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International Journal of Molecular... Nov 2022Aldehydes, particularly acetaldehyde, are carcinogenic molecules and their concentrations in foodstuffs should be controlled to avoid upper aerodigestive tract (UADT)... (Review)
Review
Aldehydes, particularly acetaldehyde, are carcinogenic molecules and their concentrations in foodstuffs should be controlled to avoid upper aerodigestive tract (UADT) and liver cancers. Highly reactive, acetaldehyde forms DNA and protein adducts, impairing physiological functions and leading to the development of pathological conditions. The consumption of aged beer, outside of the ethanol metabolism, exposes habitual drinkers to this carcinogen, whose concentrations can be over-increased due to post-brewing chemical and biochemical reactions. Storage-related changes are a challenge faced by the brewing industry, impacting volatile compound formation and triggering flavor instability. Aldehydes are among the volatile compounds formed during beer aging, recognized as off-flavor compounds. To track and understand aldehyde formation through multiple pathways during beer storage, consequent changes in flavor but particularly quality losses and harmful compound formation, this systematic review reunited data on volatile compound profiles through gas chromatography analyses from 2011 to 2021. Conditions to avoid flavor instability and successful methods for reducing beer staling, and consequent acetaldehyde accumulation, were raised by exploring the dynamic conversion between free and bound-state aldehydes. Future research should focus on implementing sensory analyses to investigate whether adding aldehyde-binding agents, e.g., cysteine and bisulfite, would contribute to consumer acceptance, restore beer flavor, and minimize acetaldehyde-related health damage.
Topics: Humans; Aged; Acetaldehyde; Aldehydes; Beer; Carcinogens; Carcinogenesis
PubMed: 36430619
DOI: 10.3390/ijms232214147 -
Medicina Oral, Patologia Oral Y Cirugia... Jan 2020Oral and pharynx cancer represent a serious global problem, reaching an incidence of half a million cases annually. The role of tobacco and alcohol have been studied and...
BACKGROUND
Oral and pharynx cancer represent a serious global problem, reaching an incidence of half a million cases annually. The role of tobacco and alcohol have been studied and proven to be one of its risk factors. We also know that mouthwashes contain a variable percentage of alcohol, so there is a reasonable concern about their role in carcinogenesis.
MATERIALS AND METHODS
To answer the PICOS (Population; Intervention; Comparison; Outcomes; Study) question: Do patients (Population) who use alcohol-based mouthwashes (Intervention) compared to those who do not use them (Comparison) have higher acetaldehyde levels in saliva or higher risk of oral cancer development? (Outcomes) Meta-analyses, systematic reviews, randomized and non-randomized clinical trials, case-control studies, and prospective and retrospective cohort studies were included (Study). Two independent authors conducted literature screening through MEDLINE, Scopus and the Cochrane Library, and they also conducted article and data extraction to undertake quality analyses. The main outcome measures were salivary acetaldehyde levels or the risk of oral cancer development. The most relevant data was extracted and the risk of bias from the studies included was also evaluated.
RESULTS
Out of 497 potentially eligible papers, 8 studies were included in the qualitative analysis which include a total of 43,499 subjects: two meta-analyses, a clinical trial, three case-control studies and two cohort studies. One study (n = 3,926) found a relationship between alcohol mouthwash and oral cancer, two studies (n = 25,033) found this relationship when a high frequency of mouthwash was present, three studies (n = 14,482) failed to find this relationship and 2 studies (n = 58) found a temporary increase of acetaldehyde levels in saliva after alcohol mouthwash.
CONCLUSIONS
It cannot be guaranteed that the use of mouthwash represents an independent risk factor for the development of head and neck cancer. However, the risk does increase when it occurs in association with other carcinogenic risk factors.
Topics: Humans; Mouth Neoplasms; Mouthwashes; Prospective Studies; Retrospective Studies; Risk Factors
PubMed: 31655832
DOI: 10.4317/medoral.23085 -
Evidence Report/technology Assessment Nov 2010The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the... (Review)
Review
OBJECTIVES
The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the risk of developing breast and colorectal cancers.
DATA SOURCES
We searched 11 external databases, including PubMed® and Embase, for studies on possible mechanisms. These searches used Medical Subject Headings and free text words to identify relevant evidence.
REVIEW METHODS
Two reviewers independently screened search results, selected studies to be included, and reviewed each trial for inclusion. We manually examined the bibliographies of included studies, scanned the content of new issues of selected journals, and reviewed relevant gray literature for potential additional articles.
RESULTS
Breast Cancer. Five human and 15 animal studies identified in our searches point to a connection between alcohol intake and changes in important metabolic pathways that when altered may increase the risk of developing breast cancer. Alterations in blood hormone levels, especially elevated estrogen-related hormones, have been reported in humans. Several cell line studies suggest that the estrogen receptor pathways may be altered by ethanol. Increased estrogen levels may increase the risk of breast cancer through increases in cell proliferation and alterations in estrogen receptors. Human studies have also suggested a connection with prolactin and with biomarkers of oxidative stress. Of 15 animal studies, six reported increased mammary tumorigenesis (four administered a co-carcinogen and two did not). Other animal studies reported conversion of ethanol to acetaldehyde in mammary tissue as having a significant effect on the progression of tumor development. Fifteen cell line studies suggested the following mechanisms: Increased hormonal receptor levels. Increased cell proliferation. A direct stimulatory effect. DNA adduct formation. Increase cyclic adenosine monophosphate (camp). Change in potassium channels. Modulation of gene expression. Colorectal Cancer. One human tissue study, 19 animal studies (of which 12 administered a co-carcinogen and seven did not), and 10 cell line studies indicate that ethanol and acetaldehyde may alter metabolic pathways and cell structures that increase the risk of developing colon cancer. Exposure of human colonic biopsies to acetaldehyde suggests that acetaldehyde disrupts epithelial tight junctions. Among 19 animal studies the mechanisms considered included: Mucosal damage after ethanol consumption. Increased degradation of folate. Stimulation of rectal carcinogenesis. Increased cell proliferation. Increased effect of carcinogens. Ten cell line studies suggested: Folate uptake modulation. Tumor necrosis factor modulation. Inflammation and cell death. DNA adduct formation. Cell differentiation. Modulation of gene expression. One study used a combination of animal and cell line and suggested intestinal cell proliferation and disruption of cellular signals as possible mechanisms.
CONCLUSIONS
Based on our systematic review of the literature, many potential mechanisms by which alcohol may influence the development of breast or colorectal cancers have been explored but the exact connection or connections remain unclear. The evidence points in several directions but the importance of any one mechanism is not apparent at this time.
Topics: Alcohol Drinking; Animals; Breast Neoplasms; Cell Proliferation; Colorectal Neoplasms; Estrogens; Ethanol; Female; Humans; Male; Mammary Neoplasms, Animal; Oxidative Stress; Prolactin; Receptors, Estrogen; Risk
PubMed: 23126574
DOI: No ID Found -
Bioscience Reports Apr 2019Alcohol consumption has been established to be a major factor in the development and progress of cancer. Genetic polymorphisms of alcohol-metabolism genes result in... (Meta-Analysis)
Meta-Analysis
Alcohol consumption has been established to be a major factor in the development and progress of cancer. Genetic polymorphisms of alcohol-metabolism genes result in differences between individuals in exposure to acetaldehyde, leading to possible carcinogenic effects. Arg47His (rs1229984 G > A) in have been frequently studied for its potential effect on carcinogenesis. However, the findings are as yet inconclusive. To gain a more precise estimate of this potential association, we conducted a meta-analysis including 66 studies from 64 articles with 31999 cases and 50964 controls. The pooled results indicated that Arg47His polymorphism is significantly associated with the decreased risk of overall cancer (homozygous model, odds ratio (OR) = 0.62, 95% confidence interval (CI) = 0.49-0.77; heterozygous model, OR = 0.71, 95% CI = 0.60-0.84; recessive model, OR = 0.83, 95% CI = 0.76-0.91; dominant model, OR = 0.62, 95% CI = 0.53-0.72; and allele comparison, OR = 0.82, 95% CI = 0.75-0.89). Stratified analysis by cancer type and ethnicity showed that a decreased risk was associated with esophageal cancer and head and neck cancer amongst Asians. In conclusion, our meta-analysis suggested that Arg47His polymorphism was significantly associated with decreased overall cancer risk. These findings need further validation in large multicenter investigations.
Topics: Alcohol Dehydrogenase; Carcinogenesis; Esophageal Neoplasms; Head and Neck Neoplasms; Models, Genetic; Neoplasm Proteins; Neoplasms; Polymorphism, Genetic
PubMed: 30872408
DOI: 10.1042/BSR20181915 -
Frontiers in Endocrinology 2024Acetaldehyde dehydrogenase 2 (ALDH2) had reported as a prominent role in the development of cardiometabolic diseases among Asians. Our study aims to investigate the... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
Acetaldehyde dehydrogenase 2 (ALDH2) had reported as a prominent role in the development of cardiometabolic diseases among Asians. Our study aims to investigate the relationship between ALDH2 polymorphism and cardiometabolic risk factors in East Asian population.
METHOD
We searched databases of PubMed, Web of Science, and Embase updated to Oct 30, 2023. We extracted data of BMI, Hypertension, SBP, DBP, T2DM, FBG, PPG, HbA1c, TG, TC, LDL-C and HDL-C.
RESULT
In total, 46 studies were finally included in our meta-analysis, containing, 54068 GG and, 36820 GA/AA participants. All outcomes related to blood pressure revealed significant results (hypertension OR=0.83 [0.80, 0.86]; SBP MD=-1.48 [-1.82, -1.14]; DBP MD=-1.09 [-1.58, -0.61]). FBG showed a significant difference (MD=-0.10 [-0.13, -0.07]), and the lipid resulted significantly in some outcomes (TG MD=-0.07 [-0.09, -0.04]; LDL-C MD=-0.04 [-0.05, -0.02]). As for subgroups analysis, we found that in populations without severe cardiac-cerebral vascular diseases (CCVDs), GG demonstrated a significantly higher incidence of T2DM (T2DM OR=0.88 [0.79, 0.97]), while the trend was totally opposite in population with severe CCVDs (T2DM OR=1.29 [1.00, 1.66]) with significant subgroup differences.
CONCLUSION
Our updated meta-analysis demonstrated that ALDH2 rs671 GG populations had significantly higher levels of BMI, blood pressure, FBG, TG, LDL-C and higher risk of hypertension than GA/AA populations. Besides, to the best of our knowledge, we first report GG had a higher risk of T2DM in population without severe CCVDs, and GA/AA had a higher risk of T2DM in population with severe CCVDs. https://www.crd.york.ac.uk/PROSPERO, identifier CRD42023389242.
Topics: Humans; Aldehyde Dehydrogenase, Mitochondrial; Asian People; Cardiometabolic Risk Factors; Cholesterol, LDL; Diabetes Mellitus, Type 2; East Asian People; Hypertension
PubMed: 38567307
DOI: 10.3389/fendo.2024.1333595