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丰云娱乐-丰云娱乐彩票
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UrFamily Labs | Mobile, web app development company with products like Mayday Alerts, AudIOfy
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CowsEatGrass | Community
cowseatgrass.org
If you read the science, you'll see that bacterial endotoxin (LPS) has been shown to promote the growth and spread of ***. But only when it comes to leukemia, melanoma, lymph node metastasis, oral squamous cell carcinoma, lung, breast, pancreatic, colo***, liver, gastric, gallbladder, esophageal, cervical, bone and prostate ***. Truth is, all ***s likely get a boost, one way or another, from endotoxin, and though you might not know it, this is good news. Maybe not the be all end all solution to every disease problem, but it means more than most realize. Endotoxin exposure is an important part of the puzzle regarding the progression of metabolic illness, and an awareness of it can open the way to better understanding of what leads to ***, and what helps prevent or treat it. I'm not a doctor, and this article is not intended as advice for the treatment of ***, or disease of any kind. I'm also not suggesting that all you need to do is deal with endotoxin, and just like that, *** is solved. But when you look at the vast amounts of high quality biological evidence relating to the subject of bacterial endotoxin (lipopolysaccharide/LPS) and ***, it makes you wonder why people don't know about it, and that includes many health professionals. If I were to say to you that stress causes ***, or that chronic low level inflammation is a powerful driver of *** spread, you probably wouldn't blink an eyelid. But mention lipopolysaccharides in conversation, and people start to look at you like you're speaking Greek or Latin, or a combination of both. (Ok, you are, but you know what I mean.) You see, there's a powerful relationship between bacterial endotoxin issues, stress, and the stimulation of chronic inflammation and metabolic dysfunction, and all these things have been shown to be directly involved in the development and metastasis of ***, as well as inflammatory disease in general. And this makes a lot of sense when you examine it more closely. And making sense of *** seems like a worthwhile objective. "...low levels of circulating Gram-negative bacterial endotoxin lipopolysaccharide (LPS) appear to be one of the key culprits in provoking a non-resolving low-grade inflammation...low-grade endotoxemia may skew host immune environment into a mild non-resolving pro-inflammatory state, which eventually leads to the pathogenesis and progression of inflammatory diseases..." "Inflammation is a potent promoter of tumor metastasis...Lipopolysaccharide (LPS) is a major structural component of the outer membrane of Gram-negative bacteria and is a potent inducer of inflammation through the production of various cytokines, growth factors and inflammatory mediators...LPS promoted lung metastasis of breast ***..." The mediators of inflammation, toll-like receptor (TLR) proteins, nuclear factor-kappa B (NF-κB) transcription factor proteins, tumor necrosis factor-α (TNF-α), interleukins and other cytokines and inflammatory things, play a role in the metabolic response to bacteria and bacterial toxins (such as endotoxin), and have been shown to be involved in *** development and progression. "TLRs, a family of pattern recognition receptors, have been shown to be closely related to *** progression...In our study, it seems that treatment of LPS, a ligand of TLR4, increased TLR4 expression, thereby promoting MCF7 breast *** cell migration or invasion. "...NF-kappaB is one of the key factors connecting inflammation with *** progression....lipopolysaccharide (LPS) promotes NF-kappaB activation in colon *** cells and pancreatic *** cells...Blockade of TLR4...decreased the LPS-dependent increased invasive ability...results suggest...TLR/NF-kappaB signaling pathway plays a significant role in connecting inflammation and *** invasion and progression." "Chronic inflammation is a well-do***ented risk for carcinogenesis, particularly in the pancreas and gastrointestinal tract...LPS...induces...cells to produce proinflammatory cytokines, such as tumor necrosis factor (TNF), interleukins, inducible nitric oxide synthase, and cyclooxygenase-2..." Although there's probably an endless number of ways that the inflammatory substances can interact with and promote each other (and knowing all of these ways would probably be useful), what I am most interested in is the overall picture. The inflammatory process can have a protective role, but nobody is suggesting (I don't think) that chronic inflammation is something to strive for, and much can be gained from a general understanding of things (like endotoxin) that can connect stress, metabolic energy system suppression and inflammation, with *** development. The thing is, you can't really talk about stress, inflammation and metabolic disease, without talking about bacterial endotoxin issues, and you can't talk about excessive endotoxin exposure, without also talking about the inflammatory stress substances like serotonin, estrogen, nitric oxide (NO), histamine and lactate. Rising levels of these and other related things are involved in the promotion of what has been referred to as the *** metabolism, and they have a tendency to rise in response to ongoing stress, thyroid suppression and inflammation, as well as being able to promote inflammation and biochemical stress. It can be a bit of a circular problem. When stress is high and blood sugar supplies run low, metabolic energy system function is interfered with in a manner which can promote bacterial excess, and which can eventually lead to rising systemic circulation of endotoxin. Endotoxin is itself directly inflammatory, as well as being able to interfere with cellular energy metabolism, increasing many of the inflammatory stress substances which have been shown to encourage ***. "Gram-negative bacteria significantly promoted lung *** development including growth and metastasis in dose dependent manner. Mechanistically, Gram-negative bacteria activate TLR4 and TLR9 signaling and enhance lipid synthesis in human lung *** cells." "TLR4 and the intestinal microbiota were...required for...HCC promotion, mediating increased proliferation...and prevention of apoptosis...the intestinal microbiota and TLR4 represent the***utic targets for HCC prevention in advanced liver disease." "TLR4 protein was increased in ESCC [esophageal squamous cell carcinoma] tumor tissues compared with the adjacent normal tissues. TLR4 over-expression was significantly correlated with tumor differentiation grade, lymph node metastasis, and UICC stage. LPS-induced activation of TLR4 signaling promoted *** cell proliferation, increased production of proinflammatory or immunosuppressive cytokines TNF-α, TGF-β and inhibited the anti-inflammatory cytokine IL-10." A suppressed thyroid metabolism is likely to promote cortisol and adrenaline release, as well as increased levels of estrogen, serotonin, NO, lactate, histamine, and greater circulation of polyunsaturated free fatty acids, encouraging the potential for systemic inflammatory issues. Subclinical hypothyroidism can activate TLR4 and can increase levels of NF-κB, TNF-α, IL-6 and IL-1β. All of these things promote inflammation and can further interfere with metabolism, creating even more opportunity for bacteria to feed and multiply, and for endotoxin to circulate through to the main system. All have been shown to be connected to *** development. As silly as it would be to argue that energy system suppression and unresolved low level inflammation is something to aim for, many of the substances of stress still get interpreted in a positive light. But don't ignore science showing how rising levels of things like NO, serotonin, estrogen, lactate and the polyunsaturated fats (PUFAs) are involved with the progression of *** and disease. And don't ignore how all of this ties in with bacterial issues, and other things like the various cytokines that also promote inflammatory conditions like ***. "Chronic inflammation is a key contributo: 2355 days ago
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