At the risk of sounding reductionist, there does appear to be an insufficient intake of magnesium by most Americans. The latest data indicates that 68% of Americans do not consume the recommended daily intake of magnesium (420 mg per day) and 19% of Americans do not consume even half the government’s recommended daily intake of magnesium.
Would a serious whole-food varied-plant diet provide adequate magnesium? Maybe. But thinking of by-gone millennia in which greens were the food of choice (and spring water/ rain water the only beverage) does raise some doubts. As an example, consider spinach and oat bran, both considered good sources of magnesium.
A dose of 30 grams (one cup) of spinach minus the 27.4 grams of water content has 23.7 mg of magnesium; 96 grams of oats (one and a half cups) minus 2 grams of water has 96 mg of magnesium. But on a per calorie basis spinach has 3.4 mg magnesium compared to 0.45 mg for oats. On a per dry weight comparison spinach has 3.4 mg/g of magnesium compared to 1.7 mg/g for oats. That’s more than five times the magnesium content in spinach compared to oats.
Magnesium, one of the most essential minerals in the human body, is a co-factor in more than 600 known enzymatic reactions. Magnesium is widely connected with brain biochemistry and, as a result, a deficiency is associated with a variety of neuromuscular and psychiatric symptoms such as depression, psychosis, agitation and irritability, headaches, seizures, muscular weakness, anxiety, insomnia, fatigue, confusion and cognitive changes; this is reversible with restoration of sufficient magnesium levels.
The diets of those clinically depressed is correlated with low intake of magnesium; research indicates an inverse relationship between dietary magnesium content and depressive symptoms. Suicidal depression particularly appears to be related to magnesium insufficiency; for example, data indicate that magnesium concentration in cerebrospinal fluid was low in patients with history of suicidal behavior.
The take-home here is to eat your greens. A magnesium level may be useful as an initial clinical workup for psychiatric symptoms. If your magnesium level is verified to be low and there are accompanying psychiatric symptoms, your provider may choose to add a supplement of 600 – 800 mg per day of any of the various forms of magnesium available (except magnesium oxide, which is not bioavailable).
 King, D. E., Mainous, A. G., Geesey, M. E., & Woolson, R. F. (2005). Dietary Magnesium and C-reactive Protein Levels. Journal of the American College of Nutrition, 24(3), 166-171. doi:10.1080/ 07315724. 2005.10719461.
 Kantak, K. M. (1988). Magnesium deficiency alters aggressive behavior and catecholamine function. Behavioral Neuroscience, 102(2), 304-311. doi:10.1037//0735-7044.102.2.304.
 Papadopol V, Tuchendria E, Palamaru I: Magnesium and some psychological features in two groups of pupils (magnesium and psychic features) (2001). Magnes Res, 14, 27–32.
 Jacka, F. N., Overland, S., Stewart, R., Tell, G. S., Bjelland, I., & Mykletun, A. (2009). Association between magnesium intake and depression and anxiety in community-dwelling adults: The Hordaland Health Study. Australian and New Zealand Journal of Psychiatry, 43(1), 45-52. doi:10.1080/00048670802534408.
 Banki, C. M., Arató, M., & Kilts, C. D. (1986). Aminergic Studies and Cerebrospinal Fluid Cations in Suicide. Ann NY Acad Sci Annals of the New York Academy of Sciences, 487(1 Psychobiology), 221-230. doi:10.1111/j.1749-6632.1986.tb27901.x.
 Banki, C. M., Vojnik, M., Papp, Z., Balla, K. Z., & Arató, M. (1985). Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. Biological Psychiatry, 20(2), 163-171. doi:10.1016/0006-3223(85)90076-9.
My latest book live today on Amazon, Neurodietetics – food for flourishing. How to prevent and reverse mental disorders. Latest etiologic explanations for cognitive, emotional, and behavioral disorders and their relation to phytonutrition. Beyond happy to eudemonia!
According to ancient Greek mythology, Hermes and his friend Krokos were horse-playing and Hermes accidentally killed Krokos through a head injury, with three blood drops from his head falling on the top of a flower, creating three stigmata and naming this plant thereafter Krokos (Crocus). Thus the ancient and godly identification of this plant and saffron.
Saffron is the dried stigma (the top part in the center of a flower which receives the pollen and on which germination takes place) of the blue-purple flower Crocus sativus L., and it has a long history of use as a spice, coloring agent, and medicine. Due to how saffron is grown and harvested, saffron is considered one of the world’s most expensive spices (upwards of $11,000 per kg, requiring 450,000 hand-picked stigmas). Apart from its traditional value as a spice and coloring agent (originally for the Persian carpet industry), saffron has a long history of medicinal use spanning over 2,500 years.
This use of saffron in traditional medicine included for cramps, asthma, menstruation disorders, liver disease, and painful dysmenorrhoea, among many other uses. Evidence from recent in vitro and in vivo research indicates that saffron has potential anti-carcinogenic, anti-mutagenic, antioxidant, and memory-enhancing properties .
Administration of saffron 30 mg/day (15 mg twice daily) was found to be as effective as a leading medication for mild to moderate Alzheimer’s disease (donepezil) in a placebo-controlled double bind for treatment in subjects of 55 years and older but with a better side effect profile. Although there are a growing number of non-human animal studies and theories why saffron could be neuroprotective for Alzheimer’s Disease and other neurodegenerative conditions, clinical studies are too few to make any tentative conclusions to date.
In two randomized, double-blind, placebo-controlled trials, saffron was effective for the treatment of mild to-moderate depression .
A systematic review of randomized control trials examining the effectiveness of saffron in mood disorders revealed a statistically significant effect on improved mood on subjects clinically diagnosed with depression; the dosing was typically 30 mg/ day.
In clinical studies, the use of saffron extract at doses of 20–30 mg/day twice daily for the treatment of mild to moderate depression has been compared with currently marketed antidepressants such as fluoxetine (20 mg/day twice daily) and imipramine (100 mg/day three times daily). So these comparative evaluations revealed that saffron was equally effective as chemically synthesized marketed pharmaceutics, in mild or moderate depression without causing the typical side effects of the artificial preparations.
Saffron may act in a manner similar to antidepressants to improve mood by inhibiting serotonin reuptake or there could be multiple pathways involving, for example, its antioxidant, anti-inflammatory properties.
Saffron contains in excess of 150 volatile and aroma-yielding compounds and many non-volatile active components, many of which are carotenoids . Safranal is the compound primarily responsible for saffron’s aroma. Safranal has shown to have anti-convulsant and anxiolytic effects as well as antidepressant properties
Premenstrual Syndrome (PMS)
One randomized controlled trial examined the effects of saffron supplementation on premenstrual syndrome. It was found that found that women with regular menstrual cycles experiencing premenstrual syndrome who took 30 mg/d of saffron supplementation for eight weeks reported relief in premenstrual symptoms and depression levels compared to placebo. Remarkably, just the aroma alone – without otherwise any oral intake of saffron was itself found effective in relief of PMS symptoms in another placebo controlled double blind study, indicating effectiveness at very small does and the likely active component being Safranal.
 Koulakiotis, N., Pittenauer, E., Halabalaki, M., Skaltsounis, L., Allmaier, G., & Tsarbopoulos, A. (2011). Isolation and Tandem Mass Spectometric Characterization of Selected Crocus sativus L. (Saffron) Bioactive Compounds.Planta Med Planta Medica, 77(12). doi:10.1055/s-0031-1282560
 Gohari, A., Saeidnia, S., & Mahmoodabadi, M. (2013). An overview on saffron, phytochemicals, and medicinal properties. Pharmacognosy Reviews Phcog Rev,7(1), 61. doi:10.4103/0973-7847.112850
 Srivastava, R., Ahmed, H., Dixit, R., D., & Saraf, S. (2010). Crocus sativus L.: A comprehensive review. Pharmacognosy Reviews, 4(8), 200. doi:10.4103/0973-7847.70919
 Kianbakht, S., & Ghazavi, A. (2011). Immunomodulatory Effects of Saffron: A Randomized Double-Blind Placebo-Controlled Clinical Trial. Phytother. Res. Phytotherapy Research, 25(12), 1801-1805. doi:10.1002/ptr.3484
 Abdullaev, F., & Espinosa-Aguirre, J. (2004). Biomedical properties of saffron and its potential use in cancer therapy and chemoprevention trials. Cancer Detection and Prevention, 28(6), 426-432. doi:10.1016/j.cdp.2004.09.002
 Bathaie, S. Z., & Mousavi, S. Z. (2010). New Applications and Mechanisms of Action of Saffron and its Important Ingredients. Critical Reviews in Food Science and Nutrition, 50(8), 761-786. doi:10.1080/10408390902773003
 Akhondzadeh, S., Sabet, M. S., Harirchian, M. H., Togha, M., Cheraghmakani, H., Razeghi, S., . . . Moradi, A. (2010). ORIGINAL ARTICLE: Saffron in the treatment of patients with mild to moderate Alzheimer’s disease: A 16-week, randomized and placebo-controlled trial. Journal of Clinical Pharmacy and Therapeutics, 35(5), 581-588. doi:10.1111/j.1365-2710.2009.01133.x
 Akhondzadeh, S., Tahmacebi-Pour, N., Noorbala, A., Amini, H., Fallah-Pour, H., Jamshidi, A., & Khani, M. (2005). Crocus sativus L. in the treatment of mild to moderate depression: A double-blind, randomized and placebo-controlled trial.Phytother. Res. Phytotherapy Research, 19(2), 148-151. doi:10.1002/ptr.1647
 Moshiri, E., Basti, A. A., Noorbala, A., Jamshidi, A., Abbasi, S. H., & Akhondzadeh, S. (2006). Crocus sativus L. (petal) in the treatment of mild-to-moderate depression: A double-blind, randomized and placebo-controlled trial.Phytomedicine, 13(9-10), 607-611. doi:10.1016/j.phymed.2006.08.006
 Hausenblas, H. A., Heekin, K., Mutchie, H. L., & Anton, S. (2015). A systematic review of randomized controlled trials examining the effectiveness of saffron (Crocus sativus L.) on psychological and behavioral outcomes. Journal of Integrative Medicine, 13(4), 231-240. doi:10.1016/s2095-4964(15)60176-5
 Noorbala, A., Akhondzadeh, S., Tahmacebi-Pour, N., & Jamshidi, A. (2005). Hydro-alcoholic extract of Crocus sativus L. versus fluoxetine in the treatment of mild to moderate depression: A double-blind, randomized pilot trial. Journal of Ethnopharmacology, 97(2), 281-284. doi:10.1016/j.jep.2004.11.004
 Akhondzadeh, S., Fallah-Pour, H., Afkham, K., Jamshidi, A., & Khalighi-Cigaroudi, F. (2004). Comparison of Crocus sativus L. and imipramine in the treatment of mild to moderate depression: A pilot double-blind randomized trial [ISRCTN45683816]. BMC Complementary and Alternative Medicine BMC Complement Altern Med, 4(1). doi:10.1186/1472-6882-4-12
 Hausenblas, H. A., Saha, D., Dubyak, P. J., & Anton, S. D. (2013). Saffron (Crocus sativus L.) and major depressive disorder: A meta-analysis of randomized clinical trials. Journal of Integrative Medicine, 11(6), 377-383. doi:10.3736/jintegrmed2013056
 Sampathu, S. R., Shivashankar, S., Lewis, Y. S., & Wood, A. B. (1984). Saffron ( Crocus Sativus Linn.) — Cultivation, processing, chemistry and standardization.C R C Critical Reviews in Food Science and Nutrition, 20(2), 123-157. doi:10.1080/10408398409527386
 Hosseinzadeh, H., & Talebzadeh, F. (2005). Anticonvulsant evaluation of safranal and crocin from Crocus sativus in mice. Fitoterapia, 76(7-8), 722-724. doi:10.1016/j.fitote.2005.07.008
 Hosseinzadeh, H., Karimi, G., & Niapoor, M. (2004). Antidepressant Effect Of Crocus Sativus L. Stigma Extracts And Their Constituents, Crocin And Safranal, In Mice. Acta Hortic. Acta Horticulturae, (650), 435-445. doi:10.17660/actahortic.2004.650.54
 Agha-Hosseini, M., Kashani, L., Aleyaseen, A., Ghoreishi, A., Rahmanpour, H., Zarrinara, A., & Akhondzadeh, S. (2008). Crocus sativus L. (saffron) in the treatment of premenstrual syndrome: A double-blind, randomised and placebo-controlled trial. BJOG: Int J O & G BJOG: An International Journal of Obstetrics and Gynaecology, 115(4), 515-519. doi:10.1111/j.1471-0528.2007.01652.x
 Fukui, H., Toyoshima, K., & Komaki, R. (2011). Psychological and neuroendocrinological effects of odor of saffron (Crocus sativus).Phytomedicine, 18(8-9), 726-730. doi:10.1016/j.phymed.2010.11.013
The fourth vitamin to be discovered, vitamin D, is technically not a vitamin as one’s body can produce it – it just requires sunlight. No one is suggesting that sunlight is a vitamin per se. And only a relatively short span of radiation from the sun is involved, the so-called UVB of the ultraviolet spectrum. The intensity of UVB available depends on the weather, season, location on earth, and time of day; in the United States it maximizes between 10 am and 4 pm between April and October.
With moderate direct exposure to the summer sun (say 5 – 30 minutes twice a week), the body will make 10,000 to 20,000 IU. Sunscreen can effectively block UVB absorption; for an individual with frequent sun exposure (greater than twice per week), it might be prudent to place sunscreen after the first 10 – 15 minutes of sun exposure to avoid skin cancer but allow vitamin D production. As our bodies can store vitamin D, it is thought that sufficient exposure during spring, summer, and early fall should be sufficient to provide needed vitamin D during the winter months.
So this is another recent modification in our evolution – to stay indoors a lot more than our ancestors, decreasing our vitamin D production. The National Academies Institute of Medicine has no guidelines for vitamin D through sun exposure; they do have RDA but it is based on food intake.
The reaction of cholesterol (in the form of 7-dehydrocholesterol) in the skin with sunlight actually produces several fat-soluble related compounds, the most important being cholecalciferol, vitamin D3, and ergocalciferol, vitamin D2. The term “vitamin D” includes both of these compounds.
Very few foods in nature contain vitamin D, although some food products have vitamin D as an additive. To manufacture vitamin D industrially, 7-dehydrocholesterol, a substance typically obtained from fish liver,or lanolin extracted from shorn sheep wool, is exposed to UVB light, producing vitamin D3. Vitamin D cannot be manufactured directly; it requires the photochemical process.
To become biologically active, vitamin D has to undergo two transformative reactions, one in the liver, then another in the kidney.
Vitamin D deficiency to the extent of causing rickets or osteomalacia is rare in the developed world but what we might call vitamin-D insufficiency, a lower than ideal biologically active form of vitamin D, appears to be quite common, particularly in the elderly.
Vitamin D toxicity is also rare. There is a feedback loop associated with vitamin D production in the skin that lowers its production as adequate amounts are reached. This natural regulatory mechanism doesn’t apply to supplementation but for daily supplemental intake of 2,000 IU (about 50 micrograms) per day, there is very little risk of toxicity.
As vitamin D is fat soluble, it requires the presence of fat for absorption; some supplements encapsulate cholecalciferol, vitamin D3, with fat; otherwise often it is recommended to take with a meal containing some degree of fat.
We have learned relatively recently that vitamin D has a lot larger effect on the body than just calcium absorption; for example, it has to do with modulation of cell growth, neuromuscular and immune function, and reduction of inflammation. And mood states.
Vitamin D and psychiatric disorders
Vitamin D acts on receptors in a variety of regions in the brain such as the prefrontal cortex, hippocampus, cingulate gyrus, thalamus, hypothalamus, and substantia nigra and as such can influence neurochemistry cognition, emotion, and behavior. Vitamin D deficiency in early life affects neuronal differentiation, and brain structure and function and appears to have some influence on disorders with a developmental basis, such as autistic spectrum disorder and schizophrenia ontogeny and brain structure and function.
The initial suggestion that vitamin D may be linked to clinical depression was based on the relation between low vitamin D and high prevalence of seasonal affective disorder (now considered to be a depressive disorder with seasonal pattern) in winter at high latitudes. One treatment modality for clinical depression with seasonal pattern is light therapy, although no ultra-violet light is used. Vitamin D insufficiency is not considered to be directly causative for this disorder.
However, vitamin D concentrations have been shown to be low in many patients suffering from mood disorders and have been associated with poor cognitive function . For example, data from the third National Health and Nutrition Examination Survey were used to assess association between serum vitamin D and depression in 7,970 residents of the United States. In that study, the likelihood of having depression in persons with vitamin D deficiency was found to be significantly higher compared to those with vitamin D sufficiency.
One thorough systematic review and meta-analysis of observational studies and randomized controlled trials was conducted and found that vitamin D insufficiency was strongly associated with clinical depression. Another systematic review and meta-analysis showed a statistically significant improvement in depression with Vitamin D supplements.
Use of vitamin D as adjunctive therapy, i.e. together with an antidepressant medication in patients with vitamin D insufficiency has shown to be superior to an antidepressant alone
What to do
This is another situation where recent changes in human lifestyle – here being indoors more than outdoors, can lead to a nutrient deficiency. Because it is so common to have a vitamin D insufficiency and the health consequences, specifically mood states, I recommend more time in the outdoors, including some limited time (say 10 minutes a day) with face and arms without sunscreen.
If you do not spend regular time in the sun, I do recommend a vitamin D3 supplement to be taken before, during, or directly after a meal. I think it wise to take these supplements during the winter months in any case.
Should you question whether or not you may be clinically depressed, professional assessment certainly is recommended as always; initial workup may include serum vitamin D levels (usually 25(OH)D is measured but various labs use different techniques resulting in varying “normal” level ranges).
A strict ethical vegan, however, faces a dilemma as the sources of vitamin D3 supplementation (and all “fortified products such as almond milk and tofu) are animal-based. Some literature supports vitamin D2 intake as sufficient, but good studies are too scarce to suggest this as the sole source for supplementation; vitamin D2 can be obtained from certain mushrooms set out in the sun for 10 minutes or so prior to consumption and there are supplements available from this source. It would appear that lifestyle emphasis on “fun in the sun” is indicated for vegans.
 Takeuchi A, Okano T, Sayamoto M, Sawamura S, Kobayashi T, Motosugi M, Yamakawa T; Okano; Sayamoto; Sawamura; Kobayashi; Motosugi; Yamakawa (1986). “Tissue distribution of 7-dehydrocholesterol, vitamin D3 and 25-hydroxyvitamin D3 in several species of fishes”. Journal of nutritional science and vitaminology. 32 (1): 13–22.
 Ross, A. C., Manson, J. E., Abrams, S. A., Aloia, J. F., Brannon, P. M., Clinton, S. K., . . . Shapses, S. A. (2011). The 2011 Dietary Reference Intakes for Calcium and Vitamin D: What Dietetics Practitioners Need to Know⁎⁎This article is a summary of the Institute of Medicine report entitled Dietary Reference Intakes for Calcium and Vitamin D (available at http://www.iom.edu/Reports/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D.aspx) for dietetics practitioners; a similar summary for clinicians has also been published (Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, Durazo-Arvizu RA, Gallagher JC, Gallo RL, Jones G, Kovacs CS, Mayne ST, Rosen CJ, Shapses SA. The 2011 report on Dietary Reference Intakes for calcium and vitamin D from the Institute of Medicine: What clinicians need to know. J Clin Endocrinol Metab. 2011;96:53-58).Journal of the American Dietetic Association, 111(4), 524-527. doi:10.1016/j.jada.2011.01.004
 DRI – Dietary Reference Intakes – Calcium and Vitamin D20122 DRI – Dietary Reference Intakes – Calcium and Vitamin D . Institute of Medicine of the National Academies, , ISBN: 13‐978‐0‐309‐16394‐1. (2012). Nutrition & Food Science, 42(2), 131-131. doi:10.1108/nfs.2012.42.2.131.2
 Yue, W., Xiang, L., Zhang, Y., Ji, Y., & Li, X. (2014). Association of Serum 25-Hydroxyvitamin D with Symptoms of Depression After 6 Months in Stroke Patients. Neurochem Res Neurochemical Research, 39(11), 2218-2224. doi:10.1007/s11064-014-1423-y
 Eyles, D. W., Burne, T. H., & Mcgrath, J. J. (2013). Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease. Frontiers in Neuroendocrinology, 34(1), 47-64. doi:10.1016/j.yfrne.2012.07.001
 Gabbard, Glen O. Treatment of Psychiatric Disorders. 2 (3rd ed.). Washington, DC: American Psychiatric Publishing. p. 1296.
 Stumpf WE, Privette TH: Light, vitamin D and psychiatry. Role of 1,25 dihydroxyvitamin D3 (soltriol) in etiology and therapy of seasonal affective disorder and other mental processes. Psychopharmacology (Berl) 1989, 97:285–294.
 Wilkins, C. H., Sheline, Y. I., Roe, C. M., Birge, S. J., & Morris, J. C. (2006). Vitamin D Deficiency Is Associated With Low Mood and Worse Cognitive Performance in Older Adults. The American Journal of Geriatric Psychiatry, 14(12), 1032-1040. doi:10.1097/01.jgp.0000240986.74642.7c
 Przybelski, R. J., & Binkley, N. C. (2007). Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Archives of Biochemistry and Biophysics, 460(2), 202-205. doi:10.1016/j.abb.2006.12.018
 Ganji, V., Milone, C., Cody, M. M., Mccarty, F., & Wang, Y. T. (2010). Serum vitamin D concentrations are related to depression in young adult US population: The Third National Health and Nutrition Examination Survey. Int Arch Med International Archives of Medicine, 3(1), 29. doi:10.1186/1755-7682-3-29
 Anglin, R. E., Samaan, Z., Walter, S. D., & Mcdonald, S. D. (2013). Vitamin D deficiency and depression in adults: Systematic review and meta-analysis. The British Journal of Psychiatry, 202(2), 100-107. doi:10.1192/bjp.bp.111.106666
 Spedding, S. (2014). Vitamin D and Depression: A Systematic Review and Meta-Analysis Comparing Studies with and without Biological Flaws. Nutrients, 6(4), 1501-1518. doi:10.3390/nu6041501
 Khoraminya, N., Tehrani-Doost, M., Jazayeri, S., Hosseini, A., & Djazayery, A. (2012). Therapeutic effects of vitamin D as adjunctive therapy to fluoxetine in patients with major depressive disorder. Australian & New Zealand Journal of Psychiatry, 47(3), 271-275. doi:10.1177/0004867412465022
Perhaps the first plant nutraceutic modified slightly to become a large commercial success was salicylic acid, found in particularly high amounts in the inner lining of white willow tree bark and central to defense mechanisms in plants against pathogen attack and environmental stress. It is the principal metabolite of the medication aspirin, which works through a completely different pathway in humans to affect an anti-inflammatory and antipyretic response. However, dosing in isolated concentrated form resulted in severe gastrointestinal distress, so that a buffered form was developed – and patented – in 1900 as Aspirin (acetylsalicylic acid) by Bayer. This approach to acquiring medicinal benefits from salicylic acid is still flawed by the fact that there is an increased risk of bleeding even for low-dose therapy. About one in ten people on chronic low-dose aspirin develop stomach or intestinal ulcers, which can perforate the gut and cause life-threatening bleeding.
There is a better way to take advantage of the healing properties of salicylic acid: eating plants. All plants contain salicylic acid and vegetarians have as much in their blood as omnivores who take aspirin supplements – but without the risk. Apparently this has been known empirically since the third millennium BC.
This is another recurring theme: plant-based diets can obviate the need for many supplements and prescribed medications. Plant-based diets are anti-inflammatory not only because of salicylic acid but because of their many other anti-inflammatory phytonutrients that help prevent the body from overproducing inflammatory compounds. Of course plant-based diets minimize one’s intake of inflammatory precursors present in meat and dairy products in the first place. More on that later.
Just to review, this amazing substance, salicylic acid, the active metabolite of aspirin and a plant hormone, plays a central role in the immune system of plants by activating the production of pathogen-fighting proteins. It can transmit the distress signal throughout the plant and even to neighboring plants. But the amazing fact is its crossover and apparent inverse role that it has in humans: it reduces the immune response, i.e. serves as an anti-inflammatory. This has an important role then in chronic inflammatory states such as cardio- and cerebrovascular disease, stroke, arthritis, even certain cancers. Recently, mental disorders have been linked to chronic inflammatory states and aspirin is finding a use for disorders ranging from mood disorders to schizophrenia.
So this remarkable agent helps prevent disease in both plants and animals but by completely different mechanisms.
 Interestingly, Aspirin ® and Heroin ® were once trademarks belonging to Bayer. After Germany lost World War I, Bayer was forced to give up both trademarks as part of the Treaty of Versailles in 1919.
 Yeomans, N., Lanas, A., Talley, N., Thomson, A., Daneshjoo, R., Eriksson, B., . . . Hawkey, C. (2005). Prevalence and incidence of gastroduodenal ulcers during treatment with vascular protective doses of aspirin. Aliment Pharmacol Ther Alimentary Pharmacology and Therapeutics, 22(9), 795-801.
 Paterson, J., Baxter, G., Dreyer, J., Halket, J., Flynn, R., & Lawrence, J. (2008). Salicylic Acid sans Aspirin in Animals and Man: Persistence in Fasting and Biosynthesis from Benzoic Acid. Journal of Agricultural and Food Chemistry J. Agric. Food Chem., 56(24), 11648-11652.
 Pieterse, C., Van Der Does, C., Zamioudis, C., Leon-Reyes, A., & Van Wees, S. (2012). Hormonal modulation of plant immunity. Annu Rev Cell Dev Biol.
 Taiz, L., & Zeiger, E. (2002). Plant physiology (3rd ed., p. 306). New York: W.H. Freeman
 Berk, M., Dean, O., Drexhage, H., McNeil, J. J., Moylan, S., O’Neil, A., … Maes, M. (2013). Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness. BMC Medicine, 11, 74. doi:10.1186/1741-7015-11-74
Ayorech, Z., Tracy, D., Baumeister, D., & Giaroli, G. (2015). Taking the fuel out of the fire: Evidence for the use of anti-inflammatory agents in the treatment of bipolar disorders. Journal of Affective Disorders, 174, 467-478.
 Keller, W., Kum, L., Wehring, H., Koola, M., Buchanan, R., & Kelly, D. (2012). A review of anti-inflammatory agents for symptoms of schizophrenia. Journal of Psychopharmacology (Oxford, England), 27(4), 337-342.