Depression is the leading cause of disability in the United States among people ages 15-44. Major Depressive Disorder (MDD) affects more than 16.1 million adults in the U.S; that is roughly 6.7% of the population over 18 years of age.1 Persistent Depressive Disorder (PDD) affects about 3.3 million adults, which is approximately 1.5% of the population.2
As surprising as these numbers are, they do not necessarily include all the people suffering from anxiety, Obsessive-Compulsive Disorder (OCD), phobias, panic disorders, or Post Traumatic Stress Disorder (PTSD) although many of these disorders are also present in people suffering with depression.
The following descriptions of depression are taken directly from the Anxiety and Depression Association of America. “Major depression is characterized by at least five of the diagnostic symptoms of which at least one of the symptoms is either an overwhelming feeling of sadness or a loss of interest and pleasure in most usual activities. The other symptoms that are associated with major depression include decrease or increase in appetite, insomnia or hypersomnia, psycho motor agitation or retardation, constant fatigue, feelings of worthlessness or excessive and inappropriate guilt, recurrent thoughts of death and suicidal ideation with or without specific plans for committing suicide, and cognitive difficulties, such as, diminished ability to think, concentrate and take decisions. The symptoms persist for two weeks or longer and represent a significant change from previous functioning. Social, occupational, educational, or other important functioning is also impacted. For instance, the person may start missing work or school, or stop going to classes or their usual social activities.”1
“Another type of depression is called Persistent depressive disorder (dysthymia). The essential feature of this mood disorder is a low, dark or sad mood that is persistently present for most of the day and on most days, for at least 2 years (children and adolescents may experience predominantly irritability and the mood persist for at least 1 year). For the individual to receive the diagnosis of persistent depressive disorder they should also have two of the diagnostic symptoms which include poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low self-esteem, poor concentration, difficulty making decisions, or feelings of hopelessness. During this period, any symptom-free intervals last no longer than two months. The symptoms are not as severe as with major depression. Major depression may precede persistent depressive disorder, and major depressive episodes may also occur during persistent depressive disorder.”1
Prior to the first antidepressant being developed, less than 1% of the population was clinically diagnosed as suffering from depression. The rapid increase in diagnosis since then is at least, by some, partially attributed to a “change in our concepts of depressive illness brought about by a widening of our experience with depression, seeing it for the first time in new (outpatient) settings”.3 While this may be true, others attribute the increase to multiple factors, including side effects of the drugs themselves.
Although the field of psychiatry has been around since the early 1800s, it was reserved for institutionalized individuals who could not function in society. For individuals not living in mental institutions, their treatment was handled by neurologists.4
Neuropathologist Sigmund Freud was fascinated with the operation of the human mind. His work around the turn of the 20th century earned him the title of Founding Father of Psychoanalysis. Freud’s work dominated the outpatient field of psychiatry up until the 1950s. The accidental discoveries of the first anti-psychotic drug and, consequently the first antidepressant drug created a permanent riff between biological psychiatry and psychotherapy/psychoanalysis.4
In the 1950s, chemists were trying to develop a drug that was effective against tuberculosis. The drug iproniazid was a synthesized version of isoniazid, another drug used to treat patients with tuberculosis, which was found to have interesting side effects. Iproniazid appeared to induce euphoria, was stimulating to the mind, increased appetite, and improved sleep. This drug became the first MAO (monoamine oxidase) inhibitor. Iproniazid was later removed from the market due to safety concerns.5
In the years since then, other types of antidepressant drugs have been developed; they include SSRI (selective serotonin reuptake inhibitors), SNRI (serotonin-norepinephrine reuptake inhibitors), tricyclic, and atypical (which don’t fit into any of the other categories).6 These drugs affect one or more neurotransmitters (chemical messengers) in the brain.
Sadly, despite all the research done since the accidental “discovery” of the first antidepressant, little is understood about the function of neurotransmitters or how the brain actually works. One of the reasons for this is that serotonin cannot be measured in a living human brain. Study consists primarily on brains of deceased individuals, levels of metabolized serotonin, and in animal models.7
Study after study have revealed conflicting results of whether the targeted neurotransmitters of the depressed individual were actually low. A review published in 2008 in the New England Journal of Medicine states “Numerous studies of norepinephrine and serotonin metabolites in plasma, urine, and cerebrospinal fluid as well as postmortem studies of the brain of patients with depression, have yet to identify the purported deficiency reliably.”8
These facts combined with a major misunderstanding of how the brain uses and regulates neurotransmitters, specifically serotonin, should bring a halt to research and development of drugs which continue to chase a very dangerous theory down the seemingly bottomless rabbit hole. In fact, it is now understood that serotonin production increases in response to excessive excitability and an overstimulated mind, or to help facilitate other normal functions in the body such as sleep and learning. Serotonin also functions to help regulate body temperature, the immune system, muscle contractions, pain intensity, memory, appetite, digestion and blood clotting by inhibiting excessive neurotransmitter firing in the brain.9 In other words, serotonin is downer, not an upper.
So, when an SSRI is prescribed for depression in an attempt to increase serotonin in the brain, the serotonin receptors become bombarded with too much serotonin. In an effort lessen excessive neurotransmitter firing, the receptors become less sensitive to serotonin; this is known as downregulation.
In a paper published by McMasters University, Paul Andrews, an assistant professor of Psychology, Neuroscience & Behavior at McMaster wrote, “When depressed patients on SSRI medication do show improvement, it appears that their brains are actually overcoming the effects of anti-depressant medications, rather than being assisted directly by them. Instead of helping, the medications appear to be interfering with the brain’s own mechanisms of recovery.”7
“We’ve seen that people report feeling worse, not better, for their first two weeks on anti-depressants,” Andrews says. “This could explain why.”7 Clearly, even short-term use of an SSRI can worsen depression and lead to suicidal thoughts or actions. A 2014 study from the Max Planck Institute in Leipzig, Germany revealed through brain imaging that a single dose of the SSRI escitalopram alters the brain’s architecture, connectivity, and activity across the entire brain within 3 hours after administration. The length of time and the extent to which these changes persist are unknown.10
Documented efficacy of antidepressants for MDD are often skewed by drug companies by neglecting proper placebo comparisons, and due to the fact that clinical trials do not adequately simulate real life stressors. In actuality, treatment resistant depression is a relatively common occurrence in clinical practice, up to 50% to 60% of the patients are not achieving adequate response following antidepressant treatment.11
There is little doubt that depression and depression related illnesses are at an all-time high not only in the United States but across the world. Even children are at risk. Despite the fact that FDA warnings were first added to antidepressant drugs in 2004 research from the CDC reveals that in 2008 nearly 5% of girls between 12 and 17 and 3% of boys used antidepressant drugs.12
What could be causing so many cases of depression across such a broad range of ages? What, besides the antidepressants themselves could be causing the steady increase of depression since the mid-1950s to the current near epidemic rate? There is emerging evidence to indicate that the modern Western lifestyle greatly contributes to it.
As far back as 400 BC depression started being looked at as a symptom of something much larger happening; this idea started with Hippocrates. Hippocrates, often called the father of modern medicine, was a philosopher as well as a physician. It was his belief that mental illness stemmed from imbalances in the body.13 He held the belief that the body must be treated as a whole and not just a series of parts. He also believed in the natural healing process of rest, a good diet, fresh air and cleanliness. These concepts are at the core of holistic treatment and lifestyle.
Research is beginning to reveal that most, if not all, diseases are the result of elevated levels of inflammation. Inflammation in the body can be measured by testing for the number and types of cytokines, which are peptides produced by the immune system for the purpose of mediating and regulating the immune response, inflammation and hematopoiesis.
A meta-analysis of 24 studies involving patients meeting criteria for major depression revealed significantly higher concentrations of the proinflammatory cytokines TNF-α and IL-6 in depressed subjects compared with control subjects.14
Another study of 50 unmedicated patients diagnosed with MDD, along with 34 healthy controls, had levels of nine cytokines (IL-1Ra, IL-6, IL-7, IL-8, IL-10, G-CSF, and IFNγ) tested and a baseline established. “After 12 weeks of treatment, the plasma levels of seven of these nine…had decreased significantly compared to baseline and did not differ from those in the healthy controls. The depressive symptoms were simultaneously significantly reduced. In addition, the reduction to normal cytokines levels occurred only in those who met the recovery criteria.”15
Well documented sources of inflammation include unmitigated stress, toxicants both in our food and in our environment, certain medications, highly processed foods, and gut dysbiosis. In reality, all these things lead to gut dysbiosis.
What is interesting is that 70% of our immune system is in our gut; it is referred to as GALT, Gut Associated Lymphatic Tissue. Also, 90% of serotonin is made in the digestive tract. You can start to see how gut health, the immune system, and depression are tied together. This association of the gut and the brain is called the Gut-Brain Axis.
To take things even farther, hormone balance is also dependent on these interactions. Cortisol is a hormone that is produced during times of stress, and stress has a direct effect on the Hypothalamic-Pituitary-Adrenal Axis (essentially, the driver for the endocrine system). Proper balance of all hormones is critical is good mental health.
And that’s not all, people taking antidepressants have a 33% higher chance of death than non-users. Antidepressants block neurons from absorbing serotonin which affects all major organs in the body. Without the ability to absorb and use serotonin, they may not function properly. There is a 14% higher risk of cardiovascular events, such as heart attacks and strokes for antidepressant users.16
Given all that we now know about depression, and given the fact that many people suffer terribly when trying to stop taking antidepressants, the first plan of treatment should involve a thorough analysis of the patient’s diet and lifestyle. Processed and sugary foods need to be removed from the diet, sleep patterns brought into alignment with normal circadian rhythm, a routine exercise program implemented, and stress reduction techniques practiced daily.
Any medications currently being used, both prescription and over the counter, should be reviewed for causing side effects of depression, increasing inflammation, or interfering with the body’s normal functioning. These include proton pump inhibitors and NSAIDs.
Likewise, toxic substances in the individual’s food and environment need to be identified and removed. This includes artificial flavorings, colors, sweeteners, and fragrances.
Certain supplements may be added which are proven to reduce symptoms of depression. Also, blood tests can be done to identify other contributing factors such as hormone imbalance in the thyroid. Strengthening the digestive system is also important. We will take a more in-depth look at natural ways to treat depression next month.
If desired results are not achieved psychotherapy can be added to the modified diet and lifestyle to address any unresolved traumatic experiences that may have occurred during childhood or later in life.
If, after all these things have been accomplished depression is still present only then should an antidepressant be considered.
Hippocrates was right about the body. Everything is connected within our body, and must be treated as a whole and not just a series of parts. Sigmund Freud would add that the mind and spirit are also connected to the body.
Only by getting to the true root of depression can the problem be truly solved. Depression is merely a symptom of a much larger imbalance in the body. The simplest solution is always the best, and this means returning to a holistic diet and lifestyle that nourishes our body and activates the innate healing, and restoration of balance, that lies within each one us.
Please check back for next month’s follow-on article that will cover natural ways to treat depression as well as tips for avoiding a depressive episode.
References
1. Depression. (n.d.). Retrieved from Anxiety and Depression Association of America: https://adaa.org/understanding-anxiety/depression
2. Facts and Statistics. (n.d.). Retrieved from Anxiety and Depression Association of America: https://adaa.org/about-adaa/press-room/facts-statistics
3. Ban, T. A. (2014, March 06). From Melancholia to Depression A History of Dianosis and Treatment. Retrieved from International Network for the History of Neuropsycopharmacology: inhn.org/fileadmin/previews_news/From_Melancholia_to_Depression_March_6_2014.pdf
4. Reidbord, S. (2014, October 20). A Brief History of Psychiatry. Retrieved from Psychology Today: https://www.psychologytoday.com/us/blog/sacramento-street-psychiatry/201410/brief-history-psychiatry
5. Hillhouse, T. M., & Porter, J. H. (2015, February 23). A brief history of the development of antidepressant drugs: From monoamines to glutamate. Retrieved from National Center for Biotechnology Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428540/
6. Depression (major depressive disorder). (2018, February 03). Retrieved from Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/depression/diagnosis-treatment/drc-20356013
7. University, M. (2015, February 17). Science behind commonly used anti-depressants appears to be backwards, researchers say. Retrieved from Science Daily: https://www.sciencedaily.com/releases/2015/02/150217114119.htm
8. Belmaker, R., & Agam, G. (2008). Major Depressive Disorder. New England Journal of Medicine, 358:55-68. Retrieved from https://www.nejm.org/doi/full/10.1056/NEJMra073096
9. Neurotransmitters. (n.d.). Retrieved from Parkinson’s Clinic International: https://parkinsonsclinicinternational.com/neurotransmitters/
10. Schaefer, A., Burmann, I., Regenthal, R., Arelin, K., Barth, C., Pampel, A., . . . Sacher, J. (2014, October 06). Serotonergic Modulation of Intrinsic Functional Connectivity. Retrieved from Cell: https://www.cell.com/current-biology/fulltext/S0960-9822(14)01037-9
11. Fava, M. (2003). Diagnosis and definition of treatment-resistant depression. Biological Pschiatry, 53:649–659. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12706951
12. Karter, J. (2016, April 24). Suicide Rates Rise While Antidepressant Use Climbs. Retrieved from Mad in America: https://www.madinamerica.com/2016/04/suicide-rates-rise-with-increased-antidepressant-use/
13. Stanley, T. (2015, March 14). A Beautiful Mind: The History of the Treatment of Mental Illness. Retrieved from Historu Cooperative: https://historycooperative.org/a-beautiful-mind-the-history-of-the-treatment-of-mental-illness/
14. Dowlati, Y., Herrmann, N., Swardfager, W., Liu, H., Sham, L., Reim, E. K., & Lanctôt, K. L. (2010, March 1). A Meta-Analysis of Cytokines in Major Depression. Retrieved from Science Direct: https://www.sciencedirect.com/science/article/pii/S0006322309012293
15. Dahla, J., Ormstad, H., Aass, H. C., Malt, U. F., Bendz, L. T., Sandvik, L., . . . Andreassen, O. A. (2014, July). The plasma levels of various cytokines are increased during ongoing depression and are reduced to normal levels after recovery. Retrieved from Science Direct: https://www.sciencedirect.com/science/article/pii/S0306453014001152?via%3Dihub
16. University, M. (2017, September 14). Antidepressants associated with significantly elevated risk of death, researchers find. Retrieved from Science Daily: https://www.sciencedaily.com/releases/2017/09/170914152238.htm
