Posttraumatic stress disorder (PTSD) is precipitated by experiencing or witnessing a traumatic or terrifying life event, such as a serious accident, a violent crime, or a natural disaster. People with PTSD may relive the event in nightmares or have disturbing recollections of it during waking hours. Ordinary events can trigger flashbacks that may result in a loss of reality, causing the person to believe the event is happening again. Approximately 5.2 million Americans are affected by PTSD, which can occur at any age (Narrow WE et al 2002; Margolin G et al 2000).
Symptoms associated with PTSD include inability to sleep, hypersensitivity to external stimuli, feelings of detachment or numbness, and loss of memory of the time surrounding the traumatic experience. In addition to the presence of these symptoms, doctors considering a diagnosis of PTSD consider whether a patient persistently re-experiences the traumatic event, such as by recollecting it, dreaming about it, experiencing hallucinations or flashbacks, or physically reacting to internal or external cues that symbolize or resemble an aspect of it. For a diagnosis of PTSD, symptoms must be present for more than one month but may occur years after the traumatic event (American Psychiatric Association 2000).
By now, it is well known that most steroid hormones (e.g., pregnenolone, estrogen, progesterone, testosterone, and DHEA) are neurologically active. In fact, large quantities of DHEA, as well as estrogen and progesterone receptors are found in the brain. These hormones have a number of effects within the brain, including regulation of mood. Accordingly, a number of studies have linked abnormalities in hormone levels to various anxiety disorders (Birzniece V et al 2006; Cohen H et al 2006; Strous RD et al 2006). In addition, studies have documented that abnormalities in the hypothalamic-pituitary-adrenal axis, which controls the body’s response to stress through the release of cortisol and DHEA, can predispose a person to anxiety and depression (Leonard BE 2005). During times of stress and anxiety, the balance between cortisol and DHEA is altered in favor of cortisol.
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Understanding risk factors for heart disease, Part I: Lipids and C-reactive protein, by William Davis, MD
Well before coronary heart disease itself gets underway, so-called risk factors for heart disease declare themselves. Atherosclerotic plaque initiates and grows for good reason. Risk factors identify some of those reasons.
This is the role of risk factors: To provide an indication that potential for atherosclerosis is present.
If you’ve become a bit confused about this conversation over the past few years, you are not alone. Controversy over the importance of risk factors, the overselling of cholesterol drugs, and the emergence of newly identified risk factors for heart disease has made this a rapidly changing, and often difficult to follow, discussion.
The understanding of risk factors for heart disease has come a long way since the 1940s, when it was not at all clear just what aspects of diet, lifestyle, or genetics lay behind the disease. Even cigarette smoking was still being advertised as a healthy habit: “Camels: Smoked by more doctors than any other brand!”
But, even after nearly 60 years of research and heated debate, there is not uniform agreement on what causes heart disease. We’ve zigzagged around the role of diet, cholesterol, and fats, while newly appreciated phenomena like inflammation, genetic factors, and vitamin D deficiency emerge and even further transform the discussion.
We might regard it as 60 years of confusion—or 60 years of wisdom gained. Despite the controversies and persistent uncertainties, surely there are some nuggets of wisdom to be learned.