The biological process that causes ptsd

Post traumatic stress disorder (PTSD) is the leading cause that contributes to the rising suicide rates, divorces, and behavioral changes in soldiers returning from war. Many doctors and psychologists believe that soldiers are undertreated and under-diagnosed after they return home, resulting in an almost exponential growth in suicide rates. Soldiers diagnosed with PTSD are struck with behavioral, cognitive, and biological changes in the brain, symptoms that are often overlooked or misdiagnosed. Post traumatic stress disorder can lead to dramatic changes in an individual’s life, inhibiting the individual from completing necessary daily tasks, often resulting in damage to the individual’s relationships, lifestyle, and so forth. The cause of PTSD is biological; the biological effects and chemicals alter the cognitive responses and behavior in the brain.

By definition, “PTSD always follows a traumatic event which causes intense fear and/or helplessness in an individual. Typically the symptoms develop shortly after the event, but may take years before they are fully developed and effecting the individual’s life dramatically. The duration for symptoms is at least one month for this diagnosis” (DSM-IV). Symptoms include re-experiencing the trauma through nightmares, obsessive thoughts, and flashbacks (feeling as if one is actually in the traumatic situation again). There is an avoidance component as well, where the individual avoids situations, people, and/or objects which remind him or her about the traumatic event For example, a person experiencing PTSD after a serious car accident might avoid driving or being a passenger in a car. An individual with PTSD will experience increased anxiety in general, possibly with a heightened startle response (e.g., very jumpy, startle easy by noises).

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However, to understand the extent of these physical symptoms that are visually observable, it is necessary to understand the biological chemistry that occurs in the brain.

The nervous system is the body’s electrochemical communication network, consisting of the Central Nervous System (CNS) and the Peripheral Nervous System (PNS). The brain and the spinal cord form the central nervous system while the peripheral nervous system links the central nervous system with the body’s sense receptors, muscles, and glands. The PNS has two components, the autonomic (controlling self-regulated action of internal organs and glands) and somatic (voluntary movements of skeletal muscles). Furthermore, the autonomic nervous system is made up of the sympathetic (arousing) nervous system and the parasympathetic (calming) nervous system.

Each brain hemisphere of the cerebral cortex is divided into four “lobes, geographic subdivisions separated by prominent fissures or folds.” They are the frontal, parietal, occipital, and temporal lobes. The frontal lobe is involved in speaking, muscle movements, and making plans and judgments. The parietal lobe receives sensory input for touch and body positions. The occipital lobe receives visual information. The temporal lobes, one lying roughly above each ear, receive auditory information.

The limbic system, a doughnut-shaped system of neural structures at the border of the brainstem and cerebral hemispheres, is associated with emotions such as fear and aggression and drives emotions such as those for food and sex. The limbic system includes the hippocampus, amygdala, and hypothalamus. The hippocampus processes memory. The amygdala influences aggression and fear. The hypothalamus directs several maintenance activities (eating, drinking, body temperature) and helps govern the endocrine system via the pituitary gland and is also linked to emotion.


In the United States, more than 30,000 persons commit suicides annually (cite source). Suicides among veterans are included in this number, but the exact proportion is unknown. Recent data show that about 20% of suicide deaths nationwide could be among veterans. (Please note that percentage does not include the rates of suicides of men and women on active duty.) Some veterans’ advocacy groups have filed a class-action lawsuit claiming that the Department of Veterans Affairs (VA) is not providing adequate and timely access to mental health care, and that this has led to an “epidemic of suicides”. It is important to note that there is a distinction between the health care system of veterans (VA) and active duty servicemen. (Department of Defense, DOD)

The Military Health System (MHS) recorded 39,365 patients who have been diagnosed with post-traumatic stress disorder. Based on Anne Tyson’s news article “Military Investigates West Point Suicides”: “The 2008 suicide rate of 20.2 per 100,000 marked a historic high for the Army, and for the first time since the Vietnam War era it surpassed the overall U.S. rate for people of similar ages and backgrounds: This rate marks a jump from the Army’s rate of 12.7 per 100,000 in 2005, 15.3 in 2006 and 16.8 in 2007.” Academies and suicide prevention programs have been passing out prevention cards, putting up posters, and reviewing its procedures, and it has ordered fresh-suicide prevention training to be completed, stated Col. Bryan Hilferty, spokesman for the U.S. Military Academy at West Point, N.Y. Although it seems like an effective technique, rates are still on the rise. The number of suicides in Afghanistan, which had ranged from none to two a year, increased to seven last year, corresponding to an increase in anxiety and expose to combat, said Col. Elspeth Ritchie, an Army psychologist. While programs are widely available the suicide rates are still rising. One student said: “They have programs here, but they are so unfriendly, and people are afraid it will affect their careers”

Veterans and active duty servicemen have a number of risk factors that increase their chance of attempting suicide. These risk factors include combat exposure, post-traumatic stress disorder and other mental health problems, traumatic brain injury (TBI), poor social support structures, and access to lethal means. The active duty servicemen are placed in a highly vulnerable environment demonstrating the active arguments occurring nationwide. Soldiers seeking help are often dismissed after only several sessions. Repeatedly, the biological effects and symptoms are overlooked (such as a predisposition to PTSD), as the cognitive behavior is the most open symptom.

The Biological Viewpoint

Other risk factors for PTSD have emphasized a possible role for a biological factor in contributing as a risk for PTSD. There is now support from several lines of evidence for a possible genetic predisposition to PTSD. True and colleagues (1993) demonstrated a greater prevalence of PTSD in individuals who had monozygotic [1] twins as trauma survivors compared with dizygotic [2] twins, demonstrating that as much as 30% of some PTSD symptoms appear to have a genetic basis (2). These findings imply that the increased prevalence in monozygotic twins is due to shared genes. Davidson and colleagues (1985) demonstrated that trauma survivors with PTSD were more likely to have parents and first-degree relatives with mood, anxiety, and substance abuse disorders compared with trauma survivors who did not develop PTSD (3).

Yehuda and colleagues (1998) stated that children of Holocaust survivors are more likely to develop PTSD in response to traumatic events compared with demographically matched subjects whose parents did not have Holocaust experiences (1). Further, Holocaust survivors with PTSD are more likely to have children who will be more easily susceptible to PTSD compared with Holocaust survivors without PTSD.

The extent to which these study findings are indicative of truly biological or even genetic phenomena as opposed to environmental ones is not yet clear. Even twin studies do not always speak directly to the issues of genetics because of the large shared environment in families. In particular, the vulnerability for developing PTSD in a trauma survivor who has lived with a chronically mentally ill family member may reflect genetics, experience, or some combination. For example, in one of the studies, children of Holocaust survivors reported feeling chronically stressed from hearing stories about the Holocaust, having to witness their parents suffer chronic pain, feeling burdened by their parents’ expectations, or experiencing losses such as the absence of grandparents and other extended family members as a result of the Holocaust (1). Thus, the increased prevalence of PTSD in family members may reflect vulnerability owing to these experiences rather than to inherited genes. But even if the diathesis for PTSD were somehow biologically transmitted to the children, the diathesis is still a consequence of the traumatic stress in the parent. Thus, even the most biological explanation for vulnerability must at some point deal with the occurrence of the traumatic event.

In the last 10 years, the field of biological studies of trauma and PTSD has grown rapidly, and there are now several strong candidates for biological “markers” of PTSD. Yehuda and colleagues (1997) stated that trauma survivors with PTSD have shown differences in several neuroendocrinological, petrochemical, psycho physiological and neuroanatomical measures compared with trauma survivors without PTSD and nonexposed comparison subjects (5).

It has been widely assumed that the biological changes in trauma survivors with PTSD are a result of trauma exposure and secondarily of PTSD. However, without any knowledge of the biological alterations in a particular trauma survivor prior to trauma exposure, it is impossible to know with certainty whether biological changes observed in PTSD truly reflect consequences of traumatic stress exposure or rather represent an underlying biological vulnerability for PTSD.

Studies of individuals who are believed to have a greater susceptibility to PTSD may be key to exploring this issue. In a landmark study, Resnick and colleagues (1995) measured Cortisol levels during the immediate aftermath (that is, within several hours) of rape. Lower Cortisol levels were observed in women who had histories of rape or assault compared with women who did not have this risk factor (6). It was the risk factor of prior trauma that was associated with a different neuroendocrine response to a subsequent traumatic event. Interestingly, the alteration observed was consistent with observations of individuals who have chronic PTSD. On the basis of this observation, Resnick and colleagues (1995) wondered if any biological variable associated with PTSD could be observed in individuals at risk for PTSD before they experienced a focal traumatic event. Yehoda and colleagues (1998) previously hypothesized that adult children of Holocaust survivors represent a high-risk group for PTSD because of the increased PTSD prevalence in this group (1).

Cortisol is a hormone that is released by the adrenal gland. In response to stress, several biological systems are activated in order to allow the body to become mobilized for the “fight-or-flight” reaction (9). During stress, the brain also signals the pituitary gland to stimulate the release of Cortisol from the adrenal gland. The function of Cortisol in response to stress is to contain the other biological reactions (that is, increased gluconeogenesis, inhibition of tissue repair, immunosuppressant) that have been activated to respond to the short-term demands of the stressor. If Cortisol did not facilitate the termination of these other reactions, they would do long-term damage to the body. Therefore, it is possible to think about Cortisol as an “anti stress” hormone. A person’s inability to produce Cortisol in sufficient amounts in response to stress would have adverse consequences.

Under conditions of acute and chronic stress and in certain types of psychiatric disorders associated with stress (such as major depression), Cortisol levels are elevated (10-12), but this sometimes reflects that the hypothalamic-pituitary-adrenal (HPA) axis [3] has grown resistant to the effects of Cortisol. The dexamethasone suppression test (DST) [4] has been used as a probe of the HPA axis (13). Dexamethasone is a synthetic glucocorticoid that mimics the effects of Cortisol to test the effectiveness of the HPA axis in shutting down the stress system. Under normal conditions, the administration of dexamethasone results in a suppression of the body’s own Cortisol. Dexamethasone acts at the level of the pituitary to shut down subsequent release of Cortisol in much the same way as Cortisol would control its own release. The decline in Cortisol following dexamethasone indicates that the negative feedback of Cortisol is intact and the body is capable of responding to stress hormones. However, under conditions in which the pituitary-adrenal system has grown resistant to the negative feedback effects of Cortisol, such as is in depression, dexamethasone may fail to shut down Cortisol levels (that is, causing them to be higher than they would normally be if negative feedback inhibition were functioning properly). A failure to suppress Cortisol levels in response to dexamethasone administration (Cortisol nonsuppression) usually implies a reduced sensitivity of the Cortisol receptors on the pituitary gland.

Trauma survivors with PTSD show a different Cortisol response from that observed under conditions of acute and chronic stress and in disorders such as major depression. Studies in various trauma survivors have shown that Cortisol levels are lower in survivors with PTSD compared with normal controls and persons with other psychiatric diagnoses.

PTSD patients also appear to have high serum levels of tyrosine and thyroxin. Thyrotoxicosis is often produced following extremely stressful events. Thyroxin increases the rate of metabolism if there are insufficient carbohydrates and fats available. Thyroxin causes rapid degradation of proteins for energy. Studies have also revealed that high thyroxin levels can be produced by a number of stressful psychological stimuli. The biological and hormonal changes, which occur in PTSD, are extensive and research indicates that significant disturbances of several areas of the brain can eventually result from the numerous alterations of the hormonal system. People without PTSD do not show the same biological alterations as those with PTSD (Henline).The intense bio-chemical changes that occur in the victim at the time of the traumatic event may lead to permanent changes in the nervous system becoming a chronic medical illness or having negative effects on learning, habituation, and stimulus discrimination.

Psychological trauma may also alter some neurotransmitters in the brain. There are five neurotransmitters which may be affected: epinephrine, Cortisol, norepinephrine, serotonin, and endorphins. Epinephrine is a by-product of the adrenal gland, which enables the body to cope with the stress of the traumatic event. Heart rate, breathing, muscles, blood sugar of energy are all regulated with this neurotransmitter. Cortisol is released by the adrenal gland when the person feels threatened. It provides a source of energy by releasing blood sugar into the bloodstream and helps repair body tissue if injured (Henline).

Norepinephrine is also a by-product of adrenaline and is transmitted through the bloodstream to the brain. It acts as the main facilitator in the brain to enhance alertness and efficient problem solving. It is released in the hypothalamus locus coeruleus and other brain areas during extreme stress (Henline). With repeated exposure to the trauma or extreme stress, a depletion of NE in the hypothalamus and hippocampus may occur.

Serotonin helps modulate NE responsiveness and arousal. The inability to modulate arousal control is due to lack of serotonin. Increased arousals in response to new stimuli, handling, or pain, are also linked to low serotonin levels. Other serotonin functions correlate with hostility, impulsivity, and self-directed aggression in patients with depression and Borderline Personality Disorder. Serotonin is a transmitter produced in the brain. Endorphins, when actively circulating and an adequate supply of serotonin produce calmness, relaxation, and contentment. When there is a deficiency, there is an increase in irritability, anger, sadness, and depression. These neurotransmitters are centrally involved in the various symptoms of PTSD (Henline).

Serotonin Reuptake Inhibitors (SSRI’s) are effective in treating both obsessive thinking and involuntary preoccupation with traumatic memories. SSRI’s may also help the behavioral inhibition system related to various problems in behavior seen in PTSD such as, impulsivity, aggressive outbursts, compulsive reenactment of trauma related behavior patterns, and the inability to learn from past mistakes (Henline).

Exposure to trauma may be associated with many different types of outcomes, one of which is PTSD. This response is associated with specific risk factors. The different types of factors associated with different responses, particularly since prospective, longitudinal studies clearly show that most trauma survivors do not develop any psychiatric disorder in the acute or chronic aftermath of an event (8). It may be appropriate to explore the nature of those who do not develop any psychiatric disorder-the less vulnerable, stress-resistant trauma survivors. On one level, resistance to PTSD may be a characteristic that is malleable by traumatic experience. Individuals who are invulnerable in certain situations may become more vulnerable with repeated stress exposure. Ultimately, knowledge not only about vulnerability but of the factors that expand or corrode resistance may be of substantial benefit to trauma survivors.

Congressional Action

After the rising suicide risks due to PTSD, depression, and other impacting factors, Congress was asked to take action. “In the 109th Congress, two measures (H.R. 5771 and S. 3808) were introduced regarding the prevention of suicide among veterans. However, these bills did not see further legislative action” (CRS). Following this the senate introduced an act that “requires the VA to establish a comprehensive program for suicide prevention among veterans” (CRS). Once again Congress made the help available but not very open to veterans or active duty servicemen. After suicide rates still did not go down, congress implemented a new policy. This policy included screening all “Operation Enduring Freedom/Operation Iraqi Freedom veterans for depression, PTSD, and alcohol abuse upon their initial visit to VA medical centers or clinics. Furthermore, screening for depression and alcohol abuse is required on an annual basis for all veterans, and screening for PTSD is required annually for the first five years after enrollment, and every five years thereafter” (CRS).


Post-traumatic stress disorder could be described as the silent but deadly disease on today’s war front. PTSD patients show a significant change of chemicals in the brain that alter their behavior and rational reasoning. One of those, as explained previously, is Cortisol. With higher levels of these the patient, or even in this case, victim, may not be able to respond quickly or reasonably at all. The “fight-or-flight” reaction has been damaged. With stress hormones raising the victim seems almost tortured by the repressing traumatic experience.

Post-traumatic stress disorder based on evidence, proven theories, tested studies, and longitudinal data is biological. It affects the biological levels of the brain and then moves on to the cognitive sections of the brain, damaging or altering them as well.

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