Water Structure, Osmolytes And Cancer

achillea

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One can easily make their own "water wand" with the information found in the book, "Dancing with water" by MJ Pangman
It took the analemma water group 14 years of their own time and money to create the testing devices and perfect the coherency and then another year to develop and ensure the efficacy of the wand,
It is not easy
 

yerrag

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I understand that there are many scams and many snake oils. I certainly don't want to be a gullible victim of such scams.

For the same reasons bzmazu has enumerated, I don't think I want to forego the chance to try the wand as it could help me greatly and the worst thing to happen to me is to lose $200.

If we added all the supplements and nootropics and pharma drugs we have spent on, and have not seen much results with, much less harm us, what really is $200? How much, for example, is an expensive blood test that got you nowhere with our voodoo doctors?,

I have a plan to use the enelemma water to increase the energy needed to overcome a systemic infectious state, with measurable metrics to gauge its effectiveness, such as wbc, neutrophils, blood pressure, as well as visible signs such as urine foaming. If enelemma can tip the balance of energy towards my healing, it will be worth every cent spent on it, and more.

If one has no idea how to evaluate the enelemma water wand objectively, it would be easy to regard spending money on it at the outset as a waste. Let somebody spend on the enelemma and test it, and when the positive results come in, and one is convinced, then one can then shell out the money for the product.
 
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yerrag

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Here is the returns policy for Analemma:


There is not much risk in trying the product.
 

yerrag

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I understand that there are many scams and many snake oils. I certainly don't want to be a gullible victim of such scams.

For the same reasons bzmazu has enumerated, I don't think I want to forego the chance to try the wand as it could help me greatly and the worst thing to happen to me is to lose $200.

If we added all the supplements and nootropics and pharma drugs we have spent on, and have not seen much results with, much less harm us, what really is $200? How much, for example, is an expensive blood test that got you nowhere with our voodoo doctors?,

I have a plan to use the anelemma water to increase the energy needed to overcome a systemic infectious state, with measurable metrics to gauge its effectiveness, such as wbc, neutrophils, blood pressure, as well as visible signs such as urine foaming. If enelemma can tip the balance of energy towards my healing, it will be worth every cent spent on it, and more.

If one has no idea how to evaluate the enelemma water wand objectively, it would be easy to regard spending money on it at the outset as a waste. Let somebody spend on the enelemma and test it, and when the positive results come in, and one is convinced, then one can then shell out the money for the product.
Sorry @achillea I was referring to you instead of bzmazu

I've started using drinking analemma water since June 11, so it's premature to say anything conclusive, but my oxygen saturation has started to go down to 97 on my oximeter. It has been on 97 more often than before. I use my oximeter many times during the day so I would know. It used to be at 98 more often. I will give it more time to see if it eventually settle on 97, and that will confirm that analemma improved my oxygen saturation. Note that I was consistently at 99 until a year ago. It was after I took a proteolytic enzyme, ZymEssence, that I saw it drop to 98, and it has stayed at 98 consistently ever since. So, now I'm hoping my oxsat could eventually stay at 97 consistently.

Another thing I notice is that I have been experiencing for the 3rd day pus forming at the two base corners of my nose above the moustache area. I've never experienced this, and I've not been bitten or have I nicked it. It's about resolved now, but I wonder if anelemma water caused the pus to form. Maybe anelemma water is enabling some healing process here?

@LLight stay put and I'll update in a month.
 
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LLight

LLight

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Another study on Drosophila. They study how some neurons which are monitoring food and water availability affect the metabolism through the production of capa neuropeptides.


Here are some of the effects of the loss of these peptides:
Loss of Capa/CapaR signaling reduces intestinal contractility, gut compartmentalization and nutrient absorption, which result in systemic metabolic defects characterized by pronounced hypoglycemia and lipodystrophy. These metabolic effects cause a gradual loss of muscle function due to dysregulated Ca2+ homeostasis in skeletal muscles, which impairs feeding behavior and cause premature death.

There is an interesting impact on digestion:
Consistent with these observations as well as our current findings, we observed frequent gut distension as well as loss of acidity in the copper-cell region (CCR) of midguts from Capa/CapaR deficient flies (Fig. 5a); a region functionally analogous to the mammalian stomach. [...] Together, our results suggest that CapaR elimination in intestinal myocytes affects the digestive and absorptive functions of the gut, which has acute effects on organismal lifespan

The lack of these neuropeptides affect glycogen stores:
These data confirmed that the major glycogen storing tissues (i.e. the fat body and skeletal muscles) are depleted of glycogen, which together with the generally lean phenotype of howts>CapaRKO animals

Now what's interesting is that, if I understand correctly (but I welcome any other interpretation of what is said/shown here), these neuropeptides seem to be mostly produced when these flies do not have access to water and/or food and released from the neurons "at high rates" when this is reversed, so that the stimulation of their production and release could be optimized with intermittent access to water and food:
Our data imply that Capa/CapaR signaling plays a central role in coordinating postprandial homeostasis, such as by increasing gut peristalsis, facilitating nutrient absorption and increasing renal secretion. We therefore tested if the Capa-expressing neurons are sensitive to internal signals related to water and nutrient availability. This hypothesis is consistent with the observation that Capa peptides accumulate in Va neurons during desiccation stress, but are subsequently released during recovery. We thus exposed flies to either desiccation or starvation for 24 hours followed by transfer to media with different water and nutrient compositions and applied complementary approaches to measure neurosecretory activity. [...] Consistent with previous findings, these data showed that Capa mRNA levels and immunoreactivity were significantly increased in Va neurons, but not SEG neurons, of desiccated flies compared to control, yet returned to steady-state levels or lower 4 hours after refeeding or rehydration. [...] These data suggest that the Va neurons are inactive during periods of water and/or nutrient restriction but are induced to release Capa neuropeptides at high rates following both refeeding and rehydration. Interestingly, however, long-term hydration of rehydrated flies led to gradual accumulation of Capa peptides, and a concomitant reduction in GFP intensity over the ensuing 24 hours, indicating that water ingestion alone is insufficient to maintain stimulation of Capa-Va neuronal activity in hydrated flies.

Also, capa peptides are countering AKH (homologue of glucagon) levels:
Our study reveal a neuroendocrine mechanism in which Capa peptides released from the CNS exert metabolic control by providing feedback regulation on AKH-mediated lipolysis in the fat body to stabilize circulating sugar levels.

Finally, these neuropeptides have a mammal homologue:
Overall, the striking functional conservation observed between insect Capa and mammalian NmU signaling further emphasizes the unique power of the Drosophila model system as a tool that may provide valuable insights into the complex regulation of metabolic and energy homeostasis in humans.

I wonder whether these results could indicate that eating without drinking water or drinking water without eating is suboptimal and that intermittent dry fasting followed by rehydration and refeeding could be optimal for digestion and metabolism via the timing/rhythmicity of capa/NmU release.
 

Cloudhands

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Another study on Drosophila. They study how some neurons which are monitoring food and water availability affect the metabolism through the production of capa neuropeptides.


Here are some of the effects of the loss of these peptides:


There is an interesting impact on digestion:


The lack of these neuropeptides affect glycogen stores:


Now what's interesting is that, if I understand correctly (but I welcome any other interpretation of what is said/shown here), these neuropeptides seem to be mostly produced when these flies do not have access to water and/or food and released from the neurons "at high rates" when this is reversed, so that the stimulation of their production and release could be optimized with intermittent access to water and food:


Also, capa peptides are countering AKH (homologue of glucagon) levels:


Finally, these neuropeptides have a mammal homologue:


I wonder whether these results could indicate that eating without drinking water or drinking water without eating is suboptimal and that intermittent dry fasting followed by rehydration and refeeding could be optimal for digestion and metabolism via the timing/rhythmicity of capa/NmU release.
Dont you think that higher intake of minerals, especially sodium, could increase osmolarity and decrease extracellular water load? Lots of the observations i just saw you make correlated with capa peptides seem to be the same observations that are made with high salt diets, i can post some studies if youd like.
 
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LLight

LLight

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Dont you think that higher intake of minerals, especially sodium, could increase osmolarity and decrease extracellular water load? Lots of the observations i just saw you make correlated with capa peptides seem to be the same observations that are made with high salt diets, i can post some studies if youd like.

I agree with you, increased osmolarity (with high salt) may play a role, for example if the FXR and LXR really happen to be linked to water homeostasis through the body and especially the gut, and probably in other ways too. By the way, the capa peptides are probably not alone, there are other peptides (some are even mentioned in the paper) and hormones.

Regarding capa, here are two other papers that add interesting things to the first one I think:

Capa mRNA levels were unchanged following immune challenge (Gram-negative or -positive), oxidative stress (H2O2 in the diet), osmotic stress (sorbitol or high salt in the diet) (Fig. 1A), or heat shock, but desiccation elicited significant increases in capa mRNA levels (more than twofold after 24 h compared with untreated controls), with expression returning to control levels within 6 h of recovery (Fig. S1A). Starvation stress in the presence of water failed to increase capa mRNA levels (Fig. 1A and Fig. S1B).
High salt diet itself might not help produce capa in the neurons. Intermittent fasting with water might not be optimal.

Our data support the hypothesis that capa-1 release regulates capaR activation and subsequent internalization, thereby also contributing to signal termination (unless the internalized receptor continues signalling). Can the physiological relevance of capaR activation and desensitization be explained by the function of the peptides? The Drosophila capa peptides have been shown to increase fluid secretion by the Malpighian tubules. However, insects generally need to retain water as much as possible; this could be achieved by releasing the capa peptides at the right physiological moment (e.g., during feeding) and once feeding is over, the diuretic action of the capa peptides needs to be terminated for the insect to conserve water. The rapid desensitization of the capaR may limit the responsiveness of the receptor to repeat agonist challenge and the physiological consequence would be to limit water loss.
This might reinforce the idea (at least for flies) that intermittent drinking is optimal because drinking continuously might desensitize the capa receptor.
 

Cloudhands

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I agree with you, increased osmolarity (with high salt) may play a role, for example if the FXR and LXR really happen to be linked to water homeostasis through the body and especially the gut, and probably in other ways too. By the way, the capa peptides are probably not alone, there are other peptides (some are even mentioned in the paper) and hormones.

Regarding capa, here are two other papers that add interesting things to the first one I think:


High salt diet itself might not help produce capa in the neurons. Intermittent fasting with water might not be optimal.


This might reinforce the idea (at least for flies) that intermittent drinking is optimal because drinking continuously might desensitize the capa receptor.
Here @zarrin77 comes to a similiar conclusion Post in thread 'Very High Salt Intake (50g A Day) Increases Metabolism, Makes People Energetic And Happy' Very High Salt Intake (50g A Day) Increases Metabolism, Makes People Energetic And Happy
 

yerrag

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@LLight Update on the Analemma Wand:

It's already past a month. I can only say I am getting more oximeter readings than before of 97%, but not all the time. I would even see the reading go to 96, 95, and then back on to 97 and 98. It's only when I get the reading to hit 96 at times that I would consider it a 97. When it would fluctuate between 97 and 98, I would consider it a 98.

I hope though, at over time, I would get to see 97 more consistently. In the same way that I went from being consistently 99 to being consistently 98.

I have an additional observation. In a pitcher of 1 liter water, I would stir the wand for about 60 times each time. When I stop to look at the water after I finish stirring, it is very perceptible that in the wake of the stirring, the water would continue to whirl visibly with mini vortexes inside the water column. I would do the exact same stirring using the staninless steel enclosure of the wand, which is slightly thicker, but I would not see the mini vortices. So, visually I can see that the wand is doing something to the water that makes its hydrodynamics different.

Since it was Tom Cowan who got us interested into the wand, I should share also his video on why the heart is not a pump, as this highlights the importance of good quality water, as coherent water purports to be, towards enabling good flow of blood in our body as it relates to the structured property of water. Here is Cown's video on why the heart is not a pump, which is very interesting :


View: https://youtu.be/kUCBEKO3IJc
 
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LLight

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It's already past a month. I can only say I am getting more oximeter readings than before of 97%, but not all the time. I would even see the reading go to 96, 95, and then back on to 97 and 98. It's only when I get the reading to hit 96 at times that I would consider it a 97. When it would fluctuate between 97 and 98, I would consider it a 98.

I hope though, at over time, I would get to see 97 more consistently. In the same way that I went from being consistently 99 to being consistently 98.
Hi Yerrag,

Thanks for your feedback.

One thing is that maybe a prolonged use may be required. Our health issues have appeared over a prolonged period of time, so the cure?
 

yerrag

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Hi Yerrag,

Thanks for your feedback.

One thing is that maybe a prolonged use may be required. Our health issues have appeared over a prolonged period of time, so the cure?
Yup, it takes time to gently effect change. How long have we been drinking incoherent water and how long has coherent water been used? A slow transition is also needed to effect a change that is gradual and not abrupt and stressful.
 
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LLight

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Interestingly, vitamin D1 (20-hydroxyecdysone) seems to be produced in insects (or plants) when they are dehydrated or subject to osmotic stress:

Dehydration triggers ecdysone-mediated recognition-protein priming and elevated anti-bacterial immune responses in Drosophila Malpighian tubule renal cells
Ecdysone titers measured from aged flies were also significantly elevated relative to young females in control (food) conditions, while desiccation increased 20E (20-hydroxyecdysone) in both young and old animals.

HYDROGEN PEROXIDE AND ECDYSONE IN THE CRYOPROTECTIVE DEHYDRATION STRATEGY OF Megaphorura Arctica (ONYCHIURIDAE: COLLEMBOLA)

Significantly elevated H2O2 and 20-HE levels were observed in M. arctica incubated at −2 °C, supporting a link between ecdysone, H2O2, and trehalose levels during cryoprotective dehydration.

NaCl induced salt adaptive changes and enhanced accumulation of 20-hydroxyecdysone in the in vitro shoot cultures of Spinacia oleracea (L.)

We also studied salt-stress induced accumulation of a bioactive compound; 20E and results showed that 200 mM salt treated shoot cultures accumulated significantly 2.9 fold higher 20E as compared to untreated shoot cultures. The results suggest that Spinacia oleracea exhibits considerable salt tolerance with better osmotic adjustment and can be considered a suitable candidate for the production of bioactive secondary metabolite.
 

Amazoniac

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- Orally Administered Betaine Has an Acute and Dose-Dependent Effect on Serum Betaine and Plasma Homocysteine Concentrations in Healthy Humans

"The urinary excretion of betaine seemed to accelerate with an increase in the betaine dose, whereas the excretion of DMG was more constant. The urinary excretion of betaine was 86 ± 43 mmol at the 1-g dose, 638 ± 637 mmol at the 3-g dose, and 2212 ± 1359 mmol at the 6-g dose. The respective values for DMG were 91 ± 49, 160 ± 80, and 261 ± 178 mmol, respectively. A very small proportion of ingested betaine was excreted via urine during the first 24 h because the calculated sum of the excreted betaine and the first metabolic product of betaine, DMG, accounted for only 3.2, 4.3, and 7.4% of the ingested amount of betaine (1, 3, and 6 g, respectively)."​
 
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Our data presents a neuronal molecular mechanism for the action of betaine, via a specific receptor, in the control of complex behaviour within the nervous system of C. elegans. This may suggest a much broader role for betaine in the regulation of animal nervous systems than previously recognised.

[...]

We also showed that animals either lacking the betaine receptor, lgc-41, or the betaine synthesis gene, alh-11, displayed defects in multiple food search behaviours.

[...]

Previous work has implicated betaine in controlling normal locomotion through the muscular cationic betaine-gated channel ACR-23.

[...]

Several types of bacteria, including E. coli, produce betaine to regulate their osmolarity23, and as such it is possible that betaine levels in bacteria may act as a marker of food quality for worms.
 
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Osmolytes are known regulators of skeletal muscle development, with the involvement of taurine and betaine already described in most detail. Taurine is essential for skeletal muscle buildup, and knockout mice lacking its transporter SLC6A6 display severe structural defects (41) and exercise intolerance (42). The trimethylglycine betaine appears also important for proper muscle functioning, although SLC6A12 knockout mice have been reported to develop only mild myopathy (34). Betaine promotes muscle fiber differentiation and myotube size (43) via stimulation of the mechanistic target of rapamycin pathway (44) and disturbed osmolyte balances have been implicated in muscle disease. Taurine levels were significantly reduced in muscle from myositis patients compared to healthy controls (45), while in urine on the other hand both taurine and betaine levels were increased in patients (46). In the murine Duchenne muscular dystrophy model, taurine content of muscle was low, mostly early in disease progression, and a reduction of its transporter SLC6A6 was observed (47). Yet, in the canine golden retriever muscular dystrophy model, muscle levels of taurine and SLC6A6 were 1.5- and 20-fold increased (48) compared to healthy dogs, pointing to possible differences between species and/or at different disease stages. Our localization studies revealed strong increases of osmolyte accumulators in small regenerating fibers. Possibly, protein replacement and refolding during the regeneration process are chaperoned by osmolytes, the latter aiding protection of functional protein conformations (49).
 

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- Extreme Urinary Betaine Losses in Type 2 Diabetes Combined with Bezafibrate Treatment are Associated with Losses of Dimethylglycine and Choline but not with Increased Losses of Other Osmolytes

Abstract said:
Purpose: Betaine deficiency is a probable cardiovascular risk factor and a cause of elevated homocysteine. Urinary betaine excretion is increased by fibrate treatment, and is also often elevated in diabetes. Does fibrate further increase betaine excretion in diabetes, and does it affect the plasma concentrations and excretions of related metabolites and of other osmolytes?

Methods: Samples from a previous study of type 2 diabetes were selected if participants were taking bezafibrate (n = 32). These samples were compared with participants matched for age and gender and not on a fibrate (comparator group, n = 64). Betaine, related metabolites, and osmolytes were measured in plasma and urine samples from these 96 participants.

Results: Median urinary betaine excretion in those on bezafibrate was 5-fold higher than in the comparator group (p < 0.001), itself 3.5-fold higher than the median reported for healthy populations. In the bezafibrate group, median dimethylglycine excretion was higher (9-fold, p < 0.001). Excretions of choline, and of the osmolytes myo-inositol, taurine and glycerophosphorylcholine, were not significantly different between groups. Some participants excreted more betaine than usual dietary intakes. Several betaine fractional clearances were >100 %. Betaine excretion correlated with excretions of the osmolytes myo-inositol and glycerophosphorylcholine, and also with the excretion of choline and N,N-dimethylglycine, but it was inconclusive whether these relationships were affected by bezafibrate therapy.

Conclusions: Increased urinary betaine excretions in type 2 diabetes are further increased by fibrate treatment, sometimes to more than their dietary intake. Concurrent betaine supplementation may be beneficial.
 
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Oxytocin might not be as bad as it is thought to be.

Oxytocin levels seem to be completely crushed to zero for animals in torpor:
1647766589701.png

Osmolyte depletion and thirst suppression allow hibernators to survive for months without water

Also, oxytocin production seems to be able to help organ regeneration:

Oxytocin is an age-specific circulating hormone that is necessary for muscle maintenance and regeneration
The regenerative capacity of skeletal muscle declines with age. Previous studies suggest that this process can be reversed by exposure to young circulation; however, systemic age-specific factors responsible for this phenomenon are largely unknown. Here we report that oxytocin--a hormone best known for its role in lactation, parturition and social behaviours--is required for proper muscle tissue regeneration and homeostasis, and that plasma levels of oxytocin decline with age. Inhibition of oxytocin signalling in young animals reduces muscle regeneration, whereas systemic administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell activation/proliferation through activation of the MAPK/ERK signalling pathway.
Oxytocin in the heart regeneration
We have demonstrated that entire oxytocin (OT) system is synthesized in the rat and human heart and this hormone is implicated in several cardiac functions including stem cells differentiation into cardiomyocytes.
Oxytocin improves proliferation and neural differentiation of adipose tissue-derived stem cells
Oxytocin treatment also upregulated the expression of oxytocin receptor mRNA. These results demonstrated for the first time that oxytocin treatment can promote neural differentiation of the ADSCs in a dose-dependent and time-dependent manner. Oxytocin has a significant role in neurogenesis, and this may have implications in regeneration of adult neurons.
Oxytocin promotes hepatic regeneration in elderly mice
In conclusion, OT promotes liver regeneration, especially in aged mice, which may be achieved by promoting autophagy. All these results support the possibility of OT and its analog being a potent anti-aging drug and promote liver rejuvenation.
Oxytocin facilitates the proliferation, migration and osteogenic differentiation of human periodontal stem cells in vitro
OT promoted proliferation, migration, and osteogenic differentiation of PDLSCs in vitro. Furthermore, the effect of OT on osteogenic differentiation was mediated through ERK and AKT pathway. Thus, OT may have potential for use in periodontal regeneration.
Oxytocin controls differentiation of human mesenchymal stem cells and reverses osteoporosis
For this purpose, we identified by transcriptomic analysis the oxytocin receptor pathway as a potential regulator of the osteoblast/adipocyte balance of human multipotent adipose-derived stem (hMADS) cells. Both oxytocin (OT) and carbetocin (a stable OT analogue) negatively modulate adipogenesis while promoting osteogenesis in both hMADS cells and human bone marrow mesenchymal stromal cells. Consistent with these observations, ovariectomized (OVX) mice and rats, which become osteoporotic and exhibit disequilibrium of this balance, have significant decreased OT levels compared to sham-operated controls. Subcutaneous OT injection reverses bone loss in OVX mice and reduces marrow adiposity. Clinically, plasma OT levels are significantly lower in postmenopausal women developing osteoporosis than in their healthy counterparts. Taken together, these results suggest that plasma OT levels represent a novel diagnostic marker for osteoporosis and that OT administration holds promise as a potential therapy for this disease.

By the way, I have heard of a testimony of someone having their thyroid regenerated after a 14 days dry fast. I thought it was completely fake but thyroid regeneration seems to be a possible thing so why not.

Could (prolonged) dry fasting be a sort of reset allowing someone to exit torpor metabolism, produce normal level of oxytocin (among other things) and heal? Testimonies I've read make me think it's possible.

 
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Hormones and Reality
Endothermy, Oxytocin, Vasopressin, and Civilization: A Narrative
A “side effect” of adrenaline stimulation of lung function is adrenalin dissolution of fat cells in the periphery, causing the release of free fatty acids into the circulation, where they provide the most efficient fuel for metabolism, consequently raising body temperature. The concomitant effects of increased oxygenation and metabolism are a powerful convergence of functions for the evolution of warm- bloodedness on an ad hoc basis. Over time, this conditional adaptation was superseded by oxytocin, a posterior pituitary neurohypophyseal hormone as the constitutively genetic regulator of body heat.
And since hypoxia is a potent stimulus for oxytocin, it may have enhanced this signaling pathway, in turn enhancing dopamine signaling in the brain, including DRD4, the “risk-taking gene,” encouraging migration behaviorally, consistent with human movement northward from Africa into Europe. Polymorphisms for the dopamine 4 gene either promote or inhibit kin selection, suggesting a balance between these genes in social systems. The climate- induced increase in oxytocin would have further promoted human imagination, creativity, and ingenuity, leading to the invention of tools, including written language as a form of toolmaking.
Furthermore, the constitutive basis for endothermy is oxytocin, a product of the posterior pituitary, which stimulates dopamine production by the brain, dopamine also being synthesized from cholesterol. In this vertical integration of our evolved capacity to ultimately thermoregulate, leading to the evolution of toolmaking and language, we see the path of our evolution from the protocell to higher and higher levels of physiology as exaptations of lipid physical chemistry, bearing in mind that pulsars produce polycyclic hydrocarbons (= lipids) and distribute them throughout the cosmos.

Oxytocin and the Warm Outer Glow: Thermoregulatory Deficits Cause Huddling Abnormalities in Oxytocin-Deficient Mouse Pups
Our results add to a growing body of work indicating that OT plays critical roles in thermoregulation and also highlight the entanglement of social and thermoregulatory processes in small mammals such as mice.

Dopamine and oxytocin interactions underlying behaviors: potential contributions to behavioral disorders
Thus, oxytocin is proposed to be a key neural substrate that interacts with central dopamine systems. In addition to psychosocial improvement, oxytocin has recently been implicated in mediating mesolimbic dopamine pathways during drug addiction and withdrawal. This bi-directional role of dopamine has also been implicated during some components of sexual behavior. This review will discuss evidence for the existence dopamine/oxytocin positive interaction in social behavioral paradigms and associated disorders such as sexual dysfunction, autism, addiction, anorexia/bulimia, and depression. Preliminary findings suggest that whilst further rigorous testing has to be conducted to establish a dopamine/oxytocin link in human disorders, animal models seem to indicate the existence of broad and integrated brain circuits where dopamine and oxytocin interactions at least in part mediate socio-affiliative behaviors. A profound disruption to these pathways is likely to underpin associated behavioral disorders. Central oxytocin pathways may serve as a potential therapeutic target to improve mood and socio-affiliative behaviors in patients with profound social deficits and/or drug addiction.

The link between thermoregulation and oxytocin might explain why the levels are totally depleted during hibernation.

It could also explain why carbohydrates (especially sugar if I remember correctly) consumption have a link with oxytocin production, because they might indicate that there is a certain temperature if we are able to eat them, and that heat production is less needed.
 
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