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MCF

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MCF last won the day on December 20 2011

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About MCF

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  • Birthday November 25

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  1. My symptoms involve worse psoriasis, intense itching post meal, very heavy, thumping rapid heart beat post meals, weakness, dizziness, fatigue, spine and neck pain, dental and facial pain, all gone unless I slip up. Turns out their are tons of mast cells in the spinal column, hence my histamine induced pinched nerve neck pains that are gone now. As for FMS, that went away for me years ago when I switched to low carb, just about overnight. Gastric dysfunction is one of the top three symptoms of HIT and small intestine bacterial overgrowth often is a cause of HIT. My case seems to be diamine oxidase deficiency related, my markers of mast cell activity don't seem to be high enough to indicate activation disorder or mastocytosis.
  2. Every single ache, pain in body, joint swellings, bloat disappeared once I began eating lower histamine. I was eating extremely high histamine, lots of high histamine veggies (check the list I posted) cooked slowly and kept unfrozen as leftovers, aged meats, braised for hours, kept unfrozen as leftovers, lots of tomatoes, pork and lamb, tons of fermented and soy based stuff in marinades and restaurant food. A great deal of shellfish and leftover fish bought unfrozen. A lot of stinky, aged cheeses. By eating only one or two ingredients per meal with nothing but salt, I identified lamb and pork as highly reactive and chicken, once, when it had been in my deep freeze for long. I can eat fresh turkey, chicken, beef and veal. I recently learned that washing off the surface is critical, since that's where most of the histamine forms. I also used almond flour, ate a lot of nuts (I tolerate macadamias and pistachios). I react much more strongly to histamine in foods than to the very few foods I tested mildly allergic to. I was gaining eating very low carb, pretty low calorie. I lost about 18lbs at first, 13 of it in 11 days, have kept it off.
  3. If is for me. This is not the same as food allergy, this is a reaction to the histamine content of foods, or foods that cause mast cells to release histamine, coupled with genetic or acquired deficiency of the enzyme that breaks down histamine in the normal gut: http://ajcn.nutrition.org/content/85/5/1185.long I've noticed that almost everyone on a histamine intolerance forum is diagnosed with Hashimoto's or "adrenal fatigue" or high cortisol and also have a lot of gut symptoms: "Histamine intolerance results from a disequilibrium of accumulated histamine and the capacity for histamine degradation. Histamine is a biogenic amine that occurs to various degrees in many foods. In healthy persons, dietary histamine can be rapidly detoxified by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity. Diamine oxidase (DAO) is the main enzyme for the metabolism of ingested histamine. It has been proposed that DAO, when functioning as a secretory protein, may be responsible for scavenging extracellular histamine after mediator release. Conversely, histamine N-methyltransferase, the other important enzyme inactivating histamine, is a cytosolic protein that can convert histamine only in the intracellular space of cells. An impaired histamine degradation based on reduced DAO activity and the resulting histamine excess may cause numerous symptoms mimicking an allergic reaction. The ingestion of histamine-rich food or of alcohol or drugs that release histamine or block DAO may provoke diarrhea, headache, rhinoconjunctival symptoms, asthma, hypotension, arrhythmia, urticaria, pruritus, flushing, and other conditions in patients with histamine intolerance. Symptoms can be reduced by a histamine-free diet or be eliminated by antihistamines. However, because of the multifaceted nature of the symptoms, the existence of histamine intolerance has been underestimated, and further studies based on double-blind, placebo-controlled provocations are needed. In patients in whom the abovementioned symptoms are triggered by the corresponding substances and who have a negative diagnosis of allergy or internal disorders, histamine intolerance should be considered as an underlying pathomechanism. Full text at the link. A food list to be used as a guide to finding if you have histamine food triggers. I was gaining a lb a day on little food until I started eating low histamine and taking diamine oxidase. Dropped a lot of weight in two weeks: http://www.histaminintoleranz.ch/download/foodlist/21_FoodList_EN_alphabetic_withCateg.pdf This is the best list online, but some folks tolerate high hist foods, and react to low ones, it's only a guide to help figure out if you have any degree of histamine intolerance. http://www.ncbi.nlm.nih.gov/pubmed/1369594 Neuroendocrinology. 1992 Dec;56(6):851-5. Histamine H1 and H2 receptor activation stimulates ACTH and beta-endorphin secretion by increasing corticotropin-releasing hormone in the hypophyseal portal blood. Kjaer A1, Knigge U, Plotsky PM, Bach FW, Warberg J. Author information AbstractHistamine (HA) stimulates the release of adrenocorticotropic hormone (ACTH) and beta-endorphin (beta-END) via activation of central postsynaptic H1 or H2 receptors. The effect of HA is indirect and may involve the hypothalamic regulating factors corticotropin-releasing hormone (CRH), arginine vasopressin, or oxytocin (OT). We studied the effect of specific HA H1 or H2 receptor agonists on the concentration of CRH and OT in hypophyseal portal blood in urethane-anesthetized male rats. In addition we investigated the effect of the agonists on ACTH and beta-END immunoreactivity in peripheral plasma in conscious male rats pretreated with antiserum to CRH. Intracerebroventricular administration of the H1 receptor agonist 2-thiazolylethylamine (2-TEA) or the H2 receptor agonist 4-methylhistamine (4-MeHA) increased the CRH concentration in pituitary portal blood by 80-90% when compared to preinfusion levels (p < 0.05). Central infusion of saline had no effect. The level of OT in the pituitary portal blood was not affected by 2-TEA or 4-MeHA when compared to saline-treated rats. Intracerebroventricular infusion of 2-TEA or 4-MeHA increased the ACTH concentration in peripheral plasma 3- or 4-fold, respectively (p < 0.01). Pretreatment with a specific CRH antiserum (abCRH) inhibited the responses by 50 and 70%, respectively (p < 0.01). Intracerebroventricular administration of 2-TEA or 4-MeHA increased the beta-END immunoreactivity in peripheral plasma 3- or 2-fold, respectively (p < 0.01). These effects were inhibited by 80-90%, when rats were pretreated with abCRH (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) PMID: 1369594 [PubMed - indexed for MEDLINE]
  4. Happy birthday to USSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSS........................! Thanks, MaryO! <*smooch*>
  5. Darlin, that's why I ALWAYS say, "those who are able" should donate. And I think it goes without saying that MaryO, by absorbing the expenses we don't cover, demonstrates it every year. Lots of us have been financially compromised by illness or unexpected life circumstances and still need the help, we all know it and understand.
  6. http://www.alltrials.net/2014/guest-post-people-with-rare-diseases-need-results-from-all-trial/ Guest Post: People with rare diseases need results from all trials 7th April 2014 By Rob Pleticha is the Online Community Manager of RareConnect.org, a EURORDIS project This is a personal opinion The International Rare Diseases Research Consortium plan to have 200 new rare diseases therapies by year 2020. In Europe a disease or disorder is defined as rare when it affects fewer than 1 in 2000 citizens.(1) Researchers studying rare diseases have difficulty gathering a sufficient number of people to join clinical trials in order to reach statistically significant results that can impact treatment. Clinical trial transparency and sharing of clinical trial data is fundamental in advancing rare disease research.
  7. http://www.healio.com/endocrinology/adrenal/news/online/%7B470d2ab6-ad4b-4b26-aa51-46822a0f261a%7D/higher-carbohydrate-intake-may-increase-intracellular-cortisol Higher carbohydrate intake may increase intracellular cortisol Stimson RH. J Clin Endocrinol Metab. 2013;doi:10.1210/jc.2013-2307. Macronutrients stimulated a postprandial rise in circulating cortisol in lean, healthy men, according to researchers in the United Kingdom. “These observations provide a novel insight into the complexity of circadian control ofglucocorticoid secretion,” researchers wrote.Plasma cortisol appeared to increase similarly after all macronutrient meals were compared with placebo, according to data. The carbohydrate meal stimulated adrenal secretion and extra-adrenal regeneration of cortisol in a similar way. Eight lean, healthy men aged 23.5 years were randomly assigned to three different liquid isocaloric single macronutrient meals (carbohydrate, protein or fat) to test the contribution of peripheral cortisol regeneration to macronutrient-induced circadian variation of plasma control, according to data. “Following the carbohydrate meal, plasma cortisol rose compared with placebo (P<.05),” researchers wrote. Eating raises cortisol, eating carbs keeps it raised by inhibiting clearance from the blood stream.
  8. The year is almost over and we've contributed only about 1/3 of the costs needed to support this site. There are plenty of folks without the means to contribute, but many folks who can spare a buck or ten. The archives on this site alone are priceless, there's nothing and nowhere that can help us save our own lives the way they have and will. If we keep the site up and running. Thanks to MaryO for not giving up on it and us.
  9. Thanks for the reminder, Robin and thanks MaryO, once again, for these boards and for keeping all this archived information online at great effort and expense. Off to Paypal you a donation right NOW.
  10. I signed the petition because I think too many people are gunea pigs for drugs whose risks are unreported until many have been injured. As one Harvard cardiologist said, "Drug companies own medicine." http://www.alltrials.net/ I It's time all clinical trial results are reported. Patients, researchers, pharmacists, doctors and regulators everywhere will benefit from publication of clinical trial results. Wherever you are in the world please sign the petition: Thousands of clinical trials have not reported their results; some have not even been registered. Information on what was done and what was found in these trials could be lost forever to doctors and researchers, leading to bad treatment decisions, missed opportunities for good medicine, and trials being repeated. All trials past and present should be registered, and the full methods and the results reported. We call on governments, regulators and research bodies to implement measures to achieve this.
  11. I agree, BDen. It's a gift to bariatric surgeons, lap band and obesity drug makers, quacks like Dean Ornish, who the Clinton's shoehorned in as paid treatment by the government and insurers. Obesity is a sign of myriad conditions and diseases, it is not a disease. It's a marker with multiple causes.
  12. Thanks for posting, I saw this somewhere yesterday but hadn't taken the time to read the summary descriptions.
  13. Actually, a lot of what's labeled recurrence is failure to attain surgical cure. Criteria and definitions of "cure" are kind of variable from surgeon to surgeon and they have an incentive to paint the rosiest picture of their own success rates. Over the years that I've been reading here and elsewhere, the cure rate from first surgeries is pretty low. That's not due to lack of surgical skill or care choosing surgeons, just the complex nature of HPA axis disorders and the lack of firm borders and definition of pituitary tumors as compared to other types of tumor. Then you have hyperplasia of the pituitary gland or in adrenals that have been overstimulated for years by an overactive pit tumor, still causing symptoms. If someone sees a cortisol rise weeks after pit surgery, it is often labeled recurrence if they had an earlier drop post op. But so many folks are cylical before and after... Conversely, research has demonstrated that folks who *are* cured may not see their cortisol drop until weeks post op, though I doubt any surgeon is failing to count those as cures, too, if they don't require additional surgery.
  14. I don't think the percentage is small at all. http://home.comcast.net/~staticnrg/Cushings/LongTermRemissionRates.pdf "Conclusions The overall remission rate of 56% (35/63) at 9·6 years follow-up is disappointing and merits some re-appraisal of the widely accepted principle that pituitary surgery must be the initial treatment of choice in pituitary-dependent Cushing’s syndrome. Following pituitary surgery, careful ongoing expert endocrine assessment is mandatory as the incidence of relapse increases with time and also with increasing rigour of the endocrine evaluation. A significant number of our patients were shown to have relapsed with a cyclical form of hypercortisolism"
  15. MCF

    High Cortisol and DHEA?

    I also think you should have other androgens, and aldosterone and renin tested. You're high all the time, could be adrenal rather than pituitary if it is Cushing's. The multiple times normal on the tests you listed is highest at midnight, suggesting that you actually do have reversal of diurnal rhythm within consistently high results all day.
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