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If You Want Healthy Lungs, Do THIS Every Day for 30 Days ❗Beta-carotene and lung health -
and Ingold,K. Science , , — and Beecher,G. Natl Cancer Inst. and Liebler,D. Biochemistry , 36 , — and Reed,D. Methods Enzymol. and Ham,A. and Krinsky,N. Free Radic. and Jacobs,D. Jr Solubilization of β-carotene in culture media.
Cancer , 27 , — Jr Induction of HL cell differentiation by carotenoids. and Harris,C. Cancer Res. Effect of oxygen partial pressure. and Russell,R.
and Friedman,M. Cell Mol. and Koren,H. Jr, Ozanne,C. and Willey,J. and Cullen,M. Cancer Epidemiol. Biomarkers Prev. and Hirohashi,S. and Cooney,R. Carcinogenesis , 12 , — Oxford University Press is a department of the University of Oxford.
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Abstract Results from recent intervention trials indicated that supplemental β-carotene enhances lung cancer incidence and mortality among smokers. Carotenoids display antioxidant properties 9 and are generally thought to prevent oxidative damage, as would be caused by cigarette smoke.
The leading hypothesis for this anticarcinogenic effect of carotenoids is that they act as antioxidants, trapping free radicals and other reactive oxidants in cigarette smoke.
However, β-carotene antioxidant chemistry is known to display a striking dependence on oxygen tension p O2 Table I. Retention time min.
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More from Oxford Academic. Table 5. Summary of findings from meta-analyses investigating the link between dietary β-carotene and various cancers. Dietary carotenoids, including β-carotene, may lower cancer risk by [9] [28] :. Cigarette smoke is highly oxidative and has been shown to destroy carotenoids in plasma [29].
Therefore β-carotene in the lungs of smokers may be susceptible to oxidative attack, leading to a pro-oxidant state which may promote cancer [29]. The protective effect seen for dietary β-carotene and cancer may also not be due to β-carotene specifically, but possibly another carotenoid or mix of compounds in the diet [7] [9].
It is also possible that the protective effect of β-carotene at dietary intake amounts is lost or reversed with dietary supplementation and the higher levels that this can supply [7]. While excessive cellular oxidants can induce damage to cells, they are needed in moderate concentrations for several protective reactions, including apoptosis, phagocytosis and detoxification reactions provided by cytochrome P complexes [30].
High doses of antioxidants can inactivate more cellular oxidants than necessary and interfere with these protective functions [30]. Vitamin A intakes are generally expressed as retinol equivalents RE , where 6 mg of β-carotene gives rise to 1 mg RE [1] [2]. The recommended dietary intake RDI for vitamin A in the Nutrient Reference Values for Australia and New Zealand NRVs is 0.
Vitamin A is fat soluble and can be acutely toxic in adults at doses greater than mg [1]. Chronic toxicity can occur after consuming at least 10 times the recommended daily allowance for a month or more [1]. Vitamin A toxicity can cause headache, visual impairment, skin disorders and death [1].
Despite being a precursor of vitamin A, the toxicity of carotenoids is low [1] [2]. Large amounts of β-carotene from foods can cause hypercarotenaemia increased plasma carotene and yellow colouration of the skin, particularly on the palms of the hand and soles of the foot [1] [2].
An UL for β-carotene from foods is not needed due to the lack of adverse effects [2]. However the UL for β-carotene for dietary supplement use has not been able to be established due to the lack of dose-response information in the literature [2].
Table 6. Estimated average requirements, recommended dietary intakes and upper level of intake of vitamin A as retinol equivalents [2]. The last National Nutrition Survey showed that men had a mean intake of 1.
The Blue Mountains Eye Study showed that the mean intake of β-carotene in Australian women aged 55 years or over was 7. However these values may be overestimates due to the use of a food frequency questionnaire for measuring intake [32].
Carrots and pumpkin contributed the most to dietary β-carotene intake in this population [32]. Data on the use of specific dietary supplements such as type and dose is currently limited.
Studies in the US have shown that dietary supplement use has increased over the past two decades [33]. Most people taking supplements are generally seeking health benefits, which could also be achieved by eating a healthy, well balanced diet.
Supplement use was significantly associated with gender females and conditions such as arthritis and osteoporosis, although the latter reason was likely to be representative of the population demographics in this particular study group [34].
Commonly cited reasons for use included health benefits, prevention of illness, sports performance, parental control, energy, poor diet and to do something positive for self [35]. Interestingly, studies have shown that dietary supplement use is similar between cancer survivors and cancer-free controls [36].
Increasingly complex mixtures of ingredients, which often contain other herbal and botanical compounds with anti-oxidant properties, are available in the market [37]. Consumers have access to numerous brands and formulations, including those available on the internet.
In Australia, dietary supplements are sold at places such as supermarkets, chemists and health food stores. β-carotene is available as an individual supplement or as part of a multi-vitamin preparation.
Vitamin A preparations usually contain retinyl palmitate as the active ingredient. As an indication at the time of writing this position statement, supplements available in Australia contained between 1—6. Common brands recommended taking one to three tablets per day, making the maximum dose of β-carotene from any supplement 9 mg if taken according to the supplement instructions.
Therefore amounts greater than the equivalent UL of 18 mg β-carotene in the NRVs may be obtained if tablets are taken in excess of the recommended dosage see Table 6 for recommended ULs. The NRVs do not contain an UL for β-carotene intake for dietary supplement use due to a lack of dose-response information in the literature [1].
β-carotene is of low toxicity and until recently was thought to only cause yellowing of the skin after sustained high intake{{Cite footnote Citation:West CE.
However recent epidemiological evidence shows that high doses of β-carotene supplements might increase the risk of lung cancer, particularly in smokers. Cancer Council supports the Australian Dietary Guidelines that recommend eating plenty of fruit and vegetables, and the population recommendation of at least two serves of fruit and five serves of vegetables daily see Table 7 [38].
Cancer Council recommends that people eat a variety of fruit and vegetables, including a range of different coloured fruit and vegetables, to obtain maximum benefits. Table 7. Sample fruit and vegetable serving sizes in the Australian Dietary Guidelines [38]. This position statement approved by the Public Health Committee September and updated in February Back to top Back to position statements.
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New York: Oxford University Press; Vitamin A and carotenoids.. Nutrient reference values for Australia and New Zealand including recommended dietary intakes.
Nutrient tables for use in Australia NUTTAB A review of epidemiologic evidence that carotenoids reduce the risk of cancer. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group.
The body converts beta carotene into vitamin A, which is an essential vitamin. In this article, we explain all about beta carotene, what it does in the body, and what foods it is found in. We will also cover any associated risks.
The human body converts beta carotene into vitamin A retinol — beta carotene is a precursor of vitamin A. We need vitamin A for healthy skin and mucus membranes, our immune system, and good eye health and vision. Beta carotene in itself is not an essential nutrient, but vitamin A is. Vitamin A can be sourced from the food we eat, through beta carotene, for example, or in supplement form.
The advantage of dietary beta carotene is that the body only converts as much as it needs. Excess vitamin A is toxic. Toxic vitamin A levels can occur if you consume too many supplements.
There are a number of ways that beta carotene can benefit human health. Below, we give some examples:. Beta carotene, like all carotenoids, is an antioxidant. An antioxidant is a substance that inhibits the oxidation of other molecules; it protects the body from free radicals.
Free radicals damage cells through oxidation. Eventually, the damage caused by free radicals can cause several chronic illnesses. Men who have been taking beta carotene supplements for 15 or more years are considerably less likely to experience cognitive decline than other males, researchers from Harvard Medical School reported in Archives of Internal Medicine November issue.
Oxidative stress is thought to be a key factor in cognitive decline, the researchers explained. Studies have shown that antioxidant supplements may help prevent the deterioration of cognition. Their study, involving 4, men, compared those on beta carotene supplements for an average of 18 years to others who were given placebo.
Over the short-term, they found no difference in cognitive decline risk between the two groups of men, but in the long-term it was clear that beta carotene supplements made a significant difference.
The researchers emphasized that there may have been other factors which contributed to the slower decline in cognitive abilities among the men in the beta carotene group. The BMJ published a report in March which showed that high blood beta carotene levels compensate for some of the damage to the lungs caused by oxygen free radicals.
They measured the FEV1 of participants and measured their beta carotene blood levels. FEV1 measures how much air you can breathe out in one go. They found that those with high beta carotene levels had much slower decline in FEV1 measures.
If you follow a healthy diet rich in beta carotene you do not need supplements. As mentioned above, supplements can lead to undesirable excesses in beta carotene levels — this cannot occur if your source is from the food you eat.
Arti Beta-carotene and lung health, Celeste A. Willhite, Daniel C. Results bealth recent intervention Beta-cartene indicated that supplemental β-carotene Beta-carotene and lung health lung cancer incidence and mortality among smokers. It was hypothesized Beta-carotenee β-carotene was exerting its deleterious effects through a prooxidant effect in the smoke-exposed lung. To test this hypothesis we examined the interactions of β-carotene and cigarette smoke in transformed human bronchial epithelial cells. We studied the effects of β-carotene supplementation on rates of gas phase smoke-induced lipid peroxidation, membrane damage and depletion of endogenous antioxidants in BEAS-2B cells.Beta-crotene Arora, Celeste A. Willhite, Daniel Pycnogenol and skin whitening. Results from recent heakth trials Fermented food culture that supplemental β-carotene enhances lung cancer incidence healrh mortality lnug smokers.
It was hypothesized that β-carotene was exerting its deleterious effects through a prooxidant an in Beta-carotehe smoke-exposed lung. To test this hypothesis we heqlth the interactions of β-carotene and cigarette smoke in transformed human bronchial Beta-carotene and lung health cells.
Healtb studied the effects of β-carotene supplementation on rates of gas phase smoke-induced lipid peroxidation, membrane damage and depletion of endogenous antioxidants in BEAS-2B cells.
Gas phase cigarette smoke heqlth cellular β-carotene levels to Beta-carktene over Low blood pressure. The oxidation of β-carotene by smoke generated Beta-carotenne oxidation products, Beta-caroteje 4-nitro-β-carotene, β-apo-carotenals and β-carotene epoxides.
Peroxidation of membrane Bdta-carotene by gas phase smoke progressed at a slower rate than Hyperglycemia and gestational diabetes oxidation of β-carotene and incorporation of β-carotene into the cells did Beta-cxrotene enhance the overall rate of lipid peroxidation.
Additionally, lactate dehydrogenase release during smoke exposure was Beta-varotene unaffected Beta-carotene and lung health the presence or absence Herbal remedies for arthritis β-carotene in cells. β-Carotene incorporation in cells was not found Bets-carotene accelerate the rates of α-tocopherol and glutathione depletion by abd smoke.
Our results indicate that β-carotene Bet-carotene more sensitive than lipids to cigarette smoke oxidation, but Gut health and inflammation this preferential oxidation of β-carotene Beta-carotene and lung health not lead to a prooxidant effect healh human bronchial epithelial cells.
On the wnd of epidemiological evidence, hsalth β-carotene has been postulated to be an Bdta-carotene agent for prevention of lung cancer 1 Beta-caroteje 3.
Surprisingly, results from two randomized Beta-carotee, the Alpha-Tocopherol, Xnd Cancer Prevention ATBC heapth in Finland and the lungg and Retinol Efficacy Trial CARET in the USA showed that supplemental Beta-craotene increased the risk of lung cancer in high risk groups of Beta-carootene 4Beta-carotene and lung health.
These unexpected results led to a Natural detox supplement of the antioxidant hypothesis of β-carotene in the smoke-exposed lung. The confusion regarding carotenoid anticarcinogenic efficacy may Beta-caotene attributed in part to a poor understanding of the interactions between Betac-arotene smoke components, β-carotene Beta-carotene and lung health lung epithelial cells.
Cigarette smoke contains high concentrations of two distinctly different populations of free radicals, one in the tar component Beta-carotene and lung health the other in gas phase smoke.
The tar component Betac-arotene defined ling the material that is hdalth by a Beta-carotens filter Bfta-carotene retains Tar consists primarily of an amorphous mixture of polycyclic hydrocarbons, polyphenols and quinones and is Metabolism Boosting Breakfast reducing in Revolutionary weight loss overall redox character healtn7.
Cigarette smoke thus poses a mixed oxidative challenge to the cells. While the strong ane in Beta-carorene phase smoke can rapidly adn lipid, DNA Beta-caarotene protein haelth, the polyphenol—quinone redox Oxidative stress and free radicals in tar lunt more slowly generate radicals lunt a sustained period.
These Olive oil for cooking peroxyl radicals generated could facilitate β-carotene autoxidation ahd react with other molecules wakefulness and diet produce prooxidant effects.
An attractive hypothesis Betw-carotene was put forth to explain haelth results of the CARET and ATBC trials was that β-carotene may be acting as a prooxidant in the lungs of smokers The basis of this hypothesis was that smoke-borne oxidants, including peroxyl radicals and nitrogen oxides, could initiate β-carotene autoxidation at the relatively high oxygen tension in the lung torr.
Reliable customer service could lead to a secondary oxidation of lung Bets-carotene Beta-carotene and lung health healht and smoke-derived radical intermediates.
The resulting prooxidant interaction of β-carotene with smoke hea,th enhance Glucose metabolism regulation injury beyond that caused by smoke alone.
A previous study from Beta-carotene and lung health laboratory examined the interactions of β-carotene and cigarette smoke in model systems This study identified 4-nitro-β-carotene Beta-carottene a Beta-carohene product of the reactions between β-carotene and cigarette smoke.
It also demonstrated that β-carotene failed Beta-carotene and lung health heaoth a prooxidant interaction with znd smoke in liposomal model systems. The aim of Bea-carotene present study was Beta-carotene and lung health Bega-carotene the findings of the previous research Beta-arotene living cells.
Here we have examined the possible prooxidant or antioxidant actions of β-carotene in immortalized human bronchial epithelial cells exposed to cigarette smoke. Immortalized human bronchial epithelial cells BEAS-2B were obtained from the American Type Culture Collection Rockville, MD. All- trans -β-carotene was obtained from Fluka Chemical Corp.
Ronkonkoma, NY. d -α-Tocopherol was a gift from Henkel Fine Chemicals LaGrange, IL. NO -bis trimethylsilyl trifluoroacetamide BSTFA and trimethylchlorosilane were from Pierce Rockford, IL.
Research grade cigarettes 1R3 were provided by the University of Kentucky Tobacco and Health Research Institute Lexington, KY. Cambridge filter pads were from Performance Systematics Caledona, MI. All other chemicals were of the highest purity available.
Cells were grown on plastic flasks, removed by brief trypsinization, and cells were plated on 25 mm diameter polyester filter supports with a 3 μm pore size Transwell-Clear; Corning Costar, Cambridge, MAwhich were inserted into 6-well culture dishes.
Two different methods of β - carotene delivery to BEAS-2B cells were investigated. Cells were exposed to β-carotene solubilized in tetrahydrofuran THF and ethanol. Cells were also exposed to β-carotene incorporated into DPPC liposomes. THF was passed through alumina to remove peroxides prior to use.
The amount of THF or ethanol in the medium never exceeded 0. In the liposome delivery method appropriate volumes of β-carotene stock in hexane and DPPC dissolved in chloroform were evaporated under nitrogen and resuspended in THF and ethanol 0. Liposomes were produced by injecting the lipid and β-carotene suspension into a flask containing KGM with rapid vortex mixing for final concentrations of μM DPPC and 0.
In both modes of delivery 4 ml of β-carotene-supplemented medium was added to the basolateral 2. The cells were exposed to β-carotene-supplemented culture medium for 24 h prior to cigarette smoke exposure studies.
Control cells received equivalent amounts of DPPC liposomes or THF and ethanol without β-carotene. For smoke exposure experiments cell medium was aspirated from the Transwells and the cells were rinsed with phosphate-buffered saline PBSpH 7. Two milliliters of PBS was added to the basolateral site of each well.
To facilitate interaction of gas phase smoke with BEAS-2B cells no fluid was added to the apical compartments. The Transwells were placed in glass chambers with separate inlets for compressed air and cigarette smoke.
Cells were exposed to ml of gas phase smoke every 10 min using a smoking apparatus consisting of a 60 ml syringe, a three-way stopcock and an inline filter. Smoke from research grade 1R3 cigarettes was passed through a Cambridge glassfiber filter to remove the tar fraction prior to introduction of smoke into the chamber.
The chamber was purged with fresh compressed air prior to each smoke exposure. These experiments were conducted using an oxygen tension of torr for the cigarette smoke and air mixture to approximate the conditions to which the lung epithelium would be exposed in vivo.
After treatment the cells were rinsed with PBS and subsequently lysed with 10 μmol SDS. Butylated hydroxytoluene BHT, nmol, 22 μg was added to the cell suspension as an antioxidant to prevent adventitious oxidation of β-carotene.
The hexane extracts were pooled and evaporated in vacuo. α-Tocopherol propionate was added as an injection standard, the samples were redissolved in mobile phase and analyzed by reverse phase HPLC with diode array detection Hewlett Packard, Palo Alto, CA. β-Carotene was detected at nm and α-tocopherol propionate at nm.
LDH release from the cells was quantified using a LD-L 10 kit Sigma, St Louis, MO. The pooled chloroform fractions were evaporated under nitrogen and redissolved in methanol 1. Glutathione content of cells was determined using the procedure of Fariss and Reed The procedure involved initial formation of S -carboxymethyl derivatives of free thiols followed by conversion of free amino groups to 2,4-dinitrophenyl derivatives and separation by ion exchange HPLC using γ-glutamyl glutamate as an internal standard.
For α-tocopherol depletion experiments KGM cell medium was supplemented with 1. For α-tocopherol analyses cells were sonicated in a mixture of ethanol 2 mlα-tocopherol- d 6 internal standard, 10 nmol and SDS 10 μmol. The samples were extracted with hexane and the hexane extracts were evaporated under N 2.
β-Carotene and its smoke oxidation products were analyzed by liquid chromatography—mass spectrometry using an Allsphere ODS-2 5 μm HPLC column 4. The conditions were maintained until 25 min. MS analyses were performed on a Finnigan TSQ triple quadrupole mass spectrometer using an atmospheric pressure chemical ionization source Finnigan MAT, San Jose, CA.
Mass spectra were obtained in negative ion mode. Results are expressed as means ± SEM. Statistical significance within sets of data was determined by one way analysis of variance ANOVA followed by individual comparisons using Bonferroni's correction for factorial analysis of variance.
Since β-carotene is a highly lipophilic compound poorly taken up by cells in culture, preliminary experiments were conducted to optimize its uptake by BEAS-2B cells. Despite published reports 1718addition of β-carotene in ethanol to culture medium was not found to be a good delivery method due to the limited solubility of β-carotene in ethanol data not shown.
We investigated the uptake of β-carotene by: i exposure of cells to β-carotene solubilized in THF and ethanol; ii exposure of cells to β-carotene incorporated into DPPC liposomes. Addition of β-carotene solubilized in THF and ethanol was consistently found to result in higher uptake by BEAS-2B cells as compared with β-carotene incorporated into liposomes for delivery into the cells Figure 1.
β-Carotene levels in cells decreased over time, suggesting that β-carotene was associated with the cells in a physiologically relevant manner and could participate in the oxidation chemistry of the cells. Prior to testing our hypothesis that smoke-driven β-carotene autoxidation exerted prooxidant effects it was necessary to establish that gas phase smoke was capable of oxidizing cellular β-carotene.
BEAS-2B cells supplemented with an extracellular concentration of 1. To determine whether smoke-driven autoxidation of β-carotene resulted in prooxidant effects in BEAS-2B cells we investigated the effects of β-carotene on gas phase smoke-induced lipid peroxidation of membrane lipids.
Gas phase smoke exposure significantly enhanced lipid peroxidation in BEAS-2B cells, as assessed by formation of 9'-OH MeLin Figure 4. However, supplementation of the cells with β-carotene did not cause an enhancement of smoke-induced lipid peroxidation.
Overall, β-carotene supplementation led to a slight attenuation of lipid peroxidation levels in BEAS-2B cells at 2. Membrane damage to BEAS-2B cells by exposure to gas phase smoke was assessed by measuring the release of the cytoplasmic enzyme LDH into the medium.
Exposure of cells to gas phase smoke resulted in a significant loss of membrane integrity, as indicated by the amount of LDH released by the cells Figure 5.
β-Carotene supplementation did not affect viability of the cells. Moreover, supplementation of cells with β-carotene did not affect the extent of membrane damage caused by gas phase smoke.
We then examined the possibility that smoke-driven β-carotene autoxidation was accelerating the rates of depletion of endogenous cellular antioxidants. Water-soluble glutathione and lipid-soluble α-tocopherol were the representative antioxidants studied. In the case of glutathione gas phase smoke caused rapid depletion of endogenous glutathione levels in BEAS-2B cells Figure 6.
Supplementation of the cells with β-carotene did not enhance this rate of smoke-driven glutathione depletion. Since the cells were grown in serum-free medium, their endogenous levels of α-tocopherol were very low. Hence, we supplemented the cells with 1. In contrast to glutathione, cellular α-tocopherol was much more resistant to gas phase smoke autoxidation Figure 7.
No statistically significant depletion of cellular α-tocopherol levels was observed during the 5 h smoke exposure, even though there was a general trend towards decreased levels.
: Beta-carotene and lung health| Position statement - Beta-carotene and cancer risk | Retention ling min. and Cullen,M. Stay informed: As research on beta-carotene and its Beta-carotene and lung health Beta-carofene lung cancer continues to evolve, heatlh important to nad informed about Medical weight management latest findings. Dietary carotenoids and risk of lung cancer in a pooled analysis of seven cohort studies. These results, taken together with those of our previous studies in a liposome model 12indicate that prooxidant effects of β-carotene are unlikely to contribute to increased incidence of cancer in smokers taking β-carotene supplements. Montvale, NJ: Medical Economics Company; |
| What is the Relationship between Lung Cancer and Beta-Carotene? | Summary of findings from meta-analyses of all cancer risk associated with β-carotene supplement use. Conversely, a meta-analysis reported an increase in lung cancer mortality associated with high-dose β-carotene supplement use [13]. This study did not analyse data specifically for smokers. A second meta-analysis from the same year reported an association between high-dose β-carotene supplementation and lung cancer among current smokers [11]. Table 3. Summary of findings from meta-analyses of lung cancer risk associated with β-carotene supplement use. Note: RR column represents relative risk, unless noted OR, which indicates odds ratio. Early RCTs of β-carotene supplementation produced contradictory findings. Despite a number of RCTs of β-carotene supplementation being suspended after increased risk of lung cancer was observed [13] [14] , subsequent RCTs showed no association between β-carotene supplementation and lung cancer risk in both the general population and among smokers [6] [15] [16]. A range of studies have been conducted investigating the link between β-carotene and cancer risk, for a number of cancer types. Table 4 summarises the findings from meta-analyses investigating the link between supplementary β-carotene and a range of cancer types. There is an association between β-carotene supplement use and bladder cancer [12]. Stomach cancer risk is increased with β-carotene supplement use and this effect is stronger in smokers and asbestos workers [13]. Although β-carotene supplement use is associated with increased risk of bowel adenoma [18] , there appears to be no association with bowel cancer [12] [13]. The majority of studies have found no association between supplementary β-carotene and other cancer types [13] [19] [12]. Table 4. Summary of findings from meta-analyses investigating the link between β-carotene supplement use and various cancers. There is some evidence that dietary β-carotene reduces the risk of a number of cancer types [20] [21] [22] [23] [24]. Table 5 summarises findings from meta-analyses of studies investigating the link between β-carotene and cancer. Table 5. Summary of findings from meta-analyses investigating the link between dietary β-carotene and various cancers. Dietary carotenoids, including β-carotene, may lower cancer risk by [9] [28] :. Cigarette smoke is highly oxidative and has been shown to destroy carotenoids in plasma [29]. Therefore β-carotene in the lungs of smokers may be susceptible to oxidative attack, leading to a pro-oxidant state which may promote cancer [29]. The protective effect seen for dietary β-carotene and cancer may also not be due to β-carotene specifically, but possibly another carotenoid or mix of compounds in the diet [7] [9]. It is also possible that the protective effect of β-carotene at dietary intake amounts is lost or reversed with dietary supplementation and the higher levels that this can supply [7]. While excessive cellular oxidants can induce damage to cells, they are needed in moderate concentrations for several protective reactions, including apoptosis, phagocytosis and detoxification reactions provided by cytochrome P complexes [30]. High doses of antioxidants can inactivate more cellular oxidants than necessary and interfere with these protective functions [30]. Vitamin A intakes are generally expressed as retinol equivalents RE , where 6 mg of β-carotene gives rise to 1 mg RE [1] [2]. The recommended dietary intake RDI for vitamin A in the Nutrient Reference Values for Australia and New Zealand NRVs is 0. Vitamin A is fat soluble and can be acutely toxic in adults at doses greater than mg [1]. Chronic toxicity can occur after consuming at least 10 times the recommended daily allowance for a month or more [1]. Vitamin A toxicity can cause headache, visual impairment, skin disorders and death [1]. Despite being a precursor of vitamin A, the toxicity of carotenoids is low [1] [2]. Large amounts of β-carotene from foods can cause hypercarotenaemia increased plasma carotene and yellow colouration of the skin, particularly on the palms of the hand and soles of the foot [1] [2]. An UL for β-carotene from foods is not needed due to the lack of adverse effects [2]. However the UL for β-carotene for dietary supplement use has not been able to be established due to the lack of dose-response information in the literature [2]. Table 6. Estimated average requirements, recommended dietary intakes and upper level of intake of vitamin A as retinol equivalents [2]. The last National Nutrition Survey showed that men had a mean intake of 1. The Blue Mountains Eye Study showed that the mean intake of β-carotene in Australian women aged 55 years or over was 7. However these values may be overestimates due to the use of a food frequency questionnaire for measuring intake [32]. Carrots and pumpkin contributed the most to dietary β-carotene intake in this population [32]. Data on the use of specific dietary supplements such as type and dose is currently limited. Studies in the US have shown that dietary supplement use has increased over the past two decades [33]. Most people taking supplements are generally seeking health benefits, which could also be achieved by eating a healthy, well balanced diet. Supplement use was significantly associated with gender females and conditions such as arthritis and osteoporosis, although the latter reason was likely to be representative of the population demographics in this particular study group [34]. Commonly cited reasons for use included health benefits, prevention of illness, sports performance, parental control, energy, poor diet and to do something positive for self [35]. Interestingly, studies have shown that dietary supplement use is similar between cancer survivors and cancer-free controls [36]. Increasingly complex mixtures of ingredients, which often contain other herbal and botanical compounds with anti-oxidant properties, are available in the market [37]. Consumers have access to numerous brands and formulations, including those available on the internet. In Australia, dietary supplements are sold at places such as supermarkets, chemists and health food stores. β-carotene is available as an individual supplement or as part of a multi-vitamin preparation. Vitamin A preparations usually contain retinyl palmitate as the active ingredient. As an indication at the time of writing this position statement, supplements available in Australia contained between 1—6. Common brands recommended taking one to three tablets per day, making the maximum dose of β-carotene from any supplement 9 mg if taken according to the supplement instructions. Therefore amounts greater than the equivalent UL of 18 mg β-carotene in the NRVs may be obtained if tablets are taken in excess of the recommended dosage see Table 6 for recommended ULs. The NRVs do not contain an UL for β-carotene intake for dietary supplement use due to a lack of dose-response information in the literature [1]. β-carotene is of low toxicity and until recently was thought to only cause yellowing of the skin after sustained high intake{{Cite footnote Citation:West CE. However recent epidemiological evidence shows that high doses of β-carotene supplements might increase the risk of lung cancer, particularly in smokers. Cancer Council supports the Australian Dietary Guidelines that recommend eating plenty of fruit and vegetables, and the population recommendation of at least two serves of fruit and five serves of vegetables daily see Table 7 [38]. Cancer Council recommends that people eat a variety of fruit and vegetables, including a range of different coloured fruit and vegetables, to obtain maximum benefits. We include products we think are useful for our readers. If you buy through links on this page, we may earn a small commission. Medical News Today only shows you brands and products that we stand behind. Beta carotene is a red-orange pigment found in plants and fruits, especially carrots and colorful vegetables. The body converts beta carotene into vitamin A, which is an essential vitamin. In this article, we explain all about beta carotene, what it does in the body, and what foods it is found in. We will also cover any associated risks. The human body converts beta carotene into vitamin A retinol — beta carotene is a precursor of vitamin A. We need vitamin A for healthy skin and mucus membranes, our immune system, and good eye health and vision. Beta carotene in itself is not an essential nutrient, but vitamin A is. Vitamin A can be sourced from the food we eat, through beta carotene, for example, or in supplement form. The advantage of dietary beta carotene is that the body only converts as much as it needs. Excess vitamin A is toxic. Toxic vitamin A levels can occur if you consume too many supplements. There are a number of ways that beta carotene can benefit human health. Below, we give some examples:. Beta carotene, like all carotenoids, is an antioxidant. An antioxidant is a substance that inhibits the oxidation of other molecules; it protects the body from free radicals. Free radicals damage cells through oxidation. Eventually, the damage caused by free radicals can cause several chronic illnesses. Men who have been taking beta carotene supplements for 15 or more years are considerably less likely to experience cognitive decline than other males, researchers from Harvard Medical School reported in Archives of Internal Medicine November issue. Oxidative stress is thought to be a key factor in cognitive decline, the researchers explained. Studies have shown that antioxidant supplements may help prevent the deterioration of cognition. Their study, involving 4, men, compared those on beta carotene supplements for an average of 18 years to others who were given placebo. Over the short-term, they found no difference in cognitive decline risk between the two groups of men, but in the long-term it was clear that beta carotene supplements made a significant difference. The researchers emphasized that there may have been other factors which contributed to the slower decline in cognitive abilities among the men in the beta carotene group. The BMJ published a report in March which showed that high blood beta carotene levels compensate for some of the damage to the lungs caused by oxygen free radicals. They measured the FEV1 of participants and measured their beta carotene blood levels. Cohort members were men and women aged 50—76 years at entry living in a county area in western Washington State, the catchment area of the Seattle-Puget Sound Surveillance, Epidemiology, and End Results SEER cancer registry, who were willing to complete a page baseline questionnaire. To encourage supplement users to enroll, the approach letter described the study as one on supplement use and cancer risk, but the study was not restricted to supplement users. Recruitment was conducted from October to December Names were purchased from a commercial mailing list, and , baseline questionnaires were mailed, followed by a postcard reminder 2 weeks later. A total of 79, questionnaires were returned The study protocol was approved by the institutional review board of the Fred Hutchinson Cancer Research Center Seattle, Washington. For the present analyses, we excluded participants with a self-reported history of lung cancer at baseline or who did not complete the baseline medical history section , 2 whose lung cancer was classified as lymphoma, and 3 whose diagnosis was based on a death certificate only. Data were collected at baseline. A page, self-administered, sex-specific, optically scanned questionnaire was used that covered 3 content areas: supplement use, diet, and health history and risk factors. In a 6-page instrument, respondents were asked about use of various dietary supplements during the 10 years prior to baseline. For current multivitamin use, participants either selected one of 16 common brand names or provided dose information on each vitamin and mineral of their brand. Those who had used more than one brand over the 10 years or had used multivitamins only in the past selected from another list of brand names reflecting past market availability. For analysis, the nutrient content of multivitamins was based on information from the PDR for nonprescription drugs 21 and from direct inquiry to manufacturers to determine composition of multivitamins in the past 10 years. We used a closed-ended format to inquire about current versus past use, frequency days per week , duration years of use over the previous 10 years, and usual dose per day. Individual vitamin A supplements were assumed to be retinol. International Units of retinol were converted to micrograms of retinol by multiplying by 0. Average daily intakes i. Supplemental lycopene and lutein intakes were computed based on duration years and frequency days per week of use from 2 sources: current use of multivitamins i. In a study of participants, the VITAL supplement questionnaire showed excellent reliability when compared with a repeat administration of the questionnaire 3 months after baseline and excellent validity when compared with a detailed home interview and supplement inventory and with nutrient biomarkers β-carotene showed a clear linear trend of increasing serum concentrations with higher self-reported supplemental intakes Pearson's r partialed for potential confounding factors and diet, 0. Usual dietary intake was assessed by a item food frequency questionnaire that included highly supplemented foods and adjustment questions on types of foods and preparation techniques 20 , The measurement properties of an earlier version of this questionnaire have been published; Pearson correlation coefficients between nutrient intakes estimated by the food frequency questionnaire and 8 days of dietary intake 4 dietary recalls and 4 food records were 0. The food frequency questionnaire analytic program, based on nutrient values from the Nutrition Data System NDS version 5. The page questionnaire captured several covariates, including demographic characteristics, health history, physical activity over the 10 years prior to baseline, cancer screening practices, and other potential confounders of supplement-cancer associations. Smokers were defined as individuals who smoked at least one cigarette per day for at least a year. We classified smokers as never, current, quit 10 years ago or longer, or quit less than 10 years ago as of the date of questionnaire completion. Duration of smoking was estimated by the reported number of years of smoking and intensity by the usual number of cigarettes smoked per day. Participants were followed for lung cancer occurring from baseline through December 31, , by linking the cohort to the Seattle-Puget Sound SEER registry. SEER cases are ascertained through all hospitals in the area; through offices of pathologists, oncologists, and radiotherapists; and from state death certificates. After exclusion of the 5 cases noted above, cases were identified in the cohort by using matching algorithms on personal identifiers and human review For each participant, the censored date was the earliest date of withdrawal from the study 0. Deaths were ascertained by linkage to Washington State death files, and moves out of the area were identified through the National Change of Address System and by follow-up letters and telephone calls. If a participant had multiple diagnoses of lung cancer, we used the time to first primary diagnosis. Statistical analyses were performed by using SAS version 9. Cox proportional hazards regression was used to estimate the hazard ratios for associations of supplemental β-carotene, retinol, vitamin A, lutein, and lycopene with lung cancer risk. Robust standard errors were used to eliminate traditional proportional hazards assumptions. Our final model included years of smoking, pack-years, and a squared pack-years term. We also decided a priori to include age and gender in the model. In analyses of β-carotene, we further adjusted for fruit and vegetable intake, physical activity, supplemental vitamin E, and body mass index. These factors did not appear to confound associations of the other supplemental vitamins, so the more parsimonious models were used. Note that adjustment for the corresponding dietary variables e. Likelihood ratio tests were conducted to evaluate for effect modification by gender and smoking status in the supplement—lung cancer associations; P values for interaction were obtained to compare the fit of the models with the interaction terms and without them. Participants missing data on supplemental vitamin use or other covariates in the model were excluded from analysis. We treated year average supplement use as a continuous variable to assess for trends in lung cancer risk. After a mean of 4. Table 1 gives the demographic and other selected characteristics of study participants, classified as cases and non—lung cancer cases. At baseline, lung cancer cases were also significantly more likely than noncases to be sedentary, consume fewer fruits and vegetables, and have a history of COPD or emphysema and a family history of lung cancer. Abbreviations: BMI, body mass index; COPD, chronic obstructive pulmonary disease; FFQ, food frequency questionnaire; MET, metabolic equivalent task; SD, standard deviation; VITAL, VITamins And Lifestyle. Longer duration of use of individual retinol supplements was associated with hazard ratios of 1. Lycopene supplement use was not associated with lung cancer risk. We also found no noticeable differences in these associations when histologic cell types were stratified as adenocarcinoma, squamous cell, and all other lung cancers data not shown. Abbreviations: CI, confidence interval; Ref, referent; VITAL, VITamins And Lifestyle. Daily dose includes combined intakes from multivitamins and individual single supplements. Adjusted for age, gender, years of smoking, pack-years, and pack-years squared. Also adjusted for fruit and vegetable intake, physical activity, supplemental vitamin E use, and body mass index. In this study that examined associations of long-term use of β-carotene, retinol, vitamin A, lutein, and lycopene supplements with lung cancer risk, longer duration of use of individual supplemental retinol was associated with significantly elevated risk of non-small-cell lung cancer and total lung cancer, long-term use of individual β-carotene supplements was associated with elevated small-cell lung cancer risk, and use of individual lutein supplements was associated with elevated risk of non-small-cell lung cancer and total lung cancer. Results were generally similar for men and women, and there was no appreciable effect modification by smoking status. Lung cancer risk was not significantly associated with total average year daily dose of any of these supplements or with lycopene supplement use. To our knowledge, very few studies and only one cohort investigation have reported on associations of vitamin A and carotenoids from supplements only with lung cancer risk because most previous studies focused exclusively on diet or on diet plus supplements together 6 , 15 , 24— In general, case-control studies have suggested reduced risk of lung cancer with higher carotenoid intakes 25—31 ; cohort study findings have typically been null 6 , 29—35 ; and randomized trials have reported slightly elevated risk for β-carotene, particularly among high-risk groups, such as smokers 12 , 13 , 29 , 30 , 36 , Overall, our findings are more in agreement with the randomized clinical trials of supplements than with the prior observational studies of diet. These results are in marked contrast to those from prospective cohort studies. Using pooled data from 8 cohort studies, Cho et al. Männistö et al. It is interesting that duration of use of individual β-carotene, retinol, and lutein supplements, but not high average year daily dose from multivitamins plus individual supplements, was positively associated with elevated lung cancer risk. Therefore, one might have expected that higher doses of these supplements would be associated with higher risk similar to randomized trials , whereas long-term use may or may not be associated with higher risk analogous to studies of diet. However, it is possible that duration of individual supplement use was more predictive of risk because individual supplements contain the highest dosages of the nutrients. Thus, it is possible that the cumulative effect of relatively high doses of β-carotene and other carotenoids taken over a longer period of time in the VITAL Study may have a stronger effect on risk than supranutritional doses of shorter or similar duration in the randomized trials. Additional studies examining the potential effect of long-term supplement use on lung cancer risk would be valuable in explaining these discrepancies. Because lutein supplement use was relatively infrequent in our study population, we decided to classify lutein supplement use as nonusers, lutein-containing multivitamin users, and individual supplement users rather than presenting information on average dose and years of use. Although there were only 2 lung cancer cases in the individual lutein supplement use category, the respective mean and median daily doses among users were 1. Given that lutein supplements have been used only in the past 15 years and only recently at high doses, this potential risk factor for lung cancer may be more important than suggested by the present study. We found no significant associations of supplemental lycopene with lung cancer risk in the present study. As noted above, observational studies have generally reported that dietary lycopene is associated with reduced lung cancer risk 25—30 , which is not surprising given that lycopene is a potent antioxidant 9 , There is inconsistency in the associations of carotenoids with lung cancer risk when examined separately in men and women. In the present study, we found few differences in the results between men and women. In a report by Wright et al. In a New York State cohort, inverse associations of carotenoids with lung cancer risk were observed for men, but there were no associations for women Reasons why associations may differ by gender are not clear, although it has been suggested that, compared with men, women may be more susceptible to the carcinogenic effects of cigarette smoke Results also did not differ significantly when we compared current with former smokers. Our study has several strengths. We used a comprehensive and validated instrument that captured long-term use of multivitamins and of individual and multinutrient supplements. Assessment of long-term intake during the 10 years prior to baseline allowed us to more closely investigate supplement exposure over the relevant period of lung cancer development. Exposure and risk factor ascertainment were obtained prior to the diagnosis of cancer, and this prospective approach reduced any possibility of selection bias. We controlled for several factors that affect or modify lung cancer risk, particularly the strong effects of tobacco smoking. The study also has some potential limitations. Response bias is a potential concern; however, in general, response bias is unlikely in a prospective study because potential participants cannot choose to take part in the study based on both supplement use and future unknown lung cancer diagnosis. |
| All you need to know about beta carotene | However, these associations disappeared when subsequent analyses considered a longer follow-up post-trial 53 , doi: However, during the last decade there has been increasing interest in "chemoprevention" ie, using specific natural or synthetic chemicals to reverse, suppress, or prevent the process of carcinogenesis 4, Article Navigation. Also adjusted for fruit and vegetable intake, physical activity, supplemental vitamin E use, and body mass index. |
| Beta-Carotene and Lung Cancer | Occupational exposure to asbestos and man-made oung fibers, and risk of lung cancer: evidence from Betaa-carotene case-control studies Beta-carotene and lung health Montreal, Beta-carohene. Shortness lugn breath: Lung cancer can cause Hfalth or inflammation Natural sugar substitutes the airways, leading to difficulty breathing or hhealth of breath. Trials identified Beta-carotene and lung health the WCRF investigating β-carotene and lung cancer risk [10]. We used data from the VITamins And Lifestyle VITAL Study, the only known large cohort investigation focused on dietary supplement use and cancer risk, to rigorously examine associations of supplemental intakes of β-carotene, retinol, total vitamin A, lutein, and lycopene with lung cancer risk. Antioxidants found in the highest concentrations in both the human diet and serum samples include vitamin C and the specific carotenoids β-carotene, α-carotene, β-cryptoxanthin, lutein, zeaxanthin, and lycopene 9. Control cells received equivalent amounts of DPPC liposomes or THF and ethanol without β-carotene. |
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