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Severely Depressed from Die-Off/Herx? Probiotics? Virus? Lyme? Co Infection? What's Happening?

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by Lotus97, Feb 9, 2013.

  1. Hip

    Hip Senior Member

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    The antidepressant remedies I find very useful when depression hits, as it seems to do on random weeks with me, are:

    Inositol powder 1 to 3 heaped teaspoons.
    Saffron 60 mg of stamens (has to be Spanish or Iranian saffron). Some small-scale studies have shown saffron to be as potent an Prozac, but without the side effects of SSRIs.
    NADH 5 to 10 mg.
    Raw chocolate 2 to 4 heaped teaspoons — a strong energy booster that has anti-depressant effects. Raw chocolate is like regular chocolate on steroids!
    Pregnenolone 50 mg — pregnenolone boosts hormone levels in general, which I find helps pick up your mood.

    Wolfberries (Goji berry) — eating a handful of dried nice wolfberries gives a nice mood boosting, antidepressant effect, but higher doses can cause diarrhea.
    Ravensara essential oil drops diluted in 30 ml carrier oil (like baby oil) and rubbed on the skin, where it gets absorbed. This herb creates a happier mood, and is also antiviral.
    Imipramine 25 mg — imipramine is an excellent TCA antidepressant like amitriptyline, but has lower side effects. Vitamin B6 may improve effectiveness of TCA antidepressants. It is best to take vitamin B2 with TCA antidepressants, as TCAs can deplete vitamin B2.
    Amisulpride 12.5 to 25 mg daily works very well to combat depression, though it reduces libido.

    I went through one or two years when depression was a constant battle, and I would take several of the above simultaneously. Nowadays my depression only comes back now and then, and to a lesser degree, but I still use the above remedies when it does.
     
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  2. Lotus97

    Lotus97 Senior Member

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    That's good to know about tricylic antidepressants. I've been on amitriptyline for years (as a sleep aid). I was actually planning on upping my dose of B2 anyways. I'm switching to the coenzymated form after someone told me you can only absorb around 30 mg of the non-active B2 at a time.
     
  3. Lotus97

    Lotus97 Senior Member

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    I've been taking probiotics for a couple of days and I'm getting depressed again. Although I am going to stop the probiotics, there is another possibility. I didn't share my original hypothesis because it seemed unlikely. When I first got depressed 2 months ago it happened around 8 days after I started a new bottle of Prozac. Although the Prozac was by the same generic company as before I wondered if it was a bad batch. When I had gone off Prozac in the past it took about 8 days before I got depressed because Prozac has such a long half life. When I switched to taking 20 mg capsules my mood improved. Now I've been off the 20 mg Prozac for about 8 days (I switched to Paxil) and I'm getting depressed. I will see if stopping the probiotics for a few weeks makes a difference, but I don't want to rule out the other possibility.
     
  4. triffid113

    triffid113 Day of the Square Peg

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    Yes, you read me right. I may be wrong, but it was at least 3.5 g / day. I am guessing she is supplying all the carnitine she needs via supplement rather than via the methyl cycle. It makes me think maybe she needed TMG and did not take it. Or maybe she was hyperthyroid and using up carnitine faster than normal. Or??? She specualted that she has a - well I forget - I think she might have said some sort of fat metabolism issue. Once she foud what worked she stuck with it. It worked for her sister too.
     
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  5. Lotus97

    Lotus97 Senior Member

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    It seems with me there's some kind of herx going on which is causing the depression rather than the cytokine flare that some people suggested. For anyone following this thread who does suspect a cytokine induced depression for themselves I found what seems to be a pretty good explanation as to why it happens
    The psychoneuroimmuno-pathophysiology of cytokine-induced depression in humans
    by
    Wichers M, Maes M.
    Department of Psychiatry and Neuropsychology,
    Maastricht University, 6200 MD Maastricht, The Netherlands.
    Int J Neuropsychopharmacol 2002 Dec;5(4):375-88

    ABSTRACT
    Administration of the cytokines interferon-alpha and interleukin-2 is used for the treatment of various disorders, such as hepatitis C and various forms of cancer. The most serious side-effects are symptoms associated with depression, including fatigue, increased sleepiness, irritability, loss of appetite as well as cognitive changes. However, great differences exist in the prevalence of the development of depressive symptoms across studies. Differences in doses and duration of therapy may be sources of variation as well as individual differences of patients, such as a history of psychiatric illness. In addition, sensitization effects may contribute to differential responses of patients to the administration of cytokines. In animals administration of pro-inflammatory cytokines induces a pattern of behavioural alterations called 'sickness behaviour' which resembles the vegetative symptoms of depression in humans. Changes in serotonin (5-HT) receptors and in levels of 5-HT and its precursor tryptophan in depressed people support a role for 5-HT in the development of depression. In addition, evidence exists for a dysregulation of the noradrenergic system and a hyperactive hypothalamic-pituitary-adrenal (HPA) axis in depression. Some mechanisms exist which make it possible for cytokines to cross the blood-brain barrier. Pro-inflammatory cytokines such as IL-1beta, IFN-alpha, IFN-gamma and TNF-alpha affect the 5-HT metabolism directly and/or indirectly by stimulating the enzyme indoleamine 2,3-dioxygenase which leads to a peripheral depletion of tryptophan. IL-1, IL-2 and TNF-alpha influence noradrenergic activity and IL-1, IL-6 and TNF-alpha are found to be potent stimulators of the HPA axis. Altogether, administration of cytokines may induce alterations in the brain resembling those found in depressed patients, which leads to the hypothesis that cytokines induce depression by their influence on the 5-HT, noradrenergic and HPA system.
     
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  6. Lotus97

    Lotus97 Senior Member

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    Someone just started a thread saying curcumin caused a herx with them. One person suggested in that thread suggested that it was because curcumin was a Th2 stimulant and many people here are Th2 dominant. I was also reading that probiotics can initiate a Th2 immune response so I'm considering that a possibility to why I had the reaction I did. I also found out that some of the cytokines mentioned in that article about cytokine-induced depression are associated with Th2 responses (also others are associated with Th1 responses). I noticed this mentioned monocytes and my monocytes were high last time I was tested.
    SP32-20130227-165511.png
     
  7. Lotus97

    Lotus97 Senior Member

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    I recently found out that ginger and turmeric both have antibacterial, antifungal, antimicrobial, and antiviral properties. I've been taking Zyflamend PM twice a day (4 capsules total) which has very potent full spectrum extracts of ginger and turmeric. I guess I'll stop those for awhile too.
     
  8. Jarod

    Jarod Senior Member

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    Lotus97 I started dumping heavy metals from methylation startup which made me terribly depressed. This was measured with a pee test.

    I may have been going too fast, but dumping metals (especially during the initial startup) can make one terribly depressed.
     
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  9. Lotus97

    Lotus97 Senior Member

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    I wasn't going to post any more in this thread unless I thought there was information I thought would be useful to others. It seems with me, the depression was (and is) due to inflammatory cytokines. Part of this was from the probiotics causing a herx which can cause inflammatory cytokines. I confirmed this after taking various antibacterial/fungal/microbial supplements and experiencing the same depression. There seems to be more, however. I was taking immune supplements that stimulate Th1 and Lyme can also cause an overactive Th1 immune response. I posted about it in this thread:
    http://forums.phoenixrising.me/inde...in-late-stage-lyme-and-buhner-protocol.22068/
    Part of the inflammatory Th1 response seems to be due to microglia. The first article talks about microglia in regards to infectious diseases in general, but does have a section specifically about Lyme. The second and third are about microglia and Lyme specifically. The last article (which the diagram is from) talks about inflammation in regards to glutamate, microglia, and depression. Except for the third article, there is a lot more information than what I'm posting here so anyone who wants to learn more about this subject I'd recommend following the links to the full articles. Only the second and third article are specifically about Lyme. The first and fourth article are broader in their scope (although the first one does have a section devoted specifically to Lyme as I mentioned earlier).
    ===========================
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847353/
    Microglia in Infectious Diseases of the Central Nervous System
    Abstract

    Microglia are the resident macrophage population in the central nervous system (CNS) parenchyma and, as such, are poised to provide a first line of defense against invading pathogens. Microglia are endowed with a vast repertoire of pattern recognition receptors that include such family members as Toll-like receptors and phagocytic receptors, which collectively function to sense and eliminate microbes invading the CNS parenchyma. In addition, microglial activation elicits a broad range of pro-inflammatory cytokines and chemokines that are involved in the recruitment and subsequent activation of peripheral immune cells infiltrating the infected CNS. Studies from several laboratories have demonstrated the ability of microglia to sense and respond to a wide variety of pathogens capable of colonizing the CNS including bacterial, viral, and fungal species. This review will highlight the role of microglia in microbial recognition and the resultant antipathogen response that ensues in an attempt to clear these infections. Implications as to whether microglial activation is uniformly beneficial to the CNS or in some circumstances may exacerbate pathology will also be discussed.
    Keywords: microglia, bacterial meningitis, brain abscess, Lyme neuroborreliosis, Toxoplasmaencephalitis, cerebral malaria, fungal infections, review
    Microglial recognition of Borrelia burgdorferi and Lyme neuroborreliosis

    The spirochete B. burgdorferi (sensu lato) is the etiologic agent of Lyme disease, the most frequently occurring vector-borne infection in the USA (Hengge et al. 2003; Rupprecht et al. 2008). B. burgdorferitransmission occurs through Ixodes ticks and is also endemic in Europe and parts of Asia. Lyme disease initially propagates in the skin before it disseminates through the blood stream to other organ systems. In addition, B. burgdorferi displays tissue tropism for the nervous system, where neurologic involvement occurs in up to 20% of patients who present with cranial neuritis, meningoradiculitis, or encephalitis (Pfister et al. 1994; Rupprecht et al. 2008). Colonization of the CNS with B. burgdorferifrom the blood is associated with inflammation of the meninges, nerve roots, brain, and spinal cord resulting in the clinical manifestations of neuroborreliosis (Pfister and Rupprecht 2006; Rupprecht et al. 2008). Furthermore, marked levels of pro-inflammatory molecules such as IL-6 and TNF-α are associated with Lyme disease, as well as the induction of an important inflammatory enzyme, cyclooxygenase-2 (COX-2; Ramesh et al. 2008; Rasley et al. 2002). However, the inflammatory mechanisms that are involved in the CNS immune responses to B. burgdorferi are not currently well understood based on the limited availability of an adequate animal model. To date, the only animal model where evidence of Lyme neuroborreliosis has been demonstrated is in rhesus macaques (Pachner et al. 2001).
    ===========================
    http://www.ncbi.nlm.nih.gov/pubmed/12225885
    Borrelia burgdorferi induces inflammatory mediator production by murine microglia.

    Abstract

    Lyme disease has been associated with damaging inflammation within the central nervous system. In the present study, we demonstrate that Borrelia burgdorferi is a significant stimulus for the production of IL-6, TNF-alpha, and PGE(2) by microglia. This effect is associated with induction of NF-kappaB, and increased expression of Toll-like receptor 2 and CD14, receptors known to underlie spirochete activation of other immune cell types. These studies identify microglia as a previously unappreciated source of inflammatory mediator production following challenge with B. burgdorferi. Such production may play an important role during the development of Lyme neuroborreliosis.
    ===========================
    http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000659
    Microglia Are Mediators of Borrelia burgdorferi–Induced Apoptosis in SH-SY5Y Neuronal Cells
    Abstract

    Inflammation has long been implicated as a contributor to pathogenesis in many CNS illnesses, including Lyme neuroborreliosis. Borrelia burgdorferi is the spirochete that causes Lyme disease and it is known to potently induce the production of inflammatory mediators in a variety of cells. In experiments where B. burgdorferi was co-cultured in vitro with primary microglia, we observed robust expression and release of IL-6 and IL-8, CCL2 (MCP-1), CCL3 (MIP-1α), CCL4 (MIP-1β) and CCL5 (RANTES), but we detected no induction of microglial apoptosis. In contrast, SH-SY5Y (SY) neuroblastoma cells co-cultured with B. burgdorferiexpressed negligible amounts of inflammatory mediators and also remained resistant to apoptosis. When SY cells were co-cultured with microglia and B. burgdorferi, significant neuronal apoptosis consistently occurred. Confocal microscopy imaging of these cell cultures stained for apoptosis and with cell type-specific markers confirmed that it was predominantly the SY cells that were dying. Microarray analysis demonstrated an intense microglia-mediated inflammatory response to B. burgdorferi including up-regulation in gene transcripts for TLR-2 and NFκβ. Surprisingly, a pathway that exhibited profound changes in regard to inflammatory signaling was triggering receptor expressed on myeloid cells-1 (TREM1). Significant transcript alterations in essential p53 pathway genes also occurred in SY cells cultured in the presence of microglia and B. burgdorferi, which indicated a shift from cell survival to preparation for apoptosis when compared to SY cells cultured in the presence of B. burgdorferi alone. Taken together, these findings indicate that B. burgdorferi is not directly toxic to SY cells; rather, these cells become distressed and die in the inflammatory surroundings generated by microglia through a bystander effect. If, as we hypothesized, neuronal apoptosis is the key pathogenic event in Lyme neuroborreliosis, then targeting microglial responses may be a significant therapeutic approach for the treatment of this form of Lyme disease.
    ===========================
    http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=1590
    Inflammation, Glutamate, and Glia in Depression: A Literature Review
    Abstract
    Multiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-α treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.
    Introduction
    Depression is a common and debilitating disorder for which current treatments are inadequate. The pathogenesis of depression is not well understood. The annual prevalence of depression is 7% and the lifetime prevalence is 16%.1,2 In addition to significant disability,3depression is associated with excess mortality,4,5 particularly from cardiovascular disease.6 Current antidepressants, which target monoamines, only produce remission in 30% of patients. Part of the problem lies in the fact that the pathophysiology of depression has not been elucidated, and treatments are based on empirical data, not mechanisms of action. It remains unclear how these drugs actually work, since their ability to increase synaptic concentrations of monoamines is immediate, while their clinical effects take 2–4 weeks to become apparent.7 The aim of this article is to provide an overview of studies implicating inflammation in depression, and propose a model of how excess inflammation may interact with glutamate and glia to cause depression.
    [​IMG]
     
  10. adreno

    adreno 3% neanderthal

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    Tundras of Europa
    I'm on Candex which is an antifungal, and the die-off seems to cause severe depression for me as well. Perhaps this is common in herxing.
     
  11. Lotus97

    Lotus97 Senior Member

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    It seems like the depression from die-off/herx is caused by inflammation, but I wonder if the same thing is going on with the metal dumping. Besides Jarod, I've heard from one or two other people with metal toxicity who say they've experienced depression from too much methylation.
    http://www.ncbi.nlm.nih.gov/pubmed/9707512
    Toxic metals stimulate inflammatory cytokines in hepatocytes through oxidative stress mechanisms.
    Abstract
    Hepatocytes, as well as nonparenchymal cells, secrete proinflammatory cytokines and chemokines that are involved in the pathology of many liver diseases. In particular, tumor necrosis factor-alpha (TNFalpha), as well as members of the CXC family of chemokines, including interleukin (IL)-8 in humans and macrophage inflammatory protein (MIP)-2 in rodents, have been implicated in both damage and repair processes associated with various hepatotoxins. In the liver, cytokine secretion is usually associated with nonparenchymal cells, particularly Kupffer cells. In the present studies, cytokine gene expression and secretion were investigated in hepatocytes treated with cadmium chloride (CdCl2) or vanadium pentoxide (V2O5). Using human Hep G2 cells and freshly isolated rodent hepatocytes, it was demonstrated that metals increase gene expression and secretion of CXC chemokines and TNFalpha. IL-8 and MIP-2 secretion induced either by the metals or H2O2 were inhibited by antioxidants such as tetramethyl-thiourea and N-acetyl-cysteine. In vitro neutralization experiments with TNFalpha and in vivo studies with TNFalpha receptor knockout mice indicated that the metals directly stimulate CXC chemokine secretion without the need for TNFalpha. Taken together these studies indicate that, in addition to other inflammatory mediators and acute phase proteins, cytokines and chemokines are produced by hepatocytes, which may participate in hepatotoxic responses. The events responsible for their expression involve cellular redox changes.
     
  12. Lotus97

    Lotus97 Senior Member

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    I found this from Wikipedia. Among the ones mentioned, tumor necrosis factor (TNF) and interleukin-6 (IL-6) are both linked to depression in the articles I posted earlier.
    http://en.wikipedia.org/wiki/Jarisch-Herxheimer_reaction
    Also from an article on Herxheimer reaction. IL-1 and interferons (such as IFN-alpha and IFN-gamma) are also linked to depression.
    http://www.jemsekspecialty.com/lyme_detail.php?sid=10
    Just as a side note I've had my monocytes tested twice. Both times they were high, but during the period where I had been making a recovery they were lower (from 9.4 to 7.7). Also, my sedimentation rate was high both times, but it was also lower during the period where I was making a recovery.
     
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  13. merylg

    merylg Senior Member

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    I found I could not tolerate the amines in Sauerkraut.
     

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