@springsnow haiduts arguments are that most of the benefit comes from restricting inflammatory amino acids like methionine. This seems to be in line with studies that show all the benefits of calorie restriction just with protein restriction.

@DavidPS the satiety one is interesting since milk has been traditionally considered a breakfast item. Another piece of evidence as to why people used to be much leaner.

See the reference 3 Glutathione Depletion Prevents Diet-Induced Obesity and Enhances Insulin Sensitivity Hannes M. Findeisen et al. 2012 https://doi.org/10.1038/oby.2011.298 Abstract Excessive accumulation of reactive oxygen species (ROS) in adipose tissue has been implicated in the development of insulin resistance and type 2 diabetes. However, emerging evidence suggests a physiologic role of ROS in cellular signaling and insulin sensitivity. In this study, we demonstrate that pharmacologic depletion of the antioxidant glutathione in mice prevents diet-induced obesity, increases energy expenditure and locomotor activity, and enhances insulin sensitivity. These observations support a beneficial role of ROS in glucose homeostasis and warrant further research to define the regulation of metabolism and energy balance by ROS. Excerpt (…) Since glutathione peroxidase (GPx) constitutes the principal antioxidant defense system to scavenge physiological concentrations of H2O2 in mammals (6), we investigated in this study the role of pharmacological glutathione depletion on diet-induced obesity and insulin sensitivity. Surprisingly, depletion of endogenous glutathione protected mice from obesity, preserved insulin sensitivity, and increased energy expenditure, pointing to a more complex role of endogenous ROS in diabetes and energy balance than previously anticipated. => There is a contradiction and a bias in the title as well in the abstract. To be reminded: too much of a good thing is bad. No need for more than 2x/wk 100 mcg. Diet with meat and eggs brings +/ 50 % of the RDA. Supplement is only bioavailable at +/ 60%. More info (In French, translator needed) https://mirzoune-ciboulette.forumactif.org/t1953-selenium-too-much-of-a-good-thing-is-bad#27971 => Selenium forms, bioavailability, enzymatic functions, synergy with other antioxidants, Sources and References.

OJ for the Win !

@stag wtf i love emf now

@LucH Thanks. There are caveats and gotchas and fine prints as well as times when these are overlooked by sellers, marketers, YouTube "experts" that are a dime a dozen, and there are people who just wing it and cross their fingers and go banzai. And unknowingly commit harikiri. Just hoping they don't.

@alfredoolivas ok, I will try. I have only tried in milk and in cooking with smaller amounts of hot water and it didn't work well.

@otto -Awesome

@NoeticJuice lovely reply boss

@rpc There is a lot of truth to the idea of persistency in microbial infections, especially when we deal with symbiotic microbes that can evade our immune system. These symbiotes evolve to a stronger colony as they gain more microbes to give them more armor from the newfound strength from new microbes in the colony. Which is to say that if we practice good hygiene and know how to provide our own preemptive defenses we essentially are nipping at the bud the ability of pathogenic microbes to be persistent. But our body themselves are a mixture of microbes that in a good environment can coexist together and balance each other out to keep any microbes from dominating. It is when the terrain is not a healthy one that some microbes could become dominant, and a microbe that used to be harmless and healthfully useful could become pathogenic when the terrain condition favor it far more than the rest of the community of microbes, called the microbiome. I see this kind of dynamic in my pet cats. When we'll cared for, I do not have to worry about an infestation of ticks even when these cats do their fair share of getting outside my home. This contrasts a lot with when I knew nothing about caring for pets and my cat and dog were always infested, and I had to give them shampoos which later on I found out made them did early because they had poisons in them. I can draw a parallel in my experience with my pets to my own experience. Knowing the right principles goes a long way in keeping us free from whatever disease, whether it is infectious or degenerative (as they are distinguished conventionally from one another but the line is blurred but I digress). Reddit has a lot of techies and techies cater towards the thinking of people like Dave Asprey and less to people like Ray Peat. Though each have their share of redemptive qualities as irredeemable faults, but that a matter of opinion, as I would say when I believe in things considered controversial. And health and medicine tend to bring people into irreconcilable differences. You agree with Ray Peat about viruses- that they exist. The article expounds on viruses, and favors the use of vaccines. I do not, as I find in nature already mechanisms that bring about the balance that makes viruses and vaccines an unnecessary appendage of a vibrant ecosystem that continually develops towards superior beings over time, as we were made by God to become.

New Therapeutic Strategies for Brain Edema and Cell Injury 2 Bradykinin is a mediator of edema formation Bradykinin is a well-known mediator of the brain edema formation and BBB disruption (Gröger et al., 2005; Plesnila et al., 2001; Schulz et al., 2000). However, its role in BSCB permeability is still not clear (Bannister et al., 2014; Ma et al., 2019; Mandadi et al., 2016; Pan, Kastin, Gera, & Stewart, 2001; Sharma, 2000; Wahl, Görlach, Hortobágyi, & Benyó, 1999; Xu et al., 2008; Yan-Feng, Gang, & Yan-Ting, 2008). Increased bradykinin content following brain injury has been demonstrated. Bradykinin has 2 receptors such B1 and B2. The detail mechanisms of B1 and B2 receptors in mediating the BBB permeability however, is still not well known (Görlach et al., 2001; Görlach, Benyó, & Wahl, 1998; Görlach & Wahl, 1996; Gröger et al., 2005; Plesnila et al., 2001; Schulz et al., 2000; Schürer, Temesvari, Wahl, Unterberg, & Baethmann, 1989; Unterberg, Wahl, & Baethmann, 1984; Wahl et al., 1996; Wahl, Young, Edvinsson, & Wagner, 1983; Whalley & Wahl, 1983). Both bradykinin and its receptors are present in healthy human brain and altered in disease processes such as ischemic brain injury (Bannister et al., 2014; Xu et al., 2008; Yan-Feng et al., 2008). Increased bradykinin concentration in the cerebrospinal fluid (CSF) is well documented for traumat6ic brain injury, ischemic stroke and intracerebral hemorrhages (Gröger et al., 2005; Kunz et al., 2013; Ma et al., 2019; Plesnila et al., 2001; Schulz et al., 2000; Schürer et al., 1989;Unterberg et al., 1984; Wahl et al., 1983; Whalley & Wahl, 1983). Increased bradykinin concentration correlates well with the severity of brain edema (Kunz et al., 2013; Unterberg et al., 1984; Unterberg, Polk, Ellis, & Marmarou, 1990; Wahl et al., 1983; Whalley & Wahl, 1983). Brain edema following increased bradykinin concentrations in the brain is largely due to bradykinin-induced vasodilatation together with venous constriction (Unterberg et al., 1984; Wahl et al., 1983; Whalley & Wahl, 1983). Bradykinin also increases microvascular permeability to plasma proteins causing fluid retention and development of cerebral edema (Pan et al., 2001; Sharma, 2000; Xu et al., 2008; Yan-Feng et al., 2008). Several in vitro studies suggest that blockade of B2 receptors decreases the permeability of isolated cerebral endothelial cells and increased the electrical resistance. (Liu, Xue, Liu, & Wang, 2008; Raslan et al., 2010; Schöller, Feiler, Anetsberger, Kim, & Plesnila, 2011; Trabold et al., 2010). This suggest that blockade of B2 receptors somehow strengthen the endothelial cell permeability (Baethmann et al., 1983, 1988; Wahl et al., 1993, 1988, 1990). There are reports that activation of bradykinin B2 receptors increases the size of the lesion in stroke and enhances BBB breakdown resulting in local neuroinflammation (Görlach et al., 1998, 2001; Görlach & Wahl, 1996; Kunz et al., 2013; Pan et al., 2001; Schürer et al., 1989; Sharma, 2000; Unterberg et al., 1984; Wahl et al., 1999, 1996, 1983; Whalley & Wahl, 1983). Upregulation of bradykinin B2 receptors is seen as early as 2 h after the onset of ischemic stroke that continue to be elevated up to 24 h after the primary insult (Dobrivojević, Špiranec, & Sinđić, 2015; Gauberti, Potzeha, Vivien, & Martinez de Lizarrondo, 2018; Smeda & Daneshtalab, 2017). Interestingly, role of bradykinin and its receptors in SCI are still unclear and require further investigation (see Pan et al., 2001; Sharma, 2000). 2.1 Bradykinin stimulates nitric oxide production Bradykinin induced vasodilatation is largely caused by endothelial production of nitric oxide (NO) (Genaro, Stranieri, & Borda, 2000; Landmesser & Drexler, 2006). Nitric oxide (NO) is a free radical gas and when produced in vivo could also affect microvascular permeability disturbances and cell injury (Sharma, 1998, 1999; Sharma, Alm, & Westman, 1998; Sharma, Drieu, Alm, & Westman, 2000). Our previous studies show that SCI leads to upregulation of neuronal nitric oxide synthase (nNOS) in the traumatized cord and the adjacent rostral and caudal segments (Sharma et al., 1998; Sharma, Westman, Olsson, & Alm, 1996). Upregulation of nNOS is well known to induce NO production that is responsible for cell injury and microvascular permeability disturbances (Sharma, 1998; Sharma & Alm, 2004; Sharma, Alm, & Westman, 1998; Sharma, Nyberg, Westman, et al., 1998; Sharma et al., 1996). This is further substantiated by our findings that when nNOS antibodies were applied topically over the injured spinal cord, cell changes, edema formation and nNOS upregulation in the spinal cord were absent (Sharma et al., 1996; Sharma, Nyberg, Westman, et al., 1998). In cell culture studies, bradykinin stimulated nitric oxide production by twofold within 30 min after its application. This NO stimulation by bradykinin is blocked by bradykinin B2 receptor antagonist HOE-140 (Sesti, Martino, Mazzulla, & Chimenti, 2005; Zhang, Nasjletti, Xu, & Hintze, 1998). This observation clearly suggests that bradykinin induced endothelial NO production is mediated by bradykinin B2 receptors. 2.2 Bradykinin B2 receptors in spinal cord injury Bradykinin is implicated in spinal network, neuropathic pain, rhizotomy, inflammatory hyperalgesia and neuroinflammation in the spinal cord (Bannister et al., 2014; Ma et al., 2019; Mandadi et al., 2016; Pan et al., 2001; Sharma, 2000; Xu et al., 2008; Yan-Feng et al., 2008). Very few report deal with bradykinin in spinal cord injury (Pan et al., 2001; Sharma, 2000). There are reports of significant elevation of bradykinin after experimental spinal cord injury (see Pan et al., 2001). Also interaction of bradykinin with aquaporin4 in spinal cord ischemic injury to the cord was described. (Xu et al., 2008) We reported reduction in BSCB breakdown by B2 receptor antagonist HPE-140 in cord injury indicating involvement of bradykinin in SCI (see Sharma, 2000). However, detailed investigations on bradykinin involvement in SCI require further investigations. With view of bradykinin interacting with dynorphin and nitric oxide in the CNS it is important to understand the modulating roles of bradykinin in SCI that upregulated both nitric oxide and dynorphin after trauma (see Bannister et al., 2014; Sharma, Nyberg, Gordh, et al., 1998; Sharma, Nyberg, & Olsson, 1992; Sharma, Olsson, & Nyberg, 1995; Sharma et al., 1996; Stålberg et al., 1998; Winkler, Sharma, Stålberg, & Westman, 1998). Peat on Bradykinin Direct mentions are sparse: "Bacterial endotoxin increases serotonin release from the intestine, and increases its synthesis in the brain (Nolan, et al., 2000) and liver (Bado, 1983). It also stimulates its release from platelets, and reduces the lungs' ability to destroy it. The formation of serotonin in the intestine is also stimulated by the lactate, propionate and butyrate that are formed by bacteria fermenting fiber and starch, but these bacteria also produce endotoxin. The inflammation-producing effects of lactate, serotonin, and endotoxin are overlapping, additive, and sometimes synergistic, along with histamine, nitric oxide, bradykinin, and the cytokines." "Y. Kuraishi (2015) said that noradrenaline inhibits pain by inhibiting the release of substance P and glutamate (the excitatory amino acid), and that the suppression of cancer pain results in the inhibition of tumor growth and lung metastasis..., apparently by inhibiting the release of substances from cancer cells (e.g., ATP, endothelin-1, and bradykinin). Things that activate and enliven the patient, and that at the same time decrease pain, seem to be therapeutically appropriate." A role for bradykinin signaling in chronic vulvar pain​ Chronic vulvar pain is alarmingly common in women of reproductive age and is often accompanied by psychological distress, sexual dysfunction, and a significant reduction in quality of life. Localized provoked vulvodynia (LPV) is associated with intense vulvar pain concentrated in the vulvar vestibule (area surrounding vaginal opening). To date, the origins of vulvodynia are poorly understood, and treatment for LPV manages pain symptoms, but does not resolve the root causes of disease. Until recently, no definitive disease mechanisms had been identified; our work indicates LPV has inflammatory origins, although additional studies are needed to understand LPV pain. Bradykinin signaling is one of the most potent inducers of inflammatory pain and is a candidate contributor to LPV. We report that bradykinin receptors are expressed at elevated levels in LPV patient versus healthy control vestibular fibroblasts, and patient vestibular fibroblasts produce elevated levels of proinflammatory mediators with bradykinin stimulation. Inhibiting expression of one or both bradykinin receptors significantly reduces proinflammatory mediator production. Finally, we determined that bradykinin activates NFκB signaling (a major inflammatory pathway), while inhibition of NFκB successfully ablates this response. These data suggest that therapeutic agents targeting bradykinin sensing and/or NFκB may represent new, more specific options for LPV therapy. Bradykinin in Pain & Inflammation + How to Decrease It Positive Effects of Bradykinin Although bradykinin may cause problems, it also serves an important purpose in the body. Bradykinin protects your heart and your nerves from damage. In the heart, it widens vessels and lowers blood pressure, which prevents heart failure and damage caused by high blood pressure. When the spinal cord or other nerves are injured, bradykinin protects nerve cells and prevents them from dying [15, 16]. 1) Heart Health and Blood Pressure High blood pressure can lead to heart failure. Bradykinin widens blood vessels and decreases blood pressure, which can protect the heart and keep it functioning after congestive heart failure [17, 18]. Doctors often take advantage of the protective effects of bradykinin to help patients with heart conditions. Angiotensin-converting-enzyme inhibitors, or ACEIs, are often prescribed to prevent heart failure in people with high blood pressure. ACEIs stop bradykinin from being broken down, and the increased concentration of bradykinin decreases blood pressure [15, 19]. 2) Insulin Sensitivity Bradykinin makes fat and muscle cells more sensitive to insulin, possibly by increasing the activity of insulin receptors on these cells [20]. Insulin resistance, the condition in which cells are not sensitive enough to insulin, develops before and often predicts type 2 diabetes. Because bradykinin increases the insulin sensitivity of certain cells, it may reduce the risk of developing type 2 diabetes. In turn, drugs which increase bradykinin, such as ACEIs, may prevent type 2 diabetes from developing [21, 20].