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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
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  ...  35  36  37  38  39  40   
 

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Dmitry
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 Posted: Sun Mar 10th, 2019 07:01

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My vote goes to ferritin. If one can compare his/her ferritin value on and off caffeine(and any other commonly used palliative drug/measure) that would be very interesting. Ferritin corresponds to MAF(macrophage activation syndrome) among other things and there is a new study which shows a rise of endogenous lactoferrin production together with ferritin (https://cyberleninka.ru/article/n/svoystva-i-kliniko-diagnosticheskoe-znachenie-opredeleniya-laktoferrina-i-ferritina-pri-ostrom-pankreatite use google translate) and lactoferrin(dual anti and pro infl. effects) by itself activate macrophages(recent Pubmed research for what it's worth). And I'd choose CRP as a second best marker. Then hemoglobin, monocytes, ESR(SED).

Last edited on Sun Mar 10th, 2019 07:21 by Dmitry



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 Posted: Mon Mar 11th, 2019 22:16

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"Tests" from MPKB.org and web you can look up and discuss with your physician. (One warning: Choose wisely. Excessive testing can trigger a mandatory script or action outcomes by many physicians working on a tight leash to act within standard of care boundaries per payer, clinic, or hospital. Some more common tests do not cause problems.)

Inflammation/Disease Markers
C-Reactive Protein (CRP)
The Complete Thyroid Report
Cholesterol and triglycerides (lipids)
Fasting Insulin
A1C
Serum Ferritin
Red Blood Cell Width (RDW)

Other tests
liver function/enzymes other than CRP
"Unfiltered coffee (boiled or pressed) may cause elevations of serum liver enzyme levels."
(Chronic Hepatitis Tina M. St. John MD, in Integrative Medicine (Fourth Edition), 2018, https://www.sciencedirect.com/topics/neuroscience/chlorogenic-acid)

Also remember that some advanced tests often come with "advanced" followup procedures/therapies/scripts that may not always be compatible with the MP, so when working with a physician/payer/etc network that monitors/insures/tracks/licenses physician, work to track test results without taking the same level of alarm often associated with standard-of-care expectations, and won't unusually draw undue attention to your Dr or his/her career over the span of many years.

Some on the MP have tracked objective markers with their physicians and identified returning to healthy markers on the MP alone. Do searches on this site and MPKB.org and find those reports to help you prepare and negotiate options with your physcian.

Choose wisely (repeating this on purpose), specifically markers that have to do with your unique diagnosis (not someone else's on the MP).

Just because a test tracks inflammation doesn't mean it is very specific or helpful. Also, the Dr may need to justify any frequent test if it is expensive, even if you pay out of pocket but that might be a way to stay off payer or actuary table alerts.

Other choices for tests might include markers that rarely return to normal ranges even with standard-of-care palliative options, but have done so with the MP. Watch Dr Marshall's international presentations and others from the ARF to see objective markers that may be of value as you make a objective marker testing decisions with your physician.

Wikipedia summary on Coffee: Research indicates coffee is considered generally "healthy" to drink, except for an increased risk in women having bone fractures, and a possible increased risk in pregnant women of fetal loss or decreased birth weight (MP olmesartan also not advised for pregnancy). Also, studies suggest that anxiety is amplified by coffee and consumption of 2 cups per/day was associated with a 14% increased risk of developing lung cancer, but only among people who smoke.

__________________
Side note
My personal opinion of any one dietary item consumed for centuries of mankind being the end all be all autoimmune poison or panacea is that we aren't going to see just one item on either list. Instead, what seems to be the pattern is a complex set of factors acting at the same time for a long period of time, usually including ongoing stress and anxiety, for immune collapse.

The return to health also seems to include a complex solution set. That meas a couple of quarts or so of coffee a week is not going to be the reason people get well or Finland, that boasts a whopping 12kg per capita per year coffee consumption, might land a little higher toward the top of the longevity list or list of most healthiest nations.

Best to all--Janet



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 Posted: Wed Mar 13th, 2019 07:26

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Adenosine plasma level correlates with homocysteine and uric acid concentrations in patients with coronary artery disease
https://www.nrcresearchpress.com/doi/abs/10.1139/cjpp-2015-0193
The role of hyperhomocysteinemia in coronary artery disease (CAD) patients remains unclear. The present study evaluated the relationship between homocysteine (HCys), adenosine plasma concentration (APC), plasma uric acid, and CAD severity evaluated using the SYNTAX score. We also evaluated in vitro the influence of adenosine on HCys production by hepatoma cultured cells (HuH7). Seventy-eight patients (mean age ± SD: 66.3 ± 11.3; mean SYNTAX score: 19.9 ± 12.3) and 30 healthy subjects (mean age: 61 ± 13) were included. We incubated HuH7 cells with increasing concentrations of adenosine and addressed the effect on HCys level in cell culture supernatant. Patients vs. controls had higher APC (0.82 ± 0.5 μmol/L vs 0.53 ± 0.14 μmol/L; p < 0.01), HCys (15 ± 7.6 μmol/L vs 6.8 ± 3 μmol/L, p < 0.0001), and uric acid (242.6 ± 97 vs 202 ± 59, p < 0.05) levels. APC was correlated with HCys and uric acid concentrations in patients (Pearson‘s R = 0.65 and 0.52; p < 0.0001, respectively). The SYNTAX score was correlated with HCys concentration. Adenosine induced a time- and dose-dependent increase in HCys in cell culture. Our data suggest that high APC is associated with HCys and uric acid concentrations in CAD patients. Whether the increased APC participates in atherosclerosis or, conversely, is part of a protective regulation process needs further investigations.

Heavy coffee consumption and plasma homocysteine: a randomized controlled trial in healthy volunteers.
https://www.ncbi.nlm.nih.gov/pubmed/11063436
RESULTS:
The mean (+/-SD) plasma concentration of total homocysteine in fasting blood was 8.1 +/- 1.8 micromol/L after abstention from coffee and 9.6 +/- 2.9 micromol/L after 3-4 wk of coffee drinking, a difference of 1.5 micromol/L (95% CI: 0.9, 2.1 micromol/L) or 18% (P: < 0.001). Coffee increased homocysteine concentrations in 24 of 26 individuals. Circulating concentrations of vitamin B-6, vitamin B-12, and folate were unaffected.
CONCLUSION:
Drinking large quantities of paper-filtered coffee raises fasting plasma concentrations of total homocysteine in healthy individuals.


Caffeine and Selective Adenosine Receptor Antagonists as New Therapeutic Tools for the Motivational Symptoms of Depression
https://www.frontiersin.org/articles/10.3389/fphar.2018.00526/full
Caffeine is a non-selective adenosine antagonist for A1/A2A receptors, and has been demonstrated to modulate behavior in classical animal models of depression. Moreover, selective adenosine receptor antagonists are being assessed for their antidepressant effects in animal studies. This review focuses on how caffeine and selective adenosine antagonists can improve different aspects of depression in humans, as well as in animal models. The effects on motivational symptoms of depression such as anergia, fatigue, and psychomotor slowing receive particular attention. Thus, the ability of adenosine receptor antagonists to reverse the anergia induced by dopamine antagonism or depletion is of special interest. In conclusion, although further studies are needed, it appears that caffeine and selective adenosine receptor antagonists could be therapeutic agents for the treatment of motivational dysfunction in depression.
...
Caffeine is a naturally occurring methylxanthine that acts mainly as a non-selective A1 and A2A adenosine receptor antagonist (Fredholm et al., 1999). This methylxanthine is found in common beverages including coffee, tea, soft drinks, and products containing cocoa, as well as a variety of medications and dietary sources (Barone and Roberts, 1996; Wikoff et al., 2017), ranking as one of the most commonly consumed dietary ingredients throughout the world (Heckman et al., 2010). Daily intake of caffeine among consumers in United States is about 280 mg, and higher intakes are estimated in some European countries (Barone and Roberts, 1996). Caffeine is typically consumed in order to increase alertness, arousal and energy (Malinauskas et al., 2007). Its consumption has been related to changes in cognitive performance and mood in normal population (Smith, 2013; Pasman et al., 2017). However, it enhances performance more in fatigued than well-rested subjects (Lorist et al., 1994; Childs and de Wit, 2008).
...
Multiple reports have lent support to the idea that depressed people could use caffeine as self-medication. It has been reported that psychiatric patients show a relatively high degree of caffeine consumption compared to the normal population (Greden et al., 1978; Leibenluft et al., 1993; Rihs et al., 1996). This appears to be particularly true in patients that have experienced depressive symptoms (Leibenluft et al., 1993). Different profiles of patients (i.e., with alcohol dependence, seasonal affective disorder, and people with MDD) have been shown to have higher levels of caffeine consumption after experiencing depressive symptoms (as shown by the Hamilton Rating Scale for depression) (Hamilton, 1967; Leibenluft et al., 1993). Specially, among youth with depression, there generally is higher caffeine consumption that in the general population (Whalen et al., 2008). Moreover, the degree of caffeine consumption seems to be a predictor of improvement of somatic symptoms (fatigue among them), and hostility in depressed patients medicated with fluoxetine (Worthington et al., 1996), suggesting that caffeine could be an effective co-treatment for some of the symptoms of depression. However, it is important to note that, at high doses or in people with susceptibility, caffeine is also known to increase anxiety and insomnia (for a review Temple et al., 2017), two side effects that can contribute to worsen MDD. At high doses, however, it has been demonstrated that caffeine may not act as an adenosine receptor antagonist, and other underlying mechanisms seem responsible of its negative effects (for a recent review Fredholm et al., 2017).
...
In addition, a broad range of studies have reported effects of caffeine withdrawal on different markers of motivation using descriptors such as fatigue, decreased energy or vigor, lethargy, amotivation for work, etc. (for a review see Juliano and Griffiths, 2004). For example, in controlled studies, after 10 days of high levels of caffeine consumption (1,250 mg/day), withdrawal results in increased subjective ratings of headache, sleepiness, laziness, and fatigue, as well as decreased alertness, activation and vigor (Juliano et al., 2012). Abstinence from intermediate doses in daily coffee and cola consumers (579 mg/day), increased ratings of drowsy/sleepy, fatigue/tired, lazy/sluggy/slow-moving, decreased ratings of active/energetic/excited and motivation to work, and impaired performance on psychomotor tasks (Liguori and Hughes, 1997). Even at low quantities (100 mg/day, in a controlled study), caffeine withdrawal increased ratings of lethargy, fatigue, tiredness, and sluggishness, and decreased ratings of energy, motivation and urge to work (Griffiths et al., 1990).

A2A Receptor Antagonists have Therapeutic Actions on Cytokine-Induced Fatigue

Cytokines are signaling molecules for the immune system mediating physiological responses to infection (Dantzer, 2001). These molecules also mediate a set of behavioral signs that include depressed activity and loss of interest or motivation (Kent et al., 1992). Compared to the general population, depressed patients have elevated levels of proinflammatory cytokines such as tumor necrosis factor alpha (TN-alpha) interleukin-1β (IL-1β), and IL-6 (Dowlati et al., 2010; Hiles et al., 2012). Fatigue, loss of energy and psychomotor slowing are reported to occurred in patients receiving treatment with IFN-α or with high levels of IL-6 (Miller et al., 2009; Goldsmith et al., 2016b). Moreover, many inflammatory stimuli have been found to target reductions in ventral striatal neural function, and decreased synthesis of striatal DA, which is possibly related to symptoms of reduced motivation and motor retardation (Felger and Treadway, 2017). Studies with IL-6 indicate that this cytokine is responsive to stress, and is implicated in the production of depression-like effects in mice, including actions on traditional tests such as the FST, TST, and social interaction tests (Sukoff Rizzo et al., 2012). In anergia related studies, IL-6 and IL-1β reduced the tendency to work for food when an alternative food source (concurrently available chow) could be obtained through minimal effort (Nunes et al., 2014; Yohn et al., 2016a).
...
Brain cytokine signaling involves adenosine signaling at adenosine A2A receptors (Hanff et al., 2010). These receptors regulate IL-1β and LPS linked to pathological behavioral and physiological responses such as anxiety (Chiu et al., 2014) or neuroinflammation (Brothers et al., 2010; Simões et al., 2012). Adenosine A2A receptor signaling provides inhibitory feedback on proinflammatory cytokine signaling in peripheral immune cells (Sitkovsky and Ohta, 2005). Thus, the effects of IL-6 and IL-1β were attenuated through co-administration of the adenosine A2A receptor antagonist MSX-3, as well as the major stimulant methylphenidate, which blocks catecholamine uptake (Nunes et al., 2014; Yohn et al., 2016c). Though previous work has shown that MSX-3 had no effect of FR5/chow-feeding choice performance when administered on its own (Farrar et al., 2007), MSX-3 produced a very robust reversal of the behavioral effects of IL-6 and IL-1β, restoring the baseline behavioral pattern of responding (i.e., increasing lever pressing and decreasing chow consumption) to a normal level (Nunes et al., 2014; Yohn et al., 2016c). These results highlight the therapeutic potential of adenosine A2A receptor antagonism for pathologies related to neuroinflammation (Simões et al., 2012; Cunha, 2016).


...

Involvement of TLR2 and TLR9 in the anti-inflammatory effects of chlorogenic acid in Herpes Simplex Virus-1-infected microglia.
https://www.ncbi.nlm.nih.gov/pubmed/25744394
CGA[chlorogenic acid] inhibits the inflammatory reaction in HSE(Herpes Simplex Virus Encephalitis) via the suppression of TLR2/TLR9-Myd88 signaling pathways.
...
Moreover, CGA could attenuate HSV-induced TNF-α and IL-6 release into the supernatant. The mRNA levels of TNF-α and IL-6 were also significantly inhibited by CGA. The expression of NF-κB p65 increased significantly in the nucleus in HSV-1-stimulated microglia but could be reduced by CGA.
...
CGA inhibits the inflammatory reaction in HSE via the suppression of TLR2/TLR9-Myd88 signaling pathways.


Distinct Roles for MyD88 and Toll-Like Receptors 2, 5, and 9 in Phagocytosis of Borrelia burgdorferi and Cytokine Induction
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2423091/
The contribution of Toll-like receptors (TLRs) to phagocytosis of Borrelia burgdorferi has not been extensively studied. We show that bone marrow-derived macrophages (BMDM) from MyD88−/− mice or Raw cells transfected with a dominant-negative MyD88 were unable to efficiently internalize B. burgdorferi. Knockouts of TLR2 and TLR9 or knockdown of TLR5 by small interfering RNA produced no defects in phagocytosis of B. burgdorferi. Production of inflammatory cytokines was greatly diminished in MyD88−/− BMDM but only partially affected in TLR2−/− BMDM or knockdown of TLR5 and unaffected in TLR9−/− BMDM. Cytochalasin D reduced cytokine induction, but not to the level of the MyD88−/−BMDM. Addition of cytochalasin D to TLR2−/− BMDM inhibited inflammatory responses to B. burgdorferi to the level of MyD88−/− BMDM, consistent with a role for TLR2 in both recognition of extracellular products and lysosomal sampling by TLR2 after processing of the organism. Cytochalasin D had no impact on cytokine production in cells undergoing TLR5 knockdown. These results suggest that MyD88, but not TLR2, TLR5, and TLR9, is important for the uptake of B. burgdorferi and that MyD88 affects inflammatory responses through both its effects on phagocytosis and its role in transducing signals from TLR2 and TLR5.

MyD88 in Mycobacterium tuberculosis infection
https://link.springer.com/article/10.1007/s00430-017-0495-0
MyD88 adaptor protein mediates numerous biologically important signal transduction pathways in innate immunity. MyD88 signaling fosters bacterial containment and is necessary to raise an adequate innate and acquired immune response to Mycobacterium tuberculosis (Mtb). The phagosome is a crucial cellular location not only for Mtb replication, but it is also where components of the Myddosome and inflammasome are recruited. Besides its function as a TLR-adaptor protein, MyD88 may help stabilizing cytosolic receptors that are recruited to the phagosome. MyD88 plays a critical role not only in the generation of an inflammatory response, but also in inducing regulatory signals to prevent excessive inflammation and cellular damage in the lung.

Dual Role of MyD88 in Rapid Clearance of Relapsing Fever Borrelia spp.
https://iai.asm.org/content/74/12/6750
MyD88-deficient mice display defective clearance of many pathogens; however, the IgM response to persistent infection is essentially normal. Therefore, MyD88−/− mice provided a unique opportunity to study the effect of nonantibody, innate host defenses to relapsing fever Borrelia. Infected MyD88−/− mice harbored extremely high levels of B. hermsii in the blood compared to wild-type littermates. In the comparison of MyD88−/− mice and B- and T-cell-deficient scid mice, two features stood out: (i) bacterial numbers in blood were at least 10-fold greater in MyD88−/− mice than scid mice, even though the production of IgM still occurred in MyD88−/− mice; and (ii) many of the MyD88−/− mice were able to exert partial clearance, although with delayed kinetics relative to wild-type mice, a feature not seen in scid mice.

Ferulic acid may target MyD88-mediated pro-inflammatory signaling - Implications for the health protection afforded by whole grains, anthocyanins, and coffee.
https://www.ncbi.nlm.nih.gov/pubmed/30037596
FA[Ferulic acid], a precursor for lignan synthesis, is widely distributed in plant-based whole foods, mostly in conjugated form; whole grains are a notable source.
Coffee ingestion boosts plasma FA[Ferulic acid] owing to gastrointestinal metabolism of chlorogenic acid.

Could MyD88 be the target of ferulic acid anti-inflammatory activity?

There is a substantial literature evaluating the antioxidant and anti inflammatory effects of FA[ferulic acid] both in cell culture studies and in rodents.
...
A recent study by Ren and colleagues has yielded a most intriguing insight in this regard [74]. These investigators confirmed that FA[ferulic acid] administration provides important protection from ischemia-reperfusion induced brain injury in rats. They followed this up with in vitro studies employing PC-12 cells (derived from a pheochromocytoma) in which ischemia was simulated by exposure to sodium dithionite. FA dosedependently protected PC-12 cells from dithionite-induced apoptosis, and also reversed the impact of simulated ischemia on expression of a number of pro-inflammatory or pro-apoptotic genes. Curiously, if the PC-12 cells were pre-treated with overexpression plasmids coding for MyD88 – a protein which plays a key mediating role in many pro-inflammatory signaling pathways that activate NF-kappaB – the protection afforded from simulated ischemia by FA was nearly abolished. This finding strongly suggests that FA somehow interferes with MyD88 function, in a manner that can be offset by a marked increase in MyD88 expression.

Last edited on Wed Mar 13th, 2019 18:52 by Dmitry



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 Posted: Fri Mar 15th, 2019 12:35

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regarding depression this is from the book
https://b-ok.cc/book/2315436/ae595b


CASE STUDY

A clinical report published in the Journal of Affective Disorders graphically illustrates the connection between caffeine and depression. A woman suffered for twenty years with recurrent depression. She was treated with a variety of drugs, including lithium, chlorpromazine, haloperidol, and Valium. After years of drug therapy, she decided to quit drinking coffee. Within one month, she was able to eliminate the Valium and all but one of her medications. At the time the clinical report was published, she had gone five years without a single episode of depression.30



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 Posted: Sat Mar 23rd, 2019 21:21

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Chronic caffeine ingestion causes microglia activation, but not proliferation in the healthy brain
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112016/
Caffeine is the most popular psychoactive drug in the world which contributes to behavioral and metabolic changes when ingested. Within the central nervous system (CNS), caffeine has a high affinity for A1 and A2a adenosine receptors. Serving as an antagonist, caffeine affects the ability for adenosine to bind to these receptors. Caffeine has been shown to alter neuronal functioning through increasing spontaneous firing. However, the effects of caffeine on non-neuronal cells in the CNS has been not been studied extensively. Microglia are one phenotype of non-neuronal glia within the CNS. Acting as phagocytes, they contribute to the immune defense system of the brain and express A1 and A2a adenosine receptors. Caffeine, therefore, may affect microglia. In order to test this hypothesis, CD-1 mice were randomly placed into one of three groups: control, low caffeine (0.3g/L water) and high caffeine (1.0g/L water) and were allowed to drink freely for 30 days. Following 30 days, brain sections were stained to reveal microglia. Morphological reconstructions and density measurements were examined in cortical and subcortical areas including the primary sensory cortex, primary motor cortex and striatum. Results indicate that microglial density throughout the brain is decreased in the caffeine groups as compared to the control. Caffeine also impacted microglia morphology shortening process length and decreasing branching. These results suggest that chronic caffeine ingestion has a systemic impact on microglia density and their activation.
...
While microglia has been most associated with immune response, there is evidence that microglia play an important role in the active maintenance of the brain. Recent studies have revealed that microglia are capable of removing weak synapses (Bialas and Stevens, 2013; reviewed by Šišková and Tremblay, 2013) as well as weak, but still viable, neurons (Brown and Neher, 2014). Within the healthy brain, microglia regulates synaptic activity and aides in the reorganization of neuronal circuits (Trembly et al., 2011). In this resepect we should reconsider the role of microglia, and examine how microglia function, and how that function can be altered, within the healthy brain.

As microglia contain A1 and A2a receptors, we believe caffeine can exert an effect on these cells. Indeed, it was found that caffeine suppresses the proinflammatory response that occurs during prolonged activation of microglia (Lee et al., 2013; Ruiz-Medina et al., 2013; Kang et al., 2012; Brothers et al., 2010) and therefore may be neuroprotective in neurodegenertive diseases such as Parkinson's disease and multiple sclerosis (Yadav et al., 2012, Tsuitsui et al., 2004). Caffiene also increases microglia reactivity when treated with 3,4-methylenedioxy-N-methylamphetamine (MDMA) (Khairnar et al., 2009). However, the afforementioned studies examined caffiene's effect on mircoglia following brain insult. The purpose of the current study is to better understand how caffeine affects microglia in the healthy brain.

Last edited on Sat Mar 23rd, 2019 21:30 by Dmitry



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 Posted: Wed Mar 27th, 2019 20:31

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JRFoutin,
Just wanted to say (belatedly) that I think your response of Mar 11 is very wisely and expertly said.



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 Posted: Thu Mar 28th, 2019 09:13

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Dmitry so from this paper, caffeine suppresses brain phagocytosis ? I think the conclusions are wrong that caffeine protects against neuro diseases. I saw brains of MS completely repair itself on caffeine free diet, called watercure of Dr Batmanghelidj.

Last edited on Thu Mar 28th, 2019 09:21 by wrotek



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 Posted: Thu Mar 28th, 2019 09:53

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I think the conclusions are wrong that caffeine protects against neuro diseases.
Yeah, they did not count the possible long-term consequences of extra protection.

I saw brains of MS completely repair itself on caffeine free diet
Nice.


so from this paper, caffeine suppresses brain phagocytosis ?


Sort of indirectly? By cutting away a response to certain immune system signals(applying hyporesponsiveness to them).

Also the fact that coffee blunts a feedback from LPS(endotoxin) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905864/ like D3/mino/LDN and almost every anti-inflammatory supplement do could be net-negative(on the years distance) for balanced phagocytosis too.

Since low levels of endotoxin seem to improve phagocytosis:

https://www.ncbi.nlm.nih.gov/pubmed/6350191
Enhancement of phagocytosis was observed with a low concentration of endotoxin (1 microgram/ml) from S. typhi, S. typhimurium and S. flexneri. Higher concentrations (2.5 and 5 micrograms/ml) depressed phagocytosis to varying extents, except for S. typhi lipopolysaccharide

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC414456/
Furthermore, low concentrations of LPS stimulate phagocytosis in macrophages derived for C3H/HeJ mice

(I assume we all have relatively low levels of endotoxin in our bodies).

P.S.:

Bacterial Endotoxin Activity in Human Serum Is Associated With Dyslipidemia, Insulin Resistance, Obesity, and Chronic Inflammation
http://care.diabetesjournals.org/content/34/8/1809

Last edited on Thu Mar 28th, 2019 09:58 by Dmitry



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 Posted: Sun Apr 7th, 2019 18:04

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If caffeine decreases cerebral blood flow by 40 percent, how good can it be ? It is nonsense. That is why u get such a headache after quitting...



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 Posted: Mon Apr 22nd, 2019 13:48

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https://www.pechakucha.com/presentations/this-is-your-brain-on-coffee

Last edited on Mon Apr 22nd, 2019 13:51 by wrotek



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 Posted: Fri May 3rd, 2019 08:36

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Caffeine Stimulation of Cortisol Secretion Across the Waking Hours in Relation to Caffeine Intake Levels
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2257922/
Objective
Caffeine increases cortisol secretion in people at rest or undergoing mental stress. It is not known whether tolerance develops in this response with daily intake of caffeine in the diet. We therefore tested the cortisol response to caffeine challenge after controlled levels of caffeine intake.

Methods
Men (N = 48) and women (N = 48) completed a double-blind, crossover trial conducted over 4 weeks. On each week, subjects abstained for 5 days from dietary caffeine and instead took capsules totaling 0 mg, 300 mg, and 600 mg/day in 3 divided doses. On day 6, they took capsules with either 0 mg or 250 mg at 9:00 AM, 1:00 PM, and 6:00 PM, and cortisol was sampled from saliva collected at 8 times from 7:30 AM to 7:00 PM.

Results
After 5 days of caffeine abstinence, caffeine challenge doses caused a robust increase in cortisol across the test day (p < .0001). In contrast, 5 days of caffeine intake at 300 mg/day and 600 mg/day abolished the cortisol response to the initial 9:00 AM caffeine dose, although cortisol levels were again elevated between 1:00 PM and 7:00 PM (p = .02 to .002) after the second caffeine dose taken at 1:00 PM. Cortisol levels declined to control levels during the evening sampling period.

Conclusion
Cortisol responses to caffeine are reduced, but not eliminated, in healthy young men and women who consume caffeine on a daily basis.


Cortisol modulates inflammatory responses in LPS-stimulated RAW264.7 cells via the NF-κB and MAPK pathways
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5789647/
Background
The uteruses of most dairy cattle are easily infected by bacteria, especially gram-negative bacteria, following parturition. Macrophages are important cells of the immune system and play a critical role in the inflammatory response. In addition, cortisol levels become significantly increased due to the stress of parturition in dairy cattle, and cortisol is among the most widely used and effective therapies for many inflammatory diseases. In this study, we assessed the anti-inflammatory effects and potential molecular mechanisms of cortisol using a Lipopolysaccharide (LPS)-induced RAW264.7 macrophage cell line.

Results
Cortisol significantly suppressed the production of prostaglandin E2 (PGE2) and decreased the gene and protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Moreover, cortisol inhibited the mRNA expression of pro-inflammatory cytokines including tumor necrosis factor alpha (TNFα), interleukin-1β (IL-1β), and interleukin-6 (IL-6) and decreased IL-1β secretion in an LPS-treated RAW264.7 macrophage cell line. Moreover, we found that cortisol suppressed nuclear factor-kappa B (NF-κB) signaling in RAW264.7 macrophages stimulated with LPS. This suppression was mediated by the inhibition of IκBα degradation and NF-κB p65 phosphorylation. In addition, cortisol also suppressed the phosphorylation of mitogen-activated protein kinases (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK).

Conclusions
These results suggest that high cortisol levels can attenuate LPS-induced inflammatory responses in the RAW264.7 macrophage cell line by regulating the NF-κB and MAPK signaling pathways.

Last edited on Fri May 3rd, 2019 09:12 by Dmitry



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