<shortened url>1: J Spinal Cord Med. 2008;31(2):157-65.Links
Neurotoxin treatments for urinary incontinence in subjects with spinal cord injury or multiple sclerosis: a systematic review of effectiveness and adverse effects.MacDonald R, Monga M, Fink HA, Wilt TJ.
Center for Chronic Disease Outcomes Research, Minneapolis Veterans Affairs Medical Center, Minneapolis, Minnesota, 55417, USA. email@example.com
BACKGROUND/OBJECTIVE: The objective was to evaluate the effectiveness of neurotoxin treatments of urinary incontinence (UI) in individuals with spinal cord injury (SCI) or multiple sclerosis (MS). METHODS: Studies were included if published in English, presented randomized adults with SCI or MS, and reported UI outcomes. RESULTS: Ten trials randomizing 288 subjects with SCI (43%), MS (52%), or other spinal conditions (5%) and UI refractory to oral antimuscarinics were included. The overall mean age was 41 years, and 46% were women. Study durations ranged from 1 to 18 months. Treatments included botulinum toxin-A (BTX-A, 2 trials) and 2 vanilloid compounds, capsaicin (6 trials) and resiniferatoxin (4 trials). BTX-A was superior to placebo and resiniferatoxin in reducing daily UI episodes, mainly in individuals with SCI, although significant reductions vs placebo were not evident throughout the study duration. There were 1.1 fewer daily UI episodes in the BTX-A 200 unit group vs 0.1 fewer for the placebo group at the final week 24 assessment. Capsaicin was generally superior to placebo. The weighted difference between capsaicin and placebo in a pooled analysis of 2 trials enrolling subjects with either paraplegia or tetraplegia (n = 32) was -3.8 daily UI episodes [95% Cl -4.7 to -2.9] after 30 days. Capsaicin was comparable to resiniferatoxin. Pelvic pain and facial flushing were associated with capsaicin. CONCLUSION: Neurotoxins may improve refractive UI in adults with SCI or MS, although trial results were inconsistent. Trials were small in size and relatively short in duration. Further studies are needed to determine the efficacy and tolerability of long-term application.
<shortened url>1: Neurourol Urodyn. 2006;25(7):752-7. Links
Intravesical glucidic capsaicin versus glucidic solvent in neurogenic detrusor overactivity: a double blind controlled randomized study.de Sèze M, Gallien P, Denys P, Labat JJ, Serment G, Grise P, Salle JY, Blazejewski S, Hazane C, Moore N, Joseph PA.
Physical Medicine and Neurorehabilitation Unit, Bordeaux University Hospital, Bordeaux, France. firstname.lastname@example.org
AIMS: Many studies report the use of alcoholic capsaicin instillation to treat neurogenic detrusor overactivity (NDO) in spinal cord injured (SCI) and multiple sclerosis (MS) patients. However, poor tolerability due to the irritative effect of the ethanol solvent limits its use. Our study aimed to evaluate the efficacy and tolerability of a new formulation of capsaicin in a glucidic solution in a multicenter clinical trial. MATERIALS AND METHODS: Thirty-three patients (26MS/7SCI) suffering from urinary incontinence due to refractory NDO were prospectively enrolled in a double-blind placebo controlled study and randomized to capsaicin group (CG, N = 17) or solvent group (SG, N = 16). They respectively received an intravesical instillation of 100 ml capsaicin diluted in glucidic solvent (CG) or glucidic solvent alone (SG). Efficacy (voiding chart, maximum cystometric capacity (MCC)) and tolerability were evaluated on days 0 (D0), 30 and 90. RESULTS: On D0, groups were homogeneous. On D30, significant improvement of overactive bladder syndrome and an increase in MCC were shown in CG, whereas there were no improvement in SG. No significant improvement was shown on D90 in both groups. There were no significant differences between groups regarding prevalence, duration, or intensity of side effects, except for short duration pubic pain during instillation more often reported in CG (58.8%) than in SG (12.5%) (P < 0.01). CONCLUSION: This placebo controlled study using glucidic capsaicin confirms its short-term efficacy in NDO patients. Global tolerance of glucidic capsaicin appeared satisfactory. Long-term efficacy and tolerance of repeated glucidic capsaicin instillations need to be evaluated. (c) 2006 Wiley-Liss, Inc.
<shortened url>1: J Neuroimmunol. 2006 Feb;171(1-2):110-9. Epub 2005 Oct 18. Links
Arvanil inhibits T lymphocyte activation and ameliorates autoimmune encephalomyelitis.Malfitano AM, Matarese G, Pisanti S, Grimaldi C, Laezza C, Bisogno T, Di Marzo V, Lechler RI, Bifulco M.
Dipartimento di Scienze Farmaceutiche, Universita' di Salerno, Via Ponte don Melillo 84084 Fisciano (Salerno), Italy.
This study examined the immunomodulatory effect of arvanil, a synthetic capsaicin-anandamide hybrid. Arvanil inhibits lymphocyte proliferation and IFN-gamma production. The phenotype of activated CD4+T cells treated with arvanil shows a down-regulation of T cell activation markers such as CD25, HLA-DR and CD134/OX40. Arvanil and anandamide do not induce apoptosis on CD4+T cells. Arvanil blocks the G1/S phase transition of the cell cycle in stimulated peripheral blood mononuclear cells, inducing activation of p21waf-1/cip-1 and phosphorylation of Akt/PKB. In vivo, arvanil ameliorates experimental autoimmune encephalomyelitis in the SJL/J mouse. Our findings have relevance for the use of arvanil and related compounds as a novel immunotherapeutic approach in the treatment of multiple sclerosis.
<shortened url>1: Eur J Pharmacol. 2002 Mar 29;439(1-3):83-92. Links
Arvanil-induced inhibition of spasticity and persistent pain: evidence for therapeutic sites of action different from the vanilloid VR1 receptor and cannabinoid CB(1)/CB(2) receptors.Brooks JW, Pryce G, Bisogno T, Jaggar SI, Hankey DJ, Brown P, Bridges D, Ledent C, Bifulco M, Rice AS, Di Marzo V, Baker D.
Pain Research Group, Department of Anaesthetics, Faculty of Medicine, Imperial College, Chelsea and Westminster Hospital Campus, London, UK.
Activation of cannabinoid receptors causes inhibition of spasticity, in a mouse model of multiple sclerosis, and of persistent pain, in the rat formalin test. The endocannabinoid anandamide inhibits spasticity and persistent pain. It not only binds to cannabinoid receptors but is also a full agonist at vanilloid receptors of type 1 (VR1). We found here that vanilloid VR1 receptor agonists (capsaicin and N-N'-(3-methoxy-4-aminoethoxy-benzyl)-(4-tert-butyl-benzyl)-urea [SDZ-249-665]) exhibit a small, albeit significant, inhibition of spasticity that can be attenuated by the vanilloid VR1 receptor antagonist, capsazepine. Arvanil, a structural "hybrid" between capsaicin and anandamide, was a potent inhibitor of spasticity at doses (e.g. 0.01 mg/kg i.v.) where capsaicin and cannabinoid CB(1) receptor agonists were ineffective. The anti-spastic effect of arvanil was unchanged in cannabinoid CB(1) receptor gene-deficient mice or in wildtype mice in the presence of both cannabinoid and vanilloid receptor antagonists. Likewise, arvanil (0.1-0.25 mg/kg) exhibited a potent analgesic effect in the formalin test, which was not reversed by cannabinoid and vanilloid receptor antagonists. These findings suggest that activation by arvanil of sites of action different from cannabinoid CB(1)/CB(2) receptors and vanilloid VR1 receptors leads to anti-spastic/analgesic effects that might be exploited therapeutically.
<shortened url>1: Clin Cancer Res. 2007 May 15;13(10):3024-32. Links
Capsaicin is a novel blocker of constitutive and interleukin-6-inducible STAT3 activation.Bhutani M, Pathak AK, Nair AS, Kunnumakkara AB, Guha S, Sethi G, Aggarwal BB.
Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
PURPOSE: Capsaicin, a constituent of green and red peppers, has been linked with suppression of tumorigenesis through a mechanism that is not well understood. Because the transcription factor signal transducer and activator of transcription 3 (STAT3) has been closely linked with tumorigenesis, we investigated the effect of this vanilloid on the STAT3 pathway in human multiple myeloma cells. EXPERIMENTAL DESIGN: The effect of capsaicin on both constitutive and interleukin-6-induced STAT3 activation, associated protein kinases, and STAT3-regulated gene products involved in proliferation, survival and angiogenesis, cellular proliferation, and apoptosis in multiple myeloma cells was investigated. RESULTS: We found that capsaicin inhibited constitutive activation of STAT3 in multiple myeloma cells in a dose- and time-dependent manner, with minimum effect on STAT5. Capsaicin also inhibited the interleukin-6-induced STAT3 activation. The activation of Janus-activated kinase 1 and c-Src, implicated in STAT3 activation, was also inhibited by the vanilloid, with no effect on extracellular signal-regulated kinase 1/2 activation. Pervanadate reversed the capsaicin-induced down-regulation of STAT3, suggesting the involvement of a protein tyrosine phosphatase. Capsaicin down-regulated the expression of the STAT3-regulated gene products, such as cyclin D1, Bcl-2, Bcl-xL, survivin, and vascular endothelial growth factor. Finally, capsaicin induced the accumulation of cells in G(1) phase, inhibited proliferation, and induced apoptosis, as indicated by caspase activation. Capsaicin also significantly potentiated the apoptotic effects of Velcade and thalidomide in multiple myeloma cells. When administered i.p., capsaicin inhibited the growth of human multiple myeloma xenograft tumors in male athymic nu/nu mice. CONCLUSION: Overall, these results suggest that capsaicin is a novel blocker of the STAT3 activation pathway, with a potential role in the prevention and treatment of multiple myeloma and other cancers.
<shortened url>1: J Immunol. 2008 May 1;180(9):6070-6. Links
Loss of STAT3 in CD4+ T cells prevents development of experimental autoimmune diseases.Liu X, Lee YS, Yu CR, Egwuagu CE.
Section of Molecular Immunology, Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.
Th17 cells are implicated in CNS autoimmune diseases. We show that mice with targeted-deletion of Stat3 in CD4(+) T cells (CD4(Stat3)(-/-)) do not develop experimental autoimmune uveoretinitis (EAU) or experimental autoimmune encephalomyelitis. Defective Th17 differentiation noted in CD4(Stat3)(-/-) mice is compensated by exaggerated increases in Foxp3-, IL-10-, IL-4-, and IFN-gamma-expressing T cells, suggesting critical roles of STAT3 in shaping Ag-specific CD4(+) T cell repertoire. In mice with EAU, a high percentage of IL-17-expressing T cells in their peripheral lymphoid organs also secrete IFN-gamma while these double-expressors are absent in CD4(Stat3)(-/-) and wild-type mice without EAU, raising the intriguing possibility that uveitis maybe mediated by Th17 and IL-17-expressing Th1 cells. Resistance of Stat3-deficient mice to EAU derives in part from an inability of uveitogenic Th17 and Th1 cells to enter eyes or brain of the CD4(Stat3)(-/-) mouse because of the reduction in the expression of activated alpha4/beta1 integrins on CD4(Stat3)(-/-) T cells. Adoptive transfer of activated interphotoreceptor retinoid-binding protein-specific uveitogenic T cells induced in CD4(Stat3)(-/-) mice a severe EAU characterized by development of retinal folds, infiltration of inflammatory cells into the retina, and destruction of retinal architecture, underscoring our contention that the loss of STAT3 in CD4(+) T cells results in an intrinsic developmental defect that renders CD4(Stat3)(-/-) resistant to CNS inflammatory diseases. STAT3 requirement for IL-17 production by Th17, generation of double positive T cells expressing IL-17 and IFN-gamma, and for T cell trafficking into CNS tissues suggests that STAT3 may be a therapeutic target for modulating uveitis, sceritis, or multiple sclerosis.
<shortened url>1: J Neurosci Res. 2006 Oct;84(5):1027-36. Links
pSTAT1, pSTAT3, and T-bet expression in peripheral blood mononuclear cells from relapsing-remitting multiple sclerosis patients correlates with disease activity.Frisullo G, Angelucci F, Caggiula M, Nociti V, Iorio R, Patanella AK, Sancricca C, Mirabella M, Tonali PA, Batocchi AP.
Institute of Neurology, Department of Neuroscience, Catholic University, Rome, Italy.
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system, and it is considered to be a T helper 1 (Th1) cell-mediated autoimmune disease. T-bet has been identified as a key transcription factor for the development of Th1 cells and the induction of interferon (IFN)-gamma production. T-bet is induced during T-cell activation by the IFN-gamma signal transducer and activator of transcription (STAT)-1 signalling pathway. In this study we found an up-regulation of T-bet and pSTAT1 in peripheral blood CD4+ and CD8+ T cells and monocytes from relapsing-remitting MS patients in relapse compared with patients in remission and with healthy subjects. The increased expression of pSTAT1 strongly correlated with T-bet expression in CD4+ and CD8+ cells and monocytes from patients in relapse and was associated with an increased production of IFN-gamma by peripheral blood mononuclear cells (PBMCs). pSTAT3 was also up-regulated in CD4+ and CD8+ cells and monocytes from patients in relapse and was associated with an increased production of interleukin (IL)-10 but not of IL-6. pSTAT1, pSTAT3, and T-bet expression strongly correlated with Gd-DTPA-enhanced lesions on brain and spinal cord magnetic resonance imaging. Our data show for the first time that there is an up-regulation of type 1 immunity-correlated transcription factors such as STAT1 and T-bet in peripheral blood subpopulations of MS patients in the active phase of disease. The evaluation of T-bet and pSTAT1 expression in peripheral blood CD4+, CD8+ T cells and monocytes could be used as a marker of disease activity in relapsing-remitting MS. Copyright 2006 Wiley-Liss, Inc.
PMID: 16865709 [PubMed - indexed for MEDLINE]
Sharon, that one is interesting. Its worth its own thread when you find your links. Meanwhile, I found this one (advertising) http://www.ultimateimmune.com/articles/lions-mane.phpSharon wrote:Have you tried or researched the mushroom, Lion's Mane? ... The Lion's Mane mushroom is supposed to be good for neurotransmission and also for regrowth of neurons.
and it goes on (as advertising normally does...)Dr. Hirokazu Kawagishi of Shizoka University Japan, a recognized authority on Lion's Mane for the past 15 years, showed the mushroom to have the remarkable activity of stimulating the synthesis of Nerve Growth Factor (NGF).
Medical sleuthing without an MRI
As a medical student in the early 1960s, trained at Bart’s Hospital (founded in 1123), I was extremely frustrated by some aspects of the teaching of clinical medicine. What I wanted to learn was exciting facts about the causes of illness, modern biochemistry, and the latest treatments. A number of years later when I worked as an intern for the late Dr Alan Spence, I felt confident enough to express my concerns. He replied that “50% of what I would have taught you would be wrong by the time you are middle aged, and biochemical tests change every 10 years.” His job, he thought, was to teach me to use clinical judgment and to keep asking why does this happen, why are we doing this? I asked myself what motivated physicians in the past to carry out procedures, such as total dental extraction for colitis and rheumatoid arthritis!
Perhaps the most important person to ask “why” was William Harvey, the first physician appointed in Bart’s. For the first 500 years of Bart’s existence, they thought they could make do without physicians, running the hospital with nurses and administrators. At that time, Galenic philosophy was deeply carved in stone and taught as the basis of human physiology. Harvey, with only minimal support and apparatus, provided about 90% of the proof that blood circulates. It is difficult to understand that the idea of a heart acting as a pump was totally foreign at the time.
Analogously, I am certain there are many things that are wrong in modern medicine, even though great breakthroughs have been made in genetics, transplants, electrophysiology, and so on. In particular, I have a gut feeling that we have shied away from truly confronting the origins of a great puzzle—the so-called autoimmune diseases.
For the last 100 years, little progress has been made in understanding the true etiology and specific treatment of autoimmune diseases, such as rheumatoid arthritis, ulcerative colitis, Crohn disease, and disseminated lupus. These illnesses are thrown into a rat bag labeled “autoimmune.” While admittedly there are design flaws in the human body, it does seem unusual that evolution has allowed the continuation of a mechanism whereby the body attacks itself. (In passing, some thought should be given to the concept that most organisms have a purpose. Bacteria and viruses, although they might kill the host, do carry out the basic tenet of nature: they reproduce and spread, thus fulfilling their goal. Such a goal is missing in all forms of cancer, which kill the host, and in the self-destructive autoimmune diseases.)
Over the last 80 years or more, great attention has been focused on the inflammatory cascade mechanisms of autoimmune disorders. We have nonsteroidal anti-inflammatory drugs, which suppress some of the pathology, disease-modifying agents that inhibit inflammation, and now the new anti–tumour necrosis factor agents. These all focus on the inflammation underlying autoimmune disorders, but none of them really address the underlying cause, the specific triggers that set the self-destructive autoimmune process in motion. The common factor in autoimmune diseases is that their true etiology remains unknown—we might be on the wrong track and persist in going down the wrong road.
A typical example of this frustrating situation is rheumatoid arthritis. Why is it symmetrical in distribution? It’s not likely that the joints classically affected differ in cartilage structure from those that aren’t. Moreover, why does a stroke prevent the development of the disease in the paralyzed limb? In animal studies, either surgically or chemically destroying the afferent nerves to joints prevents the appearance of arthritis in those joints.1 As Harvey might have noted, the same blood circulates around these joints—so why the sparing? I was surprised to observe that a great many papers in the peer-reviewed medical literature refer to a phenomenon that is virtually ignored in clinical medicine—the neurogenic origins of arthritis.2
The final stimulus that motivated me to write this letter was encountering reports from the early part of the 20th century that sectioning the sympathetic nervous system often provided amazing relief in arthritis. Not double-blind studies, but great work by great medical scientists.
There is considerable evidence that substance P (SP) is a key trigger for arthritic inflammation.3,4 Substance P is found in the terminals of afferent nerves densely innervating the joints affected by rheumatoid arthritis. The puzzle that no one can solve is why small afferent nerves carry 2-way traffic—sending sensory impulses centrally while at the same time releasing vesicles of SP antidromically. (The author will donate a case of wine for the first correct answer!) In rodents, neonatal depletion of SP from afferent joint nerve endings markedly reduces the induction of arthritis with Freund adjuvant—the classic experimental model of autoimmune arthritis.2,5,6
The neurogenic theory of arthropathy might explain why anticonvulsants often appear to exert a positive effect on so-called autoimmune diseases. Patients with epilepsy taking phenytoin seem to be at lower risk for autoimmune disorders.7 Scleroderma, very difficult to treat, was reported to respond to anticonvulsant drugs in studies conducted in the 1970s.8,9 Moreover, scleroderma might not afflict paralyzed limbs; a similar observation has been made with psoriasis.10
Our treatment of the so-called inflammatory cascade is passable: it provides pain relief and some disease modification—but it does not deal with the underlying cause of the cascade. Animal experimentation points clearly to the direct effect of a neurogenic influence, which I would humbly suggest is the initial stimulus. All of our attention in the past has been focused on the inflammatory cascade—its effect on blood chemistry and its response to therapeutic agents, such as steroids or nonsteroidal anti-inflammatory drugs—but we continue to ignore the cause.
Perhaps the greatest defect in modern medicine is that once we have gone down the wrong path, it is difficult to change direction or admit failure. Better sooner than later! Most have forgotten that for centuries we got the circulation of the blood wrong. A modern example is the hilarity and disdain that greeted the scientists who dared to propose that infection with Helicobacter pylori was the fundamental cause of ulcers. To quote a popular song—When will we ever learn?
The critical test is to electrically stimulate the afferent nerves innervating joints in animals to see if this can trigger inflammatory arthropathy—a very fast, very cheap experiment. Would anticonvulsant drugs provide protection also?
—Alan Russell MD MB MRCP
1. Glick EN. Asymmetrical rheumatoid arthritis after poliomyelitis. BMJ 1967;3:26-9.
2. Levine JD, Dardick SJ, Roizen MF, Helms C, Basbaum AI. Contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis. J Neurosci 1986;6(12):3423-9.
3. Holzer P. Local effector functions of capsaicin-sensitive sensory nerve endings: involvement of tachykinins, calcitonin gene-related peptide and other neuropeptides. Neuroscience 1988;24(3):739-68.
4. Levine JD, Moskowitz MA, Basbaum AI. The contribution of neurogenic inflammation in experimental arthritis. J Immunol 1985;135(2 Suppl):843s-7s.
5. Maggi CA, Meli A. The sensory-efferent function of capsaicin-sensitive sensory neurons. Gen Pharmacol 1988;19(1):1-43.
6. Niissalo S, Hukkanen M, Imai S, Tornwall J, Konttinen YT. Neuropeptides in experimental and degenerative arthritis. Ann N Y Acad Sci 2002;966:384-99.
7. Bobrove AM. Possible beneficial effects of phenytoin for rheumatoid arthritis. Arthritis Rheum 1983;26:118-9.
8. Morgan RJ. Scleroderma: treatment with diphenylhydantoin. Cutis 1971;8:278-82.
9. Neldner HK. Treatment of localized linear scleroderma with phenytoin. Cutis 1978;22:569-72.
10. Sethi S, Sequeira W. Sparing effect of hemiplegia on scleroderma. Ann Rheum Dis 1990;49(12):999-1000.
<shortened url>1: J Neurosurg. 2005 Mar;102(3):522-5.Links
Selective ablation of nociceptive neurons for elimination of hyperalgesia and neurogenic inflammation.Tender GC, Walbridge S, Olah Z, Karai L, Iadarola M, Oldfield EH, Lonser RR.
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1414, USA.
OBJECT: Neuropathic pain is mediated by nociceptive neurons that selectively express the vanilloid receptor 1 (VR1). Resiniferatoxin (RTX) is an excitotoxic VR1 agonist that causes destruction of VR1-positive neurons. To determine whether RTX can be used to ablate VR1-positive neurons selectively and to eliminate hyperalgesia and neurogenic inflammation without affecting tactile sensation and motor function, the authors infused it unilaterally into the trigeminal ganglia in Rhesus monkeys. METHODS: Either RTX (three animals) or vehicle (one animal) was directly infused (20 microl) into the right trigeminal ganglion in Rhesus monkeys. Animals were tested postoperatively at 1, 4, and 7 weeks thereafter for touch and pain perception in the trigeminal distribution (application of saline and capsaicin to the cornea). The number of eye blinks, eye wipes, and duration of squinting were recorded. Neurogenic inflammation was tested using capsaicin cream. Animals were killed 4 (one monkey) and 12 (three monkeys) weeks postinfusion. Histological and immunohistochemical analyses were performed. Throughout the duration of the study, response to high-intensity pain stimulation (capsaicin) was selectively and significantly reduced (p < 0.001, RTX-treated compared with vehicle-treated eye [mean +/- standard deviation]): blinks, 25.7 +/- 4.4 compared with 106.6 +/- 20.8; eye wipes, 1.4 +/- 0.8 compared with 19.3 +/- 2.5; and squinting, 1.4 +/- 0.6 seconds compared with 11.4 +/- 1.6 seconds. Normal response to sensation was maintained. Animals showed no neurological deficit or sign of toxicity. Neurogenic inflammation was blocked on the RTX-treated side. Immunohistochemical analysis of the RTX-treated ganglia showed selective elimination of VR1-positive neurons. CONCLUSIONS: Nociceptive neurons can be selectively ablated by intraganglionic RTX infusion, resulting in the elimination of high-intensity pain perception and neurogenic inflammation while maintaining normal sensation and motor function. Analysis of these findings indicated that intraganglionic RTX infusion may provide a new treatment for pain syndromes such as trigeminal neuralgia as well as others.
[/quote]Resiniferatoxin (RTX) is a naturally occurring, ultrapotent capsaicin analog that activates the vanilloid receptor in a subpopulation of primary afferent sensory neurons involved in nociception (the transmission of physiological pain). RTX causes a novel ion channel in the plasma membrane of sensory neurons — the transient receptor potential vanilloid 1 — to become permeable to cations, most particularly the calcium cation; this evokes a powerful irritant effect followed by desensitization and analgesia.
I started on 6-8 tablets last time, and had no problems. Its been a couple of days, and haven't had an issue as yet. If you want to see "extreme" bowel movements, try Homozone powder!gibbledygook wrote:Be cautious on the bowel. I plunged in with a fairly hefty dose and my bowel movements were, um, extreme!
Mine contains "Capsicum annum Fruit Powder", but has on the package "Also known as Cayenne" written on it in italics. I have also broke open a capsule, and it smells like cayenne to me. I love that spice, and found it hard to resist tasting it. It tasted the same to me, only maybe hotter.DenverCO wrote:Is cayenne pepper the same thing?
The heat in chillies is not only from capsaicin. So the heat of the product, does not directly equate to capsaicin content. Also, you can ingest considerably more when its wrapped in a plastic shell (ie a capsule), as opposed to trying to swallow the smallest amount of rocket fuel.NHE wrote:... A few drops of this stuff is probably the equivalent of an entire handful of cayenne peppers.
Wiki wrote:The substances that gives chili peppers their intensity when ingested or applied topically are capsaicin (8-methyl-N-vanillyl-6-nonenamide) and several related chemicals, collectively called capsaicinoids. Capsaicin is the primary ingredient in pepper spray.
From reading your posts, I have been cautious with these, but also try to have two during every meal. The way I do it is to have a few bites of the meal, take 1 tablet, finish nearly all the meal, take the second tablet, then finish the last 1 or 2 bites of my meal. I see this as keeping the little "depth charges" apart, and provide "padding" around each tablet. So far its worked a charm.gibbledygook wrote:When I have two pills for breakfast I have to eat protein otherwise I get a burning stomach
<shortened url>1: Biol Psychiatry. 1999 Aug 15;46(4):551-6. Links
Cerebrospinal fluid somatostatin, mood, and cognition in multiple sclerosis.Roca CA, Su TP, Elpern S, McFarland H, Rubinow DR.
Behavioral Endocrinology Branch, National Institute of Mental Health, Bethesda, Maryland, USA.
BACKGROUND: Cerebrospinal fluid (CSF) somatostatin (SS) levels have been shown to be decreased in multiple sclerosis (MS) during relapse as well as in disorders characterized by depression or cognitive impairment. Since MS is often associated with depression and cognitive impairment, we examined both the effect of course of illness on CSF SS as well as the variance in SS attributable to associated features (e.g., depression or cognitive impairment). METHODS: Fifteen patients with chronic progressive MS participating in a 2-year cyclosporine trial underwent lumbar punctures for CSF SS at baseline and at 12 and 24 months. Additionally, patients were evaluated by neuropsychological testing, and physical disability and mood ratings. Baseline CSF SS levels were also obtained in a group of control subjects (n = 10). RESULTS: At baseline, CSF SS levels were lower in MS patients than control subjects (p < .001). Decreased CSF SS at 24 months was correlated with decreased cognitive performance on several measures and was best and significantly predicted by cognitive deterioration at 24 months. CONCLUSIONS: Our data support those from previous studies that found lower levels of CSF SS in MS during relapse and suggest that changes in CSF SS are related to the process responsible for diminished cognitive function in MS.
<shortened url>1: Brain Res Bull. 1990 Sep;25(3):411-3. Links
Lumbar cerebrospinal fluid concentrations of somatostatin and neuropeptide Y in multiple sclerosis.Vécsei L, Csala B, Widerlöv E, Ekman R, Czopf J, Pàlffy G.
Department of Psychiatry and Neurochemistry, University of Lund, Sweden.
The cerebrospinal fluid (CSF) concentrations of somatostatin and neuropeptide Y were investigated by use of radioimmunoassay in patients suffering from chronic progressive multiple sclerosis. The somatostatin level was significantly decreased in the CSF of patients with multiple sclerosis compared to the control group. The magnitude of this change was more pronounced in patients with severe clinical symptoms of the illness. The CSF neuropeptide Y concentration did not differ from the control values. These findings suggest a selective involvement of somatostatin neurotransmission in multiple sclerosis.
<shortened url>1: Pharmacol Ther. 2006 Nov;112(2):440-56. Epub 2006 Jun 9. Links
Inhibitory effect of somatostatin on inflammation and nociception.Pintér E, Helyes Z, Szolcsányi J.
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, H-7624 Pécs, Szigeti u. 12, Hungary. email@example.com
The present review focuses on promising new opportunities for anti-inflammatory and analgesic therapy. The theoretical background is an original observation based on our own experimental results. These data demonstrate that somatostatin is released from capsaicin-sensitive, peptidergic sensory nerve endings in response to noxious heat and chemical stimuli such as vanilloids, protons or lipoxygenase products. It reaches distant parts of the body via the circulation and exerts systemic anti-inflammatory and analgesic effects. Somatostatin binds to G-protein-coupled membrane receptors (sst(1)-sst(5)) and diminishes neurogenic inflammation by prejunctional action on sensory-efferent nerve terminals, as well as by postjunctional mechanisms on target cells. It decreases the release of pro-inflammatory neuropeptides from sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory and immune cells. Analgesic effect is mediated by an inhibitory action on peripheral terminals of nociceptive neurons, since circulating somatostatin cannot exert central action. Somatostatin itself is not suitable for drug development because of its broad spectrum and short elimination half life, stable, receptor-selective agonists have been synthesized and investigated. The present overview is aimed at summarizing the physiological importance of somatostatin and sst receptors, pharmacological significance of synthetic agonists and their potential in the development of novel anti-inflammatory and analgesic drugs. These compounds might provide novel perspectives in the pharmacotherapy of acute and chronic painful inflammatory diseases, as well as neuropathic conditions.
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