Nutrition and Stress
A Well-Nourished Brain = A Calmer Mind
Some say humans have walked the earth for a hundred thousand years. Others say it's a million. Others six thousand. It depends on which version of events one finds credible ... and if one buys what most scientists tell us, where one draws the line between humans and pre-humans.
Our cellular machinery is much older however, as old as life itself - and the scientists tell us that's about a billion and half years.
Take that billion and half year period and compress it into a 24-hour day - the twelve thousand years that've passed since we started growing our own food is a little less than seven tenths of a second. That agricultural revolution ... at the dawn of history ... irrevocably changed the way our species eats. Our bodies and brains have largely not had sufficient time to evolve in response to these changes.1,2,3,4,5
Human diets have gone through another revolution in just the last 120 years. In the blink of an evolutionary eye large-scale industrialization has taken over food production - less than seven thousandths of a second in our evolutionary "day."
It takes half a second to blink one's eyes.
Let's look at some of the issues that arise from these changes in human nutrition and how they contribute to stress.
Trace Mineral Depletion:
Humans began growing food and taming animals only 10-13,000 years ago. Before then, everything we ate was wild and organic. After we began settling in one place, herding animals and growing crops, the nutrient content and quality of our food began to slowly decline in a few crucial respects. Certain agricultural practices common today are accelerating this decline.
Undisturbed, plants absorb minerals from the soil as they pass through their life cycle and return those minerals to the soil when they die ... typically only a few feet from where those minerals were first absorbed. This ensures that those minerals are available to future generations of plants.
This is crucial in tropical regions. Jungle soils tend to be so poor in minerals that plants suck them all up. In order to farm, the jungle must be burned, returning those minerals to the earth. Even then, soil so prepared stays fertile for only a few growing seasons.
We suffer a bit less obviously from this problem in the northern hemisphere. The reason: we had ice ages. Glaciers grind granite mountains into the soil that rains and rivers deposit in fertile floodplains. That's why the best farmland is always "bottomland."
But the first thing humans do when we start farming is build water projects. Dams and dikes are built to make the water supply more reliable and to the yearly flooding of farms and towns. But this practice also has the unfortunate side effect of stopping the natural remineralization of soil that regular flooding brings.
So Nutrient Mining occurs every year when crops are harvested and their mineral content ends up landfills or flushed out to sea. This nutrient mining drains the soil every year flooding is prevented. Simply resting the soil doesn't restore minerals, and neither do most fertilizers.
Case-in-point: magnesium. Magnesium is critical to the relaxation of muscle and nerve tissue.6 In the late nineteen eighties dairy farmers in the midwest began noticing something they'd never seen before. If they had heavy rains in the late winter or early spring with an abundant growth of lush grass, turning their cattle out to pasture caused some to have fatal seizures. Autopsies on these cattle determined that the cattle were dying of magnesium deficiency, resulting in a condition that came to be called grass tetany.7 The farmers found that only by supplementing cattlefeed with magnesium could they keep their stock alive.
- Magnesium (Mg) is often low in children with Attention Deficit Hyperactivity Disorder (ADHD) and supplementing with Mg can sometimes help these kids focus their minds.8,9
- Mg helps ordinary schoolkids reduce neurotic acting out.10
- Without enough Mg elders are more prone to developing age-related brain deficits.11,12
- Mg is crucial to carbohydrate (sugars, breads, chips, vegetables, grains) metabolism. It activates a number of enzymes that help the body burn its fuel.13
- Mg helps maintain electrical charges across cell membranes in the nervous system and throughout the body.
- Mg also plays a critical role in preventing the over-release of the stress hormones like adrenaline and noradrenaline. These same stress chemicals lower Mg levels: less Mg means more stress hormones and that means even less Mg.14
Whenever our cells do anything they usually do it by making proteins or related compounds, peptides. Neurotransmitters, hormones, digestive enzymes, cell structure itself - all proteins. When it's time for a cell to make a protein DNA transfers the information stored in its patterns to RNA molecules, which then build the actual proteins.15 This process is called RNA transcription and can't take place without adequate magnesium.
- Magnesium can help control appetite and sweet cravings in premenstrual women.16
- By controlling stress hormones and relaxing arterioles Mg can lower blood pressure.
- Mg helps insulin regulate blood sugar levels.
- Magnesium is a critical part of the enzymes that make serotonin, the stress-calming neurotransmitter. Many prescription anti-depressants (SSRIs) work by boosting serotonin levels. Since many carb addicts crave their carbs in order to get the serotonin boost carb binging can bring, adequate Mg can reduce carb cravings.17
Magnesium may be the most important mineral from a stress perspective but others are important, too.
- Zinc is also critical to RNA transcription18 which means that adequate zinc is required for the generation of neurotransmitters. This makes it vital to the maintenance of optimistic, focused and clear frames of mind.19
- Adding zinc to the diet of Iranian students (Middle Eastern soils tend to be zinc depleted) helped them get better grades.20
- Zinc and manganese work together to help the body control excess copper.21 Since the 1920s it's been noticed that schizophrenics have elevated levels of copper in their bodies.22,23
- Zinc is critical to proper thyroid function; some researchers think there may be a relationship between the suboptimal zinc levels in the population and high rates of depression and chronic fatigue related to hypothyroid disease.24
- The part of the brain with the richest concentration of zinc is the hippocampus, the seat of memory and also an important regulator of the body's stress-response.25 When enough hippocampal neurons die we start forgetting things and either can't turn on or off our stress responses (depending on the individual.)26
- Because zinc is vital to digestion zinc deficiency can contribute to disorders of assimilation and immunity that set the stage for allergies and the emotional/cognitive disorders that result from allergic brain inflammation.27,28
These are just two of the trace minerals vital to mental and emotional health - others also play critical roles.
- Manganese is essential in trace amounts as an enzyme activator. It is also essential for nerve and brain function. It is required for the synthesis of two key neurotransmitters: acetylcholine (learning) and dopamine (motivation).
- Diabetics often have low manganese levels in their bodies.
- Adequate chromium is necessary for insulin to work. Insulin lowers blood sugar by pushing it into our cells. Brain cells are fueled almost exclusively by blood sugar.
- Insulin resistance is a diabetes-related condition in which cells and neurons stop responding to insulin. Diabetes can cause a heightened sensitivity to stress hormones,29 and "cerebral diabetes" has been suggested as one possible cause of behavioral disorders and emotional distress.30,31
So I'm convinced that it can be very difficult to obtain adequate amounts of trace minerals from modern diets because of the nutrient mining of soils.32,33,34 This is why I tell patients that no matter how organic or fresh the food they eat, they may not be getting adequate mineral intake unless the folks growing their food are spreading ground granite, mineral-enriched fertilizer or pot ash on their fields (and no newspapers with colored ink in that ash, please ... they contain toxic heavy metals.)
It's important to take special care in sourcing one's supplement. Most multivitamin and even most trace mineral supplements contain oxides, sulphates, sulfides or carbonates, forms that are not well absorbed in the gut.35,36
and B Vitamins
Another shift that occurred as we graduated from hunter-gatherers to settled farmers and herders, a shift that's also accelerated over the last 120 years, is a dramatic increase in carbohydrate consumption - largely grain and sugar. Grain foods require grinding and cooking. The first stone mortars, bowls and cup holes appeared 40-12,000 years ago.39 It appears that humans had little or no experience with widespread consumption of cereal grains before that time. In any event nomadic hunter-gatherers would rarely have been able to rely on cereal grains as year-round staples.37,38
In the late 19th century the invention of steel roller mills and automated sifting devices brought about another revolution.40 Until that time grain products were typically consumed with the B-vitamin rich germ, bran and outer shell intact. Now the outer bran could be removed, "refining" the grain. "Refined" foods became associated in the public mind with "refined" people. Consuming them became a status symbol even among those who couldn't afford them. (In much the same way sub-Saharan mothers were until recently being convinced to use baby formula - inherently less nourishing than their own breast milk, but associated with success ad modernity.)
Soon, along with widespread adoption of "refined" grain foods, a new disease appeared. It was especially prevalent in poor people with sedentary lifestyles and whose diets contained large quantities of refined grains. This disease, which ultimately came to be called dry beri-beri, typically appears with neurological symptoms such as irritability, difficulty in concentration, fatigue and depression.41 It was eventually shown to be caused by a deficiency of thiamin, vitamin B1.
Shortly thereafter another strange new disease appeared with skin lesions, gastrointestinal disturbances and mental symptoms remarkably similar to what would later be known as schizophrenia. This disease, termed pellagra, ultimately came to be linked with deficiencies of niacin, vitamin B3.42 Other B vitamins, all of which are milled out of refined grain products, were soon identified - deficiencies of which were linked to emotional disorders including, most frequently, depression.43,44,45 This makes sense. B vitamins are essential to the construction of neuronal cells walls46 and their protective myelin sheaths.47 They catalyze the enzymes that make neurons fire.48 They help create the enzymes that assemble neurotransmitters and disable them once they've done their jobs.49
Today over 85% of the cereals consumed in the US today are highly processed, refined grains.50,51 While some B vitamins are added back into some of these products in a process called fortification, the author's clinical experience has consistently been that almost all of my patients experience substantial improvements in their complaints when supplementing their diets with high-potency B vitamins.
Resupplying Bs can be a tricky process however, particularly in people who have never taken B supplements. If this describes you, please review the instructions here.
The most highly refined carbohydrate is, of course, sugar. Devoid of any mineral, fiber or vitamin content, refined sugar is another relatively recent contribution of the industrial revolution to our food supply.52 The amount of sugar consumed in England rose from a little under 15 lbs/person/year in 1815 to close to 120 lbs/person/year in 1970;53 in the U.S. it' s risen from 122 lbs/person/year in 1970 to 152 lbs/person/year in 2000.54
The routine consumption of refined carbohydrates like sugar forces the body to release insulin in response in surges of a frequency and size larger than would have been experienced by any creature in the pre-modern age. In at-risk individuals these insulin surges have a marked potential to produce stress-inducing changes in hormonal balance55,56,57 particularly in children.58,59 Sugar is highly addictive. The consumption of sugar produces surges in dopamine,60,61,62 the same "reward" neurotransmitter involved in addictions to cocaine, heroin, alcohol and amphetamine.63
As already noted, brain cells are dependent upon a steady supply of glucose in order to function. Insulin resistance is a condition that can develop in response to regular excessive sugar consumption, particularly when that consumption is combined with diets low in critical trace minerals and B vitamins. Insulin resistance contributes to the development of diabetes.
A wide variety of psychological disorders has been linked to altered glucose metabolism in the brain.64,65,66,67,68,69 While it's possible that the altered glucose metabolism results from the psychological disorder rather than the other way around, there is evidence suggesting that, at least in some people, chronic excess sugar consumption and associated insulin resistance can be the precipitating factor.70,71
Altered Essential Fatty Acid Ratios
Essential fatty acids (EFAs) are relatively short, highly reactive molecules essential to our health. Even though they're fats they have opposite chemical properties to the long-chain animal fats that most people think about first when they think about fat.
The most interesting EFAs are the omega-3 (w3) and omega-6 (w6) EFAs, so-named because they have double (unsaturated) carbon bonds 3 and 6 atoms from their respective ends. W3/W6 ratios play a vital role in mental health for a number of reasons.
- W3 EFAs are involved in the construction of neurotransmitter receptor sites, small structures on neuron call walls designed to bond with messenger molecules released when neurons want to chat.
- They' re also critical to second messenger systems. These special molecules carry signals from the receptor sites on cell walls to the nucleus. There they signal the DNA to begin making proteins. When cells want to do something they generally do it by making specialized proteins.
- W3/w6 ratios are important in another sense - w3s are the raw materials the body uses to make anti-inflammatory prostaglandins; w6s are used to make prostaglandins that cause inflammation.72
- Altered w3/w6 EFA ratios have been linked with depression,73,74 bipolar disorder,75 schizophrenia,76,77,78,79 impaired learning abilities80 and cognitive disorders.81
Historically humans consumed most of their EFAs in meat. Wild animals typically have a much higher protein to fat ratio than domesticated animals because they spend so much more of their time in motion. Large animals store more fat in their bodies than smaller ones82,83 but even so there would typically have been only a few months of the year when wild animals would have had substantial amounts of fatty deposits in their bodies. Our ancestors ate meat generally much leaner than the meat we eat today.84
The content of the fat in that meat has also changed. Range foods have high w3 levels; grains are higher in w6s. Wild animals eating naturally-occurring forage have a much more favorable w3/w6 ratio than modern feedlot fed cattle who subsist largely on a diet of grain.
This is yet another reason w3/w6 ratios are altered in modern diets: the widespread consumption of refined seed oils such as the corn, safflower, sunflower and cottonseed oils in salad dressings and fried foods. These oils are low in anti-inflammatory w3s and rich instead in w6s.85 W6s contribute to a tendency toward chronic inflammation, linked with the development of psychological distress.86,87 Diets high in w6s also contribute to the development of diabetes88 and therefore sugar-metabolism related emotional stress and cognitive disorders.
W3 essential fatty acids can be difficult to obtain from diet alone in the quantities required to optimize mental health because they are highly reactive and oxidize easily. The main supplemental sources are fish oils and flax seed oil. The problem with fish oil is the possibility of contamination with food-chain concentrated toxins, varying according to where the fish was obtained and how long its life (longer life=increased risk of toxic accumulations.) The problem with flax oil products is that the most common metal used to make fittings for commercial oil pressing and bottling equipment is brass. Brass oxidizes w3 molecules when they come into contact. W3s are then so reactive that the oxidation, once started, becomes a chain reaction. Before long an entire product made with brass fittings can be spoiled.89
This review touches on only some of the most important connections between modern diets and stress. Others issues include low anti-oxidant levels, allergic reactions caused by additives and/or compromised digestive processes as we age, the substantially reversed sodium/potassium ratios characteristic of modern diets when compared to ancient ones, higher acid content of processed foods and the bizarre world of industrially altered fats.
1. Cordain, L., Eaton, S.B., et al. 2005. Origins and evolution of the Western diet: health implications for the 21st century. American Journal of Clinical Nutrition. 81:341-354. Much of the early part of this webpage is condensed from this review, and many of the references are drawn from same.
2. Boaz, N.T. 2002. Evolving Health: the Origins of Illness and How the Modern World is Making us Sick. New York: Wiley & Sons, Inc.
3. Nesse, R.M, Williams, G.C. 1994. Why we get sick. The new science of Darwinian medicine. New York: Times Books.
4. Eaton S.B., Konner, M.J. 1985. Paleolithic nutrition. A consideration of its nature and current implications. New England Journal of Medicine. 312:283-289.
5. Eaton, S.B., Konner, M., Shostak, M. 1988. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. American Journal of Medicine. 84:739-49.
6. Underwood, E.J. 1977. Trace Elements in Human and Animal Nutrition. Fourth Edition. New York: Academic Press.
7. Robinson, D.L. et al. 1989. Management Practices to Overcome the Incidence of Grass Tetany. Journal of Animal Science. 67(12):3470-3484.
8. Starobrat-Hermelin B. 1998. The effect of deficiency of selected bioelements on hyperactivity in children with certain specified mental disorders. Annales Academiae Medicae Stetinensis. 44:297-314.
9. Kozielec T, Starobrat-Hermelin B. 1997. Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD). Magnesium Research. 10(2): 143.148.
10. Papadopol V, Tuchendria E, Palamaru I. 2001 Magnesium and some psychological features in two groups of pupils (magnesium and psychic features). Magnesium Research. 14(1-2): 27-32.
11. Durlach J. et al. 1997. Are age-related neurodegenerative diseases linked with various types of magnesium depletion? Magnesium Research. 10(4): 339-353.
12. Durlach, J. 1990 Magnesium depletion and pathogenesis of Alzheimer's disease. Magnesium Research. 3(3):217-8.
13. Passwater, R. 1983. Trace Elements, Hair Analysis and Nutrition. New Canaan: Keats. 64.
14. Seelig MS. 1994. Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review). Journal of the American College of Nutrition. 13(5): 426-429.
15. Venon, W.B. 1988. The role of magnesium in nucleic-acid and protein metabolism. Magnesium. 7(5-6): 234-248.
16. Abraham, G.E. 1983. Nutritional factors in the etiology of the premenstrual tension syndromes. Journal of Reproductive Medicine. 28(7): 446-464.
17. See also l-glutamine for this purpose.
18. Passwater, R. Ibid. 123-127.
19. Kanarek, R., and Marks-Kaufman, R. 1991. Nutrition and Behavior. New York: Van Nostrand Reinhold. 59.
20. Ronaghy, H.A. 1972. Chemical Engineering News. July 10.
21. Pfeiffer, C. 1974. Journal of Orthomolecular Psychiatry. 3(4):259-264.
22. Reiter, P. 1927. Z. Neur. 108:464-480.
23. English, W. 1929. American Journal of Psychiatry. 569-580.
24. Passwater, R. Ibid. 172.
25. Lombard, J. Ibid. 44-45.
26. Sapolsky, R. Why Zebras Don't Get Ulcers. 1998. New York: Freeman. 206-207.
27. Horrobin, D. 1980. Possible role of prostaglandin E1 in the affective disorders and in alcoholism. British Medical Journal. 280(6228): 1363-1366.
28. Philpott, W., Kalita, D. 2000. Brain Allergies: the Psychonutrient and Magnetic Connections. Chicago: Keats. 38.
29. Magarinos, A.M., McEwen, B.S. 2000. Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress. PNAS. 20:11056-11061.
30. Newman, J.C., Holden, R.J. 1993. The 'cerebral diabetes' paradigm for unipolar depression. Medical Hypotheses. 41(5):391-408.
31. McEwen, B.S., Magarinos, A.M., Reagan, L.P. 2002. Studies of hormone action in the hippocampal formation: possible relevance to depression and diabetes. Journal of Psychosomatic Research. 53(4):883-890.
32. Briefel, R. 2000. Zinc intake of the U.S. population: findings from the third National Health and Nutrition Examination Survey, 1988-1994. Journal of Nutrition. 130(5S Suppl):1367S-73S.
33. Marier JR. Magnesium content of the food supply in the modern-day world. Magnesium. 1986 5(1): 1-8.
34. Morgan KJ, Stampley GL. 1988. Dietary intake levels and food sources of magnesium and calcium for selected segments of the US population. Magnesium. 7(5-6): 225-233.
35. Firoz M, Graber M. 2001. Bioavailability of US commercial magnesium preparations. Magnesium Research. 14(4):257-62.
36. Lindberg, J.S. et al. 1990. Magnesium bioavailability from magnesium citrate and magnesium oxide. Journal of the American College of Nutrition. 9(1):48-55.
37. Keeley, L.H. 1992, The use of plant foods among hunter-gatherers: a crosscultural survey. In: Anderson, P.C., ed. Prehistoire de l'agriculture. Nouvelles approches experimentales et ethnographiques. (Prehistoric agriculture. New experimental approaches and ethnography.) Paris: National Center for Scientific Research,. 29-38.
38. Harlan, J.R. 1992. Wild grass seed harvesting and implications for domestication. In: Anderson, P.C, ed. Ibid. 21-27.
39. Wright, K. 1991. The origins and development of ground stone assemblages in Late Pleistocene Southwest Asia. Paleorient. 17: 9-45.
40. Storck, J., Teague, W.D. 1952. Flour for Man's Bread, a History of Milling. Minneapolis: University of Minnesota Press.
41. Kanarek, R., Marks-Kaufman, R. 1991. Nutrition and Behavior. New York: Van Nostrand Reinhold. 39.
42. Frostig, J.P., Spies, T.D. 1940. The initial syndrome of pellagra and associated deficiency diseases. American Journal of Medical Science. 199:268.
43. Lombard, J., Germano, C. 2000. The Brain Wellness Plan. New York: Kensington Books. 238-239.
44. Bell, I.R., et al. 1991. B complex vitamin patterns in geriatric and young adult inpatients with major depression. Journal of the American Geriatric Society. 39(3):252-257.
45. Parnetti, L. 1997. Role of homocysteine in age-related vascular and non-vascular diseases. Aging (Milano). 9(4):241-257.
46. Parkhomets, P.K., et al. 1995. Role of nicotinic acid and its derivatives in disorders of nervous system function. Ukrainskii Biokhimicheskii Zhurnal. 67(4):3-11.
47. Aaron, S. et al. 2005. Clinical and laboratory features and response to treatment in patients presenting with vitamin B12 deficiency-related neurological syndromes. Neurology India. 53(1):55-58.
48. Guse, A.H. 2004. Biochemistry, biology, and pharmacology of cyclic adenosine diphosphoribose (cADPR). Current Medical Chemistry. 11(7):847-855.
49. Gibson, G.E., Blass, J.P. 1985. Oxidative metabolism and acetylcholine synthesis during acetylpyridine treatment. Neurochemical Research. 10(4):453-467.
50. Gerrior S, Bente L. 2002. Nutrient content of the U.S. food supply, 1909-99: a summary report. Washington, DC: US Department of Agriculture, Center for Nutrition Policy and Promotion, (Home Economics report no. 55.)
51. US Department of Agriculture, Agricultural Research Service. 1997. Data tables: results from USDA's 1994-96 Continuing Survey of Food Intakes by Individuals and 1994-96 Diet and Health Knowledge Survey. ARS Food Surveys Research Group.
52. Galloway, J.H. 2000. Sugar. In: Kiple, K.F., Ornelas, K.C., eds. The Cambridge World History of Food. Vol 1. Cambridge: Cambridge University Press. 437-449.
53. Cleave, T.L. 1974. The saccharine disease. Bristol, United Kingdom: John Wright & Sons, Ltd. 6-27.
54. US Department of Agriculture, Economic Research Service. 2002. Food Consumption (per capita) data system, sugars/sweeteners. Internet: http:/www.ers.usda.gov/Data/foodconsumption/datasystem.asp
55. Genter, P., Ipp, E. 1994. Plasma glucose thresholds for counterregulation after an oral glucose load. Metabolism. 43(1):98-103.
56. Thayer, R.E. 1987. Energy, tiredness, and tension effects of a sugar snack versus moderate exercise. Journal of Personality and Social Psychology. 52(1):119-125.
57. Kirschbaum, C., et al. 1997. Effects of fasting and glucose load on free cortisol responses to stress and nicotine. The Journal of Clinical Endocrinology and Metabolism. 82(4):1101-1105.
58. Jones, T.W., et al. Enhanced adrenomedullary response and increased susceptibility to neuroglycopenia: mechanisms underlying the adverse effects of sugar ingestion in healthy children. The Journal of Pediatrics. 126(2):171-177.
59. Girardi, N.L., et al. 1995. Blunted catecholamine responses after glucose ingestion in children with attention deficit disorder. Pediatric Research. 38(4):539-542.
60. Smith, G.P. 2004. Accumbens dopamine mediates the rewarding effect of orosensory stimulation by sucrose. Appetite. 43(1):11-13.
61. Hajnal, A. et al. 2004. Oral sucrose stimulation increases accumbens dopamine in the rat. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 286(1):R31-37.
62. Rada, P., Avena, N.M., Hoebel, B.G. 2005. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 134(3):737-744.
63. Cannon, C.M., Bseikri, M.R. 2004. Is dopamine required for natural reward? Physiology and Behavior. 81(5):741-748.
64. Ketter, T.A., et al. 2001. Effects of mood and subtype on cerebral glucose metabolism in treatment-resistant bipolar disorder. Biological Psychiatry. 49(2):97-109.
65. Grandinetti, A., et al. 2000. Delineating the relationship between stress, depressive symptoms, and glucose intolerance. Diabetes Care. 23(8):1443-1444.
66. Videbech, P. 2000. PET measurements of brain glucose metabolism and blood flow in major depressive disorder: a critical review. Acta Psychiatrica Scandinavica. 101(1):11-20.
67. Delvenne, V., et al. 1997. Brain hypometabolism of glucose in bulimia nervosa. International Journal of Eating Disorders. 21(4):313-320.
68. Hurwitz, T.A., et al. 1990. Regional cerebral glucose metabolism in major depressive disorder. Canadian Journal of Psychiatry. 35(8):684-688.
69. Kishimoto, H., et al. 1987. 11C-glucose metabolism in manic and depressed patients. Psychiatry Research. 22(1):81-88.
70. Newman, J.A., et al. 1993. The "cerebral diabetes" paradigm for unipolar depression. Medical Hypotheses. 41(5):391-408.
71. Holden, R.J. 1995. Schizophrenia, suicide and the serotonin story. Medical Hypotheses. 44(5):379-391.
72. Calder, P.C. 1997. N-3 polyunsaturated fatty acids and cytokine production in health and disease. Annals of Nutrition and Metabolism. 41(4):203-234.
73. Colin, A., et al. 2003. Lipids, depression and suicide. Encephale. 29(Pt 1):49-58.
74. Hibbeln, J.R. 2002. Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis. Journal of Affective Disorders. 69(1-3):15-29.
75. Kidd, P.M. 2004. Bipolar disorder and cell membrane dysfunction. Progress toward integrative management. Alternative Medicine Review. 9(2):107-135.
76. Richardson, A.J., et al. 2003. Omega-3 and omega-6 fatty acid concentrations in red blood cell membranes relate to schizotypal traits in healthy adults. Prostaglandins, Leukotrienes and Essential Fatty Acids. 69(6):461-466.
77. Emsley, R. et al. 2003. Clinical potential of omega-3 fatty acids in the treatment of schizophrenia. CNS Drugs. 17(15):1081-1091.
78. Peet, M. 2003. Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins, Leukotrienes and Essential Fatty Acids. 69(6):477-485.
79. Ross, B.M. 2003. Phospholipid and eicosanoid signaling disturbances in schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids. 69(6):407-412.
80. Alessandri, J.M., et al. 2004. Polyunsaturated fatty acids in the central nervous system: evolution of concepts and nutritional implications throughout life. Reproduction, Nutrition, Development. 44(6):509-538.
81. Doyle, M., Egan, J. 2001. The impact of the supply of glucose to the brain on mood and memory. Nutrition Reviews. 59(1):S20-21.
82. Cordain, L., et al. 2002. The paradoxical nature of hunter-gatherer diets: meat based, yet non-atherogenic. European Journal of Clinical Nutrition. 56(suppl):S42-52.
83. Pitts, C.G., Bullard, T.R. 1968. Some interspecific aspects of body composition in mammals. In: Body Composition in Animals and Man. Washington, DC: National Academy of Sciences. 45-70. (Publication 1598.)
84. Shackleton, C.M., Granger, J.E. 1989. Bone marrow fat index and kidney-fat of several antelope species from Transkei. South African Journal of Wildlife Research. 19:129-34.
85. Bourre, J.M. 2004. Roles of unsaturated fatty acids (especially omega-3 fatty acids) in the brain at various ages and during ageing. Journal of Nutrition in Health Aging. 8:163-174.
86. Sobczak, S., et al. 2004. Lower high-density lipoprotein cholestrol and increased omega-6 polyunsaturated fatty acids in first-degree relatives of bipolar patients. Psychological Medicine 34(1):103-112.
87. Colin, A., et al. 2003. Lipids, depression and suicide. Encaphale 29(Pt 1):49-58.
88. Challem, J. 2000. Syndrome X. New York: Wiley & Sons. 72.
89. Erasmus, Udo. 1993. Fats that Heal, Fats that Kill. British Columbia:Burnaby:Alive Books.