According to the National Institutes of Health, depression is one of the most important causes of disability worldwide, and yet the high rate of inadequate treatment of the disorder remains a serious concern (Kessler, 2013). There are several possible reasons for this, such as resistance to treatment, difficulty in adequate diagnosis, and compliance with medication. However, one very large prevailing factor is the way in which depression affects our brains.
To date, the most relevant theory of depression is what is known as the monoamine deficiency hypothesis. According to this theory, monoamine acts like a brain regulator, affecting several brain functions, including mood, attention, reward processing, sleep, appetite, and cognition. This theory has been supported by the fact that almost every compound that inhibits monoamine reuptake, leading to an increased concentration of monoamines in the synaptic cleft, has been proven to be a clinically effective antidepressant (Belmaker, 2008).
Further, when the enzyme monoamine oxidase, which increases the availability of monoamines in presynaptic neurons, is inhibited, antidepressant effects are observed.
From the monoamine-deficiency theory emerged the understanding of depression as a depletion of the neurotransmitters serotonin, norepinephrine or dopamine in the central nervous system.
Of the neurotransmitters involved in depression, serotonin is the most studied. Evidence for abnormally low functioning of the serotonin system in depressed patients comes from studies using tryptophan depletion, which reduces central serotonin synthesis.
When tryptophan was reduced in subjects at increased risk of depression (those with a family history, or with MDD -major depressive disorder- in full remission) depression symptoms increased (Neumeister, 2014).
Further, experimentally reduced central serotonin has been associated with mood congruent memory bias, altered reward-related behaviors, and disruption of inhibitory affective processing (Hasler, 2014). Serotonin receptors – which regulate serotonin function – also appear to work abnormally in depressed people, as decreased availability of receptors have been found in multiple brain areas of patients with MDD (Drevets, 2011).
A classic feature of depression is low energy; dysfunction of the central noradrenergic system has been hypothesized to play a role in the pathophysiology of depression. Several studies have found decreased norepinephrine metabolism, increased activity of tyrosine hydroxylase, and decreased density of norepinephrine transporter in the locus ceruleus in depressed patients (Charney, 2014). In addition, decreased density of adrenergic receptors have been found in the post-mortem brains of depressed suicide victims (Pandey, 2015).
Dopamine, which is typically associated with the reward system and evidenced in cases of addiction, also appears to play a significant role in the neurobiology of depression. When dopamine reuptake is suppressed (through reuptake inhibitors) anti-depressant effects are observed (Goldberg, 2014). In patients with MDD, dopamine transporter binding and uptake were both reduced, suggesting a depletion of the dopamine system as an important feature of depression (Meyer, 2011).
Course excerpt from:
Nutrition and Depression: Advanced Clinical Concepts is a 3-hour online continuing education (CE) course that examines how what we eat influences how we feel – and what we can do to improve both.
Depression is an increasingly common, complex, inflammatory condition that co-occurs with a host of other conditions. This course will examine how we can combat depression through nutrition, starting with an exploration of the etiology of depression – taking a look at the role of neurotransmitters, the HPA axis and cortisol, gene expression (epigenetics), upregulation and downregulation, and the connections between depression and immunity and depression and obesity. We will then turn our attention to macronutrients and investigate how factors such as regulating blood sugar, achieving amino acid balance, consuming the right fats, and eating fruits and vegetables can enhance mood, improve our decision-making, enhance cognitive processes, and reduce inflammation. From there, we will look at just how we go about the process of building a better brain – one neurotransmitter at a time. Exercises you can use with clients are included. Course #31-02 | 2018 | 42 pages | 20 posttest questions
Our online courses provide instant access to the course materials (PDF download) and CE test. Successful completion of the online CE test (80% required to pass, 3 chances to take) and course evaluation are required to earn a certificate of completion. Click here to learn more. Have a question? Contact us. We’re here to help!
Professional Development Resources is a nonprofit educational corporation 501(c)(3) organized in 1992. We are approved to sponsor continuing education by the American Psychological Association (APA); the National Board of Certified Counselors (NBCC); the Association of Social Work Boards (ASWB); the American Occupational Therapy Association (AOTA); the American Speech-Language-Hearing Association (ASHA); the Commission on Dietetic Registration (CDR); the Alabama State Board of Occupational Therapy; the Florida Boards of Social Work, Mental Health Counseling and Marriage and Family Therapy, Psychology & School Psychology, Dietetics & Nutrition, Speech-Language Pathology and Audiology, and Occupational Therapy Practice; the Ohio Counselor, Social Worker & MFT Board and Board of Speech-Language Pathology and Audiology; the South Carolina Board of Professional Counselors & MFTs; the Texas Board of Examiners of Marriage & Family Therapists and State Board of Social Worker Examiners; and are CE Broker compliant (all courses are reported within a few days of completion).
Target Audience: Psychologists, Counselors, Social Workers, Marriage & Family Therapist (MFTs), Speech-Language Pathologists (SLPs), Occupational Therapists (OTs), Registered Dietitian Nutritionists (RDNs), School Psychologists, and Teachers