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My 66 Year Old Bipolar Story

R

RonPrice

Well-known member
Joined
Oct 10, 2009
Messages
94
Location
George Town Tasmania Australia
BIPOLAR DISORDER:
A Personal Analysis of My Chaos Narrative

A Longitudinal Context: October 1943 To March 2010
10th Edition

By
Ron Price of George Town Tasmania Australia
(125 Pages: Font 14—50,000 words)

1. Preamble and Introduction:

1.1 This is a small book. Ten years ago it started out as a brief essay and it is now an appendix to my memoirs, a five volume 2600 page opus found in whole and in part at various places on the internet. Both this small book and my memoirs could benefit from the assistance of one, Rob Cowley, affectionately known in publishing circles back in the seventies and early eighties as “the Boston slasher.” His editing was regarded in some circles as constructive and deeply sensitive. If he could amputate several dozen pages, several thousand words, of this exploration of my life experience of bipolar disorder(BPD) with minimal agony to my emotional equipment I’m sure readers would be the beneficiaries. But, alas, I think Bob is dead.


1.2 This is a longitudinal, retrospective account going back to my conception in the last half of October 1943. Neurobiological, neuropsychiatric and affective disorders like BPD have diverse manifestations and symptomatology as well as a broad range of age of onset and specificity of symptoms. Little is still known about its pathogenesis, that is, the origin and development of the disease. What follows is one person’s story, one person’s life experience of BPD. It is my personal life-narrative with the diverse manifestations, the symptomology of BPD as I experienced it.

1.3 I make reference to a strong genetic contribution to the aetiology of BPD, a genetic predisposition, a genetic susceptibility as a factor in the pathogenesis of BPD. A family history, what is sometimes referred to as a family pedigree, of affective disorder in a first-degree relative, in my case my mother(1904-1978) is relevant to this narrative. My mother had a mild case of what may very well have been BPD, at least I have come to think of her mood swings as falling into a significantly high place in what is sometimes called the BPD spectrum during her 75 year life. Her mood-swing disability or affective disorder, though, was never given the formal medical diagnosis manic-depressive(MD), a term which was replaced in 1980 after she died by the term BPD.

1.3.1 All manifestations of BPD share uncertain etiologies, with often opaque relationships between genes and environment. Some medical experts and theorists in the field of such studies posit latent changes in the expression of specific genes initially primed at the developmental stage of life. Some studies and some experts emphasize that certain environmental agents disturb gene regulation in a long-term manner, beginning at early developmental stages in the lifespan perhaps even in utero. But these disturbances, these perturbations as they are sometimes called, might not have pathological results until significantly later in life. In retrospect, as I look back from these middle years(65-75) of late adulthood, the years 60 to 80 as some developmental psychologists call these years of the lifespan, these perturbations and pathological results were clearly manifested at the age of 18. I could easily theorize an earlier onset on the basis of behavioural perturbations manifested in early childhood and into adolescence and I do such theorizing later in this account(see sections 2.7.1 and 2.7.2 below).

1.4 The new diagnostic term, BPD, is now found in the Diagnostic and Statistical Manual of Mental Disorders published by the American Psychiatric Association (DSM-III). DSM-III had 300 disorders twice as many as in the DSM-II. The DSM is considered the bible by specialists and by the various professions and other interest groups. It is considered by many as an information source, a major scientific instrument in the field of mental health. In the DSM the term maniac was deleted and a one-size-fits-all classification system for MD and BPD was more finely tuned by the 4th edition published in 1994. The exact discourse that has come to have jurisdiction in this labelling process, the circumstances that have come to result in a person given some mental illness label are due to: (a) norms and expectations as well as (b) medical, psychological, physiological and (c) most recently, neurochemical and electrical brain activity as seen in brain imaging.

1.5 About half of all patients with BPD have one parent who also has some form of mood disorder. There is then, or so it seems to me, a clinical significance in my mother’s mood disorder in the explanation of the origins and diagnosis of my own BPD. The high heritability of BPD has been well-documented through familial incidence, twin and adoption studies. There is an unquestionable justification for the inclusion of my family in the understanding of my BPD. No specific gene has yet been identified as the one bipolar gene. It appears likely that BPD is caused by the presence of multiple genes conferring susceptibility to BPD when combined with psychosocial stressors. I make this point as an opening remark and pass on to my story.

1.6 This account also provides a statement of my most recent experiences in the last two years, 2007-2010, with manic-depression(MD) or BPD as it has come to be called since 1980. Some prospective analysis of my illness is also included with the view to assessing: potential short term, medium term and long-term strategies, appropriate lifestyle choices and activities in which to engage in the years ahead in these middle years(65-75) of late adulthood(60-80) and old age(80++), if I last that long. For the most part, though, this account, this statement I have written here in some 50,000 words, is an outline, a description, of this partially genetically predisposing family-based illness and of my experience with it throughout my life. I would, though, discourage others from blaming their parents for their genetic contribution to the disorders. I would also discourage them from blaming other family members for their contributions in the form of stress and conflict and failure to understand. Rather than wasting time and energy in finger-pointing or bemoaning the fact that they have BPD, I would encourage them to learn how to best use available treatment modalities to minimize their symptoms and to find success and satisfaction in their lives despite their disorder.

This lengthy account has various treatments over 6 decades and i will post ore of my story after some feedback....Ron in Australia
 
R

RonPrice

Well-known member
Joined
Oct 10, 2009
Messages
94
Location
George Town Tasmania Australia
Here is a little more of my story.-Ron
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1.6 The goal of what is sometimes called ‘personalized medicine’ is to utilize a person's genetic makeup for appropriate disease diagnosis and treatment, an idea conceptualized initially in the recent years of the Human Genome Project. The current conceptualisation of MD/BPD can be traced back, as I indicated briefly above, to the 1850s, although its history can be traced as far back as ancient history in Turkey. Both terms, MD and psychosis, were coined in 1875 by Jules Falret, a French psychiatrist and he recognized its genetic link. German psychiatrist Emil Kraepelin (1856–1926), the founder of modern psychopharmacology, also made a major contribution to the early understanding of MD/BPD, only one of the many disorders in the general mood disorder category, but a cyclical mood disorder associated with a circularity between D and euphoria.

1.7 About 37,000 years ago Neanderthals arguably intermingled with modern humans and thus a new gene entered the human genome, the DRD4 7R gene. This gene arguably originated from Neanderthals. This gene is associated with risk-taking, sensation-seeking and novelty-seeking, and correlated with openness to new experiences, intolerance to monotony, and exploratory behavior, features of Neanderthal behaviour. About 10% of the population have the activated DRD4 7R gene. So goes yet another theory on the genetic predisposition to BPD.

1.8 All manifestations of BPD share uncertain etiologies, with often opaque, obscure, relationships between genes and environment. Some medical experts and theorists in the field of such studies posit latent changes in the expression of specific genes initially primed at the developmental stage of life. Some studies and some experts emphasize that certain environmental agents disturb gene regulation in a long-term manner, beginning at early developmental stages in the lifespan perhaps even in utero. There may be, in fact, pervasive developmental disorders that involve a triad of deficits in social skills, communication and language. For the underlying neurobiology of these symptoms, disturbances in neuronal development and synaptic plasticity have been discussed, but I don’t want to comment on this area of complexity, this puzzling area and the aetiology of BPD.

1.8.1 These disturbances, these perturbations, as they are sometimes called, might not have pathological results until significantly later in life. In retrospect, as I look back from these middle years(65-75) of late adulthood, the years 60 to 80 as some developmental psychologists call these years of the lifespan, these perturbations and pathological results were clearly manifested at the age of 18. I could easily theorize an earlier onset on the basis of behavioural perturbations manifested in early childhood and into adolescence and I do such theorizing later in this account(see sections 2.7.1 and 2.7.2 below). The change from psychodynamic models of psychiatry to neurobiological models that dominate the discipline today has been a critical determinant in both my story and its treatment by the psychiatric profession.

1.9 I received three diagnoses between 1963 and 1980 from psychiatrists, friends, family, GPs and concerned others. The diagnosis that was made in 1980, namely, BPD, is a diagnosis that is standardized according The Diagnostic and Statistical Manual of Mental Disorders (DSMMD-III: 1980 and DSM-IV: 1994) which provides diagnostic criteria for mental disorders. I use the term BPD not MD throughout this document and I use that acronym. In the DSM-IV MD is a 5 axis/level system of diagnosis that is used.

1.9.1 In my case, axis/level 1 is for clinical disorders that are mood disorders. Axis 3 in this system is for what they refer to as acute medical concerns that relate to BPD; axis-4 is for psycho-social and environmental problems that contribute to BPD and axis-5 is an overall caregiver’s assessment of my functioning on a scale 1 to 100. Most of the successful diagnoses and treatment of my BPD have come from psychopharmacology and its roots in physiological assumptions. In the last decade, say, 2001 to 2011, talking cures and behaviour modification techniques like cognitive behaviour therapy with their roots, their emphasis on assumptions in the domain of intrapsychic experience have also been successful as adjuncts to medications or separate from them.
-------------MORE OF MY STORY IF DESIRED------------or just google: RonPrice BPD-----------
 
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