Journal of the American Osteopathic Assoc., March 2004 vol.104 S2-S5
Diagnosis and Management of Anxiety Disorders
Charles Shelton, Doctor of Osteopathy
Before posting the article, I think it’s important to at least try to explain the difference between an MD and a DO. There is info online, but it’s not very clear except to say that the two are genuine medical doctors, but osteopathy has a different “philosophy and practice” style than “allopathic” medical doctors.
Info from the article: This article was developed from a lecture presented by Dr Shelton at a symposium sponsored by Wyeth Pharmaceuticals at the 108th Annual AOA Convention and Scientific Seminar on October 15, 2003, in New Orleans, La. Dr Shelton is a national speaker on the visiting speakers bureau of Wyeth Pharmaceuticals. He is also on the speakers bureaus of GlaxoSmithKline; Pfizer Inc; Cephalon, Inc; and Bristol-Myers Squibb Company. Dr Shelton is also on the CNS advisory panels of Pfizer Inc and Elan Pharmaceuticals.
What is a DO? From The American Osteopathic Assoc.
“Doctors of Osteopathic Medicine, or DOs, are fully licensed physicians who practice in all areas of medicine. Emphasizing a whole-person approach to treatment and care, DOs are trained to listen and partner with their patients to help them get healthy and stay well. (Comment; the average person might think that all doctors had some training in patient interaction, but as many of know from experience, apparently not!)
DOs receive special training in the musculoskeletal system, your body’s interconnected system of nerves, muscles and bones. (Hence osteo-bone) By combining this knowledge with the latest advances in medical technology, they offer patients the most comprehensive care available in medicine today.
Osteopathic physicians focus on prevention, tuning into how a patient’s lifestyle and environment can impact their wellbeing. DOs strive to help you be truly healthy in mind, body and spirit — not just free of symptoms. (See article for lists of pharmaceuticals “used for” each anxiety disorder)-
Major anxiety disorders are more prevalent in women than in men. Although the tendency toward anxiety disorders appears familial, other factors such as environmental influences can play a role in the risk for anxiety. This clinical review focuses on the pathophysiologic basis for anxiety disorders. It provides brief overviews of panic disorder, generalized anxiety disorder, social anxiety disorder, obsessive-compulsive disorder, and posttraumatic stress disorder. It also summarizes treatment options for patients with anxiety disorders. (Specific pharmaceuticals for each anxiety “type” Informative IF you’ve been correctly diagnosed – a very big IF!)
The Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (Text Revision) (DSM-IV-TR)1 defines the five major anxiety disorders as social anxiety disorder (SAD), panic disorder (PD), obsessive-compulsive disorder (OCD), generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD). Panic attacks, which represent an extreme form of anxiety, can occur in association with most of these anxiety disorders, though they are not typically associated with GAD. Lifetime prevalence rates of the major anxiety disorders range between approximately 3% (OCD) and 12% (SAD) and are approximately two times greater among women than among men.2,3
Pathophysiology of Anxiety Disorders
In the same way that behavioral traits are passed from parent to child, anxiety disorders tend to run through family structures. Studies comparing the risk of psychiatric illness in identical twins (who share 100% of their DNA) have found that in general, if one identical twin has a psychiatric condition, the risk that the other twin will have the same condition is approximately 50%.4 It therefore appears that nongenetic factors, including environmental influences occurring throughout the lifespan, must also contribute to the risk of developing an anxiety disorder.2,3
The human body attempts to maintain homeostasis at all times. Anything in the environment that disturbs homeostasis is defined as a stressor. Homeostatic balance is then reestablished by physiologic adaptations that occur in response to the stress response. (Comment: The dangerous American social belief that “superior humans” actually “thrive on more and more stress” is highly dysfunctional! The current idiotic belief is that the practice of increasing the stress that the average person must “deal with” every day, somehow (mystical natural selection) “improves” performance is abusive and a perversion of “survival of the fittest.” It’s DEADLY and accounts for the increase in poor health outcomes for Americans. But if it increases profits – it “must be good”!
The stress response in humans involves a cascade of hormonal events, including the release of corticotropin-releasing factor (CRF), which, in turn, stimulates the release of corticotropin, leading to release of the stress hormones (glucocorticoids and epinephrine) from the adrenal cortex. The glucocorticoids typically exert negative feedback to the hypothalamus, thus decreasing the release of CRF.6
The stress response is hardwired into the brain of the typical mammal and is most often triggered when survival of the organism is threatened. The primate stress response, however, can be triggered not only by a physical challenge, but also by the mere anticipation of a homeostatic challenge. As a result, when humans chronically and erroneously believe that a homeostatic challenge is about to occur, they enter the realm of neurosis, anxiety, and paranoia. (This is not an “erroneous belief” – it is the purposeful and chronic state of the American social power structure to ensure that “homeostatic challenge” occurs 24/7 FEAR and conflict are promoted as the constant state of human reality by government and the media; by unstable employment and skewed presentations of threats from violence and crime via “news” programs and entertainment)
The amygdala is the primary modulator of the response to fear- or anxiety-inducing stimuli. It is central to registering the emotional significance of stressful stimuli and creating emotional memories.7 The amygdala receives input from neurons in the cortex. This information is mostly conscious and involves abstract associations. Being stuck in traffic, in a crowded shopping mall, or on an airplane may serve to trigger the anxiety response in a susceptible individual via this mechanism. (Yeah – that’s almost every one; and “corporate policies” (the airline industry) are pushing this stress to the MAX for passengers.)
The amygdala also receives sensory input that bypasses the cortex and thus tends to be subconscious. An example is that of a victim of sexual abuse who suddenly finds herself acutely anxious when interacting with a number of friendly people. It may take her a few moments to realize that characteristics of the individuals with whom she is interacting remind her of the person who abused her.
When activated, the amygdala stimulates regions of the midbrain and brain stem, causing autonomic hyperactivity, which can be correlated with the physical symptoms of anxiety. (You cannot “turn it off”) Thus, the stress response involves activation of the hypothalamic-pituitary-adrenal axis. This axis is hyperactive in depression and in anxiety disorders.8,9
Corticotropin-releasing factor, a 41 amino acid peptide, is a neurotransmitter within the central nervous system (CNS) that acts as a key mediator of autonomic, behavioral, immune, and endocrine stress responses. The peptide appears to be anxiogenic, depressogenic, and proinflammatory and leads to increased pain perception.10 γ-Aminobutyric acid (GABA) inhibits CRF release.6
Glucocorticoids activate the locus caeruleus, which sends a powerfully activating projection back to the amygdala using the neurotransmitter norepinephrine. The amygdala then sends out more CRF, which leads to more secretion of glucocorticoids, and a vicious circle of feedback between the mind (brain) and the body results.5 Repeated stimulation of the amygdala results in strengthened communication across its synapses with other regions of the brain (ie, long-term potentiation) (So- the damaging results of stress don’t go away, but are cumulative)
Prolonged exposure of the CNS to glucocorticoid hormones eventually depletes norepinephrine levels in the locus caeruleus. As norepinephrine is an important neurotransmitter involved in attention, vigilance, motivation, and activity, the onset of depression may subsequently occur. (Bad outcomes such as depression are PHYSICAL and not “hooky-spooky magical psychology”)
Serotonin appears to be involved in the pathogenesis of anxiety disorders as well. Agents that enhance serotonin neurotransmission may stimulate hippocampal 5-HT1A receptors, thus promoting neuroprotection and neurogenesis and exerting an anxiolytic effect.11
GABA, the primary inhibitory neurotransmitter in the CNS, is another neurotransmitter believed to be inherently involved in the pathophysiology of anxiety disorders. Levels of GABA appear to be decreased in the cortex of patients with PD, compared with those in control subjects.12 Benzodiazepines facilitate GABA neurotransmission and therefore can improve anxiety. (This is where the “rubber meets the road” – the assumption that medication can “treat” anxiety – it may effectively (or not) “mask symptoms” BUT pharmaceuticals “for brain pain” de facto create more problems in the form of side effects and changes to “the brain” – that’s how they work. They change the brain. It’s a crap shoot for the individual taking the drug; it’s wildly uncontrolled testing on humans. Drugs do not REMOVE the source of stress that is causing anxiety! They OVERRIDE the brain-body alarm system, not only for “erroneous threats” but for actual threats such as toxic environments, unhealthy conflict-driven work environments, destructive relationships and anything that is “too stressful” in the person’s environment. They provide “negative adaptation” that allows for the damage to the person to continue.
The remainder of the articles deals with the specific DSM disorders and “drug” treatment …