Good carotenoids, bad carotenoids
FunkOdyssey 09 Jan 2009
Am J Cardiol. 2008 May 22;101(10A):20D-29D.
Biologic activity of carotenoids related to distinct membrane physicochemical interactions.
McNulty H, Jacob RF, Mason RP.
Elucida Research, Beverly, MA 01915, USA.
Carotenoids are naturally occurring organic pigments that are believed to have therapeutic benefit in treating cardiovascular disease (CVD) because of their antioxidant properties. However, prospective randomized trials have failed to demonstrate a consistent benefit for the carotenoid beta-carotene in patients at risk for CVD. The basis for this apparent paradox is not well understood but may be attributed to the distinct antioxidant properties of various carotenoids resulting from their structure-dependent physicochemical interactions with biologic membranes. To test this hypothesis, we measured the effects of astaxanthin, zeaxanthin, lutein, beta-carotene, and lycopene on lipid peroxidation using model membranes enriched with polyunsaturated fatty acids. The correlative effects of these compounds on membrane structure were determined using small-angle x-ray diffraction approaches. The nonpolar carotenoids, lycopene and beta-carotene, disordered the membrane bilayer and stimulated membrane lipid peroxidation (>85% increase in lipid hydroperoxide levels), whereas astaxanthin (a polar carotenoid) preserved membrane structure and exhibited significant antioxidant activity (>40% decrease in lipid hydroperoxide levels). These results suggest that the antioxidant potential of carotenoids is dependent on their distinct membrane lipid interactions. This relation of structure and function may explain the differences in biologic activity reported for various carotenoids, with important therapeutic implications.
PMID: 18474269
So I interpret this to mean, in the context of lipid peroxidation, nonpolar carotenoids (lycopene, beta-carotene) = bad, polar carotenoids (astaxanthin, lutein) = good.
Am J Clin Nutr. 2000 Apr;71(4):878-84.
The vitamin A spectrum: from deficiency to toxicity.
Russell RM.
US Department of Agriculture, Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA. russell@hnrc.tufts.edu
PMID: 10731492
...........excerpt:
b-CAROTENE TOXICITY
About the same time that these studies were published, b-carotene toxicity was described by Leo et al (30) in the livers of alcohol-fed animals, which showed swollen mitochondria after b-carotene feeding. Of interest is the possibility that retinoid metabolites of b-carotene could also have biological and possibly toxic potential. Wang et al (31) showed that b-carotene molecules in an in vitro system, in addition to splitting into retinal, could also be split at several double bonds, yielding apo carotenals and
apo carotenoic acids. They showed that at low doses, these carotenoic acids could be converted directly to retinoic acid (32–34). That is, for retinoic acid to be formed, b-carotene need not be converted to retinal first because in the presence of citral, which blocks the oxidation of retinal to retinoic acid, retinoic acid was still detected (35). Yeum et al (36) showed that this eccentric cleavage of b-carotene could occur by a cooxidation mechanism in the cytosol. These investigations showed that when lipoxyge-
nase was incubated with b-carotene alone, very small amounts of eccentric cleavage products of b-carotene appeared; however, when the substrate linoleic acid was added to the system, the cleavage metabolites of b-carotene increased dramatically. Thus, it appears that eccentric cleavage can be initiated in tissues by a cooxidation mechanism and then possibly completed by either conversion to retinaldehyde to form retinoic acid or by a mitochondrial mechanism, as Wang et al (37) described, to form retinoic acid. However, the question arises as to what happens when these eccentric cleavage products accumulate in large amounts? Do they have biological activity of their own? Could these metabolites interfere with the action of retinoic acid? This may, in fact, partially explain the results from 2 carotene intervention trials in which the effects of high doses of b-carotene supplements were studied in smokers and in asbestos-exposed workers (38, 39). These studies showed a higher incidence of lung cancer in smokers who consumed high doses of b-carotene than in smokers who did not take b-carotene supplements.
An animal model was used to try to mimic the results of these studies in humans (40). Ferrets were divided into 2 groups: b-carotene supplemented and non-b-carotene supplemented (control group). The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials. The b-carotene–supplemented and non-b-carotene–supplemented groups were further divided into smoke-exposed and non-smoke-exposed groups. The smoke-exposed group was exposed to cigarette smoke within a chamber twice in the morning and twice in the afternoon for 30 min each time, providing an exposure equivalent to that from 1.5 packs of cigarettes/d in humans. The animals tolerated this exposure well; they experienced no decrease in appetite or weight and behaved no differently from non-smoke-exposed animals. Animals were treated for 6 mo and then killed. b-Carotene concentrations in the plasma and lungs were greater in the b-carotene–supplemented ferrets than in the non-supplemented ferrets; however, b-carotene concentrations in the lungs were significantly lower in the smoke-exposed ferrets than in the non-smoke-exposed ferrets in both the b-carotene–supplemented and nonsupplemented control animals. Retinoic acid concentrations in the lung tissue were also significantly lower in all 3 treatment groups than in the control group (Table 3). The dramatic decreases in lung and blood b-carotene concentrations as a result of smoke exposure correlated with the enhanced breakdown of b-carotene into eccentric cleavage oxidation products.
When the lung sections of the 4 groups of ferrets were examined, it was found that smoke exposure alone caused mild aggregation and proliferation of macrophages. However, localized proliferation of alveolar cells and alveolar macrophages and keratinized squamous epithelial cells were observed in the ferrets in the 2 b-carotene–sup-
plemented groups. The most severe proliferation of alveolar cells and squamous metaplasia was observed in the b-carotene–supplemented, smoke-exposed ferrets. Keratinized squamous metaplasia was confirmed by immunohistochemical staining with anti-keratin antibody in the lung sections of all ferrets in the b-carotene–supplemented, smoke-exposed and non-smoke-exposed groups. Retinoic acid concentrations were lower in the smoke-exposed ferrets than in the non-smoke-exposed ferrets, presumably because of increased oxidative breakdown. In turn, the expression of RAR b (a subtype of RAR) activity was down-regulated in the lungs of the 3 treatment groups compared with that in the control group. RAR b is known to play an important role in normal lung development, and primary lung tumors and lung cancer cell lines lack RAR b expression (41–46). Thus, a role for RAR b as a tumor suppressor gene in the lung has been proposed (47). Because lung carcinogenesis is also associated with an alteration in retinoid signaling involving the AP-1 complex, AP-1 transcriptional activity was studied in these ferrets (48). c-Fos and c-Jun expression were up-regulated in the b-carotene–supplemented, smoke-exposed group. Additionally, AP-1 expression in this study was positively correlated with squamous metaplasia and inversely with RAR b expression in these animals.
Thus, it appears that high doses of b-carotene under highly oxidative conditions result in many eccentric cleavage oxidative breakdown products, which could have biological activity of their own. One possibility is that these products interfere with retinoic acid binding to retinoid receptors, but another likely possibility is
that these metabolites induce local enzymes in the lung, such as P450 enzymes, which increase the catabolism of retinoic acid and thus diminish retinoic acid signaling. A local deficiency of retinoic acid can then result in squamous metaplasia. Salgo et al (49) reported that b-carotene oxidation products promote the binding of benzo[a]pyrene (a smoke-borne carcinogen) to calf thymus DNA. Incubation of DNA with intact b-carotene decreased such binding, whereas incubation with b-carotene oxidation products (eg, 5,6-epioxide) for 1, 2, 3, and 4 h significantly increased the binding. These are all possible explanations for why toxicity occurs after high doses of b-carotene and may explain the increased incidence of lung cancers observed in the 2 large intervention trials mentioned previously (38, 39).
Here we have beta-carotene inducing proliferation of alveolar cells and keratinized squamous metaplasia in ferrets without smoke exposure at human equivalent doses.
nameless 09 Jan 2009
Here is another ferret study, same study authors (I think):
http://www.ars.usda....q_no_115=165739
This study shows low dose beta carotene having a benefit (in ferrets, anyway). For the high dose study, I also think C + E minimized some of the beta carotene problems, although I can't recall where I read this, or what doses were used (sorry for a useless statement).
I just stick to a half dose of my multi + whatever I get from diet for beta carotene anyway. I see no need to megadose the stuff.
Edited by nameless, 09 January 2009 - 07:20 PM.
ajnast4r 09 Jan 2009
on my quick browse through that text it doesn't appear to say, and i believe chirality is an important factor that will determine whether one receives health benefit or detriment from b-carotene supplementation... also 30mg/d is somewhere around 50,000iu which is way more than any normal person would be consuming, and is way beyond excessive for such a small animal.
b-carotene is SO widely spread in the plant world, and in high amounts in fruits & vegetables that have known health benefits, that's its very hard for me to believe that reasonable doses could cause any harm.
rwac 09 Jan 2009
The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials.
This is bad. the dosage is within an order of magnitude of the dosage in Ortho-core (6mg).
nameless 09 Jan 2009
The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials.
This is bad. the dosage is within an order of magnitude of the dosage in Ortho-core (6mg).
Odd coincidence, although perhaps not a coincidence if AOR did their research -- 6 mg is the equivalent dose given ferrets for the low beta carotene group. And that is the group that demonstrated potential benefits from beta carotene.
----
In the present study, ferrets were given a physiological (low) dose or a pharmacological (high) dose of ß-carotene supplementation (0.43 mg versus 2.4 mg/kg body wt/day, which is equivalent to 6 mg versus 30 mg/day in humans) and exposed to cigarette smoke for 6 months.
----
http://carcin.oxford...ract/21/12/2245
kai73 09 Jan 2009
wasn't licopene supposed to be the best antioxidant of all caretinoids (protecting also the skin and preventing cancer)? now it increase peroxidation
FunkOdyssey 09 Jan 2009
The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials.
This is bad. the dosage is within an order of magnitude of the dosage in Ortho-core (6mg).
Odd coincidence, although perhaps not a coincidence if AOR did their research -- 6 mg is the equivalent dose given ferrets for the low beta carotene group. And that is the group that demonstrated potential benefits from beta carotene.
----
In the present study, ferrets were given a physiological (low) dose or a pharmacological (high) dose of ß-carotene supplementation (0.43 mg versus 2.4 mg/kg body wt/day, which is equivalent to 6 mg versus 30 mg/day in humans) and exposed to cigarette smoke for 6 months.
----
http://carcin.oxford...ract/21/12/2245
Look what happens to 6mg of beta-carotene from food:
Am J Clin Nutr. 2001 Sep;74(3):348-55.Click here to read Links
A novel extrinsic reference method for assessing the vitamin A value of plant foods.
Edwards AJ, You CS, Swanson JE, Parker RS.
Division of Nutritional Sciences and the Department of Food Science, Cornell University, Ithaca, NY 14853, USA.
BACKGROUND: The amounts of vitamin A that are metabolically derived from specific carotene-containing foods are largely unknown. OBJECTIVE: We sought to develop an improved method for estimating the metabolic vitamin A potential of provitamin A carotenoids by using [2H4]retinyl acetate (d4-RA) as an extrinsic reference standard. DESIGN: Healthy subjects consumed a standardized test meal containing 6 mg beta-carotene as either raw carrot or spinach, either 20 or 1 g added fat, and 6.0 micromol d4-RA. Concentrations of unlabeled (d0) retinyl esters (RE), labeled (d4) RE, and carotenoids in the plasma triacylglycerol-rich lipoprotein fraction (d < 1.006 kg/L) were determined in serial blood samples with HPLC and gas chromatography-mass spectrometry. Baseline-corrected areas under the curve for d0-RE, d4-RE, and carotenoids were calculated, and the masses of absorbed d0-retinol and carotenes were estimated assuming 80% absorption of the d4-RA reference dose. RESULTS: In trials with ample (20 g) fat (n = 6), 7 +/- 4% of the 6 mg beta-carotene ingested was taken up as beta-carotene plus RE with 0.3 +/- 0.1 mg as retinol. Test meals without carotenes yielded no beta-carotene or d0-RE response and there was no effect of treatment (either fat amount or vegetable, n = 6) on the mean d4-RE area under the curve. The lower-than-expected vitamin A yields were attributed to poor intestinal uptake rather than to low conversion of beta-carotene to RE. CONCLUSION: The triacylglycerol-rich lipoprotein and d4-RA method, which controls for variation in chylomicron kinetics in vivo and RE recovery during analysis, is useful for obtaining quantitative estimates of the vitamin A potential of single meals.
Only 7% was absorbed, compared to 80% of a retinyl ester which the intestines were eager to gobble up. Hmm. Of course, we can override our natural inclination not to absorb much beta-carotene from a normal diet by consuming purified beta-carotene supplements which enhance bioavailability about 300% in this study:
J Nutr. 2000 Mar;130(3):534-40.
The bioavailability of beta-carotene in stir- or deep-fried vegetables in men determined by measuring the serum response to a single ingestion.
Huang C, Tang YL, Chen CY, Chen ML, Chu CH, Hseu CT.
Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, College of Agriculture National Taiwan University, Taipei, Taiwan.
To evaluate the bioavailability of beta-carotene from plant foods, the serum beta-carotene response to a single ingestion of various beta-carotene sources was determined in 10 healthy men. Tested beta-carotene sources included stir-fried shredded carrot, stir-fried water convolvulus leaves, deep-fried sweet potato ball, purified beta-carotene in a capsule (beadlets) and beadlets with beta-carotene free oriental radish (beadlets + radish). The maximal change in serum beta-carotene concentration occurred at 24 or 32 h post ingestion. This response to beadlets was significantly higher than that to the other four tested beta-carotene sources (P < 0.05). The maximal serum response to beadlets + radish was also significantly higher than that to the three food beta-carotene sources (P < 0.05). The maximal serum response to sweet potato was significantly higher than that to water convolvulus leaves (P < 0. 05). The bioavailability relative to beta-carotene beadlets was calculated by dividing the maximal change in serum concentration to each test meal of each subject by his own serum maximal change in response to beadlets. Accordingly, the bioavailability was 65% for beadlets + radish, 33% for carrots, 26% for water convolvulus leaves and 37% for sweet potatoes. Concurrent ingestion of oriental radish reduced the bioavailability of beadlets to two-thirds of its original value, which partially accounted for the difference between the bioavailability of beadlets and natural foods. The relative bioavailability of beta-carotene from stir-fried and deep-fried vegetables was about one-third to one-fourth that of the purified beta-carotene beadlets. These bioavailabilities are higher than previously reported values.
PMID: 10702581
So maybe 6mg of beta-carotene in supplements is more like 18mg in regular food? My discomfort grows.
Edited by FunkOdyssey, 09 January 2009 - 08:15 PM.
nameless 09 Jan 2009
A novel extrinsic reference method for assessing the vitamin A value of plant foods.
Edwards AJ, You CS, Swanson JE, Parker RS.
I think this study is showing the conversion of beta carotene to retinol, not absorption of beta carotene? Or am I misreading it?
While: The bioavailability of beta-carotene in stir- or deep-fried vegetables in men determined by measuring the serum response to a single ingestion.
Concerns just how bioavailable beta carotene is, based on the form taken? So each study is testing different things. I think beta carotene from foods is decreased if cooked (usually), although it can also increase it. So in the latter study, since the foods were cooked, perhaps their beta carotene bioavailabilty was lower than the supplement form?
-----
How do cooking, storage, or processing affect beta-carotene?
In certain cases, cooking can improve the availability of carotenoids in foods. Lightly steaming carrots and spinach improves your body's ability to absorb carotenoids in these foods.
It is important to note, however, that in most cases, prolonged cooking of vegetables decreases the availability of carotenoids by changing the shape of the carotenoid from its natural trans-configuration to a cis-configuration. For example, fresh carrots contain 100% all-trans beta-carotene, while canned carrots contain only 73% all-trans beta-carotene.
Which I pasted from : http://www.whfoods.c...n...nt&dbid=125
Edited by nameless, 09 January 2009 - 08:42 PM.
ajnast4r 09 Jan 2009
I really believe studies that don't control for chirality are useless...
ajnast4r 09 Jan 2009
http://findarticles....i_68727251/pg_7
FunkOdyssey 09 Jan 2009
Edited by FunkOdyssey, 09 January 2009 - 10:44 PM.
rwac 09 Jan 2009
I'm not taking AOR Ortho-Core any more, it was too expensive and had too many ingredients in token amounts that I was already taking separately. What I have decided to do is obtain a much lower dose of natural beta-carotene, 1.43mg from this product: http://www.iherb.com...px?pid=153&at=0. It has the other major carotenoids in nice ratios and has a better ratio of beta:alpha carotene than Ortho-Core. I will depend on real Vitamin A from fish liver oil for the majority of my Vitamin A intake (read this before objecting: http://www.westonapr...mina-osteo.html)
Funk, what Multi do you take ?
FunkOdyssey 09 Jan 2009
Shepard 09 Jan 2009
I'm not taking AOR Ortho-Core any more, it was too expensive and had too many ingredients in token amounts that I was already taking separately. What I have decided to do is obtain a much lower dose of natural beta-carotene, 1.43mg from this product: http://www.iherb.com...px?pid=153&at=0. It has the other major carotenoids in nice ratios and has a better ratio of beta:alpha carotene than Ortho-Core. I will depend on real Vitamin A from fish liver oil for the majority of my Vitamin A intake (read this before objecting: http://www.westonapr...mina-osteo.html)
I've gone a similar route, and dropped Ortho-Core in favor of individual supplementation. That is the Vitamin A product that I take, and the rest I provide from diet.
Edited by shepard, 09 January 2009 - 11:15 PM.
DukeNukem 09 Jan 2009
This is one of those topics that deserves deep investigation. I personally rely on healthy foods to get my A and carotenes, because supplementation appears to be frought with peril. Except, I do take 8mg of astaxanthin daily, and a zeaxanthin/lutein formulation.All of this Weston Price stuff has started to influence my thinking about what constitutes a healthy source of Vitamin A, and I find myself viewing beta-carotene with some newfound suspicion. The carotenoids have different properties: a few can be converted into retinol (most can't), and they are either protective or damaging to lipids depending on their structure.
Am J Cardiol. 2008 May 22;101(10A):20D-29D.
Biologic activity of carotenoids related to distinct membrane physicochemical interactions.
McNulty H, Jacob RF, Mason RP.
Elucida Research, Beverly, MA 01915, USA.
Carotenoids are naturally occurring organic pigments that are believed to have therapeutic benefit in treating cardiovascular disease (CVD) because of their antioxidant properties. However, prospective randomized trials have failed to demonstrate a consistent benefit for the carotenoid beta-carotene in patients at risk for CVD. The basis for this apparent paradox is not well understood but may be attributed to the distinct antioxidant properties of various carotenoids resulting from their structure-dependent physicochemical interactions with biologic membranes. To test this hypothesis, we measured the effects of astaxanthin, zeaxanthin, lutein, beta-carotene, and lycopene on lipid peroxidation using model membranes enriched with polyunsaturated fatty acids. The correlative effects of these compounds on membrane structure were determined using small-angle x-ray diffraction approaches. The nonpolar carotenoids, lycopene and beta-carotene, disordered the membrane bilayer and stimulated membrane lipid peroxidation (>85% increase in lipid hydroperoxide levels), whereas astaxanthin (a polar carotenoid) preserved membrane structure and exhibited significant antioxidant activity (>40% decrease in lipid hydroperoxide levels). These results suggest that the antioxidant potential of carotenoids is dependent on their distinct membrane lipid interactions. This relation of structure and function may explain the differences in biologic activity reported for various carotenoids, with important therapeutic implications.
PMID: 18474269
So I interpret this to mean, in the context of lipid peroxidation, nonpolar carotenoids (lycopene, beta-carotene) = bad, polar carotenoids (astaxanthin, lutein) = good.Am J Clin Nutr. 2000 Apr;71(4):878-84.
The vitamin A spectrum: from deficiency to toxicity.
Russell RM.
US Department of Agriculture, Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA. russell@hnrc.tufts.edu
PMID: 10731492
...........excerpt:
b-CAROTENE TOXICITY
About the same time that these studies were published, b-carotene toxicity was described by Leo et al (30) in the livers of alcohol-fed animals, which showed swollen mitochondria after b-carotene feeding. Of interest is the possibility that retinoid metabolites of b-carotene could also have biological and possibly toxic potential. Wang et al (31) showed that b-carotene molecules in an in vitro system, in addition to splitting into retinal, could also be split at several double bonds, yielding apo carotenals and
apo carotenoic acids. They showed that at low doses, these carotenoic acids could be converted directly to retinoic acid (32–34). That is, for retinoic acid to be formed, b-carotene need not be converted to retinal first because in the presence of citral, which blocks the oxidation of retinal to retinoic acid, retinoic acid was still detected (35). Yeum et al (36) showed that this eccentric cleavage of b-carotene could occur by a cooxidation mechanism in the cytosol. These investigations showed that when lipoxyge-
nase was incubated with b-carotene alone, very small amounts of eccentric cleavage products of b-carotene appeared; however, when the substrate linoleic acid was added to the system, the cleavage metabolites of b-carotene increased dramatically. Thus, it appears that eccentric cleavage can be initiated in tissues by a cooxidation mechanism and then possibly completed by either conversion to retinaldehyde to form retinoic acid or by a mitochondrial mechanism, as Wang et al (37) described, to form retinoic acid. However, the question arises as to what happens when these eccentric cleavage products accumulate in large amounts? Do they have biological activity of their own? Could these metabolites interfere with the action of retinoic acid? This may, in fact, partially explain the results from 2 carotene intervention trials in which the effects of high doses of b-carotene supplements were studied in smokers and in asbestos-exposed workers (38, 39). These studies showed a higher incidence of lung cancer in smokers who consumed high doses of b-carotene than in smokers who did not take b-carotene supplements.
An animal model was used to try to mimic the results of these studies in humans (40). Ferrets were divided into 2 groups: b-carotene supplemented and non-b-carotene supplemented (control group). The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials. The b-carotene–supplemented and non-b-carotene–supplemented groups were further divided into smoke-exposed and non-smoke-exposed groups. The smoke-exposed group was exposed to cigarette smoke within a chamber twice in the morning and twice in the afternoon for 30 min each time, providing an exposure equivalent to that from 1.5 packs of cigarettes/d in humans. The animals tolerated this exposure well; they experienced no decrease in appetite or weight and behaved no differently from non-smoke-exposed animals. Animals were treated for 6 mo and then killed. b-Carotene concentrations in the plasma and lungs were greater in the b-carotene–supplemented ferrets than in the non-supplemented ferrets; however, b-carotene concentrations in the lungs were significantly lower in the smoke-exposed ferrets than in the non-smoke-exposed ferrets in both the b-carotene–supplemented and nonsupplemented control animals. Retinoic acid concentrations in the lung tissue were also significantly lower in all 3 treatment groups than in the control group (Table 3). The dramatic decreases in lung and blood b-carotene concentrations as a result of smoke exposure correlated with the enhanced breakdown of b-carotene into eccentric cleavage oxidation products.
When the lung sections of the 4 groups of ferrets were examined, it was found that smoke exposure alone caused mild aggregation and proliferation of macrophages. However, localized proliferation of alveolar cells and alveolar macrophages and keratinized squamous epithelial cells were observed in the ferrets in the 2 b-carotene–sup-
plemented groups. The most severe proliferation of alveolar cells and squamous metaplasia was observed in the b-carotene–supplemented, smoke-exposed ferrets. Keratinized squamous metaplasia was confirmed by immunohistochemical staining with anti-keratin antibody in the lung sections of all ferrets in the b-carotene–supplemented, smoke-exposed and non-smoke-exposed groups. Retinoic acid concentrations were lower in the smoke-exposed ferrets than in the non-smoke-exposed ferrets, presumably because of increased oxidative breakdown. In turn, the expression of RAR b (a subtype of RAR) activity was down-regulated in the lungs of the 3 treatment groups compared with that in the control group. RAR b is known to play an important role in normal lung development, and primary lung tumors and lung cancer cell lines lack RAR b expression (41–46). Thus, a role for RAR b as a tumor suppressor gene in the lung has been proposed (47). Because lung carcinogenesis is also associated with an alteration in retinoid signaling involving the AP-1 complex, AP-1 transcriptional activity was studied in these ferrets (48). c-Fos and c-Jun expression were up-regulated in the b-carotene–supplemented, smoke-exposed group. Additionally, AP-1 expression in this study was positively correlated with squamous metaplasia and inversely with RAR b expression in these animals.
Thus, it appears that high doses of b-carotene under highly oxidative conditions result in many eccentric cleavage oxidative breakdown products, which could have biological activity of their own. One possibility is that these products interfere with retinoic acid binding to retinoid receptors, but another likely possibility is
that these metabolites induce local enzymes in the lung, such as P450 enzymes, which increase the catabolism of retinoic acid and thus diminish retinoic acid signaling. A local deficiency of retinoic acid can then result in squamous metaplasia. Salgo et al (49) reported that b-carotene oxidation products promote the binding of benzo[a]pyrene (a smoke-borne carcinogen) to calf thymus DNA. Incubation of DNA with intact b-carotene decreased such binding, whereas incubation with b-carotene oxidation products (eg, 5,6-epioxide) for 1, 2, 3, and 4 h significantly increased the binding. These are all possible explanations for why toxicity occurs after high doses of b-carotene and may explain the increased incidence of lung cancers observed in the 2 large intervention trials mentioned previously (38, 39).
Here we have beta-carotene inducing proliferation of alveolar cells and keratinized squamous metaplasia in ferrets without smoke exposure at human equivalent doses.
Vitamin A and D appear to have significant hand-in-hand protective qualities--you need both to protect from toxicity.
http://wholehealthso...ty-concern.html
Edited by DukeNukem, 09 January 2009 - 11:32 PM.
david ellis 10 Jan 2009
Bausch&Lomb sells Ocuvite(same ingredients/quantities as the AREDS ICAPS-approved by NIH) formula for eyes that has 28,640 IU's of beta-carotene which if I am doing calculations correctly is about 16 mg of beta-carotene. According to my doctor the formula has been tested and proven beneficial in reducing the progress of macular degeneration. Because the beta-carotenes are not label identified, they possibly are the "bad" carotenes you found on WestonAPrice.org.
Edited by david ellis, 10 January 2009 - 12:05 AM.
health_nutty 10 Jan 2009
balance 10 Jan 2009
which combo lef supplement are u referring to that has 42mg of beta-carotene?
Edited by piet3r, 10 January 2009 - 11:39 PM.
rwac 11 Jan 2009
This supplement.
Lutein is still supposed to be good, because it's a polar carotenoid.
I don't know about Zeaxanthin and Meso-Zeaxanthin.
My guess would be they are polar too.
Not quite as bad as you think.
david ellis 11 Jan 2009
This supplement.
Lutein is still supposed to be good, because it's a polar carotenoid.
I don't know about Zeaxanthin and Meso-Zeaxanthin.
My guess would be they are polar too.
Not quite as bad as you think.
Yeah, I have been taking the 42 mg supplement for over 5 years. It is the only supplement that I regularly buy from LEF. Nobody else competes by delivering comparable doses of lutein, zeaxanthin and meso-zeaxanthin. It didn't 100% protect me from macular generation, but I don't blame the supplement. I got a macular pucker, and that put a lot of stress on the macula, resulting in lots of inflammation. I have a little bit of degeneration in the puckered eye. The surgery removed the cause of the stress and my eyes may recover to 20/25 vision. Evidently I have the gene that causes macular degeneration.
I have made a mistake, I thought lutein & zeaxanthin were in the beta-carotenes class and thus pro-vitamin A. It seems like all of the vitamin A I get is in my diet.
Edited by david ellis, 11 January 2009 - 03:51 AM.
woly 11 Jan 2009
This is one of those topics that deserves deep investigation. I personally rely on healthy foods to get my A and carotenes, because supplementation appears to be frought with peril. Except, I do take 8mg of astaxanthin daily, and a zeaxanthin/lutein formulation.
Vitamin A and D appear to have significant hand-in-hand protective qualities--you need both to protect from toxicity.
http://wholehealthso...ty-concern.html
I was reading the Alternative medicine review on vitamin D and they mention that high retinol antagonises the action of vitamin D and blunts its protective effect on colorectal adenomas. Maybe itd be a better idea to just lower the dose of retinol and consume vit A precursors instead?
woly 11 Jan 2009
like this one and this one
Edited by woly, 11 January 2009 - 01:31 PM.
graatch 13 Jan 2009
Edited by graatch, 13 January 2009 - 06:20 AM.