![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 5 of 5. This is the beginning of the thread.
Posted by tealady on September 6, 2003, at 23:42:54
In reply to Re: Larry what do you think about lithium orotate? » tealady, posted by Larry Hoover on September 4, 2003, at 9:48:48
Starting thread on the "2nd bit" of the minerals we take.
Someone asked which are "best" forms to take.
Answer..it depends,
on individual needs, some are better absorbed than others, and even this will vary greatly among different people depending on their age, stomach acid level, what they are taken with other supplements, food,etc Some have question marks over their safety.... like picolinate and orotate.Link to orotate is here (also below)
http://www.dr-bob.org/babble/20030902/msgs/256876.html> > >Glomerular filtration rate and urine flow were markedly lower in rats given lithium orotate than in rats given lithium carbonate, sodium chloride or a sham injection.
> >
> > Is this the filtration rate overall is lowered by the lithium oratate, meaning I assume that kidney function is impaired??
>
> That's what it means. Overall kidney function is impaired (decreased filtration rate), and fluid is being retained (decreased urine output), suggesting edema.
>
> > OR the amount of lithium filtered out is lower than with a placebi...
>
> Lithium clearance was also impaired, meaning that the ratio of plasma lithium to urine lithium has increased. I see that as a consequence of the decreased filtration rate. Other substances which should have left the body in urine would also be retained to a greater degree.
>
> The article in question was comparing equal amounts of lithium, supplied as the carbonate or orotate. Just to put that into context, Serenity's proponents are suggesting that a vastly lower supply of lithium, as the orotate salt, is equivalent to the more typical dose of lithium carbonate. I can find no evidence of dose-ranging studies of that equivalence. Lithium orotate was tried in human trials back in the 70's, and was abandoned, although I'm having trouble finding out exactly why (modern references are far more informative).
>
> > so do we have lithium in our blodd normally if we don't supplement?
>
> Yes, but at nowhere near the concentrations seen after the use of lithium salts.
>
> > <The renal lithium clearance was significantly lower, >
> > Lar, I only understand a glimmer of this and of the equilibrium between intra, inter cellular and blood stream and ion transfer etc..
>
> Without revisiting those concepts literally, I was describing processes which are driven by laws of nature. Wherever a high concentration of something exists, that concentration will tend to dissipate, via entropy. Wherever high concentrations of e.g. lithium ions exist in the body, that concentration will tend to be reduced by osmosis between compartments, and diffusion. So, as the kidneys dump lithium, concentrations of lithium will fall everywhere. The way the body gets around these laws of entropy is by employing transporters, energy-consuming ion pumps, in the case of lithium.
>
> If there wasn't very much lithium to begin with (even the proponents of lithium orotate acknowledge there is little in the blood at any one time), then the brain cells will lose what little they have obtained (even if the orotate somehow navigates to the brain). Even the ion pumps will fail if there isn't very much lithium around to pump. There are other organs that have very high affinities for orotic acid (liver, kidney and heart), so there is little likelihood, IMHO, that the brain will get any sort of preferential delivery. Nor will it retain lithium when the concentration gradient runs "downhill" towards the bloodstream, and away from the brain.
>
> > It seems they are saying that with oratate, the kidneys do not filter out the lithium as much, and yet there is MORE lithium in the heart, kidneys and presumably other organs..like brain, thyroid etc..and the kidney WEIGHT is increased..presumably as it is not functioning as well??
>
> Probably edema, but I don't that's a good thing.
>
> You will recall that I mentioned that the rat study used equivalent amounts of the two lithium salts. By whatever mechanism more lithium is retained in these tissues, current human dosage recommendations (as given at the Serenity site, for example) are so very low relative to therapeutic doses of the carbonate or citrate prescribed for mood stabilization, I cannot see how the orotate could possibly work, as described.
>
> > <the kidney weight and the lithium concentrations in serum, kidney and heart significantly higher after injection of lithium orotate than after injection of lithium carbonate. The higher lithium concentrations could be accounted for by the lower kidney function.>
> >
> > So it looks like they may be saying you do get highrr levels in the organs but the kidneys are no longer filtering the blood efficiently, so the lithium stays in the kidney, brain, thyroid, heart etc and doesn't get removed as fast?
>
> That's what they're suggesting. Rather than a higher delivery/uptake rate, they're saying that the higher retention is due to kidney toxicity.
>
> > Does this mean the kidnys themselves are not removing other things as fast also?..I'm assuming so..
>
> I would make the same assumption.
>
> > I have heard many folks swear that orotates were better and the way to go..eg. calcium orotate, magnesium oratate, potassium orotate.
> > Does the oratate itself affect the kidneys ? and is this why the orotate form of minerals "works" better
>
> Quite possibly. There is one profound form of ignorance carried over from generation to generation, which is epitomized by the existence of lists such as GRAS (generally recognized as safe), used for food additives, for example. Substances on that list have probably never been tested for safety. That we have used them for years, and no one has *obviously* died from their use, does not mean they are safe. Absence of evidence is not evidence of absence.
>
> At present, I will scrupulously avoid two forms of salts, those with orotate, and those with piccolinate.
>
> > Like should we AVOID orotates as it may harm kidney function.
>
> You anticipate me well. :-)
>
> > For other begiiners like me who have no idea on the kidneys , I came across this, which helps explain kidbey function
> > http://rarediseases.about.com/gi/dynamic/offsite.htm?site=http%3A%2F%2Fwww.niddk.nih.gov%2Fhealth%2Fkidney%2Fpubs%2Fglomer%2Fglomer.htm
>
>
Posted by tealady on September 7, 2003, at 0:16:04
In reply to mineral forms...orotate, posted by tealady on September 6, 2003, at 23:42:54
>>> At present, I will scrupulously avoid two forms of salts, those with orotate, and those with piccolinate.
>I have just been taking large doses of magnesium carbonate and ascorbic acid(a heaped teaspoon of each) mixed together with a little water, and zinc picolinate, B6.. parsley (I hate cilantro), chlorella, selenium as well as normal vitamins. I have had amalgam removed and was doing what I thought was a safe mild "chelation".I thought the thing against picolinate forms was their ability to chelate?
Here they reckon that as a metal chelator the picolinate chelates out more zinc than the tablets puts in?? Of course it's written by the folks who own the patent on the glycine chelated form.... nah, that wouldn't influence the research...
http://www.albionlabs.com/human/Newsletter/2000October.html
says zinc "glycine (amino acid)" chelate is good and zinc picolinate chelate is bad as picolinate is NOT USABLE BY BODY as well as chelating more zinc than you take in the tablet and other minerals from your body...hopefully mercury!
"absorption of zinc, in vivo, did not vary in favor of the use of picolinate or citrate, when compared to zinc sulfate"
All I can say is my taste is so much stronger now afer a few days on zinc picolinate compared to zinc sulphate at comparable doses (50mg-90mg per day)..backing down from today, so that would indicate that picolinate does have greater effect"the use of picolinic acid led to an increase in urinary and fecal output of zinc. In addition, the residual zinc levels in the tissues of the animals were reduced in the picolinate fed animals, even in the animals that were fed diets containing 0.8 mmol Zn/Kg. These observations indicated that picolinic acid increased the turnover of endogenous zinc and it enhances the excretion of ingested (supplemental) zinc. This gives cause to question the use of picolinate as a chelating ligand for supplemental zinc."
"The urinary zinc, copper and magnesium increased with increasing picolinate supply."
Then I came across a thread where they were discussing picolinate forms causing cancer ..in chromium picolinate
http://forums.about.com/ab-thyroid/messages?msg=50658.3Lar, I have only scanned this so far, but I was wondering why you were against picolinate forms.
Haven't tried any chromium as yet, unless it is in a multi.Thanks as always, Jan
Posted by tealady on September 7, 2003, at 1:52:31
In reply to mineral forms...picolinate ... to Lar, posted by tealady on September 7, 2003, at 0:16:04
"Unlike other forms of trivalent chromium, chromium picolinate was
shown to cause DNA damage in mammalian cells in vitro. Additionally, two case reports have associated
renal failure with the use of chromium picolinate supplements."
http://www.foodstandards.gov.uk/multimedia/pdfs/evm_chromium.pdf
Posted by Larry Hoover on September 7, 2003, at 9:15:40
In reply to mineral forms...picolinate ... to Lar, posted by tealady on September 7, 2003, at 0:16:04
> >>> At present, I will scrupulously avoid two forms of salts, those with orotate, and those with piccolinate.
> >I have just been taking large doses of magnesium carbonate and ascorbic acid(a heaped teaspoon of each) mixed together with a little water, and zinc picolinate, B6.. parsley (I hate cilantro), chlorella, selenium as well as normal vitamins. I have had amalgam removed and was doing what I thought was a safe mild "chelation".If you're worried about mercury, I'd suggest that you ensure that your selenium intake is at the higher end of the normal range. Mercury forms a strong ionic bond with selenium, with a solubility that can only be estimated, it's so low (less than one molecule per liter of water). Even though that salt will be retained in your body, it will have no further effect, except if you are cremated.
> I thought the thing against picolinate forms was their ability to chelate?
You have to be very careful about chelation, in any form, as the ligand (the chelator molecule) will bind any ions with the appropriate charge, or the ability to hybridize the electron orbitals. Any chelator that will bind mercury will preferentially bind other ions that you need for normal biochemical processes. IMHO, chelation is useful in acute exposure (i.e. while the blood concentration is very high, before it's taken up by tissues), but counterproductive in chronic exposure.
> Here they reckon that as a metal chelator the picolinate chelates out more zinc than the tablets puts in?? Of course it's written by the folks who own the patent on the glycine chelated form.... nah, that wouldn't influence the research...
> http://www.albionlabs.com/human/Newsletter/2000October.htmlThat link didn't work for me. I'll take your word for it, though. Was the excretion in feces or urine?
> says zinc "glycine (amino acid)" chelate is good and zinc picolinate chelate is bad as picolinate is NOT USABLE BY BODY as well as chelating more zinc than you take in the tablet and other minerals from your body...hopefully mercury!
See above. Picolinic acid is usable by the body (it's an intermediate), but it isn't found in high concentrations, floating around in the blood.
> "absorption of zinc, in vivo, did not vary in favor of the use of picolinate or citrate, when compared to zinc sulfate"
> All I can say is my taste is so much stronger now afer a few days on zinc picolinate compared to zinc sulphate at comparable doses (50mg-90mg per day)..backing down from today, so that would indicate that picolinate does have greater effectYour increase in taste sensitivy is de facto evidence that the picolinate has provided you with an enhanced zinc supply, but why the sulphate had failed to do so is beyond me. Any chance you're achlorhydric (no stomach acid), or hypochlorhydric (low stomach acid)? I use amino chelates myself.
Just for full comprehension here, a chelator has more than one charged area on its surface (the word derives from the scientific name for a lobster claw). That permits it to bind polyvalent cations (those with a charge greater than 1+, e.g. Mg++, Zn++, Cu++, Cr+++, etc.), especially.
> "the use of picolinic acid led to an increase in urinary and fecal output of zinc. In addition, the residual zinc levels in the tissues of the animals were reduced in the picolinate fed animals, even in the animals that were fed diets containing 0.8 mmol Zn/Kg. These observations indicated that picolinic acid increased the turnover of endogenous zinc and it enhances the excretion of ingested (supplemental) zinc. This gives cause to question the use of picolinate as a chelating ligand for supplemental zinc."And runs contrary to your experience. <shrug>
> "The urinary zinc, copper and magnesium increased with increasing picolinate supply."
....because they exist in the blood as divalent (i.e. ++ ) cations. Chelators are stupid critters. They'll velcro onto anything with the right charge.
> Then I came across a thread where they were discussing picolinate forms causing cancer ..in chromium picolinate
> http://forums.about.com/ab-thyroid/messages?msg=50658.3
>
> Lar, I have only scanned this so far, but I was wondering why you were against picolinate forms.It's the genetic damage issue. Picolinic acid is the culprit. See:
Toxicology. 2002 Oct 30;180(1):5-22.
Comment in:
Toxicology. 2003 Apr 15;186(1-2):171-3; author reply 175-7.
Cytotoxicity and oxidative mechanisms of different forms of chromium.Bagchi D, Stohs SJ, Downs BW, Bagchi M, Preuss HG.
Department of Pharmacy Sciences, Creighton University School of Pharmacy and Health Professions, 2500 California Plaza, Omaha, NE 68178, USA. debsis@creighton.edu
Chromium exists mostly in two valence states in nature: hexavalent chromium [chromium(VI)] and trivalent chromium [chromium(III)]. Chromium(VI) is commonly used in industrial chrome plating, welding, painting, metal finishes, steel manufacturing, alloy, cast iron and wood treatment, and is a proven toxin, mutagen and carcinogen. The mechanistic cytotoxicity of chromium(VI) is not completely understood, however, a large number of studies demonstrated that chromium(VI) induces oxidative stress, DNA damage, apoptotic cell death and altered gene expression. Conversely, chromium(III) is essential for proper insulin function and is required for normal protein, fat and carbohydrate metabolism, and is acknowledged as a dietary supplement. In this paper, comparative concentration- and time-dependent effects of chromium(VI) and chromium(III) were demonstrated on increased production of reactive oxygen species (ROS) and lipid peroxidation, enhanced excretion of urinary lipid metabolites, DNA fragmentation and apoptotic cell death in both in vitro and in vivo models. Chromium(VI) demonstrated significantly higher toxicity as compared with chromium(III). To evaluate the role of p53 gene, the dose-dependent effects of chromium(VI) were assessed in female C57BL/6Ntac and p53-deficient C57BL/6TSG p53 mice on enhanced production of ROS, lipid peroxidation and DNA fragmentation in hepatic and brain tissues. Chromium(VI) induced more pronounced oxidative damage in multiple target organs in p53 deficient mice. Comparative studies of chromium(III) picolinate and niacin-bound chromium(III), two popular dietary supplements, reveal that chromium(III) picolinate produces significantly more oxidative stress and DNA damage. Studies have implicated the toxicity of chromium picolinate in renal impairment, skin blisters and pustules, anemia, hemolysis, tissue edema, liver dysfunction; neuronal cell injury, impaired cognitive, perceptual and motor activity; enhanced production of hydroxyl radicals, chromosomal aberration, depletion of antioxidant enzymes, and DNA damage. Recently, chromium picolinate has been shown to be mutagenic and picolinic acid moiety appears to be responsible as studies show that picolinic acid alone is clastogenic. Niacin-bound chromium(III) has been demonstrated to be more bioavailable and efficacious and no toxicity has been reported. In summary, these studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis. The safety of chromium(III) is largely dependent on the ligand, and adequate clinical studies are warranted to demonstrate the safety and efficacy of chromium(III) for human consumption.
FASEB J. 1995 Dec;9(15):1643-8.
Chromium(III) picolinate produces chromosome damage in Chinese hamster ovary cells.
Stearns DM, Wise JP Sr, Patierno SR, Wetterhahn KE.
Department of Chemistry, Dartmouth College, Hanover, New Hampshire 03755-3564, USA.
Chromium(III) complexes currently being sold as dietary supplements were tested for their ability to cause chromosomal aberrations in Chinese hamster ovary cells. Complexes were tested in soluble and particulate forms. Chromium picolinate was found to produce chromosome damage 3-fold to 18-fold above control levels for soluble doses of 0.050, 0.10, 0.50, and 1.0 mM after 24 h treatment. Particulate chromium picolinate doses of 8.0 micrograms/cm2 (corresponding to a 0.10 mM solublized dose) and 40 micrograms/cm2 (0.50 mM) produced aberrations 4-fold and 16-fold above control levels, respectively. Toxicity was measured as a decrease in plating efficiency relative to controls. The above treatments produced > or = 86% survival for all doses except 1.0 mM chromium picolinate, which produced 69 +/- 10% survival. Chromium nicotinate, nicotinic acid, and chromium(III) chloride hexahydrate did not produce chromosome damage at equivalent nontoxic doses. Damage was inferred to be caused by the picolinate ligand because picolinic acid in the absence of chromium was clastogenic. Data are evaluated in terms of their relevance to human exposure based on pharmacokinetic modeling of tissue accumulation and are discussed in terms of literature reporting toxic effects of picolinic acid.
> Haven't tried any chromium as yet, unless it is in a multi.
>
> Thanks as always, JanYou're welcome.
Lar
Posted by Dr. Bob on September 7, 2003, at 13:27:49
In reply to Re: mineral forms...picolinate ... to Lar » tealady, posted by Larry Hoover on September 7, 2003, at 9:15:40
[reposted with language set to "English"]
> > >>> At present, I will scrupulously avoid two forms of salts, those with orotate, and those with piccolinate.
> > >I have just been taking large doses of magnesium carbonate and ascorbic acid(a heaped teaspoon of each) mixed together with a little water, and zinc picolinate, B6.. parsley (I hate cilantro), chlorella, selenium as well as normal vitamins. I have had amalgam removed and was doing what I thought was a safe mild "chelation".
>
> If you're worried about mercury, I'd suggest that you ensure that your selenium intake is at the higher end of the normal range. Mercury forms a strong ionic bond with selenium, with a solubility that can only be estimated, it's so low (less than one molecule per liter of water). Even though that salt will be retained in your body, it will have no further effect, except if you are cremated.
>
> > I thought the thing against picolinate forms was their ability to chelate?
>
> You have to be very careful about chelation, in any form, as the ligand (the chelator molecule) will bind any ions with the appropriate charge, or the ability to hybridize the electron orbitals. Any chelator that will bind mercury will preferentially bind other ions that you need for normal biochemical processes. IMHO, chelation is useful in acute exposure (i.e. while the blood concentration is very high, before it's taken up by tissues), but counterproductive in chronic exposure.
>
> > Here they reckon that as a metal chelator the picolinate chelates out more zinc than the tablets puts in?? Of course it's written by the folks who own the patent on the glycine chelated form.... nah, that wouldn't influence the research...
> > http://www.albionlabs.com/human/Newsletter/2000October.html
>
> That link didn't work for me. I'll take your word for it, though. Was the excretion in feces or urine?
>
> > says zinc "glycine (amino acid)" chelate is good and zinc picolinate chelate is bad as picolinate is NOT USABLE BY BODY as well as chelating more zinc than you take in the tablet and other minerals from your body...hopefully mercury!
>
> See above. Picolinic acid is usable by the body (it's an intermediate), but it isn't found in high concentrations, floating around in the blood.
>
> > "absorption of zinc, in vivo, did not vary in favor of the use of picolinate or citrate, when compared to zinc sulfate"
> > All I can say is my taste is so much stronger now afer a few days on zinc picolinate compared to zinc sulphate at comparable doses (50mg-90mg per day)..backing down from today, so that would indicate that picolinate does have greater effect
>
> Your increase in taste sensitivy is de facto evidence that the picolinate has provided you with an enhanced zinc supply, but why the sulphate had failed to do so is beyond me. Any chance you're achlorhydric (no stomach acid), or hypochlorhydric (low stomach acid)? I use amino chelates myself.
>
> Just for full comprehension here, a chelator has more than one charged area on its surface (the word derives from the scientific name for a lobster claw). That permits it to bind polyvalent cations (those with a charge greater than 1+, e.g. Mg++, Zn++, Cu++, Cr+++, etc.), especially.
>
> > "the use of picolinic acid led to an increase in urinary and fecal output of zinc. In addition, the residual zinc levels in the tissues of the animals were reduced in the picolinate fed animals, even in the animals that were fed diets containing 0.8 mmol Zn/Kg. These observations indicated that picolinic acid increased the turnover of endogenous zinc and it enhances the excretion of ingested (supplemental) zinc. This gives cause to question the use of picolinate as a chelating ligand for supplemental zinc."
>
> And runs contrary to your experience. <shrug>
>
> > "The urinary zinc, copper and magnesium increased with increasing picolinate supply."
>
> ....because they exist in the blood as divalent (i.e. ++ ) cations. Chelators are stupid critters. They'll velcro onto anything with the right charge.
>
> > Then I came across a thread where they were discussing picolinate forms causing cancer ..in chromium picolinate
> > http://forums.about.com/ab-thyroid/messages?msg=50658.3
> >
> > Lar, I have only scanned this so far, but I was wondering why you were against picolinate forms.
>
> It's the genetic damage issue. Picolinic acid is the culprit. See:
>
> Toxicology. 2002 Oct 30;180(1):5-22.
>
> Comment in:
> Toxicology. 2003 Apr 15;186(1-2):171-3; author reply 175-7.
>
> Cytotoxicity and oxidative mechanisms of different forms of chromium.
>
> Bagchi D, Stohs SJ, Downs BW, Bagchi M, Preuss HG.
>
> Department of Pharmacy Sciences, Creighton University School of Pharmacy and Health Professions, 2500 California Plaza, Omaha, NE 68178, USA. debsis@creighton.edu
>
> Chromium exists mostly in two valence states in nature: hexavalent chromium [chromium(VI)] and trivalent chromium [chromium(III)]. Chromium(VI) is commonly used in industrial chrome plating, welding, painting, metal finishes, steel manufacturing, alloy, cast iron and wood treatment, and is a proven toxin, mutagen and carcinogen. The mechanistic cytotoxicity of chromium(VI) is not completely understood, however, a large number of studies demonstrated that chromium(VI) induces oxidative stress, DNA damage, apoptotic cell death and altered gene expression. Conversely, chromium(III) is essential for proper insulin function and is required for normal protein, fat and carbohydrate metabolism, and is acknowledged as a dietary supplement. In this paper, comparative concentration- and time-dependent effects of chromium(VI) and chromium(III) were demonstrated on increased production of reactive oxygen species (ROS) and lipid peroxidation, enhanced excretion of urinary lipid metabolites, DNA fragmentation and apoptotic cell death in both in vitro and in vivo models. Chromium(VI) demonstrated significantly higher toxicity as compared with chromium(III). To evaluate the role of p53 gene, the dose-dependent effects of chromium(VI) were assessed in female C57BL/6Ntac and p53-deficient C57BL/6TSG p53 mice on enhanced production of ROS, lipid peroxidation and DNA fragmentation in hepatic and brain tissues. Chromium(VI) induced more pronounced oxidative damage in multiple target organs in p53 deficient mice. Comparative studies of chromium(III) picolinate and niacin-bound chromium(III), two popular dietary supplements, reveal that chromium(III) picolinate produces significantly more oxidative stress and DNA damage. Studies have implicated the toxicity of chromium picolinate in renal impairment, skin blisters and pustules, anemia, hemolysis, tissue edema, liver dysfunction; neuronal cell injury, impaired cognitive, perceptual and motor activity; enhanced production of hydroxyl radicals, chromosomal aberration, depletion of antioxidant enzymes, and DNA damage. Recently, chromium picolinate has been shown to be mutagenic and picolinic acid moiety appears to be responsible as studies show that picolinic acid alone is clastogenic. Niacin-bound chromium(III) has been demonstrated to be more bioavailable and efficacious and no toxicity has been reported. In summary, these studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis. The safety of chromium(III) is largely dependent on the ligand, and adequate clinical studies are warranted to demonstrate the safety and efficacy of chromium(III) for human consumption.
>
> FASEB J. 1995 Dec;9(15):1643-8.
>
> Chromium(III) picolinate produces chromosome damage in Chinese hamster ovary cells.
>
> Stearns DM, Wise JP Sr, Patierno SR, Wetterhahn KE.
>
> Department of Chemistry, Dartmouth College, Hanover, New Hampshire 03755-3564, USA.
>
> Chromium(III) complexes currently being sold as dietary supplements were tested for their ability to cause chromosomal aberrations in Chinese hamster ovary cells. Complexes were tested in soluble and particulate forms. Chromium picolinate was found to produce chromosome damage 3-fold to 18-fold above control levels for soluble doses of 0.050, 0.10, 0.50, and 1.0 mM after 24 h treatment. Particulate chromium picolinate doses of 8.0 micrograms/cm2 (corresponding to a 0.10 mM solublized dose) and 40 micrograms/cm2 (0.50 mM) produced aberrations 4-fold and 16-fold above control levels, respectively. Toxicity was measured as a decrease in plating efficiency relative to controls. The above treatments produced > or = 86% survival for all doses except 1.0 mM chromium picolinate, which produced 69 +/- 10% survival. Chromium nicotinate, nicotinic acid, and chromium(III) chloride hexahydrate did not produce chromosome damage at equivalent nontoxic doses. Damage was inferred to be caused by the picolinate ligand because picolinic acid in the absence of chromium was clastogenic. Data are evaluated in terms of their relevance to human exposure based on pharmacokinetic modeling of tissue accumulation and are discussed in terms of literature reporting toxic effects of picolinic acid.
>
>
> > Haven't tried any chromium as yet, unless it is in a multi.
> >
> > Thanks as always, Jan
>
> You're welcome.
> Lar
>
>
This is the end of the thread.
Psycho-Babble Alternative | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.