Re: Further questioning the vitamin D ratio test.

[Guest guest]

Mark

What do you think all this should be tied to- and what do you prefer

an ARB or ace inhibitor- these are questions that we'll need up our

sleeve as we age.I also feeel strongly that we need a package and

unfortunatel;y as much as I initially liked arb's they are

absolutely useless and possably dangerous drugs in my own case when

they no longer clamp inflammation.

> Ken Lassesen has well argued the lack of scientific basis for using

> the ratio of 1,25-D3 to 25-D3 as a means of determining TH1

production

> of 1,25-D3. The following study shows yet another example of that:

>

> J Clin Endocrinol Metab. 1995 Jul;80(7):2227-32.

> Calcium-regulating hormones across the menstrual cycle: evidence

of a

> secondary hyperparathyroidism in women with PMS.

>

> This study confirms another study that was previously mentioned

here,

> which is that vitamin D levels can significantly vary during the

> menstrual cycle. However, more interestingly is that in PMS

patients,

> 1,25-D3 was significantly increased, and 25-D3 was significantly

> decreased.

>

> When this occurs, doctors will test PTH levels, as PTH can increase

> renal production of 1,25-D3. This can occur due to a calcium

> deficiency. However, PTH levels also vary significantly during the

> menstrual cycle, and only during certain days were PTH levels

> significantly increased in PMS patients, compared to controls. On

> many days, PTH levels were normal, so that one could easily test

such

> people, and on the basis of the vitamin D ratio, claim that they

had

> TH1 production of vitamin D. In fact, in half of the PMS patients,

> PTH levels looked quite normal during almost the whole cycle. This

> anomoly is likely due to estrogen, which can directly influence

> 1,25-D3 levels.

>

> This is just one of many possible factors which influence 1,25-D3

levels.

> It's one of the reasons why 25-D3 is mainly used to test for a

vitamin

> D deficiency, as too many factors influence 1,25-D3 levels.

>

> In the above study, one of the PMS patients was treated with

calcium

> and vitamin D supplementation, and this corrected the high 1,25-D3

and

> low 25-D3 levels.

>

> Calcium is known to suppress normal renal production of vitamin D.

> Calcium supplementation, or loading, is a common and much more

valid

> way of determining whether increased 1,25-D3 levels is due to

either

> non-renal or extra-renal production. In fact, this was suggested

in

> the following study:

>

> J Clin Invest. 1993 Apr;91(4):1396-8.

> Increased calcium intake does not suppress circulating

> 1,25-dihydroxyvitamin D in normocalcemic patients with

sarcoidosis.

>

> To determine if increased Ca intake suppresses serum 1,25(OH)

2D in

> normocalcemic patients and to identify those at risk, 17 normal

> subjects and 11 patients were studied on a metabolic ward for

two

> and one-half days while receiving first 400 and then 1,000

mg/d of Ca.

> On the low Ca intake, serum angiotensin-converting enzyme

(ACE), an

> index of disease activity, was higher in only three of the

patients

> than in the controls, mean serum 1,25(OH)2D was higher in the

> patients, and mean serum total Ca, serum Ca++, and urinary Ca

weren't

> different in the two groups. On the higher Ca intake, mean

urinary Ca

> increased in both groups, but mean serum 1,25(OH)2D was

suppressed

> only in the normal subjects. Thus, 1,25(OH)2D production is

> abnormally regulated, indicating that (a) normocalcemic

patients with

> sarcoidosis are at risk for developing abnormal Ca metabolism,

and (

> a better index of disease activity is provided by the oral Ca

> suppression test than by serum ACE.

>

>

> As for people who claim that using an ARB like Benicar can reduce

> vitamin D levels, and that that is proof of TH1 vitamin D

production,

> that is not so clear either. For example, here's an interesting

study

> on angiotensin II's effects on calcium metabolism and vitamin D

levels:

>

>

> Am J Hypertens. 2003 Jun;16(6):453-9.

> Effect of quinapril, quinapril-hydrochlorothiazide, and

enalapril on

> the bone mass of hypertensive subjects: relationship with

> angiotensin converting enzyme polymorphisms.

>

>

> Few studies have been conducted on the relationship between

> angiotensin II and its effects on calcium metabolism. I could not

> find a study that used ARBs, but in the above study which used ACE

> inhibitors on people with hypertension, they found that these drugs

> caused a decrease in 1,25-D3 levels. They concluded:

>

>

> " This therapeutic group acts by blocking angiotensin II

synthesis.

> Consequently, it has a beneficial effect on the skeleton

because there

> is a decrease in angiotensin concentration. It has been

hypothesized

> that angiotensin can indirectly act on bone cells by

regulating the

> flow of bone marrow capillaries or directly by binding to AT1

> receptors located on osteoblasts, thus promoting the mediator

release

> that would activate the osteoclasts. " " The reduction of

angiotensin

> II levels has a beneficial effect of inhibiting bone

resorption and

> promoting mineralization.

>

> Angiotensin II can interfere with calcium metabolism. The

> administration of this peptide in a group of healthy

volunteers caused

> a decrease in ionic calcium levels and an increase in PTHi

levels.

> The decrease of calcemia was not related to an increase in

calciuria,

> but it could be caused by an increase in calcium uptake by

vascular

> smooth muscle cells. In our patients, ACE inhibitors increased

the

> level of calcium, although the concentration of PTHi was not

modified.

> These data suggest a beneficial effect on the blockage of the

> synthesis of angiotensin in calcium metabolism. "

>

> If AT1 receptors are responsible for this effect, then one could

> easily speculate that ARBs should have at least a strong, if not

much

> stronger effect, on calcium metabolism, than ACE inhibitors. So

even

> if it was determined that ACE inhibitors do not exhibit a similar

> effect on non-hypertensives, an ARB with a much stronger ability to

> block angiotensin II, might still be able to have an significant

effect.

>

> Therefore, even if Benicar actually could lower vitamin D levels,

it

> still would not be positive proof of TH1 vitamin D production.

Other

> testing methods would need to be used, such as calcium loading,

which

> have been shown by studies to be useful in detecting TH1 vitamin D

> production.

>

> Mark

[Guest guest]

Mark London <mrl@...> wrote:

Ken Lassesen has well argued the lack of scientific basis for usingthe ratio of 1,25-D3 to 25-D3 as a means of determining TH1 productionof 1,25-D3. The following study shows yet another example of that: J Clin Endocrinol Metab. 1995 Jul;80(7):2227-32. Calcium-regulating hormones across the menstrual cycle: evidence of a secondary hyperparathyroidism in women with PMS.This study confirms another study that was previously mentioned here,which is that vitamin D levels can significantly vary during themenstrual cycle. However, more interestingly is that in PMS patients,1,25-D3 was significantly increased, and 25-D3 was significantlydecreased.When this occurs, doctors will test PTH levels, as PTH can increaserenal production of 1,25-D3. This can occur due to a calciumdeficiency.

However, PTH levels also vary significantly during themenstrual cycle, and only during certain days were PTH levelssignificantly increased in PMS patients, compared to controls. Onmany days, PTH levels were normal, so that one could easily test suchpeople, and on the basis of the vitamin D ratio, claim that they hadTH1 production of vitamin D. In fact, in half of the PMS patients,PTH levels looked quite normal during almost the whole cycle. Thisanomoly is likely due to estrogen, which can directly influence1,25-D3 levels.This is just one of many possible factors which influence 1,25-D3 levels.It's one of the reasons why 25-D3 is mainly used to test for a vitaminD deficiency, as too many factors influence 1,25-D3 levels.In the above study, one of the PMS patients was treated with calciumand vitamin D supplementation, and this corrected the high 1,25-D3 andlow 25-D3 levels.Calcium is known to

suppress normal renal production of vitamin D. Calcium supplementation, or loading, is a common and much more validway of determining whether increased 1,25-D3 levels is due to eithernon-renal or extra-renal production. In fact, this was suggested inthe following study: J Clin Invest. 1993 Apr;91(4):1396-8. Increased calcium intake does not suppress circulating 1,25-dihydroxyvitamin D in normocalcemic patients with sarcoidosis. To determine if increased Ca intake suppresses serum 1,25(OH)2D in normocalcemic patients and to identify those at risk, 17 normal subjects and 11 patients were studied on a metabolic ward for two and one-half days while receiving first 400 and then 1,000 mg/d of Ca. On the low Ca intake, serum angiotensin-converting enzyme (ACE),

an index of disease activity, was higher in only three of the patients than in the controls, mean serum 1,25(OH)2D was higher in the patients, and mean serum total Ca, serum Ca++, and urinary Ca weren't different in the two groups. On the higher Ca intake, mean urinary Ca increased in both groups, but mean serum 1,25(OH)2D was suppressed only in the normal subjects. Thus, 1,25(OH)2D production is abnormally regulated, indicating that (a) normocalcemic patients with sarcoidosis are at risk for developing abnormal Ca metabolism, and ( a better index of disease activity is provided by the oral Ca suppression test than by serum ACE.As for people who claim that using an ARB like Benicar can reducevitamin D levels, and that that is proof of TH1 vitamin

D production,that is not so clear either. For example, here's an interesting studyon angiotensin II's effects on calcium metabolism and vitamin D levels: Am J Hypertens. 2003 Jun;16(6):453-9. Effect of quinapril, quinapril-hydrochlorothiazide, and enalapril on the bone mass of hypertensive subjects: relationship with angiotensin converting enzyme polymorphisms.Few studies have been conducted on the relationship betweenangiotensin II and its effects on calcium metabolism. I could notfind a study that used ARBs, but in the above study which used ACEinhibitors on people with hypertension, they found that these drugscaused a decrease in 1,25-D3 levels. They concluded: "This therapeutic group acts by blocking angiotensin II synthesis. Consequently, it has a

beneficial effect on the skeleton because there is a decrease in angiotensin concentration. It has been hypothesized that angiotensin can indirectly act on bone cells by regulating the flow of bone marrow capillaries or directly by binding to AT1 receptors located on osteoblasts, thus promoting the mediator release that would activate the osteoclasts." "The reduction of angiotensin II levels has a beneficial effect of inhibiting bone resorption and promoting mineralization. Angiotensin II can interfere with calcium metabolism. The administration of this peptide in a group of healthy volunteers caused a decrease in ionic calcium levels and an increase in PTHi levels. The decrease of calcemia was not related to an increase

in calciuria, but it could be caused by an increase in calcium uptake by vascular smooth muscle cells. In our patients, ACE inhibitors increased the level of calcium, although the concentration of PTHi was not modified. These data suggest a beneficial effect on the blockage of the synthesis of angiotensin in calcium metabolism."If AT1 receptors are responsible for this effect, then one couldeasily speculate that ARBs should have at least a strong, if not muchstronger effect, on calcium metabolism, than ACE inhibitors. So evenif it was determined that ACE inhibitors do not exhibit a similareffect on non-hypertensives, an ARB with a much stronger ability toblock angiotensin II, might still be able to have an significant effect.Therefore, even if Benicar actually could lower vitamin D levels, itstill would not be positive proof of

TH1 vitamin D production. Othertesting methods would need to be used, such as calcium loading, whichhave been shown by studies to be useful in detecting TH1 vitamin Dproduction.Mark

for Good Click here to donate to the Hurricane Katrina relief effort.

[Guest guest]

Mark, thank you for this. It's very impressive. And very logical. If

you want, you should post it in the files section.

I'm still doing great with the Benicar but am starting to need even

less than the 2 pills (40mg each) per day. At this point, I'm

sometimes going much longer than 12 hours before realizing I haven't

taken the Benicar, usually because one of the old symptoms starts

creeping up. Usually it's a tenseness in the neck muscles that is

the reminder (a symptom that's been with me since childhood) or some

stiffness when getting up from a chair (amazing how Benicar makes

that disappear). The teeth chattering only happens rarely now, as do

almost all the other symptoms I've struggled with for so long.

I'll probably have to start splitting the Benicars in half and

figure out another dosing schedule to get myself down to around 60

mg per day, rather than the 80 I've been taking for a few months

now. I am so encouraged that the benefits of the drug are lasting

and that I'm gradually decreasing the amount needed for the same

effect. I'm sure this may fluctuate depending on other treatments.

I've been doing great on penicillin, but started a new anti-fungal,

and apparently the die off is creating a little more inflammation

(achiness), so I seem to need to take the benicar a little more

frequently since starting the V-fend.

I wonder how they'll prescribe this drug in the future, so that

people can use as needed? That freedom has been a godsend for me.

penny

> Ken Lassesen has well argued the lack of scientific basis for using

> the ratio of 1,25-D3 to 25-D3 as a means of determining TH1

production

> of 1,25-D3. The following study shows yet another example of that:

>

> J Clin Endocrinol Metab. 1995 Jul;80(7):2227-32.

> Calcium-regulating hormones across the menstrual cycle: evidence

of a

> secondary hyperparathyroidism in women with PMS.

>

> This study confirms another study that was previously mentioned

here,

> which is that vitamin D levels can significantly vary during the

> menstrual cycle. However, more interestingly is that in PMS

patients,

> 1,25-D3 was significantly increased, and 25-D3 was significantly

> decreased.

>

> When this occurs, doctors will test PTH levels, as PTH can increase

> renal production of 1,25-D3. This can occur due to a calcium

> deficiency. However, PTH levels also vary significantly during the

> menstrual cycle, and only during certain days were PTH levels

> significantly increased in PMS patients, compared to controls. On

> many days, PTH levels were normal, so that one could easily test

such

> people, and on the basis of the vitamin D ratio, claim that they

had

> TH1 production of vitamin D. In fact, in half of the PMS patients,

> PTH levels looked quite normal during almost the whole cycle. This

> anomoly is likely due to estrogen, which can directly influence

> 1,25-D3 levels.

>

> This is just one of many possible factors which influence 1,25-D3

levels.

> It's one of the reasons why 25-D3 is mainly used to test for a

vitamin

> D deficiency, as too many factors influence 1,25-D3 levels.

>

> In the above study, one of the PMS patients was treated with

calcium

> and vitamin D supplementation, and this corrected the high 1,25-D3

and

> low 25-D3 levels.

>

> Calcium is known to suppress normal renal production of vitamin D.

> Calcium supplementation, or loading, is a common and much more

valid

> way of determining whether increased 1,25-D3 levels is due to

either

> non-renal or extra-renal production. In fact, this was suggested

in

> the following study:

>

> J Clin Invest. 1993 Apr;91(4):1396-8.

> Increased calcium intake does not suppress circulating

> 1,25-dihydroxyvitamin D in normocalcemic patients with

sarcoidosis.

>

> To determine if increased Ca intake suppresses serum 1,25(OH)

2D in

> normocalcemic patients and to identify those at risk, 17 normal

> subjects and 11 patients were studied on a metabolic ward for

two

> and one-half days while receiving first 400 and then 1,000

mg/d of Ca.

> On the low Ca intake, serum angiotensin-converting enzyme

(ACE), an

> index of disease activity, was higher in only three of the

patients

> than in the controls, mean serum 1,25(OH)2D was higher in the

> patients, and mean serum total Ca, serum Ca++, and urinary Ca

weren't

> different in the two groups. On the higher Ca intake, mean

urinary Ca

> increased in both groups, but mean serum 1,25(OH)2D was

suppressed

> only in the normal subjects. Thus, 1,25(OH)2D production is

> abnormally regulated, indicating that (a) normocalcemic

patients with

> sarcoidosis are at risk for developing abnormal Ca metabolism,

and (

> a better index of disease activity is provided by the oral Ca

> suppression test than by serum ACE.

>

>

> As for people who claim that using an ARB like Benicar can reduce

> vitamin D levels, and that that is proof of TH1 vitamin D

production,

> that is not so clear either. For example, here's an interesting

study

> on angiotensin II's effects on calcium metabolism and vitamin D

levels:

>

>

> Am J Hypertens. 2003 Jun;16(6):453-9.

> Effect of quinapril, quinapril-hydrochlorothiazide, and

enalapril on

> the bone mass of hypertensive subjects: relationship with

> angiotensin converting enzyme polymorphisms.

>

>

> Few studies have been conducted on the relationship between

> angiotensin II and its effects on calcium metabolism. I could not

> find a study that used ARBs, but in the above study which used ACE

> inhibitors on people with hypertension, they found that these drugs

> caused a decrease in 1,25-D3 levels. They concluded:

>

>

> " This therapeutic group acts by blocking angiotensin II

synthesis.

> Consequently, it has a beneficial effect on the skeleton

because there

> is a decrease in angiotensin concentration. It has been

hypothesized

> that angiotensin can indirectly act on bone cells by

regulating the

> flow of bone marrow capillaries or directly by binding to AT1

> receptors located on osteoblasts, thus promoting the mediator

release

> that would activate the osteoclasts. " " The reduction of

angiotensin

> II levels has a beneficial effect of inhibiting bone

resorption and

> promoting mineralization.

>

> Angiotensin II can interfere with calcium metabolism. The

> administration of this peptide in a group of healthy

volunteers caused

> a decrease in ionic calcium levels and an increase in PTHi

levels.

> The decrease of calcemia was not related to an increase in

calciuria,

> but it could be caused by an increase in calcium uptake by

vascular

> smooth muscle cells. In our patients, ACE inhibitors increased

the

> level of calcium, although the concentration of PTHi was not

modified.

> These data suggest a beneficial effect on the blockage of the

> synthesis of angiotensin in calcium metabolism. "

>

> If AT1 receptors are responsible for this effect, then one could

> easily speculate that ARBs should have at least a strong, if not

much

> stronger effect, on calcium metabolism, than ACE inhibitors. So

even

> if it was determined that ACE inhibitors do not exhibit a similar

> effect on non-hypertensives, an ARB with a much stronger ability to

> block angiotensin II, might still be able to have an significant

effect.

>

> Therefore, even if Benicar actually could lower vitamin D levels,

it

> still would not be positive proof of TH1 vitamin D production.

Other

> testing methods would need to be used, such as calcium loading,

which

> have been shown by studies to be useful in detecting TH1 vitamin D

> production.

>

> Mark

[Guest guest]

That's great news Penny.

You may be getting to the point in your therapy where STARTED

his (lower dose, or intermittant Benicar).

Maybe the inflammatory condition has been improved to the point where

your abx really got in there and wipe out alot of bad bugs.

If the researchers figure out how to monitor progress on Benicar,

(maybe some sort of test marker) then there should be a systematic

way to change the dose as needed. I think there's alot of research

going on in that area because there's alot of money to be made.

Barb

> > Ken Lassesen has well argued the lack of scientific basis for

using

> > the ratio of 1,25-D3 to 25-D3 as a means of determining TH1

> production

> > of 1,25-D3. The following study shows yet another example of

that:

> >

> > J Clin Endocrinol Metab. 1995 Jul;80(7):2227-32.

> > Calcium-regulating hormones across the menstrual cycle:

evidence

> of a

> > secondary hyperparathyroidism in women with PMS.

> >

> > This study confirms another study that was previously mentioned

> here,

> > which is that vitamin D levels can significantly vary during the

> > menstrual cycle. However, more interestingly is that in PMS

> patients,

> > 1,25-D3 was significantly increased, and 25-D3 was significantly

> > decreased.

> >

> > When this occurs, doctors will test PTH levels, as PTH can

increase

> > renal production of 1,25-D3. This can occur due to a calcium

> > deficiency. However, PTH levels also vary significantly during

the

> > menstrual cycle, and only during certain days were PTH levels

> > significantly increased in PMS patients, compared to controls. On

> > many days, PTH levels were normal, so that one could easily test

> such

> > people, and on the basis of the vitamin D ratio, claim that they

> had

> > TH1 production of vitamin D. In fact, in half of the PMS

patients,

> > PTH levels looked quite normal during almost the whole cycle.

This

> > anomoly is likely due to estrogen, which can directly influence

> > 1,25-D3 levels.

> >

> > This is just one of many possible factors which influence 1,25-D3

> levels.

> > It's one of the reasons why 25-D3 is mainly used to test for a

> vitamin

> > D deficiency, as too many factors influence 1,25-D3 levels.

> >

> > In the above study, one of the PMS patients was treated with

> calcium

> > and vitamin D supplementation, and this corrected the high 1,25-

D3

> and

> > low 25-D3 levels.

> >

> > Calcium is known to suppress normal renal production of vitamin

D.

> > Calcium supplementation, or loading, is a common and much more

> valid

> > way of determining whether increased 1,25-D3 levels is due to

> either

> > non-renal or extra-renal production. In fact, this was suggested

> in

> > the following study:

> >

> > J Clin Invest. 1993 Apr;91(4):1396-8.

> > Increased calcium intake does not suppress circulating

> > 1,25-dihydroxyvitamin D in normocalcemic patients with

> sarcoidosis.

> >

> > To determine if increased Ca intake suppresses serum 1,25(OH)

> 2D in

> > normocalcemic patients and to identify those at risk, 17

normal

> > subjects and 11 patients were studied on a metabolic ward for

> two

> > and one-half days while receiving first 400 and then 1,000

> mg/d of Ca.

> > On the low Ca intake, serum angiotensin-converting enzyme

> (ACE), an

> > index of disease activity, was higher in only three of the

> patients

> > than in the controls, mean serum 1,25(OH)2D was higher in the

> > patients, and mean serum total Ca, serum Ca++, and urinary Ca

> weren't

> > different in the two groups. On the higher Ca intake, mean

> urinary Ca

> > increased in both groups, but mean serum 1,25(OH)2D was

> suppressed

> > only in the normal subjects. Thus, 1,25(OH)2D production is

> > abnormally regulated, indicating that (a) normocalcemic

> patients with

> > sarcoidosis are at risk for developing abnormal Ca

metabolism,

> and (

> > a better index of disease activity is provided by the oral Ca

> > suppression test than by serum ACE.

> >

> >

> > As for people who claim that using an ARB like Benicar can reduce

> > vitamin D levels, and that that is proof of TH1 vitamin D

> production,

> > that is not so clear either. For example, here's an interesting

> study

> > on angiotensin II's effects on calcium metabolism and vitamin D

> levels:

> >

> >

> > Am J Hypertens. 2003 Jun;16(6):453-9.

> > Effect of quinapril, quinapril-hydrochlorothiazide, and

> enalapril on

> > the bone mass of hypertensive subjects: relationship with

> > angiotensin converting enzyme polymorphisms.

> >

> >

> > Few studies have been conducted on the relationship between

> > angiotensin II and its effects on calcium metabolism. I could not

> > find a study that used ARBs, but in the above study which used ACE

> > inhibitors on people with hypertension, they found that these

drugs

> > caused a decrease in 1,25-D3 levels. They concluded:

> >

> >

> > " This therapeutic group acts by blocking angiotensin II

> synthesis.

> > Consequently, it has a beneficial effect on the skeleton

> because there

> > is a decrease in angiotensin concentration. It has been

> hypothesized

> > that angiotensin can indirectly act on bone cells by

> regulating the

> > flow of bone marrow capillaries or directly by binding to AT1

> > receptors located on osteoblasts, thus promoting the mediator

> release

> > that would activate the osteoclasts. " " The reduction of

> angiotensin

> > II levels has a beneficial effect of inhibiting bone

> resorption and

> > promoting mineralization.

> >

> > Angiotensin II can interfere with calcium metabolism. The

> > administration of this peptide in a group of healthy

> volunteers caused

> > a decrease in ionic calcium levels and an increase in PTHi

> levels.

> > The decrease of calcemia was not related to an increase in

> calciuria,

> > but it could be caused by an increase in calcium uptake by

> vascular

> > smooth muscle cells. In our patients, ACE inhibitors

increased

> the

> > level of calcium, although the concentration of PTHi was not

> modified.

> > These data suggest a beneficial effect on the blockage of the

> > synthesis of angiotensin in calcium metabolism. "

> >

> > If AT1 receptors are responsible for this effect, then one could

> > easily speculate that ARBs should have at least a strong, if not

> much

> > stronger effect, on calcium metabolism, than ACE inhibitors. So

> even

> > if it was determined that ACE inhibitors do not exhibit a similar

> > effect on non-hypertensives, an ARB with a much stronger ability

to

> > block angiotensin II, might still be able to have an significant

> effect.

> >

> > Therefore, even if Benicar actually could lower vitamin D levels,

> it

> > still would not be positive proof of TH1 vitamin D production.

> Other

> > testing methods would need to be used, such as calcium loading,

> which

> > have been shown by studies to be useful in detecting TH1 vitamin D

> > production.

> >

> > Mark

[Guest guest]

> Mark, thank you for this. It's very impressive. And very logical. If

> you want, you should post it in the files section.

>

> I'm still doing great with the Benicar but am starting to need even

> less than the 2 pills (40mg each) per day. At this point, I'm

> sometimes going much longer than 12 hours before realizing I haven't

> taken the Benicar, usually because one of the old symptoms starts

> creeping up. Usually it's a tenseness in the neck muscles that is

> the reminder (a symptom that's been with me since childhood) or some

> stiffness when getting up from a chair (amazing how Benicar makes

> that disappear).

This effect makes sense, considering that there are AT1 receptors in

skeletal muscls, and ARBs have been shown to decrease muscle

sympathetic activity, increase insulin sensitivity, and increase blood

flow, all things that could affect muscle tightness. Hmm... Now I can

see why it might be helping some people with fibromyalgia, an effect I

hadn't considered.

Mark