American adolescents now face a staggering burden of mental illness. It is an epidemic without precedent. An estimated 32 percent of United States teens have already experienced at least one DSM-based anxiety disorder, and over 14 percent have suffered from a major mood disorder (Merikangas et al., 2010). Their parents mirror the pattern—one out of every six adults takes daily psychiatric medication (Moore & Mattison, 2017)—and yet prevalence rates continue to rise relentlessly in virtually every major category of psychological disorder.
Particularly alarming is the recent spike in adolescent suicide. The rate at which American teens end their own lives has increased over 300 percent since the early 1950s (Scherff, Eckert, & Miller, 2005), and suicide now stands as the second leading cause of adolescent death (Heron, 2017). Among girls ages ten to fourteen, the suicide rate has tripled over just the past two decades alone. And the Los Angeles Unified School District recently reported a remarkable eighteen-fold increase in self-harm and suicidal behavior since the year 2010 (Schrobsdorff, 2016).
Although such dire statistics can be dispiriting, especially for those of us who work as mental health professionals, they also point to an urgent need to better understand the origins of the burgeoning mental health crisis and to discover ways of addressing it with greater effectiveness. Clearly, the prevailing paradigm of adolescent psychiatry, which might be glibly characterized as “throwing meds at the problem and hoping for the best,” has not delivered reductions in the overall burden of teen mental illness. Although medications have doubtless been of great benefit to many, they have not been truly game-changing in the sense of providing complete and enduring recovery for the overwhelming majority of those who take them.
We believe, accordingly, that it is time for a fresh look at the epidemic of teen psychological disturbance. In so doing, we draw upon several other relevant scientific domains—including medical epidemiology, cognitive neuroscience, nutritional medicine, and evolutionary biology—to tackle the pressing questions: Why are we seeing such an increase in mental illness? And what, if anything, can be done about it?
Diseases of Civilization
In recent decades, medical epidemiologists have identified an array of diseases and pathological syndromes—including diabetes, obesity, atherosclerosis, asthma, allergies, and many forms of cancer—which are highly prevalent in affluent, industrialized, Western societies, but much less common among more traditional agrarian societies, and almost completely unknown among even less technologically advanced aboriginal groups. These “diseases of civilization” appear to be caused to a large degree by characteristic features of modern life, including a heavily processed diet, physical inactivity, reduced sleep, excessive stress, low sunlight exposure, and increasing social isolation. As such, they may be regarded as diseases of lifestyle.
From the vantage point of evolutionary medicine (Williams & Nesse, 1991), diseases of civilization may arise from a fundamental mismatch between the twenty-first-century postindustrial landscape and the much different ancestral, largely Pleistocene (Stone Age) environment in which the human species evolved. Simply put: we were never designed for the sedentary, indoor, socially isolated, fast-food-laden, sleep-deprived, screen-addicted, frenzied pace of modern life. The radical pace of “environmental mutation” since the industrialization has delivered us to a lifestyle for which the human genome, which builds our bodies and brains, is not always well adapted. The result is an epidemic of lifestyle-based illness.
Importantly, some of the most prevalent and debilitating forms of mental illness—including clinical depression, bipolar disorder, generalized anxiety, and social anxiety disorder—appear to fit the basic pattern of diseases of civilization. In fact, we propose that the typical twenty-first-century American lifestyle contains numerous features that are psychologically toxic, and particularly so for adolescents.
Most of our ancestors inhabited a very different world from the one we now face. For over 99 percent of hominid history, until about ten thousand years ago, our forebears lived in intimate, tight-knit, hunter-gatherer communities that typically numbered between thirty and fifty. In effect, they were on a lifelong camping trip with their closest friends and loved ones.
Notably, most of the natural selection pressure on the human genome occurred during this epoch. In many respects, our genes are still sculpting Pleistocene bodies and Pleistocene brains in expected adaptation to a Stone Age world. Although there has certainly been additional evolutionary change since the advent of agriculture and livestock herding in the interim (for example, mutations that now give people the ability to digest lactose even after weaning), such changes are often quite minor and narrow in scope.
With the onset of the Industrial Revolution about two hundred years ago, the pace of environmental mutation quickened even further. And despite dramatic changes in human lifestyle over the past two centuries—a span of about eight generations—there has simply been too little time for any significant evolutionary change to occur. The resulting mismatch between the human genome and our present environment is profound. This genomic mismatch now takes an immense toll, both physically and psychologically, on those facing the twenty-first-century milieu.
Mental Illness and the Runaway Stress Response
The genome-environment mismatch is particularly evident in the body’s reaction to stress, especially in the dramatic “fight-or-flight” response to perceived danger. This reaction, mediated hormonally by the hypothalamic-pituitary-adrenal axis (HPA axis), prepares the body to respond with intense physical activity to acute threats. Among other things, it involves an increased release of the stress hormone cortisol, which sharply raises blood sugar (fuel for muscles) and helps shift the brain into threat-response mode. Although such adaptations are metabolically costly, they represent a small price to pay for ensured survival.
In the ancestral human environment, of course, most threats were physical in nature—whether in the form of predatory animals, dangerous weather, or hostile out-groups—and they typically required only brief bouts of intense stress axis activation. But the modern world presents a relentless stream of threats that are nonphysical in nature, and yet still quite capable of activating the brain’s stress response circuitry: unsettling news events, social-media-provoked envy, crowded urban landscapes, noise pollution, work deadlines, competitive pressures, and so on.
In fact, twenty-first-century life appears almost perversely designed to engender chronic stress reactions, including the long-term elevation of cortisol and related hormones. And long-term stress tends to be toxic both to the brain and the rest of the body.
The psychopathological consequences of chronic-threat-linked arousal are mediated to a large degree by the powerful neurohormone CRH (corticotropin releasing hormone), secreted by the hypothalamus at the nexus of the brain’s stress response circuitry. During stressful episodes, CRH is released into the brain’s pool of cerebrospinal fluid, where it can travel to influence circuits throughout the brain.
When chronically elevated, CRH can induce a number of harmful neurological changes including:
- Perturbed serotonergic signaling, with a corresponding increase in behavioral withdrawal and the risk of depressive illness
- Decreased activation of dopamine-based reward circuits
- Disrupted sleep architecture, including a decline in restorative slow-wave sleep that can in turn induce lethargy, decreased cognitive performance, and many depressive symptoms
- Increased signaling in norepinephrine-mediated sympathetic nervous system pathways, with a corresponding surge in anxious arousal
- Reduced brain expression of BDNF, a neural growth hormone essential to memory function and overall brain health
Because long-term surges in CRH release can be so maladaptive—with the potential to induce depressive illness, clinical anxiety, attentional disturbance, social dysfunction, and cognitive deficits—the brain has protective feedback mechanisms designed to keep the stress response from continuing at length. However, when such safeguards fail, the resulting runaway stress response can be devastating in its effects.
Despite leading what we might regard as difficult lives, aboriginal groups appear to have lower overall stress levels than those of us living in industrialized societies. Consistent with this observation: their circulating levels of cortisol tend to be remarkably low by Western standards (Berger et al., 2017). Although they doubtless spike, as designed, whenever a threat presents itself, they quickly normalize once the threat has passed. In contrast, ours tend to remain elevated. In fact, many American adolescents appear to be living in a perpetual state of hyperarousal.
Numerous features of contemporary life contribute to the problem. Smartphones, for example, are now a ubiquitous presence for teens, with a robust potential to amplify stress. Via social media, they can cultivate invidious social comparison (Shakya & Christakis, 2017), cyberbullying, and paradoxical feelings of isolation (Twenge, 2017). These addictive devices have also begun crowding out stress-reducing activities such as in-person interaction with friends and sleep time (Twenge, 2017); they are also intruding into physical activity. For many, adolescence is also now marked by relentless achievement pressure, and the nagging ever-present thought of “I must do more.”
In contrast with teens of previous generations, those of the post-9/11 era have come of age in a world often perceived as fundamentally unsafe. In this context, helicopter parenting has become common, in tandem with the relative disappearance of “free-range childhood.” Although doubtless well-intended, this overprotective style can serve to strengthen core beliefs about the dangerousness of the world. By depriving children of the freedom to explore their environment, it can also impede their developing sense of agency and control, which can in turn increase their perceived vulnerability and proneness to anxiety (Segrin, Woszidlo, Givertz, & Montgomery, 2013).
Therapeutic Lifestyle Change
The impact of lifestyle on brain function is something of a double-edged sword. Although we have focused thus far on the many ways in which modern American life promotes the brain’s runaway stress response—which in turn carries the potential to trigger depressive illness, clinical anxiety, sleep disturbance, neurocognitive deficits, and various related forms of mental illness—we now turn our attention to many ways in which targeted lifestyle modifications may help address these debilitating syndromes. Among the numerous lifestyle domains worthy of consideration, we focus on seven for which the research support is particularly robust.
Exercise is Medicine
It is now well-established that vigorous physical activity triggers a wide array of beneficial physiological changes throughout the body, including many in the brain. In fact, if it were possible to capture this panoply of exercise-induced benefits in pill form, such a drug—perhaps branded as Exerzac—would doubtless become an instant blockbuster.
The range of salubrious exercise effects with respect to mental illness is truly staggering. Among the more notable:
- Reduced activity in the brain’s stress response circuitry (Lehmann & Herkenham, 2011)
- Enhanced signaling in dopamine-based reward circuitry (Sutoo & Akiyama, 2003)
- Effective acute treatment of depressive illness (Blumenthal et al., 1999)
- Enhanced sleep quality (Driver & Taylor, 2000)
- Increased production of BDNF, a critical neural growth hormone with neuro-protective and memory-enhancing effects (Wrann et al., 2013)
- Improved attentional function (Gomez-Pinilla & Hillman, 2013)
Even at a rather modest exercise “dose” such as brisk walking for thirty minutes at an aerobic pace three times per week, physical activity has been found to have equally efficacious in the acute treatment of depression as an antidepressant medication (Blumenthal et al., 1999), with lower rates of subsequent relapse (Babyak et al., 2000). Similar results have now been reported by multiple teams of clinical researchers, and the antidepressant impact of exercise is supported by rigorous meta-analysis (Schuch et al., 2016).
Unfortunately, contemporary life is largely sedentary, as technological advances have eliminated much of the need for physical activity in the modern world. Most of our time is now spent sitting, and adolescents are particularly prone to screen-induced inactivity. The contrast with the physically active lives of our hunter-gatherer forebears is striking. Of course, our ancestors were not really trying to stay fit per se, and they certainly never set out to get exercise for its own sake. Instead, they were simply active in the service of meaningful goals, engaging in vigorous movement because it was necessary for them to survive and flourish.
There is pretty good evidence that humans, like most species, have an innate tendency to minimize physical effort, to save on caloric expenditure (i.e., to be lazy) whenever possible, and the adaptive significance of such default programming is obvious in ancestral world in which food scarcity was an ever-present risk. So, not surprisingly, the ethnographic record is filled with accounts of aboriginal groups eagerly embracing the labor-saving technological advances introduced by Western anthropologists and missionaries.
Because modern life has effectively removed the demand for vigorous movement for most of us, including most teens, we face a difficult dilemma. We know that exercise is good for us, and we desperately need its beneficial effects on our physical and mental well-being, and yet most find it surprisingly challenging to expend physical effort when it does not really seem to be required. When we look up at a piece of exercise equipment, it is as if a primitive neural subroutine begins crying out, “Do not do it! You are not going anywhere on that thing, and it is a huge waste of energy!”
Fortunately, most people find it much easier to be physically active when the activity feels meaningful, when it feels engaging, and when it feels fun. The typical visitor to Walt Disney World, for example, ends up walking many miles each day, but they do so simply because they are engaged in the fun of reaching meaningful destinations. Likewise, we have found in our clinical research (Ilardi, 2009) that even severely depressed patients are capable of becoming physically active, especially when we brainstorm with them to develop a list of activities they might find meaningful or engaging, and provide the requisite social support and encouragement, typically in the form of a personal trainer.
Omega-3 Fatty Acids
The human brain is mostly made up of fat. The body is able to manufacture most of the key fats needed by the brain, but two varieties known as essential fatty acids can only be derived from diet: omega-3s and omega-6s. Omega-6 fats tend to promote systemic inflammation, and as such they carry the potential to exacerbate the brain’s stress response. Conversely, omega-3s are generally anti-inflammatory in their impact, with a commensurate array of neurological benefits that include enhanced fidelity of neurotransmitter signaling and a potential reduction in symptoms of depression (Logan, 2003), anxiety (Ross, 2009), and ADHD (Hawkey & Nigg, 2014).
Proper neurological function actually requires the presence of all molecular forms of fatty acid in relative balance, and it has been suggested that a dietary omega-6, omega-3 ratio of about 1:1 is ideal (Simopoulos, 2011). Interestingly, this is approximately the ratio one might encounter in a hunter-gatherer diet (Simopoulos, 2011). But the typical American diet now delivers a ratio of nearly 20:1, supplying far too many inflammatory omega-6 fats. They are abundant, for example, in processed foods and fast foods, often in the form of seed-based and grain-based oils.
Omega-3 fats—found in grasses, leaves, algae, and the animals that eat them—are increasingly uncommon in contemporary diets. Most animals in the meat supply are primarily grain-fed, and thus chock-full of omega-6s. In previous eras, fish would have been an excellent source of omega-3s, but much of the fish sold in today’s supermarkets have been farm-raised and grain-fed as well. Accordingly, it can difficult to consume an adequate quantity of omega-3s through diet alone, so we often recommend supplementing with a high-quality fish oil to reach an amount that will provide clinical benefit. For example, there is now considerable evidence that supplementation with the omega-3 fatty acid EPA (eicosapentaenoic acid) at a dose of at least 1,000 mg per day can be of benefit in the treatment of depression (Freeman et al., 2006).
The human body is host to an estimated one hundred trillion microbes, often collectively known as the “microbiome.” Because our species has coevolved with these microbial symbionts over the millennia, the relationship is mutually beneficial, at least for the most part. The great bulk of our microbes live in the gut, where they extract nutrients and help regulate immune function. They also have the ability to influence brain function, and recent evidence suggests that they may help soothe anxiety and combat depression (Allen et al., 2016).
But two features of modern American life have combined to wreak havoc on the microbiome: the widespread use of antibiotics and the shift to a processed-food-based diet. Whenever we go on a round of antibiotic therapy (and the average American has done so over a dozen times) the drugs not only wipe out the unwanted bacterial intruders that cause symptoms of infection, but they also eliminate broad swaths of the microbiome. To make matters worse, the ecological niches in the gut vacated by beneficial species can be taken up by harmful, parasitic microbes following antibiotic therapy, and these interlopers can promote inflammation and damaging overall physical and neurological well-being. In contrast, beneficial microbes tend to flourish on a diet laden with soluble plant fiber, which is often in perilously short supply in the dietary intake of contemporary teens.
Although research on strategies for enhancing microbiome health is still in its infancy, a few interventions already have empirical support. Among the most useful: probiotic supplementation, the consumption of foods that are fermented (Selhub, Logan, & Bested, 2014) or rich in plant fiber (Tuohy, Conterno, Gasperotti, & Viola, 2012), supplementation with soluble fiber sources such as psyllium husk or inulin (Slavin, 2013), and avoidance of antibiotic therapy whenever it is not medically indicated.
For countless generations our ancestors spent the lion’s share of each day outside in natural sunlight, which is typically several hundred times brighter than the best indoor lighting. Modern life, on the other hand, is increasingly lived indoors.
But our eyes and brains were designed by natural selection to derive the benefits that follow from regular bright light exposure. Such light stimulates specialized photoreceptors in the retina, which in turn signal to the suprachiasmic nucleus deep in the brain, with a cascade of downstream effects that include setting the internal body clock, increasing arousal, enhancing sleep architecture, and regulating various hormone levels. Extreme bright light deprivation—as often occurs during the short, cold, gloomy days of winter, when many people see little if any sunlight—can induce numerous adverse effects, including a serious form of depression often known as seasonal affective disorder (SAD).
Fortunately, when natural sunlight is not conveniently available, its neurological and psychological benefits can be simulated effectively with the use of an artificial light box, often at a surprisingly reasonable cost. Many commercially available boxes now sell for under $100.
The key is to ensure that the device yields luminance of at least 10,000 lux, by far the most research-supported light “dosage” (Terman & Terman, 2005). Not only does thirty minutes of morning light exposure at 10,000 lux help reverse symptoms of SAD, but it has also been found to be useful in the treatment of more common nonseasonal depression (Al-Karawi & Jubair, 2016), ADHD (Terman, 2007), and elevated anxiety (Baxendale, O’Sullivan, & Heaney, 2013).
The typical teen needs at least nine hours of sleep each night for optimal neurological functioning (Orzech, 2013), but most now fall far below this requirement. It is not uncommon for sleep to be regarded as optional and dispensable, something that can be sacrificed whenever there is extra schoolwork to be done, or even just the lure of a smartphone screen or a new show to binge-watch on Netflix. Our ancestors, of course, lacked such distractions. Prior to the advent of electric lighting a few generations ago, they often went to bed soon after the sun went down—much to their benefit.
Inadequate sleep has profoundly negative consequences for physical, neurological, and psychological health. Not only is sleep essential to repairing neuronal damage and clearing out accumulated toxins and metabolites from the brain, but adequate sleep also helps boost mood, reduce stressful arousal, improve attention, restore energy, and enhance mental clarity.
Many American teens (and their adult counterparts) would derive enormous benefit from improving both the quantity and quality of their sleep. Doing so typically requires putting into practice robust habits of healthy sleep, among them:
- Going to bed at the same time each night
- Getting up at the same time each morning
- Dimming the lights and disengaging from all interactive devices an hour before bedtime
- Developing a quiet “bedtime ritual” such as reading, taking a soothing bath, or watching a relaxing show in a darkened room
- Using the bed only for sleep to help classically condition the body to shift into sleep mode upon crawling into bed, much as Pavlov famously conditioned his dog to salivate involuntarily upon hearing a bell
- Turning down the thermostat at least five degrees
- Avoiding work or any other highly stimulating activities the hour bedtime
- Avoiding caffeine and other stimulants for at least ten hours before going to sleep
Rumination, the repetitive process of brooding on negative thoughts and turning them over and over again in the mind, is common when we experience either depression or anxiety, and it only serves to ramp up the brain’s stress response. Rumination occurs most often when we are alone and mentally disengaged. Although our remote ancestors were often far too busy and socially connected to spend much time ruminating, those who inhabit the modern environment generally have ample opportunity to ruminate.
For many, and particularly for those battling various forms of mental illness, rumination can become a pervasive daily practice. But it is a habit that can be effectively countered, especially with skillful guidance. The first step in combatting rumination is simply learning to recognize (i.e., be mindful of) its occurrence. Although it may seem impossible not to notice what we are thinking about, rumination can become such an overlearned process that it occurs in a state of cognitive autopilot, almost completely outside of any attentional regulation.
Once aware of rumination, one must then decide to redirect attention elsewhere, preferably to something engaging. This is often best accomplished through interacting with other people, ideally in shared activity together. Shared conversation can be helpful, as well, provided it does not devolve into a state corumination, in which both partners end up ruminating together out loud. Other viable antiruminative strategies include exercise, playing an instrument, reading, watching an engaging video, being immersed in nature, journaling, or interacting with pets.
Our ancestors generally lived in tight-knit groups that provided a strong sense of companionship and belonging. They rarely spent time alone—reliance on others was essential for their entertainment, comfort, safety, and survival. And because the human species is highly social by nature, the support and companionship of others still remains essential to our sense of well-being. The physical presence of a close friend or loved one even helps to soothe the brain’s stress response circuitry.
But contemporary American life is increasingly characterized by social isolation, with roughly one in four adults reporting the absence of any meaningful emotional support from others (McPherson, Smith-Lovin, & Brashears, 2006). The problem extends to adolescents as well. Following the advent of social media, today’s graduating high school seniors spend dramatically less time with friends in comparison with those who graduated a generation ago (Eagan et al., 2015), and teens now report feelings of loneliness and isolation with alarming frequency (Twenge, 2017).
Although there is certainly no “magic bullet” solution to the pervasive problem of social disconnection, we note that for many the remedy may lie, at least in part, in a reordering of priorities. Simply put: Americans often live out their lives as if achievement and affluence were more important to them than the quality of their relationships, despite the fact that few people would endorse such priorities if asked point-blank. Inasmuch as it can be a bit counter-cultural, cultivating a deep, rich sense of social connection in the twenty-first century may require some degree of conscious intentionality in consistently placing the highest priority on meaningful face-to-face interaction with the people who matter to us most.
As we have seen, the modern American epidemic of adolescent mental illness may reflect, to a large degree, the psychological toxicity of life in the affluent postindustrial Western world, which appears almost perversely designed to keep the brain’s stress response circuitry engaged. It is a lifestyle largely devoid of the protective, beneficial habits of the past, including regular physical activity, plentiful dietary omega-3 fats, abundant sleep, healthy microbiomes, daily sunlight exposure, and rich social connectedness.
Fortunately, extensive research evidence suggests that the reacquisition of such modifiable lifestyle practices can be of great benefit in countering many of the most prevalent forms of psychological disorder. We believe that a lifestyle-based approach to treatment—modified and adapted to the exigencies of other common forms of adolescent mental illness—carries potential to help stem the scourge of mental illness now plaguing the current generation of young Americans. Given its seriousness, and the disappointing efficacy of the more mainstream approaches used to date, we believe the time has come to try addressing the problem at its source.
Al-Karawi, D., & Jubair, L. (2016). Bright light therapy for nonseasonal depression: Meta-analysis of clinical trials. Journal of Affective Disorders, 198, 64–71.
Allen, A. P., Hutch, W., Borre, Y. E., Kennedy, P. J., Temko, A., Boylan, G., … Clarke, G. (2016). Bifidobacterium longum 1714 as a translational psychobiotic: Modulation of stress, electrophysiology, and neurocognition in healthy volunteers. Translational Psychiatry, 6(11), e939.
Babyak, M., Blumenthal, J. A., Herman, S., Khatri, P., Doraiswamy, M., Moore, K. A., … Krishnan, K. R. (2000). Exercise treatment for major depression: Maintenance of therapeutic benefit at ten months. Psychosomatic Medicine, 62(5), 633–8.
Baxendale, S., O’Sullivan, J., & Heaney, D. (2013). Bright light therapy for symptoms of anxiety and depression in focal epilepsy: Randomised controlled trial. The British Journal of Psychiatry, 202(5), 352–6.
Berger, M., Leicht, A., Slatcher, A., Kraeuter, A. K., Ketheesan, S., Larkins, S., & Sarnyai, Z. (2017). Cortisol awakening response and acute stress reactivity in first nations people. Scientific Reports, 7, 41760.
Blumenthal, J. A., Babyak, M. A., Moore, K. A., Craighead, W. E., Herman, S., Khatri, P., … Krishnan, K. R. (1999). Effects of exercise training on older patients with major depression. Archives of Internal Medicine, 159(19), 2349–56.
Driver, H. S., & Taylor, S. R. (2000). Exercise and sleep. Sleep Medicine Reviews, 4(4), 387–402.
Eagan, K., Stolzenberg, E. B., Ramirez, J. J., Aragon, M. C., Suchard, M. R., & Hurtado, S. (2015). The American freshman: National norms fall 2014. Retrieved from https://www.heri.ucla.edu/monographs/TheAmericanFreshman2014.pdf
Freeman, M. P., Hibbeln, J. R., Wisner, K. L., Davis, J. M., Mischoulon, D., Peet, M., … Stoll, A. L. (2006). Omega-3 fatty acids: Evidence basis for treatment and future research in psychiatry. The Journal of Clinical Psychiatry, 67(12), 1954–67.
Gomez-Pinilla, F., & Hillman, C. (2013). The influence of exercise on cognitive abilities. Comprehensive Physiology, 3(1), 403–28.
Hawkey, E., & Nigg, J. T. (2014). Omega-3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials. Clinical Psychology Review, 34(6), 496–505.
Heron, M. (2017). Deaths: Leading causes for 2015. National Vital Statistics Reports, 66(5). Retrieved from https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_05.pdf
Ilardi, S. (2009). The depression cure: The six-step program to beat depression without drugs. Cambridge, MA: Da Capo Press.
Lehmann, M. L., & Herkenham, M. (2011). Environmental enrichment confers stress resiliency to social defeat through an infralimbic cortex-dependent neuroanatomical pathway. The Journal of Neuroscience, 31(16), 6159–73.
Logan, A. C. (2003). Neurobehavioral aspects of omega-3 fatty acids: Possible mechanisms and therapeutic value in major depression. Alternative Medicine Review, 8(4), 410–25.
McPherson, M., Smith-Lovin, L., & Brashears, M. E. (2006). Social isolation in America: Changes in core discussion networks over two decades. American Sociological Review, 71(3), 353–75.
Merikangas, K. R., He, J. P., Burstein, M., Swanson, S. A., Avenevoli, S., Cui, L., … Swendsen, J. (2010). Lifetime prevalence of mental disorders in US adolescents: Results from the national comorbidity study-adolescent supplement (NCS-A). Journal of the American Academy of Child and Adolescent Psychiatry, 49(10), 980–9.
Moore, T. J., & Mattison, D. R. (2017). Adult utilization of psychiatric drugs and differences by sex, age, and race. JAMA Internal Medicine, 177(2), 274–5.
Orzech, K. M. (2013). A qualitative exploration of adolescent perceptions of healthy sleep in Tucson, Arizona, USA. Social Science & Medicine, 79(1), 109–16.
Ross, B. M. (2009). Omega-3 polyunsaturated fatty acids and anxiety disorders. Prostaglandins, Leukotrienes, and Essential Fatty Acids, 81(5–6), 309–12.
Segrin, C., Woszidlo, A., Givertz, M., & Montgomery, N. (2013). Parent and child traits associated with overparenting. Journal of Social and Clinical Psychology, 32(6), 569–95.
Selhub, E. M., Logan, A. C., & Bested, A. C. (2014). Fermented foods, microbiota, and mental health: Ancient practice meets nutritional psychiatry. Journal of Physiological Anthropology, 33(1), 2.
Scherff, A. R., Eckert, T. L., & Miller, D. N. (2005). Youth suicide prevention: A survey of public school superintendents’ acceptability of school-based programs. Suicide and Life-Threatening Behavior, 35(2), 154–69.
Schrobsdorff, S. (2016). There’s a startling increase in major depression among teens in the US. Time. Retrieved from http://time.com/4572593/increase-depression-teens-teenage-mental-health/
Schuch, F. B., Vancampfort, D., Richards, J., Rosenbaum, S., Ward, P. B., & Stubbs, B. (2016). Exercise as a treatment for depression: A meta-analysis adjusting for publication bias. Journal of Psychiatric Research, 77, 42–51.
Shakya, H. B., & Christakis, N. A. (2017). A new, more rigorous study confirms: The more you use Facebook, the worse you feel. Harvard Business Review. Retrieved from https://hbr.org/2017/04/a-new-more-rigorous-study-confirms-the-more-you-use-facebook-the-worse-you-feel
Simopoulos, A. P. (2011). Evolutionary aspects of diet: The omega-6/omega-3 ratio and the brain. Molecular Neurobiology, 44(2), 203–15.
Slavin, J. (2013). Fiber and prebiotics: Mechanisms and health benefits. Nutrients, 5(4), 1417–35.
Sutoo, D., & Akiyama, K. (2003). Regulation of brain function by exercise. Neurobiology of Disease, 13(1), 1–14.
Terman, M. (2007). Evolving applications of light therapy. Sleep Medicine Reviews, 11(6), 497–507.
Terman, M., & Terman, J. S. (2005). Light therapy for seasonal and nonseasonal depression: Efficacy, protocol, safety, and side effects. CNS Spectrums, 10(8), 647–63.
Tuohy, K. M., Conterno, L., Gasperotti, M., & Viola, R. (2012). Up-regulating the human intestinal microbiome using whole plant foods, polyphenols, and/or fiber. Journal of Agricultural and Food Chemistry, 60(36), 8776–82.
Twenge, J. M. (2017). Have smartphones destroyed a generation? The Atlantic. Retrieved from https://www.theatlantic.com/magazine/archive/2017/09/has-the-smartphone-destroyed-a-generation/534198/
Williams, G. C., & Nesse, R. M. (1991). The dawn of Darwinian medicine. The Quarterly Review of Biology, 66(1), 1–22.
Wrann, C. D., White, J. P., Salogiannnis, J., Laznik-Bogoslavski, D., Wu, J., Ma, D., … Spiegelman, B. M. (2013). Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway. Cell Metabolism, 18(5), 649–59.