Grieving is about loss; usually most painfully about the loss of love or a loved one. Even small losses may result in the emotional pain known as grieving. Sadness and grieving respond well to therapy and are most likely to dissipate on their own overtime. These states are often diagnosed inaccurately as depression, they are not. Nor will they respond to antidepressants, because there is no significant chemical imbalance, for the antidepressant to address.

Depression is a whole different thing. Depression may eventually result from multiple underdressed grief and sadness issues that have rotted for so long they have become the homeostatic condition of the biochemistry of individual. In this case antidepressants and therapy are both appropriate. But that’s not the only kind of depression there is. Many people, usually the descendents of biochemically depressed individuals are born biochemically depressed individuals. All the therapy in the world will not do any good. If the person is fortunate they may find antidepressants or a combination of antidepressants that effectively lift their mood and allow them to operate on a whole different, non-depressed, level. These people could also benefit from significant therapy after the depression has lifted, but not until then. Why therapy after the depression has lifted? Because a person who is primarily depressed and has always been primarily depressed will be confronted with whole new ways of being in the world that would benefit from and be supported by a therapeutic relationship. This is the best way to prevent relapse. Rarely is a person who has been depressed for a significant amount of time, that is years or decades, in a financial position to maintain the medication and therapy necessary to stay well.

25 years ago, when I was being treated for depression, I had excellent insurance. I worked for the County of Santa Barbara psychiatric inpatient unit and had access to the best psychiatrist, the best resources. I had the privilege of being a patient of Dr. Joseph Johnson, who would on a weekly basis, spend an hour with me. At that time, that was the standard. I had the best medications and excellent therapy. Consequently, it was one of my most “well” periods. Then came managed care. Dr. Johnson was permitted 15 minutes per patient. He could no longer do psychotherapy; he could no longer even do a decent medication assessment. He went from being a very happy appearing person to being a very frustrated, border on angry appearing, person. Just before resigning from the clinic, he briefly expressed to me that he could no longer work under those conditions, that wasn’t fair to his patients. Nothing has been the same since managed care and as far as I can see none of it is good.

Recently in the New York Times there have been several articles on the inability of antidepressants to address mild and moderate depression. Some of that information is provided in the post just prior to this one. I will be commenting on that for the next couple days. I will say, at this time, the issue of depression has become much too simplistic. Saying “depression” is like saying “cancer”. There are hundreds if not thousands of types, severities and causes. In general, every successful treatment starts with an accurate diagnosis. Spare no cost in getting an accurate diagnosis, it is your life you are wasting if you don’t.

Now here’s the challenge, if I’m treated for a disorder someone needs to get paid. If there is going to be a payment through some type of insurance, there must be an ICD code, specifically a selection from ICD-9 codes 290-319: mental disorders, in the case of a mental illness. This code does not contain sadness or grieving, consequently, anyone who is sad or grieving will be given a depression or anxiety code. We are now comparing apples to oranges in any study and getting poor inaccurate results.
Let’s take a look at this on a very basic level. I’m running antidepressant trial. Included are 6 individuals who are really sad, 10 individuals who are grieving, and 15 individuals who are truly clinically depressed. Just to complicate matters, five of the 15 depressed individuals actually had a bipolar disorder, which is usually first diagnosed as depression. In short form, the result of my trial will be useless. The result of a meta-analysis based on a number of such trials will be just as useless. You begin to see why we have made such poor progress with the treatment of depression in the past 50 years.

Lifting the Curtain on Depression         By BENEDICT CAREY

via Depression – Reporter’s File – Lifting the Curtain on Depression – NY Times Health.

In Brief:

Each patient experiences depression differently, and the symptoms can vary significantly from case to case.

Available treatments do not work for as many as half of chronically depressed patients.

Researchers have long focused on the role of serotonin, but new therapeutic paradigms are needed.

Recent brain imaging studies may have uncovered surprising targets for intervention.

Depression is no monochromatic black veil, no shared melancholy, as is often claimed. Instead, the disorder is more like a virus that amplifies each sufferer’s particular vulnerabilities, whether anxiety, helplessness, self-doubt, anger or some combination of these. The subjective experience varies from person to person, yet treatment is far from personalized.

Progress has slowed as researchers grapple with one of the most difficult aspects of the disorder: it is impossible to predict who will respond to what therapy, and many sufferers find no relief from anything now available, including medication. While depression appears in many forms, therapeutic options remain worryingly limited.

“We’re at a point where we need to find new treatments, because it’s very clear that the old ones simply don’t work well for many people,” said Dr. Thomas Insel, director of the National Institute of Mental Health. “Our thinking about depression has to change, and it is changing.”

Some people are genetically predisposed to react more strongly than others to life’s inevitable blows. Scientists have traced this susceptibility in part to how the body processes a neural messenger called serotonin, which is linked to mood, and helps cells learn and communicate. For the past 20 years, depression researchers have focused heavily on this connection, both to understand the disorder and find better treatments. A serotonin “deficit” or “imbalance” has become synonymous with depression itself in the public consciousness, an easy catch-all explanation reinforced in drug ads and awareness campaigns.

But it is increasingly clear that serotonin is only one piece of the puzzle. Even when used aggressively by psychiatrists, selective serotonin reuptake inhibitors like Prozac and Zoloft, which prolong the action of the neurotransmitter in the brain, speed recovery in only about half of seriously afflicted patients. In a small number of young people, these drugs seem to backfire, making patients more likely to harm themselves or to think about it.

Indeed, many sufferers of moderate depression may be more likely to recover with talk therapy, particularly cognitive behavior therapy, in which patients learn techniques for defusing their own reflexive, self-defeating thoughts.

Despite the clear need, better therapies for depression have been slow coming. Newer alternatives, like Effexor and Cymbalta, are not S.S.R.I.’s but so-called S.N.R.I.’s; they prolong the activity of a brain messenger called norepinephrine, as well as serotonin. But this extra effect does not seem to make much difference for most patients, and experts consider these drugs to be essentially an extension of S.S.R.I. therapy, not a real departure.

“We really need to find better, more precise targets” for depression drugs, Dr. Insel said.

Assaults on depression based primarily on serotonin have hit a wall, in effect, forcing psychiatrists and researchers to explore entirely new notions about the causes of the disorder and possible options for treatment.

Recently investigators have explored the role of the hippocampus, an area deep in the brain critical to memory formation, in severe depression. They have looked more closely at the activity of the glutamate system, a brain messenger that jump-starts activity along neural networks. And they have used brain imaging to try to pinpoint areas in the brain that flare up or go quiet when people are suffering from spasms of despair.

Brain imaging has already paid off in an unexpected way. In a series of brain-imaging experiments performed at the University of Toronto and at Emory University in Atlanta, Dr. Helen Mayberg, a neurologist, has found that activity in a part of the brain known as Brodman area 25 is strongly associated with the experience of despair.

Brodman area 25 is uncharted territory; before these studies appeared, no one suspected it was linked to depression. But the researchers went one step further, implanting electrodes into the brains of severely and chronically depressed patients in an effort to quiet this area. The results were encouraging. Depression this severe can seem unbreakable, but most of the patients treated — more than a dozen have had the surgery — have improved enough that they have been able to return to work and to reconnect with family, friends and children. Most continue on drug therapy, as well.

It is a radical experiment, but it has made the darkness of depression visible, a first for psychiatry. If there are many different permutations of depression, then imaging techniques like these should soon help doctors differentiate them. Dr. Mayberg’s work already suggests that depression looks different in the brains of people who respond to talk therapy, compared with those who do well on antidepressants.

Scientists also are rethinking the pharmaceutical approach to depression, and in striking ways. Ketamine, a narcotic better known in nightclubs as “Special K,” has shown antidepressant effects in animal studies, but because of its reputation as a street drug it was never taken seriously as a potential therapy.

But last year scientists at the National Institutes of Health reported in a small study that some severely depressed patients recovered within hours after taking the drug intravenously. Most of them remained in improved condition for more than a week. Now the N.I.H. is running a large-scale study to determine how long the therapeutic effect lasts, and in whom.

The sudden scientific interest in ketamine has been criticized as a desperate stab at what has been an unsolvable medical puzzle, the treatment of chronic depression. But there is hope in the paradigm shift that has led to ketamine’s re-evaluation, and a welcome sign of change. The research already has scientists scrambling to find related compounds that don’t have the side effects of ketamine, as well as drugs that could sustain its effects once the initial treatment was stopped.

After reporting results from the 2006 ketamine study, the lead author, Dr. Carlos Zarate, chief of the mood and anxiety disorders research unit of the National Institute of Mental Health, summed up the findings this way: “What the study tells us is that we can break the sound barrier.”

He wasn’t just talking about breaking the hold of a devastating chronic disorder. He was talking about the science of depression itself, which was badly in need of a shake-up.

            Four and  1/2 years ago, after going into yet another devastating depression, I was put on Wellbutrin by the Primary Care Provider of the year. ZIP, ZOOM, ZAP!!! I was no longer depressed! I was also no longer working-I was PLAYING!! -three months and a few (about 3) thousand dollars later, I came down to a ‘reasonable’ level and for the first time I recalled every bit (I think) of my-disconcerting is a good word, dis·con·cert·ed, dis·con·cert·ing, dis·con·certs

1. To upset the self-possession of; ruffle. See Synonyms at <embarrass>.

2. To frustrate (plans, for example) by throwing into disorder; disarrange.

-behavior. Upset the self-possession of / throwing into disorder/ upset the self-possession of /throwing into disorder/ upset the self-possession of/ throwing into disorder…shit and it really scared me.  Somewhere in there, I acquired an additional diagnosis of anxiety disorder and was put on, BuSpar. It took me another few months to admit the impact of the experience to myself and tell the Primary Care Provider of the year.  I got my long overdue, nearly 3 decades long overdue, bipolar disorder diagnosis.

            It was becoming the year of disconcerting experiences.  It was not okay for me to have a bipolar disorder diagnosis to ‘be’ bipolar.  In my mind that made me like, put me in a category with – my crazy violent father, the ex-boyfriend who kept breaking into my apartment and tried to choke me and all the former psychiatric patients, I had helped restrain and shot up with Haldol or some other highly sedating med to bring them down.  It could not be, but it was.

            That’s where the Lamictal came in.  I was prescribed the Lamictal to stabilize my mood, no more scary up, no more crushing down.  Quite simply, it didn’t work-or did it?  It’s like praying, can’t tell what would’ve or would not have happened if you hadn’t done it.  However, things did not get smooth and when the Wellbutrin was discontinued, I quickly crashed into another horrible depression.  I couldn’t even call for help until I restarted the Wellbutrin for about 10 days.  I continued to have intermittent hypomanic spikes that only lasted for a few days to a week or so.  I didn’t really have time to get into tooooooo much trouble.  I got my medical records and made a chart.  I still bounced up and down-all the time.  As far up?  As far down?  Who knows?  Overall-I felt less well than I had on the original  Wellbutrin and Lamictal combo.  Adding a thyroid med didn’t seem to make any difference.  The next time I became  horribly depressed we added lithium and that didn’t seem to make much difference either-it just made me so shaky I couldn’t use my cell phone.  We got it down to the 300 mg brain preserving dose I could tolerate.

            Then the primary care provider of the year went away, just as the primary care provider of the year before her had gone away-and I got a real Doctor!  This Dr. is actually an experienced specialist, and I am privileged and grateful to have him.  Value of hope.  He had seen miraculous results with Seroquel, so I tried it.  It is the best sleep med I’ve ever experienced, but I didn’t have a sleep problem.  It also had somewhat of a mind organizing quality, not dramatic but noticeable.  Although my mind certainly could use some organizing, I’ve never thought of its lack of organization as a particularly big problem.  I just compensate by organizing my environment to make up for the deficit.  I’ve gotten by pretty well that way from a very long time.  It did not stop the depression’s and I gained 35 lbs in two months!  The next time I took a big dive we tried the new SSNI (selective serotonin norepinephrine reuptake inhibitor) Pristique.  I had some reason to be hopeful about that.  It’s an Effexor spinoff and Effexor works well for my younger brother, who has a bipolar 2 diagnosis.  It flips him out of his depression the way Wellbutrin flips me out if mine-but it doesn’t keep him from becoming hypomanic and it doesn’t keep him from eventually going back into a depression, just as I do.  Pristique didn’t appear to do anything for me but like praying…  Then I ran into a glitch at the clinic, that I won’t go into (because I could rave on and on about the deficiencies of the clinic) where I couldn’t get the Pristique and had to be out for the weekend.  I had become increasingly forgetful to a frightful degree and was developing severe word finding problems.  I had been on line trying to find the source of the problem or some type of solution, when I started coming across multiple blogs by people on Lamictal-who were having the same problem.  I trashed the Lamictal and I decided since I already had to do the Pristique withdrawal I may as well trash the Seroquel also.  So I did. This may be evidence of my deteriorated mental state or just commentary on my way of doing things. 

            That was last April and for the first time in 14 years I became very scary suicidal. Part of my brain was thinking up painless ways to kill myself that would not impact other people while the other part was saying “BAD Idea! We need more meds! Go get more meds!”  So I went and told the Dr. what I did. He wanted me to go back on the Seroquel, but I refused.  I went back on the Wellbutrin.  It allows me to function most of the time.  To be continued, in three parts, this week.

“There’s no guarantee on anything in life. Approximately 10 people per year are killed by vending machines falling down on them. You can be killed or maimed every time you drive a car. The computer you’re using can explode. Bad weather, earthquakes, lightning and terrorists can kill. The electricity in your home can cause a fatal fire in your house. Your car can explode. You can be killed by lightning hitting your telephone line.”

[Then there is MY reality...  expressed so well by the Doctor.   Diane]

“Being depressed increases the risk of a heart attack by 600%. There are more suicides per year than the combination of homicide and automobile accidents combined. Anxiety dramatically increases the risk of immune system disease, cancer, heart attacks, strokes, high blood pressure and others.

There is no absolute prevention of risk. What we do with everything in life is make an attempt to balance the risks versus the benefits.

I would not be concerned if any of my loved ones took BuSpar (buspirone) and Prozac…”

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