How Ketosis May Have Managed My Pain.
GaleHawkins
Posts: 8,159 Member
alzheimersnewstoday.com/2015/02/24/dieting-produces-compound-that-may-drive-inflammation-in-alzheimers-disease/
"In a new study entitled “The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease,” researchers report to have found a natural body producing metabolite – β-hydroxybutyrate (BHB) — capable of blocking NLRP3 inflammasome activation, a multi protein complex that promotes secretion of pro-inflammatory cytokines and is a key mediator in inflammatory diseases and conditions that are known to be driven by states of inflammation, such as Alzheimer’s Disease. The study was published in the journalNature Medicine."
It was the line, "β-hydroxybutyrate (BHB) — capable of blocking NLRP3 inflammasome activation".
Google then found the below article which near the bottom covers diseases that may be trigger by NLRP3 inflammasome activation. We all know β-hydroxybutyrate (BHB) is the main ketone produced by the liver when in ketosis burning fats.
Folks I am tired but excited and I want to get home so I have copied some key remarks. It is a research paper of research so I am not sure how helpful it may be. I have been reading this kind of stuff researching my AS since 1976. Scan to the bottom where you see the names of diseases.
hindawi.com/journals/mi/2015/846782/
Role of Genetic Alterations in the NLRP3 and CARD8 Genes in Health and Disease
Studies have shown that the formation of amyloid β plaques is associated with the activation of NLRP3 inflammasome (Alzheimer's related)
To our knowledge, the study made by Kastbom et al. is the only investigation conducted on the association of genetic alteration in the NLRP3 inflammasome components with the AS susceptibility. (Ankylosis Spondylitis)
However, a significant amount of research remains to be performed on the genetic and functional aspects of NLRP3 inflammasome variants in the predisposition to the risk of celiac disease. (IBS/IBD related)
Given that the DAMPs are well-known direct activators of NLRP3 inflammasome and IL-1β production, further studies on variants responsible for the dysregulation of the NLRP3 inflammasome may provide an insight on the susceptibility of developing gout. (Gout)
Altogether, these findings reflect that the dysregulation of NLRP3 inflammasome might have a prominent role in the pathogenesis of IBD.
"In a new study entitled “The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease,” researchers report to have found a natural body producing metabolite – β-hydroxybutyrate (BHB) — capable of blocking NLRP3 inflammasome activation, a multi protein complex that promotes secretion of pro-inflammatory cytokines and is a key mediator in inflammatory diseases and conditions that are known to be driven by states of inflammation, such as Alzheimer’s Disease. The study was published in the journalNature Medicine."
It was the line, "β-hydroxybutyrate (BHB) — capable of blocking NLRP3 inflammasome activation".
Google then found the below article which near the bottom covers diseases that may be trigger by NLRP3 inflammasome activation. We all know β-hydroxybutyrate (BHB) is the main ketone produced by the liver when in ketosis burning fats.
Folks I am tired but excited and I want to get home so I have copied some key remarks. It is a research paper of research so I am not sure how helpful it may be. I have been reading this kind of stuff researching my AS since 1976. Scan to the bottom where you see the names of diseases.
hindawi.com/journals/mi/2015/846782/
Role of Genetic Alterations in the NLRP3 and CARD8 Genes in Health and Disease
Studies have shown that the formation of amyloid β plaques is associated with the activation of NLRP3 inflammasome (Alzheimer's related)
To our knowledge, the study made by Kastbom et al. is the only investigation conducted on the association of genetic alteration in the NLRP3 inflammasome components with the AS susceptibility. (Ankylosis Spondylitis)
However, a significant amount of research remains to be performed on the genetic and functional aspects of NLRP3 inflammasome variants in the predisposition to the risk of celiac disease. (IBS/IBD related)
Given that the DAMPs are well-known direct activators of NLRP3 inflammasome and IL-1β production, further studies on variants responsible for the dysregulation of the NLRP3 inflammasome may provide an insight on the susceptibility of developing gout. (Gout)
Altogether, these findings reflect that the dysregulation of NLRP3 inflammasome might have a prominent role in the pathogenesis of IBD.
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Replies
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Looks like NLRP3 has a role in a variety of inflammatory diseases. Another article for you, Gale:
Inflammasomes: mechanism of action, role in disease, and therapeutics
It's a recent review (with pretty pictures) that cites the Yale study you mentioned:
The ketone body β-hydroxybutyrate (BHB), which serves as an alternative source of ATP during energy-deficit status, was found to specifically inhibit a variety of stimuli triggering NLRP3 inflammasome activation but not NLRC4 or AIM2 inflammasome activation141. Importantly, in animal models of NLRP3-mediated diseases such as Muckle-Wells syndrome, familial cold autoinflammatory syndrome and urate crystal–induced peritonitis, BHB-complexed nanolipogels and a ketogenic diet strikingly attenuated caspase-1 activation and IL-1β secretion. It was shown that BHB inhibits the NLRP3 inflammasome by preventing potassium efflux and reducing ASC oligomerization and speck formation, although the direct target of BHB is still under exploration141.
You have to pay to view the Yale study, but some of it is here:
http://www.nature.com/nm/journal/v21/n3/abs/nm.3804.html0 -
wabmeser that is an awesome article and drives home how if one can manage Type 2 Diabetes by diet then one may sidestep major health issues.
"NLRP3 inflammasome and atherosclerosis.
Chronic inflammation plays an essential role in the initiation and progression of metabolic disorders such as type 2 diabetes (T2D), obesity, gouty arthritis and atherosclerosis86. Atherosclerosis accounts for 70% of morbidity in T2D patients and is a chronic disease that results in progressive narrowing of arterial vessels due to imbalanced lipid metabolism. Cholesterol crystals and white blood cells accumulate on the arterial wall, limiting the flow of oxygen-rich blood to the organs87. Atherosclerosis is commonly referred to as a hardening or furring of the arteries and can lead to life-threatening complications such as heart attack and stroke."0
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