And God said, “Behold, I have given you every plant yielding seed that is on the face of all the earth, and every tree with seed in its fruit. You shall have them for food.”
—Genesis 1:29
Self-maintenance systems play a major role in gene expression and immune system functioning. A nutritionally impoverished diet, lack of exercise, and poor-quality sleep are associated with unhealthy gene expression and shortened telomeres, all undermining mental health. This combination of factors represents the foundation of health. Without addressing these factors immediately, the traditional psychotherapy interventions fail to gain traction.
Like first responders, the self-maintenance systems must be addressed right away to stabilize and ensure that no more damage is done—for this reason this chapter is up front rather than tucked away in an appendix. In fact, people who work as first responders cannot respond effectively if these self-maintenance factors are undermined.
For example, Mike, who worked as a police officer, came in to see me because of his irritability, decreased stress tolerance, and restless sleep. “I’m just not myself,” Mike told me. “I’ve turned into one of those grumpy old cops you see on TV.” Serving in a high-crime neighborhood, Mike found his job extremely stressful and exhausting. He often joked that that while his trips to the donut shop were a cliché, he needed the “extra boost” the sugar gave him but complained about “crashing” two hours later. Mike’s wife, Molly, worked as a dispatcher for the police department and was well aware of the gang violence and drive-by shootings on his beat. They both agreed that he should work his current beat for one more year in order to earn promotion to detective. In the meantime, it was essential that Mike learn to take better care of himself.
Molly told me during a phone call that Mike started the day with an energy bar and a cup of coffee with three spoonfuls of sugar. She described his typical lunch as a few fried egg rolls or chicken nuggets. He insisted on bringing home fish and chips, fried chicken, and cake.
During our third session, when we reviewed his diet, Mike told me that what he ate had nothing to do with his grumpiness. He stared at me and said, “I hope you’re not a health nut like my wife!” When I told him that I hoped to help him deal with his stress at work, he seemed to slightly lower his guard. As a sarcastic joke, he said that he would shift from donuts to blueberry muffins at the donut shop, thinking that they were healthier. With a playful smile I pointed out that the muffins were loaded not only with empty calories but also trans-fatty acids. He replied, “I thought you food fanatics say that blueberries are good for you!” We both had a good laugh.
Mike’s stress level was higher than that of police officers in small towns with less violence. His resistance slowly dissolved by my asking if his poor diet was undermining his stress tolerance. The short answer was that Mike’s body was not prepared for the constant onslaught of stress that triggered his need for cheap energy.
It is important to keep in mind that our bodies did not evolve to consume processed foods. Prior to eleven thousand years ago, our ancestors lived a hunter-gatherer subsistence lifestyle, with a diet consisting of plants, nuts, berries, fish, and lean game. While our bodies have not changed since the Paleolithic era, our diets have, with negative results. The Western diet—Mike’s diet—consists of deep fried foods, refined carbohydrates, and processed foods containing sugar and high-fructose corn syrup, which spike glucose levels. When the body digests carbohydrates, it produces glucose, which accumulates in the bloodstream. In response, the pancreas releases insulin, which signals the liver and muscles to convert glucose into a starch-like molecule called glycogen. We also possess an enzyme called uricase that stores up energy is fat cells. This efficient method of energy storage worked quite well with a Paleolithic diet and a small supply of food. Mike, like too many people, was excessively “storing energy” in the form of extra fat cells. In his case, he had an extralarge belly, leaching out pro-inflammatory cytokines.
In addition to consuming fast food with empty calories, he drank one, sometimes two Big Gulp sodas. A couple of hours after Mike’s brain was assaulted with surges of glucose from the simple carbohydrates he consumed, his blood sugar and energy level took a nose dive. And so was there a loss of fuel for his prefrontal cortex—the CEO of his brain. With less energy for his executive network, his default-mode network replayed all the mishaps of the day. Nervously focused on the past instead of the present and anticipating what he might encounter in the immediate future made him prone to make mistakes, sometimes dangerous ones.
When blood sugar (glucose) drops below 50 milligrams per milliliter, the following symptoms may occur:
Fructose, unlike other sugars, produces uric acid when it is broken down in cells and blunts the effect of leptin, the hormone that tells the brain to stop eating. Elevated fructose essentially flips a switch in the body, causing it to hoard fat and raising blood sugar and blood pressure. A diet high in refined, processed carbohydrates and fats is associated with high levels of C-reactive protein, a common measure of inflammation (Liu et al., 2002).
Many processed foods and many “fruit” drinks contain fructose. Fructose has been shown to increase lipopolysaccharide by as much as 40 percent (Benros et al., 2013). As noted in Chapter 4, the combination of lipopolysaccharide and the gut bacteria Firmicutes, which feed on simple carbohydrates, increases gut permeability—leaky gut contributes to chronic inflammation.
Soon after our first session, Mike was involved a shooting during a robbery and was reassigned for six months to a desk job. Thinking he no longer needed help with stress, he did not return until six months later. In the meantime his diet, high in simple carbohydrates, combined with a sedentary lifestyle contributed to insulin resistance and obesity, which led to a host of health problems affecting his mental health, including metabolic syndrome and type 2 diabetes. The associated increases in blood pressure, cholesterol, and triglycerides elevated his risk for developing heart disease. In addition, a rise in uric acid increased his blood pressure by oxidative stress, which constricted his blood vessels, forcing his heart to pump harder. Also, the increased uric acid caused low-grade injury and inflammation in his kidneys, which made them less able to excrete salt and increased his blood pressure even more.
Glucose must be balanced so that the pancreas, liver, thyroid, adrenals, pituitary, and brain function properly. Keeping glucose levels in balance is critical so that the pancreas can deliver the right amount of insulin to regulate fuel delivery to cells. If glucose is elevated too long, a reaction called glycation occurs that causes sugars to attack proteins, causing inflammation in cell membranes and impairing interactions between neurons (Epstein, 1996). Advanced glycation end products (AGEs) additionally shorten the life span of cells by causing inflammation and creating free radicals, which result in cognitive and emotional deficits. AGEs also lead to structural damage to mitochondria, the energy factories within cells, which produce cellular energy in the form of ATP (Kikuchi et al., 2003).
Mike not only complained about fatigue and depression but was also referred to a neuropsychologist because of persisting and increasing memory problems. He thought he was developing Alzheimer’s disease but was actually elated when the neuropsychologist described the detrimental effects of his diet and his sedentary job. It was at that point that he returned to me to address his self-maintenance.
A useful measure of glucose level, glycemic load (GL), relates to the expected rise in blood sugar caused by a particular food. Foods with a high GL, such as white bread, instant oatmeal, French fries, and fruit juices, lead to greater inflammation, which can have destructive effects on the brain and impact cognition, memory, and mood. Consistent with these findings, a diet high in simple carbohydrates is associated with increased swelling and decreased brain-derived neurotrophic factor (BDNF) in the hippocampus, which is central to explicit memory. This is one of the reasons that people with diabetes are at increased risk for developing memory problems.
In the last forty years the standard Western diet has been marked by an exponential increase in soft drinks and fruit drinks. They contain sugar or high-fructose corn syrup, which trigger free radical products of damaged fatty acids, called isoprostanes, which rise 34 percent just ninety minutes after consumption (Sampson et al., 2002). When fatty acids such as arachidonic acid are damaged, isoprostanes appear in tissues and cause free radical activity, which chips away at the cell membrane. To put this in perspective, levels of isoprostanes are nine times higher one day after a brain injury than before the injury (Pratico et al., 2002). High levels of isoprostanes are found in the cerebral spinal fluid, plasma, and urine of people with Alzheimer’s disease, which implies that they are a possible predictor of the disease.
An increase in glycemic load and a blood marker of oxidative stress, malondialdehyde, have been shown to damage essential fatty acids (Hu et al., 2006). Because essential fatty acids are critical to the structure and health of our brain, this combination of inflammatory factors and oxidative stress is corrosive to the brain and thus to mood and cognition.
After helping Mike stabilize his diet, I was invited to give a presentation on brain health and stress tolerance to the entire police department. Just to get the discussion started, I told the officers that the next time someone called them fat heads, say thanks! A large proportion of the brain is composed of fats, so despite the food fads, fat consumption is critical to a healthy diet. However, during the past century the amount of healthy fats in the form of essential fatty acids in the Western diet has dramatically declined. In the place of good fats we are now consuming destructive fats, including animal fats, trans-fatty acids, vegetable oils, and processed foods.
A diet high in saturated fat has increasingly been associated with cardiovascular disease and dementia, and the World Health Organization has reported its association with cancer. When combined with social stress, a diet high in saturated fat leads to deterioration of the hippocampus associated with the retraction of dendrites (Baran et al., 2015).
We all had a good laugh when caterers began to set up. The lunch buffet featured hamburgers, French fries, onion rings, and fried fish patties. One of the lieutenants said that the menu was not an anomaly. Like Mike, many of the officers admitted to consuming fried foods at home on a regular basis, not knowing of the multiple adverse consequences. Trans-fatty acids are formed when an unsaturated vegetable fat is heated for long periods of time in a metal container, such as deep frying. Trans-fats, which are structured differently than essential fatty acids, tend to be solid at body temperature and act like saturated fat, all of which are corrosive to cell membranes. Consuming trans-fatty acids decreases the levels of healthy fats, so the uptake of trans-fatty acids into the brain doubles.
The Destructive Effects of Trans-Fatty Acids
Despite our good laugh together over the menu, most of the officers went up for seconds. If we eat more calories than we burn, our triglycerides levels rise. Triglycerides are a type of fat found in the blood. The body converts calories the body does not need right away into triglycerides, which it stores in fat cells. Between meals, hormones release triglycerides for energy. Elevated triglycerides are associated with multiple health problems, including depression, while lowering the triglyceride level is associated with the alleviation of depression.
When essential fatty acids are not balanced, pro-inflammatory cytokines become overactivated, turning the immune system against cells, such as occurs with autoimmune disorders. As noted in Chapter 4, increases in pro-inflammatory cytokines are associated with cognitive problems, anxiety, and depression.
Omega-3 fish oil supplementation is associated with decreased pro-inflammatory cytokines and free radical damage. Some of the anti-inflammatory effects of omega-3s appear to be related to altered expression of genes encoding inflammatory mediators, as well as lower oxidative stress.
Omega-3 Essential Fatty Acids and Functions in the Brain
Eicosapentaenoic acid (EPA)
Docosahexaenoic acid
Omega-3s have been associated with promoting BDNF, which as noted in Chapter 4 plays a critical role in neurogenesis and neuroplasticity, serves as a neuroprotective agent, and is critical for memory and new learning. While inflammation and oxidative stress interfere with BDNF production, omega-3s can lower both inflammation and oxidative stress. Low levels of BDNF are associated with neurological damage and depression, and the omega-3 EPA can help maintain BDNF. On the other hand, the combination of high cortisol, disrupted gut microbiota, high levels of inflammation in the gut, systemic inflammation, and lower levels of BDNF has been consistently associated with anxiety and depression (Glaus et al., 2014).
Excessive doses of omega-3 are counterproductive—lower doses are more effective than higher doses. Consumption of over 2 grams per day is related to higher levels of depression (Pect & Stokes, 2005).
Essential fatty acids can also help the brain facilitate the so-called second-messenger system that activates when neurotransmitters penetrate the fatty membrane of the cell and trigger secondary emissaries that reach into the nucleus of the cell, where they turn genes off or on, to send chemicals back outside the cell and create yet even more reactions.
Brains capable of generating balanced moods and clear thinking need a diet containing essential amino acids, vitamins, and minerals to produce the cornucopia of brain chemistry optimal for the brain. Because neurotransmitters are synthesized from precursor amino acids that serve as their building blocks, a diet lacking these critical amino acids diminishes neurochemistry, contributing to deficits in memory, attention, and mood. Specific amino acids serve as the building blocks for neurotransmitters.
Amino Acid Precursors to Neurotransmitters
Amino Acid | Neurotransmitter | Effects |
L-Trytophan | Serotonin | Improves sleep, calmness, and mood |
L-Glutamine | GABA | Decreases tension and irritability |
L-Phenylalanine | Dopamine | Increases feelings of anticipation of pleasure and drives motivation |
L-Phenylalanine | Noreprinephrine | Increases energy, feelings of pleasure, and memory |
Given the huge amount of information available about foods, and the food fads that have come and gone, what can we consider the most consistently supported recommendations? A diet with low levels of saturated fat and high in fruits and vegetables, such as the Mediterranean diet, has been associated with a lower risk of age-related cognitive impairment (Feart et al., 2009). When comparing the Mediterranean diet alone or in combination with regular exercise, the addition of exercise lowers the risk of developing dementias such as Alzheimer’s disease (Scarmeas et al., 2009). People who adhere to a Mediterranean diet, consisting of fresh fruits and vegetables, anti-inflammatory fats, and proteins have been found to have a lower rate of depression (Sanchez-Villegas et al., 2009).
Adherence to the Mediterranean diet has been associated with telomere maintenance and associated health status and longevity (Boccardi et al., 2013). The Asian equivalent, sometimes called the Okinawan diet, which consists of high consumption of fish, seaweed, and vegetables and low consumption of simple carbohydrates and red meats, is also associated with telomere maintenance (Lee et al., 2015). A “plants plus” diet oriented around vegetables with only “sensible carbohydrates” and minimal saturated fats is best for mental health (Borysenko, 2014).
Diet plays a major role in stress tolerance, which depends on a healthy microbiome. The serotonin-containing cells in the enteric nervous system play a role in linking the food we consume and activity in our gut to our brain. The microbes that feed on the food influence our mood through gut-brain interactions. For example, a diet low in tryptophan, the amino acid precursor to serotonin, results in less serotonin and potentially depressed mood. The gut bacterium Bifidobacterium infantis plays a role of making tryptophan available to be synthesized into serotonin. Microbial metabolites can increase the production of serotonin in the enterochromaffin cells in the gut. The vagus nerve signals the brain when enough is available, having an effect on mood and stress tolerance.
Though so-called comfort foods do provide momentary comfort during periods of stress, a chronically stressed person experiences only a temporary inhibition of the stress response system. The benefits are short-lived and are followed by many more hours of emotional discomfort, as well as cognitive fog, the growth of fats cells, and even obesity (Tomiyama et al., 2011).
Various gut hormones act through feedback loops to the reward pathways in the brain that boost appetite. Those associated with overeating include dopamine-containing cells, which increase appetite, while certain appetite-suppressing signals decrease dopamine release. These dopamine pathways follow the main route through which all addictive behaviors activate: the nucleus accumbens. The reward system and the appetite cycle worked well together for hunter-gatherers to promote motivation for food seeking. However, with constant food availability, many people find it difficult to resist the temptation to eat out of habit and addiction. If the food is salty, fatty, and/or sugary, it becomes even a greater source of addiction. Fast food outlets build their menus to incorporate these factors and yield great profits. Consistent with our vulnerability to fast foods, many processed food companies have developed recipes that we “cannot eat just one.” The consequences of regular consumption of such empty-calorie foods include dysbiosis of the microbiome, low-grade inflammation (metabolic endotoxemia), autoimmune disorders, and anxiety and depression.
Shifting the microbiome to promote mental health is consistent with the benefits of the Mediterranean or Okinawan diet. For example, healthy microbes in the colon metabolize many of the undigested plant-derived carbohydrates into short-chain fatty acids. Among them is butyrate, so named because of its buttery odor. It plays a key role in providing nutrients for the cells lining the colon and protects the brain against the destructive effects of low-grade inflammation caused by a high-fat diet and artificial sweeteners (Mayer, 2016). Butyrate aids in plugging the leaks in the gut by acting as a messenger to turn up the volume on genes to make more protein chains in the gut wall to tighten it. Butyrate causes the release of leptin for satiety, which plays an important part in preventing obesity.
Prior to 11,000 years ago, our ancestors walked approximately 10 miles per day in search of food. Because the portion of the human genome that determines our basic physiology has remained unchanged, it leaves us poorly adapted to our current sedentary lifestyle and diet (Cordain, Gotshall, & Eaton, 1998). Many of the genes selected for the survival of our ancestors now impair our health. The result is that physical inactivity makes us more susceptible to chronic illnesses. This largely accounts for the increase in the prevalence of such illnesses as atherosclerosis, certain cancers, obesity, and type 2 diabetes (Booth & Neufer, 2005). During my presentation to the police officers I was informed that the department gave them free membership to local gyms. By a show of hands, only two indicated they took advantage of this perk. Not coincidently, those two looked the healthiest, with bright eyes and taking frequent notes during the seminar.
Well over 60 percent of Americans are overweight, and only 25 percent are physically active. More troubling is that only 10 percent are active enough to achieve fitness. The critical point that must be addressed in psychotherapy is that exercise is a key component of improving mental health.
Regular exercise not only burns off excess calories and weight but also increases the insulin receptor sites throughout the body to aid in the metabolism of glucose. The initial burst of pro-inflammatory cytokines after exercise seems to trigger the body’s anti-inflammatory mechanisms to keep inflammation in check (Goebel et al., 2000). As we age the potential for inflammation rises. However, with older adults, resistance training, flexibility training, and aerobic exercise all lead to improved levels of optimism and the lifting of depression, but only aerobic exercise led to lowering of inflammation as measured by reduced levels of C-reactive protein and interleukin-6.
Exercise offers one of the best antidepressant and antianxiety treatments. It costs nothing and offers only good “side effects.” A wide variety of factors contribute to these positive effects. Exercise promotes increased efficiency of the neurotransmitters serotonin and dopamine, which are the very neurotransmitters targeted by the major antidepressant medications. Exercise upregulates these neurotransmitters, in contrast to medications, which downregulate them. In other words, exercise promotes their activity long afterward, promoting less relapse, in contrast to medications, which are notorious for relapse of depression after “treatment.”
In addition, as described in Chapter 9, depression is associated with abnormal default-mode activity. Exercise has been shown to decrease and normalize default-mode network activity (McFadden et al., 2013). Meanwhile, exercise has been shown to bolster executive network activity across all age groups.
Exercise as a Treatment for Depression
Because our genes evolved with the expectation of a certain threshold of physical activity for normal gene expression, regular exercise restores the homeostatic feedback mechanisms toward the normal physiological range of our ancestors. Daily exercise normalizes gene expression critical for not only general health but also mental health.
Movement alone is a step in the right direction (pun intended). The trend toward weakening of skeletal muscle has been estimated to range from 8.8 percent in people under seventy years of age to 17.5 percent in people older than eighty years. People with weak muscles have a greater risk of mortality and health problems. Whereas contracting muscles increases their glucose uptake, reduced physical activity is associated with a rapid development of insulin resistance.
A large number of genes in the skeletal muscles are activated after exercise. Based on the duration of the exercise, the genes fall in three categories. “Stress-response genes” are activated during the later phases of exercise. Their protein concentrations rise quickly to high levels and return to normal levels very quickly after exercise. These acutely sensitive genes encode proteins that are part of the general response to stress in all types of cells and include heat-shock proteins and some transcription factors—immediate-early genes. The second category is referred to as “metabolic-priority genes” that are required as a consequence of metabolic stress, such as when muscle glycogen and blood glucose levels are low. These genes can also be expressed at high levels, usually peaking after a few hours and returning to normal levels after twenty-four hours. The third category is referred to as “metabolic/mitochondrial enzyme genes.” These genes encode protein whose function is to convert food to energy. They produce much lower concentrations but do not return to normal levels for up to one week. These genes play a role in muscle plasticity, which involve the increase in mitochondrial and capillary concentration.
There are multiple ways that exercise serves as an effective treatment for anxiety. At the most basic level, the buildup of stress increases muscle tension, whereas exercise relaxes the resting tension of muscle spindles, breaking the stress feedback loop to the brain. Exercise lowers blood pressure by increasing the efficiency of our cardiovascular system, pumping healthy levels of oxygen to the brain and increasing the health of the capillaries. (Swain et al., 2003). As our heart rate increases during exercise, so does the hormone atrial natriuretic peptide, which tempers our body’s stress response by going through the blood-brain barrier and attaching to receptors in the hypothalamus to tone down the hypothalamic-pituitary-adrenal axis activity. It also acts on our amygdala and the locus ceruleus to dampen the effects of corticotropin-releasing hormone, part of the neuroendocrine stress system that can induce anxiety.
Exercise upregulates a variety of neurotransmitters and neurohormones to buffer stress and lower anxiety. During and after exercise there is a release of endorphins and neuropeptides that bind to opioid receptors in the brain, inducing the so-called runner’s high, with potent analgesic effects and feelings of easiness. Serotonin levels increase when our body breaks down fatty acids to fuel our muscles.
Exercise upregulates GABA. Simply moving the body triggers the release of GABA, whereas benzodiazepines downregulate the GABA system after targeting their receptors. They contribute to tolerance and withdrawal, the hallmarks of addiction. When they wear off the ill-informed patient experiences “anxiety sensitivity” and feels more anxiety during early withdrawal, sometimes prompting the mistaken assumption that the patient “needs” the drug. Benzodiazepines also contribute to depression. The bottom line is that taking these drugs is similar to wading into a warm pit of quicksand. He feels good initially, but soon he is sucked down into the abyss of depression and, ironically, more anxiety.
Exercise promotes multiple brain enhancing mechanisms, which are critical for brain health. They include neurotrophic factors that rebuild brain structure and enhance blood flow. The two neurotrophic factors which have received the most attention are BDNF and glial-cell-derived neurotrophic factor. Both are involved in neuroplasticity and neurogenesis. BDNF has been shown to produce new neurons in the hippocampus and prefrontal cortex. Glial-cell-derived neurotrophic factor (GDNF) is involved in new glial cells. Both are released after exercise, and both enhance cognition and diminish depression.
Brain Health and Exercise
Mechanism | Impact |
Gene expression | Neuroplasticity |
Brain-derived neurotrophic factor (BDNF) | Neuroplasticity, neurogenesis (Adlard, Perreau, & Cotman, 2005) |
Insulin-like growth factor-1 (IGF-1) | Neural energy utilization (Carro, Trejo, Busiguina, & Torres-Aleman, 2001) |
Nerve growth factor (NGF) | Enhanced neuroplasticity (Neeper, Gomez-Pinilla, Choi, & Cotman, 1996) |
Vascular endothelial growth factor (VEGF) | Strengthening blood vessels. Also, enhanced neurogenesis (Fabel et al., 2003) |
These repair factors also help prevent the damaging effects of chronic psychological stress by keeping the stress hormone cortisol in check. High levels of cortisol have a corrosive effect on the hippocampus, resulting in its atrophy. Because the hippocampus is critical for laying down new memories, chronically high stress can result in a memory deficit and the inability to turn off the hypothalamic-pituitary-adrenal axis.
The bottom line is that exercise is an indispensable adjunct to therapy. Clients who do not engage in regular exercise undermine their recovery. Exercise reduces stress, anxiety, and depression by pumping up the levels of neurotransmitters GABA, acetylcholine, serotonin, dopamine, and norepinephrine that keep us calm, positive, and energized. It also increases the repair factors to maintain and build a healthy brain.
When I asked the police officers about their sleep, most reported that they had too little of it because of insomnia or frequent awakenings during the night. Sleep medication, either prescribed or over the counter, were common, and the officers reported diminishing benefits after a few days. Many of the officers reported waking up in the morning feeling groggy and then going directly to coffee or energy drinks.
When I informed them that there were a variety of sleep hygiene techniques that can help them get good-quality sleep. One said, “Crappy sleep is a hazard of the job.” The rest nodded, punctuated with sarcastic laughs.
We spend one-third of our lives asleep. The quality of that sleep plays a major role in our cognitive and emotional experience during the other two-thirds of our lives. Failure to follow a healthy sleep schedule increases mortality risks, mood disorders, and even cancer prevalence (Evans & Davidson, 2013). Many companies and, surprisingly, health care programs have failed to heed the results of research on rotating shift work, which show not only major health risks but also a wide range of work performance problems: not just more accidents and health costs but also cognitive deficits such as poor and risky decisions (Venkatraman, Chuah, Huettel, & Chee, 2007).
Sleep provides a means through which the brain can clear out toxins. During sleep a plumbing system for cerebral spinal fluid called the glymphatic system opens up, letting fluid flow more efficiently through the brain. Glia cells control the flow through the glympathatic system by shrinking or swelling. Norepinephrine, an arousing neurotransmitter, controls cell volume: with a low level of norepinephrine, such as during healthy sleep, fluid flow increases because of the greater space between the cells. Because toxic molecules, including beta-amyloid involved in neurodegenerative disorders, tend to accumulate in the space between brain cells, a healthy glymphatic system provides a method to clear them out (Xie et al., 2013).
As an illustration of the importance of good-quality sleep, chronic insomnia is associated with shorter telomeres (Blackburn & Epel, 2017). In other words, sleep is critical for the overall maintenance of the brain, and without good-quality sleep we age quicker and suffer cognitive and mood regulatory deficits.
Functions of Sleep
The Whitehall Study of thousands of British civil servants found that men who slept five or fewer hours most nights had shorter telomeres than those who slept more than seven hours. These results were independent of obesity, socioeconomic status, and depression (Jackowska et al., 2012). Studies suggest that an average of seven hours of good-quality sleep per evening is optimal (Ferrie, et al, 2011). Six hours of sleep is reported as the minimum biological requirement and for this reason is referred to as the “core sleep.” However, people who sleep more than nine or less than six hours, while not constituting a sleep disorder, are at greater risk of cardiovascular disorders, hypertension, type 2 diabetes, and other disorders correlated with inflammation.
Sleep deprivation causes
•Heightened risk of type 2 diabetes
Sleep deprivation results in a drop in the ability to clear glucose through insulin, decrease leptin (which would normally inhibit hunger), and increase ghrelin (which increases hunger). Taken as a whole, these factors are consistent with the overall concept that sleep deprivation contributes to weight gain, a fact now supported by at least fifty studies (Strickgold, 2015). Sleep deprivation, even after one week, can promote weight gain through an increase production of ghrelin, matched by a decline in the production of the hormone leptin. The increased appetite associated with sleep loss tends to promote the consumption of foods high in simple carbohydrates and calories, at the expense of hunger for fruits, vegetables, and high-protein foods. Sleep-deprived people may consume up to 33–45 percent more calories than non-sleep-deprived people.
Sleep deprivation destabilizes the functioning of mental operating networks, for example, with deficits in attention and task completion of the executive network. There appears to be abnormal “resting state” activity associated with the default-mode network (Gujar, Yoo, Hu, & Walker, 2010). Correspondingly, sleep deprivation reduces default-mode network (DNM) connectivity (De Havas, Parimal, Soon, & Chee, 2012). Sleep deprivation has been shown to alter the activation of the salience network, and its reward process is associated with overeating (Fang et al., 2015).
Given that when memory is reenacted it becomes unstable, the mood that we are in during sleep reconsolidates memories within the context of that mood. In fact, the concept of memory reconsolidation has itself changed to memory evolution. When sleep deprived, we form twice as many memories of negative events as positive events. Coupled with decreased executive network activity and increased DMN activity, this fuels the DMN tendency to ruminate on negative memories and increase depression. Sleep can result in memory evolution of traumatized feelings that increase with nightmares, such that acute stress disorder evolves into posttraumatic stress disorder (PTSD).
People who suffer from trauma generally experience fragmented sleep and less slow-wave (stage 4) sleep. Slow-wave sleep is critical for consolidating explicit memory, while REM sleep is critical for consolidating procedural memory. Sleep deprivation results in impairments in attention, new learning, and memory. During sleep unstable memory traces are reconfigured into more permanent ones for long-term storage (Frank, Issa, & Stryker, 2001).
In addition to insomnia, people who suffer from trauma wake up feeling sleep deprived as well as fatigued. They also have reduced time in REM sleep, in part because of the increase in norepinephrine. Because norepinephrine is generally inactive during REM for people without PTSD, the failure to shut down norepinephrine in people with PTSD leads to an incomplete entry to REM sleep. And as noted above, high levels of norepinephrine impair the glymphatic system’s ability to clear out toxins.
One night of sleep deprivation can negatively shape emotional memories, impairing a person’s ability to recognize positive or neutral words by 50 percent (Strickgold, 2015). In other words, when sleep deprived we are prone to lay down twice as many memories of negative events as positive ones, which contributes to depression.
Sleep loss, as well as sleep disturbances, tends to result in impairments in the immune system. It has long been known that people who experience less than 6 hours of sleep tend to be more susceptible to illness, such as viral infections. Sleep loss and disturbances have been associated with the reduction in lymphocyte responses and natural killer cell activity. Insomnia has been associated with elevations in inflammatory markers such as interleukin-6 and tumor necrosis factor alpha (Vgontzas, et al., 2002). Pro-inflammatory cytokines are associated with inducing sleep, particularly slow-wave deep sleep. Cortisol levels are the lowest during slow-wave sleep, and the levels rise late in the sleep cycle during REM periods.
This may be one of the reasons that not just daytime sleepiness and fatigue but also achiness and depressed mood follow a night with insomnia. Inflammatory biomarkers such as C-reactive protein and interleukin-6 are associated with metabolic disorders and have been shown to be associated with sleep dysregulation.
As noted throughout this book, for many people health problems that disrupt the length and quality of sleep tend to be associated with mental health problems. For example, people with sleep-disordered breathing tend to be overweight. Common and obstructive sleep apnea is often associated with fat buildup or loss of muscle tone. Sleep-impaired breathing represents a range of sleep disorders that tend to be underdiagnosed and strongly associated with cognitive decline and mood disorders. People with sleep apnea are especially vulnerable. They suffer from an increased risk of coronary heart disease, hypertension, type 2 diabetes, mental health disorders, cognitive impairment, and dementia. Likewise, all of these health problems, as well as sleep dysregulations, are associated with increased levels of inflammation. However, when people with sleep apnea are put on a continuous positive airway pressure (CPAP) device, cognitive decline and depression can be arrested (Osorio et at., 2015).
When not complicated by artificial light, our sleep pattern and circadian rhythm follow the daylight length. When full-spectrum light hits our retina, this signals our pineal gland that it is daytime. Our pineal gland responds by suppressing its release of melatonin, signaling that it is not time to sleep. Alternatively, when it is dark, our pineal gland releases melatonin to induce sedation.
Resetting the circadian rhythm represents a key part of treating insomnia. Because the amount of light to which we are exposed during the daytime affects sleep, clients with insomnia should maximize exposure to bright light in the daytime to set the body clock to match the natural day/night cycle. Exposure to bright natural light in the late morning encourages lower body temperature in the middle hours of the sleep cycle and promotes staying asleep. With early morning awakening, clients should expose themselves to bright light, helping ensure that the pineal gland does not produce melatonin throughout the day and that his body temperature will be the lowest during sleep. If clients suffer from insomnia they should not use a computer in the late evening because this is essentially looking at light, which tricks the brain into adjusting to a daytime pattern, suppressing the pineal gland’s secretion of melatonin. Clients with insomnia need soft light a few hours before going to sleep.
The circadian rhythm for cortisol involves approximately ten bursts every day, with most of the pulsations occurring between 4 a.m. and noon. This rhythm served an evolutionary purpose, aiding our ancestors to be alert first thing in the morning, because safety required vigilance around dawn, when most predators were on the prowl. Ideally, during a six-hour period prior to 4 a.m. the absence of cortisol bursts allows for a restful sleep. In contrast, with chronic stress, cortisol levels do not level out, resulting in greater potential for insomnia.
A healthy circadian rhythm involves regulating body temperature. Insomnia can result from difficulty in regulating nighttime body temperature. Body temperature may actually increase at night when it should be going down, which may occur if the person fails to get any exercise in the daytime. During the early sleep cycle our body temperature should be in the process of dropping. Just before rising from bed our body temperature rises, as do cortisol levels.
A key way to keep body temperature cool at night, to achieve the deepest sleep, is to make sure the bedroom is cool. Warm bedrooms promote light and/or disrupted sleep. Taking a hot bath helps not only as a wind-down activity but also by raising body temperature while in the tub, which then drops sharply by bedtime.
Despite the folklore about alcohol promoting sleep, it suppresses slow wave sleep. Three hours after drinking alcohol, the induced glutamate blockade wears off, contributing to “sleep maintenance” insomnia, also referred to as mid-sleep cycle awakening. This type of insomnia occurs during the middle of the sleep cycle, and it takes one to two hours to get back to sleep. Also, many people who suffer from insomnia resort to over-the-counter sleep drugs or physician-prescribed benzodiazepines. However, these drugs contribute to shallow sleep, minimizing slow-wave (deep) sleep, and lead to dependence and tolerance.
This chapter began by noting that self-maintenance comprises the first responders to mental health crises, as the critical stabilizers. Self-care behaviors must be addressed immediately, without which the traditional psychotherapy interventions may be fruitless.
Mental health studies have shown that lifestyle factors, diet, cognitive challenge, exposure to new environments, social engagement, and exercise on a regular basis are all associated with boosts of cognition and mood (Butler, Forette, & Greengross, 2004). I have used the mnemonic SEEDS—social, exercise, education, diet, and sleep factors—to help people remember to “plant” and cultivate them on a daily basis (Arden, 2014).
SEEDS:
S –Social
E –Exercise
E –Educate
D –Diet
S –Sleep