Water Structure, Osmolytes And Cancer

[LLight]

(PDF) Vasopressin and oxytocin release and the thyroid function

PDF | The aim of the present investigations was to examine the effects of the states of hypothyroidism or hyperthyroidism on vasopressin (AVP) and... | Find, read and cite all the research you need on ResearchGate

www.researchgate.net

Water restriction (but not salt loading) seems to boost T3 production in this model of hypothyroidism.

From another paper (see below), we know that a transcription factor called CREB3L1 is involved both in thyroid iodine metabolism and vasopressin (the antidiuretic hormone) production. CREB3L1 is also know to be activated by TSH. This seems to be how TSH initiates thyroid hormone production : CREB3L1 increases the expression of the NIS (iodine symporter) in the thyroid.

Transcription Factor CREB3L1 Regulates the Expression of the Sodium/Iodide Symporter (NIS) in Rat Thyroid Follicular Cells

Here, we analyzed the role of CREB3L1 as a TSH-dependent transcriptional regulator of the expression of the sodium/iodide symporter (NIS), a major thyroid protein that mediates iodide uptake. We show that overexpression and inhibition of CREB3L1 induce an increase and decrease in the NIS protein and mRNA levels, respectively. This, in turn, impacts on NIS-mediated iodide uptake. Furthermore, CREB3L1 knockdown hampers the increase the TSH-induced NIS expression levels. Finally, the ability of CREB3L1 to regulate the promoter activity of the NIS-coding gene (Slc5a5) was confirmed. Taken together, our findings highlight the role of CREB3L1 in maintaining the homeostasis of thyroid follicular cells, regulating the adaptation of the secretory pathway as well as the synthesis of thyroid-specific proteins in response to TSH stimulation.
[...]
Our findings argue in favor of the notion that, under physiological conditions, CREB3L1 may contribute to thyroid cell differentiation promoting the production of thyroid hormones.

Participation of CREB3L1 in a hormone synthetic pathway has been also reported in pituitary gland where CREB3L1 not only regulates transcription of the gene coding for antidiuretic hormone arginine vasopressin (AVP), but also its processing via increased Pcsk1 expression, revealing its role as a key molecular component of AVP biosynthesis.

So we can wonder whether this transcription factor couldn't also be activated in the thyroid by hyperosmolarity (which is a signal for vasopressin production), promoting iodine metabolism and thyroid hormones production. It would fit with the data about water restricted rats improving their hypothyroidism and the other study where water restricted rats had slightly lower TSH than the control group.

 

[LLight]

Liver X receptors and copper metabolism: New frontiers for the oxysterol receptors

We read with great interest the article by Hamilton et al.1 showing that treatment with the liver X receptor (LXR) agonist, T0901317, ameliorates disease manifestation in a mouse model of Wilson disease (WD), but only with a partial effect in inducing the predicted LXR target genes.

It should be noted that T0901317 is a synthetic LXR ligand that has a weak LXR specificity given that it can also bind to and activate other nuclear receptors, such as farnesoid X receptor (FXR) and pregnane X receptor.2, 3 Interestingly, the activity of the bile acid receptor, FXR, has recently been shown to be down-regulated in both patients and an animal model of WD, exhibiting elevated serum bile acids and bilirubin levels.4 Therefore, the beneficial effects of T0901317 may be attributed to a simultaneous activation of both FXR and LXR in livers affected by WD.

Nevertheless, what is the link between a selective LXR activation and copper homeostasis?

First, copper may bind with high affinity to the DNA-binding domain of several nuclear receptors, including LXRs, inducing a conformational change that prevents DNA binding and, in turn, their transcriptional activity.4

Second, and most interestingly, microarray studies in wild-type mice treated with the more selective LXR agonist, GW3965, showed an up-regulation of a cluster of genes involved in copper homeostasis, such as metallothionein 1 and 2, the copper transport protein, Atcx1, and ceruloplasmin.5

Taken together, all those studies open new perspective for the oxysterol receptors, LXRs, involved not only in controlling lipid metabolism, inflammation, water transport, and cell proliferation, but also in regulating copper homeostasis.

These data make think that activation of LXR and/or FXR might improve copper metabolism. Copper metabolism issues seems to be involved in lots of disease, like Alzheimer's or cardiovascular diseases for example. Copper could also be impairing the functioning of these transcription factors, which seems rather bad.

Copper is also involved in the antioxidant enzymes SOD 1 and 3, which might find useful in case of osmotic stress.
Dietary supplementation with copper oxide nanoparticles ameliorates chronic heat stress in broiler chickens

Finally, it seems like copper can form complexes with antidiuretic hormones (oxytocin and vasopressin) and potentiates their effect (or do nothing it), which is intriguing. Maybe this could serve to bring copper to certains places like the mitochondria?

Binding of Cu+ and Cu2+ with peptides: Peptides = oxytocin, Arg8-vasopressin, bradykinin, angiotensin-I, substance-P, somatostatin, and neurotensin

Oxytocin, arg8-vasopressin, bradykinin, substance-P, and somatostatin show the binding of 5Cu+, and angiotensin-I and neurotensin show the binding of 7Cu+ from both CuI and Cu targets, while bradykinin shows the binding of 2Cu2+, oxytocin, arg8-vasopressin, angiotensin-I, and substance-P; somatostatin shows the binding of 3Cu2+; and neurotensin shows 4Cu2+ binding.

Cu(II) complexation potentiates arginine vasopressin action on nonpregnant human myometrium in vitrohttps://pubmed.ncbi.nlm.nih.gov/12814818/

 

[LLight]

The MnSOD (an antioxidant enzyme located in the mitochondria that uses manganese) could be important regarding the fluid restriction response, and detoxification of xenobiotics/endobiotics/ROS specifically.
​

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Transcriptional profiling of MnSOD-mediated lifespan extension in Drosophilareveals a species-general network of aging and metabolic genes​

Lifespan extension by MnSOD appears to proceed through a retrograde signal of increased hydrogen peroxide that involves an intricate network of genes that modulate energetic efficiency, purine biosynthesis, apoptotic pathways, endocrine signals, and the detoxification and excretion of metabolites.​

Taken together with results from C. elegans, the data suggest a model in which MnSOD is a direct transcriptional target of the FOXO transcription factor and MnSOD catalyzed detoxification of superoxide results in increased intracellular hydrogen peroxide levels that mediate numerous signaling events.​

In a Drosophila model where MnSOD was upregulated, it was shown that detoxification pathways are increased due to the fact that this enzyme catalyzes the production of superoxide to hydrogen peroxide, a signaling molecule.​

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Molecular strategies of the Caenorhabditis elegans dauer larva to survive extreme desiccation​

These data show that the desiccation response is activated by hygrosensation (sensing the desiccative environment) via head neurons. This leads to elimination of reactive oxygen species and xenobiotics, expression of heat shock and intrinsically disordered proteins, polyamine utilization, and induction of fatty acid desaturation pathway.​

The data also indicated strong activation of the ROS defense pathway. Additionally, many enzymes with cytochrome P450 and glutathione S-transferase (GST) activity were enriched among the upregulated genes. These enzymes not only accept endogenous substrates but also contribute to degradation of xenobiotics. Thus, detoxification may be another general strategy of desiccation tolerance.​

In a model of anhydrobiosis (organisms surviving extreme dehydration), the C. elegans sod-3 enzyme (a MnSOD) was increased (along with other SOD enzymes) following extreme desiccation. Xenobiotics detoxification pathways were upegulated too.​

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Water restriction increases renal inner medullary manganese superoxide dismutase (MnSOD)​

Water restriction, which elevates renal medullary NaCl and urea, increases MnSOD protein, accompanied by a proportionate increase in MnSOD enzymatic activity in the inner medulla, but not in the cortex or the outer medulla.​

Kidneys needs MnSOD to sustain water restriction.​

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Farnesoid X receptor activation by chenodeoxycholic acid induces detoxifying enzymes through AMP-activated protein kinase and extracellular signal-regulated kinase 1/2-mediated phosphorylation of CCAAT/enhancer binding protein β​

Effects of FXR Agonists on the Induction of Detoxifying Enzymes.
Oxidative stress promotes the progression of various diseases by altering intracellular redox homeostasis, thereby sometimes causing cell death when the stress persists or exceeds the range of cellular antioxidative capacity (Shaw et al., 2004). In a continuing effort to define the functional outcome of CDCA treatment in terms of antioxidant capacity, we measured the effect of CDCA treatment on the levels of glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, and MnSOD transcripts from the genes containing the C/EBP-RE (Maehara et al., 1999; Yang et al., 2001).

As expected, CDCA treatment significantly increased all of the transcript levels in a time-dependent manner (Fig. 6A).​

In this study, the FXR transcription factor (which was already shown to participate in xenobiotic detoxification and water homeostasis) activation increased detoxification genes including the MnSOD enzyme.​

 

[aliml]

ClinicalTrials.gov

clinicaltrials.gov

Effect of Salt Solution Immersion Bath on Cancer in Vivo​

Study Description:
Many previous studies have shown that the Cancer cells are over-hydrated, and that Hyponatraemia exists in many cases of Cancer. The Cancer cell's viability depends on Angiogenesis and formation of blood vessels that carry water and nutrient to the rapidly-dividing Cancer cells. This study tests the hypothesis that disrupting the water content of blood could lead to increasing its Tonicity and hence withdrawing water from the Cancer cells by Osmosis, which can result in disrupting the growth of the Cancer cell itself. This disruption of Blood Water content can be achieved using Osmotic Pressure differential via immersing the whole body in Hypertonic Saline Solution for a certain amount of time, thus making the Blood more Hypertonic relative to the cells of the body and of the cancer, leading to water withdrawal from the cells of the body and of the cancer. While body's cells can sustain temporary dehydration, Cancer cells could be negatively affected.
Study Design:
A pilot randomized blinded controlled study, whereas a number of patients with clinically-diagnosed Cancer (any type, any location and any stage), and who were poorly responsive to at least one cycle of conventional and standard therapy (Chemotherapy or Radiation therapy), are equally divided into 2 groups, Active and Control groups. The Active group patients will separately have an immersion bath in 25% Sea Salt in Water solution at a temperature comfortable to every patient, whereas the bath solution is in direct contact with the skin, for 30 minutes once daily for 7 consecutive days, in addition to their standard treatments they receive from their health care providers. The Control group's patients will separately have a bath in 0.9% Sea Salt in Water at a comfortable temperature whereas the bath solution is in direct contact with the skin, for 30 minutes once daily for 7 consecutive days, in addition to their standard treatments they receive from their health care providers.
Additional Information:
Synthetic ion transporters can induce apoptosis by facilitating chloride anion transport into cells.
High Salt Inhibits Tumor Growth by Enhancing Anti-tumor Immunity.
The osmotic passage of water and gases through the human skin.
Permeability Of The Skin: A Review Of Major Concepts And Some New Developments.
Cell swelling, softening and invasion in a three-dimensional breast cancer model.
Cell Stiffness May Indicate Likelihood of Cancer Metastasis.
The Dysfunction of Metabolic Controlling of Cell Hydration Precedes Warburg Phenomenon in Carcinogenesis.
Publications:
Cell hydration as the primary factor in carcinogenesis: A unifying concept.
The relationship between transepidermal water loss and skin permeability.

 

[yerrag]

Synthesis of the cathelicidins is
dependent on vitamin D. - July 2021 RP Newsletter

Currently getting as much sunshine as possible to get my Vitamin D levels to at least 50 ng/ml. Weather permitting, getting 2 hours exposure of peak sunshine daily to get 20,000 IU each day.

I have not been taking any D supps at all, and I had not been consciously getting direct sunshine these past years so I am aiming for achieving serum D levels of 50ng/ml solely off sunlight. I would need probably 1-2 weeks more of sunlight exposure to attain minimum serum vitamin D levels. Since exposure to sunlight does not lead to vitamin D excess (unlike D supplementation), I would be assured of sufficient D levels to maximize my production of cathelicidins, especially LL-37, which are needed to help kill microbes that are responsible for my blood pressure condition (as I suspect).

I would then be able to further maximize LL-37 production on a 5-day dry fast, which I believe I am fit enough now to do, given that my recent blood sugar testing using a 5 hr OGTT (oral glucose tolerance test) points to.

Here is a study Peat referenced to on vitamin D being needed for cathelicidin production:

The role of cathelicidin and defensins in pulmonary inflammatory diseases - PubMed

Antimicrobial peptides (AMPs) protect the epithelia of mucosal organs like the respiratory or the gastrointestinal tract from invading microorganisms. As an integral part of the innate immune system they display antimicrobial activity against gram- and gram-negative bacteria as well as against...

pubmed.ncbi.nlm.nih.gov

 

[LLight]

ClinicalTrials.gov

clinicaltrials.gov

Effect of Salt Solution Immersion Bath on Cancer in Vivo​

Study Description:
Many previous studies have shown that the Cancer cells are over-hydrated, and that Hyponatraemia exists in many cases of Cancer. The Cancer cell's viability depends on Angiogenesis and formation of blood vessels that carry water and nutrient to the rapidly-dividing Cancer cells. This study tests the hypothesis that disrupting the water content of blood could lead to increasing its Tonicity and hence withdrawing water from the Cancer cells by Osmosis, which can result in disrupting the growth of the Cancer cell itself. This disruption of Blood Water content can be achieved using Osmotic Pressure differential via immersing the whole body in Hypertonic Saline Solution for a certain amount of time, thus making the Blood more Hypertonic relative to the cells of the body and of the cancer, leading to water withdrawal from the cells of the body and of the cancer. While body's cells can sustain temporary dehydration, Cancer cells could be negatively affected.
Study Design:
A pilot randomized blinded controlled study, whereas a number of patients with clinically-diagnosed Cancer (any type, any location and any stage), and who were poorly responsive to at least one cycle of conventional and standard therapy (Chemotherapy or Radiation therapy), are equally divided into 2 groups, Active and Control groups. The Active group patients will separately have an immersion bath in 25% Sea Salt in Water solution at a temperature comfortable to every patient, whereas the bath solution is in direct contact with the skin, for 30 minutes once daily for 7 consecutive days, in addition to their standard treatments they receive from their health care providers. The Control group's patients will separately have a bath in 0.9% Sea Salt in Water at a comfortable temperature whereas the bath solution is in direct contact with the skin, for 30 minutes once daily for 7 consecutive days, in addition to their standard treatments they receive from their health care providers.
Additional Information:
Synthetic ion transporters can induce apoptosis by facilitating chloride anion transport into cells.
High Salt Inhibits Tumor Growth by Enhancing Anti-tumor Immunity.
The osmotic passage of water and gases through the human skin.
Permeability Of The Skin: A Review Of Major Concepts And Some New Developments.
Cell swelling, softening and invasion in a three-dimensional breast cancer model.
Cell Stiffness May Indicate Likelihood of Cancer Metastasis.
The Dysfunction of Metabolic Controlling of Cell Hydration Precedes Warburg Phenomenon in Carcinogenesis.
Publications:
Cell hydration as the primary factor in carcinogenesis: A unifying concept.
The relationship between transepidermal water loss and skin permeability.

Interesting, thanks you! I will wait for the results but 7 days might be a little short

Synthesis of the cathelicidins is
dependent on vitamin D. - July 2021 RP Newsletter

Currently getting as much sunshine as possible to get my Vitamin D levels to at least 50 ng/ml. Weather permitting, getting 2 hours exposure of peak sunshine daily to get 20,000 IU each day.

I have not been taking any D supps at all, and I had not been consciously getting direct sunshine these past years so I am aiming for achieving serum D levels of 50ng/ml solely off sunlight. I would need probably 1-2 weeks more of sunlight exposure to attain minimum serum vitamin D levels. Since exposure to sunlight does not lead to vitamin D excess (unlike D supplementation), I would be assured of sufficient D levels to maximize my production of cathelicidins, especially LL-37, which are needed to help kill microbes that are responsible for my blood pressure condition (as I suspect).

I would then be able to further maximize LL-37 production on a 5-day dry fast, which I believe I am fit enough now to do, given that my recent blood sugar testing using a 5 hr OGTT (oral glucose tolerance test) points to.

Here is a study Peat referenced to on vitamin D being needed for cathelicidin production:

The role of cathelicidin and defensins in pulmonary inflammatory diseases - PubMed

Antimicrobial peptides (AMPs) protect the epithelia of mucosal organs like the respiratory or the gastrointestinal tract from invading microorganisms. As an integral part of the innate immune system they display antimicrobial activity against gram- and gram-negative bacteria as well as against...

pubmed.ncbi.nlm.nih.gov

Hi Yerrag,

If I remember correctly the LL-37 production due to osmotic regulation wasn't directly linked to the vitamin D "pathway". I suppose it cannot be counterproductive though.

The link of Peat is interesting, I didn't know that AMP were useful for tissue repair.

I don't know if you still have blood oxygen dips during the night but I thought about this issue the other day while I was reading comments about a manganese supplement. A guy was saying that he was monitoring his O2 during the night (with a Fitbit if I remember correctly, and that may not be the perfect device to do that) and that supplementing with it fixed his O2 dips during the night one week after having started taking the supplement. He even posted screen shots showing the difference of his nights before and after. You might not be deficient in manganese though.

 

[yerrag]

Interesting, thanks you! I will wait for the results but 7 days might be a little short


Hi Yerrag,

If I remember correctly the LL-37 production due to osmotic regulation wasn't directly linked to the vitamin D "pathway". I suppose it cannot be counterproductive though.

The link of Peat is interesting, I didn't know that AMP were useful for tissue repair.

I don't know if you still have blood oxygen dips during the night but I thought about this issue the other day while I was reading comments about a manganese supplement. A guy was saying that he was monitoring his O2 during the night (with a Fitbit if I remember correctly, and that may not be the perfect device to do that) and that supplementing with it fixed his O2 dips during the night one week after having started taking the supplement. He even posted screen shots showing the difference of his nights before and after. You might not be deficient in manganese though.

How I wish that would be the case, regarding manganese. I'm not likely deficient in manganese, as I've been eating a variety of food ever since I left the US.

I still have those large drops in spO2 though, and I'm still not sure whether they are as bad as they appear to be.

 

[LLight]

An interesting property of oxytocin (and vasopressin too) is that it seems to be able to carry silver atoms.

I don't know if it's something that really happens in vivo but if it's the case, could it be a way silver is distributed to cells?

https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/abs/10.1002/rcm.7562

We have investigated Ag+ binding of six biologically important peptides in the mass range 1–2 kDa to determine their intrinsic binding ability. The [Peptide-(Ag)n] + complexes were prepared and characterized by MALDI-MS. The peptides show the binding of 5–7 Ag+ and the possible amino acids responsible for the binding are analyzed based on the DFT-calculated relative binding energies of Ag+ with individual amino acids. The peptides OT and AVP show the formation of their dimers and its Ag+ complexes. In addition, the mass spectra also show fragment ion formation of the intact peptide and its complexes due to the in-source decay phenomenon. The binding of more Ag+ with these peptides indicates the greater affinity for Ag+ as compared to other studied singly/doubly charged metal ions. Thus, it is expected that these peptides become more effective with their respective receptors when tagged with Ag due to their change in conformation. Hence, they may be used as carriers for AgNPs in targeted drug delivery as well as an alternate for iodinated contrasting agents in the dual energy X-ray imaging technique.

Now what is also interesting is that silver and oxytocin seem to be both involved in tissue regeneration via stem cells stimulation. They can also both act against infections.

Oxytocin promotes epicardial cell activation and heart regeneration after cardiac injury

Cardiovascular disease (CVD) is one of the leading causes of mortality worldwide, and frequently leads to massive heart injury and the loss of billions of cardiac muscle cells and associated vasculature. Critical work in the last 2 decades demonstrated that these lost cells can be partially...

www.frontiersin.org

Here, we show that oxytocin (OXT), a hypothalamic neuroendocrine peptide, induces epicardial cell proliferation, EMT, and transcriptional activity in a model of human induced pluripotent stem cell (hiPSC)-derived epicardial cells.

Induced dedifferentiation: A possible alternative to embryonic stem cell transplants - IOS Press

Induction of local tissue regeneration in the human would best be accomplished if the patient's own cells at the desired site could be caused to dedifferentiate into the required embryonic stem cells. A system involving the electrical iontophoretic i

content.iospress.com

Induction of local tissue regeneration in the human would best be accomplished if the patient's own cells at the desired site could be caused to dedifferentiate into the required embryonic stem cells. A system involving the electrical iontophoretic introduction of free silver ions into human wounds for their antibiotic effect has been in clinical use since 1975. In addition to a major antibiotic effect, the technique was found to produce the regeneration of all local tissues, apparently by stimulating dedifferentiation of mature human cells. More recently the use of a newly developed silvered nylon fabric has been found to have similar results without the need for electrical parameters. The results of a preliminary laboratory and clinical study of this material are presented.

 

[yerrag]

After a 2-day dry fast (sugar every few hours, when needed: in case my blood sugar falls low), my blood pressure only went down to 182/120. It wasn't a great improvement over the 179/129 a few days ago on a 1-day dry fast. I had a much higher heart rate, with heart rates ranging from 85-93, as in the two previous 1-day fasts.

I'll have to do another 2-day dry fast, but without sugar assist to see if that makes a big difference. I wonder how low blood sugar can get in a fast though, as it seems to me that in a fast, I can still carry on at a blood sugar of 60 (although I can sense it's low) while regularly (without a fast) I may have a harder time.

A good thing to try. I may try that in between dry fasts, just skipping breakfast and not drinking water until lunch. And during the other times, to drink only when I thirst.

It's the norm for people to keep drinking water throughout the day, and without ever dry fasting, the habit could be making thing worse for people.

I wonder how healthy and hardy wild animals are who go through the extreme seasons of water abundance and scarcity in some parts of Africa. There was a thread here about how animals who are less hydrated go to the watering holes being more peaceful. The idea was that this is an adaptation to make possible less conflicts given the proximity of animals sharing a space. Hard to know though if the lack of excessive hydration has anything to do with it, or that it was a survival adaptation to make animals co-exist and share a resource.




Not so sure on the role of vasopression. The stools could be "dehydrated" because the colon will tend to absorb more water from the colon wastes, leaving a smaller stool. And my sleep could be less interrupted by urination because water has to be conserved even more in a dry fast? But I'm still interested in knowing the effect of dry fasting on vasopressin as it relates to sleep and digestion.

@LLight

I was on a 2 day fast, one on water and the next day on juice..Each of these days my BP went down. Then On the third day I ate a meal of rice and ground beef. Then my BP shot up.

I now suspect it is the dietary iron in beef that is feeding the bacteria in my blood vessels that is causing my BP to increase.

Will have to try fasting from meat to see if this approach would be helpful in lowering my BP.

 

[LLight]

Will have to try fasting from meat to see if this approach would be helpful in lowering my BP.

Could proteins also be involved in your high BP?
Might be an interesting hypothesis along with the one involving iron, because fasting is also a total protein restriction.

Was your BP after the fast more elevated than before it?

 

[yerrag]

@LLight Yes.

 

[LLight]

@yerrag this adds to the conundrum indeed.

 

[yerrag]

@LLight Yes, so many twists and turns. The author of GOT would be as easily perplexed.

 

[LLight]

@yerrag Out of curiosity, do you tend to have a good memory or not?

I'm currently researching the benefits of colloidal silver and colloidal gold. I see a lot of testimonies of people improving their memory with gold (which makes me very interested in it because my memory tends to be bad at times). I think gold could associate with the vasopressin peptide and improve its function (it seems like vasopressin is linked with memory) as it was theorized in the last publications I posted here regarding silver atoms and vasopressin/oxytocin.

I thought that vasopressin being connected to blood pressure (I've also seen someone saying that his BP was improved with colloidal gold but it's highly anecdotal) and water retention (you mentioned being awakened to go to the WC many times some nights), it could be an interesting idea. However vasopressin is rather known to increase BP if I'm not mistaken so it might have an inverse effect, who knows. Maybe water fasting has an impact on vasopressin and creates this rebound when you restart eating (not only juices). I don't know, this is a complete hypothesis.

 

[yerrag]

I've had two episodes of memory loss each associated with taking supplements that do some kind of lysing. The first one was with using a proteolytic enzyme. This was 4 years ago.

The second one was about two months ago involving taking a supplement that improves capillary health that contains fucoidan, hyaluron, and glucosamine. It is supposed to restore the glycocalyyx, which is a gel layer lining the insides of our capillaries.

I would have a hard time with word recollection. It is what we commonly call "tip of the tongue." But thankfully, each episode was temporary, though it would just fade off without me realizing it.

I think of it as perhaps the brain being under reconstruction to restore operation in the near but uncertain future. Can't tell though if there was renewal in the form of becoming better.

The first time my BP shot up from 180/120 to 240/150 and held on and took a long time to lower, about 2 years to settle at 200/130.

The second one didn't have such an effect, but wasn't lowering my BP.

 

[LLight]

Interesting but it's hard to make a firm conclusion about it.

 

[LLight]

This publication seems rather on topic.

Structured Water and Cancer: Orthomolecular Hydration Therapy | Journal of Cancer Research Updates

It is a common practice to envision cancer exclusively as a genetic disease, however, in our perspective, changes in gene expression leading to malignancy are secondary to biochemical disturbances and at its core we consider cancer as a metabolic energetic disease. In this regard, incongruence with the concept of the bioenergetic theory of carcinogenesis, we propose structured water (EZ water), as an element that facilitates the correction of the fundamental energy disruption and the reestablishment of health. The prime approach for this therapy would be to infuse kosmotropic osmolytes by the intravenous route to improve the physiological conditions and promote the reduction of cancer growth with no side effects. By doing so, we could expect that the cells will regain their communication ability with a functioning Ras and p53 proteins and other metabolic and transcription factors. The end goal is to support the cell in overcoming its low-energy anaerobic glycolytic metabolism that favors uncontrolled growth and regain the full energetic potential of oxidative phosphorylation that supports controlled cell division and differentiation. To achieve this goal, we propose the use of metabolic correction to improve the membrane function of the mitochondria. The use of precursors, enzymatic cofactors, and a variety of biological response modifiers which includes structured water and its kosmotropic properties in enzyme dynamics are part of the metabolic correction concept.

Recently, I have been interested in IP6 (inositol hexaphosphate) which has been shown to be useful against cancer (and other diseases like diabetes or blood vessels calcification) and which is connected to osmolytes (inositol being an important one).

 

[LLight]

Here is a publication about hyperosmolarity, structured water, osmolytes and cancer, which is basically the same as the first one having been posted in this thread, but in a proper format and with some additional data I believe.

 

[LLight]

I've begun to write some ideas in a Substack. Nothing really new but I think it could also be helpful to organize these ideas while writing them down.

Here is the last one:

Osmolytes as anti-aging compounds

Less water, more osmolytes please!

open.substack.com

 

[LLight]

Two new posts about the glymphatic system and Chronic Fatigue Syndrome:

Glymphatic system

The brain's cleansing system and its link with water homeostasis

open.substack.com

Chronic Fatigue Syndrome (& long covid) and NFAT5

An intriguing series of associations

open.substack.com