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Cortisol, cytokines and the brain/ gut axis

Discussion in 'Adrenal Rx and Leaky Gut Rx' started by chocolate, Apr 5, 2012.

  1. chocolate

    chocolate Silver


    Wow, you think folks might have chance of getting off the 2k a month psych meds? Atypical treatment is good (usually means cheap). Wonder how much pharmaceutical companies make on it? Or the "good" shrinks? They decide what to kill your brain with.... I wonder how long til this stuff is mainstream? There is a cortisol communication problem if I am reading properly. The organ clocks are all timed differently....I think. I need to go back and read Docs blog.
  2. chocolate

    chocolate Silver

  3. nonchalant

    nonchalant Silver

    I don't think Dr. Kruse's protocols will make the drug companies very happy.
  4. LinD

    LinD New Member

  5. chocolate

    chocolate Silver

    I read that metformin is like calorie restriction and stops oxidative stress.


    Its listed in a wikipedia article as one of the things that helps. I just can't find the one.

    I've never heard anyone complain about metformin. I was afraid of it until I learned and am thinking about it. I am sure there are demyelination issues around my house. I will keep looking for it.


    there is a better article elsewhere, but this mentions it all.
  6. chocolate

    chocolate Silver


    This is pretty good about fructose intolerance.... dietary fructose intolerance, not hereditary. The zinc gets isolated and causes depression

    and all kinds of bad stuff, I guess fructose is a really bad anti-nutrient. Anyway, its a hospital guide that's short and sweet. Its seems like if you just got liquored up, you'd know what to expect. This is worse, IMO. I was a terrible mother with all the garbage yogurt and fruit.
  7. LinD

    LinD New Member

    I hear ya, Chocolate. (re: fruit a yogurt) :-( One of the areas for a needed do-over.
  8. I still kick myself that I thought I was helping my kids by insisting any juice they had was 100% juice, no sugar.
  9. Destiny

    Destiny New Member

    Most of us did, Merri.
  10. chocolate

    chocolate Silver

    avatar Jack Says: (CT-9 #210)

    April 13th, 2012 at 9:19 am

    @Russ LDL -pregnenlone conversion is for every steroid hormone…..and is needed for survival. That is how important it is.
  11. chocolate

    chocolate Silver

    avatar Jack Says:(CT-9 #235)

    April 13th, 2012 at 5:20 pm

    @Mark read this too…….From a summary of Nora Gegaudas talk at Paleo FX (and more insight into stress and inflammation and the importance of continuing on this path for our mental health as well as our physical!): (from: http://roosclues.blogspot.co.nz/2012…-function.html)… (thanks to Jennifer for posting on the Leptin RX thread)

    These notes are for one section of a talk given by Nora Gedgaudas during the Paleo Summit. She was refuting the idea of safe starches, put forward by Paul Jaminet (author of The Perfect Health Diet), and discussing hypoglycemia. She explains that hypoglycemia only occurs in people who are (unnaturally) temporarily adapted to getting glucose from dietary sugars and starches, and that for people who are fat burners- which is what the human body is adapted for- mood and cognitive functioning are not dependent on blood sugar levels. The human body can make all of the glucose it needs in the liver from amino acids, there is no need to get it from the diet.

    The exception to this, she explains, is when people have chronically depressed cortisol levels. What really caught my attention is that she says that this low cortisol production is not because the adrenals themselves have been “exhausted” by stress, which she says is an outdated idea. She says that cortisol output is not controlled by the glad itself, but by the brain. It is mitigated by the HPA (Hypothalamus Pituitary Axis), specifically by a group of cells inside the hypothalamus called the Paraventricular Nuclear cells (PVN). The level of cortisol that we produce depends on how these cells are stimulated- whether the balance of neurochemicals leans towards excitatory or inhibitory, but in particular by the presence of inflammatory cytokines. To rephrase that, low cortisol levels are caused by inflammation in the brain. Various stressors on the body result in the release of these cytokines, including chronic infection. This process can also impact our balance of neurotransmitters.
  12. chocolate

    chocolate Silver


    Using L-Tyrosine For Cortisol Fluctuation May Reduce Your Level Of Stress!


    When the body is under any type of stress, chemical and hormone reactions occur that leave the body susceptible to modification, which may be resolved with the medicinal use of L-Tyrosine for cortisol fluctuation. This is a substance which is released...

    L-tyrosine is in soy
  13. chasee33

    chasee33 Silver

    Chocolate your post about adrenal issues being tied to the HPA axis is very true. This is why phosphatidylserine is such a great supplement for people with "adrenal problems". PS breaks down in to small amounts of acetylcholine which have a high activity in the temporal lobes where part of this feed back occurs. This is also why many patients with "adrenal fatigue" also start to have difficulty with their memory. Salivary cortisol rhythm tests are shown in the literature to be great predictors of alzheimer's and dementia due to feedback cycle.
  14. Souldanzer

    Souldanzer Banned

  15. chocolate

    chocolate Silver


    Melatonin in mitochondrial dysfunction and related disorders.

    Srinivasan V, Spence DW, Pandi-Perumal SR, Brown GM, Cardinali DP.


    Sri Sathya Sai Medical, Educational and Research Foundation, Prashanthi Nilayam 40, Kovai Thirunagar Coimbatore 641014, India.


    Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.
  16. chocolate

    chocolate Silver


    Sleep Deprivation Blocks Hippocampal Neurogenesis Through Steroid Effect

    NEW YORK (Reuters Health) Nov 28 - Sleep deprivation causes a rise in glucocorticoid levels that works to inhibit neurogenesis in the hippocampus, results of an animal study suggest.

    This finding may help explain the adverse cognitive effects associated with sleep deprivation, according to the report in the November 28th Early Edition of the Proceedings of the National Academy of Sciences.

    In the new study, Dr. Elizabeth Gould and colleagues, from Princeton University in New Jersey, show that 72 hours of sleep deprivation in rats causes a drop in hippocampal neurogenesis, which coincides with an elevation in circulating levels of corticosterone.

    When corticosteroid levels were maintained at a normal level, the sleep-deprived animals no longer showed a reduction in hippocampal neurogenesis, the report indicates.
  17. chocolate

    chocolate Silver


    mt1 Melatonin Receptor in the Primate Adrenal Gland: Inhibition of Adrenocorticotropin-Stimulated Cortisol Production by Melatonin

    The pineal hormone melatonin participates in circadian, seasonal, and reproductive physiology. The presence of melatonin binding sites in human brain and peripheral tissues is well documented. However, in the mammalian adrenal gland, low-affinity melatonin binding sites have been detected only in the rat by some but not all authors. Conflicting evidence for a regulatory role of melatonin on adrenal cortisol production, prompted us to investigate this possibility in a New World primate, the capuchin monkey. Expression of melatonin receptors in the adrenal cortex was demonstrated through pharmacological characterization and autoradiographic localization of 2-[125I]iodomelatonin binding sites (dissociation constant = 96.9 ± 15 pm; maximal binding capacity = 3.8 ± 0.4 fmol/mg protein). The mt1 identity of these receptors was established by cDNA sequencing. Melatonin treatment of dispersed cells and explants from adrenal gland did not affect basal cortisol production. However, cortisol production stimulated by 100 nm ACTH was significantly inhibited by low melatonin concentrations (0.1–100 nm); this inhibitory effect was reversed by the mt1/MT2 melatonin antagonist luzindole. Melatonin also inhibited dibutyril-cAMP-stimulated cortisol production, suggesting that melatonin acts through a cAMP-independent signaling pathway. The present data demonstrate that the primate adrenal gland cortex expresses functional mt1 melatonin receptors and shows that melatonin inhibits ACTH-stimulated cortisol production.
  18. chocolate

    chocolate Silver


    Melatonin enhances endogenous heme oxygenase-1 and represses immune responses to ameliorate experimental murine membranous nephropathy.

    Idiopathic membranous nephropathy (MN), an autoimmune-mediated glomerulonephritis, is one of the most common causes of nephrotic syndrome in adults. Therapeutic agents for MN remain ill defined. We assessed the efficacy of melatonin therapy for MN. Experimental murine MN was induced with cationic bovine serum albumin, and the mice were immediately administered 20 mg/kg melatonin or phosphate-buffered saline subcutaneously once a day. Disease severity was verified by examining serum and urine metabolic profiles and renal histopathology. The expression of cytokines and oxidative stress markers, cell apoptosis, and the associated mechanisms were also determined. Mice treated with melatonin displayed a significant reduction in proteinuria and a marked amelioration of glomerular lesions, with attenuated immunocomplex deposition. The subpopulations of T cells were not altered, but the CD19(+) B-cell subpopulation was significantly reduced in the MN mice treated with melatonin. The expression of cytokine mRNAs in splenocytes indicated that melatonin reduced the expression of proinflammatory cytokines and increased the expression of anti-inflammatory cytokines (interleukin 10). The production of reactive oxygen species and TUNEL-positive apoptotic cells in the kidney were also significantly reduced in the melatonin-treated MN mice. Melatonin also upregulated heme oxygenase 1 (HO1) and ameliorated MN. The blockade of HO1 expression with SnPP, a HO1 inhibitor, attenuated HO1 induction by melatonin and thus mitigated its renoprotective effects during MN. Our results suggest that melatonin treatment ameliorates experimental MN via multiple pathways, including by its antioxidative, antiapoptotic, and immunomodulatory effects. Melatonin should be considered a potential therapeutic intervention for MN in the future

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