Survival Poem

I am not dreaming

Of a hope-victory-life.

I am just dreaming

Of a hope-survival-life.

~

Yesterday my need was world-conquest.

I failed.

Today my need is my own survival.

I am failing.

Tomorrow my need will be a surrendered life.

I shall fail.

By: Sri Chinmoy

via Survival Poem — Sri Chinmoy Poetry.

Almost every day feels like a fight against that “surrendered life”. As I fight I try not to think about it, how that “surrended life” would look, dependency, poverty, SSI disability. Trapped face-to-face with the term second-class citizen, no transportation no escape. Perhaps sharing a room with someone I don’t know and have no interest in getting know-and then a succession of someones. The glance is so bleak only suicide comes to mind to comfort me. They do that-they do that all the time. That is how it has been.
Then on Monday-I started crying-because I knew everything was OK. More precisely because I felt everything was okay. For decades I lived in some state of anxiety all the time and even when inside my head, I knew everything was okay, my body and my emotions could never be convinced. We are tight, we are afraid, we are ready, it will never really be okay. Monday my brain said everything is okay and my body said yes, everything is okay and my emotional body took a deep breath and whispered yes, everything is okay. I cried tears of overwhelming relief. I think my new medication is working.
Diane

Quotes on Pain                           by: Sri Chinmoy

“Adversity makes you dynamic. Adversity forces your eyes wide open. Adversity teaches you the meaning of patience. Adversity endows you with faith in yourself. Adversity opens the secret door through which you can see the ultimate future fulfilment of God’s Will.”

“There is a general notion that if we go through suffering, tribulations and physical pain then our system will be purified. This idea is not founded upon reality.”

“To think that pain is a well-deserved punishment is wrong. To think that pain is an unavoidable heritage of karma is worse. To think that pain can never be surmounted is worst of all. Pain is a momentary experience of one’s limited self before it enters into the sea of Bliss.”

via Quotes on Pain — Poet Seers.

The part you do not get to see-my depression:
The back of my head, my neck, my spine feel like they’re in a clamp. I can’t see the windows from where I am lying on the mattress on the floor. I don’t know if it’s day or night. There is a bright light beyond the sliding doors to my room. I can see the light through the crack. I may have been in bed for days. I have no idea. Time doesn’t exist inside my head when I’m this depressed. Except for that crack of light, the rest of the room is black and the pain in my back and neck are becoming unbearable. I have to send it someplace else, separate myself from it. I pull my elbows back and under me and rest my forearms on the bed, forming a high arch between my lower back and the back of the head. I close my eyes and pretend all that energy clamping down on my back and neck is running down my body down my legs out my feet and through the crack in the doors, where it is keeping the light on in the living room. I channel the energy and my neck begins to loosen. I keep channeling and my back starts to relax, the pain is decreasing. I continue to channel the pain away with the energy, until I can pull my arms out from behind me, collapse and sleep some more. Diane

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.

Bipolar Disorder in DSM-V (Part II): Diseases or Comorbidities?
Nassir Ghaemi, MD, Psychiatry/Mental Health, 01:33PM Oct 15, 2009
Thank you Dr.Nassir Ghaemi for helping us stay updated. Amoung other things (ex psychiatric nurse, business owner, Teacher for the National Alliance on Mental Illness Family to Family Program, Mentor for NAMI Peer to Peer Program, Bipolar NOS/Anxiety Disorder patient, recovered alcoholic X 35 years, creator of the Anhedoniablog.com …) I am a devoted “groupie” of you and Dr. Akiskal. Knowing there are a few people trying to do more than throw a hand full medications at my various symptoms gives me hope.
In my family my father had a bipolar disorder self medicated with alcohol and reports would indicate his father probably had the same thing. His only sibling, my aunt, was involuntarily hospitalized many times, starting at about 14 years old, due to violence associated with her schizophrenic diagnosis. My older brother has spent the last 25 years in a locked psychiatric forensic Hospital in New York after having killed my grandmother. One of my younger sisters is severely dysthymic with regular cycles into major depressive disorder, she is also a recovered alcoholic. She refuses all treatment, has obviously been depressed for so long she doesn’t remember anything else. My younger brother has been treated fairly successfully for a bipolar two disorder for many years, he is also a recovered alcoholic.
I see my illness as very much of a mix, the genetic contributions are obvious and they were likely exacerbated and magnified by the living situation characteristic of a household led by a very mentally ill alcoholic.
It appears to me there is a thin line between the diagnosis of bipolar disorder, at least bipolar one and schizophrenia, primarily identified by degree of remission and resilience. Certainly this would be supported by the current use of antipsychotic medications in bipolar stabilization. Then what of the effective use of anticonvulsants, it is apparent message there?
We have come a long ways with symptom relief for which I am very grateful however I believe it’s time to start looking at the brain as a total system and supporting the whole system in hope of being able to heal and rebalance that system. Like I say in my blog “HELP MY HPA AXIS HAS CRASHED!” Thank you all for being here we need all the help we can get.

“Philosophy Dictionary: apathy

Although it is the particular enemy of teachers and sports coaches, apathy often gets a good philosophical press, especially in ethical systems that regard desire and worldly interest as low and unworthy. Plato recognizes the need for passion or eros even in the advanced contemplative state of the philosopher, but Hindu, Buddhist, Stoical and some Christian traditions have all looked askance at desire, equating the summum bonum with a kind of torpid vacuity. Hobbes shrewdly points out that while we live we have desires and Alexander Pope sides with the energetic: ‘In lazy Apathy let Stoics boast, Their Virtue fix’d; ‘tis fix’d as in a frost’ (An Essay on Man, ii). However, like Stoics and Buddhists, Kant found apathy to be particularly excellent: bliss is a state of ‘complete independence from inclinations and desires’ and this freedom is both itself a virtue and presupposed by other virtues. Aquinas, however, recognizes the desolation involved in turning away from what is good, and classifies it as a leading or capital sin. See accidie, ataraxia, autonomy/heteronomy, love.”

How then do they differ, apathy and anhedonia? I say, there is no choice in anhedonia. Only passionate souls-who know they are missing something important to THEM- experience anhedonia. Diane

via apathy: Definition, Synonyms from Answers.com.

This kind of thing makes me sick, it makes me afraid of our “experts” and it’s all too typical.  Not only in terms of denial and avoidance of responsibility, but arrogance, dismissal of people in dire need, insensitivity, stigmatization, marginalization, devaluation….I too thought they were full of crap-lazy, avoidant, whiney-until my symptoms started getting worse and worse…

Op-Ed ContributorA Case of Chronic Denial Sign in to Recommend

by HILLARY JOHNSON

Published: October 20, 2009

EARLIER this month, a study published in the journal Science answered a question that medical scientists had been asking since 2006, when they learned of a novel virus found in prostate tumors called xenotropic murine leukemia virus-related virus, or XMRV: Was it a human infection?

Health Guide: Chronic Fatigue XMRV is a gammaretrovirus, one of a family of viruses long-studied in animals but not known to infect people. In animals, these retroviruses can cause horrendous neurological problems, immune deficiency, lymphoma and leukemia. The new study provided overwhelming evidence that XMRV is a human gammaretrovirus — the third human retrovirus (after H.I.V. and human lymphotropic viruses, which cause leukemia and lymphoma). Infection is permanent and, yes, it can spread from person to person (though it is not yet known how the virus is transmitted).

That would have been news enough, but there was more. XMRV had been discovered in people suffering from chronic fatigue syndrome, a malady whose very existence has been a subject of debate for 25 years. For sufferers of this disease, the news has offered enormous hope. Being seriously ill for years, even decades, is nightmarish enough, but patients are also the targets of ridicule and hostility that stem from the perception that it is all in their heads. In the study, 67 percent of the 101 patients with the disease were found to have XMRV in their cells. If further study finds that XMRV actually causes their condition, it may open the door to useful treatments. At least, it will be time to jettison the stigmatizing name chronic fatigue syndrome.

The illness became famous after an outbreak in 1984 around Lake Tahoe, in Nevada. Several hundred patients developed flu-like symptoms like fever, sore throat and headaches that led to neurological problems, including severe memory loss and inability to understand conversation. Most of them were infected with several viruses at once, including cytomegalovirus, Epstein-Barr and human herpesvirus 6. Their doctors were stumped. The Centers for Disease Control and Prevention, the nation’s presumed bulwark against emerging infectious diseases, dismissed the epidemic and said the Tahoe doctors “had worked themselves into a frenzy.” The sufferers, a C.D.C. investigator told me at the time, were “not normal Americans.”

When, by 1987, the supposed hysteria failed to evaporate and indeed continued erupting in other parts the country, the health agency orchestrated a jocular referendum by mail among a handful of academics to come up with a name for it. The group settled on “chronic fatigue syndrome” — the use of “syndrome” rather than “disease” suggested a psychiatric rather than physical origin and would thus discourage public panic and prevent insurers from having to make “chronic disbursements,” as one of the academics joked.

An 11th-hour plea by a nascent patient organization to call the disease by the scientific name used in Britain, myalgic encephalomyelitis, was rejected by the C.D.C. as “overly complicated and too confusing for many nonmedical persons.”

Had the agency done nothing in response to this epidemic, patients would now be better off. The name functioned as a kind of social punishment. Patients were branded malingerers by families, friends, journalists and insurance companies, and were denied medical care. (It’s no coincidence that suicide is among the three leading causes of death among sufferers.) Soon the malady came to be widely considered a personality disorder or something that sufferers brought upon themselves. A recent study financed by the C.D.C. suggested that childhood trauma or sexual abuse, combined with a genetic inability to handle stress, is a key risk factor for chronic fatigue syndrome.

Many people don’t realize how severe this illness can be. It is marked by memory and cognition problems, and physical collapse after any mental or physical exertion. The various co-infections that occur only make matters worse. Many patients are bedridden. And recovery is rare. A significant number of patients have been ill for more than two decades.

Dr. Nancy Klimas, an immunologist at the University of Miami School of Medicine who treats AIDS and chronic fatigue syndrome, remarked in The Times last week that if given the choice she would prefer to have AIDS: “My H.I.V. patients for the most part are hale and hearty,” she said, noting that billions of dollars have been spent on AIDS research. “Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families.”

Congress has appropriated money for research on chronic fatigue syndrome, too, though in far smaller amounts, but the C.D.C. has seemed unwilling to spend it productively. A decade ago, investigations by the inspector general for the Department of Health and Human Services and what was then called the General Accounting Office revealed that for years government scientists had been funneling millions meant for research on this disease into other pet projects.

As public health officials focused on psychiatric explanations, the virus apparently spread widely. In the new study, active XMRV infections were found in 3.7 percent of the healthy controls tested. Roughly the same degree of infection in healthy people has been found in the prostate research. If this is representative of the United States as a whole, then as many as 10 million Americans may carry the retrovirus.

It is estimated that more than a million Americans are seriously ill with the disease. (Not everyone infected with XMRV will necessarily get chronic fatigue syndrome — in the same way that not all of the 1.1 million Americans infected with H.I.V. will get AIDS.)

Hints that a retroviral infection might play a role in chronic fatigue syndrome have been present from the beginning. In 1991, Dr. Elaine DeFreitas, a virologist at the Wistar Institute in Philadelphia, found retroviral DNA in 80 percent of 30 chronic fatigue patients. The C.D.C. went so far as to try to replicate her effort, but refused to follow her exacting methods for finding the virus. In addition, the centers’ blood samples became contaminated, and some people at the agency said that administrators ended the research prematurely. Rather than admit any such failure, the C.D.C. publicly criticized Dr. DeFreitas’s findings.

That episode had a chilling effect on other researchers in the field, and the search for the cause was largely abandoned for 20 years.

Now, Judy Mikovits, the retrovirus expert at the Whittemore Peterson Institute, in Reno, Nev., who led the recent study, has revisited the cold case. Not surprisingly, the institute is private, created by the parents of a woman who suffers from chronic fatigue syndrome. But Dr. Mikovits collaborated with scientists at the National Cancer Institute and the Cleveland Clinic.

When she began her work on this disease in 2006, Dr. Mikovits, a 22-year veteran of the National Cancer Institute, knew little about chronic fatigue syndrome. But she was intrigued that an unusually high number of patients being followed by a Nevada doctor were suffering rare lymphomas and leukemias; at least one had died. And she was also impressed that the doctor, Dan Peterson, had built an extraordinary repository of more than 8,000 chronic fatigue syndrome tissue samples going back as far as 1984.

“My hypothesis was, ‘This is a retrovirus,’ and I was going to use that repository to find it,” Dr. Mikovits told me.

What she found was live, or replicating, XMRV in both frozen and fresh blood and plasma, as well as saliva. She has found the virus in samples going back to 1984 and in nearly all the patients who developed cancer. She expects the positivity rate will be close to 100 percent in the disease.

“It’s amazing to me that anyone could look at these patients and not see that this is an infectious disease that has ruined lives,” Dr. Mikovits said. She has also given the disease a properly scientific new name: X-associated neuroimmune disease.

For patients who have been abandoned to quackish theories and harsh ideologies about their illness for 25 years, the dismantling of “chronic fatigue syndrome” can’t come soon enough.

From a book I have written on my experience:   20 years ago….

The ground under me, it’s nicer, but I am still crawling through the world.  When I feel bad I feel terrible.  When I feel good, I only feel bad.  I don’t see any end to this.  I only go for help, I only let someone know how I feel, when I don’t think I can take it for another day, but I have become so good at looking good, that when I will admit how bad I feel, how desperate I am, no one believes me.  They seem to think something must have just happened that I won’t talk about, some tragedy or overblown disappointment that I can identify and define.  Nothing bad has happened, not this week, not this month, probably not even this year.  It may have happened 30 or 40 years ago, but I’ve been over that stuff over and over and going over it again is not going to help.  I think if I have to talk to one more damn useless archaeological therapist I’ll scream.  I’m stuck in emotional overdrive without a definable catalyst.  I can’t see how I got here, I can’t see what keeps me here, and I can’t see how to get out-it’s hopeless.

MY problem-or one of MY problems as I see it…

“ Depression, stress and the adrenal axis

Carmine M. Pariante

Institute of Psychiatry, King’s College London

Download the briefing as a PDF file

Depression is characterised by an over activity of the hypothalamic-pituitary-adrenal (HPA) axis that resembles the neuro-endocrine response to stress. These abnormalities participate in the development of depressive symptoms. Moreover, antidepressants directly regulate HPA axis function. These novel findings are reshaping our understanding of the causes and treatment of this disabling disorder.

Major depression – major importance

Costing more than 30 billion pounds every year in the UK and the US alone, major depression is a significant cause of disability and the most important cause of suicide worldwide. Why should neuro-endocrinologists bother with depression? Depression is characterised by an over activity of the hypothalamic-pituitary-adrenal (HPA) axis that resembles the neuro-endocrine response to stress. In this Briefing I will claim that HPA axis hyperactivity is not a mere epiphenomenon of depression, but rather a crucial biological mechanism in the pathogenesis of this disorder and a fundamental target for its successful treatment.

HPA axis activity is governed by the secretion of corticotropin-releasing hormone (CRH) from the hypothalamus. CRH activates the secretion of adrenocorticotropic hormone (ACTH) from the pituitary. ACTH, in turn, stimulates the secretion of glucocorticoids (cortisol in humans) from the adrenal glands. Glucocorticoids interact with their receptors – the corticosteroid receptors – in almost every tissue in the body, and the best known effect is the regulation of energy metabolism. By binding to corticosteroid receptors in the brain, glucocorticoids also inhibit the further secretion of CRH from the hypothalamus and ACTH from the pituitary (negative feedback).

Three lines of evidence demonstrate the link between stress, depression and the HPA axis. First, depression, in its core symptoms of dysphoric or low mood, inability to take pleasure and low energy, is a universal cross-cultural response to stressful events, particularly when the stress is chronic or the individual has no control over the situation. Second, stress activates the HPA axis, leading to a powerful release of glucocorticoids into the bloodstream; depression, especially when severe, is also characterised by over activity of the HPA axis. Third, treatments that modify the stress response, like “talking therapies” improving the ability to cope with stress, have an antidepressant effect; moreover, known antidepressants directly decrease HPA axis activity.

Facts and questions

The HPA axis abnormalities in patients with major depression are remarkably similar to those present in animals experiencing chronic stress. Depressed patients have an increased drive to the HPA axis, as shown by the larger production of CRH in the brain. They also have an impaired negative feedback by glucocorticoids. Finally, they have an increased volume of the adrenal and pituitary glands. One accepted explanation for the HPA axis over activity in depression is that, because of the reduced function of the corticosteroid receptors, circulating cortisol is unable to successfully inhibit HPA axis activity (“glucocorticoid resistance”). Consistent with this, antidepressants directly increase the expression and function of corticosteroid receptors in the brain, thus enhancing the negative feedback and reducing HPA axis activity.

“One way to conceptualise depression is a pathological stress response gone awry”…Charles B. Nemeroff, 1996

There is, however, a big unanswered question (see Figure). Does the fact that depressed patients have a hyperactive HPA axis actually mean that a lot of cortisol is flooding their brain, and that the depressive symptoms are consequence of this putative “toxic” effect of cortisol (Pathway A)? Or is the opposite true: that patients have a hyperactive HPA axis as a compensatory mechanism, because their brain is resistant to the effects of circulating cortisol (Pathway B)? The question is not trivial, especially in our quest for a more effective treatment. In the first scenario, our recommendation should be the lowering of cortisol levels. In the second scenario, our recommendation should be the administering of more cortisol. The situation is complicated by the fact that increased cortisol levels in the bloodstream do not necessarily translate into increased effects of glucocorticoids on the brain, because the brain sensitivity to cortisol is also regulated by the function of the corticosteroid receptors as well as by efflux systems at the blood-brain barrier. In what seems to be a clear effort of nature to tease us all, depression has been described in endocrine disorders characterised by elevated cortisol levels, like Cushing’s disease, but also in disorders characterised by low cortisol levels, like Addison’s disease. Moreover, high and low levels of cortisol give similar functional and morphological changes in the brain. Even more strikingly, both the lowering of cortisol levels and the administering of cortisol have antidepressant effects in depressed patients.

LIKE CANCER, DEPRESSION HAS BEEN ESTABLISHED TO BE NOT JUST ONE, BUT MANY DISORDERS-NO DOUBT THERE ARE MANY FACTORS AND COMBINATIONS OF FACTORS INVOLVED.  UNDER TREATMENT IS A KILLER !  MY HPA AXIS HAS CRASHED!  IT MAY NEED MULTIPLE SUPPORTS AND REHABILITATIVE TREATMENTS, IF IN FACT IT EVER CAN BECOME HEALTHY.  I WILL SETTLE FOR A LOT OF SYMPTOM RELIEF!  ANY IDEAS??

read more here>>>via British Society for Neuroendocrinology – 19. Depression, stress and the adrenal axis.

I see many things in drawings, spatial terms, distances inside my head.  Everything is neatly measured on graphs, often with colors for emotion.  That’s how I see the issue of quality of life.  Quality life is such a broad ill-defined term tossed about with regard to health or finances in general.  It’s inherent subjectivity makes objective assessments feel vague, everyone holding different values and tolerances.  For me the bottom line in quality of life would be the pure desire to live.  Anything above that line is a movement toward health and anything below a movement toward death.   The line itself-is made of ANHEDONIA.   Moving up from the anhedonic line into quality-of-life is not a step into happiness it is a step in to struggle, possibly a very long struggle, possibly a losing battle.  We might think of anhedonia as a place to rest. The problem with resting in anhedonia is its proximity to the wish to die and the ease of falling or slipping into that territory. 

Drs., the mental health profession, they ask the wrong question.  The truly relevant question is not “do you want to hurt yourself ? Are you thinking of suicide?  The question should be “do you want to live”.  That is where to start a conversation about how a person really feels. 

Right now I’m taking BuSpar for anxiety, Wellbutrin for depression, lithium to augment the Wellbutrin, stabilize my mood and rehabilitate my brain, Levothyroxine to augment the Wellbutrin, Metformin to protect my brain, Chlorpheniramine Maleate to sleep (OTC) and Cetitizine Hydrochloride for allergy (OTC), as well as melatonin for sleep, fish oil and vitamin D.  I quit taking my B complex because it makes me gag for some reason.  B vitamins have always made me gag and I finally decided that was a good reason not to take them.  I go on and off 5-HTP, Acetyl L-Carniterine with Alpha Lipoic Acid and St. John’s wort, they never seem to be particularly effective.  This week I’m in the process of lowering / eliminating the Wellbutrin and the melatonin in preparation for starting the Selegiline that I ordered from Mexico. 

            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.

Main Entry: in·do·lent Pronunciation: \-lənt\Function: adjective Etymology: Late Latin indolent-, indolens insensitive to pain, from Latin in- + dolent-, dolens, present participle of dolēre to feel painDate: 16631 a : causing little or no pain b : slow to develop or heal 2 a : averse to activity, effort, or movement : habitually lazy b : conducive to or encouraging laziness c : exhibiting indolence synonyms see lazy— in·do·lent·ly adverb

via indolent – Definition from the Merriam-Webster Online Dictionary.