It was 1534, and the crew of French explorer Jacques Cartier were in trouble. They had been ship-bound for months and surviving off meagre rations during their exploration of the eastern Canadian coastline for what would become the French empire’s vast claims to North America. The inevitabilities of life at sea had caught up with them in devastating fashion: Cartier’s men had scurvy. For many seafaring adventurers in that Age of Exploration, the cumulative effects of scurvy were intensifying and worsening preludes to a horrible disease, and often death. Vasco da Gama had lost two-thirds of his crew to scurvy in 1499, and in 1520, while attempting a trans-Pacific voyage, Ferdinand Magellan watched his ranks thin by 80% as scurvy claimed the lives of his men (Lamb, 2011).
However, it seems that luck was on Cartier’s side, as he had befriended a tribe of Quebecois Native Americans in his explorations. Wise in the plant lore of their ancestors, they offered Cartier and his men a medicinal tea brewed from the needles and bark of special pine trees. To Cartier, the healing of his crew surely was not insignificant, and his journal entries are testament to the fact that this mysterious tea saved his men. The ramifications of the Quebecois’ kindness also led to one of the most exciting breakthroughs in the field of nutritional psychiatry: the ancient wisdom of the Native Americans shared with Jacques Cartier in the 1500s has been shown by modern science to be an effective treatment for attention-deficit/hyperactivity disorder (ADHD).
According to data from the Centers for Disease Control and Prevention (2017), an estimated 6.4 million children aged 4 to 17 are diagnosed with ADHD at some point in their lives, reflecting a 41% increase in the last decade alone. ADHD is characterized by an ongoing pattern of inattention and/or hyperactivity–impulsivity that interferes with an individual’s functioning and development. Despite the thousands of scientific research papers published on the illness and diagnosis of ADHD, the etiology and treatment recommendations from medical and psychiatric professionals have changed little over the years.
The prevalence of ADHD today has given rise to widespread professional and public awareness, as well as a myriad of treatment approaches ranging from behavioral to pharmaceutical, while the concomitant surge in research churns out new scientific data that seem to upend every firmly held assumption on which these treatments have been based. Studies from around the globe are impressively united in their contradiction of the long-held belief that ADHD is a “kids’ disorder”. While ADHD typically manifests before puberty, new research has revealed that the disorder is lifelong, with prevalence rates amongst adults being nearly identical to those observed in children.
Perhaps most fascinating is the ongoing research exploring the genetic and biologic underpinnings of ADHD. While parents are primarily concerned with the behavioral manifestations of ADHD and strategies for symptom management, researchers have identified multiple biological changes associated with the behavioral and cognitive issues associated with ADHD. There is a growing body of unequivocal empirical evidence that validates ADHD as a neurologic, brain-based disorder represented by numerous biological abnormalities, so that what is observed as atypical behavior is merely the tip of a very large ADHD iceberg, the base of which can extend to an individual’s genetic blueprint and biochemical makeup. A comprehensive list of the neurobiological changes that have been found to be associated with ADHD exceeds the scope of this article; however, a sampling of such a list would include the following:
- Several studies employing magnetic resonance imaging (MRI) technology have revealed abnormalities within the motivational circuitry of individuals with ADHD (Seymour, Reinblatt, Benson, & Carnell, 2015); neuroimaging studies have found unusual patterns of brain activation in individuals with ADHD, particularly within those networks involved in reward processing.
- A study examining the volume and quality of electrochemical signaling (communication) between brain regions found that ADHD children had atypical functional connections as compared with non-ADHD children (Costa Dias et al., 2013).
- Studies have revealed a genetic component to ADHD susceptibility; recent research investigating the incidence of ADHD amongst family members has yielded a heritability estimate of 76% in the general population (Faraone et al., 2005).
- Individuals with ADHD consistently display neurologic symptoms characteristic of insufficient dopamine. Dopamine plays a critical role in brain functions such as movement, attention, learning, and the reinforcing effects of many drugs. Researchers found that by administering a drug that enhances the release of dopamine in the brain of ADHD patients, symptoms were significantly relieved, thus confirming that ADHD symptoms are associated with insufficient dopamine (Carlson, 2014).
- In our clinic, we have found many nutritional and metabolic disturbances related to the symptoms of ADHD, such as heavy metal toxicity, fatty acid imbalances, deficiencies of magnesium, iron, and zinc, and carbohydrate intolerance.
The emerging research on the pathophysiology and neurobiology of ADHD has consequently forced us to reexamine the ways in which we approach ADHD treatment. No longer can ADHD be thought of as a behavioral disorder. We now know that ADHD involves changes and functional abnormalities in specific brain regions, brain networks, biochemical processes, and even systemic metabolic processes. A disorder this complex requires a treatment approach that is equally multifaceted. Unfortunately, however, the reigning ADHD therapeutic paradigms utilized today are largely one-dimensional.
The administration of stimulant medications has long been the first-line treatment for ADHD, and drugs such as methylphenidate and dextroamphetamine are commonly prescribed to children as young as 3 or 4 years old to control restlessness, agitation, and impulsivity. By stabilizing dopamine levels in the brain, stimulants can affect an ADHD patient’s scholastic performance and social functioning, and they have been successful at improving grades, self-esteem, and social relationships. Although the administration of pharmaceutical drugs treats the symptoms of the disorder, it fails to address the causes of ADHD. For some, the eradication of “problem behaviors” in the ADHD child is sufficient; yet stimulant medications may also carry a host of risks and negative side-effects including tics, insomnia, nausea and dizziness, as well as delayed growth, impaired vision, heart problems, and psychosis (Rubio et al., 2016).
The number of treatments available for ADHD can be overwhelming for patients and caregivers alike; these range from parent training, psychotherapy, medications, neurofeedback, and behavior therapy, some of which have been proven effective. Methods such as neurofeedback target imbalances and cognitive abnormalities that underlie adverse ADHD symptomatology.
If we return to the 1500s, we now know that Cartier’s men were actually given a natural compound by the Quebecois that is found to have significant neurophysiological properties that improve symptoms observed in ADHD. These plant-derived compounds are known as oligomeric proanthocyanidins (OPCs), and while it may be premature for us to call them a miracle cure, mounting empirical evidence demonstrates that OPCs are a safe, natural, and efficacious treatment strategy in supporting cognitive function in clients with ADHD. To the ADHD patient, practitioner or parent, OPCs are a beacon of hope, substantiated by modern science to effectively address many of the root biologic causes of ADHD.
A Brief History of OPCs
OPCs (i.e., oligomeric proanthocyanidins—sometimes known as proanthocyanidins or proanthocyanidolic oligomers), are a variety of polyphenol, a compound that plants produce as a defense against environmental harm. Polyphenol is a plant pigment that appears as red in cranberries, blueberries, and grapes; green in green tea; and the brown hue of dark chocolate. OPCs are also found in grapeseed, gingko biloba, plums, peaches, pine needles, and pine bark. For humans, the most beneficial molecular components of OPCs are flavonols, a type of antioxidant.
By the time Cartier and his men were introduced to the healing properties of pine tea, OPC-rich plant extracts had already been used as medicine in China and India for millennia. Between 1100 BC and 200 BC, Chinese physicians ardently supported the drinking of green tea (Camellia sinensis) to maintain health, and by the Tang Dynasty (AD 618–907), tea had become an object of medicinal veneration. According to practitioners of traditional Chinese medicine, green tea possesses cooling (yin) properties that help to refresh the mind, boost mental alertness, eradicate excess heat (yang), promote digestion, and relieve headaches. Passages from ancient Indian texts also demonstrate a rich history of using OPC-containing plants for therapeutic purposes: two plants that are prominently featured in Ayurvedic literature—Cedrus deodara, or Himalayan cedar, and Pinus roxburghii, or Indian longleaf pine—have been described as possessing central nervous system effects and have traditionally been used in Ayurvedic medicine to treat disorders of the mind (Chaudhary, Ahmad, & Mazumder, 2013).
In 1947, a French doctor by the name of Jacques Masquelier happened upon Cartier’s journal, and became interested in the special properties of the pine tea that had been used to treat the explorer’s company (Carper, 1998). As the needles of the pine used for the tea are rather low in vitamin C, Masquelier suspected another chemical was in fact responsible for saving Cartier’s men (Passwater, 1991).
He was right: the pine needles and bark used to brew the scurvy-conquering tea were rich in OPCs. OPCs with small amounts of vitamin C had cured Cartier’s crew of scurvy, and Masquelier promptly set out to learn as much as he could about this fascinating compound. He went on to extract OPCs from the skin of peanuts, and in 1950, OPCs derived from peanut skins were marketed as a blood-vessel protectant. Several years later, Masquelier discovered another rich source of OPCs in grape seeds. He was subsequently granted a patent for the extraction and medical application of OPCs in 1969 (Passwater, 1991).
Masquelier’s work provided valuable insight for a possible explanation of the curious paradox concerning the epidemiological observation that French people exhibit lower incidences of coronary heart disease despite consuming a diet rich in saturated fats. Crediting the OPCs present in red wine, scientists found that OPCs exert multiple cardio-protective effects, as evidenced by their ability to decrease lipid peroxidation of low-density lipoprotein (Fuhrman, Lavy, & Aviram, 1995). Soon after this discovery, pharmaceutical companies developed drugs such as Endotelon to treat atherosclerosis and other cardiovascular diseases with OPCs from grape seeds as the active ingredient.
Today, OPCs are widely available to the public as a dietary supplement, with Pycnogenol most prominent among them. Pycnogenol is the registered trademark name of a nutritional supplement derived from Pinus pinaster, and is commonly used for treating circulation problems, asthma, tinnitus, high blood pressure, osteoarthritis, diabetes, female menstrual disorders, and retinopathy.
In keeping with the ancient traditions of Chinese medicine, Indian Ayurveda, and Native American plant medicine, OPCs show great promise as a nutritional biomedical therapy for ADHD. Based on observations spanning decades of clinical experience, OPCs can be incredibly useful in the treatment of ADHD for children and adults, either as an augmentation strategy for medications or as a stand-alone therapy.
OPCs as a Treatment for ADHD
A preliminary experiment conducted by psychologist Marion Sigurdson, involving 30 subjects with ADHD, found that attention and concentration (as measured by tests before and after the experiment) improved just as much with a daily regimen of pine bark-derived OPCs as with traditional ADHD stimulant medications (Carper, 1998). Additionally, the subjects reported experiencing better sleep and improved mood while taking the OPC supplement, corroborating centuries’ worth of accumulated evidence from traditional systems of medicine that OPCs positively affect brain function.
Sigurdson’s experimental outcomes were echoed in later research, including a randomized controlled trial seeking to investigate the effects of Pycnogenol on attention, oxidative DNA damage, and antioxidant status in ADHD patients and healthy controls. In a 2006 study, 61 children with ADHD aged 6–14 were randomly assigned to receive either Pycnogenol (1 mg/kg of body weight) or a placebo daily for one month, without any additional medications or supplements. Baseline measures taken at the start of the trial revealed that children with ADHD had significantly more oxidative DNA damage than their non-ADHD counterparts; after the study, markers of DNA damage were significantly lower in the group that had received Pycnogenol, even compared to measures taken from the non-ADHD controls (Chovanová et al., 2006). At the end of the study, children who had taken Pycnogenol displayed significantly elevated measures of antioxidant status. Within a month of discontinuing the supplement, however, subjects displayed increased levels of DNA damage. The data generated by this randomized controlled trial points to a strong association between DNA oxidation, total antioxidant status, and inattention.
Additional evidence in support of the efficacy of OPCs for ADHD comes from psychologist Dr. Steven Tenenbaum, who was diagnosed with ADHD as a child and lived with the disorder through adulthood. In addition to being a practicing clinical psychologist, Tenenbaum was an aviation enthusiast. Due to regulations of the Federal Aviation Administration, he was unable to utilize pharmaceutical treatments for his ADHD, and the use of stimulant drugs would cost him his pilot’s license. He therefore turned to alternative therapies, and in 1995, initiated a regimen of Pycnogenol three times daily (Carper, 1998). According to Tenenbaum, the results were impressive: with Pycnogenol, he reported increased attention, improved focus, decreased emotional volatility, and elevated mood. Without Pycnogenol, Tenenbaum reported that ADHD symptoms would return immediately.
Tenenbaum’s and Sigurdson’s results with Pycnogenol supplementation are by no means unusual: numerous case reports, documented and anecdotal, have recorded substantial improvements in attention and focus, decreased restlessness and aggression, and emotional resiliency in ADHD patients who have been administered OPCs, and add to the body of literature supporting Pycnogenol supplementation as an alternative treatment for ADHD. For example, the case of a 10-year-old boy with ADHD, having experienced only marginal success on a regimen of stimulant drugs, was successfully treated with Pycnogenol was described in a letter to the editor of the Journal of the American Academy of Child and Adolescent Psychiatry (Heimann, 1999). The boy’s parents noted significant improvements in his symptoms while the Pycnogenol regimen was maintained. When Pcynogenol was stopped, the boy experienced a significant exacerbation of ADHD symptoms.
The effects of OPCs have been tested in both ADHD patients and healthy, non-ADHD individuals, and the results from investigations into the latter are no less impressive than those of the former. For example, Luzzi et al. (2011) explored the effects of Pycnogenol on the cognitive abilities and emotional status of 53 healthy students aged 18–27. The students were tested before and after a regimen of Pycnogenol (100 mg/day) on measures of attention, memory, alertness, executive functioning, and mood, and showed significant improvements across-the-board after eight weeks of Pycnogenol supplementation. A more recent study from Exeter University (Bowtell, Aboo-Bakkar, Conway, Adlam, & Fulford, 2017) has documented the positive effects of drinking blueberry juice (rich in OPC flavonols) upon brain function in older adults. In this study, healthy participants aged 65–77 were randomly assigned to one of two experimental groups: members of the first group drank 30 ml/day of blueberry juice concentrate for 12 weeks, while members of the second group were given a placebo. Before and after the 12-week period, participants underwent a battery of cognitive tests while an MRI scanner monitored their brain function and resting brain blood flow. Compared to the placebo group, those who took the blueberry supplement showed improvements in cognitive function, working memory, blood flow to the brain, and brain activation while carrying out cognitive tests. Finally, a noteworthy study from the University of Reading examined the effects of blueberry extract consumption on cognition in children, and found that every measure of mental ability, including memory, improved in those children who drank blueberry extract (Whyte & Williams, 2015).
These data emphatically underscore what the wisdom from ancient Chinese, Indian, and Native American medical traditions has long recognized: OPCs can benefit the human brain, and powerfully enough to combat, minimize, and in some cases eliminate ADHD symptoms. Furthermore, OPCs can enhance cognitive performance, reduce anxiety, and improve mood in healthy individuals and ADHD sufferers alike. From the bark of the humble pine, the fruit of grape and blueberry plants, the fragrant leaves of green tea, and so many more abundant plant sources, we have a natural, plant-based therapy that may not only support those who struggle with ADHD but also large-scale approaches to the maintenance of general cognitive health.
This has been an excerpt from The Neuropsychotherapist's Essential Guide to the Brain Part 16. To download the full article, and more excellent material for the psychotherapist, please subscribe to our monthly magazine.
Ahn, S. H., Kim, H, J., Jeong, I., Hong, Y. J., Kim, M. J., Rhie, D. J., . . . Yoon, S. H. (2011). Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neurons. BMC Neuroscience, 12, 78. doi:10.1186/1471-2202-12-78
Arnold, L. E., & DiSilvestro, R. A. (2005). Zinc in attention-deficit/hyperactivity disorder. Journal of Child and Adolescent Psychopharmacology, 15, 619–627. doi:10.1089/cap.2005.15.619
Arnold, L. E., Disilvestro, R. A., Bozzolo, D., Bozzolo, H., Crowl, L., Fernandez, S., . . . Joseph, E. (2011). Zinc for attention-deficit/hyperactivity disorder: Placebo-controlled double-blind pilot trial alone and combined with amphetamine. Journal of Child and Adolescent Psychopharmacology, 21, 1–19.
Bilici, M., Yildirim, F., Kandil, S., Bekaroğlu, M., Yildirmiş, S., Değer, O., . . . Aksu, H. (2004). Double-blind, placebo controlled study of zinc sulfate in the treatment of attention deficit hyperactivity disorder. Progress in Neuropsychopharmacology & Biological Psychiatry, 28, 181–190. doi:10.1016/j.pnpbp.2003.09.034
Boris, M., & Mandel, F. S. (1994). Foods and additives are common causes of the attention deficit hyperactivity disorder in children. Annals of Allergy, 72, 462–468.
Bowtell, J. L., Aboo-Bakkar, Z., Conway, M., Adlam, A. R., & Fulford, J. (2017). Enhanced task related brain activation and resting perfusion in healthy older adults after chronic blueberry supplementation. Applied Physiology, Nutrition, Metabolism. Advance online publication. doi:10.1139/apnm-2016-0550
Carlson, N. R. (2014). Foundations of behavioral neuroscience (9th ed.). Upper Saddle River, NJ: Pearson Education.
Carper, J. (1998). Miracle cures: Dramatic new scientific discoveries revealing the healing power of herbs, vitamins, and other natural remedies. New York, NY: HarperPerennial.
Centers for Disease Control and Prevention. (2017, February 14). Attention deficit/hyperactivity disorder (ADHD). Retrieved from https://www.cdc.gov/ncbddd/adhd/data.html.
Chaudhary, A. K., Ahmad, S., & Mazumder, A. (2013). Cognitive enhancement in aged mice after chronic administration of Cedrus deodara Loud. and Pinus roxburghii Sarg. with demonstrated antioxidant properties. Journal of Natural Medicines, 68, 274–83. doi:10.1007/s11418-013-0775-y
Chovanová, Z., Muchová, J., Sivonová, M., Dvoráková, M., Zitnanová, I., Waczulíková, I., . . . Duracková. Z. (2006). Effect of polyphenolic extract, Pycnogenol, on the level of 8-oxoguanine in children suffering from attention deficit/hyperactivity disorder. Free Radical Research, 40, 1003–1010. doi:10.1080/10715760600824902
Comim, C. M., Gomes, K. M., Réus, G. Z., Petronilho, F., Ferreira, G. K., Streck, E. L., . . . Quevedo, J. (2014). Methylphenidate treatment causes oxidative stress and alters energetic metabolism in an animal model of attention-deficit hyperactivity disorder. Acta Neuropsychiatrica, 26, 96–103. doi:10.1017/neu.2013.35
Costa Dias, T. G., Wilson, V. B., Bathula, D. R., Iyer, S. P., Mills, K. L., Thurlow, B. L., . . . Fair, D. A. (2013). Reward circuit connectivity relates to delay discounting in children with attention-deficit/hyperactivity disorder. European Neuropsychopharmacology, 23, 33–45. doi:10.1016/j.euroneuro.2012.10.015
Duric, N. S., Assmus, J., Gundersen, D., & Elgen, I. B. (2012). Neurofeedback for the treatment of children and adolescents with ADHD: A randomized and controlled clinical trial using parental reports. BMC Psychiatry, 12, 107. doi:10.1186/1471-244X-12-107
Dvoráková, M., Sivonová, M., Trebatická, J., Skodácek, I., Waczuliková, I., Muchová, J., & Duracková, Z. (2006). The effect of polyphenolic extract from pine bark, Pycnogenol, on the level of glutathione in children suffering from attention deficit hyperactivity disorder (ADHD). Redox Report, 11, 163–72. doi:10.1179/135100006X116664
Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., & Sklar, P. (2005). Molecular genetics of attention-deficit/hyperactivity disorder. Biological Psychiatry, 57, 1313–1323.
Fuhrman, B., Lavy, A., & Aviram, M. (1995). Consumption of red wine with meals reduces the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation. The American Journal of Clinical Nutrition, 61, 549–554.
González-Castro, P., Cueli, M., Rodríguez, C., García, T., & Álvarez, L. (2016). Efficacy of neurofeedback versus pharmacological support in subjects with ADHD. Applied Psychophysiology and Biofeedback, 41, 17–25. doi:10.1007/s10484-015-9299-4
Greenblatt, J. M. (1999). Nutritional supplements in ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 1209–1211.
Greenblatt, J. M. (2016, March). Oligomeric proanthocyanidins as an alternative treatment for ADHD. Integrative Medicine for Mental Health. Retrieved from http://www.integrativemedicineformentalhealth.com/articles/greenblatt_oligomeric_proanthocyanidins.html
Heimann, S. W. (1999). Pycnogenol for ADHD? Journal of the American Academy of Child and Adolescent Psychiatry, 38, 357–358.
Johansson, J., Landgren, M., Fernell, E., Vumma, R., Åhlin, A., Bjerkenstedt, L., & Venizelos, N. (2011). Altered tryptophan and alanine transport in fibroblasts from boys with attention-deficit/hyperactivity disorder (ADHD): An in vitro study. Behavioral and Brain Functions, 7, 40. doi:10.1186/1744-9081-7-40
Karege, F., Perret, G., Bondolfi, G., Schwald, M., Bertschy, G., & Aubry, J. (2002). Decreased serum brain-derived neurotrophic factor levels in major depressed patients. Psychiatry Research, 109, 143–8.
Kodoma, G., Fujisawa, C., & Bhadhprasit, W. (2012). Inherited copper transport disorders: Biochemical mechanisms, diagnosis, and treatment. Current Drug Metabolism, 13, 237–250. doi:10.2174/138920012799320455
Lamb, J. (2011, February 17). Captain Cook and the scourge of scurvy. BBC History. Retrieved from http://www.bbc.co.uk/history/british/empire_seapower/captaincook_scurvy_01.shtml
Luzzi, R., Belcaro, G., Zulli, C., Cesarone, M. R., Cornelli, U., Dugall, M., . . . Feragalli, B. (2011). Pycnogenol® supplementation improves cognitive function, attention and mental performance in students [Supplemental material]. Panminerva Medica, 53, 75–82.
Mann, C., Lubar, L. F., Zimmerman, A. W., Miller, C. A., & Muenchen, R. A. (1992). Quantitative analysis of EEG in boys with attention-deficit-hyperactivity disorder (ADHD): A controlled study with clinical implications. Pediatric Neurology, 8, 30–36.
Meisel, V., Servera, M., Garcia-Banda, G., Cardo, E., & Moreno, I. (2013). Neurofeedback and standard pharmacological intervention in ADHD: A randomized controlled trial with six-month follow-up. Biological Psychology, 94, 12–21. doi:10.1016/j.biopsycho.2013.04.015
Passwater, R. A. (1991). Pycnogenol (proanthocyanidins). WholeFoods Magazine, 3, 83–98.
Robert, A. M., Tixier, J. M., Robert, L., Legeais, J. M., & Renard, G. (2001). Effect of procyanidolic oligomers on the permeability of the blood-brain barrier. Pathologie Biologie, 49, 298–304. doi:10.1016/S0369-8114(01)00148-1
Rubio, B., Boes, A. D., Laganiere, S., Rotenberg, A., Jeurissen, D., & Pascual-Leone, A. (2016). Noninvasive brain stimulation in pediatric attention-deficit hyperactivity disorder (ADHD): A review. Journal of Child Neurology, 31, 784–796. doi:10.1177/088307381561567
Russo, A. J. (2010). Decreased serum Cu/Zn SOD associated with high copper in children with ADHD. Journal of Central Nervous System Disease, 2, 9–14.
Schwartz, J. C. (2011). The histamine H3 receptor: From discovery to clinical trials with pitolisant. British Journal of Pharmacology, 163, 713–721. doi:10.1111/j.1476-5381.2011.01286.x
Serafini, M., Maiani, G., & Ferro-Luzzi, A. (1998). Alcohol-free red wine enhances plasma antioxidant capacity in humans. The Journal of Nutrition, 128, 1003–1007.
Seymour, K. T., Reinblatt, S. P., Benson, L., & Carnell, S. (2015). Overlapping neurobehavioral circuits in ADHD, obesity, and binge eating: Evidence from neuroimaging research. CNS Spectrums, 20, 401–411. doi:10.1017/S1092852915000383
Shin, D. W., Kim, E. J, Oh, K. S., Shin, Y. C., & Lim, S. W. (2014). The relationship between hair zinc and lead levels and clinical features of attention-deficit hyperactivity disorder. Journal of Korean Academy of Child and Adolescent Psychiatry, 25, 28–36. doi:10.5765/jkacap.2014.25.1.28
Steiner, N. J., Frenette, E. C., Rene, K. M., Brennan, R. T., & Perrin, E. C. (2014). In-school neurofeedback training for ADHD: Sustained improvements from a randomized control trial. Pediatrics, 133, 483–492. Retrieved from http://pediatrics.aappublications.org/content/pediatrics/early/2014/02/11/peds.2013-2059.full.pdf
Szewczyk, B., Kubera, M., & Nowak, G. (2011). The role of zinc in neurodegenerative inflammatory pathways in depression. Progress in Neuropsychopharmacology and Biological Psychiatry, 35, 693–701. doi:10.1016/j.pnpbp.2010.02.010
Takeda, A., Sakamoto, K., Tamano, H., Fukura, K., Inui, N., Suh, S. W., . . . Yokogoshi, H. (2011). Facilitated neurogenesis in the developing hippocampus after intake of theanine, an amino acid in tea leaves, and object recognition memory. Cellular and Molecular Neurobiology, 31, 1079–88. doi:10.1007/s10571-011-9707-0
Toomim, H., Mize, W., Yeekwong, P., Toomim, M., Marsh, R., Kozlowski, G. P., & Remond, A. (2004). Intentional increase of cerebral blood oxygenation using hemoencephalography: An efficient brain exercise therapy. Journal of Neurotherapy, 8, 5–21. doi:10.1300/J184v08n03_02
Uhlig, T., Merkenschlager, A., Brandmaier, R., & Egger J. (1997). Topographic mapping of brain electrical activity in children with food-induced attention deficit hyperkinetic disorder. European Journal of Pediatrics, 156, 557–561.
Viktorinova, A., Ursinyova, M., Trebaticka, J., Uhnakova, I., Durackova, Z., & Masanova, V. (2015). Change plasma levels of zinc and copper to zinc ratio and their possible associations with parent- and teacher-rated symptoms in children with ADHD. Biological Trace Element Research, 169, 1–7. doi:10.1007/s12011-015-0395-3
Whyte, A. R., & Williams, C. M. (2015). Effects of a single dose of a flavonoid-rich blueberry drink on memory in 8- to 10-year-old children. Nutrition, 31, 531–534. doi:10.1016/j.nut.2014.09.013
About the Authors
James M. Greenblatt, MD, is the author of Finally Focused: The Breakthrough Natural Treatment Plan for ADHD that Restores Attention, Minimizes Hyperactivity, and Helps Eliminate Drug Side Effects (with Bill Gottlieb, Harmony Books, 2017). He currently serves as Chief Medical Officer and Vice-President of Medical Services at Walden Behavioral Care, and he is an Assistant Clinical Professor of Psychiatry at Tufts University School of Medicine and Dartmouth Geisel School of Medicine. An acknowledged expert in integrative medicine, Dr. Greenblatt has lectured throughout the United States on the scientific evidence for nutritional interventions in psychiatry and mental illness.
For more information, visit www.JamesGreenblattMD.com
Jennifer C. Dimino, MS (Psychology), is a freelance writer who has produced blogs and consumer articles for Dr. Greenblatt’s new book Finally Focused (Harmony Books, 2017). She has specific research interests in integrative and holistic psychology and neuroscience.
Winnie T. Lee, RN, has provided research and editorial assistance for several book publications by James Greenblatt, including Finally Focused (Harmony Books, 2017), Answers to Binge Eating (with Virginia Ross-Taylor, 2014), and Integrative Therapies for Depression (edited by James Greenblatt & Kelly Brogan, CRC Press, 2016). She is a coauthor (with James Greenblatt) of Breakthrough Depression Solution: Mastering Your Mood with Nutrition, Diet and Supplementation (2nd ed., Sunrise River Press, 2016). She is currently pursuing a master’s in nursing to become a psychiatric nurse practitioner.