Tristan Loscha
Member
- Joined
- Dec 18, 2018
- Messages
- 2,206
These Data-Hamsters are unhinged,let them entertain us though.Allegedly excess NaCl and concomitant rise of Sodium sensing Glucocorticoid-Kinase1,Interleukine liberation,NFKB induction etc, is a major driver of inflammation.
Link To Full Study:https://www.researchgate.net/profil...athogenesis-of-neuropsychiatric-disorders.pdf
In the astronaut training(?) study that was also posted at rpf,the rise of inflammatory cytokines was 6-fold,supression of antiinflammatory pathways 4-fold.
My take is that Ray Peat is right on NaCl in hypothyroidism,but for semi-healthy peeps maybe there is risk involved.
the IL17-secreted-by-Th17-cells-cascade is pretty damn evil,and evil isnt aloud o.o..salt is pretty tasty though..
In Depression there is higher residual natrium in one study,IL17 antagonists are used in psoriasis,colitis i think..
IL17 is highly expressed in nervous tissue also,and sodium retention is increased in older age,i saw that sentiment in another one.
i know what the man has to say about salt,but this is new research,unknown to peat in his formative years.
Low Dose salt dosage would be 2-3g total Nacl,
Thoughts?
Abstract
Salt is an important macronutrient that plays pivotal roles in physiological
and pathophysiological conditions. High salt intake is an important cause of
hypertension, cardiovascular disease and stroke. However, recent investigations
uncovered the role of excessive salt intake in the induction of severe
inflammatory reactions through augmentation of T helper-17 pathway and
their inflammatory cytokines. In contrast, numerous studies have shown the
role of inflammation in the pathophysiology of neuropsychiatric disorders
(NPD). Here, it is hypothesized that high salt intake can increase the risk of
NPD through salt-derived neural inflammations. Therefore, this hypothesis
suggests that low-salt intake can decrease the risk of NPD. The present
review discusses the potential role of excessive salt intake in the pathophysiology
of NPD.
Link To Full Study:https://www.researchgate.net/profil...athogenesis-of-neuropsychiatric-disorders.pdf
In the astronaut training(?) study that was also posted at rpf,the rise of inflammatory cytokines was 6-fold,supression of antiinflammatory pathways 4-fold.
My take is that Ray Peat is right on NaCl in hypothyroidism,but for semi-healthy peeps maybe there is risk involved.
the IL17-secreted-by-Th17-cells-cascade is pretty damn evil,and evil isnt aloud o.o..salt is pretty tasty though..
In Depression there is higher residual natrium in one study,IL17 antagonists are used in psoriasis,colitis i think..
IL17 is highly expressed in nervous tissue also,and sodium retention is increased in older age,i saw that sentiment in another one.
i know what the man has to say about salt,but this is new research,unknown to peat in his formative years.
Low Dose salt dosage would be 2-3g total Nacl,
Thoughts?
Abstract
Salt is an important macronutrient that plays pivotal roles in physiological
and pathophysiological conditions. High salt intake is an important cause of
hypertension, cardiovascular disease and stroke. However, recent investigations
uncovered the role of excessive salt intake in the induction of severe
inflammatory reactions through augmentation of T helper-17 pathway and
their inflammatory cytokines. In contrast, numerous studies have shown the
role of inflammation in the pathophysiology of neuropsychiatric disorders
(NPD). Here, it is hypothesized that high salt intake can increase the risk of
NPD through salt-derived neural inflammations. Therefore, this hypothesis
suggests that low-salt intake can decrease the risk of NPD. The present
review discusses the potential role of excessive salt intake in the pathophysiology
of NPD.