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
>
>
poster:Dr. Bob
thread:257732
URL: http://www.dr-bob.org/babble/alter/20030903/msgs/257834.html