Supplementation for general well-being

[neonhypoxia]

Oh, well in that case the CMZ would be pretty pointless. The Calcium will almost completely block the uptake of the other minerals.

[dinoiii]

Originally Posted by neonhypoxia

I'm sure this is a stupid question, but by CMZ are you meaning Calcium, Mangesium, and Zinc? If so just be sure to not take them together.

So not to be a complete dick, I'm going to disagree with supplementing beta-carotene. In several studies long term intake of beta-carotene has been shown to cause an increase in the rate of cancers and general mortality. Retinyl palmitate, the other common form of vitamin A in supplements has not shown an increase in cancer risk or mortality rate. However supplementing with beta-carotene has been shown in a few, but not completely conclusive, studies to help slow mental decline in old age, and retinyl palmitate has not. Also retinyl palmitate is subject to overdosing, and with the exception of turning you orange beta-carotene is not. Now that we've made things confusing...

I'de say don't supplement long term with beta-carotene if you have cancer, or are in a high risk group for it. If however you have a condition which causes mental decline or are in a group with a high risk for it go for beta-carotene. If you have both then... I'm just stumped.

Personally I go with retinyl palmitate at 8000 I.U. (160% RDA) on M T T F and none on the other three days of the week.

A considerable number of epidemiologic studies conducted in the 1970s and 1980s indicated that an inverse relationship exists between estimated intakes of ß-carotene and the risk of developing various types of cancer, especially lung cancer. These studies have led to the suggestion that dietary ß-carotene can reduce human cancer rates (1,2). Subsequent observational cohort and nested case-control studies based on measurement of carotenoids in blood and tissues showed consistent inverse association between blood ß-carotene and risk of lung cancer (1). Initially, it was thought that the conversion of ß-carotene to retinol (1,3) is the mechanism of its cancer preventive effects. However, the inability to demonstrate a consistent negative association between plasma retinol levels and cancer risk has led to the proposal that ß-carotene itself might exert chemopreventive effects. Several mechanisms have been proposed for such effects: 1) action as an antioxidant, 2) induction of cytochrome P450 xenobiotic detoxifying enzymes, 3) enhancement of gap-junctional communication, and 4) metabolism to retinoic acid that could exert biologic effects by activating nuclear retinoic acid receptors (RARs) (1,4,5). This metabolism occurred through either central cleavage to retinal and subsequent oxidation to retinol and retinoic acid or excentric cleavage to form ß-apocarotenoic acids and subsequently retinoic acids (4,5).

Several large-scale intervention studies were then designed to test the ability of ß-carotene alone or combined with -tocopherol or retinyl palmitate to prevent lung cancer (6-10). Unexpectedly, these studies failed to demonstrate prevention of lung cancer. Furthermore, both the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study conducted in Finland (6,7) and the ß-Carotene and Retinol Efficacy Trial study conducted in the United States (8,9) demonstrated a higher incidence of lung cancer in current smokers, alcohol drinkers, and individuals exposed to asbestos who received ß-carotene. In contrast, ex-smokers not exposed to asbestos showed no increased risk upon supplementation with ß-carotene.

The mechanism by which ß-carotene increased lung cancer risk in heavy smokers and asbestos workers is not clear. It has been suggested that the relatively high partial oxygen pressure in the lung combined with reactive oxygen species derived from tobacco smoke or induced by asbestos is conducive for ß-carotene auto-oxidation and that the oxidative metabolites can act as propagators of free-radical formation in smokers' lungs (11-13).


1 International Agency for Research on Cancer (IARC) Working Group on the Evaluation of Cancer Preventive Agents. IARC handbooks of cancer prevention. Vol. 2. Carotenoids. Lyon (France): IARC; 1998.

2 Peto R, Doll R, Buckley JD, Sporn MB. Can dietary beta-carotene materially reduce human cancer rates? Nature 1981;290:201-8.[CrossRef][Medline]cancerlit;81148840

3 Moore T, editor. Vitamin A. Amsterdam (The Netherlands): Elsevier; 1957.

4 Krinsky NI. Carotenoids and cancer: basic research studies. In: Frei B, editor. Natural antioxidants in human health and disease. New York (NY): Academic Press; 1994. p. 239-61.

5 Wang XD, Krinsky NI, Chun L, Peacocke M, Russell RM. ß-Apo-14'-carotenoic acid transactivates the response element of retinoic acid receptor 2 gene via its conversion into retinoic acid [abstract]. FASEB J 1997;11:A181.

6 The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029-35.[Abstract/Free Full Text]cancerlit;94173292

7 Albanes D, Heinonen OP, Taylor PR, Virtamo J, Edwards BK, Rautalahti M, et al. -Tocopherol and ß-carotene supplements and lung cancer incidence in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study: effects of base-line characteristics and study compliance. J Natl Cancer Inst 1996;88:1560-70.[Abstract/Free Full Text]cancerlit;97057515

8 Omenn GS, Goodman G, Thornquist M, Barnhart S, Balmes J, Cherniack MG, et al. Chemoprevention of lung cancer: the ß-Carotene and Retinol Efficacy Trial (CARET) in high-risk smokers and asbestos-exposed workers. IARC Sci Publ 1996;136:67-85.cancerlit;96383254

9 Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med 1996;334:1150-5.[Abstract/Free Full Text]cancerlit;96185731

10 Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med 1996;334:1145-9.[Abstract/Free Full Text]cancerlit;96185730

11 Palozza P, Calviello G, Bartoli GM. Prooxidant activity of ß-carotene under 100% oxygen pressure in rat liver microsomes. Free Radic Biol Med 1995;19:887-92.[CrossRef][ISI][Medline]

12 Mayne ST, Handelman GJ, Beecher G. ß-Carotene and lung cancer promotion in heavy smokers—a plausible relationship? [editorial].J Natl Cancer Inst 1996;88:1513-5.cancerlit;97057508

13 Omaye ST, Krinsky NI, Kagan VE, Mayne ST, Liebler DC, Bidlack WR. Beta-carotene: friend or foe? Fundam Appl Toxicol 1997;40:163-74.[CrossRef][ISI][Medline]cancerlit;98110538

Originally Posted by neonhypoxia

Oh, well in that case the CMZ would be pretty pointless. The Calcium will almost completely block the uptake of the other minerals.

Not true. Calcium when used as a amino acid chelate is actually absorbed like the constituent amino acid; the absorptive issues do NOT tend to occur.



D_

[dinoiii]

Originally Posted by thesinner

What are your thoughts on Zinc Gluconate Glycine (Zincum Gluconicum) products such as Cold-eeze or Zicam?

I got hooked on using these when I got a cold way back in the day when they first came out and didn't have any flavoring (and dammit, if you had to suffer through that, you'd better get over your cold :yuck:.).

Zinc gluconate gives higher Zn concentrations than other zinc salts in the blood in the first 6 hours post-administration but also shows greater losses in the feces. If you take it consistently enough, I could assume a high enough serum concentration to potentially offset fecal losses, so why not.



D_

[neonhypoxia]

So I swear I'm not trying to be a dick and just disagree with you for no reason, but...

My primary issue with beta-carotene is that almost (almost, not all) ever cancer group, both within and outside the U.S. recomends not taking beta-carotene. I have to assume they have more expertese with this subject than I do. I also know that these proposed mechanism are only proposed, there is really alot about cancer formation on the whole that we don't know so... *shrugs* I just plan on agreeing with the people that I think know more than me.

As for the absoption of metals in chelate form, I don't know much about that. I could be completely mistaken on this, but if I remember from my chem classes amino acid chelates don't bind as well to metal ion in acidic environments as say EDTA. So while some of the calcium might stay as a chelate, not all will and you'll still end up with some in solution which could block absorption of other free ions. The other metals of course would have the same issue with not all of them staying in chelate form. So the free calcium would atleast block the absorption of the other free minerals wouldn't it?

[neonhypoxia]

Actually I think we both may be over or heads on this one considering how complicated cancer formation can be. I work with several oncologist and I'll just ask on when I see them on Friday. I'de like to have the opinions of several different people in the field on this too instead of just one or two.

[GotTest]

Recommended dosing for P-5-P?
Is it really better than B6?

[neonhypoxia]

Originally Posted by GotTest

Recommended dosing for P-5-P?
Is it really better than B6?

I have no idea what the recommended dosing is, but it would be easier to reach overdose levels. B6 should probably be kept at 200mg or less a day if you are using it everyday althought many people don't have problems with doses as high as 1g.

Pyridoxal-5'-Phosphate [(4-formyl-5-hydroxy-6-methyl-3-pyridyl) methoxyphosphonic acid, Pyridoxal-phosphate,P-5-P, P5P, or PLP] is simply what you get after your liver has metabolized B6, its basicly the active form. As long as you aren't taking certain drugs (I'm not sure which ones fall under the category), you don't have certain metabolic disorders (again not sure which ones are in this category), and you aren't too old you should be converting B6 perfectly fine. So B6 and Pyridoxal-5'-Phosphate would get the same job done but with the B6 being cheaper. Pyridoxal-5'-Phosphate also has a shorter half life than B6. So in a very simplified way B6 could be considered a limited storage method.

Simple answer: I'de go with B6 unless there are other issues at play.

[dinoiii]

Originally Posted by neonhypoxia

So I swear I'm not trying to be a dick and just disagree with you for no reason, but...

My primary issue with beta-carotene is that almost (almost, not all) ever cancer group, both within and outside the U.S. recomends not taking beta-carotene. I have to assume they have more expertese with this subject than I do. I also know that these proposed mechanism are only proposed, there is really alot about cancer formation on the whole that we don't know so... *shrugs* I just plan on agreeing with the people that I think know more than me.

Interesting prefaces always being returned to. I didn't reference your being any part of the normal male anatomy, so when you have to begin with that sentiment, it is likely that what will follow is probably just that.

In any event, the populations that seemingly suggest (as I stated above) anti-beta-carotene sentiments are already diseased populaces and/or those who are smoking. For a person who is functioning "normally" this is actually splitting hairs. Your consistent contention is interesting though.

As for the absoption of metals in chelate form, I don't know much about that. I could be completely mistaken on this, but if I remember from my chem classes amino acid chelates don't bind as well to metal ion in acidic environments as say EDTA. So while some of the calcium might stay as a chelate, not all will and you'll still end up with some in solution which could block absorption of other free ions. The other metals of course would have the same issue with not all of them staying in chelate form. So the free calcium would atleast block the absorption of the other free minerals wouldn't it?

Well, I am curious what kind of chemistry class taught you about amino acid chelates and absorptive capacity in the first place as they certainly weren't in my various course catalogs - of course, perhaps that is just how it is taught further East?

The ideal chelating agent is one which:

Provides a bond strong enough to hold the mineral chelate together while it is in the stomach, yet not so strong as to make its central mineral ion unavailable for absorption, and allows the creation of a mineral chelate which carries a zero electrical charge so that the mineral ion encased therein might be attracted to the villi to a degree sufficient to permit assimilation into the bloodstream.

It has been established that amino acids, especially those producing neutral chelates, fulfill all essential characteristics required as chelating agents. Since the mineral is embedded in a cyclic or ring-like molecular configuration comprised of amino acids which bear no electrochemical charges, and the intestinal villi have receptors with the affinity to absorb 95% of all amino acids*. Properly absorbed amino acid chelated minerals will be absorbed through the villi intact (* some minerals may enter the bloodstream through the receptor sites of the amino acids simply by being "hidden" within the amino acid). This form of chelate cannot cause the intestinal problems sometimes encountered with prolonged use of mineral gluconates, citrates, sulphates or carbonates.

CMZ is likely a fine product; or at least when compared to the rest of the mineral formulas available - the "best" we have.


D_

[neonhypoxia]

Alright, if you want to get into a pissing contest that's fine, we can do that.

As for the CMZ I'm holding off on that one. Why you might ask, because I work at Eli Lilly and one of my coworkers in an expert on GI drug absorption and I would like her opinion on it. If it is in fact well absorbed I would consider it a good product, especially considering it has a nice quantity of boron in it. The is