Water Structure, Osmolytes And Cancer

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LLight

LLight

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New post summarizing some data already posted here:
  1. There exist theoretical arguments allowing us to hypothesize that hyperosmolarity, induced by water restriction for example, could facilitate the synthesis of thyroid hormones while potentially lowering the requirement for TSH stimulation.
  2. Rats (with an animal model of hypothyroidism) put under water restriction got an increase in their T3 levels, bringing them almost back to the control group’s levels.
  3. It was found that, in rabbits, vasopressin itself seems to play a role similar to TSH regarding thyroid hormone synthesis.
  4. Two studies on rats found that water restriction or deuterium depleted water (which might be interpreted by the body as water restriction) tend to lower TSH levels.
  5. Finally, bile acids could be related both to the TSH and metabolic rate of tissues involved in thermogenesis, but are also related to water homeostasis as the bile acid TGR5 receptor (along with the FXR transcription factor) is involved in kidneys’ function. From this data, we can hypothesize that a TSH decrease itself could boost T3 systemic levels as it might increase bile acids synthesis and thus peripheral deiodinase enzymes.

Thus, water restriction (or deuterium depletion) could lead to a TSH decrease while keeping thyroid hormones levels maintained or increased. The TSH decrease could be explained by an increase in vasopressin, which could play the role of a TSH surrogate and stimulate bile acids synthesis and thus the conversion of T4 to T3 in peripheral tissues.

Another explanation could be that hyperosmolarity itself, by activating the NFAT5 transcription factor which would upregulate the uptake of inositol by the thyroid, or activating the CREB3L1 transcription factor, would increase the sensitivity of the thyroid gland to TSH and optimize thyroid hormones output.

Upping intake of inositol, selenium and intermittently restricting water intake to achieve hyperosmolarity may improve the function of the thyroid system.
 

Regina

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New post summarizing some data already posted here:
  1. There exist theoretical arguments allowing us to hypothesize that hyperosmolarity, induced by water restriction for example, could facilitate the synthesis of thyroid hormones while potentially lowering the requirement for TSH stimulation.
  2. Rats (with an animal model of hypothyroidism) put under water restriction got an increase in their T3 levels, bringing them almost back to the control group’s levels.
  3. It was found that, in rabbits, vasopressin itself seems to play a role similar to TSH regarding thyroid hormone synthesis.
  4. Two studies on rats found that water restriction or deuterium depleted water (which might be interpreted by the body as water restriction) tend to lower TSH levels.
  5. Finally, bile acids could be related both to the TSH and metabolic rate of tissues involved in thermogenesis, but are also related to water homeostasis as the bile acid TGR5 receptor (along with the FXR transcription factor) is involved in kidneys’ function. From this data, we can hypothesize that a TSH decrease itself could boost T3 systemic levels as it might increase bile acids synthesis and thus peripheral deiodinase enzymes.

Thus, water restriction (or deuterium depletion) could lead to a TSH decrease while keeping thyroid hormones levels maintained or increased. The TSH decrease could be explained by an increase in vasopressin, which could play the role of a TSH surrogate and stimulate bile acids synthesis and thus the conversion of T4 to T3 in peripheral tissues.

Another explanation could be that hyperosmolarity itself, by activating the NFAT5 transcription factor which would upregulate the uptake of inositol by the thyroid, or activating the CREB3L1 transcription factor, would increase the sensitivity of the thyroid gland to TSH and optimize thyroid hormones output.

Upping intake of inositol, selenium and intermittently restricting water intake to achieve hyperosmolarity may improve the function of the thyroid system.
Excellent. Thank you!
 

BearWithMe

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New post summarizing some data already posted here:
  1. There exist theoretical arguments allowing us to hypothesize that hyperosmolarity, induced by water restriction for example, could facilitate the synthesis of thyroid hormones while potentially lowering the requirement for TSH stimulation.
  2. Rats (with an animal model of hypothyroidism) put under water restriction got an increase in their T3 levels, bringing them almost back to the control group’s levels.
  3. It was found that, in rabbits, vasopressin itself seems to play a role similar to TSH regarding thyroid hormone synthesis.
  4. Two studies on rats found that water restriction or deuterium depleted water (which might be interpreted by the body as water restriction) tend to lower TSH levels.
  5. Finally, bile acids could be related both to the TSH and metabolic rate of tissues involved in thermogenesis, but are also related to water homeostasis as the bile acid TGR5 receptor (along with the FXR transcription factor) is involved in kidneys’ function. From this data, we can hypothesize that a TSH decrease itself could boost T3 systemic levels as it might increase bile acids synthesis and thus peripheral deiodinase enzymes.

Thus, water restriction (or deuterium depletion) could lead to a TSH decrease while keeping thyroid hormones levels maintained or increased. The TSH decrease could be explained by an increase in vasopressin, which could play the role of a TSH surrogate and stimulate bile acids synthesis and thus the conversion of T4 to T3 in peripheral tissues.

Another explanation could be that hyperosmolarity itself, by activating the NFAT5 transcription factor which would upregulate the uptake of inositol by the thyroid, or activating the CREB3L1 transcription factor, would increase the sensitivity of the thyroid gland to TSH and optimize thyroid hormones output.

Upping intake of inositol, selenium and intermittently restricting water intake to achieve hyperosmolarity may improve the function of the thyroid system.
That's super interesting, thanks for sharing!

The study says the rats were "deprived of water for two days" with no further details, does it mean they were getting no water at all?
 
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LLight

LLight

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@BearWithMe

Yes possibly. The T3 may be helpful to boost fat utilization and to produce metabolic water to compensate for the lack of water. So in some ways, it might be a response to a stressful situation.

Moreover, I've read testimonies on this forum stating that their T3 supplementation caused them health issues (the theory being that their nutrition was deficient).

Would I advise someone not to drink for 2 days? No except if their nutrition is rather "moist" and with plenty of fat. But this data is helpful to illustrate the concept that water restriction could be helpful.
 
OP
LLight

LLight

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In a previous study by Parodi et al., it was observed that autophagy was actively occurring in hair matrix keratinocytes during the anagen phase of organ-cultured hair follicles [7]. Conversely, not only was autophagy found to be impaired during the catagen phase, but inhibiting autophagy actually promoted catagen development [7]. These findings suggest that one strategy for promoting hair growth in humans is to stimulate intrafollicular autophagy. We reasoned that topically applied magnetized saline water could act as a potential strategy to promote autophagy in the scalp because salinity-alkaline stress may exert autophagy-stimulating effects [15]. Another possibility is the local induction of hyperosmotic stress by magnetized saline water, which has been shown to upregulate aquaporin 3 (AQP3), a channel that primarily transports water, glycerol, and hydrogen peroxide [23,24]. AQP3 not only plays a crucial role in maintaining skin hydration, water retention, and barrier repair, but it also possesses the unique ability to directly bind to Beclin-1, thereby activating autophagy [25]. However, it remains to be answered whether the topical application of magnetized saline water enhances AQP3 expression. Despite the poorly understood mechanisms of autophagy activation by magnetized saline water, the significant positive correlations observed between the increase in Beclin-1 and LC3B expression in the scalp, along with the notable improvements in hair density and HMI, strongly indicate that the clinical effects induced by the lotion were primarily autophagy-dependent. However, we cannot exclude that magnetized saline water may also promote hair growth through autophagy-independent mechanisms. Accordingly, magnetic fields can modify conductivity, dielectric constant, pH, surface tension, and dissolved oxygen levels, leading to enhanced nutrient and gas supply to the scalp [11,18]. To fully harness the clinical benefits of magnetized saline water, further research is needed to clarify its mechanisms of action. When evaluating the benefits of an intervention for treating androgenetic alopecia, it is also important to consider the impact it has on patients. In our study, we found that 80% of participants rated the topical lotion as excellent or good, indicating a high level of satisfaction.
 
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