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Prof Trevor Marshall
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For an overview, here is a blog article describing the study:
http://arstechnica.com/science/2014/12/immune-cells-tweak-the-bodys-metabolism-to-help-control-obesity/

while the study itself is in Nature: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14115.html

I have read the fulltext and it is detailed and thorough. I think the authors knew the resistance they would be likely to experience... This study is also interesting because it is an integrated murine/human study where the phenomenon was discovered in mice and immediately cross-checked with human biology. Excellent work, in fact, from Weil Cornell and a host of collaborating institutions and funding sources. The "Acknowledgments section alone runs to 250 words. Quite amazing, and a wonderful challenge as we start the New Year....



..Trevor..


Joyful
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For a long time I have suspected that bad science was the cause of obesity myself ...

wrotek
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Dr Marshall, does insulin take part in driving inflammation ?

eClaire
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I have noticed significant weight gain every time I've crashed. When I felt better in 2012 than I had since total disability, my weight stabilized at 22 pounds less than where I am now and I could eat with impunity. Then, I went through an extremely stressful time (Mom became sick and died and her home flooded when she died) and crashed heavily. This weight is stuck on me. (Goes right to my middle, but mostly my butt.) It doesn't matter how much or how little I eat.

I'd always noticed, pre-total disability, that even though I have always been unwell, it was always easier to maintain my weight when I felt relatively better. (I've always eaten a relatively healthy, non-processed diet low in carbs because carbs equaled fat for me.)

Last edited on Thu Jan 8th, 2015 22:00 by eClaire

wrotek
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eClaire wrote:
I went through an extremely stressful time

So stress hormones, right ?

eClaire
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That could be it Wrotek. And I have no clue what to do about it (to get the weight off) other than meditate.

I don't appear to be killing off a lot of bacteria.

Two measures of major bacteria die off for me has been plaque on teeth (I never had any pre-MP) and ear wax production (also did not have). At one point during the MP, I had to scrape my teeth daily because of plaque (gross amounts) and just about the same for my ears.

Although plaque production eventually slowed down to a more manageable level, I have had virtually no plaque build up again (like pre-MP) at all since moving and much less ear wax (though more than pre-MP). This concerns me a bit because I wonder if my immune response has shut down due to stress despite the olmesartan. Or perhaps my continued disability has to do with neuro damage that has yet to heal.

Last edited on Sat Jan 10th, 2015 04:48 by eClaire

Cairo123
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how does plaque relate to immune activation? At my last two or three dental visits it was noted that I have minimal plaque on my teeth.

eClaire
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I don't know how plaque relates. I don't think it is seen as being part of the immune response, but I know that ear wax is.

Regardless, at some point on the MP when I was having extreme IP, my plaque was absolutely ridiculous. I see no explanation for it other than my immune system killing off bacteria.

Plaque in the mouth is supposed to be a build up of bacterial film. I think -- given my own experience :D -- that it is created by the immune system killing off bacteria. Most people are at the losing end of that war and may develop gum disease over time just as they are at the losing end of the fight with other bacteria in their bodies as they age.

I don't think my immune system was killing off much of anything until I got on the MP. I imagine over time, as bacteria is killed off on the MP, then plaque would decrease. I just wonder if I am there or artificially there as a result of stress suppressing my immune system.

That's my own theory.

Last edited on Mon Jan 12th, 2015 05:36 by eClaire

Cynthia S
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How about the idea that bacteria are escaping the immune system thru our salivary ducts and taking up residence on our teeth?

But I think this is getting off topic.

Cynthia

Paula Bennett
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What can generate group 2 innate lymphoid cells? I would like some of my white fat to be converted to the brown calorie burning fat!!

Sallie Q
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I do not know where to go for an answer to that, Paula
but
I do hate those blame-the-victim ideas that flourish: sort of "I'm all right, Jack, so there must be something wrong with you" :( "eat less! / get some running shoes / a gym instructer".

a bit like a doctor who rationalises 'I do not know what, if anything, I can do for you, so I will refer you to a psychiatrist'
and thinks you must have an over-active imagination, or unlucky ancestral genes, not a cranial microbe imbalance somewhere within the envelope of the brain's immune system- something that science has only recently made clear.

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I have been reading more and more information put forth by functional medicine doctors that state that inflammation begins in the gut. The more I read on the subject the more it made sense to me. I had done an Elimination Diet many years ago and found I had food sensitivities to dairy, corn, and peanuts. Once I stopped eating the foods I began to feel better. The new information put forth by these doctors state that it is virtually impossible to lose weight when one is eating food to which they are intolerant. The biggest culprit for causing inflammation is gluten. I never believed myself to be gluten-intolerant, but I decided to go off gluten to see if I had any good results after coming off of it. I have always had a healthy diet, but I decided to try. A month after cutting gluten I had lost 25 lbs, decreased my inflammation, and drastically reduced my Vit D level. It has been been 4 months since then and I have lost another 10 lbs. I am now in my ideal weight range and feel better than I have in years. I think it is something that is worth looking into for those with chronic inflammation.

Prof Trevor Marshall
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Gluten avoidence also helps avoid the major sources of GMO food in the USA - corn and wheat. When you travel internationally, the benefits of gluten avoidance become less obvious, as other countries are still growing wheat and corn without the 'efficiencies' introduced by new 'strains' in the USA and Australia.

..trevor... (in Moscow, gutsing all the local food with gusto)..

k1075
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That's very interesting! Gust away! All the best....

Cynthia S
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At this point on the MP, almost 8 years, I am extremely sensitive to carbohydrates.  So, over the last 2 years, with a strict very low carbohydrate life style, I have lost 45 pounds.  This includes, of course, no grains of any kind.

After a roughly 9 month break from olmesartan because of extreme immune activity (brought on using serrapeptase),  causing my cortisol to go well above range in reaction to the high immune activity, I will be back on olmesartan and hoping that I will eventually not have this high sensitivity to carbs.  But it looks like what ever is going on does not respond quickly to the immune enhancement of the olmesartan.

Cynthia

Prof Trevor Marshall
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Cynthia,
Sadly, the activities of olmesartan are being partially offset by the immune suppression of the electrosmog which has proliferated these last few years. Nothing is static in this world, all is dynamic...

Lee
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I eat many organic non gmo grains.  I do avoid try and avoid most corn though.  My weight has stayed the same, docs consider me thin yet well nourished and my inflammation levels and pain stay low.  I have grains with 2 out of 3 meals and found the more healthy organic non gmo grain I eat the less sugar cravings I have ...:D  Lee

Dmitry
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Zonulin(protein) modulates the permeability of tight junctions between digestive tract cells was discovered only in 2000.

I've been eating a lot of gluten before being diagnosed with Celiac back in 2008 - must me a ton of inflammation hitting me through this route for years, since skin dermatitis disappeared with gluten avoidance diet but probably too late - I could only imagine how many bugs traveled(in the immune cells and directly) through "leaky gut" to the blood -> tissues... along with being constantly exposed to unproductive inflammation :(
(I had both HLA)

Zonulin, regulation of tight junctions, and autoimmune diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384703/
Among the several potential intestinal luminal stimuli that can trigger zonulin release, we identified small intestinal exposure to bacteria and gluten as the two more powerful triggers (18,23,28). Enteric infections have been implicated in the pathogenesis of several pathological conditions, including allergic, autoimmune, and inflammatory diseases, by causing impairment of the intestinal barrier. We have generated evidence that small intestines exposed to enteric bacteria secrete zonulin (28).
...
Celiac disease
Celiac disease (CD) is an immune mediated chronic enteropathy with a wide range of presenting manifestations of variable severity. It is triggered by the ingestion of gliadin fraction of wheat gluten and similar alcohol-soluble proteins (prolamines) of barley and rye in genetically susceptible subjects with subsequent immune reaction leading to small bowel inflammation and normalization of the villous architecture in response to a gluten-free diet (31). CD is a unique model of autoimmunity in which, in contrast to most other autoimmune diseases, a close genetic association with HLA genes, a highly specific humoral autoimmune response against tissue transglutaminase auto-antigen, and, most importantly, the triggering environmental factor (gliadin), are all known. It is the interplay between genes (both HLA and non-HLA associated) and environment (i.e. gluten) that leads to the intestinal damage typical of the disease (32). Under physiological circumstances this interplay is prevented by competent intercellular TJ. Early in CD, TJs are opened (33–36) and severe intestinal damage ensues.
...
There are at least 50 toxic epitopes in gluten peptides exerting cytotoxic, immunomodulatory, and gut permeating activities (38). The effect of the permeating gliadin peptides in vivo was confirmed by the analysis of intestinal tissues from patients with active CD and non-CD controls probed for zonulin expression (23). Quantitative immunoblotting of intestinal tissue lysates from active CD patients confirmed the increase in zonulin protein compared to control tissues (23). Zonulin upregulation during the acute phase of CD was confirmed by measuring zonulin concentration in sera of 189 CD patients using a sandwich ELISA (Fig. 3A) (13).
...
oof of concept for the pathogenic role of zonulin-dependent intestinal barrier defect in celiac disease and type 1 diabetes
CD and T1D autoimmune models suggest that when the finely tuned trafficking of macromolecules is deregulated in genetically susceptible individuals, autoimmune disorders can occur (53). This new paradigm subverts traditional theories underlying the development of autoimmunity, which are based on molecular mimicry and/or the bystander effect, and suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the intestinal barrier function. To challenge this hypothesis, zonulin inhibitor AT1001 was used with encouraging results in the BBDP rat model of autoimmunity (16). Beside preventing the loss of intestinal barrier function, the appearance of auto-antibodies, and the onset of disease, pre-treatment with AT1001 protected against the insult of pancreatic islets and, therefore, of the insulitis responsible for the onset of type 1 diabetes.

This prove-of-concept in an animal model of autoimmunity provided the rationale to design human clinical trials in which AT1001 was initially tested in an inpatient, double-blind, randomized placebo controlled trial to determine its safety, tolerability, and preliminary efficacy (54). No increase in adverse events was recorded among patients exposed to AT-1001 as compared to placebo. Following acute gluten exposure, a 70% increase in intestinal permeability was detected in the placebo group, while no changes were seen in the AT-1001 group (54). After gluten exposure, IFN-γ levels increased in 4 out of 7 patients (57.1%) of the placebo-group, but only in 4 out of 14 patients (28.6%) of the AT-1001-group. Gastrointestinal symptoms were significantly more frequent among patients of the placebo group as compared to the AT-1001 group (54). Combined, these data suggest that AT-1001 is well tolerated and appears to reduce pro-inflammatory cytokine production and gastrointestinal symptoms in CD patients. AT1001 has now been tested in approximately 500 subjects with excellent safety profile and promising efficacy as concern protection against symptoms caused by gluten exposure in CD patients (55).


Restoration of impaired intestinal barrier function by the hydrolysed casein diet contributes to the prevention of type 1 diabetes in the diabetes-prone BioBreeding rat.
https://www.ncbi.nlm.nih.gov/pubmed/20853098

Higher Levels of Serum Zonulin May Rather Be Associated with Increased Risk of Obesity and Hyperlipidemia, Than with Gastrointestinal Symptoms or Disease Manifestations.
https://www.ncbi.nlm.nih.gov/pubmed/28282855

Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5214347/
The two major triggers of zonulin release that have been described so far are bacteria and gliadin. It is well described that many enteric pathogens are able to produce enterotoxins that affect the intestinal tight junction of the host. In addition to enteroxins, several enteric pathogens, including commensal Eschericha coli, lab E. coli, virulent E. coli, and Salmonella typhi have been shown to cause a release of zonulin from the intestine when applied to the apical surface.84 Following the release of zonulin, the intestine showed increased permeability and disassembly of ZO-1 from the tight junction complex. 84



https://www.doctorsdata.com/zonulin/
Restoration of the gastrointestinal mucosal barrier may include dietary changes, treatment of dysbiosis, digestive supports, and anti-inflammatory therapies. These may include supplements such as quercetin, vitamin C, curcumin, gamma-linoleic acid, omega-3 fatty acids (EPA, DHA), and aloe vera.

^ hmm, typical anti-inflammatory drugs

How to Become Gluten Intolerant ;)
https://www.youtube.com/watch?v=Oht9AEq1798

Last edited on Wed Oct 31st, 2018 20:35 by Dmitry

Dmitry
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https://www.sciencemag.org/news/2018/11/do-gut-bacteria-make-second-home-our-brains
Roberts wondered whether bacteria from the gut could have leaked from blood vessels into the brain in the hours between a person’s death and the brain’s removal. So she looked at healthy mouse brains, which were preserved immediately after the mice were killed. More bacteria. Then she looked at the brains of germ-free mice, which are carefully raised to be devoid of microbial life. They were uniformly clean.

RNA sequencing revealed that most of the bacteria were from three phyla common to the gut: Firmicutes, Proteobacteria, and Bacteroidetes. Roberts doesn’t know how these bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose.


Butyrate-producing Firmicutes feast on fiber:

https://www.ncbi.nlm.nih.gov/pubmed/26011307
'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens).

Bacteroidetes and Proteobacteria seem to be associated with carnivore diet:

https://onlinelibrary.wiley.com/doi/full/10.1002/mbo3.677
The phyla Firmicutes and Bacteroidetes are highly abundant, and Fusobacteria, Actinobacteria, and Proteobacteria also feature prominently. Proteobacteria is the most diverse bacterial phylum and commonly features in the fecal microbiota of healthy dogs and cats, although its reputation is often sullied as its members include a number of well‐known opportunistic pathogens, such as Escherichia coli, Salmonella, and Campylobacter, which may impact the health of the host and its owner. Furthermore, in other host species, high abundances of Proteobacteria have been associated with dysbiosis in hosts with metabolic or inflammatory disorders. In this review, we seek to gain further insight into the prevalence and roles of the Proteobacteria within the gastrointestinal microbiomes of healthy dogs and cats.

Bacteroidetes feats of fiber too...

https://www.sciencedaily.com/releases/2014/11/141118125552.htm
Hannah Holscher, a U of I postdoctoral researcher and registered dietitian in animal sciences, said what was most surprising and novel in the recent study was a shift in the Bacteroidetes:Firmicutes ratio toward more Bacteroidetes, something the researchers had not seen previously.

"This was of particular interest to us because other research has shown that having more Bacteroidetes may be beneficial because the higher that proportion is, the individual tends to be leaner. With higher Firmicutes, that individual tends to be more obese," Holscher said. "We don't know if there is any causality for weight loss, but studies have shown that having a higher fiber diet is protective against obesity. It's an exciting shift and helps to drive researchers to study these fibers as part of a weight loss diet."


No matter what we eat we always feed one species or another. ;)

Last edited on Sun Nov 11th, 2018 13:01 by Dmitry

Joyful
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Nice diagram in your second to last post Dmitry!

Dmitry
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Links between insulin resistance, adenosine A2B receptors, and inflammatory markers in mice and humans.
https://www.ncbi.nlm.nih.gov/pubmed/21270276
OBJECTIVE:
To determine the mechanisms by which blockade of adenosine A(2B) receptors (A(2B)Rs) reduces insulin resistance.

RESEARCH DESIGN AND METHODS:
We investigated the effects of deleting or blocking the A(2B)R on insulin sensitivity using glucose tolerance tests (GTTs) and hyperinsulinemic-euglycemic clamps in mouse models of type 2 diabetes. The effects of diabetes on A(2B)R transcription and signaling were measured in human and mouse macrophages and mouse endothelial cells. In addition, tag single nucleotide polymorphisms (SNPs) in ~42 kb encompassing the A(2B)R gene, ADORA2B, were evaluated for associations with markers of diabetes and inflammation.

RESULTS:
Treatment of mice with the nonselective adenosine receptor agonist 5'-N-ethylcarboxamidoadensoine (NECA) increased fasting blood glucose and slowed glucose disposal during GTTs. These responses were inhibited by A(2B)R deletion or blockade and minimally affected by deletion of A(1)Rs or A(2A)Rs. During hyperinsulinemic-euglycemic clamp of diabetic KKA(Y) mice, A(2B)R antagonism increased glucose infusion rate, reduced hepatic glucose production, and increased glucose uptake into skeletal muscle and brown adipose tissue. Diabetes caused a four- to sixfold increase in A(2B)R mRNA in endothelial cells and macrophages and resulted in enhanced interleukin (IL)-6 production in response to NECA due to activation of protein kinases A and C. Five consecutive tag SNPs in ADORA2B were highly correlated with IL-6 and C-reactive protein (CRP). Diabetes had a highly significant independent effect on variation in inflammatory markers. The strength of associations between several ADORA2B SNPs and inflammatory markers was increased when accounting for diabetes status.

CONCLUSIONS:
Diabetes affects the production of adenosine and the expression of A(2B)Rs that stimulate IL-6 and CRP production, insulin resistance, and the association between ADORA2B SNPs and inflammatory markers. We hypothesize that increased A(2B)R signaling in diabetes increases insulin resistance in part by elevating proinflammatory mediators. Selective A(2B)R blockers may be useful to treat insulin resistance.


Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice.
https://www.ncbi.nlm.nih.gov/pubmed/28654087
Caffeine, an antagonist of the adenosine receptor A1R, is used as a dietary supplement to reduce body weight, although the underlying mechanism is unclear. Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance. These data suggest that caffeine inhibits A1Rs expressed on PVN oxytocin neurons to negatively regulate energy balance in DIO mice.

Interaction between saliva's adenosine and tick parasitism: effects on feeding and reproduction.
https://www.ncbi.nlm.nih.gov/pubmed/28693553
BACKGROUND:
It has recently been demonstrated that saliva from Rhipicephalus sanguineus ticks contains adenosine (ADO) and prostaglandin E2 (PGE2), two non-protein molecules that have significant immunomodulatory properties. These molecules can inhibit cytokine production by dendritic cells (DCs), while also reducing the expression of CD40 in these cells. However, more studies are needed for a better understanding of their participation in the feeding of ticks in vivo. This work, therefore, evaluated the importance of ADO during tick infestations. Mice were infested with adult ticks (3 couples/mouse), and their skin was collected at the tick-infested site (3rd and 7th day), and mRNA for receptors of ADO was quantified by real-time PCR.

RESULTS:
Tick infestation increased by four and two times the expression of the A2b and A3v1 receptors on day 3, respectively, while expression of other ADO receptors was unaltered. In addition, we treated mice (n = 10/group) daily with 8-(p-Sulfophenyl)theophylline, 8-pSPT, 20 mg/kg, i.p.), a non-selective antagonist of ADO receptors, and evaluated the performance of ticks during infestations. Female ticks fed on 8-pSPT-treated mice presented a reduction in their engorgement, weight and hatching rates of egg masses, and survival times of larvae compared to the same parameters presented by ticks in the control group. To investigate if these 8-pSPT-treated mice presented altered immune responses, we performed three tick infestations and collected their lymph node cells to determine the percentages and activation state of DCs and cytokine production by lymphocytes by flow cytometry (Cytometric Bead Array technique, CBA). Our data showed that 8-pSPT-treated mice presented an increase in the percentage of DCs as well as of their stimulatory and co-stimulatory molecules (CD40, CD80 and MHCII). Regarding production of T cell cytokines, we observed a significant increase in the levels of IL-2 and a significant decrease in IL-10, IL-17, TNF-α and IFN-γ cytokines.

CONCLUSIONS:
These results suggest that ADO produced by ticks helps them feed and reproduce and that this effect may be due to modulation of host DCs and T cells.


...

Regulation of leukocyte function by adenosine receptors
https://www.ncbi.nlm.nih.gov/pubmed/21586357

Adenosine production: a common path for mesenchymal stem-cell and regulatory T-cell-mediated immunosuppression
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124006/

Adenosine A2B receptor activation stimulates glucose uptake in the mouse forebrain
https://www.ncbi.nlm.nih.gov/pubmed/26446689

The macrophage A2B adenosine receptor regulates tissue insulin sensitivity
https://www.ncbi.nlm.nih.gov/pubmed/24892847

Health benefits of methylxanthines in cacao and chocolate.
https://www.ncbi.nlm.nih.gov/pubmed/24145871

Adenosine, adenosine receptors and their role in glucose homeostasis and lipid metabolism
https://www.ncbi.nlm.nih.gov/pubmed/23460239
Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage. The role of adenosine in glucose homeostasis has been attributed to its ability to regulate, through its membrane receptors, processes such as insulin secretion, glucose release and clearance, glycogenolysis, and glycogenesis. Additionally, adenosine and its multiple receptors have been connected to lipid metabolism by augmenting insulin-mediated inhibition of lipolysis, and the subsequent increase in free fatty acids and glycerol levels. Furthermore, adenosine was reported to control liver cholesterol synthesis, consequently affecting plasma levels of cholesterol and triglycerides, and the amount of fat tissue. Alterations in the balance of glucose and lipid homeostasis have implications in both cardiovascular disease and diabetes. The ability of different adenosine receptors to activate and inhibit the same signaling cascades has made it challenging to study the influence of adenosine, adenosine analogs and their receptors in health and disease. This review focuses on the role and significance of different adenosine receptors in mediating the effect of adenosine on glucose and lipid homeostasis.

Last edited on Thu Feb 7th, 2019 09:39 by Dmitry

Dmitry
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Your Gut Bacteria Are Controlling Your Appetite, Study Finds
https://www.sciencealert.com/your-gut-bacteria-appear-to-be-controlling-your-appetite
Bacteria in the gut produce appetite-suppressing proteins about 20 minutes after a meal, a new study has found, suggesting that we have less control over how much we eat than we thought.

Scientists investigated the role that colonies of Escherichia coli (E.coli) bacteria living in our intestines play in what we eat. They discovered that the proteins these bacteria release when they’ve had enough nutrients influence the signals sent between the gut and the brain, and can even activate appetite-related neurons to make you feel full.
...
Makes you feel like even more of a big, dumb animal than you did before, right? It might be kind of embarrassing that tiny bacteria appear to be having a rather large say in how much we eat and when, but there is some good news.

Not only is there the possibility of one day treating obese patients with extra doses of ClpB, but by better understanding the relationship between us, our gut bacteria, and our food, we could get to the bottom of why so many of us are prone to overeating.

So the next time you muster the strength to say no to a slice of dessert you really don't need, remember to thank your E. coli overlords for their service.

Prof Trevor Marshall
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:)

wrotek
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In a year i have lost weight from 120kilos to 100 kilos. The key was loosing wheat, which makes mine appetite high ( just stopped being hungry) and i eat mostly meat. That is mine experience

Last edited on Fri Jan 10th, 2020 12:14 by wrotek



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