Is Vitamin D Supplementation Even Neccessary

[Travis]

I'll drill a hole in one of the pineapples and fill it with rum...just for those who still enjoy a little "drink"... I'll supply the straws too!

That's is so . . . cool—like in a Jimmy Buffet-sort-of-way, only cooler.

(I made a martini with an icicle once.)

 

[Braveheart]

That's is so . . . cool—like in a Jimmy Buffet-sort-of-way, only cooler.

(I made a martini with an icicle once.)

Actually it is quite common to do that with a watermelon here...works perfectly. watermelon filled with rum - Buscar con Google

 

[Travis]

Vitamin D is involved in thermoregualtion, and it's actually the molecule most suitable for the role. In addition to telling us how much sun we are exposed to, vitamin D₃ also tells-us how much heat we are exposed to: After the photolysis of the 9–10 carbon bond of 7-dehydrocholesterol, only the inactive cis-vitamin D₃ is formed lacking the precise stereochemistry needed to activate the vitamin D receptor. The conversion of cis-vitamin D₃ to active trans-vitamin D₃ is strictly a thermal process and can be accomplished by heating previtamin D₃ at 125° celsius, in octane, for one hour.⁽¹⁾

Although the precise amount of heat required for the thermally-induced cis-trans isomerizaion of vitamin D₃ in aqueous solution is not presently known, I'd imagine that it occurs at around body temperature—and it must, really, or else it would never form in our body. The hydroxylations of vitamin D₃ could play a role in lowering the energy barrier for cis-trans isomerization, and it's easy to see how the 1α-hydroxylation could facilitate this by making the 'head' more water-soluble —'allowing water to get a better grip' by adding a polar group, or pulling it into solution. Vitamin D₃ (calcitriol) is actually the only 1-hydroxylated steroid produced by mammals.

Assuming that small changes in body heat can effects the cis ⇌ trans equilibrium, this means that retinoids and calcitriol are the prime molecular candidates for regulating thermogenesis. There is actually no need to speculate any further, however, as Vitamin D₃ has recently been proven to be more than a mere putative 'heat switch.' Calcitriol has been shown to suppress uncoupling protein, a mitochondrial protein that intimately regulates thermogenesis. This is in fact the proteins classic function, and it had originally been called 'thermogenin' in dedication of this fact (before David Nicholls had created its current name). I am not sure about the retinoids, but I do know that photo-induced cis-trans isomerization of retinal is the first step in eyesight.

'Some [molecules] are born great, some achieve greatness, and some have greatness thrust upon them.' ―William Shakespeare (obviously talking about calcitriol)​

So what effect does this have? The presence of vitamin D₃—acting through its nuclear receptor—suppresses the induction of uncoupling protein, a protein most powerfully upregulated by thyroid hormone and catecholamines.⁽²⁾ This has the effect of lowering metabolism and causing weight gain, something can be demonstrated by using genetically engineered mice: Mice lacking the vitamin D receptor (VDR) always have a higher metabolic rate, higher oxygen consumption, and a lower body weight despite consuming the same amount of food as the control mice.⁽³⁾ Conversely, mice having additional vitamin D receptor expressed in their cells invariably have a higher body weight.⁽⁴⁾

So after vitamin D₃ is sensed by our cells, our metabolism will be decrease with intent of lowering body temperature. This means that taking additional vitamin D₃ is tantamount to tricking the body into thinking that it's warmer than it really is, and too much of this vitamin–hormone should lower metabolism through this mechanism—by suppressing uncoupling proteins (UCP2 & UCP3). I think this is only confusing if you are chained to semantics, or that is: This is only confusing if you think that 'uncoupling protein' is accurately named. The unfortunate name 'uncoupling protein' had been spawned from the imagination of David Nicholls in the early '80s. Doctor Nicholls had imagined, quite wrongly, that body heat could actually be created by 'uncoupling' Mitchell's chemi-osmotic force from ATP production. What really happens to Nicholl's 'uncoupled protons' is never explained, although numerous Rube Goldberg cycling events had been proposed. I do maintain that David Nicholls was laboring under a false assumption, or that is that ADP⟳ATP cycling is a not thermodynamically-neutral process:

'Consequently the heat evolved by the oxidation of a substrate such as palmitate will be the same for a direct chemical combustion as for when a brown adipocyte catalyzes the same overall reaction through a cascade of some 30 enzymatic steps. Further, because any ATP synthesized by mitochondria within a cell is immediately recycled and does not appear in the final equation of reactants and products, there is no inherent difference in the thermodynamic efficiency of hypothetical mechanisms involving “coupled” or “uncoupled” mitochondria. In practice any thermogenic process that occurs without performing useful work, accumulating intermediates, or concentrating ions can be said to have an efficiency of zero from the standpoint of energy conservation (or 100% for the purposes of thermogenesis).' ―David Nicholls⁽⁵⁾​

Of course the ADP⟳ATP cycling is thermodynamically neutral if you assume that the proton released is released back inside the cell, but this really is not the case: Adenosine triphosphate is repelled from the mitrochondria's negative membrane potential (ψ ≈ −180·mV) do to its high negative charge and the proton (H⁺) formed upon hydrolysis is actually released into the extracellular space. This process releases heat, as entropy, outside of the system.

ATP + H₂O ⟶ ADP + PO₄²⁻ + H⁺

ΔG ≈ −30·kJ/mol.​

The only reason why Nicholls hadn't observed a higher mitochondrial proton gradient was simply because he had used the wrong nucleotides.⁽⁶⁾⁽⁷⁾ The 'uncoupling protein,' or thermogenin, has a high affinity GDP binding domain yet appears to require cAMP for rapid proton transport.⁽⁸⁾⁽⁹⁾⁽¹⁰⁾ This protein very likely is why phosphodiesterase inhibitors such as caffeine—which increase cAMP by limiting its degradation—reliably increase the metabolic rate. What 'uncoupling proteins' appear to be, really, are mitochondrial proteins which accept cAMP specifically—the smallest and least charged nucleotide capable of rapid proton cycling and hence capable of maintaining the highest metabolic rate. Doctor Nicholls also had also failed to test whether cyclic CTP, cyclic GMP, cyclic TMP, or cyclic UTP are mitochondrial substrates capable of accepting his so-called 'leaked protons.'

Perhaps coincidentally, but most likely not, is the simple fact that retinoic acid—the only other vitamin hormone capable of cis-trans isomerization—has been shown capable of modifying the conductance of 'uncoupling protein' (i.e. thermogenin).⁽¹¹⁾

The only way to increase heat is to increase metabolism, not by decreasing it as 'proton-leakage' implies. Protons do little to create heat—you can demonstrate this yourself using water and a cell phone charger—and that created through metabolism is made by the kinetic energy of molecules and nucleotyde cycling heats of hydrolysis (ΔG). Mammals having more 'uncoupling protein,' thermogenin, or cAMP-linked mitochondria always have a higher oxygen consumption & glucose utilization than controls; this would be frankly impossible under the Nicholls paradigm. We can control both our metabolic rate and our metabolism—which are always linked and never 'uncoupled'—by increasing cyclic AMP (caffeine, catecholamines), by increase the conductance of said protein (retinoids), or by regulating the expression of same (calcitriol, triiodothyronine). As a molecular indicator of heat it is teleologically-plausible and that vitamin D₃ should act to lower body temperature, something which cannot be accomplished in any way other besides lowering metabolism.

[1] Jacobs, H. "Photochemistry of vitamin D and its isomers and of simple trienes." Advances in Photochemistry, Volume 11 (1979)
[2] Gong, D. "Uncoupling protein-3 is a mediator of thermogenesis regulated by thyroid hormone, β3-adrenergic agonists, and leptin." Journal of Biological Chemistry (1997)
[3] Wong, K. "Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins." American Journal of Physiology-Endocrinology and Metabolism (2009)
[4] Wong, K "Targeted expression of human vitamin D receptor in adipocytes decreases energy expenditure and induces obesity in mice." Journal of Biological Chemistry (2011)
[5] Nicholls, D. "Thermogenic mechanisms in brown fat." Physiological reviews (1984)
[6] Nicholls, D. "The control of respiration and the proton electrochemical potential gradient by possible physiological effectors of the proton conductance..." European journal of biochemistry (1974)
[7] Nicholls, D. "The effective proton conductance of the inner membrane of mitochondria from brown adipose tissue." The FEBS Journal (1977)
[8] McQuaid, T. "cAMP-mediated signaling normalizes glucose-stimulated insulin secretion in uncoupling protein-2 overexpressing β-cells." Journal of Endocrinology (2006)
[9] Cao, W. "β-adrenergic activation of p38 MAP kinase in adipocytes cAMP induction of the uncoupling protein 1 (UCP1) gene requires p38 map kinase." Journal of Biological Chemistry (2001)
[10] Cao, W. "p38 mitogen-activated protein kinase is the central regulator of cyclic AMP-dependent transcription of the brown fat uncoupling protein 1 gene." Molecular and cellular biology (2004)
[11] Rial, E. "Retinoids activate proton transport by the uncoupling proteins UCP1 and UCP2." The EMBO journal (1999)​

 

[Dolomite]

Vitamin D is involved in thermoregualtion, and it's actually the molecule most suitable for the role. In addition to telling us how much sun we are exposed to, vitamin D₃ also tells-us how much heat we are exposed to: After the photolysis of the 9–10 carbon bond of 7-dehydrocholesterol, only the inactive cis-vitamin D₃ is formed lacking the precise stereochemistry needed to activate the vitamin D receptor. The conversion of cis-vitamin D₃ to active trans-vitamin D₃ is strictly a thermal process and can be accomplished by heating previtamin D₃ at 125° celsius, in octane, for one hour.⁽¹⁾

View attachment 9285

Although the precise amount of heat required for the thermally-induced cis-trans isomerizaion of vitamin D₃ in aqueous solution is not presently known, I'd imagine that it occurs at around body temperature—and it must, really, or else it would never form in our body. The hydroxylations of vitamin D₃ could play a role in lowering the energy barrier for cis-trans isomerization, and it's easy to see how the 1α-hydroxylation could facilitate this by making the 'head' more water-soluble —'allowing water to get a better grip' by adding a polar group, or pulling it into solution. Vitamin D₃ (calcitriol) is actually the only 1-hydroxylated steroid produced by mammals.

Assuming that small changes in body heat can effects the cis ⇌ trans equilibrium, this means that retinoids and calcitriol are the prime molecular candidates for regulating thermogenesis. There is actually no need to speculate any further, however, as Vitamin D₃ has recently been proven to be more than a mere putative 'heat switch.' Calcitriol has been shown to suppress uncoupling protein, a mitochondrial protein that intimately regulates thermogenesis. This is in fact the proteins classic function, and it had originally been called 'thermogenin' in dedication of this fact (before David Nicholls had created its current name). I am not sure about the retinoids, but I do know that photo-induced cis-trans isomerization of retinal is the first step in eyesight.

'Some [molecules] are born great, some achieve greatness, and some have greatness thrust upon them.' ―William Shakespeare (obviously talking about calcitriol)​

So what effect does this have? The presence of vitamin D₃—acting through its nuclear receptor—suppresses the induction of uncoupling protein, a protein most powerfully upregulated by thyroid hormone and catecholamines.⁽²⁾ This has the effect of lowering metabolism and causing weight gain, something can be demonstrated by using genetically engineered mice: Mice lacking the vitamin D receptor (VDR) always have a higher metabolic rate, higher oxygen consumption, and a lower body weight despite consuming the same amount of food as the control mice.⁽³⁾ Conversely, mice having additional vitamin D receptor expressed in their cells invariably have a higher body weight.⁽⁴⁾

View attachment 9286

So after vitamin D₃ is sensed by our cells, our metabolism will be decrease with intent of lowering body temperature. This means that taking additional vitamin D₃ is tantamount to tricking the body into thinking that it's warmer than it really is, and too much of this vitamin–hormone should lower metabolism through this mechanism—by suppressing uncoupling proteins (UCP2 & UCP3). I think this is only confusing if you are chained to semantics, or that is: This is only confusing if you think that 'uncoupling protein' is accurately named. The unfortunate name 'uncoupling protein' had been spawned from the imagination of David Nicholls in the early '80s. Doctor Nicholls had imagined, quite wrongly, that body heat could actually be created by 'uncoupling' Mitchell's chemi-osmotic force from ATP production. What really happens to Nicholl's 'uncoupled protons' is never explained, although numerous Rube Goldberg cycling events had been proposed. I do maintain that David Nicholls was laboring under a false assumption, or that is that ADP⟳ATP cycling is a not thermodynamically-neutral process:

'Consequently the heat evolved by the oxidation of a substrate such as palmitate will be the same for a direct chemical combustion as for when a brown adipocyte catalyzes the same overall reaction through a cascade of some 30 enzymatic steps. Further, because any ATP synthesized by mitochondria within a cell is immediately recycled and does not appear in the final equation of reactants and products, there is no inherent difference in the thermodynamic efficiency of hypothetical mechanisms involving “coupled” or “uncoupled” mitochondria. In practice any thermogenic process that occurs without performing useful work, accumulating intermediates, or concentrating ions can be said to have an efficiency of zero from the standpoint of energy conservation (or 100% for the purposes of thermogenesis).' ―David Nicholls⁽⁵⁾​

Of course the ADP⟳ATP cycling is thermodynamically neutral if you assume that the proton released is released back inside the cell, but this really is not the case: Adenosine triphosphate is repelled from the mitrochondria's negative membrane potential (ψ ≈ −180·mV) do to its high negative charge and the proton (H⁺) formed upon hydrolysis is actually released into the extracellular space. This process releases heat, as entropy, outside of the system.

ATP + H₂O ⟶ ADP + PO₄²⁻ + H⁺

ΔG ≈ −30·kJ/mol.​

The only reason why Nicholls hadn't observed a higher mitochondrial proton gradient was simply because he had used the wrong nucleotides.⁽⁶⁾⁽⁷⁾ The 'uncoupling protein,' or thermogenin, has a high affinity GDP binding domain yet appears to require cAMP for rapid proton transport.⁽⁸⁾⁽⁹⁾⁽¹⁰⁾ This protein very likely is why phosphodiesterase inhibitors such as caffeine—which increase cAMP by limiting its degradation—reliably increase the metabolic rate. What 'uncoupling proteins' appear to be, really, are mitochondrial proteins which accept cAMP specifically—the smallest and least charged nucleotide capable of rapid proton cycling and hence capable of maintaining the highest metabolic rate. Doctor Nicholls also had also failed to test whether cyclic CTP, cyclic GMP, cyclic TMP, or cyclic UTP are mitochondrial substrates capable of accepting his so-called 'leaked protons.'

Perhaps coincidentally, but most likely not, is the simple fact that retinoic acid—the only other vitamin hormone capable of cis-trans isomerization—has been shown capable of modifying the conductance of 'uncoupling protein' (i.e. thermogenin).⁽¹¹⁾

The only way to increase heat is to increase metabolism, not by decreasing it as 'proton-leakage' implies. Protons do little to create heat—you can demonstrate this yourself using water and a cell phone charger—and that created through metabolism is made by the kinetic energy of molecules and nucleotyde cycling heats of hydrolysis (ΔG). Mammals having more 'uncoupling protein,' thermogenin, or cAMP-linked mitochondria always have a higher oxygen consumption & glucose utilization than controls; this would be frankly impossible under the Nicholls paradigm. We can control both our metabolic rate and our metabolism—which are always linked and never 'uncoupled'—by increasing cyclic AMP (caffeine, catecholamines), by increase the conductance of said protein (retinoids), or by regulating the expression of same (calcitriol, triiodothyronine). As a molecular indicator of heat it is teleologically-plausible and that vitamin D₃ should act to lower body temperature, something which cannot be accomplished in any way other besides lowering metabolism.

[1] Jacobs, H. "Photochemistry of vitamin D and its isomers and of simple trienes." Advances in Photochemistry, Volume 11 (1979)
[2] Gong, D. "Uncoupling protein-3 is a mediator of thermogenesis regulated by thyroid hormone, β3-adrenergic agonists, and leptin." Journal of Biological Chemistry (1997)
[3] Wong, K. "Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins." American Journal of Physiology-Endocrinology and Metabolism (2009)
[4] Wong, K "Targeted expression of human vitamin D receptor in adipocytes decreases energy expenditure and induces obesity in mice." Journal of Biological Chemistry (2011)
[5] Nicholls, D. "Thermogenic mechanisms in brown fat." Physiological reviews (1984)
[6] Nicholls, D. "The control of respiration and the proton electrochemical potential gradient by possible physiological effectors of the proton conductance..." European journal of biochemistry (1974)
[7] Nicholls, D. "The effective proton conductance of the inner membrane of mitochondria from brown adipose tissue." The FEBS Journal (1977)
[8] McQuaid, T. "cAMP-mediated signaling normalizes glucose-stimulated insulin secretion in uncoupling protein-2 overexpressing β-cells." Journal of Endocrinology (2006)
[9] Cao, W. "β-adrenergic activation of p38 MAP kinase in adipocytes cAMP induction of the uncoupling protein 1 (UCP1) gene requires p38 map kinase." Journal of Biological Chemistry (2001)
[10] Cao, W. "p38 mitogen-activated protein kinase is the central regulator of cyclic AMP-dependent transcription of the brown fat uncoupling protein 1 gene." Molecular and cellular biology (2004)
[11] Rial, E. "Retinoids activate proton transport by the uncoupling proteins UCP1 and UCP2." The EMBO journal (1999)​

Thank you for this.

 

[InChristAlone]

Then why did Peat say vitamin D is parallel to thyroid?

 

[Mito]

As a molecular indicator of heat it is teleologically-plausible and that vitamin D₃ should act to lower body temperature, something which cannot be accomplished in any way other besides lowering metabolism.

Doesn't this suggest that spending time in the sun will effectively lower the metabolic rate?

 

[Travis]

Thank you for this.

I'm telling you that thermally-induced cis-trans isomerization of vitamin D₃ and retinoic acid are our biochemical 'heat sensors.' Although cis-trans isomerization is an established way of transducing thermal energy into molecular transformation, its application to biochemical heat sensing—coupled with stereospecific receptors—has gone entirely unmentioned.. .

Imagine cis-retinoic acid isomerizing into the all-trans form at around 99° F, a configuration allowing it to bind to a 'mitochondrial uncoupling protein.' This could induce a decrease in the mitochondrial proton gradient, then cAMP cycling, oxygen consumption, and finally glucose consumption because NADH can only donate hydrides (∶H⁻) as fast as the electron transport chain will allow. This leads to lower metabolism, increased weight, and lower body temperature . . . or exactly what had caused the cis-trans isomerization in the first place.

The cis-trans isomerization of retinoic acid could be entirely self rectifying loop; a self rectifying loop could also be retinoic acid's trans-cis isomerization.​

What exactly is our molecular thermostat if not retinoids and vitamin D₃? I suppose person could imagine a transcription factor in the nucleus serving this role, or perhaps even a receptor somewhere, but I challenge anyone to think of anything besides cis-trans isomerization directing the process.

 

[Travis]

Doesn't this suggest that spending time in the sun will effectively lower the metabolic rate?

But shouldn't it? I mean, if your metabolic rate doesn't decrease with increasing ambient temperature then you will overheat.

 

[Travis]

Then why did Peat say vitamin D is parallel to thyroid?

I din't know that he had said that. Do you know if he had said that in one of his articles? . . or if he had said that in an interview?

 

[Mito]

I din't know that he had said that. Do you know if he had said that in one of his articles? . . or if he had said that in an interview?

HD: [...] How do you see fibromyalgia in terms of vitamin D3 deficiency?

RP: I think, it's parallel, almost identical to the hypothyroid condition. All of the inflammations that you get with low thyroid function are structurally and functionally similar to those you get from a vitamin D deficiency. And the thyroid stimulating hormone is an agent of those inflammatory processes, actually more than the direct effect of thyroxin which lowers TSH. The TSH directly activates and causes tissue to release the inflammatory cytokines, interleukins and so on, and parathyroid hormone does that. And just by taking vitamin D or increasing your calcium intake or decreasing your phosphate relative to the calcium: all of these cases in your diet will lower both TSH and parathyroid hormone. And both of these hormones are directly involved in things such as mast cell activation, releasing histamine and serotonin, increasing all of the cytokines, tumor necrosis factor, nitric oxide: all of the things that promote degenerative inflammatory processes. And so functionally vitamin D and thyroid are really parallel. You can't quite separate them.

Vitamin D - KMUD, 2016-11-18

 

[Travis]

HD: [...] How do you see fibromyalgia in terms of vitamin D3 deficiency?

RP: I think, it's parallel, almost identical to the hypothyroid condition. All of the inflammations that you get with low thyroid function are structurally and functionally similar to those you get from a vitamin D deficiency. And the thyroid stimulating hormone is an agent of those inflammatory processes, actually more than the direct effect of thyroxin which lowers TSH. The TSH directly activates and causes tissue to release the inflammatory cytokines, interleukins and so on, and parathyroid hormone does that. And just by taking vitamin D or increasing your calcium intake or decreasing your phosphate relative to the calcium: all of these cases in your diet will lower both TSH and parathyroid hormone. And both of these hormones are directly involved in things such as mast cell activation, releasing histamine and serotonin, increasing all of the cytokines, tumor necrosis factor, nitric oxide: all of the things that promote degenerative inflammatory processes. And so functionally vitamin D and thyroid are really parallel. You can't quite separate them.

Vitamin D - KMUD, 2016-11-18

He's not comparing them under a metabolic paradigm, but seems focused through an entirely different lens—perhaps one made of calcium. He appears to be functionally equating the two on account of their effects on immunity and also on parathyroid inhibition, something vitamin D₃ can do through its classic effect or increasing calcium absorption. However! vitamin D₃ does little to increase calcium absorption in adipose tissue and in skeletal muscle—where UCP3 is expressed—and exerts there a metabolic effect in diametric opposition to that of thyroid hormone. This effect is of course the suppression or induction of uncoupling proteins, responses which have been fully-demonstrated as being reliable. So although calcitriol's effects in the kidneys and intestines can have the ultimate effect of achieving the same end as thriiodothyronine, the same cannot be said when considering their respective effects on adipose and skeletal tissue:

Shi, H. "1α,25-dihydroxyvitamin D₃ inhibits uncoupling protein 2 expression in human adipocytes." The FASEB Journal (2002)
Gong, D. "Uncoupling protein-3 is a mediator of thermogenesis regulated by thyroid hormone, β3-adrenergic agonists, and leptin." Journal of Biological Chemistry (1997)​

 

[Travis]

In humans, there appears to be no studies examining this effect explicitly. However, if you search Google™ for the clause 'vitamin D makes me tired' you may be forced into considering its general metabolic effects. In fact, you don't even have to do that: you merely have type in the clause 'vitamin D makes...' and the rest auto-suggests itself, both saving the effort required to type the entire clause while also informing you of the most common way to finish it.

 

[Terma]

This is in fact the proteins classic function, and it had originally been called 'thermogenin' in dedication of this fact (before David Nicholls had created its current name). I am not sure about the retinoids, but I do know that photo-induced cis-trans isomerization of retinal is the first step in eyesight.

That whole post is fantastic and deserves its own thread.

I tried to look into the Retinoic acid -> UCP (and also PPARdelta, probably important) question a few times, but ultimately this stood in the way and made some of what I read invalid:
Retinoic acid has different effects on UCP1 expression in mouse and human adipocytes

There seemed to be another lesser-researched relation between Retinaldehyde and UCP:
Retinaldehyde represses adipogenesis and diet-induced obesity
But again it's all in damn rodents (to my knowledge, maybe there's more in human cells somewhere) so who knows.

[I supposed there's this one: Expression of Uncoupling Proteins in Human Skin and Skin-Derived Cells - ScienceDirect I wasn't very interested in it due to cell type, but you might be; naturally the animal vs human problem extends to cell type distinction in human cells as well]

 

[Obi-wan]

Ever go to the beach and observe how many people are sleeping in the late afternoon. Also ever feel tired after leaving the beach. I layed out by the pool yesterday and...fell asleep! So @Travis is correct in "Vitamin D is involved in thermoregulation" Just add a couple cans of beer and you will sleep like a baby. One way to wake up was to jump in the ocean. Another negative for supplemental Vit D. Buy a cheap brand in Soy oil and really start yawning...I wonder if @Travis will stop applying it trandermally?

 

[jb116]

Ever go to the beach and observe how many people are sleeping in the late afternoon. Also ever feel tired after leaving the beach. I layed out by the pool yesterday and...fell asleep! So @Travis is correct in "Vitamin D is involved in thermoregulation" Just add a couple cans of beer and you will sleep like a baby. One way to wake up was to jump in the ocean. Another negative for supplemental Vit D. Buy a cheap brand in Soy oil and really start yawning...I wonder if @Travis will stop applying it trandermally?

Why is it a negative?

 

[Obi-wan]

Why is it a negative?

Why would you want to slow your metabolism throughout the day? Not very Peaty except when you are out in the sun. Nothing like a dip in cool water to get it started again...

 

[Obi-wan]

you are right Charlie!

PUFA Required/essential For Cancer; Stearic Acid Is A PUFA Antagonist & Anti-cancer This post is a great read!

 

[jb116]

Why would you want to slow your metabolism throughout the day? Not very Peaty except when you are out in the sun. Nothing like a dip in cool water to get it started again...

Why is there an assumption that is slows metabolism?

 

[Obi-wan]

Why is there an assumption that is slows metabolism?

Read Travis's post's above

 

[HDD]

And despite being deficient in vitamin D, the sucrose-fed rats had strong bones. SARAH JOHANNESEN MURRAY: So sugar doesn’t weaken your bones SARAH JOHANNESEN MURRAY: like we’re told. RAY PEAT: No, it actually works parallel to thyroid and vitamin D for stimulating the metabolism, which calcium – T3 component of the thyroid hormone and fructose all have some overlapping effects activating respiratory metabolism.



“Well, that is one of the factors in sunlight. The vitamin D allows us to absorb and use calcium and calcium holds down some of the basic stress hormones that tend to put us into a torpid hibernation stage when it’s too dark. The hormones that make people depressed and sick in the winter are the same hormones that allow animals and nature to go into torpor or hibernation when the days are very short, and progesterone is the main anti-stress hormone that is inhibited if we’re deficient in either calcium or vitamin D. When vitamin D and calcium are not adequate in either the diet or the exposure to the environment, cells go into an excited inefficient state and they have to be quieted and put into a torpor...


I believe napping while sunbathing is a sign of increased metabolism, allowing the body to relax. Sunbathing can raise temperatures.