Calcium Antagonists May Completely Reverse Diabetes

haidut

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The study used animals and a specific calcium antagonist (verapamil). However, if the principle is correct and the clinical trial in humans works well, then I don't see why other calcium antagonists like magnesium and cyproheptadine would not work as well.
Could a common blood pressure drug completely reverse diabetes?
"...However, in animal models, the team has found that verapamil – used to treat high blood pressure, irregular heartbeat and migraine headaches – lowers TXNIP levels in beta cells. In fact, in mice with established diabetes and blood sugars over 300 mg/dL, verapamil “eradicated” the disease."

Btw, eugeno is a great calcium antagonist that can be bought from many vendors dirt cheap, and the doses are similar to verapamil - 100mg-150mg daily.
 
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docall18

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The study used animals and a specific calcium antagonist (verapamil). However, if the principle is correct and the clinical trial in humans works well, then I don't see why other calcium antagonists like magnesium and cyproheptadine would not work as well.

Could a common blood pressure drug completely reverse diabetes?

So does this imply that dairy such as milk that is high in calcium might cause diabetes?

I find magnesium beneficial and often wonder if my lifelong high milk consumption could have been detrimental.
 

Tarmander

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I can attest that taking egg shell calcium makes blood sugars much more chaotic...but it's good for me right? Right?
 

Nighteyes

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Is this due to The wrong placement/utilization of calcium as in poor removal from The blood stream due to imbalance in fat soluble vitamins (K2)? I am guessing calcium does not always have this effect in all people, so something must Explain it.
 

haidut

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Is this due to The wrong placement/utilization of calcium as in poor removal from The blood stream due to imbalance in fat soluble vitamins (K2)? I am guessing calcium does not always have this effect in all people, so something must Explain it.

Calcium is crucial for the proper functioning of the Krebs cycle where most of the CO2 is produced. However, calcium overload is the common pathway for all cellular death. Controlling calcium requires proper energy but without calcium it is difficult to get that energy. So, it's a bit of Catch 22 but Peat has said that calcium is one of the least dangerous nutrients for a hypothyroid person even though "everything is dangerous when you are hypothyroid".
 

tyw

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We need to be more specific here, and de-complect :arghh: the different contexts in which calcium is referred to.

(And as usual, the first word in my signature is ASSERT .... what I write here are assertions of models that I propose. These models are put forth with the intention of being falsified; they may not be correct, but proving them wrong helps us gain more knowledge)


----

(a) Verapamil, magnesium, etc .... are Calcium Channel Blockers -- Calcium channel blocker - Wikipedia, the free encyclopedia

This refers to a very specific mechanism, wherein calcium is taken it from outside the cell, into the cell cytosol.

Note that just because there is Calcium in the cell cytosol, it does not imply that there will be a lot of calcium in other components of the cell (like the mitochondria, which are touched on in point (c))

(b) Dietary calcium may or may not affect calcium balance

Example study -- What serum calcium can tell us and what it can't

The Article was specifically about how serum calcium cannot predict calcium status at all, but goes into some mechanics of calcium balance.

Whatever the case, there are lots of regulatory mechanisms for calcium.


(c) Association between Calcium Influx into Mitochondrial, and Cell Apoptosis (Death of the Cell)

I have a hunch that prevention of this mechanism is the reason for the apparent curing of Type 1 diabetes seen in the original article referenced by Haidut.

First, some of the studies that claim to show that "High Calcium in cell => apoptosis" use really high concentrations of calcium :banghead:.

As the authors of this study correctly state -- http://www.jbc.org/content/278/16/14134.full

It has been shown that high [Ca2+] (100–500 μM) is necessary for PTP opening in isolated mitochondria (1), but this [Ca2+] is not attained in the cytosol of intact cells.

[TYW note: we're usually talking hundreds of nano-Moles as normal baseline levels .... though some cells like neurons do get up into the tens of micro-Moles. 1000 nano-Mole = 1 micro-Mole, so 100-500 micro-moles that we're talking about here is sign of some serious dys-regulation to begin with. Of course, diabetes is by definition, a dysregulated state whereby levels of ATP and NAD+ and probably chronically deficient]

It has been proposed that mitochondrial Ca2+overload in intact cells can trigger the opening of PTP and release of proapoptotic factors during neuronal ischemic and/or excitotoxic cell death (4, 5), but the downstream events that couple the rise in calcium to cell death are unknown.

Mitochondrial Ca2+ overload would be a side result of the rise in the cytosolic Ca2+concentration ([Ca2+]c) promoted by Ca2+entry through plasma membrane receptor-operated and voltage-dependent Ca2+ channels.

When the [Ca2+]c increases, Ca2+ is taken up into the mitochondria via the mitochondrial Ca2+ uniporter (MCU), a low affinity, high capacity Ca2+ transport system driven by the ΔψM. Since uptake through MCU is a function of ([Ca2+]c) (6), its extent critically depends on both the magnitude and duration of the [Ca2+]c rise (7).​


While really high levels of excessive calcium is key for this cascade to apoptosis, it is only one element in a line of interactions.

Another paper shows how many different scenarios can affect the apparent requirement for Ca2+ to be present during Mitochondrial Transition Pore permeability associated apoptosis -- Mitochondrial calcium and the permeability transition in cell death

I think Figure 1 is useful (specific to calcium-overloading in Hepatocytes / Liver cells):

1-s2.0-S0005272809002229-gr1.jpg


Quotes from the section with that figure:

The short-chain hydroperoxide, tert-butylhydroperoxide (TBH), is an analog of the lipid hydroperoxides that form during oxidative stress and ischemia–reperfusion

Thus, NAD(P)H oxidation leads to mitochondrial Ca2+ loading, which in turn promotes ROS formation and the MPT. Indeed, Ca2+ loading of isolated mitochondria promotes ROS formation, although the mechanism for this remains obscure.

[TYW Note: "NAD(P)H oxidation" directly generates superoxide. Under normal situations, this should be a signal to do something -- eg: shutdown insulin function. Under chronic stress conditions, bad things happen. I personally see Ca2+ as "tagging along for the ride", rather than ]​

Again, note the common factors here ;):
  • High Reactive Oxygen Species production
  • Decreased delta-psi (membrane potential)
  • Low ATP production

I am tempted to say that if energetics is good in the first place, then this cascade with involves calcium all the way to cell death, also does not occur.

Blocking calcium may then just be forcibly blocking a cascade that is normally a good thing (you want to get rid of bad cells ASAP). Of course, is a chronic disease state, there are so many "bad cells", then allowing this natural cascade to occur may kill off too many cells, and compromise viable of entire systems. Blocking the cascade in that context may then be a good thing (for until metabolic health is restored)


(d) Calcium as it is used in metabolism.

This is a topic for which I have no clear answers. All I know are a couple of isolated mechanics, and I do not know yet how they fit together.

Haidut's observations of the U-shaped relationship between calcium concentration and Pyruvate Decarboxylase activity.

I want to more to a more fundamental level than that, and re-visit Gilbert Ling's premise of Ca2+ as a potent Electron Withdrawing Cardinal Adsorbent (EWC).

This is exactly what both ATP and Carbon Dioxide do -- withdraw electrons from proteins -- and we may want to ask if Calcium is acting as a substitute for the function of ATP, in places where ATP cannot be used for whatever reason.

SIDENOTE: ATP is likely the "most powerful" EWC, meaning that it can most readily withdraw charge from a protein.

SIDENOTE: Carbon Dioxide may also be called a "Lewis Acid" based on it's electron withdrawing properties. I think the only reason it is recognised as a generic Lewis Acid, is because it is such a simple molecule, and can perform its electron withdrawing behaviour in almost any context. (larger molecules require more specific orientations to work, and specific regulatory pathways in the body to control)​

The observed behaviour of calcium, which is generally viewed as an "excitatory ion", is actually consistent with this Electron-Withdrawing behaviour, but probably not in the way the mainstream thinks.

By Ling's Model, the "resting potential" is Highly Charged -- potential energy which can maybe be used for great good :borg:.

The "action potential", which the mainstream will say "involves the use of calcium", is a lowered charge state. What is actually happening is:

- a dissipation of an existing charge potential
- opening of voltage-gated calcium channels
- calcium moves into cell
- (and then if you believe Ling) calcium adsorbs onto proteins, withdrawing electrons from them, aligning them again to allow for Charge-separated water formation and re-establishment of a higher energy potential (It is the water that holds the charge)

From my biased perspective, this assigns Ca2+ ions the role of "The Initial Mobile Restorative Squad" -- small ions that benefit from quick transport to re-order intracellular (and intra-mitochondrial) proteins to be ready for the next potential phase of action.


I have a hunch that this is directly linked to Mitochondrial Electron Chain Transport, and likely the plasma membrane calcium ATPases -- Calcium signaling around Mitochondria Associated Membranes (MAMs) | Cell Communication and Signaling | Full Text . But for now, I dunno. So I won't comment about this yet.

-----

Will eating more calcium on it's own restore good metabolism? IMO, likely not. Too many endogenous regulatory pathways to bypass. I think Ca2+ is a slave to metabolism, rather than a driver of it.

The exception would be a true Calcium deficiency scenario, which was very prevalent in the past (even if Ca2+ is a slave, you still need the slaves to run your machine :banghead:).

The issue today is what is considered a "calcium deficiency". In cases of malnutrition, the answer is obvious, but with today's stress, we may have "acute times of Calcium unavailability to tissues", which prompt systemic calcium increases (eg: by giving it up from the bones).

Another major confounder, Vitamin D status plays a large role in calcium regulation at the fundamental metabolic level -- Regulation of Pyruvate Carboxylase Activity by Calcium in Intact Rat Liver Mitochondria

Will eating too much calcium lead to bad energetics? If regulatory systems (either storage or excretion) are not working properly, then maybe excess dietary calcium is not well dealt with. How to tell if this is the case for you? Dunno.

Personally, I do not worry too much about Calcium. Metabolic fixes take priority.

Though of course, I'm South Chinese, and there is some data to suggest that people from different ancestry probably do better on higher calcium intakes. PTH measures are probably more useful than absolute daily calcium intake recommendations.

.....
 
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haidut

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We need to be more specific here, and de-complect :arghh: the different contexts in which calcium is referred to.

(And as usual, the first word in my signature is ASSERT .... what I write here are assertions of models that I propose. These models are put forth with the intention of being falsified; they may not be correct, but proving them wrong helps us gain more knowledge)


----

(a) Verapamil, magnesium, etc .... are Calcium Channel Blockers -- Calcium channel blocker - Wikipedia, the free encyclopedia

This refers to a very specific mechanism, wherein calcium is taken it from outside the cell, into the cell cytosol.

Note that just because there is Calcium in the cell cytosol, it does not imply that there will be a lot of calcium in other components of the cell (like the mitochondria, which are touched on in point (c))

(b) Dietary calcium may or may not affect calcium balance

Example study -- What serum calcium can tell us and what it can't

The Article was specifically about how serum calcium cannot predict calcium status at all, but goes into some mechanics of calcium balance.

Whatever the case, there are lots of regulatory mechanisms for calcium.


(c) Association between Calcium Influx into Mitochondrial, and Cell Apoptosis (Death of the Cell)

I have a hunch that prevention of this mechanism is the reason for the apparent curing of Type 1 diabetes seen in the original article referenced by Haidut.

First, some of the studies that claim to show that "High Calcium in cell => apoptosis" use really high concentrations of calcium :banghead:.

As the authors of this study correctly state -- http://www.jbc.org/content/278/16/14134.full

It has been shown that high [Ca2+] (100–500 μM) is necessary for PTP opening in isolated mitochondria (1), but this [Ca2+] is not attained in the cytosol of intact cells.

[TYW note: we're usually talking hundreds of nano-Moles as normal baseline levels .... though some cells like neurons do get up into the tens of micro-Moles. 1000 nano-Mole = 1 micro-Mole, so 100-500 micro-moles that we're talking about here is sign of some serious dys-regulation to begin with. Of course, diabetes is by definition, a dysregulated state whereby levels of ATP and NAD+ and probably chronically deficient]

It has been proposed that mitochondrial Ca2+overload in intact cells can trigger the opening of PTP and release of proapoptotic factors during neuronal ischemic and/or excitotoxic cell death (4, 5), but the downstream events that couple the rise in calcium to cell death are unknown.

Mitochondrial Ca2+ overload would be a side result of the rise in the cytosolic Ca2+concentration ([Ca2+]c) promoted by Ca2+entry through plasma membrane receptor-operated and voltage-dependent Ca2+ channels.

When the [Ca2+]c increases, Ca2+ is taken up into the mitochondria via the mitochondrial Ca2+ uniporter (MCU), a low affinity, high capacity Ca2+ transport system driven by the ΔψM. Since uptake through MCU is a function of ([Ca2+]c) (6), its extent critically depends on both the magnitude and duration of the [Ca2+]c rise (7).​


While really high levels of excessive calcium is key for this cascade to apoptosis, it is only one element in a line of interactions.

Another paper shows how many different scenarios can affect the apparent requirement for Ca2+ to be present during Mitochondrial Transition Pore permeability associated apoptosis -- Mitochondrial calcium and the permeability transition in cell death

I think Figure 1 is useful (specific to calcium-overloading in Hepatocytes / Liver cells):

1-s2.0-S0005272809002229-gr1.jpg


Quotes from the section with that figure:

The short-chain hydroperoxide, tert-butylhydroperoxide (TBH), is an analog of the lipid hydroperoxides that form during oxidative stress and ischemia–reperfusion

Thus, NAD(P)H oxidation leads to mitochondrial Ca2+ loading, which in turn promotes ROS formation and the MPT. Indeed, Ca2+ loading of isolated mitochondria promotes ROS formation, although the mechanism for this remains obscure.

[TYW Note: "NAD(P)H oxidation" directly generates superoxide. Under normal situations, this should be a signal to do something -- eg: shutdown insulin function. Under chronic stress conditions, bad things happen. I personally see Ca2+ as "tagging along for the ride", rather than ]​

Again, note the common factors here ;):
  • High Reactive Oxygen Species production
  • Decreased delta-psi (membrane potential)
  • Low ATP production

I am tempted to say that if energetics is good in the first place, then this cascade with involves calcium all the way to cell death, also does not occur.

Blocking calcium may then just be forcibly blocking a cascade that is normally a good thing (you want to get rid of bad cells ASAP). Of course, is a chronic disease state, there are so many "bad cells", then allowing this natural cascade to occur may kill off too many cells, and compromise viable of entire systems. Blocking the cascade in that context may then be a good thing (for until metabolic health is restored)


(d) Calcium as it is used in metabolism.

This is a topic for which I have no clear answers. All I know are a couple of isolated mechanics, and I do not know yet how they fit together.

Haidut's observations of the U-shaped relationship between calcium concentration and Pyruvate Decarboxylase activity.

I want to more to a more fundamental level than that, and re-visit Gilbert Ling's premise of Ca2+ as a potent Electron Withdrawing Cardinal Adsorbent (EWC).

This is exactly what both ATP and Carbon Dioxide do -- withdraw electrons from proteins -- and we may want to ask if Calcium is acting as a substitute for the function of ATP, in places where ATP cannot be used for whatever reason.

SIDENOTE: ATP is likely the "most powerful" EWC, meaning that it can most readily withdraw charge from a protein.

SIDENOTE: Carbon Dioxide may also be called a "Lewis Acid" based on it's electron withdrawing properties. I think the only reason it is recognised as a generic Lewis Acid, is because it is such a simple molecule, and can perform its electron withdrawing behaviour in almost any context. (larger molecules require more specific orientations to work, and specific regulatory pathways in the body to control)​

The observed behaviour of calcium, which is generally viewed as an "excitatory ion", is actually consistent with this Electron-Withdrawing behaviour, but probably not in the way the mainstream thinks.

By Ling's Model, the "resting potential" is Highly Charged -- potential energy which can maybe be used for great good :borg:.

The "action potential", which the mainstream will say "involves the use of calcium", is a lowered charge state. What is actually happening is:

- a dissipation of an existing charge potential
- opening of voltage-gated calcium channels
- calcium moves into cell
- (and then if you believe Ling) calcium adsorbs onto proteins, withdrawing electrons from them, aligning them again to allow for Charge-separated water formation and re-establishment of a higher energy potential (It is the water that holds the charge)

From my biased perspective, this assigns Ca2+ ions the role of "The Initial Mobile Restorative Squad" -- small ions that benefit from quick transport to re-order intracellular (and intra-mitochondrial) proteins to be ready for the next potential phase of action.


I have a hunch that this is directly linked to Mitochondrial Electron Chain Transport, and likely the plasma membrane calcium ATPases -- Calcium signaling around Mitochondria Associated Membranes (MAMs) | Cell Communication and Signaling | Full Text . But for now, I dunno. So I won't comment about this yet.

-----

Will eating more calcium on it's own restore good metabolism? IMO, likely not. Too many endogenous regulatory pathways to bypass. I think Ca2+ is a slave to metabolism, rather than a driver of it.

The exception would be a true Calcium deficiency scenario, which was very prevalent in the past (even if Ca2+ is a slave, you still need the slaves to run your machine :banghead:).

The issue today is what is considered a "calcium deficiency". In cases of malnutrition, the answer is obvious, but with today's stress, we may have "acute times of Calcium unavailability to tissues", which prompt systemic calcium increases (eg: by giving it up from the bones).

Another major confounder, Vitamin D status plays a large role in calcium regulation at the fundamental metabolic level -- Regulation of Pyruvate Carboxylase Activity by Calcium in Intact Rat Liver Mitochondria

Will eating too much calcium lead to bad energetics? If regulatory systems (either storage or excretion) are not working properly, then maybe excess dietary calcium is not well dealt with. How to tell if this is the case for you? Dunno.

Personally, I do not worry too much about Calcium. Metabolic fixes take priority.

Though of course, I'm South Chinese, and there is some data to suggest that people from different ancestry probably do better on higher calcium intakes. PTH measures are probably more useful than absolute daily calcium intake recommendations.

.....

Thank you for the extensive analysis. As far as the calcium tests I think that only by doing PTH, serum calcium, vitamin D3, calcitriol, phosphorus, and maybe even thyroid can one get an idea of true calcium status in the cell.
 

paymanz

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i never understand peat's recommendation for high milk intake, maybe because its cheap and highly available.its so high in phosphorous.

with a diet high in fruit and vegs you get little phosphorous and so need less calcium.even if you replace the fruit with white rice.and getting some protein from gelatin or bone broth.+ you get much higher magnesium in diet like that.
 

Vinero

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You can also skip dairy and just supplement with calcium carbonate which is what I'm doing. I think calcium carbonate is even more effective than dairy to bring PTH and prolactin under control since it's pure calcium without any phosphate, which dairy products are also high in.
 
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You can also skip dairy and just supplement with calcium carbonate which is what I'm doing. I think calcium carbonate is even more effective than dairy to bring PTH and prolactin under control since it's pure calcium without any phosphate, which dairy products are also high in.

My preferred choice is egg shell powder for calcium carbonate. Peat's other points for using dairy/milk has to do with food-sustainability and his hedge against the filler and toxin pumped food that is the US food supply. He reasons that he prefers the cow doing the filtering and processing of his foods rather than man.
 

tyw

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Thank you for the extensive analysis. As far as the calcium tests I think that only by doing PTH, serum calcium, vitamin D3, calcitriol, phosphorus, and maybe even thyroid can one get an idea of true calcium status in the cell.

Yup, agree.

If people want more of the mechanical details, I liked Chris Masterjohn's recent podcast on Calcium and Phosphorous ratios -- The Daily Lipid: The Daily Lipid Podcast 9: Balancing Calcium and Phosphorus in the Diet, and the Importance of Measureing Parathyroid Hormone (PTH)

Example: he will talk about how 1,25-hydroxy-D is probably just a "currency", that has variable inputs (Sun, diet), and variable outputs (Calcitriol, and ultimately PTH). Measuring this alone, which a lot of people do, doesn't tell you much about calcium status at all.

....
 

skycop00

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Yup, agree.

If people want more of the mechanical details, I liked Chris Masterjohn's recent podcast on Calcium and Phosphorous ratios -- The Daily Lipid: The Daily Lipid Podcast 9: Balancing Calcium and Phosphorus in the Diet, and the Importance of Measureing Parathyroid Hormone (PTH)

Example: he will talk about how 1,25-hydroxy-D is probably just a "currency", that has variable inputs (Sun, diet), and variable outputs (Calcitriol, and ultimately PTH). Measuring this alone, which a lot of people do, doesn't tell you much about calcium status at all.

....
That was a great podcast!
 

Makrosky

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You can also skip dairy and just supplement with calcium carbonate which is what I'm doing. I think calcium carbonate is even more effective than dairy to bring PTH and prolactin under control since it's pure calcium without any phosphate, which dairy products are also high in.
But the thing is that dairy comes packed with a great ammount of nutrients, for instance milk : sat fat, 30gr. protein per liter, micronutrients, 50gr of carbs per liter. All of that easily digestible assuming you aren't lactose intolerant. So it's not only about the calcium. It's about choosing a good food. Peat's purpose is provide nutrition from food, not from supplements.
 

narouz

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But the thing is that dairy comes packed with a great ammount of nutrients, for instance milk : sat fat, 30gr. protein per liter, micronutrients, 50gr of carbs per liter. All of that easily digestible assuming you aren't lactose intolerant. So it's not only about the calcium. It's about choosing a good food. Peat's purpose is provide nutrition from food, not from supplements.

Despite drinking a lot of milk myself,
I think taking a lot of eggshell calcium over a period of a few months
helped me in the past.
I'm not sure what it did--I was thinking mainly of "quieting the parathyroid gland,"
as Peat put it, when I did it.
 

Makrosky

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Despite drinking a lot of milk myself,
I think taking a lot of eggshell calcium over a period of a few months
helped me in the past.
I'm not sure what it did--I was thinking mainly of "quieting the parathyroid gland,"
as Peat put it, when I did it.
What did you notice?? Do you notice anything when the parathyroid is calmed??
 
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