Thursday, December 31, 2009

Acute Stress Leaves Epigenetic Marks on the Hippocampus

Yesterday I posted two long articles of PTSD (PTSD and the Military and The Science of PSTD and its Future as a DSM-V Diagnosis), and in the second, in talking about the science, I mentioned that one of the features is shrinking of hippocampus while the amygdala tends to enlarge.

So, of course, today Science Daily posts an article on new research that shows the impact of acute stress on the hippocampus is mediated by epigenetics. It's interesting that a single 30-minute exposure caused such drastic changes, and more so that the brains did not adapt to the stress over a 21-day period of chronic stress.

And once again, anti-depressants like Prozac (fluoxetine) show an ability to mitigate the damage not through serotonin channels, as the drug companies have promoted, but through reversing some of the methylation effects caused by chronic stress.

Other studies have shown fluoxetine's ability (paroxetine [paxil] appears to do the same thing, in PTSD specifically) to generate neurogenesis in the hippocampus. The mounting evidence that these drugs are effective pieces of the treatment puzzle, but also that they appear to increase hippocampal volume in non-PTSD brains suggests a possible prophylactic use for those who are going into acute or chronic stress situations.

Acute Stress Leaves Epigenetic Marks on the Hippocampus

ScienceDaily (Dec. 31, 2009) — In trying to explain psychiatric disorders, genes simply cannot tell the whole story. The real answers are in the interaction of genes and the environment. Post-traumatic stress disorder requires some trauma, for instance, and people, for the most part, aren't born depressed. Now research has revealed one mechanism by which a stressful experience changes the way that genes are expressed in the rat brain. The discovery of "epigenetic" regulation of genes in the brain is helping change the way scientists think about psychiatric disorders and could open new avenues to treatment.

Richard Hunter, a postdoc in Rockefeller University's Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, found that a single 30-minute episode of acute stress causes a rapid chemical change in DNA packaging proteins called histones in the rat hippocampus, which is a brain region known to be especially susceptible to the effects of stress in both rodents and humans.

The chemical change Hunter examined, called methylation, can either increase or decrease the expression of genes that are packaged by the histones, depending on the location of the methylation. He looked for methylation on three regions of histone H3 that have been shown to actively regulate gene expression. In experiments published this month in Proceedings of the National Academy of Sciences, he shows that methylation of one mark, H3K9 trimethyl, roughly doubled in the hippocampus. Methylation of a second mark, H3K27 trimethyl, dropped by about 50 percent in the same area. Changes associated with the third mark were minor.

"The hippocampus is involved in episodic memory, so you would expect it to be sensitive to episodic experiments like this, more so than the motor regions, for instance," says Hunter, who worked on the project with Rockefeller scientists Bruce S. McEwen and Donald W. Pfaff. "But what is surprising is the magnitude and regional specificity of these patterns." The sheer size of the change in histone methylation suggests that it is important to the brain's response to acute stress, although its exact role remains a mystery. The two methyl marks that changed are both thought to repress gene expression usually, but methylation increased in one and decreased in the other.

Hunter also checked for similar changes as a result of chronic stress -- exposure to a 30-minute stress each day for 21 days. He did not find a major effect, which could reflect the animals' adjusting to the stress. However, when he treated the rats with fluoxetine, the generic form of the popular antidepressant Prozac, he reversed some methylation effects associated with chronic stress.

It's becoming increasingly evident, Hunter says, that the epigenetic changes like the methyl marks he observed and others, such as acetylation and phosphorylation, could play a significant role in the brain's response to stress and the treatment of stress related diseases, such as post-traumatic stress disorder.

"There was a thought that the genome project would reveal all in neuropsychiatric disease, but that has proven not to be the case," he says. "Epigenetics has become much more interesting because it allows us to look at how gene expression is changed by environmental events, explainable in part by histone modifications."

Journal Reference:

  1. Hunter et al. Regulation of hippocampal H3 histone methylation by acute and chronic stress. Proceedings of the National Academy of Sciences, 2009; 106 (49): 20912 DOI: 10.1073/pnas.0911143106

Working Through Grief: It's Different For Everyone

More and more, the old K├╝bler-Ross Model of grief that was so long taken for granted, is being dismantled. While it is true that some people do go through the five stages (below) in order, many more people do not.

Stages of Grief

  1. Denial"I feel fine."; "This can't be happening, not to me."
    Denial is usually only a temporary defense for the individual. This feeling is generally replaced with heightened awareness of situations and individuals that will be left behind after death.[1]
  2. Anger"Why me? It's not fair!"; "How can this happen to me?"; "Who is to blame?"
    Once in the second stage, the individual recognizes that denial cannot continue. Because of anger, the person is very difficult to care for due to misplaced feelings of rage and envy. Any individual that symbolizes life or energy is subject to projected resentment and jealousy.[1]
  3. Bargaining"Just let me live to see my children graduate."; "I'll do anything for a few more years."; "I will give my life savings if..."
    The third stage involves the hope that the individual can somehow postpone or delay death. Usually, the negotiation for an extended life is made with a higher power in exchange for a reformed lifestyle. Psychologically, the individual is saying, "I understand I will die, but if I could just have more time..."[1]
  4. Depression"I'm so sad, why bother with anything?"; "I'm going to die . . . What's the point?"; "I miss my loved one, why go on?"
    During the fourth stage, the dying person begins to understand the certainty of death. Because of this, the individual may become silent, refuse visitors and spend much of the time crying and grieving. This process allows the dying person to disconnect oneself from things of love and affection. It is not recommended to attempt to cheer up an individual who is in this stage. It is an important time for grieving that must be processed.[1]
  5. Acceptance"It's going to be okay."; "I can't fight it, I may as well prepare for it."
    This final stage comes with peace and understanding of the death that is approaching. Generally, the person in the fifth stage will want to be left alone. Additionally, feelings and physical pain may be non-existent. This stage has also been described as the end of the dying struggle.[1]
It helps to know the stages, and then toss them out the window. Everyone grieves in their own way, as this new article from Medical News Today makes clear. The article offers some good advice for working through the grieving process.

Working Through Grief: It's Different For Everyone

A death of a loved one, a job loss, the end of a marriage, an illness or disability. Everyone faces losses and grief, but the toll that grief can take on the mind and body can catch many people by surprise.

The December issue of Mayo Clinic Women's HealthSource provides an overview of grief -- a normal reaction to loss. In years past, grief often was described as following a certain pattern or orderly progression from one feeling to another.

But there is no one way to grieve. People who are grieving experience many different emotions in any number of combinations. They may include denial, sadness, anger, confusion, despair and even guilt. Physical reactions can include sleeping problems, changes in appetite, a drop in energy level, body aches and pain or the development or worsening of an illness.

Time spent grieving varies, too. Some people take months to fully accept or adapt to a loss. For others, the process may take years. To help cope with grief:

-- Express feelings: Suppressing thoughts and emotions may prevent working through grief. Friends, family or members of the religious community often can be a source of support and comfort. Other options are support groups or grief counselors.

-- Delay any major decisions or changes: Decisions that affect life and lifestyle, such as housing changes or new ways of handling finances, should wait a while. Advice from a trusted family member or friend, financial adviser or attorney may be helpful.

-- Take care of personal health: Eating right, getting adequate sleep and limiting alcohol are important. Regular exercise can relieve stress and anxiety.

-- Be patient: Expecting to simply "get over" grief is unrealistic. Ups and downs may last for weeks or months following a loss. Though some feelings of loss may never fully go away, the most intense signs and symptoms of grief typically diminish over time, within six months or so. Grief that is prolonged and debilitating may be a sign of depression or post-traumatic stress disorder. A doctor should be consulted for treatment options.

Source: Mayo Clinic
If you would like a more in-depth approach, one that offers tools for many different types of people, my new book, Essential10 Behaviors for Coping with a Crisis (Dealing with Change) is designed to help people find the growth opportunities hidden in these life crises we all face.

Yes, a shameless plug my book - it's only $2.99 (for either a PDF or a Kindle version) for 45 pages of information.


Stephen and Martine Batchelor - Godless Religion or Devout Atheism? (Parts 10 - 14)

Here are the final five parts of this cool series from Upaya Zen Center.

Godless Religion or Devout Atheism? Part 10 of 14 – Dharma Talk on Buddhahood & Awakening

Speaker: Martine Batchelor

Martine begins the talk urging us to look at our motivation for awakening. Is it done with wisdom and compassion or perhaps with the goal to escape from the world? She discusses sudden vs. gradual awakening and working with bad habits. She goes on to discuss the role of insight in our lives and how we can use it to change ourselves and the world. When we sit, we should work on de-grasping so that we can let go in our everyday lives.

Podcast: Play in new window [Play] | Download [Play]

Godless Religion or Devout Atheism? Part 11 of 14 – Session 5

Speaker: Stephen Batchelor

The theme of this seminar is the title of the retreat, “Godless Religion or Devout Atheism?” Stephen tells of how Brahman or God was understood at the time of the Buddha, and how the Buddha rejected this notion. The Buddha, says Stephen, was deeply rooted in the phenomenal world and instructed his followers to pay attention to this world. As Buddhism developed in time and cultures, it added superstructure that looked religious, which we often find today.

Podcast: Play in new window [Play] | Download [Play]

Godless Religion or Devout Atheism? Part 12 of 14 – Discussion and Q & A

Speakers: Stephen & Martine Batchelor

Stephen begins the Q & A by taking a question on the Tibetan people’s relationship with their land and culture. Other topics include art, impermanence and aesthetics and our relationship to the world; the Buddha’s perspective on ritual; the Buddha as atheist or agnostic; finding mystery in everyday life; music as meditation; choosing the kind of meditation one should do; and “no self” further explained.

Podcast: Play in new window [Play] | Download [Play]

Godless Religion or Devout Atheism? Part 13 of 14 – Dharma Talk on Love & Compassion

Speaker: Martine Batchelor

How can we cultivate creative, wise love without grasping? One aspect of this kind of love, says Martine, is to create relationships outside of the primary love relationship. Another aspect is not to make assumptions in relationship, but to ask ourselves, “How can I creatively engage with others?” Meditation helps us to open up to others and to such questions, thus making ourselves less self-absorbed. At the root of compassion is deep listening, which sometimes is the most we can do in a difficult situation.

Podcast: Play in new window [Play] | Download [Play]

Godless Religion or Devout Atheism? Part 14 of 14 – Session 6

Speaker: Stephen Batchelor

The Buddha’s teaching was dialogic: interactive and responsive to the present circumstances. Stephen asks us to find the foundation beneath the superstructure of culture in order to understand the Buddha’s teaching. Stephen goes on to discuss what the Buddha meant by “entering the stream,” including three things that fall away for the stream enterer. He ends the seminar and the retreat by noting principles that are distinctly the Buddha’s, and not found in the superstructure of the Buddha’s time.

Podcast: Play in new window [Play] | Download [Play]

Closer to the Truth - What is Consciousness?

Excellent, but WAY too short.
What is Consciousness? (107)



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From the Series:
Produced by:
University of Southern California

08/08/2004

Description:
What is Consciousness -- our inner thoughts, feelings, personalities -- the hidden 'Stuff' of our Private Selves? Is there something special about Consciousness, something of the mind not in the brain? This is self awareness, the interior mental experience we call Consciousness. What is the importance of studying Consciousness? The panel discusses the concept of human consciousness.

Related Links:
Closer to Truth

Speaker(s):
James Trefil, professor of physics, George Mason University; author of fifteen books

David Chalmers, professor of philosophy, co-head, Center for Consciousness, University of Arizona

John Searle, professor of philosophy, University of California, Berkeley

Marilyn Schlitz, director of Research, Institute of Noetic Science; senior scientist, Geraldine Brush Cancer Research Institute, California Pacific Medical Center

Fred Alan Wolf, theoretical physicist, international lecturer on consciousness and the new physics; award-winning author of eight books

Robert Lawrence Kuhn, Ph.D., UCLA; Closer to Truth host

Runtime:00:27:53

Rating:TV-PG


New Year Resolutions?

http://happylists.files.wordpress.com/2009/01/new-years-resolutions.jpg

Do you make resolutions for the New Year? Many people do, and few people ever succeed with them. About 15 years ago I resolved to never make another New Year resolution, and it's the only one that has ever lasted.

But if you make New Year resolutions, here are two articles worth considering. First, Add Spiritual Renewal to your list of New Year's Resolutions and more importantly, A Guide to Making Change Stick in the New Year.

Doing the right thing for body, mind, and spirit includes spiritual renewal

by Thomas Plante, PhD

Many people make New Year resolutions to eat and drink less as well as exercise more. Why not add spiritual renewal to the list?

Regardless of your religious and spiritual traditions and beliefs, quality research and clinical practice shows that there are a variety of spiritual tools that can help to improve your life for body, mind, and spirit. Doing the right thing for yourself (and others) might include spiritual renewal.

In my most recent book, Spiritual Practices in Psychotherapy: Thirteen Tools for Enhacing Psychological Health published earlier this year by the American Psychological Assocition (http://books.apa.org/books.cfm?id=4317178%20), I outline spiritual tools that psychotherapists can use to improve their effectiveness with clients. All of the tools have been found in research to improve well being for body, mind, and spirit. They include the following:

1. Prayer

2. Meditation

3. Developing Meaning, Purpose, and Calling in Life

4. Bibliotherapy (Reading appropriate books and articles for renewal)

5. Attending Community Services and Rituals (e.g., Church or Temple services and events)

6. Volunteerism and Charity (Helping others means helping ourselves)

7. Ethical Values and Behavior

8. Forgiveness, Gratitude, and Kindness

9. Social Justice (working towards making the world a more just place for all especially those in need)

10. Learning from Spiritual Models (who are our spiritual models?)

11. Acceptance of Self and Others (even with faults)

12. Being Part of Something Larger than Yourself

13. Appreciating the Sacredness of Life (seeing the divine within all)

I'll discuss these in more detail in susbequent blog posts but for now think of these 13 tools as ways for you to structure your spiritual renewal. Perhaps it would be helpful as we come to a new year and decade to consider how we might work towards spiritual renewal by using some or all of the tools mentioned above. Something to consider in addition to joining the gym and passing on seconds at dinner as we begin 2010.

Now, if you want to make this resolution stick, read this article from Elisha Goldstein, Ph.D.

A Guide to Making Change Stick in the New Year

By Elisha Goldstein, Ph.D.
December 30, 2009

Recently I wrote the blog Neuroplasticity, Gratitude, and Your Mental Health: Food for Thought and thousands of people viewed it being reminded of the really powerful effects of counting blessings over burdens. So here we are, at the end of the year, answer these 4 questions for yourself right here, right now in an effort to move into 2010 with less stress and a greater sense of resiliency and well-being.

  1. Think back to when this year started-what were your expectations? What did you want/hope for?
  2. What are you grateful for in this past year?
  3. What are your intentions for this upcoming year, how would you like to be (e.g., more calm, a better listener, more focused, kinder to yourself and others, more present to friends and family?)
  4. Looking forward, what are you wishing for yourself (e.g., health, feeling safe, free from fear, happiness, a sense of peace)?

Take this into the New Year, making change stick is really about setting an intention and repeatedly coming back to review that intention as if it was a doctor’s appointment. This may actually be the most important thing to do, repeatedly coming back and reviewing your intentions.

Set a time in your calendar one week or one month from today to review your answers to this page and check back on your intentions for yourself. Really, go ahead and do it now and make it a recurring appointment. Life gets too busy and distracting, allow this to be your time to review your intentions on a more consistent basis than once a year.

May you move into this New Year with the presence and kindness to live your intentions.

Below, please share your intentions and wishes for yourself and others below. Your interactions provide a living wisdom for us all to benefit from.

Do you make resolutions? Do you have tips for making them successful? If so, please leave a note in the comments.


Precision Nutrition - Epigenetics: Feast, Famine, and Fatness

Great post from Helen Kollias writing at the Precision Nutrition blog. Understanding the science of fat accretion and fat loss is crucial, at least for those of us trying to help others.

Epigenetics: Feast, Famine, and Fatness

I have a simple Biology 101 question: How are biological traits passed down from one generation to the next?

Pretty easy, right? If you said “genetics” then you’re only half right.

The other half of the answer is surprising — so surprising, in fact, that if I’d proposed it during my undergrad years, I’d have been ridiculed as a member of the Flat Earth Society.

In the last five to ten years, there has been more and more evidence showing there is a non-genetic part that can be passed down to children and even grandchildren. As of this summer there are over 100 scientific articles documenting non-DNA inheritance, also called transgenerational epigenetics (1).

Non-DNA inheritance (aka epigenetics)

Non-DNA inheritance or epigenetics means that the sequence of the DNA doesn’t change, but access to the DNA changes biochemically. This altered DNA can then be passed down to children and grandchildren.

A brief molecular biology interlude: Access to DNA is changed by adding methyl groups to the DNA (take a look at Figure 1) or acetylating or deacetylating the histones the DNA is wrapped around (Figure 2).

For more info on histones and DNA access, read my last research review.

Methylation and gene expression. (2)

Figure 1: Methylation and gene expression. (2)

Figure 2: Two major components of epigenetics (3)

Figure 2: Two major components of epigenetics (3)

Think of the sequence of DNA as letters in a book. You can change the book’s story if you staple some of the pages together.

You didn’t change or delete a single letter in the book, but you can’t read certain pagers or an entire chapter, and that can change the entire story.

Think of methylation as a staple that stops a cell from reading genes.

What’s the big deal, DNA or non-DNA?

The big deal is that non-DNA inheritance responds to your environment. Things like diet can change your non-DNA inheritance.

The tale of two genetically identical mice

If you take a look at Figure 3 below, you see two mice that are, believe it or not, genetically identical (4).

They don’t look genetically identical — they don’t even look like the same species of mouse — but they are. They’re a breed of mouse called agouti.

Figure 3: Agouti mice

Figure 3: Agouti mice

Agouti mice are usefully for epigenetic studies for two reasons:

  1. They have a gene (a genetically modified agouti gene) that makes them obese and yellow.
  2. The agouti gene can be turned off by methylation (or staples in our book analogy).

Mice with the agouti gene turned off are genetically identical to their yellow obese kin, but are skinny and brown, because of methylation of the agouti gene.

How is this possible? Nutrition.

The mother of the skinny brown mouse ate mouse chow supplemented with folic acid (vitamin B12), choline chloride and anhydrous betaine (all chemicals that donate methyl to DNA) for two weeks before mating, though the pregnancy (about 3 weeks) and lactation.

Once the mice were weaned they ate the same food until they were 21 days old – when the picture was taken.

What about humans?

To quote Alexander Pope, “The proper study of mankind is man”; thus in this week’s review I look at a study of epigenetics (non-DNA inheritance) in people.

Heijmans BT, et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17046-9.

Methods

Boy during Dutch hunger winter

Boy during Dutch hunger winter

This study is a bit different then most studies because it uses a historical event (the Dutch hunger winter) as a way of studying non-DNA changes.

The Dutch hunger winter occurred from November 1944 to May 1945, when the Dutch in German-occupied Netherlands lived through a severe famine.

Daily rations during the famine:

  • Started at less than 1000 kcal in November 1944
  • Ended at around 500 kcal by April 1945

In May 1945 the Dutch were liberated, rationing stopped, the famine ended and everybody ate pretty much what they wanted (4).

Two things happened that makes this unfortunate event very useful scientifically:

  1. We have the health information, because registries and health care records were maintained and are still available.
  2. We know when the famine started and stopped, because implementation of rationing was sudden and the rations were well documented.

There were three groups for this study:

  1. People that were born or conceived during the famine (311 of them).
  2. Same-sex siblings that were born before or conceived after the famine (311 of them).
  3. Unrelated people as controls (349 of them).

Non-DNA changes in IGF2

For this study the researchers looked at the IGF2 gene. IGF2 is involved in human growth and development and it can be methylated.

The researchers compared how many methyl groups the IGF2 gene had in each of the three groups. More methylation means less IGF2.

Results

Six decades after being conceived during the Dutch hunger winter people had less methylation on their IGF2 gene compared to their unexposed same-sex brother or sister.

Other studies on the same group found that people conceived during the famine had impaired glucose tolerance, hypercholesterolaemia, raised blood pressure and higher rates of obesity in adulthood (6-8). However, researchers didn’t look at whether these differences were because of epigenetic changes or developmental problems caused by the famine.

Why would being conceived during a famine make you more likely to have metabolic and cardiovascular problems?

This study’s researchers think it’s because your body tries to become as efficient as possible at storing calories, since there isn’t much food around during your development. That works well, until suddenly you have all the food you need and more.

Once you have too many calories, or even simply enough calories, your body can’t stop storing calories. This causes you to have metabolic and cardiovascular problems associated with being overweight.

Conclusion

While famine is an extreme case of altered nutrition – all nutrients are scarce — it gives scientist a pretty useful tool to look at how nutrition can change our epigenetics.

This is the first study to show that the short-term environmental conditions at time of conception affects people’s epigenetics.

Not to over-dramatize, but epigenetics will be the next major biological frontier.

Don’t believe me?

What if I told you scientists found that whether or not your paternal grandfather had enough food as a teenager would change how long you lived, but only if you were male. Or that being born after your mother’s gastric bypass surgery is better for your health?

Same-sex grandparents and starvation

Swedish scientists found that if your grandfather or grandmother went through a famine as teenagers, you would have higher mortality risk ratios, but only if you were the same sex as the grandparent who starved.

Grandfather starvation only changed the grandson’s mortality risk and grandmother starvation only changed the granddaughter’s mortality risk (9). Wow.

Gastric bypass surgery and children’s obesity

Another study looked at mothers who had gastric bypass surgery and obesity in their children.

Do you think it would matter whether the children were born before or after the surgery? Since it was surgery and not a change in lifestyle, I would have guessed there would be no difference (10).

Possibly because of epigenetics, the study found that children born to women post-gastric bypass surgery were 52% less likely to be obese compared to their brothers and sisters born while their mother was obese. Wow, again.

Bottom line

We probably have more control over our DNA than we’ve been led to believe.

While you can’t change the sequence of your DNA, you may be able to change whether or not it is activated.

As it turns out, eating poorly and restrictively can have effects not just for you but your children as well.

"Zemliia (Earth)." The painting is dedicated to the memory of the 1933 famine in Ukraine.

"Zemliia" (Earth). (Commemorates the 1933 famine in Ukraine)

References

  1. Jablonka E, Raz G. Transgenerational epigenetic inheritance: prevalence,mechanisms, and implications for the study of heredity and evolution. Q Rev Biol.2009 Jun;84(2):131-76. Review.
  2. Ling C, Groop L. Epigenetics: a molecular link between environmental factors and type 2 diabetes. Diabetes. 2009 Dec;58(12):2718-25. Review.
  3. Qiu J. Epigenetics: unfinished symphony. Nature. 2006 May 11;441(7090):143-5.
  4. Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol. 2003 Aug;23(15):5293-300.
  5. Lumey LH, et al. Cohort profile: the Dutch Hunger Winter families study. Int J Epidemiol. 2007 Dec;36(6):1196-204.
  6. Roseboom TJ, et al. Coronary heart disease after prenatal exposure to the Dutch famine, 1944-45. Heart. 2000 Dec;84(6):595-8.
  7. Roseboom TJ, van der Meulen JH, Osmond C, Barker DJ, Ravelli AC, Bleker OP. Plasma lipid profiles in adults after prenatal exposure to the Dutch famine. Am J Clin Nutr. 2000 Nov;72(5):1101-6.
  8. Painter RC, Roseboom TJ, Bleker OP. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reprod Toxicol. 2005 Sep-Oct;20(3):345-52. Review.
  9. Pembrey ME, et al. ALSPAC Study Team. Sex-specific, male-line transgenerational responses in humans. Eur J Hum Genet. 2006 Feb;14(2):159-66.
  10. Kral JG, et al. Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years. Pediatrics. 2006. Dec;118(6):e1644-9.

Wednesday, December 30, 2009

PTSD - The Shadow of the Millenial Decade (Part II)

http://img.medscape.com/slide/migrated/editorial/cmecircle/2005/3793/images/susman/slide034.gif

This is Part II of two parts in my look at PTSD. Part I, which focused on PTSD in the military, can be found here. This time, we will look at the future of this diagnosis with regard to the DSM-V, the science of PTSD, and a newer approach to treatment.

PTSD in the DSM-V: The Future of a Diagnosis

The creation of the new handbook for psychiatrists, psychologists, and therapists has been subject to secrecy and scandal. Participants are overwhelmingly psychiatrists (MDs), which contributes to the ever-dominant trend toward a medical model of mental illness (which is true but partial). Many of the docs, estimated at between 2/3 and 3/4 have very strong ties to the pharmaceutical industry, again pushing the DSM toward a more medical model of only including diagnoses for which there is a pill. And to top it off, all participants have signed non-disclosure agreements, essentially swearing themselves to secrecy about the process.

Michael D. Anesti, at the Psychotherapy Brown Bag blog (a great psychology blog) offers one of the best overviews of the current discussion around how to revise this diagnosis and he provides the current diagnostic criteria from the DSM-IV-TR, which will be useful for the rest of the discussion:
Criterion A: The person has been exposed to a to a traumatic event in which both of the following were present -
  1. the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others
  2. the person's response involved intense fear, helplessness, or horror (in children, can be expressed through disorganized or agitated behavior)
Criterion B: The traumatic event is persistently reexperienced in one (or more) of the following ways:
  1. recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions (in children, repetitive play may occur in which themes or aspects of the trauma are exposed)
  2. recurrent distressing dreams of the event (in children, there may be frightening dreams without recognizable content)
  3. acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated)
  4. intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
  5. physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
Criterion C: Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
  1. efforts to avoid thoughts, feelings, or conversations associated with the trauma
  2. efforts to avoid activities, places, or people that arouse recollections of the trauma
  3. inability to recall an important aspect of the trauma
  4. markedly diminished interest or participation in significant activities
  5. feeling of detachment or estrangement from others
  6. restricted range of affect (e.g., unable to have loving feelings)
  7. sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
Criterion D: Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
  1. difficulty falling or staying asleep
  2. irritability or outbursts of anger
  3. difficulty concentrating
  4. hypervigilance
  5. exaggerated startle response

Criterion E: Duration of the disturbance (symptoms in Criteria B, C, and D) is more than 1 month

Criterion F: The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

Criteria A seems to be one of the biggest battle grounds, as you will see below. Some people think it is too limited and should include other experiences which are not defined as traumatic there. They argue that divorce or the death of a loved one can produce PTSD, but does not rise to the level of "intense fear, helplessness, or horror." The other side thinks this is just pathologizing a normal response to a "tough" experience.

The broader issue is that
at one end are those who want to do away with the diagnosis entirely (some of these people were being encouraged by the Bush Administration and have since become less vociferous) and those who want to expand the criteria to make the diagnosis more widely inclusive. Obviously the extremes are to be avoided.

Here are the real issues, as outlined by Anesti at his blog:
The criticisms of PTSD stem not from its diagnostic wordiness, but rather contentions that several people have about particular criteria, as well as the underlying nature of the disorder itself. With respect to that latter point, some individuals claim that the PTSD diagnosis pathologizes normal distress. In other words, it is perfectly natural for people to become upset after something traumatic happens, but such distress will run its course naturally. Research has shown, however, that individuals diagnosed with PTSD often still meet criteria many years later (e.g., Morgan, Scourfield, Williams, Jasper, & Lewis, 2003). Such findings indicate that, while being upset by trauma is normal, extreme responses exist that require clinical attention.

Other critiques of PTSD center on the symptom overlap it shares with other diagnoses. This, of course is not a problem unique to PTSD. Many anxiety disorders share criteria with one another (e.g., avoidance behavior) and generalized anxiety disorder and depression exhibit a substantial amount of symptom overlap. Nonetheless, the point remains that, to some degree, the PTSD diagnosis might include symptoms that are reflective of overall distress or another diagnosis rather than simply applying to this one specific disorder.

A third critique - the one that has been subject to the most attention - is the inadequacy and utility of Criterion A. In other words, a substantial number of people question whether the diagnosis of PTSD should actually require exposure to a specific traumatic event and a response to that event that was characterized by extreme fear, horror, or hopelessness. Some people argue that this criterion prevents people who meet all other criteria from receiving a legitimate diagnosis and subsequent treatment. Others argue that the broadening of the definition that occurred with the publication of DSM-IV has led to a "criterion creep," allowing for diagnoses of individuals who were exposed to traumatic events that are not viewed as legitimate causes of PTSD (e.g., watching frightening Halloween television programs, losing cattle to foot and mouth disease; Rosen & Lilienfeld, 2008). Research conducted by Breslau and Kessler (2001) revealed that the broadening of Criterion A did, in fact, result in an increased number of PTSD cases, but that the vast majority of those new cases involved individuals learning about the sudden unexpected death of a loved one.

All this being said, there is a fairly strong movement afoot to remove Criterion A in DSM-V. When I first heard this, I was highly skeptical and, in fact, in discussions I have had on this topic with my students in Abnormal Psychology, we have often come to a consensus opinion that this move would not make sense. After reading two articles (one on each side of the argument) in this special issue of the Journal of Traumatic Stress, however, I actually have now changed my opinion. My goal with the rest of this article is to explain the proposed models of these two articles and their justification so that you can make an informed decision as well and lend your voice to the discussion.

Brewin, Lanius, Novac, Schnyder, & Galea (2009)

Brewin and colleagues (2009) propose that the DSM-V should eliminate Criterion A and, in doing so, refocus the diagnosis of PTSD around a specific set of core symptoms unique to this particular disorder. They argue that no other mental illness requires a specific etiology and that, in fact, demanding that a disorder be prompted by a single environmental event while excluding the roles of characteristics of the individual and the interaction of personal characteristics with environment is an overly simplistic way of thinking about mental illness. Indeed, this does seem to discount the idea of the diathesis-stress model. Not everybody responds to the same event in the same way or views particular events as equally traumatic, so requiring a specific triggering traumatic event introduces substantial bias to the diagnostic criteria and shifts focus away from the degree of suffering being experienced by the client. They also argue that, after three revisions of this criteria, we still find ourselves unable to articulate a description that ensures that all appropriate cases are included and all inappropriate cases are excluded. There is little reason to believe this would change in DSM-V.

In the field trials for DSM-IV (Kilpatrick et al., 1998), adjusting the definition of Criterion A to include low magnitude events had almost no impact of prevalence rates. In other words, by creating a situation in which a specific trigger does not have to be identified and events not typically considered traumatic were included, the researchers running the field trial actually did not cause a steep increase in PTSD diagnoses.

Brewin and colleagues (2009) thus believe that, in the DSM-V, PTSD should be based around the core phenomenon of "re-experiencing in the present, in the form of intrusive multi-sensory images accompanied by marked fear or horror, an event now perceived as having severely threatened a person's physical or psychological well-being." In other words, if the individual is having flashbacks of past events, the core of the disorder is present whether or not the individual can identify a specific event that prompted all of his or her symptoms and a response to that event that involved specific emotions. Doing this places an emphasis on the symptoms that are present and are unique to PTSD rather than the individual's recollection of past events and feelings. In this sense, we would become more concerned with treating what is present than in discussing what occurred in the past. To me, this sounds eerily familiar to one of the main arguments for why empirically supported treatments such as cognitive behavioral therapy outperform old fashioned therapeutic approaches like psychoanalysis for so many diagnoses. If people are suffering, it does not matter why as much as it matters how they are suffering and what can be done to improve that individual's quality of life. If PTSD symptoms are induced by something that most people would not view as traumatic...who cares? Perhaps individual differences in variables such as distress tolerance cause particular individuals to experience particular events as more problematic than others. If such individuals exhibit the same core symptoms and will respond to treatment just as well, why not include them in the diagnosis?

Kilpatrick, Resnick, & Acierno (2009)

A second article in the same issue of the Journal of Traumatic Stress arrived at an entirely different conclusion. Like Brewin and colleagues (2009), Kilpatrick and colleagues (2009) acknowledged the imperfections of the PTSD diagnosis and contested the notion of "criterion creep;" however, they believe that the core nature of PTSD requires Criterion A and that revisions are a better answer than elimination.

Their rationale for this suggestion centered on a number of specific points. First, because they believe that PTSD is a disorder that does not occur spontaneously and always follows exposure to some stressful event, removing Criterion A would be inconsistent with the nature of the disorder. Second, they believe that, because the DSM-IV field trails revealed that few people meet the other criteria for PTSD without meeting Criterion A, it makes more sense to simply increase flexibility to include the few cases that might otherwise get lost rather than eliminating the criterion altogether. Third, the authors argued that the better focus is on which events are most likely to induce PTSD, rather than which events should qualify. Ultimately, the authors also argued that revision would allow for a DSM-V criteria set more consistent with prior research on the topic.

Ultimately, these authors acknowledged the imperfections, but believe that revising the criteria while remaining consistent with the research already conducted on this issue makes more sense than a massive reboot of the construct involving elimination of Criterion A.

Anesti changed his mind on Criteria A after reading these articles and agrees that Criteria A should be eliminated, which will greatly expand the possible diagnoses:
the priority should be on maximizing our ability to reliably and validly identify suffering, not on determining a particular event that prompted the symptoms in the first place. Unless research indicates that particular prompting events result in differential responses to particular treatments, what is the point in being hung up on the prompting event? If it is there, and it likely is in the vast majority of cases, it will be clear in the client's flashbacks and nightmares and can thus be adequately addressed in treatment.
I think I agree with his take on it - the most help for the most people.

However, not everyone agrees with that perspective. This article from The British Journal of Psychiatry looks at some of the issues with the PTSD diagnosis that need to be addressed (in their view) in the DSM-V. They are cynical at best - the reject a specfic etiology (Criteria A) and go on to dismantle the diagnosis on other grounds as well.
Specific aetiology?

Unlike other diagnoses in the DSM that were agnostic to aetiology, PTSD was defined as a disorder that arose after a specific set of traumatic stressors. Thus, the origins of the definition of PTSD rest on the assumption of a specific aetiology (Criterion A). This assumption, already questionable,1 has been undermined by reports that the disorder can develop after a variety of non-life-threatening events (e.g. divorce, financial difficulties).2 Further, recent studies have demonstrated the frequent occurrence of PTSD symptoms among people with depression who had not experienced Criterion A life stressors,3 and among people with social phobias who respond to failed performance situations.4 Even when an individual encounters horrific, life-threatening events (Criterion A), studies find that pre-incident vulnerability factors (e.g. psychiatric history) and post-incident social support contribute more to post-trauma morbidity than does the magnitude of the presumed aetiological trauma.5 In short, Criterion A events are neither necessary nor sufficient to produce PTSD. Instead, they appear to represent high-magnitude stressors that are otherwise indistinct from the full range of stressors that can have an impact on an individual and create risk of psychiatric morbidity. Now set apart from the general field of stress studies, PTSD might arguably be better returned to the fold.

Distinct syndrome?

In the absence of a specific aetiology, the rationale for diagnosing PTSD lies in the distinctiveness of the clinical syndrome. This is problematic when one considers that a combination of symptoms of major depression and specific phobia fully constitutes the requisite criteria for diagnosing PTSD.6 This raises the concern that PTSD, at least on some occasions, is simply an amalgam of other disorders.

Consider, for example, the case of a boat captain whose fishing vessel is lost at sea, resulting in the death of several crew. Though not physically injured, the captain starts feeling ‘on edge,’ suffers from insomnia and begins to withdraw from usual activities. Most alien to the fisherman’s self-concept, he becomes anxious when considering a return to his usual occupation. Consequently, he turns down offers to work on other vessels, and he becomes isolated from the fishing industry. Without income, this man becomes increasingly anxious and depressed. Prior to the introduction of PTSD in 1980, a psychiatrist would have conceptualised this fisherman’s problems, first, as normal bereavement over lost friends who died in the incident, and second, as a phobic disorder caused by the traumatic event. A third concern would have addressed the development of situational depression as a consequence of adjustment issues and the fisherman’s inability to return to sea. Now, in our post-DSM–III era, we can ask whether the introduction of PTSD has furthered our understanding of this patient’s reactions to a life-threatening event.

Criterion creep

It might be expected that ‘traumatologists’ would be cautious in diagnosing a person as having PTSD upon realising that it lacks a specific aetiology and is possibly not a distinct syndrome. Despite that, enthusiasm for the PTSD diagnosis has not been tempered, and the PTSD ‘model’ has been extended worldwide to encompass an increasing array of events and human reactions across diverse cultures. Individuals no longer have to directly experience or witness a traumatic event to be thought to develop PTSD. Instead, based on the DSM–IV, the diagnosis can be provided to individuals who hear of misfortunes befalling others. Peer-reviewed articles have even discussed the possibility of developing PTSD from watching traumatic events on television.7 It has been suggested that rude comments heard in the workplace can lead to PTSD because a victim might worry about future boundary transgressions: the conceptual equivalent of pre-traumatic stress disorder.8 New diagnostic categories modeled on PTSD have been proposed, including prolonged duress stress disorder, post-traumatic grief disorder, post-traumatic relationship syndrome, post-traumatic dental care anxiety, and post-traumatic abortion syndrome. Most recently, a new disorder appeared in the professional literature to diagnose individuals impaired by insulting or humiliating events – post-traumatic embitterment disorder. Even expected and understandable reactions after extreme events, such as anxiety and anger, are now referred to as ‘symptoms’. This expansion of the PTSD model, a phenomenon referred to as ‘criterion creep’, highlights a critical shortcoming of traumatology: the cross-cultural medicalisation of normal human emotions.9 Labelling situation-based emotions and upsetting thoughts as ‘symptoms’ is akin to saying that someone’s cough in a smoky tavern is a symptom of respiratory disease. Such illogical leaps increasingly inform our cultural narratives when we discuss human reactions to stressful events, possibly giving rise to iatrogenic misapprehensions and contributing to chronicity.

Not only has the PTSD model been expanded, but patients who present with psychiatric problems after traumatic events increasingly receive the diagnosis. Perhaps in this time of managed care, physicians have come to believe that without a PTSD diagnosis a patient’s reactions to traumatic stress will be denied appropriate psychiatric attention, therapeutic intervention, and proportional compensation. Pressure for a PTSD diagnosis also may arise when patients are involved in personal injury claims. Unlike depression or other psychiatric diagnoses that can be caused by multiple stressors unrelated to a legal claim, a PTSD diagnosis is incident-specific and clearly determines causation. Unfortunately, what may be best for a lawsuit is not necessarily best for the patient. By narrowing a physician’s analysis of causation to a single event, a PTSD diagnosis may downplay or even ignore crucial pathogenic features that are to be found in the broader context of a patient’s personality, developmental history, and situational context.

Implications

In light of these research and clinical considerations, psychiatrists should consider alternative perspectives and the full context of a patient’s presentation when formulating their diagnosis. The diagnosis of PTSD may be appropriate in some cases, but physicians should not provide it reflexively in the aftermath of trauma. As for the DSM–V, it is unclear how current problems can best be resolved. In observing the issues that have followed PTSD since 1980, we are not dismissing the diagnosis, nor are we ignoring a wealth of research findings spurred by the construct. Rather, we are asserting that there are reasons for concern. Defining PTSD criteria in DSM–V so that they reflect current findings, while limiting the construct’s susceptibility to misuse, expansion and reification, will be a difficult challenge.
It is good that they do not totally reject the diagnosis, especially because as we saw in Part I of this series, military veterans are exhibiting very intense symptom patterns that not only justify the diagnosis, but are teaching us a lot more about the disorder.

The Science of PTSD

Regardless of the diagnostic criteria, there is a great deal of neuroscience evidence for PTSD, including an enlarged amygdala and a shrunken hippocampus:

A great deal of research has attempted to identify those parts of the brain whose function may be altered in PTSD. Three key areas have been identified, the prefrontal cortex, amygdala and hippocampus. Much of this research has utilized PTSD sufferers from the Vietnam conflicts. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD[26]. In a study by Gurvits et al., Combat veterans of the Vietnam war with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who suffered no such symptoms.[27]

In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.

The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus particularly during extinction.[28] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[28][29] Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

The amygdala is our first order emotional processing center. It is here that events are paired with emotions - especially fear related memories. In PTSD the amygdala is over-aroused (and enlarged) and the hippocampus, which would normally modulate and contextualize the emotional memories, is less active and has been noted to shrink.

Yet how this happens is a mystery. The Wikipedia entry cited here suggests that low cortisol may be to blame, though that is unclear.

Perhaps no one is better known in the trauma treatment and research community than Bessel van der Kolk. Here is the abstract to an article he published in 2006 (Clinical Implications of Neuroscience Research in PTSD. Ann. N.Y. Acad. Sci. xxxx: 1–17):

ABSTRACT: The research showing how exposure to extreme stress affects brain function is making important contributions to understanding the nature of traumatic stress. This includes the notion that traumatized individuals are vulnerable to react to sensory information with subcortically initiated responses that are irrelevant, and often harmful, in the present. Reminders of traumatic experiences activate brain regions that support intense emotions, and decrease activation in the central nervous system (CNS) regions involved in (a) the integration of sensory input with motor output, (b) the modulation of physiological arousal, and (c) the capacity to communicate experience in words. Failures of attention and memory in posttraumatic stress disorder (PTSD) interfere with the capacity to engage in the present: traumatized individuals “lose theirway in the world.” This article discusses the implications of this research by suggesting that effective treatment needs to involve (1) learning to tolerate feelings and sensations by increasing the capacity for interoception, (2) learning to modulate arousal, and (3) learning that after confrontation with physical helplessness it is essential to engage in taking effective action.
I mention this article because he makes some important observations about the neuroscience of PTSD that has not been widely acknowledged either in treatment of the disorder or in its defintion.

Neuropsychology and neuroimaging research demonstrate that traumatized individuals have problems with sustained attention and working memory, which causes difficulty performing with focused concentration, and hence, with being fully engaged in the present. This is most likely the result of a dysfunction of frontal–subcortical circuitry, and deficits in corticothalamic integration.[22,23]

Many traumatized children and adults, confronted with chronically overwhelming emotions, lose their capacity to use emotions as guides for effective action. They often do not recognize what they are feeling and fail to mount an appropriate response. This phenomenon is called “alexithymia,”[24] an inability to identify the meaning of physical sensations and muscle activation. Failure to recognize what is going on causes them to be out of touch with their needs, and, as a consequence, they are unable to take care of them. This inability to correctly identify sensations, emotions, and physical states often extends itself to having difficulty appreciating the emotional states and needs of those around them. Unable to gauge and modulate their own internal states they habitually collapse in the face of threat, or lash out in response to minor irritations. Futility becomes the hallmark of daily life.

Psychology and psychiatry, as disciplines, have paid scant attention to the deficient orientation and action patterns that are triggered by sensory input, and, instead, tend to narrowly focus on either neurochemistry or emotional states. They thereby may have lost sight of the forest for the trees: both neurochemistry and emotions are activated in order to bring about action: either to engage in physical movements to protect, engage, or defend or displaying bodily postures denoting fear, anger, or depression that invite others to change their behavior. Pharmacotherapy helps to address some of the neurochemical problems associated with PTSD, thereby helping to modulate some of the embarrassing and upsetting behaviors and emotions, but drugs seem to not really be able to correct whatever abnormality underlies these behaviors and emotions. (pg. 4-5)

[For those interested, you can read a wonderful collection of his articles at this site (most of them are PDFs).]

According to van der Kolk, neither cognitive behavioral therapy (CBT) protocols nor psychodynamic approaches (the two main treatment approaches for trauma) pay sufficient attention to the experience and interpretation of disturbed physical sensations and preprogrammed physical action patterns. With this in mind, he has studied and advocated from more somatic-based treatments, including Eye Movement Desensitization and Reprocessing (EMDR) in treating PTSD - see here, here, and here, for example.

For more on the biological/neurological aspect of PTSD, see this great article from van der Kolk: The Body Keeps The Score: Memory & the Evolving Psychobiology of Post Traumatic Stress.

Dissociation in PTSD and its Treatment

One of the overlooked elements of the PTSD diagnosis that needs to be integrated into the definition is the degree of dissociation involved. Dissociation occurs on a spectrum from very mild (daydreaming) to very severe (dissociative identity disorder).

Some authors contend - and I agree - that dissociation has not been recognized as a central element in PTSD, or at least in Complex PTSD.

From Dissociation: An Insufficiently Recognized Major Feature of Complex PTSD by Onno van der Hart, Ellert R.S. Nijenhuis, and Kathy Steele: Journal of Traumatic Stress, 2005, 18(5).
It is difficult to determine whether “dissociation” is a central feature in complex PTSD and other trauma-related disorders because there is not uniform agreement on what constitutes the construct. The current use of the term is highly confusing (cf., Marshall, Spitzer, & Liebowitz, 1999). For example, some PTSD intrusive symptoms are referred to as “dissociative flashback episodes” (APA, 1994, p. 428), while the same flashbacks are not described as dissociative in ASD. The PTSD diagnosis does not consider avoidant or numbing symptoms to be dissociative, but in ASD these very symptoms are labeled dissociative (APA, 1994, p. 432). In the trauma literature at large, there are debates about whether or not dissociation is dimensional or a taxon, and which symptoms should be included under the rubric of dissociation. In relation to dissociation and trauma-related disorders in general, and complex PTSD specifically, we thus briefly introduce a theory regarding the processes and manifestations of dissociation that recommends a way to clarify this conceptual problem.

As part of this theory, we will define the term “personality;” describe the induction of structural dissociation of the personality during traumatizing events; illustrate the characteristics of parts of the personality that are dissociated to some extent from each other, and are fixed in enduring maladaptive behaviors and ways of perceiving, and in avoidance or reexperiencing; describe levels of complexity of this structural dissociation; and discuss the scope of dissociative symptoms stemming from structural dissociation, and distinguish them from what we consider to be related but non-dissociative phenomena. Finally, we analyze a number of symptom clusters of the proposed diagnostic category of complex PTSD/DESNOS in terms of structural dissociation of the personality, proposing that they all potentially involve dissociation. (pg. 2)
Here is how this study looks at the dissociative process in trauma survivors:
Our hypothesis is that integration between defensive and daily life action systems will fail first and most readily in a context of extreme stress that reduces integrative capacity. This integrative failure basically manifests in the prototypical alternations between functioning in daily life with avoidance/numbing (daily life action systems), and reexperiencing (defense action systems). We also hypothesize that survivors may develop a phobia of reexperiencing if they do not integrate these intrusive and intense trauma-related memories. This phobia sustains ongoing dissociation of daily life and defensive action systems. (pg. 3-4)
The way they conceptualize this happening is very similar to ego states work (Watkins & Watkins, 1997) or Internal Family Systems "part work" (Schwartz, 1995) and various other methods of working with what are variously known as complexes (Jung), ego states (the Watkins), parts (Schwartz), or subpersonalities (Rowan). [Emphasis added below.]
The basic pattern of posttraumatic stress response can be described as an alternation between a single dissociative part of the personality mediated by action systems of daily life and a second (rather limited and rudimentary) part mediated by defense. When the major dissociative part of traumatized individuals is detached from the trauma and mediated by action systems of daily life, the individual can seem rather undisturbed and able to lead a (relatively) normal life. However, this normality is only apparent, because this part of the personality physically and mentally avoids trauma-related cues, including his or her intrapsychic world, resulting in life “lived on the surface of consciousness” (Appelfeld, 1994, p. 18). Parts fixated in action systems of defense tend to intrude or become dominant when the individual is confronted with major threat cues. (pg. 5)
The first and best thing about this approach is that is does not pathologize the clients - they are wounded human beings with a dysfunctional part - the traumatized part. Yet it also provides a more somatic approach to treatment, for which van der Kolk is advocating, in that the various forms of parts work or ego states work can also work with the body.

And yet, seeing how the new DSM is being constructed, the medical model would never admit such an approach. Even in the managed care system, only treatments like CBT, which van der Kolk has shown to be inferior to somatic based approaches like EMDR, or brief therapy are covered by insurance most times.

The Future of PTSD

There is no doubt this diagnosis will survive the next few rounds of revision in the DSM. However, with the DSM becoming more and more dominated by the medical model and with treatment also quickly moving in that direction, the more effective treatments for PTSD will remain on the fringe of the therapeutic community.

On the bright side, the military is experimenting with EMDR and with Schwartz's parts work in treating soldiers. The dark side of this is that they are seeking faster ways to return their weapons of war to active duty and hoping these alternative approaches might do the job.

If they turn out to be more effective than drugs or CBT, they will likely make their way into the mainstream - or at least that is what we can hope.