Understanding Depression
Understanding Depression
Major depression is a syndrome that primarily relies on the subjective categorisation by the individual of their own behaviour. The disorder entails a self-report of negative mood, absence of enjoyment, lack of energy, feelings of worthlessness or guilt, recurrent thoughts of death, and incapacity to concentrate. Several of the behaviours contributing to the criteria for a diagnosis of depression can be measured through observation by another person: motoric agitation or motoric retardation, changes in appetite and sleeping. Ressler and Mayberg (2007) suggested that ninety per cent of individuals with depression are also anxious).
Lambert (2006) reported that the rates of depression have progressively increased across the decades in the United States. Researchers have suggested that males born near the beginning of the 20th century had a 1% probability of becoming depressed, whereas if you were born after 1960 the rate increased to 9% to 10%. If you were a female born around the turn of the 20th century, the rate of depression was 2%, rising to 25% if born after 1960 (Klerman and Weissman, 1989; Wickramaratne et al.,1989).
While the rates of depression have increased across cohorts born after World War II, suicide rates for males remain comparatively constant between 1940 and the 1980s (Maris, Berman, and Silverman, 2000). The rates of depression are acutely high in Europe and the United States in comparison with developing countries. For example, in Taiwan and China, Parker and associates (2001) suggested that less than 1% of individuals reported a mood disorder. Keller et al., (2007) documented that almost 88% of depressive events (either first or subsequent episodes) happen in response to a life event. The onset of the first episode of major depression is preceded by the incidence of a stressful life event in 70-82% of cases (Slavich, Monroe and Gotlib, 2011; Slavich et al., 2010). Personal loss is the most common type of stress associated with developing depression, especially when the loss involves rejection by another (Slavich et al., 2010, 2011). Individuals that have experienced early parental loss are more liable to become depressed after a stressor (Slavich et al., 2011). Kendler and colleagues (2003), found in a sample of 7,322 subjects, that events involving humiliation and loss were more liable to led to depression, whereas events associated with danger and loss precipitate anxiety.
Brain Imaging and EEG Outcomes
Davidson et al., (2002) reported from imaging evidence that individuals with depression exhibit greater activity in the anterior cingulate gyrus brain area. This area in the brain is linked with conflict monitoring. Treadway and Zald (2011) found that individuals with both depression and anxiety displayed increased activation of the amygdala in response to unpleasant imagery. The amygdala is a group of cells located near the base of the brain. There are two, one in each hemisphere and is part of the brain's limbic system. Studies by Johansen-Berg et al., (2008) and Ressler and Mayberg (2007) have also proposed that individuals with both depression and anxiety display stronger activation of the anterior insular cortex and the subgenual anterior cingulate. These two additional areas are associated with conflict monitoring.
The areas in the brain that are correlated with response to reward and motivated behaviour which are strongly innervated by dopamine tend to show reduced levels of activation in individuals that are depressed. Brain imaging research by Der-Avakian & Markou (2012) found lower levels of activation in the ventral striatum and orbitofrontal cortex. In a study by Pizzagalli et al., (2009) subjects with depression failed to respond to a rewarding stimulus with limited activity in the nucleus accumbens. Dunlop and Nemeroff, (2007) reported that consistent with reduced dopamine tone, individuals with depression have lower levels of dopamine metabolites in the cerebrospinal fluid.
Evidence From Hormonal Findings
Across several studies, it has been reported that between 50-70% of depressed subjects displayed elevations in cortisol (the stress hormone) (Müller and Holsboer, 2006; Pace and Miller, 2009). Individuals with depression are also more prone to be dexamethasone nonsuppressors and they typically fail to display the anticipated fluctuations in cortisol release related to circadian rhythms (Dunlop and Nemeroff, 2007). Oxytocin levels are also inclined to be lower in those with depression (Yuen et al., 2014).
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Cognitive Processing
Beck has characterised depression as a pessimistic view of oneself, the world, and the future. Forgeard et al., (2011) has suggested that depressed individuals exhibit negative involuntary thoughts, with a view that negative events are more prone to transpire. Gotlib and Joormann, (2010) suggested that depressed individuals attend to negative stimuli and recollect negative stimuli more than individuals without depression. Some researchers have debated that individuals with depression, cogitate about negative events and are less likely to engage in physical activity after a demanding day (Watkins and Nolen- Hoeksema, 2014).
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Emotional Control or Regulation
Gotlib and Joormann (2010) suggested that depressed individuals have an inability to regulate emotion in the development of a depressed mood. They exposed those individuals with depression who are less skilled at concentrating on a target and disregarding distracting negative stimuli. Task performance of those with depression is especially impaired after an error is made (Pizzagalli, 2011). Sheline et al., (2009) showed that depressed people were unable to downregulate activity in the alarm area (anterior cingulate) when asked to reappraise negative imagery.
Emotional control suggests not only the capacity for inhibiting attention to negative stimuli but also the capability to maintain a positive focus. Tomarken and Keener (1998) have debated whether those with depression have difficulty sustaining positive affect. Evidence from several studies supports the hypothesis that those with depression have an inability to sustain positive emotions. Heller et al., (2009) compared the responses in individuals instructed to enhance, suppress, or attend to positive and negative stimuli over 37-minutes. The authors reported no differences initially in activity in the nucleus accumbens between depressed and non-depressed subjects to the positive imagery in the enhanced condition. However, during the concluding half of the period, depressed subjects could not sustain the activity in the nucleus accumbens to the positive imagery. This contrasted with those without depression who could sustain activity in the nucleus accumbens.
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The notion that depressed individuals have difficulties with emotional regulation is also constant with outcomes from the investigation of the startle response. A startle response to an aversive noise is controlled by a prior presentation of positive or negative images. In nondepressed individuals, the startle reflex is diminished by positive imagery and heightened by negative imagery. Dichter and associates (2004) revealed that depressed individuals were unaffected by the pictures. On initial viewing of neutral images, depressed subjects were startled as readily to the aversive noise as the control subjects viewing the negative pictures. However, the startle response of depressed individuals was not reduced by the positive imagery. Consequently, prior context did not change the startle response of the depressed persons.
The areas of the brain involved in restraining impulses, delaying a prepotent response, restraining the amygdala after loss, and regulating mood include the dorsolateral prefrontal cortex and the ventromedial prefrontal cortex (Hartley and Phelps, 2010). There is evidence that these structures in persons with depression may be dissimilar to nondepressed individuals. Davidson et al., (2002) found that those with depression show less activity in the dorsolateral prefrontal cortex and dorsomedial prefrontal cortex. Those with depression, when asked to inhibit negative affect in response to negative imagery, demonstrated less activation of the left ventral lateral prefrontal cortex and less diminution in amygdala activity (Johnstone et al., 2007).
Conceptional Models of Depression
Learned Helplessness
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In 1967, the learned-helplessness hypothesis was introduced by Seligman and colleagues. The researchers hypothesized that animals learned that outcomes were independent of their responses. The study design is composed of three groups with one group able to escape shock where shock offset is contingent on the animal’s response. This group of dogs learned in the hammock to press a panel with their noses to turn off each shock. The second group is yoked to the escapable shock group. In this early experiment, on each trial, the yoked group dogs received the average duration of shock that the escapable shock group produced on each trial. In the inescapable shock group, shock offset and all the animal's responses are non-contingently related. A third group gets no shock.
The subsequent day the dogs were examined in a shuttle box escape environment. The outcomes reported were that two-thirds of the dogs from the inescapable shock group failed to learn to escape, while 90% of the dogs in both the escapable shock group and control groups easily learned to escape. Significantly the escapable shock and the control group learned to escape equally well. It was concluded from this result that the dogs in the inescapable shock group had learned in the hammock that shock offset was independent of their responses and when the shock occurred in the shuttle box, they expected that its offset would once again be independent of responding. This expectation challenged their trying (“response initiation”) to escape. The fact that the escapable shock group did not do better than the control group and that the main effect was that the inescapable group did worse than both other groups strongly influenced the belief that helplessness had been learned.
The brain circuitry resulting in learned helpless behaviour has been acknowledged with the uncontrollability of the shock being detected by the lateral habenula. The lateral habenula projects to the caudal dorsal raphe nucleus, which in turn projects to the amygdala to initiate anxiety-associated behaviours. The lateral habenula also projects to the ventral tegmental area to inhibit cells in this area that project to the nucleus accumbens. The net result is lowered release of dopamine from the neurons in the ventral tegmental area to the nucleus accumbens (Balcita-Pedicino, Omelchenko, Bell and Sesack, 2011; Friedman et al., 2011; Omelchenko, Bell and Sesack, 2009). While the reduction of dopamine is not a loss of pleasure as such, it does suggest a reduction of interest in and a loss of motivation for responding to both positive and negative stimuli. Therefore, there will be a failure of activation of the ventral striatum (the projection area of the ventral tegmental area) in response to rewards. Furthermore, an inability to mount an excited response is observed (Der-Avakian and Markou, 2012; Treadway, Bossaller, Shelton and Zald, 2012).
The lateral habenula is in the brain that establishes circadian rhythm and sleep-wake cycles. The increased activity in the habenula may clarify the sleep disruption that is frequently observed in those with depression (Aizawa, Cui, Tanaka, & Okamoto, 2013).
Inflammation
Controlled Research in Animal Models
Maier and Watkins, (1998) have demonstrated that exposure to uncontrollable shock also increases the level of interleukin-1β (IL-1β), an inflammatory cytokine in the brain. When an antagonist to IL-1β is placed into the hippocampi of animals exposed to uncontrollable shock, the depressive behaviours (i.e., less moving around, and less drinking of sugar water) withdraw. This finding suggests that inflammatory molecules in the brain play a fundamental role in producing the depressive profile. Maier and associates also examined whether inflammation attributable to a response to a pathogen would also result in depressive behaviour. The authors positioned part of the cell wall of a bacterium, lipopolysaccharide, into the appendage of the animal. This procedure elevated the level of inflammatory cytokine in the blood of the exterior regions. Consequently, this led to more IL-1β in the animal’s brain with the animal displaying depressive actions. When an antagonist for IL-1β was placed into the hippocampus, the depressive behaviours faded (Maier and Watkins, 1998).
Other researchers have manipulated peripheral inflammation either with lipopolysaccharide or administration of an inflammatory cytokine. In animal models, after administration of lipopolysaccharide or administration of cytokines, inflammatory cytokines increase in the brain and the animal loses preference for previously favoured foods and displays more social avoidance, less exploration, an increase in cortisol levels, and an increase in body temperature (Dantzer et al., 2011; Nadjar et al., 2005). In terms of brain responsivity, the animals are less willing to work to apply electrical stimulation in areas associated with dopamine release (Borowski et al.,1998), and increased levels of activation in the bed nucleus of the stria terminalis in the anxiety region (amygdala) are noted (Engler et al., 2011; Frenois et al., 2007).
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Research in Humans
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Results from human studies, in which inflammation is induced in the periphery, report both reduced response in reward areas and stronger response in distressed areas. The way peripheral inflammation is generated has varied across studies. For example, Eisenberger et al., (2011) reported that following lipopolysaccharide administration in the periphery, subjects displayed less activation in the ventral striatal area in response to financial reward. In those females administered lipopolysaccharide in the periphery, greater activation of the dorsal anterior cingulate cortex was found in response to social exclusion (Eisenberger et al., 2009) and higher activation was reported in the amygdala in response to fearful faces (Inagaki et al., 2012).
Harrison and associates (2009) vaccinated subjects with nonharmful bacterial proteins to induce systemic inflammation. As anticipated, the inoculated subjects exhibited activation in the anterior cingulate cortex. Inoculation with interferon-α, an inflammatory cytokine, is used to treat melanoma and hepatitis C. Subjects treated with interferon-α showed activation in the dorsal anterior cingulate cortex (Capuron et al., 2005). Capuron et al., (2012) also reported less activity in the nucleus accumbens and other brain structures activated by dopamine after interferon-α treatment. The images were almost indistinguishable from the images from Parkinson patients whose dopamine neurons die and who as a group show elevations in depressive symptoms (Miller et al., 2013).
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Correlational Research in Depressed Persons
Numerous researchers have reported that inflammatory markers are elevated in the blood of those with depression and anxiety. Elevated levels of interleukin 6, tumour necrosis factor-alpha, C-reactive protein, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1 have been acknowledged (Dowlati et al., 2010; Howren et al., 2009; Rajagopalan et al., 2001; Raison et al., 2006; Schiepers et al., 2001). There are, however, false negatives that suggest that depression is not constantly correlated with inflammation (Musselman et al., 2001). Conversely, the level of inflammatory cytokines does predict failure to respond to antidepressant treatments (O’Brien et al., 2007; Yoshimura et al., 2009).
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Stress and Inflammation Hypothesis
Investigators have also exposed subjects to stressful conditions, such as the Trier Social Stress Test. In this example, subjects are assigned to give a speech about a painful subject (e.g., your most embarrassing moment) to a hostile audience. This practice resulted in elevations in interleukin-6, with those subjects who were already depressed showing greater increases in interleukin-6 (Pace et al., 2006). Other research models have been used to evaluate the association between stress and inflammation. In response to social rejection or a laboratory stressor, levels of inflammatory cytokines increase, which relate to activation in the dorsal anterior cingulate cortex (Slavich et al., 2010).
Correlational outcomes are also obtainable for individuals undergoing specific types of stressors. For example, Cole et al., (2007) examined levels of a transcription factor for inflammatory cytokines (nuclear factor-κB [NF-κB]). The authors noted that levels are elevated in lonely individuals. The partners of individuals with Alzheimer’s disease have elevated interleukin-6 levels (Kiecolt-Glaser et al., 2003; von Känel et al., 2006). Those who are under stress in the work environment display elevations in intercellular adhesion molecule-1, inflammatory cytokines, and fibrinogen (a factor that facilitates blood clotting) (Hong et al., 2006; Ramachandruni, Handberg, and Sheps, 2004; Steptoe et al., 2003; von Känel, et al., 2001). Slavich et al., (2010) reported that those with higher levels of tumour necrosis factor-alpha at baseline showed greater activation of the dorsal anterior cingulate cortex in response to social rejection.
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Anti-Inflammation Factors and the Hygiene Hypothesis
There are several studies in which inflammatory cytokines are increased either by a psychological stressor or by presenting a pathogen, which suggests that inflammation is a proximal cause of depression. The discussion focuses on inflammatory cytokines. However, the leukocytes also produce anti-inflammatory cytokines, such as interleukin-10 and transforming growth factor-beta, following the removal of a pathogen. Correlational outcomes suggest that depressed individuals also have lower levels of interleukin-10 along with their higher levels of inflammatory cytokines (Li et al., 2010).
The hygiene premise has been suggested to describe why individuals in developed countries have higher levels of depression, anxiety, inflammatory bowel disease, and asthma. In certain environments where there is significant exposure early in life to bacteria, such as Mycobacterium vaccae from animal faeces, relatively high levels of interleukin-10 are produced. The elevations in anti-inflammatory cytokines will create resilience to the impact of future environmental stressors (Rook and Lowry, 2008).
Brain Mechanisms
The pathways through which brain inflammation and elevated cytokines can change behaviour are now beginning to be interpreted. Several new chemicals such as neutrophil gelatinase-associated lipocalin and orexin may be proximal causes. Neutrophil gelatinase-associated lipocalin is increased with inflammation and is relevant for hippocampal signalling (Naudé et al., 2014). Orexin is decreased with inflammation and is relevant for activation of appetitive structures (Weymann et al, 2014). When inflammatory cytokines increase in the brain, the activity of the habenula is increased (Hikosaka, 2010). As previously conferred, habenula activity is increased in learned helplessness. Upcoming research will hopefully provide greater specificity concerning the pathways through which inflammation influences behaviour.
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Heritability
Heritability for major depression is approximately 31- 42% (Dunlop and Nemeroff, 2007). Alleles for proteins in the dopamine pathways do predispose for depression (Dunlop and Nemeroff, 2007). Though, the most studied allele for depression is the short promoter allele for the gene for making the serotonin transporter. The short transporter predisposes to depression. With the short transporter, reduced amounts of the serotonin transporter are produced with, serotonin remaining in the synapse cleft for a longer period. In individuals without a mood disorder (those with a short transporter) show stronger amygdala response to frightening images (Hariri et al., 2002). Additionally, those with short transporters show lower volume in brain areas that regulate emotions (Pezawas et al., 2005). Those with two short transporter alleles display greater cortisol spikes following a stressor (Gotlib et al., 2008).
While most of the heritability studies have assessed how individuals with the short transporter respond to negative stimuli, Way and Taylor (2010) studied the response to positive stimuli. Those with the short transporter are more responsive to positive events. Researchers have found that those with the short promoter for serotonin transporter were less happy in unstable relationships but happier than others in supporting relationships. Therefore, the allele for the short promoter seems to convey greater responsivity to the environment, rather than depression under all conditions.
Contemporary research suggests that it is a genetic and environmental interaction that increases the risk for depression. Academics have reported that alleles only predispose to depression given a stressful environment. Uher et al., (2011) found that the short serotonin transporter only leads to depression given a stressful childhood environment. Additionally, social support can ameliorate the risk of increased depression of those with both the genetic predisposition and childhood neglect (Kaufman et al., 2004). Another genetic variation, which can lead to depression is the G allele for the oxytocin receptor. However, if an individual with one or two copies of the G allele has a positive childhood home environment, then the individual rates higher on empathy, enthusiasm, and confidence (McQuaid et al., 2013). The outcomes for various alleles, which increase the risk for depression, are greatly influenced by the environment. Given a supportive environment, risk alleles can promote positive outcomes.
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Tasks to Increase Regulatory Capability
Some researchers believe that depressed individuals may have underdeveloped regions in the brain for controlling or regulating both good and bad moods. Some researchers have developed strategies for improving regulatory control. For example, deRaedt et al., (2010) used transcranial magnetic stimulation of the dorsolateral prefrontal cortex over a succession of days, improved subjects’ mood, and enhanced inhibitory control.
An approach called cognitive rehabilitation has been established that targets the prefrontal cortex to increase capacity for emotional regulation. Siegle and colleagues (2007) stated that cognitive rehabilitation begins by isolating affected cognitive functions and brain regions through neuropsychological assessment and neuroimaging. Siegle and associates approach employs specific cognitive tasks to develop capacity through the prefrontal cortex.
Cognitive rehabilitation is dissimilar to traditional therapy, in which individuals converse their problems (which can be a painful process). The traditional approach focuses on clients externally. Siegle et al., (2007) utilise two tasks. In the first undertaking, subjects were instructed to distinguish a specific bird sound from white noise. The second task involved the presentation of numbers, one at a time, on a screen. The subject was asked to add the last two digits appearing on the screen. Therefore, the subject had to add, while keeping in short-term memory both the answer and the last digit presented so that this digit could be summated with the next digit that appeared on the screen. Following two weeks of training, depression and cogitation had decreased more in the trained group than in the control group. Furthermore, the amygdala displayed less activation in response to negative stimuli and there was an increase in prefrontal cortex activity.
The research on using cognitive tasks to increase regulatory control is consistent with animal studies. For instance, animals contained in enriched environments have greater ventromedial prefrontal cortex responses and are more resilient given social defeat (Lehmann and Herkenham, 2011).
Cognitive Behavioural Therapy
In the National Institute of Mental Health Collaborative Depression Study (1989), antidepressant treatment was compared with cognitive behavioural therapy (CBT). Antidepressants were found to produce improvement faster but by the end of the study, outcomes were comparable (Elkin et al., 1989; Shea et al., 1992, Watkins et al., 1993).
Individuals who were severely depressed had comparable outcomes for CBT and medications, although a meta-analysis demonstrated that CBT achieves a larger effect size (DeRubeis, et al., 1999). In a particular study, subjects were randomly assigned to conditions with the following outcomes reported. For the moderately to severely depressed at 16- weeks demonstrated that 58% of subjects achieved at least 50% reduction in symptoms in both the CBT and drug conditions. Furthermore, forty-six per cent of subjects were remitted in the antidepressant group compared to 40% in the CBT group. Those treated with CBT displayed lower rates of relapse than those on drugs (Evans et al., 1992; Simons et al., 1986).
Dietary Intake and Nutrition
Omega-3 Fatty Acids
Fatty acids in which the first double bond is three carbons away from the end of the methyl end of the fatty acid chain are called omega-3s. Omega-3s include docosahexaenoic acid and eicosapentaenoic acid with fish oil and walnuts suitable sources of omega- 3s. Omega-3s have been suggested to decreasing inflammation through a variety of mechanisms. For example, omega-3s increase heart rate variability (Farooqui et al., 2007) and consumption levels relate to heart rate variability in adults (Mozaffarian et al., 2008). Omega-3s are converted in the body to resolvins and protectins, which reduce inflammation. Moreover, researchers have reported that there are receptors for resolvins and omega-3s on white blood cells (Ji et al., 2011; Oh et al., 2010; Oh and Olefsky, 2012). When omega-3s bind to the GPR120 receptors on white blood cells (inflammation is inhibited and insulin sensitivity increases (Oh et al., 2010).
Omega-3s have been documented to skew the microbiota in the gut toward anti-inflammatory types (Forsythe et al., 2010). As well as having powerful anti-inflammatory effects, there are receptors for omega-3 in the hypothalamus. When the omega-3s bind to these receptors, they increase metabolic rate and reduce appetite (Cintra et al., 2012; Lam et al., 2012). The link between high levels of omega-3 consumption and a lower probability of experiencing depression has been observed (Kiecolt-Glaser, 2010). Individuals who have diets enriched with omega-3 experience fewer increases in inflammation under stress (Maes et al., 2000). They are also at reduced risk for the development of other inflammatory diseases, including cardiovascular disease and type 2 diabetes (Arita et al., 2005).
A preliminary test of omega-3s, particularly eicosapentaenoic acid, has shown potential as a monotherapy in treating depression. Although the difference between placebo and omega-3 did not reach statistical significance in this small study (n = 35; p = 0.087), there was a 45% response rate in those receiving omega-3s compared to a 23% response rate in the placebo group (Mischoulon et al., 2009). In a randomly assigned study, omega-3s decreased the stress levels of medical students during examinations (Kiecolt-Glaser et al., 2011). Further work with an adequately powered study is required before conclusions can be drawn.
Mediterranean Diet Curcumin and Vitamin D
Mediterranean diets have been associated with lower cytokine levels, less oxidative stress, and lower levels of depression (Luciano et al., 2012; Sánchez-Villegas et al., 2009). A specific protective effect has been reported for high consumption of fruits, nuts, and beans, while consumption of whole-fat dairy and meat was harmful (Sánchez-Villegas et al., 2009).
Apart from the Mediterranean diet, curcumin, which is found in turmeric, is anti-inflammatory and suppresses the activation of NF-κB, a transcription factor inducing the expression of many inflammatory cytokines (Aggarwal, 2010; Shehzad, Rehman and Lee, 2013). Curcumin has been suggested to produce antidepressant effects like fluoxetine in animals (Wang et al., 2008) and has been suggested to be better than placebo treatments in humans (Lopresti et al., 2014). According (Anand et al., 2007) Black pepper enables the absorption of curcumin.
Vitamin D
Vitamin D can assist in the differentiation of the anti-inflammatory white blood cells (T regulatory cells) as well as reducing activation of NF-κB transcription factor activity. Vitamin D is linked with higher levels of IL-10 and lower levels of inflammatory cytokines (Adler and Steinbrink, 2007; Adorini and Penna, 2009). A meta-analysis by Shaffer et al., (2014) suggests that for individuals with clinically significant levels of depression, vitamin D supplementation has a moderate effect on decreasing symptoms. however, the number of studies is limited.
Avoid Inflammatory Influences
High levels of saturated fats in the diet enhance inflammation in numerous ways. For example, in white blood cells, toll-like receptors in which saturated fats will bind result in being activated (Milanski et al., 2009). Specific proteins keep the cells lining the intestinal tract together so that microbes do not the bloodstream. However, saturated fats disrupt these cell connectors enabling the bacteria to cross the barrier. Additionally, high saturated fats in the diet will alter the composition of the microbes in the intestine toward more inflammatory species and decrease microbe species diversity (De La Serre et al., 2010; Lam et al., 2012). Gut microbiota has become a hotbed of research as stress alters the gut microbiota (Wang and Kasper, 2014). Microbiotas are a feature of obesity. In animal studies, if the faeces of lean animals are inserted into obese animals, these animals lose weight. The mechanisms through which bacteria influence hunger are multifaceted.
Saturated fat also influences the neurons in the hypothalamus, which regulate hunger and metabolic rate. A high-fat diet induces stress in these cells. In the hypothalamus, brain glial cells also release more inflammatory factors given a high-saturated-fat diet (Maric et al., 2014; Schneeberger et al., 2013). Sobesky et al., (2014) reported that a high-fat diet also increases the level of inflammatory cytokine production in the hippocampus in response to stress. The sugar contained in fruit consists of sucrose, which is a glucose molecule associated with a fructose molecule. Sucrose is not inflammatory; however, the food industry now uses carbohydrates in corn to produce highly concentrated fructose, which is inflammatory (Tappy and Lê, 2010). High-fructose corn syrup is often added to fruit juices. Reducing high-fructose corn syrup should further decrease inflammatory factors. Initial evidence suggests that preservatives added to food (e.g., bread, ice cream) to increase shelf-life alter gut microbiota and aid to gut inflammation and may be a factor in explaining the relatively high rates of inflammatory bowel disease in those eating a Western diet.
Physical Activity and Exercise
Uncontrollable shock produces escape deficits, social avoidance, and a hyperbolic fear response. Evidence from animal studies has demonstrated that allowing an animal increased time on an exercise wheel will reduce the impact of uncontrollable shock (Greenwood and Fleshner, 2011). Various studies suggest that exercise applies healthy effects by reducing inflammation and associated occurrences (Cotman et al., 2007).
Physical activity and exercise decrease inflammatory cytokine response to stress (Hamer and Steptoe, 2007; Mathur and Pedersen, 2008). Exercise increases heart rate variability (Coats et al., 1992), which diminishes inflammation. Exercise influences immune system regulators. It reduces NF-κB activation, the transcription factor for inflammatory cytokines. Exercise decreases the expression of toll-like receptor 4, which initiates an inflammatory response (Hamer and Steptoe, 2007).
It increases the reliability of the gut intestinal barrier, so the gut is less likely to allow access to harmful bacteria (Luo et al., 2014). In the brain, exercise is associated with increased brain-derived neurotrophic factors in the hippocampus and with increased neurogenesis (Trejo et al., 2001). In clinical studies, physical activity has established efficacy in improving major depression (Babyak et al., 2000; Hoffman et al., 2011) with effect sizes equivalent to pharmacological interventions (Greenwood and Fleshner, 2008). In a study in which 156 subjects were randomised either: (1) exercise; (2) Zoloft; (3) or a combination of the two. The results reported that there were no differences at 4 months among the conditions; however, at 6 months, only 15% of the exercise group stayed depressed compared with 46% in the Zoloft group and 40% in the combination group.
In relation to those who improved but then relapsed, relapse occurred in 8% in the exercise group, 38% in the medication group, and 31% in the combination group. Beyond inflammation, learning new physical skills will amalgamate the new neurons produced in the hippocampus during neurogenesis into circuits and liberate them from premature death (Curlik et al., 2013; Shors et al., 2012).
Key Points
There are numerous options available for treating individuals with depression. For example, cognitive behavioural therapy has been suggested by researchers to be as effective as antidepressants, although it may be slower to achieve results. Cognitive behavioural therapy relates to a reduced probability of relapse compared to antidepressants. Contemporary talk therapies steering towards regulatory capacity are being established. Lifestyle changes involving diet, exercise, and positive interaction with others are also effective in decreasing depression. The lifestyle changes discussed in this section are the same interventions recommended to prevent heart disease and cancer. A disadvantage to making lifestyle changes is that they require developing new habits, similar to the lifestyle changes recovering alcoholics must implement in their lives to stay sober. Although this may appear intimidating, it is also the case that small changes can yield significant payoffs.