The mean age was 62.5 years (range: 40 to 86 years), 45% were 65 years or older, 9% were 75 years or older, 25% women, 85% White, 2% Black and 10% Asian
GLP-1 Patches from Kind Patches The folks over at Kind Patches are certainly keeping things interesting
Touw, W
So, what is this interesting supplement and why should you take it
On activation, M1 macrophages release a host of pro-inflammatory cytokines, such as TNF-, IL-6, IL-1 and ROS, which are crucial in initiating and perpetuating inflammatory responses.38 In addition to cytokines, M1 macrophages secrete chemokines like C-X-C motif chemokine ligand (CXCL) 9 and CXCL10, which further recruit T helper 1 (Th1) cells and propagate inflammation in the liver.39 In contrast, M2 macrophages are associated with the resolution of inflammation and tissue repair.38 These macrophages are activated by signals indicating that the tissue injury or infection is subsiding, and they release anti-inflammatory mediators like TGF-, IL-10 and chemokines such as C-C motif chemokine ligand (CCL)17, CCL18, CCL22 and CCL24.38 These signalling molecules help attract regulatory T cells (Tregs), which contribute to suppressing immune responses and promoting tissue regeneration.35 40 The balance between M1 and M2 macrophages is crucial for maintaining liver homeostasis, as prolonged M1 activation can exacerbate liver injury, whereas M2 macrophages aid in repairing damaged tissue and resolving inflammation.34 41 In ALD, there is a notable increase in both circulating monocytes and liver macrophages, particularly in severe forms like AH and experimental models of chronic alcohol consumption.30 42 TLR4 signalling, along with its adaptor protein myeloid differentiation primary response gene 88 (MyD88), plays a central role in alcohol-induced inflammation.43 The increased intestinal permeability seen in chronic alcohol use leads to the translocation of bacterial endotoxins such as LPS into the bloodstream.43 These endotoxins activate the TLR4/MyD88 signalling pathway in KCs and infiltrating macrophages, resulting in the production of pro-inflammatory cytokines and chemokines that drive liver inflammation.43 A particularly interesting mechanism in ALD involves the complement receptor of the immunoglobulin superfamily (CRIg), which is predominantly expressed on macrophages, including KCs.44 CRIg plays a protective role in liver health by aiding the clearance of translocated pathobionts, potentially pathogenic organisms that migrate from the intestine to the liver during alcohol-induced gut permeability.44 This protective mechanism helps reduce the inflammatory burden in the liver by preventing the accumulation of harmful bacterial products.44 However, in both murine models and patients with ALD, CRIg expression is significantly reduced, leading to impaired clearance of pathobionts and sustained liver inflammation.44 The reduction in CRIg function exacerbates the inflammatory response and contributes to continued liver damage, as the inability to clear intestinal bacteria leads to persistent immune activation.44 Furthermore, strategies aimed at promoting M2 macrophage polarisation have shown promise in mitigating alcohol-induced liver injury
