (Berl). 76(2):118-121.

42. Braverman, Eric. The Healing Nutrients Within. 2003. North Bergen, NJ: Basic Health Publications. 23. This is the most current edition of the work cited in 1, above.

43. Robinson, N., and Williams, C.B., Amino acids in human brain. 1965. Clinica Chimica Acta. 12:311-317.

44. Bagchi, S.P. and Smith, T.M. Dopa and dopamine formation from phenylalanine in human brain. 1977. Biochemical Pharmacology. 26(9):900-902.

45. Ibid, 23. Tyrosine becomes epinephrine (a.k.a: adrenaline), norepinephrine (noradrenaline) and dopamine. Epinephrine and norepinephrine wake us up and focus us. If we're in a slightly different mood tyrosine can become dopamine, the neurotransmitter of love, pleasure and motivation.

46. Braverman, E. Ibid. 27.

47. Michals K. and Matalon R. 1985. Phenylalanine metabolites, attention span and hyperactivity. American Journal of Clinical Nutrition. 42(2):361-365.

48. If you can't find l-tryptophan, a somewhat smaller dose of 5-HTP should do the job.

49. Russell, A.L., McCarty, M.F. 2000. DL-phenylalanine markedly potentiates opiate analgesia - an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system. Medical Hypotheses. 55(4):283-288.

50. Ehrenpreis, S. 1985. Analgesic properties of enkephalinase inhibitors: animal and human studies. Progress in Clinical and Biological Research. 192:363-370.

51. Ehrenpreis, S. 1982. D-phenylalanine and other enkephalinase inhibitors as pharmacological agents: implications for some important therapeutic application. Acupuncture & Electrotherapeutics Research. 7(2-3) 157-172.

52. Blum, K., et al. 1989. Enkephilinase inhibition and precursor amino acid loading improves inpatient treatment of alcohol and polydrug abusers: double-blind placebo-controlled study of the nutritional adjunct SAAVE (a REWARD 6 variant). Alcohol. 5:481.

53. Budd, K. 1983. Use of d-phenylalanine, an enkephalinase inhibitor, in the treatment of intractable pain. In: Advances in Pain Research and Therapy. Bonica, J.J., Liebeskind, J.C. and Albe-Fessard, D.G. eds. New York: Raven Press. 5:305-308. Cited in Braverman

54. Braverman, E. Ibid. 30.

55. Spreen, O.,et al. 1984. Human Developmental Neuropsychology. New York: Oxford University Press.

56. Frier, L. J. and L. D. Stegink. 1989. Aspartame metabolism in normal adults, phenylketonuric heterozygotes, and diabetic subjects. Diabetes Care. 12(1):67-74.

57. Nutrition Reviews. 1979. Phenylalanine-tyrosine conversion in 1 hour in 18 families with one or more non-specific retarded children. 37(7):217.

58. Maher, T.J., Wurtman, R.J. 1987. Possible neurologic effects of aspartame, a widely used food additive. Environmental Health Perspectives. 75:53-57.

59. Erasmus, Udo. 1993. Fats That Heal, Fats That Kill. Burnaby, B.C.: Alive Books. 80-81.

60. Cernak, I., et al. 2000. Alterations in magnesium and oxidative status during chronic emotional stress. Magnesium Research. 13(1):29-36.

61. Logan, A.C. 2001. Chronic fatigue syndrome: oxidative stress and dietary modifications. Alternative Medicine Review. 6(5):450-459.

62. Tsuboi, H., et al. 2004. Depressive symptoms are independently correlated with lipid peroxidation in a female population: comparison with vitamins and carotenoids. Journal of Psychosomatic Research. 56(1):53-58.

63. McGinnis, W.R. 2004. Oxidative stress in autism. Integrative Medicine. 3(6):42-57.

64. Yao, J.K. 2000. Abnormal age-related changes of plasma antioxidant proteins in schizophrenia. Psychiatry Research. 97(2-3):137-151.

65. Sinclair, A.J., et al. 1998. Altered plasma antioxidant status in subjects with Alzheimer's disease and vascular dementia. International Journal of Geriatric Psychiatry. 13(12):840-845.

66. Dawson, R.J., et al. 1995. Excitotoxins, aging, and environmental neurotoxins: implications for understanding human neurodegenerative diseases. Toxicology and Applied Pharmacology. 134(1):1-17.

67. Draczynska-Lusiak, B., et al. 1998. Oxidized lipoproteins may play a role in neuronal cell death in Alzheimer disease. Molecular and Chemical Neuropathology. 33(2):139-148.

68. Deschamps, V., et al. 2001. Nutritional factors in cerebral aging and dementia: epidemiological arguments for a role of oxidative stress. Neuroepidemiology. 20(1):7-15.

69. Serrano, F., Klann, E. 2004. Reactive oxygen species and synaptic plasticity in the aging hippocampus. Ageing Research Reviews. 3(4):431-443.

70. Hsu, J.M. 1984. Lead toxicity as related to glutathione metabolism. Journal of Nutrition. III:26-33.

71. Jensen, L.S. and Maurice, D.V. 1979. Influence of sulfur amino acids on copper toxicity in chicks. Journal of Nutrition. 109:91-97.

72. Ballatori, N. and Clarkson, T.W. 1982. Developmental changes in the biliary excretion of methlymercury and glutathione. Science. 216(2):61-62.

73. Pfeiffer, C.C. and Bacchi, D. 1975. Copper, zinc, manganese, niacin and pyridoxine in the schizophrenias. Journal of Applied Nutrition. 27(2,3):9-39.

74. Chasseaud, L.F., 1975. The role of glutathione and gluathione S-transferases in the metabolism of chemical carcinogens and other electrophilic agents. Advances in Cancer Research. 29:176-244.

75. Giardino, N.J., Andelman, J.B. 1996. Characterization of the emissions of tricholorethylene, chloroform, and 1,2-dibromo-3-chloropropane in a full-size, experimental shower. Journal of Exposure Analysis and Environmental Epidemiology. 6(4):413-423.

76. Andelman, J.B. 1985. Human exposures to halogenated organic chemicals in indoor and outdoor air. Environmental Health Perspectives. 62:313-318.

77. Cornell University Pesticide Management Program.

78. Larsson, A., et al. 1984. Functions of glutathione, biochemical, physiological, toxicological and clinical aspects. Annals of Biochemisty. 139(1):126.

79. Braverman, Ibid. 121.

80. Germano, Carl and Lombard, J. Ibid. 28-29.

81. Williams, A.L. 2005. S-adenosylmethionine (SAMe) as treatment for depression: a systematic review. Clinical and Investigative Medicine. 28(3):132-139.

82. Mischoulon, D., Fava, M. 2002. Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence. American Journal of Clinical Nutrition. 76(5):1158S-1161S.

83. Papakostas, G.I., et al. 2003. S-adenosyl-methionine in depression: a comprehensive review of the literature. Current Psychiatry Reports. 5(6):460-466.

84. Freeman, M.P., et al. 2004. Selected integrative medicine treatments for depression: considerations for women. Journal of the American Women's Medical Association. 59(3):216-224.

85. Otero-Losada, M.E., Rubio, M.C. 1989. Acute changes in 5-HT metabolism after S-adenosyl-L-methionine administration. General Pharmacology. 20(4):403-406.

86. Curcio, M. et al. 1978. Effect of S-adenosyl-L-methionine on serotonin metabolism in rat brain. Progress in Neuropsychopharmacology. 2(1):65-71.

87. Alpert, J.E., et al. 2004. S-adenosyl-L-methionine (SAMe) as an adjunct for resistant major depressive disorder: an open trial following partial or nonresponse to selective serotonin reuptake inhibitors or venlafaxine. Journal of Clinical Psychopharmacology. 24(6):661-664.

88. Goren, J.L., et al. 2004. Bioavailability and lack of toxicity of S-adenosyl-L-methionine (SAMe) in humans. Pharmacotherapy. 24(11):1501-1507.

89. Braverman, Eric. 2003. Ibid. 166.

90. Braverman, Ibid. 167-168.

91. Braverman, Ibid. 166.

92. Rogers, L.L. et al. Amino acid supplementation and voluntary alcohol consumption by rats." 1956. Journal of Biological Chemistry. 220(1):321-323.

93. Williams, R.J. 1958. Alcoholism, the Nutritional Approach. Austin: Univ. of Texas Press. 88.

94. Rogers, L.L. 1957. Glutamine in the treatment of alcoholism". Quarterly Journal of Studies on Alcohol. 18(4):581-587.

95. I've also seen it not work for a few, but only a very few. It's important to take it correctly. Please see the second paragraph of the present article. 33(3):257-267.

96. Cowen, M.A. 1976. An electrophysiological study on the effects of tryptophan and cortisol on schizophrenic and other mentally ill patient groups and on normal subjects. Biological Psychiatry. 11(4):389-401.

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