PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Beer”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

Effect of dealcoholized beer (Bitburger Drive) consumption on hemostasis in humans.

BACKGROUND: The beneficial effect of moderate alcohol consumption in lowering the risk of cardiovascular disease has been shown in several epidemiologic studies. Such studies have also shown, however, that the protective effect of alcoholic beverages like wine and beer is not only due to the ethanol content but also to the presence of nonalcoholic constituents. The positive effect of alcoholic beverages has been attributed to changes in lipoprotein metabolism, but there is substantial evidence that effects on hemostasis play an important role. Whether the effects of alcoholic beverages on hemostasis are due exclusively to ethanol or are due, in part, to nonalcoholic components, is still under debate. METHODS: We have examined the hemostatic effects of 3 liters of beer, dealcoholized beer, and ethanol/water (v/v 4%), consumed over a period of 3 hr, in 12 young healthy volunteers. Platelet parameters CD62, PAC-1, and monocyte platelet aggregates were analyzed using flow cytometric measurements. The activity of factor VII was determined with a prothrombin time (PT) assay and plasminogen activator inhibitor activity using a chromogenic substrate. Thrombin generation was determined according to the method of Hemker. RESULTS: All three fluids administered, dealcoholized beer, beer, and ethanol, reduced the expression of activated fibrinogen receptor, the platelet activation marker CD62, and the formation of monocyte-platelet-aggregate. In addition, dealcoholized beer also showed significant inhibitory effects on thrombin generation, whereas beer and ethanol showed procoagulatory effects. CONCLUSIONS: This study has shown that the acute consumption of dealcoholized beer inhibits thrombogenic activity in young adults. This action could have a beneficial effect on the development of coronary artery disease. Thus, the consumption of dealcoholized beer could provide cardiovascular benefit without the negative effects of alcohol.

Adult↗

Beer consumption among hazardous drinkers during pregnancy.

OBJECTIVE: The objective of this study was to examine the prevalence of beer consumption among hazardous drinkers in our pregnant patient population. METHODS: This prospective clinic-based cohort study involved women who were surveyed during their first prenatal visit. Hazardous drinking was identified on alcohol surveys as frequent or binge drinking habits with related consequences. Participants completed initial and postpartum interviews about the quantity, frequency, and type (beer, wine, liquor, and/or combinations) of alcoholic beverages consumed before and after pregnancy recognition. RESULTS: Of the total 4,494 patients who completed the survey, 203 (4.52%) met criteria for hazardous drinking, met study eligibility criteria, and completed the interviews. Beer was consumed most often (n = 151, 74.4%) and in greater quantities than wine (P < .05) or liquor (P < .01). Beer continued to be consumed by 52.3% women after pregnancy recognition. Although abstinence for prolonged periods was common during pregnancy, beer was consumed more than wine and liquor per drinking episode (2.7 versus 0.9 drinking units per drinking day; P = .002) indicating a binging pattern. Very few switched to drinking either a light beer (n = 6) or a nonalcoholic beer (n = 1). CONCLUSION: Beer is the most consumed among women with hazardous drinking habits before and after pregnancy awareness. Focusing on binge beer drinking is worthwhile during routine prenatal questioning. LEVEL OF EVIDENCE: II-2.

Adult↗

Beer congener stimulates gastrointestinal motility via the muscarinic acetylcholine receptors.

BACKGROUND: Ethanol and alcoholic beverages are known to affect upper gastrointestinal motility in humans. Beer has been reported to accelerate gastric emptying compared with other beverages that contain the same ethanol concentrations. In this study, we investigated the mechanism that underlies the effects of beer congener on gastrointestinal motility. METHODS: Gastric emptying activity was measured by means of movement of a semisolid test meal (0.05% phenol red/1.5% methylcellulose) in mice. To elucidate the mechanism for the effect of beer congener on gastrointestinal motility, we conducted receptor binding assays and contraction study by using longitudinal muscle from guinea pig ileum. RESULTS: Beer congener (1 g/kg orally) enhanced gastric emptying of a semisolid meal in mice. The receptor binding assay revealed that beer congener bound to dopamine D2 receptor and 5-hydroxytryptamine (5-HT)3 receptor. These IC50 values were more than 5 mg/ml. However, beer congener bound to 5-HT2 receptor, 5-HT4 receptor, and muscarinic M3 receptor with IC50 values of 2, 0.9, and 2 mg/ml, respectively. Beer congener (0.05-2 mg/ml) induced the contraction of longitudinal muscle from guinea pig ileum in a dose-dependent manner. This effect was not affected by either tetrodotoxin (10(-6)M) or ketanserin (10(-7)-10(-5)M), an antagonist for the 5-HT2 receptor. On the other hand, 4-DAMP (10(-8)-10(-5)M), an antagonist for the muscarinic M3 receptor, inhibited the contraction of the longitudinal muscle induced by beer congener (2 mg/ml) dose dependently. CONCLUSIONS: Beer congener stimulates gastrointestinal motility via the muscarinic M3 receptor.

Animals↗

Effects of chronic dietary beer and ethanol consumption on experimental colonic carcinogenesis by azoxymethane in rats.

Epidemiological studies have shown an association between consumption of alcoholic beverages, particularly beer, and carcinoma of the large bowel, especially the rectum. We studied the effects of chronic dietary beer and ethanol consumption on experimental colonic carcinogenesis, fecal bile acid and neutral sterol levels, fecal bacterial flora, and colonic epithelial DNA synthesis. Ten-week-old male Fischer 344 rats were pair fed throughout the study with Lieber-DeCarli-type liquid diets providing comparable total carbohydrates, proteins, fats, and calories. The diets provided 23 or 12% of calories as alcohol in beer (Hi-Beer and Lo-Beer groups), 18 or 9% of calories as reagent ethanol (Hi-EtOH and Lo-EtOH groups), or no alcohol (control group). After 3 weeks of dietary acclimatization, 10 weekly s.c. injections of the bowel carcinogen azoxymethane, 7 mg/kg, were given (weeks 1-10). At necropsy in week 26, the high alcohol groups (Hi-Beer and Hi-EtOH) showed a significantly reduced incidence of tumors in the right colon (42 and 46% versus 81% in control, P less than 0.01 and P = 0.02) but no effect on left colonic tumorigenesis. By contrast, the low alcohol groups (Lo-Beer and Lo-EtOH) showed a trend toward increased incidence and proportion of tumors in the left colon (incidence of 42 and 35% versus 15% in control, P = 0.06 for Lo-Beer; 28 and 30% of tumors in left colon versus 11%, P = 0.08 and P = 0.07) but no effect on right colonic tumorigenesis. Numbers of right colonic tumors were inversely correlated with alcohol consumption of all rats (r = -0.350, P less than 0.001), but left colonic tumors were not correlated. Fecal bile acid and neutral sterol levels, fecal bacterial counts, and colonic epithelial DNA synthesis did not correlate with the effects of alcohol consumption on colonic tumorigenesis. Our findings suggest that: modulation of experimental colonic tumorigenesis by chronic dietary beer and ethanol consumption was due to alcohol rather than other beverage constituents; tumorigenesis in the right and left colon was affected differentially by the levels of alcohol consumption, reflecting complex interactions among the potential mechanisms for alcohol effects in the model used.

Alcohol Drinking↗

Mycotoxins transmitted into beer from contaminated grains during brewing.

Studies with aflatoxin B1, ochratoxin A, zearalenone, deoxynivalenol, and fumonisins B1 and B2 added at various stages of the brewing process show that these mycotoxins (or metabolites) may be transmitted from contaminated grains into beer. Citrinin does not survive the mashing step. Mycotoxins in beer could originate from the malted grain or from adjuncts. Although high incidences and concentrations of aflatoxins and zearalenone have been found in local beers brewed in Africa, aflatoxins have not been detected in European beers. Zearalenone and alpha- or beta-zearalenol (the metabolite likely to occur) have not been found in Canadian and European beers, except for one sample analyzed by thin-layer chromatography only. Ochratoxin A rarely has been detected at > 1 ng/mL in beer; liquid chromatographic methods with a 0.05-0.1 ng/mL detection limit, however, have shown moderately high incidences of trace levels. Deoxynivalenol, which survives the brewing process, has been found with high incidence in Canadian and European beers, with concentration of > 200 ng/mL reported in several German beers. Fumonisins B1 and B2 occur to a limited extent in beer.

Aflatoxin B1↗

Alcohol and beer consumption in relation to cancers of bowel and lung: an extended correlation analysis.

Some extensions to simple international correlation analyses are examined with reference to beer consumption and bowel and lung cancers in 29 countries. Simple correlation of cross-sectional data for beer consumption and rectal cancer yields a coefficient of 0.77 in males and 0.75 in females. Lagged correlation analyses show a different temporal relationship between beer and colon cancer (little change over time) and rectal cancer (maximal correlation for contemporaneous, i.e. cross-sectional, data sets). Lagged correlation analysis of beer consumption and lung cancer shows a similar pattern to that for rectal cancer and beer, and markedly different from that for lung cancer and cigarettes, the former showing maximal correlation for contemporaneous data, the latter peaking 15 yr prior to date of mortality. Changes in beer consumption over time correlate with subsequent changes in rectal cancer, particularly amongst younger age groups. The sex-ratio of rectal cancer varies from around 1 in low beer consumption countries to about 1.75 in high consumption countries. The utility of these extensions to the usual simple correlation analyses is considered. The biologic plausibility of beer-bowel cancer relationships, and possible mechanisms, are discussed in the light of the findings.

Adult↗

Acute effects of drinking beer or wine on the steroid hormones of healthy men.

Plasma Testosterone, Dihydrotestosterone and Estradiol were determined in 72 healthy volunteers, divided into 36 beer and 36 wine drinkers, who consumed between 0.9-2.1 g ethanol/kg b.wt, simulating natural patterns of drinking. Blood samples were taken 5-10 h after drinking ceased and compared with control samples withdrawn exactly 24 h previously. For a consideration of the time variation of blood sampling, the subjects were classified as fast and slow drinkers. All groups exhibited both depressed and elevated testosterone levels, depending upon the time after drinking (fast beer drinkers) and upon the amount of alcohol (fast wine drinkers). Consumption of beer and wine significantly (P less than 0.05) inhibited dihydrotestosterone biosynthesis; depending on the time after drinking (only in beer drinkers) and blood alcohol levels (slow beer drinkers). Estradiol levels were significantly elevated (P less than 0.05-less than 0.001); correlating with the amount of beer and wine/kg b.wt, with time after drinking (fast beer drinkers), and with blood alcohol levels (fast wine drinkers). Consumption of these beverages showed different dependencies for the changed hormone levels. It is discussed whether the estrogenic constituents of beer and wine might be responsible for the enhancement of estradiol, which could contribute towards clarifying the phenomenon of feminization observed with chronic abuse of alcohol.

Adult↗

The use of nonalcoholic beer as the vehicle for ethanol consumption in rats.

Adult, male rats were presented in their home cages with either a nonalcoholic beer, the nonalcoholic beer with 10% ethanol added, or a choice between the two fluids. Although alcohol intake was increased by using the beer vehicle when alcohol was presented as the only available fluid, total daily consumption was not found greater than previous studies using other tastants to mask the alcohol taste. When given a choice, the rats preferred the nonalcohol-containing nonalcoholic beer to the alcohol-containing nonalcohol beer. After prolonged ethanol exposure in the home cage using the nonalcoholic beer vehicle, a subgroup of rats was tested in an operant paradigm to determine if ethanol presentation would maintain lever press behavior. There was little indication that, after this home cage procedure, ethanol functioned as an effective reinforcer. Therefore, although it appears that the use of nonalcoholic beer as the vehicle for making alcohol solutions can increase alcohol consumption, the utility of the nonalcoholic beer is no better than that of adding sweeteners.

Animals↗

Pseudouridine, an antimutagenic substance in beer towards N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

Previously we reported that beer is antimutagenic against several food-derived mutagens including heterocyclic amines. We describe here the isolation and identification of pseudouridine from beer as an antimutagenic substance against N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). All of the 17 samples of beer tested showed inhibition of the MNNG mutagenicity in Salmonella. Extensive fractionation through chromatography of the active components from a freeze-dried beer sample gave six antimutagenic fractions. One contained pseudouridine, as characterized by the UV spectra, nuclear magnetic resonance, and co-chromatography in HPLC. Pure pseudouridine inhibited the mutagenicity of MNNG in a dose-dependent manner. The amount of pseudouridine in the beer sample, estimated at about 0.4 mg/100 ml beer, can account for 3% of the total antimutagenicity of beer. Thus, the major active components in beer remain to be identified. The role of pseudouridine in inhibiting the mutagenicity of MNNG is to be studied further. Among analogs of pseudouridine, spongouridine, but not uridine, was antimutagenic against MNNG. The bacterial mutagenicity of another methylating agent N-methyl-N-nitrosourea was also inhibited by pseudouridine. Pseudouridine is the first example among nucleosides to be shown to possess an antimutagenic property.

Antimutagenic Agents↗

Further insights into the role of methional and phenylacetaldehyde in lager beer flavor stability.

This work attempts to measure the importance of methional and phenylacetaldehyde on the flavor stability of beer, as direct participants or as indicators of aroma deterioration. A trained sensory panel identified the most important descriptors related to the typical aroma of aged beer: "malty", "honey-like", "cooked potato", and "metallic". By GC-olfactometry analysis, six aromatic zones related to the selected descriptors were highlighted, and by using GC-MS techniques it was possible to identify methional and phenylacetaldehyde as being responsible for two odor zones. The quantification of these molecules in samples submitted to forced aging treatments showed that the levels of methional and phenylacetaldehyde are dependent on the temperature of storage. Normal aged beers were also analyzed, and it was observed that these compounds accumulate with time of storage. Furthermore, these molecules were negatively correlated with the aroma quality of beer as evaluated by a sensorial panel. To validate the sensory impact of these substances, a fresh beer was spiked with these molecules and also with trans-2-nonenal, singly and in combination, and the similarity value between samples and the aged beer was then determined. The highest value from the similarity tests was 72% when the three compounds were added simultaneously. The combination of the two Strecker aldehydes increases by 54% the degree of similarity, indicating the key role played by these molecules in the aroma deterioration of beer. Finally, the kinetic parameters, Ea and k, were calculated, and it was observed that the Arrhenius equation described well the temperature dependence of the reaction rate constant. Measuring the concentration of methional and phenylacetaldehyde may provide information about the key steps along the process that most affect the flavor stability of beer, which may be useful in establishing the best storage conditions.

Acetaldehyde↗

Gastric acid secretion in dogs in response to combinations of beer, ethanol and peptone meal--the role of endogenous gastrin.

AIM: To examine the effects of beer, ethanol, peptone meal and combinations of either peptone meal and beer or peptone meal and ethanol on gastric acid secretion in vagally denervated pouch dogs. METHODS AND RESULTS: The oral administration of either 200 mL of beer, 5% ethanol or 10% peptone meal significantly stimulated gastric acid secretion for 60-90 min in these dogs. With 5% ethanol the plasma gastrin concentration was not affected for 90 min. Combinations of 10% peptone and beer (peptone-beer) or 10% peptone and 5% ethanol (peptone-ethanol) potentiated the acid secretion and increased the plasma gastrin level. While a selective cholecystokinin-B/gastrin receptor antagonist, S-0509, had no effect on ethanol-stimulated acid secretion, the compound markedly inhibited both peptone-beer-stimulated and peptone-ethanol-stimulated gastric acid secretion. Famotidine and atropine significantly inhibited gastric acid secretion stimulated by 5% ethanol, peptone-beer and peptone-ethanol. CONCLUSIONS: The mechanisms by which peptone-beer and peptone-ethanol stimulate gastric acid secretion may be mediated not only by increased plasma gastrin, but also by the action of histamine and acetylcholine coupled with the increased plasma gastrin. Ethanol-stimulated secretion appears to be unrelated to circulating gastrin, yet may be related to the acid regulatory mechanism involving histamine and acetylcholine.

Administration, Oral↗

Ochratoxin A in domestic and imported beers in Belgium: occurrence and exposure assessment.

Determination of ochratoxin A (OTA) concentration was performed in commercial beer in Belgium using immunoaffinity column (OchraTest) clean-up and liquid chromatography. The procedure was validated and fulfilled the European Committee for Standardization's criteria. It offered a detection limit of 3 ng l(-1) and a quantification limit of 10 ng l(-1). Recovery experiments carried out with the spiked samples in the range 50-200 ng OTA l(-1) showed an overall average recovery rate of 97% (RSD = 2.8%). The validated method was applied to the analysis of 62 Belgian beers and 20 commercial beers imported from Denmark, France, Germany, Ireland, Mexico, The Netherlands and Scotland. None of these beers exceeded the previously suggested EU limit of 200 ng l(-1). However, OTA was detected in 60 Belgian beers and in all imported beers. The average levels of contamination were 33 ng l(-1) (RSD = 112%) and 32 ng l(-1) (RSD = 81%), respectively. The highest level found was 185 ng l(-1). On the basis of the established tolerable daily intake (TDI) of 5 ng kg(-1) body weight, accepted by the scientific committee on food of the EU, this study indicates that beer consumption in Belgium is not likely to contribute to more than a few per cent of the TDI based on the average consumption. This study also shows variability of the OTA contamination in beer with time. Thus, there is a potential risk of having highly contaminated batches from time to time. We therefore recommend to control further the OTA contamination in brewery products and to take precautionary measures during harvest, transport and storage of the raw materials to maintain the OTA intake at the lowest achievable level.

Beer↗

Beer drinking and its effect on uric acid.

This study attempted to simulate the drinking habits of gout patients. Beer or squash was drunk over a 4-hour period on two successive days by five gouty and five normouricaemic men. Serum lactate increased with beer and squash, but elevation of plasma uric acid was confined to beer drinking. Urate clearance increased with both beverages, but 24-hour uric acid excretion was accentuated only by beer. The purine content of several beers was measured and the principal constituent found to be guanosine, which is probably the most readily absorbed dietary purine. It was concluded that the hyperuricaemic effect of beer was mediated by the digestion of purines contained by the beer and by an effect of ethanol on uric acid synthesis. There was no evidence that beer taken in usual quantities reduced the renal excretion of uric acid.

Alcohol Drinking↗

Genetic characterization of non-spoilage variant isolated from beer-spoilage Lactobacillus brevis ABBC45.

AIMS: To characterize the non-spoilage variant obtained from beer-spoilage Lactobacillus brevis ABBC45C and to identify a potential genetic marker capable of discriminating beer-spoilage L. brevis strains from non-spoilers. METHODS AND RESULTS: A non-spoilage variant was obtained from beer-spoilage L. brevis ABBC45C by repeatedly subculturing the strain at 37 degrees C. Genetic characterization of the variant revealed that 12,605 bp portion of one plasmid, designated pRH45II, was lost in the variant. The sequence analysis indicates the presence of 12 ORFs in the deleted region of pRH45II. The PCR and Southern hybridization study revealed that the homologues of ORF5 found in the deleted region were present in all of the beer-spoilage L. brevis strains examined in this study. In contrast, the homlogues appeared to be absent in non-spoilage L. brevis strains. CONCLUSIONS: The presence or absence of ORF5 homologues was found to be highly correlated with the beer-spoilage ability of L. brevis strains, indicating this ORF is potentially a useful genetic marker capable of differentiating beer-spoilage strains among L. brevis. SIGNIFICANCE AND IMPACT OF THE STUDY: A non-spoilage variant was successfully isolated from beer-spoilage L. brevis ABBC45C. This study could facilitate the understanding of mechanisms underlying beer-spoilage ability of L. brevis.

Bacterial Proteins↗

Random amplified polymorphic DNA-PCR based cloning of markers to identify the beer-spoilage strains of Lactobacillus brevis, Pediococcus damnosus, Lactobacillus collinoides and Lactobacillus coryniformis.

AIMS: Beer-spoilage ability of lactic acid bacteria such as Lactobacillus brevis is a strain-dependent phenomenon in which the mechanism has not yet been completely clarified. In order to systematically identify genes that contribute to beer-spoilage, large-scale random amplified polymorphic DNA (RAPD)-based cloning methods was carried out. METHODS AND RESULTS: A systematic RAPD polymerase chain reaction (PCR) analysis using 600 primers was performed on beer-spoilage and on nonspoilage strains of L. brevis. Among 600 primers, three were found to amplify a single locus highly specific to beer-spoilage strains. DNA sequencing of this locus revealed a three-part operon encoding a putative glycosyl transferase, membrane protein and teichoic acid glycosylation protein. PCR analysis of typical beer-spoilage lactic acid bacteria suggested that this locus is highly specific to beer-spoilage strains. CONCLUSION: The cloned markers are highly specific to identify the beer-spoilage strains not only in L. brevis but also in Pediococcus damnosus, Lactobacillus collinoides and Lactobacillus coryniformis. SIGNIFICANCE AND IMPACT OF THE STUDY: This paper proves that RAPD-PCR is an efficient method for cloning the strain-specific genes from bacteria. The markers described here is one of the most useful tools to identify the beer-spoilage strains of lactic acid bacteria.

Beer↗

horC confers beer-spoilage ability on hop-sensitive Lactobacillus brevis ABBC45cc.

AIMS: To determine whether horC confers beer-spoilage ability and to evaluate the validity of horC as a trans-species genetic marker for differentiating the beer-spoilage ability of lactic acid bacteria (LAB). METHODS AND RESULTS: Hop-sensitive Lactobacillus brevis ABBC45cc was transformed with an expression plasmid, pHYchorBC, containing putative multidrug resistance gene horC and its putative regulator horB, and the transformant was designated as ABBC45cc/pHYchorBC. As a control, ABBC45cc was transformed with pHYchorB that contains horB, and the transformed strain was designated as ABBC45cc/pHYchorB. As a result of beer-spoilage assay of these transformants, ABBC45cc/pHYchorBC exhibited beer-spoilage ability, whereas ABBC45cc/pHYchorB did not. Furthermore ABBC45cc/pHYchorBC showed higher hop resistance than ABBC45cc/pHYchorB, accounting for the differences in beer-spoilage ability observed between the two transformants. ABBC45cc/pHYchorBC also exhibited higher resistance to various structurally unrelated drugs, compared with ABBC45cc/pHYchorB. CONCLUSIONS: horC was shown to confer hop resistance and beer-spoilage ability on ABBC45cc by presumably encoding a multidrug transporter. SIGNIFICANCE AND IMPACT OF THE STUDY: The finding that horC plays an important role in hop resistance and beer-spoilage ability supports the validity of horC as a trans-species genetic marker for differentiating the beer-spoilage ability of LAB.

Bacterial Proteins↗

Isolation of a hop-sensitive variant of Lactobacillus lindneri and identification of genetic markers for beer spoilage ability of lactic acid bacteria.

We have isolated a hop-sensitive variant of the beer spoilage bacterium Lactobacillus lindneri DSM 20692. The variant lost a plasmid carrying two contiguous open reading frames (ORF s) designated horB(L) and horC(L) that encode a putative regulator and multidrug transporter presumably belonging to the resistance-nodulation-cell division superfamily. The loss of hop resistance ability occurred with the loss of resistance to other drugs, including ethidium bromide, novobiocin, and cetyltrimethylammonium bromide. PCR and Southern blot analysis using 51 beer spoilage strains of various species of lactic acid bacteria (LAB) revealed that 49 strains possessed homologs of horB and horC. No false-positive results have been observed for nonspoilage LAB or frequently encountered brewery isolates. These features are superior to those of horA and ORF 5, previously reported genetic markers for determining the beer spoilage ability of LAB. It was further shown that the combined use of horB/horC and horA is able to detect all 51 beer spoilage strains examined in this study. Furthermore sequence comparison of horB and horC homologs identified in four different beer spoilage species indicates these homologs are 96.6 to 99.5% identical, which is not typical of distinct species. The wide and exclusive distribution of horB and horC homologs among beer spoilage LAB and their sequence identities suggest that the hop resistance ability of beer spoilage LAB has been acquired through horizontal gene transfer. These insights provide a foundation for applying trans-species genetic markers to differentiating beer spoilage LAB including previously unencountered species.

Anti-Bacterial Agents↗

Traditional home-brewed beer consumption and iron status in patients with esophageal cancer and healthy control subjects from Transkei, South Africa.

Consumption of home-brewed beer is associated with dietary iron excess and a high incidence of esophageal cancer in Transkei, South Africa. We examined the relationship between home-brewed beer consumption and body iron status in 234 patients with esophageal squamous cell carcinoma and 595 control subjects residing in Transkei. Subjects were screened for iron overload using transferrin saturation >45%, and/or serum ferritin >200 microg/l for women and >300 microg/l for men. A questionnaire was administered to all subjects, and iron content of randomly selected home-brewed beer samples was determined. The iron content of home-brewed beer was 258-fold higher than the commercial Castle Lager beer produced by South African Breweries. The prevalence of home-brewed beer consumption was 30.1% in esophageal cancer patients and 15.5% in control subjects and was found not to be a risk factor for esophageal cancer after adjustment for age, sex, and tobacco consumption (male subjects, odds ratio= 1.6 (95% confidence interval [CI]: 0.7-4.5); female subjects, odds ratio=1.7 (95% CI: 0.7-4.5). Iron overload as determined by transferrin saturation and elevated serum ferritin was observed in 4.3% of patients with esophageal cancer and 0.7% of control subjects and was not associated with the consumption of home-brewed beer. Consumption of home-brewed beer is not a risk factor for esophageal cancer and is not linked with iron overload in either cancer patients or control subjects; however, iron overload is likely to result from a combination of dietary intake and a genetic component.

Aged↗