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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Chlorogenic Acid in Coffee is powerful Immune modulator


Chlorogenic Acid in Coffee is powerful Immune modulator
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wrotek
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 Posted: Mon Feb 10th, 2014 22:58

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What it means more precisely is that while caffeine blocks adenosine receptors, in the same time Chlorogenic Acids block adenosine transporter counteracting actions of caffeine.

Adenosine transporter is suppose to remove excess of adenosine, but when blocked adenosine levels stay higher and displace caffeine from receptors.



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wrotek
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 Posted: Fri Feb 14th, 2014 05:19

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Caffeine is non specific phosphodiesterase blocking agent, so is theophylline.
http://ceaccp.oxfordjournals.org/content/7/6/203.full

and there are 11 types of this enzyme
http://ceaccp.oxfordjournals.org/content/7/6/203/T1.expansion.html

Some of them are involved in immune system
like

PDE-4
Phosphodiesterase 4 Inhibition Reduces Innate Immunity and Improves Isoniazid Clearance of Mycobacterium tuberculosis in the Lungs of Infected Mice
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017091

PDE-5
Phosphodiesterase-5 inhibition augments endogenous antitumor immunity by reducing myeloid-derived suppressor cell function.
http://www.ncbi.nlm.nih.gov/pubmed/17101732

PDE-7
Ubiquitous expression of phosphodiesterase 7A in human proinflammatory and immune cells.
http://www.ncbi.nlm.nih.gov/pubmed/12388353

Last edited on Fri Feb 14th, 2014 05:22 by wrotek



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 Posted: Sat Mar 15th, 2014 07:18

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More bad news "buyer beware"
They are selling chlorogenic acid for weight control..
http://greencoffeexfatburn.com/?28/12



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 Posted: Sat Mar 15th, 2014 13:45

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The link does not work :) but i saw those pills, I actually think that chlorogenic acid may increase weight gain since it acts like a steroid.




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 Posted: Thu May 1st, 2014 22:38

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http://www.ncbi.nlm.nih.gov/pubmed/23888332

Caffeic acid regulates LPS-induced NF-κB activation through NIK/IKK and c-Src/ERK signaling pathways in endothelial cells.



Abstract

The redox sensitive, proinflammatory nuclear transcription factor NF-κB plays a key role in inflammation. In a redox state disrupted by oxidative stress, pro-inflammatory genes are upregulated by the activation of NF-κB via diverse kinases. Thus, the search and characterization of new substances that modulate NF-κB are topics of considerable research interest. Caffeic acid is a component of garlic, some fruits, and coffee, and is widely used as a phenolic agent in beverages. In the present study, caffeic acid was examined with respect to the modulation of inflammatory NF-κB activation via the redox-related c-Src/ERK and NIK/IKK pathways via the reduction of oxidative stress. YPEN-1 cells (an endothelial cell line) were used to explore the molecular mechanism underlying the anti-inflammatory effect of caffeic acid by examining its modulation of NF-κB signaling pathway by LPS. Our results show that LPS-induced oxidative stress-related NF-κB activation upregulated pro-inflammatory COX-2, NF-κB targeting gene which were all inhibited effectively by caffeic acid. Our study shows that caffeic acid inhibits the activation of NF-κB via the c-Src/ERK and NIK/IKK signal transduction pathways. Our results indicate that antioxidative effect of caffeic acid and its restoration of redox balance are responsible for its anti-inflammatory action. Thus, the study provides new information regarding the anti-inflammatory properties of caffeic acid and the roles in the regulation of LPS-induced oxidative stress induces alterations in signal transduction pathways.

Last edited on Thu May 1st, 2014 22:39 by wrotek



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 Posted: Thu May 1st, 2014 22:43

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Chlorogenic acid attenuates ventricular remodeling after myocardial infarction in mice.Kanno Y1, Watanabe R, Zempo H, Ogawa M, Suzuki J, Isobe M.Author information AbstractChlorogenic acid (CGA), which is a key component of coffee, has many biological effects such as anti-inflammation activity. However, the effects of CGA on ventricular remodeling after myocardial ischemia have not been well investigated. To test the hypothesis that CGA can attenuate chronic ventricular remodeling after myocardial ischemia, we orally administered CGA to murine myocardial ischemia models. Seven to nine week-old C57BL/6 mice were used. A myocardial infarction (MI) model was produced by permanent ligation of the left anterior descending coronary artery (LAD) using an 8-0 suture passed under the arteries. These mice were randomly assigned into 4 groups in each experimental model. Some MI mice were supplemented orally with CGA (30 mg/kg/day, MI+CGA group, n = 13) as a CGAtreated MI group, and other MI mice received vehicle (MI+vehicle group, n = 11) as a vehicle-treated MI group. Shamoperated mice without MI also received vehicle (Sham+vehicle group, n = 3) as a sham group, and sham-operated mice without MI received CGA (30 mg/kg/day, Sham+CGA group, n = 8) as a Sham+CGA group. Just before sacrifice on day 14, we measured blood pressure and heart rate and performed echocardiography. We obtained 3 transverse sections per heart for histopathologic examination. There were no differences in body weight, heart rate, or blood pressure among the groups on day 14. The vehicle-treated MI group showed significantly impaired left ventricular contraction compared to the sham-operated group. However, the CGA-treated MI group showed significantly improved ventricular contraction compared to the vehicle-treated MI group. Severe myocardial fibrosis with enhanced macrophage infiltration was observed in the vehicle-treated ischemia group on day 14. CGA attenuated these fibrotic changes with suppressed macrophage infiltration without systemic adverse effects. CGA may effectively suppress chronic ventricular remodeling after myocardial ischemia because it is critically involved in the suppression of macrophage infiltration.
Does this study say that CGA stops macrophage movement/activity ?

Last edited on Thu May 1st, 2014 22:44 by wrotek



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 Posted: Mon May 5th, 2014 04:23

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Anti-Angiogenic and Anti-Inflammatory Properties of Kahweol, a Coffee Diterpene
http://www.ncbi.nlm.nih.gov/pubmed/21858104

Last edited on Mon May 5th, 2014 04:23 by wrotek



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 Posted: Tue May 6th, 2014 00:48

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http://www.ncbi.nlm.nih.gov/pubmed/23579598

Chlorogenic acid decreases retinal vascular hyperpermeability in diabetic rat model.
from full paper
VEGF expression with immunohistochemistry and Western blot analysis. VEGF ex- pression in endothelial cells (arrows) was suppressed by chlorogenic acid administration in diabetic rats (scale bar: 50 µm). *P < 0.05 compared with control, † P < 0.05 compared with STZ. STZ, streptozotocin; CGA10, chlorogenic acid 10 mg/kg; CGA20, chlorogenic acid 20 mg/kg; GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer.



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 Posted: Thu May 8th, 2014 01:34

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So in conclusion, coffee contain 3 chemicals that prevent sprouting of a new blood vessels (they are antiangiogenic) - caffeine, chlorogenic acid, kahweol.

Angiogenesis is very important for tissues healing

Last edited on Thu May 8th, 2014 01:35 by wrotek



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 Posted: Thu May 8th, 2014 09:09

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Hmm, the western, industrialized nations seem to be coffee-addicted. Are we slowly but collectively killing ourselves by inhibiting angiogenesis then?

How important is this for currently healthy people? How important is it for those of us who are already immuno-compromised?

I use coffee to block runaway IP, but now wonder if I ought to try giving it up altogether.



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 Posted: Thu May 8th, 2014 09:15

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Well i know anecdotal stories, like this guy who avoided amputation of legs due to quitting caffeine increasing water intake etc...

There is a problem with angiogenesis in diabetes.

Imagine, how can You heal tissue if it has poor circulation, deliver drugs there etc...

Last edited on Thu May 8th, 2014 09:16 by wrotek



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 Posted: Sun May 25th, 2014 00:24

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Antiangiogenic properties of cafestol, a coffee diterpene, in human umbilical vein endothelial cells.
http://www.ncbi.nlm.nih.gov/pubmed/22525673

Last edited on Sun May 25th, 2014 00:32 by wrotek



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 Posted: Sun May 25th, 2014 05:16

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Adenosine receptors and fibrosis: a translational review
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3186039/

AbstractAdenosine—a purine nucleoside generated extracellularly from adenine nucleotides released by cells as a result of direct stimulation, hypoxia, trauma, or metabolic stress—is a well-known physiologic and pharmacologic agent. Recent studies demonstrate that adenosine, acting at its receptors, promotes wound healing by stimulating both angiogenesis and matrix production. Subsequently, adenosine and its receptors have also been found to promote fibrosis (excess matrix production) in the skin, lungs, and liver, but to diminish cardiac fibrosis. A commonly ingested adenosine receptor antagonist, caffeine, blocks the development of hepatic fibrosis, an effect that likely explains the epidemiologic finding that coffee drinking, in a dose-dependent fashion, reduces the likelihood of death from liver disease. Accordingly, adenosine may be a good target for therapies that prevent fibrosis of the lungs, liver, and skin.

Last edited on Sun May 25th, 2014 08:20 by wrotek



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 Posted: Fri May 30th, 2014 23:37

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Effects of Caffeine on Intermittent Hypoxia in Infants Born Prematurely: A Randomized Clinical Trial (2014)

http://www.ncbi.nlm.nih.gov/pubmed/24445955
http://www.medscape.com/viewarticle/825421

Study Findings

Across each postmenstrual age week, the infants who received caffeine demonstrated fewer episodes of intermittent hypoxia and spent less time, on average, below 90% oxygen saturation. For example, at 35 weeks' postmenstrual age, infants in the treatment group experienced 3.6 episodes of intermittent hypoxia per hour of recording compared with 8.4 episodes in the placebo group. This represented 52% fewer episodes. Similarly, the treatment group experienced 50.9 seconds per hour of saturation < 90% compared with 106 seconds among the placebo group.

The general pattern of less frequent episodes of intermittent hypoxia and reduced mean time with saturations < 90% was present across all postmenstrual age weeks, but the differences only reached statistical significance in the groups at 35 and 36 weeks' postmenstrual age. Although the pattern held for infants of 37, 38, and 39 weeks' postmenstrual age, the 95% confidence intervals for those differences all included 1. That said, even at 39 weeks' postmenstrual age, treatment group infants experienced 2.2 episodes of intermittent hypoxia per hour of recording vs 3.0 episodes per hour among the placebo group, but each group experienced approximately 40 seconds of oxygen saturation < 90% per hour of recording.

In 5 of the treatment infants, caffeine was discontinued as a result of tachycardia, but no other significant adverse events were noted. Rhein and colleagues conclude that extended treatment with caffeine for premature infants previously treated with caffeine can reduce the frequency and duration of intermittent hypoxia episodes.

Viewpoint

I'll go out on a limb and presume that many pediatric providers won't be thrilled at the prospect of premature infants spending even more time on caffeine, but these are results are very eyebrow-raising. The authors are very careful to comment that this study measures an intermediate outcome: reduction of potentially harmful events. In their discussion, they comment that it would be very important to demonstrate that the reduction of intermittent hypoxia actually produces clinical benefits, such as improved neurologic or other outcomes, in premature infants. They also allude to data from other studies that suggest that caffeine doses may have to be adjusted for older premature infants, those above 36 weeks' gestation, as a potential explanation for why the differences in intermittent hypoxia among the older infants did not reach statistical significance.



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 Posted: Tue Sep 23rd, 2014 23:37

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http://www.ncbi.nlm.nih.gov/pubmed/25153081

Anti-Inflammatory Activity of Odina wodier Roxb, an Indian Folk Remedy, through Inhibition of Toll-Like Receptor 4 Signaling Pathway.
Ojha D1, Mukherjee H2, Mondal S2, Jena A2, Dwivedi VP2, Mondal KC3, Malhotra B4, Samanta A5, Chattopadhyay D2.
Author information

Abstract
Inflammation is part of self-limiting non-specific immune response, which occurs during bodily injury. In some disorders the inflammatory process becomes continuous, leading to the development of chronic inflammatory diseases including cardiovascular diseases, diabetes, cancer etc. Several Indian tribes used the bark of Odina wodier (OWB) for treating inflammatory disorders. Thus, we have evaluated the immunotherapeutic potential of OWB methanol extract and its major constituent chlorogenic acid (CA), using three popular in vivo antiinflammatory models: Carrageenan- and Dextran-induced paw edema, Cotton pellet granuloma, and Acetic acid-induced vascular permeability. To elucidate the possible anti-inflammatory mechanism of action we determine the level of major inflammatory mediators (NO, iNOS, COX-2-dependent prostaglandin E2 or PGE2), and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-12). Further, we determine the toll-like receptor 4 (TLR4), Myeloid differentiation primary response gene 88 (MyD88), c-Jun N-terminal kinases (JNK), nuclear factor kappa-B cells (NF-κB), and NF-kB inhibitor alpha (IK-Bα) by protein and mRNA expression, and Western blot analysis in drug treated LPS-induced murine macrophage model. Moreover, we determined the acute and sub-acute toxicity of OWB extract in BALB/c mice. Our study demonstrated a significant anti-inflammatory activity of OWB extract and CA along with the inhibition of TNF-α, IL-1β, IL-6 and IL-12 expressions. Further, the expression of TLR4, NF-κBp65, MyD88, iNOS and COX-2 molecules were reduced in drug-treated groups, but not in the LPS-stimulated untreated or control groups, Thus, our results collectively indicated that the OWB extract and CA can efficiently inhibit inflammation through the down regulation of TLR4/MyD88/NF-kB signaling pathway.


PMID: 25153081 [PubMed - in process] PMCID: PMC4143220 Free PMC Article
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Last edited on Tue Sep 23rd, 2014 23:39 by wrotek



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 Posted: Wed Sep 24th, 2014 05:42

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Toll-like receptor 4 is a protein that in humans is encoded by the TLR4 gene.[1][2] TLR 4 is a toll-like receptor. It detects 
lipopolysaccharide from Gram-negative bacteria and is thus important in the activation of the innate immune system

http://en.m.wikipedia.org/wiki/TLR4

LPS is the major component of the outer membrane of Gram-negative bacteria, contributing greatly to the structural integrity of the bacteria, and protecting the membrane from certain kinds of chemical attack. LPS also increases the negative charge of the cell membrane 

http://en.m.wikipedia.org/wiki/Lipopolysaccharide



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 Posted: Thu Sep 25th, 2014 01:28

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Sure toll like receptor 4 was discussed many times
http://mpkb.org/home/search?cx=013271705758360138132%3A_v88fj6gxwk&cof=FORID%3A10&ie=UTF-8&q=toll+like+receptor&sa.x=51&sa.y=21&sa=Search

in alcohol
http://mpkb.org/home/food/alcohol

and innate immune system
http://mpkb.org/home/pathogenesis/innate_immunity



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 Posted: Thu Sep 21st, 2017 19:46

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I went reading all the posts in this thread, 35 pages, and found this to be salient (besides the central theme of CGA). (Bolded part I believe presumes - diet source of serum 25D - Microbiome not generating the serum 25D.)
Prof Trevor Marshall wrote:
You know, one of the problems of relying upon peer-reviewed papers is that so many of them are incorrect, and most (nearly all) are more than a few years old, and of questionable value (the translocation papers are too old to be useful, IMO).

Mouse were recently bred without the D Binding Protein (DBP), and lived perfectly normal lives, reproducing normally. Yet they had zero (yes, ZERO) circulating levels of 1,25-D in their bloodstreams.

http://www.ncbi.nlm.nih.gov/pubmed/18372326

This tells us that Adams et al's hypothesis that DBP is necessary for translocation is almost certainly not true, because the mice would not be healthy without translocation.

Secondly, this tells us that 1,25-D is not a circulating signal hormone, but a metabolite leaking through the cell wall into the bloodstream. Which is why it is at such a low concentration. Look at this diagram: (the I and V are vertical arrows, BTW)

25-D  in bloodstream at 40nanomolar
|
V
20 times attenuation
|
V
Cell Cytoplasm, 25- D and 1,25-D both at about 2 nanomolar
|
V
20 times attenuation
|
V
1,25-D transported by DBP in the bloodstream at 100 picomolar

Which implies that 25-D leaks from the bloodstream through the phospholipid bilayer (which forms the cell wall) into the cytoplasm, and 1,25-D leaches out from the cytoplasm into the bloodstream (each with about a 20 times concentration attenuation compared to the cytoplasm).

It also implies that the cell gets all the Vitamin D it needs from its own internal sources, and the circulating 25-D contribution from diet, etc, is purely collateral damage from eating and hunting, as it is ultimately immunosuppressive.


See, it's quite easy to turn the whole scientific world on its head :)

..Trevor..



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 Posted: Thu Sep 21st, 2017 20:33

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mvanwink5 wrote: I went reading all the posts in this thread, 35 pages, and found this to be salient
Indeed it is. Thanks for the re-post and sharing the conclusion of your effort Mike. :cool:

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 Posted: Thu Sep 21st, 2017 21:31

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I had been wondering why the serum 25D did not start increasing towards 18 ng/ml.
It also implies that the cell gets all the Vitamin D it needs from its own internal sources, and the circulating 25-D contribution from diet, etc, is purely collateral damage from eating and hunting, as it is ultimately immunosuppressive.
This explains it. Nearly all the serum 25D is coming from external sources (if one includes the Microbiome especially gut).



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