Guest guest Posted January 6, 2006 Report Share Posted January 6, 2006 Sally, Prozac for me and mood levelers as needed for parental visits. LMAO Ahh just had my nightly prozac. You'll probably like the Pegasys Sally. Same good old sides you missed so much but higher response rates. Probably all you can do to swing the odds higher is to take more riba or lose weight before treatment. You already have the nutrition program going. Mike > > Psychosom Med. 2005 Sep-Oct;67(5):773-7. > Click here to read > Irritability rather than depression during interferon treatment is > linked to increased tryptophan catabolism. > > Russo S, Kema IP, Haagsma EB, Boon JC, Willemse PH, den Boer JA, de > Vries EG, Korf J. > > Department of Biological Psychiatry, University Hospital Groningen, > Groningen, The Netherlands. s.r.russo@a... > > OBJECTIVE: Treatment with recombinant interferon is associated with high > rates of psychiatric comorbidity. We investigated the relation between > catabolism of the essential amino acid tryptophan, being rate- limiting of > peripheral and cerebral serotonin formation, and psychiatric symptoms in > patients undergoing combination treatment with interferon-alpha and > ribavirin. PATIENTS AND METHODS: Eighteen patients with viral hepatitis C > who received interferon were included. A psychiatrist screened patients > before and while on interferon-alpha treatment for 2 months, using a > structured diagnostic interview. Fasting plasma tryptophan and platelet > serotonin levels were measured at each visit. RESULTS: At baseline no > evident psychopathology was observed. After 2 months of interferon > treatment, 10 patients experienced increased irritability. No other > structural psychopathology was observed. Decreased plasma tryptophan level > correlated with the presence of irritability (p = .047). Platelet serotonin > levels were found to be decreased during treatment (p = .002). CONCLUSIONS: > Aggressive impulse dysregulation is highly prevalent in patients receiving > interferon treatment. This is associated with decreased plasma tryptophan > levels which may lead to attenuated peripheral and central serotonergic > neurotransmission. > > PMID: 16204437 [PubMed - in process] > > > Antidepressants suppress production of the Th(1) cytokine interferon-gamma, > independent of monoamine transporter blockade. > > Diamond M, JP, Connor TJ. > > Department of Pharmacology, National University of Ireland, Galway, Ireland. > > In this study, antidepressants with selectivity for the noradrenaline > transporter (reboxetine and desipramine), or the serotonin transporter > (fluoxetine and clomipramine) were examined in terms of their ability to > promote an anti-inflammatory cytokine phenotype in human blood. In addition, > we examined the ability of trimipramine; a tricyclic antidepressant that is > devoid of monoamine reuptake inhibitory properties on cytokine production. > Lipopolysaccharide (LPS) was used to stimulate monocyte-derived > pro-inflammatory (IL-1beta, TNF-alpha, IL-12) and anti-inflammatory (IL-10) > cytokines, whilst concanavalin A (Con A) was used to stimulate T- cell > (Th(1): IFN-gamma and Th(2/3): IL-10) cytokines. All of the antidepressants > suppressed IFN-gamma production in the 10-50 muM concentration range, > irrespective of their preference for serotonin or noradrenaline > transporters. This suppression of IFN-gamma production was paralleled by > reduced T-cell proliferation, therefore we suggest that the ability of > antidepressants to suppress IFN-gamma production may be related to their > anti-proliferative properties. The fact that trimipramine also suppressed > IFN-gamma production and T-cell proliferation indicates that these > immunomodulatory actions of antidepressants are most likely unrelated to > inhibition of monoamine reuptake. Interestingly, exposure to a lower > concentration (1 muM) of the antidepressants tended to increase > T-cell-derived IL-10 production, with significant effects elicited by the > noradrenaline reuptake inhibitors reboxetine and desipramine. In contrast to > the robust actions of antidepressants on T-cell derived cytokine production, > they failed to induce any consistent change in LPS-induced monocyte cytokine > production. Overall, our results indicate that IFN-gamma producing T-cells > (Th(1) cells) are the major target for the immunomodulatory actions of > antidepressants, and provide evidence questioning the relationship between > the monoaminergic reuptake properties of antidepressants and their > immunomodulatory effects. The potential clinical significance of the > anti-inflammatory actions of antidepressants is discussed. > > PMID: 16388933 [PubMed - as supplied by publisher] > > > Encephale. 2005 May-Jun;31(3):349-57. > Hepatitis C, interferon a and depression: main physiopathologic hypothesis > > Vignau J, Karila L, Costisella O, Canva V. > > Service d'Addictologie, CHRU de Lille. > > Imputability of thymic disorders caused by IFNalpha during the chronic > Hepatitis C treatment -- hepatitis C and depression -- the infection by the > hepatitis C virus (HCV) is a major public health concern since it affects > 1.2% in the French population. Eighty percent of those contaminated by HCV > keep bearing the virus chronically although they remain asymptomatic during > many years. HCV infection is associated with psychiatric symptoms like > depression. Together with other factors (eg the severity of hepatic > condition), depression may induce significant impairment in quality of life. > Conversely, some psychiatric conditions may increase the risk of HCV > infection. In drug-addicted subjects using intravenous route, HCV > contamination rate ranges from 74 to 100%. Compared with general population, > a higher HCV contamination rate has also been noticed in some other > subgroups of subjects (patients with alcohol abuse or dependence, with > alcohol-induced hepatic disease and psychiatric inpatients). However, no > valid explanation to this phenomenon has been established. Interferon alpha > and depression - Interferons are a variety of cytokines naturally produced > by human tissues and have also been synthesized for therapeutic purposes > (treatment of a variety of cancers and viral infections). Many > psychobehavioural symptoms are observed under IFNalpha treatment. Among > them, mood disorders are known to occur early after entry into treatment and > to be within the reach of preventive measures. The reported frequency of > depression during IFNalpha treatment ranges from 0 to 37%. This variation > reflects either methodological biases (eg differences in psychiatric > assessment) or the heterogeneity of the population of patients accepted in > therapeutic protocols. Note that the adjunction of ribavirine to IFNalpha in > therapeutic protocols has not brought any changes in the depression > frequency. The causal relationship between IFNalpha administration and the > occurrence of mood disorders has been tackled by various recent research > works focusing on the importance of the immune system in the pathophysiology > of depression. Miscellaneous pathophysiological hypotheses -- nature of the > psychobehavioural symptomatology -- in addition to depressive symptoms, > IFNalpha treatment also induces various cognitive impairments and > disruptions in EEG patterns. These symptoms are consistent with a mild > subcortical dementia. Data resulting from pharmacological trials in humans > and in animals are controversial (eg IFNalpha-induced symptoms being > alleviated by both immune and antidepressant therapies). However, the debate > about the nature of the psychobehavioural disorders observed under IFNalpha > treatment might be no longer relevant in the light of recent theories which > regard depression as a maladaptive response to a particular form of stress, > namely a deep and diffuse feeling of sickness ( " malaise " ). These theoretical > views ascribe the production of depressive symptoms to a disruption in the > immune function, mediated by the variety of cytokines. The therapeutic > effects of anti-depressive drugs are thus attributed to their analgesic > properties, reducing the " malaise " feeling underlying depressive symptoms. > Necessity of a second messanger -- accordingly to current pathophysiological > theories, depression results from disorders of various CNS functions, mainly > limbic, monaminergic and neuroendocrinal systems. Though, exogenous IFNalpha > does not cross the blood-brain barrier when unscathed and an intermediary > mechanism is necessary. First to be addressed is the cytokines system itself > since it is composed of numerous different molecules interacting in an > infinite number of possible combinations. Some of these cytokines (eg some > interleukins) both are activated by IFNalpha and can reach CNS; they are > good candidates for the role of second messenger mediating the induction of > psychobehavioural disorders. Second, keeping in mind that serotonin is a > monoaminergic neurotransmitter classically involved in depression > pathophysiology, other works have demonstrated that IFNalpha modulates the > peripheral activity of indolamine-dioxygenase -- a regulating enzyme of > serotonin metabolism -- possibly through lymphocyte T CD4 activation. Third, > other authors have postulated an immune-induced vagal mechanism to explain > depression caused by IFNalpha. Action of IFNalpha on the neuroendocrine and > on neuromodulating functions: monoaminergic hypothesis -- cytokines could > have an influence on the mood through their modulating role on the > serotoninergic system. IFNalpha treatment is reported to produce: 1) a > decrease in tryptophan availability for serotonin synthesis, 2) a decrease > in the 5-HIAA level in the LCR, and 3) a modification of the central > serotoninergic receptors. Moreover, selective inhibitors of serotonin > transporters are effective to treat or prevent depression caused by > IFNalpha. Many studies support the serotonin-transporter hypothesis: in > vitro, both IFNalpha and interleukine 4 (IL-4) increases the expression of > serotonin transporter gene, IFNalpha increases in the production of IL-4 by > mononucleus cells (not found in vivo). Serotoninergic system can also be > altered by a peripheral action of IFNalpha on trytophan catabolism by > activating a concurrent pathway (known as " kynurenine pathway " ) to serotonin > synthesis. Finally, serotonin-mediated vulnerability to the > psychobehavioural effects of IFNalpha could be underlain by a polymorphism > of serotonin transporter gene. Concerning the other monoaminergic systems, > IFNalpha seems to have an amphetamine-like effect at its first > administration, followed by a decrease in dopaminergic tone with chronic > administration. Dopaminergic depletion, subsequent to psychostimulant abuse > for instance, results in severe depressive syndromes. Interactions between > IFNalpha and noradrenergic system have also been reported. Neuroendocrinian > hypothesis -- when administered through central or peripheral way, IFNalpha > simulates/inhibits the corticotrope axis and alters endorphin system as > shown by the induction of analgesia, catatonia and behavioural slowdown that > can be suppressed by opioid antagonists. IFNalpha neurotoxic effects are > successfully treated by naltrexone. Lastly, IFNalpha is known to cause > disorders in thyroid function that are likely to contribute to the > production or aggravation of mood disorders. CONCLUSION: A better > understanding of pathophysiologic mechanisms underlying psychiatric > side-effects of IFNalpha is essential to extend access to treatment to some > categories of patients that remain excluded from the protocols. A better > management of those psychiatric side effects should help the clinician not > to draw aside patients at risk, ie patients with depression, drug and > alcohol addiction. Treating them in a pragmatic and careful way is a major > issue, since this population represents a high percentage of the potential > candidates for interferon therapy. > > Publication Types: > > * Review > > > PMID: 16142050 [PubMed - indexed for MEDLINE] > > Clin Chim Acta. 2005 Aug 31; > > Monitoring tryptophan metabolism in chronic immune activation. > > Schrocksnadel K, Wirleitner B, Winkler C, Fuchs D. > > Division of Biological Chemistry, Biocentre, Innsbruck Medical > University, Fritz Pregl Strasse 3 A-6020 Innsbruck, Austria; Ludwig > Boltzmann Institute of AIDS Research, Innsbruck, Austria. > > The essential amino acid tryptophan is a constituent of proteins and is > also a substrate for two important biosynthetic pathways: the generation of > neurotransmitter 5-hydroxytryptamine (serotonin) by tryptophan > 5-hydroxylase, and the formation of kynurenine derivatives and nicotinamide > adenine dinucleotides. The latter pathway is initiated by the enzymes > tryptophan pyrrolase (tryptophan 2,3-dioxygenase, TDO) and indoleamine > 2,3-dioxygenase (IDO). TDO is located in liver cells, whereas IDO is > expressed in a variety of cells including monocyte-derived macrophages and > dendritic cells and is preferentially induced by Th1-type cytokine > interferon-gamma. Tryptophan depletion via IDO is part of the cytostatic and > antiproliferative activity mediated by interferon-gamma in cells. In vivo > tryptophan concentration can be measured by HPLC by monitoring its natural > fluorescence (285 nm excitation and 365 nm emission wavelength). IDO > activity is characterized best by the kynurenine to tryptophan ratio which > correlates with concentrations of immune activation markers such as > neopterin. Low serum/plasma tryptophan concentration is observed in > infectious, autoimmune, and malignant diseases and disorders that involve > cellular (Th1-type) immune activation as well as during pregnancy due to > accelerated tryptophan conversion. Thus, in states of persistent immune > activation, low tryptophan concentration may contribute to immunodeficiency. > Decreased serum tryptophan can also effect serotonin biosynthesis and thus > contribute to impaired quality of life and depressive mood. As such, > monitoring tryptophan metabolism in chronic immunopathology provides a > better understanding of the association between immune activation and IDO > and its role in the development of immunodeficiency, anemia and mood > disorders. > > PMID: 16139256 [PubMed - as supplied by publisher] > > Med Hypotheses. 2005;65(1):138-44. > > 5-Hydroxytryptophan plus SSRIs for interferon-induced depression: > synergistic mechanisms for normalizing synaptic serotonin. > > EH, Blackwell AD. > > Mental Health Division, Mood Disorders Research Center, Portland VA > Medical Center, 3710 SW US Veterans Hospital Rd., Portland, OR 97239, USA. > .turner@m... > > Interferon-alpha (IFN) is widely used in the treatment of certain > cancers and viral infections, including hepatitis C (HCV). Unfortunately, > depression is a common side effect of IFN therapy, affecting approximately a > third of HCV patients receiving IFN therapy. Studies have shown that > selective serotonin reuptake inhibitors (SSRIs) can effectively treat > IFN-induced depression in only 63-75% of cases. For the remaining > percentage, depression often necessitates dose reduction of or > discontinuation from IFN therapy. Emerging evidence indicates that IFN may > cause depression by affecting brain serotonin. IFN has been shown to > increase serotonin reuptake and to decrease serotonin synthesis. We > hypothesize that SSRIs are not fully effective because they affect only > serotonin reuptake, not serotonin synthesis, and that effective treatment > must address both uptake and synthesis. 5-Hydroxytryptophan (5-HTP) > effectively increases central nervous system synthesis of serotonin. It is > the immediate precursor of serotonin and is widely available as a dietary > supplement, which is well absorbed after an oral dose. Several double-blind > studies have shown 5-HTP to be effective in the treatment of nondrug-induced > depression. We hypothesize that patients who become depressed on IFN will > respond to the synergistic combination of SSRIs plus 5-HTP. > > PMID: 15893130 [PubMed - indexed for MEDLINE] > > Dig Liver Dis. 2005 Feb;37(2):102-7. > > Interferon-induced depression: prevalence and management. > > Scalori A, Pozzi M, Bellia V, Apale P, Santamaria G, Bordoni T, Redaelli > A, Avolio A, Parravicini P, Pioltelli P, Roffi L. > > Department of Medicine, University of Milano-Bicocca, S. Gerardo > Hospital, Monza, Italy. > > BACKGROUND: Interferon-induced depression ranges from 0 to 50%. > Interferon schedule and a history of psychiatric illnesses are not enough to > predict who will develop symptoms and who will not. AIMS: To assess the > prevalence of depression during interferon therapy; to test whether > Minnesota Multiphasic Personality Inventory is useful in clinical practice > for the early identification of patients at risk of depression; whether and > how the depression can be cured. PATIENTS: One hundred and eighty- five > patients treated with interferon and ribavirin for chronic hepatitis C. > METHODS: Before therapy, all patients underwent a Minnesota Multiphasic > Personality Inventory and a clinical examination, specifically for the > identification of depressive symptoms. RESULTS: Thirty-one patients > developed a psychiatric disorder, 11 of them requiring treatment with > anti-depressant drugs. Among the 18 patients with Minnesota Multiphasic > Personality Inventory positive tests, 16 developed a psychiatric disorder, 8 > of them a severe disorder (sensitivity of 0.58; 0.73 for severe disorders). > Among the 154 who did not develop psychiatric side effects, 152 had a > negative Minnesota Multiphasic Personality Inventory (specificity: 0.99). > Severe psychiatric disorders were successfully treated with anti- depressant > drugs. CONCLUSIONS: Psychiatric side effects are easy to see during > interferon therapy. A psychiatric evaluation should be considered on all > patients before treatment. If depression develops, it should be treated > aggressively, and selective serotonin re-uptake inhibitors are the > anti-depressants of choice. > > PMID: 15733522 [PubMed - indexed for MEDLINE] > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 6, 2006 Report Share Posted January 6, 2006 Well, yeah, anyone hear of " Riba Rage " ? I warned everybody at work that it was gonna happen. I thought I'd have temper tantrums but instead I became viciously snide and nasty to people. Oh yes, I made more friends and influenced people (NOT!). Lexpro is good for me, it lets me cry when I need to (unlike Paxil) and keeps the anxiety down. Michele __________________________________________ DSL – Something to write home about. Just $16.99/mo. or less. dsl. Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.