Matters of Great Personal Importance: Depression.

My Psychologist Is Me: A Space To Learn, Grow And Heal From Within.

Tips, reflections and resources on how to take care of your mental health, improve your self-esteem and develop your potential. I do not intend to replace professional help, but rather to complement it and motivate you to be your own psychologist. I hope you like it and that it inspires you.

In life, we often face challenges that lead us to question ourselves, to look inward for answers. We become our own psychotherapists when we embrace this invitation to self-reflection, exploring the deepest corners of our minds and hearts. The idea of becoming our own healers may seem like uncharted territory, but in reality, each of us possesses the innate power to understand and heal our own emotional wounds. Without the need for complicated theorizing or incomprehensible technicalities, we can embrace a practical and humane approach to our mental well-being. Furthermore, by developing this skill of self-reflection and self-therapy, we not only benefit our own lives, but we can also become a source of support and guidance for others. With empathy and understanding, we can offer our support without psychological jargon, but with a genuine and compassionate approach to the well-being of those around us.

Depression is a set of clinical conditions in which the subjective symptom of decreased mood predominates (it may not be manifest) and a drop in interest. They occur in the course of uni or bipolar (affective) mood disorders, somatic disorders, adjustment disorders caused by difficult situations, intoxications, adverse effects to medications, other psychiatric disorders such as schizoaffective disorders, such as post-mortem depression. -psychotic, mixed depressive and anxiety disorders, neurasthenia or withdrawal syndromes.

Depression prevalence figures vary depending on the studies, depending on whether they include only major depressive disorders or other types of depressive disorders. In general, prevalence figures are usually collected in Western countries of approximately 3 percent in the general population, and for major depressive disorder, an annual incidence of 1 to 2 per thousand.

According to the WHO, there are more than 350 million people with depression in the world. Studies and statistics seem to agree that the prevalence is almost double in women than in men, although there are many studies that question this asymmetric incidence: there are studies that indicate that depression in men is much less recognized and its symptoms reports differently.

Some life stressors, such as the birth of a child, marital crises, abuse of toxic substances (mainly alcohol), or the presence of a chronic organic disease, are associated with an increased risk of developing major depressive disorder. Regarding the family association due to genetic factors, the existence of a first-degree relative with a history of major depressive disorder increases the risk between 1.5 and 3 times compared to the general population. The longer duration of the first episode and the greater number of episodes in the life of those with early-onset depression is due to the lack of early detection and treatment in young people.

CAUSES

Depression can result from many reasons:

• Genetic inheritance (it is passed on in your family).
• Other diseases.
• Certain medications.
• The use of drugs or alcohol.
• Mental (psychiatric) problems.
• Etiology

The origin of depression is complex, since genetic, biological and psychosocial factors influence its appearance. Among all of them, biological factors are those that deserve special attention, including psycho-neuro-immunology, which proposes a bridge between strictly biological and psychological approaches.

A high and growing body of evidence indicates that depressive episodes are associated not only with changes in the neurotransmission of the central nervous system, but also with structural changes in the brain, produced through neuroendocrine, inflammatory and immunological mechanisms.

Some types of depression tend to affect members of the same family, which would suggest that a biological predisposition can be inherited. In some families, severe depression occurs generation after generation. However, severe depression can also affect people who do not have a family history of depression.

Currently, there is no clear profile of biomarkers associated with depression that can be used to diagnose the disease.

INFLAMMATORY THEORY

There is a growing body of evidence demonstrating that depression is associated with a chronic low-grade inflammatory response, which results in the activation of cellular immunity and a compensatory anti-inflammatory response, characterized by negative immunoregulatory processes. New evidence shows that clinical depression is accompanied by an increase in oxidative stress and the appearance of autoimmune responses, which contribute to the progression of depression.

The theory that has aroused the greatest interest among researchers is the participation of pro-inflammatory cytokines in the behavioral changes typical of depression. Their increase and their effects on the central nervous system contribute to the development of somatic and neuropsychological depressive symptoms. In fact, in studies where healthy participants are administered infusions of endotoxin to trigger the release of cytokines, classic depressive symptoms appear that also condition the behavioral and cognitive characteristics typical of depression. For example, approximately 25% of patients receiving interferon for the treatment of hepatitis C develop significant depression.

Many studies carried out to date have demonstrated the existence of elevated levels of pro-inflammatory cytokines in the serum of patients with a severe depressive episode. An interesting phenomenon that confirms the link between inflammatory processes and symptoms of depression is the association of depressive symptoms with inflammatory, autoimmune or neuroinflammatory diseases, such as asthma, chronic obstructive pulmonary disease, cardiovascular disease, diabetes, allergy, rheumatoid arthritis, celiac disease, multiple sclerosis and Parkinson's disease.

The levels of pro-inflammatory cytokines correlate with the severity of depressive symptoms, while treatment with antidepressants and clinical improvement lead to normalization of the concentration of pro-inflammatory cytokines in patients with depression. A meta-analysis of 22 studies that evaluated the relationship between the levels of inflammatory markers and the effectiveness of antidepressant medications in the treatment of depression, demonstrated a decrease in the levels of pro-inflammatory cytokines, such as IL-1β and IL -6, associated with the use of antidepressant drugs, especially selective serotonin reuptake inhibitors.

The lack of response to antidepressant treatments is associated with persistently high levels of inflammatory markers and can be explained by the existence of chronic inflammatory processes, chronic damage due to increased oxidative stress and the appearance of autoimmune disorders.

Any factor that activates cellular immunity and inflammatory processes without a concomitant activation of the compensatory anti-inflammatory response can further aggravate the detrimental effects of activated immuno-inflammatory processes. Different environmental factors potentially connected to systemic inflammation increase the risk of developing depression; These include psychosocial stress factors, poor diet, increased intestinal permeability, food intolerances, physical inactivity, obesity, smoking, atopy, periodontal diseases, sleep and vitamin D deficiency.

ENVIRONMENTAL FACTORS

Of all possible psychosocial factors, stress and psychological trauma are the best known. Both acute trauma or sub-chronic stress factors, as well as early exposure to childhood trauma, increase the risk of developing depression and causing mood disorders, due to their impact on the immune system and the central nervous system.

Psychosocial stress can activate the production of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1), and decrease the levels of anti-inflammatory cytokines, such as interleukin-10 (IL-10). This has been shown in relation to acute or chronic stress, both in animals and humans.

Evidence from animal models has long suggested that early exposure to trauma in childhood may increase the risk of future malfunctioning of the nervous, immune, and endocrine systems. These findings have subsequently been corroborated in humans. Studies exploring the influence of stress on other inflammatory diseases, such as metabolic syndrome and cardiovascular disease, have consistently demonstrated similar trends. All of these results suggest that stress that occurs at an early age can exert persistent effects over long periods of time, causing an increased susceptibility to developing somatic and psychiatric diseases, and a potential low response to treatments.

However, this model does not completely explain the vulnerability to suffering from inflammatory diseases, but rather the use in adulthood of learned maladaptive responses to stress seems to play a fundamental role. For example, there is evidence that personality and the way a person responds to psychosocial stressors, such as job stress or exam stress, can contribute to the development of inflammatory processes.

Understanding and modifying risk factors related to stress and lifestyle is an important step in the prevention of inflammatory diseases, such as depression.

DIET

Throughout the world, since the last decades of the 20th century, important changes have been taking place in eating habits. Healthy dietary patterns, abundant in fiber, nutrient-dense foods and omega-3 fatty acids, have been replaced by diets high in saturated fats and refined sugars.

Various components of the diet can negatively influence the functioning of the immune system and increase levels of systemic inflammation, which predisposes to the development of depression. Numerous studies conducted since 2009 demonstrate inverse associations between diet quality and mental disorders such as anxiety and depression, both in adults and in children and adolescents of all cultures.

An unhealthy ("western") pattern, characterized by a high glycemic load, rich in refined carbohydrates and added sugars, red and processed meats, and other highly processed foods, is associated with an increase in inflammatory markers. A diet disproportionately high in omega-6 fatty acids (commonly used in processed foods) increases the production of pro-inflammatory cytokines. "Trans" fatty acids induce inflammation in a similar way.

In contrast, a healthy dietary pattern (such as the Mediterranean diet), characterized by greater consumption of fish, legumes, fruits, vegetables and whole grains, has been found to be associated with reduced plasma concentrations of inflammatory markers. The fiber contained in whole grain foods appears to have immune modulating functions and protects against oxidative stress, which is a consequence of inflammation and a characteristic of depressive illness. Omega-3 fatty acids, which are important components of many healthy foods, such as seafood, leafy green vegetables, legumes and nuts, work to reduce inflammation. Magnesium consumption is inversely related to serum levels of C-reactive protein (CRP), which is an important marker of inflammation at a general level.

Deficiencies of certain nutrients are also associated with the development of depression, such as decreased lycopene content in foods and decreased availability of selenium in groundwater. There is a growing body of evidence about the role that the gastrointestinal tract may play in the development of depression. Increased intestinal permeability, which consists of a dysfunction of the intestinal barrier, is one of the factors that cause systemic inflammation and elevated levels of pro-inflammatory cytokines. These findings have been documented in patients with depression.

The main role of the intestinal barrier is to regulate the passage of nutrients and block the passage of both microorganisms and antigens. When intestinal permeability is increased, the intestinal barrier loses its protective function and molecules that should not pass, such as certain intestinal bacteria, toxins and incompletely digested nutrients, pass into the bloodstream.

It has been shown that increased intestinal permeability can be caused by exposure to bacteria, drugs, stress or certain foods, such as gliadin (protein fraction of gluten). Gliadin causes an increase in intestinal permeability, regardless of the existing genetic basis, that is, both in celiac and non-celiac patients.

The passage of incompletely digested nutrients from the intestinal lumen into the blood leads to the activation of the immune system, which can initiate the production of specific antibodies of the IgG type against nutrients. As a consequence, hypersensitivity to certain foods develops (which is delayed and IgG mediated) and inflammation, which is maintained chronically by repeated consumption of allergenic foods. The role of specific antibodies of the IgG type has been confirmed in celiac patients, in whom a delayed reaction against gluten occurs.

The delayed nature of the IgG-mediated reaction, in which symptoms appear hours or even days after ingestion of the food, constitutes a major obstacle to diagnosis, since it is impossible for the patient to identify the cause of the allergy. On the contrary, IgE type antibodies are responsible for acute allergic reactions (IgE-mediated allergies), which appear immediately.

There is currently growing interest in the role of the microbiota in maintaining the proper functioning of the intestinal barrier, the gut-brain axis, and psychiatric disorders. A balanced intestinal flora is an important factor in reducing the levels of pro-inflammatory cytokines and maintaining the intestinal barrier. This is why intestinal bacterial overgrowth can lead to increased intestinal permeability, allowing bacterial lipopolysaccharides to penetrate the blood. In patients with depression, significantly elevated levels of IgA and IgM antibodies against the lipopolysaccharides of Gram-negative bacteria have been found. This observation is very important, since the metabolites of certain bacteria penetrate the blood, in addition to negatively affecting the functioning of the central nervous system.

EXERCISE

Sedentary behavior is considered an important and novel risk factor for a number of health disorders due to its relationship with increased inflammation, although the underlying physiology of sedentary behavior is not fully understood. Sarcopenia (general loss of muscle mass and strength, associated with aging or a sedentary lifestyle) is also linked to cognitive decline in the elderly, which appears to be mediated by inflammation.

Regular exercise has been shown to be an effective treatment for depression and anxiety disorders and protects against the development of new depressive illnesses. Regular exercise reduces systemic inflammation through homeostatic adaptation and decreases leptin, elevated levels of which are also implicated in the development of depression. These findings support the role of inflammation in exercise-induced mood improvement.

In contrast, physical inactivity during childhood has been shown to be associated with an increased risk of developing depression in adulthood.

OBESITY

It has been shown that obesity, which currently constitutes a growing health problem that is already reaching epidemic proportions, can predispose to the development of depressive symptoms and clinical depression. Likewise, there is evidence that depression predisposes to obesity in a bidirectional way. A recent meta-analysis found that depression increases the odds of developing obesity by 58% and that obesity increases the risk of suffering from long-term depression by 55%.

Obesity is an inflammatory state and is related to a wide range of chronic diseases. Pro-inflammatory cytokines are involved in fat metabolism. Obesity, independent of age and other potential confounders, has been shown to increase levels of inflammatory cytokines (or vice versa) across all obesity indices, particularly abdominal obesity. This fact provides a likely explanation for the observed increases in comorbidities, such as depression.

TOBACCO

Smoking rates have repeatedly been shown to be significantly higher in patients suffering from depression, although the explanation is complex. The three possible hypotheses are that smoking causes the development of depression, that depression increases smoking-inducing behaviors, and that shared vulnerability factors increase the risk of both. One important pathway is the effect that the thousands of chemicals present in tobacco smoke have on increasing systemic inflammation, exposure to oxidative stress, and immune response.

ATOPIC DISORDERS

The results of various studies demonstrate that atopic disorders, whose prevalence has been increasing steadily over the last decades, are associated with an increased risk of suffering from clinical depression and depressive symptoms. Atopy is the result of an inflammatory response to exposure to common allergens, leading to the development of allergic symptoms, such as asthma, eczema or rhinitis.

PERIODONTAL DISEASES

Periodontal diseases, including gingivitis and periodontitis, are a major public health concern. It is documented that psychiatric patients have worse oral health status. Recent studies suggest that depression in particular may be associated with periodontal disease, although other studies have found no association.

Periodontal disease is an inflammatory disease, both locally and systemically, and is associated with elevated serum levels of C-reactive protein. In addition, it has a significant predictive value for other inflammatory diseases. However, despite some evidence that periodontal infections may play a role in some neurodegenerative diseases, there is currently still a paucity of evidence about whether translocation of periodontal bacteria plays a role in some patients with clinical depression.

As such, periodontal disease can be considered a marker of a failure of the immune system to fight inflammation, increasing the risk of depression through its systemic inflammatory effects, which can enhance the symptoms of inflammatory and oxidative processes, and therefore both depressive. On the other hand, the psychosocial effects of poor oral hygiene, such as shame, loneliness or isolation, can predispose to the development of depression.

DREAM

Sleep regulation is an essential component for understanding the pathophysiology and treatment of depression. It influences mood and plays a fundamental role in the regulation of various physiological and psychological systems. Sleep disturbances are related to a number of negative health consequences, such as poorer quality of life, comorbidity, and increased risk of mortality; they often persist beyond the clinical episode of depression and increase vulnerability to relapse. Furthermore, changes in sleep predict response to depression treatment, and many antidepressant treatments influence sleep. Regulating sleep habits can be a protective factor against mental health problems.

Depressed patients frequently suffer from sleep disorders, with rates higher than those of the general population. It is estimated that up to 80-90% of people who suffer from major depression also experience sleep disorders.

Several prospective and epidemiological studies have suggested that sleep disturbances may predispose to later developing mood disorders, that insomnia symptoms often increase the risk of relapse in patients previously diagnosed with major depressive disorder, and that periods of insomnia to They often precede manic episodes in bipolar patients.

A number of changes in sleep have been observed in depressed patients, although no single sleep marker is specifically associated with depression. Among them, the most reliable include alterations in continuity (for example, delayed falling asleep and decreased efficiency), earlier onset of rapid eye movement (REM) sleep, increased activity, density and amount of the REM phase, and decrease in the slow wave phase. Some of these sleep markers have been detected in healthy people at high familial risk for depression and are associated with the later development of depression.

Both chronic and acute sleep deprivation produce deficiencies in the functioning of the immune system, characterized by increased levels of pro-inflammatory cytokines, such as C-reactive protein, tumor necrosis factor alpha (TFN-α) and interleukin-6 (IL-6). A growing body of research suggests that sleep restrictions are associated with neuroendocrine and neurobiological alterations similar to those observed in mood disorders. Increases in the pro-inflammatory cytokines TFN-α and IL-6 caused by sleep deprivation are also thought to be related to a reduction in adult neurogenesis (birth of new neurons), comparable to the alterations found in depressed patients. For this reason, it has been proposed that the inhibition of neurogenesis through the process of chronic sleep interruption may also be a cause of depression. Both successful pharmacological treatment of depression and improved nighttime sleep are associated with decreased levels of the cytokines IL-6.

VITAMIN D

In the Western population, vitamin D deficiency, especially 25-hydroxyvitamin D, is widespread. Low serum levels of vitamin D are linked to various health disorders, including cancer, osteoporosis, and depression.

Vitamin D physiology overlaps with the pathophysiology of depression. There are vitamin D receptors in key areas of the brain; and vitamin D plays a role in circadian rhythms and sleep, affects glucocorticoids, and influences neuronal growth, cell proliferation in the developing brain, and embryogenesis.

Regarding the potential antidepressant effects of vitamin D, there are contradictory results, with studies that show positive results and others, on the contrary, negative results. Vitamin D has modulating effects on immunity. Vitamin D supplementation has been shown to markedly reduce levels of the pro-inflammatory cytokines TFN-α and IL-6 (both clearly associated with depression) and oxidative stress (which is closely linked to inflammation). Vitamin D derived from safe sun exposure can reduce systemic inflammation.