I don't know if it is good news but just because you have unbearable pain that makes life not worth living does not mean you will die. You can have pain like that for years, but once the karma is exhausted it will end. When suffering is that extreme one of the best things you can do is not think about it when you do get little breaks. There is pain so intense it is like a meditative absorption and at that level it is easier than the pain where you can still think and torture yourself. Reminiscing about the life the illness has taken from you is a terrible habit.
As for medicine if you have an uncommon problem(less than 1 in 2000) you are screwed. The key in medicine and Buddhism is to understand the cause of your condition and not treat the individual symptoms. My conditions sounded incurable, but that was not the case. I had comorbid conditions that confused diagnosis and one was quite rare. Most doctors don't have time for wild goose chases.
Allergies and chronic inflammation are very interesting. The mental affliction that often accompanies them may not be mere poor mental hygiene. The correlation of inflammation and mental disorders may have massive and paradigm changing implications.
From the American Society for Clinical Psychopharmacology annual meeting 2014
INFLAMMATION AND INSULIN RESISTANCE: IMPLICATIONS FOR PATHOPHYSIOLOGY AND TREATMENT
Recent research has identified a link between cardio metabolic illnesses and mood symptoms. Insulin resistance and other cardio metabolic risk factors predict increased risk of depression and decreased response to antidepressant and mood stabilizer treatments. This panel symposium will present new findings implicating inflammation, adipocytokines, and oxidative stress to the pathophysiology of mood states and discuss the role of anti-inflammatory and insulin-sensitizingagents as potential treatments for mood disorders. Results will be presented from an open-label proof-of-concept study evaluating the effects of pioglitazone, a peroxisome proliferator-activatedreceptor-gammaagonist with insulin sensitizing properties, on bipolar depression symptomseverity. This study found significant improvement to occur in depression severity with pioglitazone treatment. Moreover, a positive correlation was identified between reduction in depression severity and decreases in levels of interleukin 6 and adiponectin. Data on the relationship between cytokines and damage associated molecular patterns (DAMPs) by mood state will also be presented from two separate samples of patients and controls. These immunogenic markers were identified to become silent during interepisode periods and represent proxies of peripheral toxicity and illness activity. Specifically, higher levels of ccf DNA (nuclear(n)DNA (p < 0.0001) and mitochondrial (mt)DNA ( p= 0.032), as well as HSP70 (p = 0.02) were found in drug free bipolar patients compared to healthy controls . After pharmacological treatment, ccf nDNA (p = 0.013) and HSPs levels (p = 0.025) decreased in those patients that achieved clinical remission. Inaddition to bipolar disorder, recent findings relating inflammation to brain structure and function will be presented from a population with major depressive disorder (MDD). It was recently discovered that the ratios of kynurenic acid (KA) to 3-hydroxykynurenine (3HK)and KA/quinolinic acid (QA), putative neuroprotective indices, were lower in an unmedicated MDD group relative to a healthy control group, and that within the MDD group, the ratio of KA/QA was inversely correlated with the concentration of IL1RA, a proxy measure of IL1ß. Further, in the MDD group, the KA/QA ratio was positively correlated with total hippocampal volume and total amygdala volume. These results raise the possibility that immune dysregulation predisposes to mood disorders via its effect on glutamatergic signaling such that abnormal NMDA receptor signaling may be the unifying mechanism underlying the glutamate and inflammation hypotheses of depression.
In summary, the panel will focus on inflammatory cytokines and indicators of cell death or apoptosis that may represent useful biomarkers for assessing burden of disease in patients with mood disorders as well as targets for novel antidepressant treatments.
To appreciate the role of inflammation and insulin resistance in the pathophysiology of mood disorders.
To understand the implications of inflammatory and cardiometabolic biomarkers on illness activity in bipolar disorder and recognize potential novel neurobiological targets for treating depression
ASSOCIATION BETWEEN KYNURENINE PATHWAY METABOLITES AND GRAY MATTER VOLUMES OF THE HIPPOCAMPUS AND AMYGDALA IN PATIENTS WITH MOOD DISORDERS
Laureate Institute for Brain Research
Major Depressive Disorder (MDD) has been associated with reductions in hippocampal and amygdalar volume that are thought to reflect dendritic atrophy and/or decreases in neurogenesis.Some patients with mood disorders display elevated levels of pro-inflammatory cytokines such as IL1ß and TNF which increase the formation of kynurenine (KYN) pathway metabolites, including kynurenic acid (KA), a potentially neuroprotective antagonist of NMDA receptors, 3-hydroxykynurenine (3HK), a free radical generator, and quinolinic acid (QA), an NMDA agonist and potential neurotoxin. Whereas an association between molecular markers of inflammation and brain structu re and/or function has been found in animal models of depression, the relationship between the peripheral concentrations of kynurenine-pathway metabolites and morphometric MRI abnormalities in mood disorders remains unclear. Here I will present data showing that the ratios of KA/3HK and KA/QA, putative neuroprotective indices, were lower in an unmedicated MDD group relative to a healthy control group, and that within the MDD group, KA/QA was inversely correlated with the concentration of IL1RA, a proxy measure of IL1ß. Further, in the MDD group, the KA/QA ratio was positively correlated with total hippocampal volume and total amygdala volume. Secondly, I will present data from an independent sample of unmedicated subjects with MDD, medicated subjects with MDD, and healthy controls both to replicate the original finding and to examine the effects of medication on the relationship between neuromorphometric abnormalities and peripheral immune markers. Since both KA and QA affect glutamate release, our results raise the possibility that immune dysregulation predisposes to mood disorders via its effect on glutamatergic signaling such that abnormal NMDA receptor signaling may be the unifying mechanism underlying the glutamate and inflammation hypotheses of depression.
The kynurenine theory of depression.