Depression Affecting 10% of Population, is Largely Chemical In Nature
Virtually all clinical reports on mood disorders identify neurotransmitter imbalances as either the root cause or as a contributor to symptoms of depression and anxiety.
Clinical symptoms of mood disorders can be grouped into three basic categories with many individuals experiencing symptoms in more than one category. A. Emotional: Depressed mood, lack of motivation, disinterest in social activity, anxiety B. Cognitive: Inability to concentrate, poor memory C. Physical: Insomnia, headache, fatigue, and stomach, back, and neck pain
Disruption within two key neurotransmitters, serotonin, and norepinephrine, represent a common neurochemical failure.
Serotonin imbalances are associated with: • Poor impulse control • Low sex drive • Decreased appetite • Painful PMS
Norepinephrine imbalances are associated with: • Poor attention and memory • Decreased concentration • Stress and Anxiety • Altered states of arousal Although serotonin and norepinephrine imbalances are primary culprits, dopamine, GABA, glutamate, estrogen, and progesterone can all play significant roles in the cause and/or affect mood. Addressing each of these neurotransmitters and hormones simultaneously is the most efficient route to wellness. has a synergistic relationship with serotonin and norepinephrine as it is responsible for regulating the pleasure/reward pathway, memory, and motor control. Many stimulants can inhibit neural transmission, reducing demand and contributing to depletion over time.
GABA’s regulates norepinephrine, epinephrine, dopamine, and serotonin. Neuroexcitatory overload can raise demand for GABA. Low GABA levels are associated with adrenal HPA axis breakdown and can contribute to anxious and reactive symptoms.
Glutamate is considered to be the major mediator of excitatory signals in the CNS, and is involved in most aspects of normal brain function including cognition, memory, and learning. Due to its excitatory role, high levels of glutamate is often associated with panic attacks, anxiety, and depression. Sex hormones play a role in mood disorders as well.
Estrogen is essential for serotonin production and is also a dopamine modulator. Estrogen increases serotonin receptor sensitivity and increases serotonin production. Estrogen fluctuations experienced by many (especially aging) women will have a rising and falling effect on serotonin.
Progesterone is a GABA agonist (a drug mimicking bodily chemical) and has a significant effect on the body’s HPAG axis to manage stress and maintain a balanced mood.
Take the first step in controlling your depression and improving your life. Testing both neurotransmitters and hormones provides a comprehensive and foundational view of the body’s functional neuroendocrine status, and brings to light factors that contribute to symptoms, allowing for defined, targeted treatments and excellent clinical success. Canary Club Neurotransmitter Tests, all with Hormone Testing Add-Ons Available: ZRT NeuroAdvanced
Health Disclaimer: All information given about health conditions, treatments, products, and dosages are not intended to be a substitute for professional medical advice, diagnosis or treatment. This is provided only as a suggested guideline. References: http://www.cdc.gov/Features/dsDepression http://www.gallup.com/poll/145868/chronic-health-conditions-prevalent-2010-2009.aspx Akiskal HS. Mood disorders: introduction and overview. In: Kaplan HI, Sadock BJ, eds. Comprehensive Textbook of Psychiatry. 6th ed. Baltimore, Md: Lippincott, Williams & Wilkins; 1995:1067-1079. Grossman F, Potter WZ. Catecholamines in depression: a cumulative study of urinary norepinephrine and its major metabolites in unipolar and bipolar depressed patients versus healthy volunteers at the NIMH. Psychiatry Res. 1999 Jul 30;87(1):21-7. Gonzales GF, Carillo C. Blood serotonin levels in postmenopausal women: effects of age and serum oestradiol levels. Maturitas. 1993;17:23-9. Kaura V, et al. The progesterone metabolite allopregnanolone potentiates GABAa receptor-mediated inhibition of 5-ht neuronal activity. Eur Neuropsychopharm. 2007; 17: 108-15