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2 Types of Inflammation You NEED to Know About- How FASTING Helps

Click Here to Subscribe: http://Bit.ly/ThomasVid Check Out Kettle & Fire's Organic Bone Broth: http://KettleandFire.com/thomas This video does contain a paid partnership with a brand that helps to support this channel. It is because of brands like this that we are able to provide the content that we do for free. The best way that you can directly support my channel, is by supporting the brands that help make this all possible. Any product that you see on my channel is a product that I also use personally, regardless of any paid promotion. Get my Free Newsletter and Downloadable Cheatsheets (eating out, travel, etc): https://www.thomasdelauer.com/life-op... Follow More of My Daily Life on Instagram:   / thomasdelauer   2 Types of Inflammation You NEED to Know About- How FASTING Helps Just DAMPing and PAMPing!! Ok, you are probably wondering, "what is DAMP & PAMP?!" In regards to IF, understanding these two can help out you get more out of your fast AND address GUT INFLAMMATION! Let's dive in and I'll see you in the COMMENTS!! Low-grade chronic inflammation might be induced by two distinct mechanisms. DAMP stands for the damage-associated molecular pattern – patterns signalling internal damage. We already mentioned one type of cellular damage –the ruptured mitochondrial membranes. Such damage allows for the release of mitochondrial DNA and this DNA acts as DAMP. The mitochondrial DNA signals damage because in the normal state it is not present outside the mitochondria. PAMP stands for pathogen-associated molecular pattern, the foreign particles signalling that there is a pathogen present. The ability to sense PAMP is integral for the immune system as the binding of the PAMP to immune receptors triggers the immune response. One such PAMP can be lipopolysaccharide (LPS), a molecule present on bacterial membranes. Our gut is full of bacteria with LPS but the mucous is preventing their contact with the gut lining. However, the western diet is associated with higher gut permeability, decreased mucous production and therefore LPS can get into the bloodstream where it triggers a response. If the gut barrier integrity is compromised continuously, LPSs are constantly leaking to the bloodstream and cause the low-grade inflammation. Intermittent fasting can help in multiple ways against the damage caused by LPS. First of all, it can stop the problem at the very beginning by improving the integrity of the gut. This mechanism was reported in a study published in Scientific Reports. In a group of 20 women, very low-calorie diet for four weeks significantly improved the gut barrier function and levels of circulating LPS were much lower after the 4-week diet. LPS can have a negative effect on our cognition. Chronic neuroinflammation significantly increases the risk of neurodegenerative diseases. Promisingly, in a study published in the Journal of Neuroinflammation, intermittent fasting (IF) was found to attenuate the LPS induced neuroinflammation. The beneficial effect is achieved by the activation of NF-kappaB. This transcription factor has a somewhat conflicting function in the brains. It can be activated by LPS and then it rapidly increases the expression of several pro-inflammatory genes. On the contrary, it can also stimulate genes involved in synaptic plasticity and cell survival. In here they reported that IF makes the NF-kB go the neuroprotective way. Further, LPS usually reduces levels of BDNF, a protein crucial for brain health. IF managed to prevent the LPS induces a decrease in BDNF. IF also prevented elevation of pro-inflammatory cytokines IL-1α, IL-1β and TNF-α levels. However, outside of the brain, the NF-kB pathway might have more detrimental effects as suggested by the study published in Free Radical Biology and Medicine. As it was discussed previously, chronic inflammation can induce fibrosis in tissues where we don’t want it. In this study, alternate day fasting was able to inhibit the inflammation and fibrosis by suppressing NF-kB pathway. The detrimental effect of NF-kB is further supported by a study published in Experimental Neurology. In ischemic stroke, inflammasomes NLRP1 and NLRP3 play a major role in motor impairment and neural cell death. In here we can describe the concept of DAMPs. After a stroke, the necrotic tissue without oxygen releases DAMPs (little pieces of the membrane) and these trigger inflammation through activation of NF-kB. In turn, NF-kB activates the NLRP1 and NLRP3 inflammasome. However, IF suppressed the activation of NF-kB and subsequently levels of expressed inflammasomes NLRP 1 and 3 were reduced as well. References https://www.ncbi.nlm.nih.gov/pmc/arti... https://pubmed.ncbi.nlm.nih.gov/19818... https://www.ncbi.nlm.nih.gov/pmc/arti... https://pubmed.ncbi.nlm.nih.gov/25686...