Food and Feelings: Nutrition and Mental Health
Download all this issues at our Academy site. [wlm_private “NPT Basic|3 Year Subscription|Standard Membership|Staff|NPT Premium|Standard Monthly”] Members get your downloads for free by clicking HERE. [/wlm_private]
Not all that long ago, the conventional wisdom was that nutrition had little to do with mental illness.
Folks spending too much money in the vitamin aisle or eating organic were health nuts. Teachers and parents who swore they saw candy producing hyperactivity in their kids had only their day-to-day experience—anecdotal evidence—to back them up. Careful research couldn't find any link.
The conventional wisdom dismissed other nutritional approaches to behavior as well. Doctors counseling allergy treatment for ADHD were quacks. Others suggesting nutrient doses wildly in excess of daily value (DV) levels for some pathologies were ridiculed.
Not any more.
By now we've had a good ten years of peer-reviewed work by a new generation documenting relationships between nutrition and mental health. This should not surprise us. In history we have the example of pellagra, a deficiency of vitamin B3 caused by diets heavy in corn. Pellagra's early symptoms include aggressiveness, confusion, insomnia and hypersensitivity.
It's not just decades of anecdotal evidence generated by parents and teachers. A nutrition/mental link makes logical sense. The brain is only 2% of the body's weight yet it consumes 20% of the body's energy.
Because of the brain's high metabolic rate, it makes intuitive sense that any prolonged interruption to the supply of crucial nutrients to the body could manifest early on in cognitive or emotional symptoms. The brain is the body's "canary in the coal mine" nutritionally.
This review highlights new research supporting relationships between nutritional and mental health.
The inflammation is hard to pin down in the lab because it can have many causes and many faces. Mineral deficiencies, omega-3/6 imbalances, diets poor in antioxidants or too high in sugar, allergies, stress—all these can create inflammation.
Think of the brain as a billion tiny soap bubbles: very energetic, complex bubbles, but essentially a globe of cytoplasm and organelles in a thin, bulging membrane. Now blow in a small handful of fine river silt.
The bubbles weaken. Some of them pop. That's close to the effect that chronic low-grade inflammation has on our brains. Cell membranes are degraded. Energy generation suffers. Communication snags. This inflammatory chaos can emerge as anxiety, depression and other behavioral disorders.
Nutrition is no panacea. But today, highly industrialized diets of restaurant and packaged food are generally not well balanced by vegetables, greens, or any food that doesn't come wrapped in paper or plastic. Well-designed (and individualized) nutrition programs may be key to achieving optimal growth and healing in individuals dependent on such diets when they present with psychopathology.
Let's look at a few of these pro-inflammatory factors.
Before the mid-20th century, farmland would often flood. Flooding replenishes farmed soil with mineral-rich waters washing down from granite-rich mountains. That's why the best farmland is always down by the river.
In the early 20th century, dams, reservoirs and other flood control measures were put in place to protect farmers. This ended the replenishing flow of mineral-rich flood water into farmed soil. For over 50 years, minerals in harvested crops have been mined from the topsoil. No regular flooding restores them.
So each year, mineral content of such farmed food diminishes a bit. That bit adds up over time.
Many people, sensing this, take multiminerals. Unfortunately the oxides and sulfate compounds found in many multimineral products don't assimilate well, particularly in the middle aged and older. Few mineral products do the job right: 100% Daily Value (DV) levels and fully chelated.
Magnesium is essential for the relaxation of muscle and nerve tissue. It's also an anti-inflammatory (antioxidant) mineral, along with zinc, and crucial for wound repair. It protects nerves while it's "cooling" and calming them.
Sixty percent of cases of clinical depression are considered to be treatment-resistant depression (TRD). Magnesium deficiency damages neurotransmitter receptors. This impairs normal nerve function, which may appear to humans as major depression. Oral administration of magnesium to animals led to anti-depressant-like effects that were comparable to those of strong anti-depressant drugs.
Magnesium halved the sleep onset time in alcoholics in withdrawal. It was found to approximate the effect of lithium in half of rapid cycling bipolar affective disorder patients. Deficiency may even be involved in the involuntary obscenity of Tourette's.
Essential Fatty Acids
Essential fatty acids (EFAs) are essential to the brain's "wiring". The body sends signals from nerve to nerve by making special molecules called neurotransmitters.
Neurotransmitters are released from one neuron and bind with receptors on the next, where new molecules (second messengers) are generated to carry the signal from the receptors to the neuron's nucleus. The nucleus responds by sending the signal on to the next neuron, and on and on.
Both the receptors and the second messengers are made from omega 3 EFAs. The brain can't think, feel or act without plenty of EFAs.
EFAs also are turned into signaling molecules for the immune system. Omega 6 EFAs turn the immune system up and omega 3s turn it down. The immune system uses inflammation to digest damaged tissue and destroy microbial invaders. It can be tricky to tell the difference between tissue that needs to be destroyed by inflammation and tissue that should be spared. When the body gets even a little too aggressive in this area, chronic low-grade inflammation results. This chronic low-grade inflammation is now understood to underlie many chronic diseases of aging: cardiovascular disease, cognitive decline, chronic pain and even dementia.
Omega 3s calm all this down; omega 6s turn it up, activating inflammation.
Green vegetables are rich in omega 3s, grains in omega 6s. The massive shift in modern diets away from vegetables and toward convenience foods that are heavy on grains is one pro-inflammatory change. Grass is rich in omega 3s, corn in omega 6s. The historic shift from grass-fed toward grain-fed beef has been another pro-inflammatory move.
This inflammation attacks the brain. The brain's high metabolic rate is undermined by this inflammation, which impacts mood and degrades.
Research shows inflammation contributes to anxiety, depression, autism,, ADHD, schizophrenia and more. Grain-heavy diets low in omega 3 essential fatty acids may an exacerbating factor in much contemporary psychopathology.
EFAs generate neuroprotective metabolites. In double-blind, randomized controlled trials, combinations of the fatty acids DHA and EPA have been shown to benefit attention deficit/hyperactivity disorder (ADHD), autism, dyspraxia, dyslexia, and aggression. For the affective disorders, meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.
Inflammation is sand in the gears of metabolism. It corrodes cell membranes and their delicate communication structures. If neurotransmitter receptors are like the dish antennas on microwave towers, inflammation is debris picked up by the wind, pitting them and knocking them out of alignment.
Antioxidants calm inflammation. Each makes its own unique contribution to soaking up corrosive extra electrons that immune cells use to inflame and digest microbes and damaged tissue. Inflammation is a gentle molecular "acid bath" dissolving intruders and debris.
Antioxidants come in a wide variety of shapes and, literally, colors. Brightly colored fruits and vegetables are rich sources of bioflavonoid and cartenoid antioxidants.
Carotene, the carotenoid that makes carrots and yellow cheese yellow, is converted by the body into vitamin A which protects our bones, skin, eyes and genes from the effects of environmental toxins. Specialized antioxidants like lutein and zeaxanthin protect the nerves at the back of the eyes that register light and help us see.
Vitamin C is the master antioxidant. It recharges all the others.
Free radicals are small molecules with an extra electron making the molecule more reactive, or oxidizing. Normally when an antioxidant (AO) molecule neutralizes an inflammatory free radical, the AO is done. It can't absorb any more. But if there's a vitamin C molecule around, the frontline AO can transfer its extra electron to vitamin C. Then the AO is "recharged" and can go back out and absorb more free radicals.
But that's not all vitamin C does. Like all nutrients, vitamin C plays multiple roles.
Vitamin C is also the raw material from which the body makes connective tissue. So not only does it absorb cell-wrecking debris in the body's inflammatory storms, it also strengthens things like the blood brain barrier (BBB). When it's healthy, the BBB acts as a filter ensuring toxins are kept out of the brain's delicate workaholic tissues.
So, not only can vitamin C keep the brain less inflamed, it can also keep out of the brain some of the toxins that would produce brain inflammation in the first place (inflaming tissue is the way many toxins work).
One of the more interesting factoids about vitamin C is that most mammals produce copious amounts of it in their own tissues, interconverting it from blood sugar. Higher primates like man, guinea pigs and fruit bats are the only mammals that don't. If we humans were producing vitamin C at the rate most mammals do, then considering our body weight we'd be making 14,000–17,000 mg/day.
The USDA recommended Daily Value (DV) level for vitamin C is only 60 mg/day.
Human trials of varying doses of vitamins E and C, including low, supplemental, and pharmacologic, have found that these nutrients may improve immunity, vascular function, and brain performance. An optimal intake of these nutrients has been associated with decreased risk of developing cognitive impairments associated with aging.
Research shows vitamin C improves the outcome of schizophrenia and that schizophrenics appear to need more than most of us. Vitamins C and E have been associated with lower incidence of Alzheimer's., Prozac works better with vitamin C.
Sugar and Other Sweeteners
The brain prefers to run solely on sugar. Historically the easiest way for the body to make sugar was by breaking down the complex carbs we consumed in greens, roots and the occasional seed.
Think about what's involved in washing off a pre-cultivated tuber like a potato and biting into it. Takes a lot of motivation, doesn't it! Eat some raw greens some day and see how tasty they are without salad dressing. (If you source your greens right it can actually taste good. But it's an acquired taste.)
For the longest time, we needed to find such fare satisfying in order to stay alert and alive. One of the most powerful reward mechanisms in the brain evolved in part to give us the motivation we needed to find and consume uncultivated, uncooked, relatively tasteless complex carbs.
Dopamine rewires the brain to repeat whatever behavior gave us a dopamine surge. Carbohydrates train us to like them by providing such a surge. Refined carbohydrates like sugar produce unnaturally powerful dopamine surges. That's not only why sugar tastes so good, it's also why it’s so easy to become addicted to it.
Dopamine receptors reset themselves to a less sensitive state when they're overloaded with dopamine frequently. That's how addictions start. We push the circuits too hard and they go numb, requiring progressively stronger stimulation to achieve sensations of pleasure.
Research shows that artificial sweeteners aren't much better. They reset the brain's dopamine pathways to numb, too.
This is a serious issue. Things are interesting to us because they're pleasurable, and dopamine pathways are important for helping us pay attention and keep our focus. When these pathways reset themselves to be less sensitive, the stage is set for attention deficit hyperactivity disorder (ADHD).
ADHD ruins many lives. Problems in school and at work, higher rates of divorce, auto accidents and drug abuse are common with ADHD.
Studies also link sugar to depression,, anxiety and schizophrenia. Along with resetting dopamine receptors, high refined carbohydrate consumption also knocks our endocrine system out of balance. If the liver and kidneys become overstressed and lose their ability to clear unnaturally large surges of insulin responding to unnaturally large blood, excess insulin can start to drive blood sugar too low.
Stress hormones like adrenalin and norepinephrine respond and convert a quick-release form of tissue sugar (glycogen) into blood sugar so we don't pass out. This stress hormone surge in response to dropping blood sugar explains why hunger makes us shake and become irritable. (It also explains why medical researchers dismiss the concept of hypoglycemia, or low blood sugar. Turns out when they go looking they usually can't find actual low blood sugar levels in people who exhibit all the classic symptoms of anxiety, fatigue etc. These are instead really symptoms stemming from the inflammation due to excessive insulin and/or the counterbalancing stress hormones secreted to keep us functioning.)
One of the ways modern diets have changed in the last few decades is that we can eat the same thing every day if we want to. The experience of seasonal availability of foods has been lost. Seasonal fruits and vegetables are flown in from around the world to keep our refrigerators full all year.
This matters, because the stress of modern life, nutrient deficiencies and the ravages of age tend to weaken digestion as we get older, as they do every other body function. One of digestion's roles is to turn the protein in our food into amino acids. Stress and all the rest can create a situation in which proteins don't break down completely. Partially digested protein fragments then enter the small intestine and can become absorbed through the gut wall into the bloodstream.
There the immune system mobilizes to meet what it perceives as a threat. It marshals its forces to produce free radicals that attack and dissolve the offending foreign protein fragments.
This creates inflammation. Not only does this localized inflammation make the gut more porous, allowing more partially digested protein fragments to create even more inflammation, but as this happens three additional issues are triggered:
1) Cytokines, immune activity-boosting immunotransmitters are released. These cytokines interact with the brain and central nervous system producing lethargy and irritability. This feels emotionally similar to the way one feels during the first few days of a cold or a flu—and for a very good reason: cytokines are also released when the body fights off invasion by the flu virus.
2) Kinins are formed. These highly inflammatory substances have near-instant access to all body tissues by circulating in the bloodstream.
3) The body interprets all of this as a stressor, and stress hormones are released. As we saw in the case of hypoglycemia, above, these stress hormones mobilize glycogen stores and turn them into circulating blood sugar. The surge in blood sugar produces a surge in dopamine.
The dopamine rewires the brain to repeat whatever behavior led to the dopamine surge. The result is that we become addicted to our favorite foods. And since we never need go without them in this modern day of cheap air transport, we can keep inflaming ourselves until our bodies break down.
But long before we develop physical illness, the mood- and energy-destroying cytokine and stress hormone surges can contribute to anorexia, anxiety, depression,, hyperactivity, and other emotional and cognitive issues.
Given its high metabolic rate and intricate physiology, it shouldn't surprise us that the human brain depends on a rich mix of nutrients. Failure to supply these nutrients in optimal quantities undermines optimal brain function. Emotional and cognitive psychopathologies can be the result. Nutritional therapies can at times deliver outcomes functionally equivalent to pharmaceuticals.
 Cordain, L., Eaton, S. B., Sebastian, A., Mann, N., Lindeberg, S., Watkins, B. A., . . . Brand-Miller, J. (2005). Origins and evolution of the Western diet: Health implications for the 21st century. American Journal of Clinical Nutrition, 81, 341–354.
 Bouayed, J., Rammal, H., & Soulimani, R. (2009). Oxidative stress and anxiety: Relationship and cellular pathways. Oxidative Medicine and Cellular Longevity, 2, 63–67. doi:10.4161/oxim.2.2.7944
 Hovatta, I., Juhila, J., & Donner, J.. (2010). Oxidative stress in anxiety and comorbid disorders. Neuroscience Research, 68, 261–275.
 Ng, F., Berk, M., Dean, O., & Bush, A. I. (2008). Oxidative stress in psychiatric disorders: Evidence base and therapeutic implications. International Journal of Neuropsychopharmacology, 11, 851–876.
 Hornyak, M., Haas, P., Veit, J., Gann, H., & Riemann, D. (2004). Magnesium treatment of primary alcohol-dependent patients during subacute withdrawal: An open pilot study with polysomnography. Alcoholism: Clinical and Experimental Research, 28, 1702–1709.
 Chouinard, G., Beauclair, L., Geiser, R., & Etienne, P. (1990). A pilot study of magnesium aspartate hydrochloride (Magnesiocard®) as a mood stabilizer for rapid cycling bipolar affective disorder patients. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 14, 171–180.
 Grimaldi, B. L. (2002). The central role of magnesium deficiency in Tourette's syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette's syndrome and several reported comorbid conditions. Medical Hypotheses, 58, 47–60.
 Yanik, M., Kocyigit, A., Tutkun, H., Vural, H., & Herken, H. (2004). Plasma manganese, selenium, zinc, copper, and iron concentrations in patients with schizophrenia. Biological Trace Element Research, 98, 109–117.
 Moylan, S., Eyre, H. A., Maes, M., Baune, B. T., Jacka, F. N., & Berk, M. (2013). Exercising the worry away: How inflammation, oxidative and nitrogen stress mediates the beneficial effect of physical activity on anxiety disorder symptoms and behaviours. Neuroscience & Biobehavioral Reviews, 37, 573–584.
 Nunes, S. O. V., Vargas, H. O., Prado, E., Barbosa, D. S., de Melo, L. P., Moylan, S., . . . Berk, M. (2013). The shared role of oxidative stress and inflammation in major depressive disorder and nicotine dependence. Neuroscience & Biobehavioral Reviews, 37, 1336–1345.
 Theoharides, T. C., Asadi, S., & Patel, A. B. (2013). Focal brain inflammation and autism. Journal of Neuroinflammation, 10, Article 46. doi:10.1186/1742-2094-10-46
 Theoharides, T. C., Asadi, S., Panagiotidou, S., & Weng, Z. The "missing link" in autoimmunity and autism: Extracellular mitochondrial components secreted from activated live mast cells. Autoimmunity Reviews, 12, 1136–1142.
 Bulut, M., Selek, S., Bez, Y., Kaya, M. C., Gunes, M., Karababa, F., . . . Savas, H. A. (2013). Lipid peroxidation markers in adult attention deficit hyperactivity disorder: New findings for oxidative stress. Psychiatry Research, 209, 638–642. doi:10.1016/j.psychres.2013.02.025
 Keller, W. R., Kum, L. M., Wehring, H. J., Koola, M. M., Buchanan, R. W., & Kelly, D. L. (2013). A review of anti-inflammatory agents for symptoms of schizophrenia. Journal of Psychopharmacology, 27, 337–342. doi:10.1177/0269881112467089
 Vargas, H. O., Nunes, S. O. V., de Castro, M. P., Bortolasci, C. C., Barbosa, D. S., Morimoto, H. K., . . . Berk, M. (2013). Oxidative stress and lowered total antioxidant status are associated with a history of suicide attempts. Journal of Affective Disorders, 150, 923–930. doi:10.1016/j.jad.2013.05.016
 Raz, R., Carasso, R. L., & Yehuda, S. (2009). The influence of short-chain essential fatty acids on children with attention-deficit/hyperactivity disorder: A double-blind placebo-controlled study. Journal of Child and Adolescent Psychopharmacology, 19, 167–177. doi:10.1089/cap.2008.070
 Kidd, P. M. (2007). Omega-3 DHA and EPA for cognition, behavior, and mood: Clinical findings and structural-functional synergies with cell membrane phospholipids. Alternative Medicine Review, 12, 207–227.
 Stonehouse, W., Conlon, C. A., Podd, J., Hill, S. R., Minihane, A. M., Haskell, C., & Kennedy, D. (2013). DHA supplementation improved both memory and reaction time in healthy young adults: A randomized controlled trial. American Journal of Clinical Nutrition, 97, 1134–1143. doi:10.3945/ajcn.112.053371
 Wu, A., Ying, Z., & Gomez-Pinilla, F. (2011). The salutary effects of DHA dietary supplementation on cognition, neuroplasticity, and membrane homeostasis after brain trauma. Journal of Neurotrauma, 28, 2113–2122. doi:10.1089/neu.2011.1872
 Pauling, L. (1968). Varying the concentrations of substances normally present in the human body may control mental disease. Science, 160, 265–271. doi:10.1126/science.160.3825.265
 Cernak, I., Savic, V., Kotur, J., Prokic, V., Kuljic, B., Grbovic, D., & Veljovic, M. (2000). Alterations in magnesium and oxidative status during chronic emotional stress. Magnesium Research, 13, 29–36.
 Sinclair, A. J., Bayer, A. J., Johnston, J., Warner, C., & Maxwell, S. R. J. (1998). Altered plasma antioxidant status in subjects with Alzheimer's disease and vascular dementia. International Journal of Geriatric Psychiatry, 13, 840–845. doi:10.1002/(SICI)1099-1166(1998120)13:12<840::AID-GPS877>3.0.CO;2-R
 Martin, A., Cherubini, A., Andres-Lacueva, C., Paniagua, M., & Joseph, J. (2002). Effects of fruits and vegetables on levels of vitamins E and C in the brain and their association with cognitive performance. Journal of Nutrition, Health & Aging, 6, 392–404.
 Dakhale, G. N., Khanzode, S. D., Khanzode, S. S., & Saoji, A. (2005). Supplementation of vitamin C with atypical antipsychotics reduces oxidative stress and improves the outcome of schizophrenia. Psychopharmacology, 182, 494–498. doi:10.1007/s00213-005-0117-1
 Engelhart, M. J., Geerlings, M. I., Ruitenberg, A., van Swieten, J. C., Hofman, A., Witteman, J. C. M., & Breteler, M. M. B. (2002). Dietary intake of antioxidants and risk of Alzheimer disease. Journal of the American Medical Association, 287, 3223–3229. doi:10.1001/jama.287.24.3223
 Frank, B., Gupta, S. (2005). A review of antioxidants and Alzheimer's disease. Annals of Clinical Psychiatry, 17, 269–286. doi:10.1080/10401230500296428
 Amr, M., El-Mogy, A., Shams, T., Vieira, K., & Lakhan, S. E. (2013). Efficacy of vitamin C as an adjunct to fluoxetine therapy in pediatric major depressive disorder: A randomized, double-blind, placebo-controlled pilot study. Nutrition Journal, 12, Article 31. doi:10.1186/1475-2891-12-31
 Johnson, R. J., Gold, M. S., Johnson, D. R., Ishimoto, T., Lanaspa, M. A., Zahniser, N. R., & Avena, N. M. (2011). Attention-deficit/hyperactivity disorder: Is it time to reappraise the role of sugar consumption? Postgraduate Medicine, 123(5), 39–49. doi:10.3810/pgm.2011.09.2458
 Varea, V., de Carpi, J. M., Puig, C., Alda, J. A., Camacho, E., Ormazabal, A., . . . Gómez, L. (2005). Malabsorption of carbohydrates and depression in children and adolescents. Journal of Pediatric Gastroenterology and Nutrition, 40, 561–565.
 Souza, C. G., Moreira, J. D., Siqueira, I. R., Pereira, A. G., Rieger, D. K., Souza, D. O., . . . Perry, M. L. S. Highly palatable diet consumption increases protein oxidation in rat frontal cortex and anxiety-like behavior. Life Sciences, 81, 198–203. doi:10.1016/j.lfs.2007.05.001
 Peet, M. (2004). International variations in the outcome of schizophrenia and the prevalence of depression in relation to national dietary practices: An ecological analysis. British Journal of Psychiatry, 184, 404–408. doi:10.1192/bjp.184.5.404
 Hayley, S., Merali, Z., & Anisman, H. (2003). Stress and cytokine-elicited neuroendocrine and neurotransmitter sensitization: Implications for depressive illness. Stress, 6, 19–32. doi:10.1080/1025389031000091167
 Plata-Salamán, C. R. (1998). Cytokines and anorexia: A brief overview. Seminars in Oncology, 25(Suppl. 1), 64–72.
 Anisman, H., & Merali, Z. (2003). Cytokines, stress and depressive illness: Brain–immune interactions. Annals of Medicine, 35, 2–11. doi:10.1080/07853890310004075
 Anisman, H., Hayley, S., Turrin, N., & Merali, Z. (2002). Cytokines as a stressor: Implications for depressive illness. International Journal of Neuropsychopharmacology, 5, 357–373. doi:10.1017/S1461145702003097
 Rucklidge, J. J., Johnstone, J., Kaplan, B. J. (2009). Nutrient supplementation approaches in the treatment of ADHD. Expert Review of Neurotherapeutics, 9, 461–476. doi:10.1586/ern.09.7
 Kronfol, Z., & Remick, D. G. (2000). Cytokines and the brain: Implications for clinical psychiatry. American Journal of Psychiatry, 157, 683–694. doi:10.1176/appi.ajp.157.5.683