喝酒脸红的人到底能喝还是不能喝
由于我是沾酒就脸红的人，而且是全身红，喝三杯就快要吐的那种人，很多人说喝酒脸红的人才是真正的能喝酒，是真的吗？来看看以下内容。
喝酒脸红的人患食管癌风险增加相关研究论文全文，这篇文章发表于2009年：
Philip J. Brooks*, Mary-Anne Enoch, David Goldman, Ting-Kai Li,Akira Yokoyama*
Citation: Brooks PJ, Enoch M-A, Goldman D, Li T-K, Yokoyama A (2009) The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption. PLoS Med 6(3): e1000050. doi:10.1371/journal.pmed.1000050
Published: March 24, 2009
This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
Funding: The authors received no specific funding for this article.
Competing interests: The authors have declared that no competing interests exist.
Abbreviations: ADH, alcohol dehydrogenase; ALDH2, aldehyde dehydrogenase 2; Glu, glutamate; Lys, lysine; OR, odds ratio; UADT, upper aerodigestive tract
To whom correspondence should be addressed. E-mail: pjbrooks@mail.nih.gov;a_yokoyama@kurihama1.hosp.go.jp
Philip J. Brooks, Mary-Anne Enoch, and David Goldman are in the Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, Maryland, United States of America. Ting-Kai Li is the former Director of the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health. He is now a Professor at the Duke–National University of Singapore Graduate Medical School, Durham, North Carolina, United States of America. Akira Yokoyama is Director of Clinical Research Unit, National Hospital Organization Kurihama Alcoholism Center, Nobi, Yokosuka, Kanagawa, Japan. Philip J. Brooks and Akira Yokoyama were participants in the 2007 International Agency for Research on Cancer Working Group on alcoholic beverage consumption.
Provenance: Not commissioned; externally peer reviewed
Approximately 36% of East Asians (Japanese, Chinese, and Koreans) show a characteristic physiological response to drinking alcohol that includes facial flushing (see Figure 1), nausea, and tachycardia [1] . This so-called alcohol flushing response (also known as “Asian flush” or “Asian glow”) is predominantly due to an inherited deficiency in the enzyme aldehyde dehydrogenase 2 (ALDH2) [2]. Although clinicians and the East Asian public generally know about the alcohol flushing response (e.g., http://www.echeng.com/asianblush/), few are aware of the accumulating evidence that ALDH2-deficient individuals are at much higher risk of esophageal cancer (specifically squamous cell carcinoma) from alcohol consumption than individuals with fully active ALDH2. This is particularly unfortunate as esophageal cancer is one of the deadliest cancers worldwide [3], with five-year survival rates of 15.6% in the United States, 12.3% in Europe, and 31.6% in Japan [4].
Figure 1. The Alcohol Flushing Response
Facial flushing in a 22-year-old ALDH2 heterozygote before (left) and after (right) drinking alcohol. The individual pictured in this figure has given written consent for publication of his picture using the PLoS consent form.
doi:10.1371/journal.pmed.1000050.g001
Our goal in writing this article is to inform doctors firstly that their ALDH2-deficient patients have an increased risk for esophageal cancer if they drink moderate amounts of alcohol, and secondly that the alcohol flushing response is a biomarker for ALDH2 deficiency. Because of the intensity of the symptoms, most people who have the alcohol flushing response are aware of it. Therefore clinicians can determine ALDH2 deficiency simply by asking about previous episodes of alcohol-induced flushing. As a result, ALDH2-deficient patients can then be counseled to reduce alcohol consumption, and high-risk patients can be assessed for endoscopic cancer screening. Based on the sizes of the Japanese, Chinese, and Korean populations and the expected frequency of ALDH2-deficient individuals in each [1], we estimate that there are at least 540 million ALDH2-deficient individuals in the world, representing approximately 8% of the population. In a population of this size, even a small reduction in the incidence of esophageal cancer could result in a substantial reduction in esophageal cancer deaths worldwide.
#### Summary Points ALDH2 eficiency resulting from the ALDH2 Lys487 allele contributes to both the alcohol flushing response and an elevated risk of squamous cell esophageal cancer from alcohol consumption.
Knowledge of the flushing response is useful clinically, as it allows doctors to identify their ALDH2-deficient patients in a simple, cost-effective, and non-invasive manner. Doctors should counsel their ALDH2-deficient patients to limit alcohol consumption and thereby reduce the risk of developing esophageal cancer.
In view of the approximately 540 million ALDH2-deficient individuals in the world, many of whom now live in Western societies, even a small percent reduction in esophageal cancers due to a reduction in alcohol drinking would translate into a substantial number of lives saved.A Primer on the Genetics of Alcohol Metabolism Top
Ethanol is first metabolized primarily by alcohol dehydrogenase (ADH) into acetaldehyde (Figure 2), a mutagen and animal carcinogen that causes DNA damage and has other cancer-promoting effects [5–7]. Acetaldehyde is subsequently metabolized to acetate, mainly by the enzyme ALDH2 [8]. In East Asian populations there are two main variants of ALDH2, resulting from the replacement of glutamate (Glu) at position 487 with lysine (Lys) [9]. The Glu allele (also designated _ALDH21_) encodes a protein with normal catalytic activity, whereas the Lys allele (ALDH2*2) encodes an inactive protein. As a result, Lys/Lys homozygotes have no detectable ALDH2 activity. Because the Lys allele acts in a semi-dominant manner, ALDH2 Lys/Glu heterozygotes have far less than half of the ALDH2 activity of Glu/Glu homozygotes; in fact, the reduction in ALDH2 activity in heterozygotes is more than 100-fold [8].
Figure 2. The Ethanol Metabolic Pathway and the Role of the ALDH2 Variants in Acetaldehyde Accumulation
It should be noted that ADH is also polymorphic, and genetic variants in ADH1B interact with the ALDH2 variant to modify risk [13].
doi:10.1371/journal.pmed.1000050.g002
Alcohol consumed by ALDH2-deficient individuals is metabolized to acetaldehyde, which accumulates in the body due to absent ALDH2 activity and results in facial flushing (Figure 1), nausea, and tachycardia [2]. These unpleasant effects are the result of diverse actions of acetaldehyde in the body, including histamine release [10]. Because of the intensity of this unpleasant response, ALDH2 Lys/Lys homozygotes are unable to consume significant amounts of alcohol. As a result, they are protected against the increased risk of esophageal cancer from alcohol consumption [11]. This observation also provided evidence for a causative role for ethanol in esophageal cancer, and a key role for acetaldehyde in mediating this effect [11].
ALDH2 Lys/Glu heterozygotes experience a less severe manifestation of the flushing response due to residual but low ALDH2 enzyme activity in their cells. As a result, some are able to develop tolerance to acetaldehyde and the flushing response and become habitual heavy drinkers, due in part to the influence of societal and cultural factors (see below). Therefore, paradoxically, it is the more common low-activity ALDH2 heterozygous genotype that is associated with greatest risk of esophageal cancer from drinking alcohol.Evidence That ALDH2 Deficiency Increases the Risk of Alcohol-Related Squamous Cell Esophageal Cancer Top
Following the first study [12], which was conducted in the Japanese population, case control studies in Japan and Taiwan have consistently demonstrated a strong link between the risk of esophageal squamous cell carcinoma (Figure 3) and alcohol consumption in low-activity ALDH2 heterozygotes, with odds ratios (ORs) ranging from 3.7 to 18.1 after adjustment for alcohol consumption. Moreover, most studies show ORs of over 10 for increased risk in heterozygotes who are heavy drinkers [13,14]. An independent meta-analysis has also confirmed an increased risk, even among moderate drinking heterozygotes [11]. In the Japanese and Taiwanese studies, a strikingly high proportion (58%–69%) of the excessive risk for esophageal cancer is attributable to drinking by low-activity ALDH2 heterozygous individuals [13,14].
Figure 3. A Late-Stage Squamous Cell Carcinoma of the Esophagus in a 51-Year-Old Male with a Known History of Flushing and Alcohol Drinking
doi:10.1371/journal.pmed.1000050.g003
Consistent with the results of case control studies, prospective studies in cancer-free alcoholics have also shown that the relative hazard for future upper aerodigestive tract (UADT) cancers in low-activity ALDH2 heterozygotes is approximately 12 times higher than in individuals with active ALDH2 [15]. (The UADT includes the oral cavity, pharynx, larynx, and esophagus.) In addition, alcohol consumption in low-activity ALDH2 heterozygotes has been associated with other cancer-related outcomes, including the presence of multiple areas of esophageal dysplasia (i.e., premalignant lesions) and multiple independent UADT cancers [13].
It is important to note that ALDH2 deficiency does not influence esophageal cancer risk in non-drinkers [11]. Furthermore, the magnitude of the ALDH2-associated esophageal cancer risk depends on the relative importance of alcohol versus other risk factors in a given population. In rural areas of China, where there is a high rate of esophageal cancer but alcohol drinking plays a less important role than in Japan and Taiwan, there is a more modest positive association (ORs, 1.7 to 3.1) between low-activity ALDH2 heterozygotes and esophageal cancer risk (e.g., [16]).
### Acetaldehyde Is Responsible for Facial Flushing and Esophageal Cancer Risk in ALDH2-Deficient Individuals Top
Acetaldehyde is responsible for the facial flushing and other unpleasant effects that ALDH2-deficient individuals experience when they drink alcohol [10]. Importantly, there is now direct evidence that ALDH2-deficient individuals experience higher levels of acetaldehyde-related DNA and chromosomal damage than individuals with fully active ALDH2 when they consume equivalent amounts of alcohol, providing a likely mechanism for the increased cancer risk. A study in Japanese alcoholics [17] showed that the amount of mutagenic acetaldehyde-derived DNA adducts (Figure 4) in white blood cells was significantly higher in ALDH2-deficient heterozygotes than in individuals with active ALDH2 (Table 1). In this study, while the two groups were matched for alcohol consumption, the ALDH2-deficient group consumed slightly less alcohol on average than the controls. Also, ALDH2 heterozygotes who drank alcohol had higher levels of white blood cells with chromosomal damage than drinkers with active ALDH2 [18]. Because of these as well as other data, the 2007 International Agency for Research on Cancer Working Group on alcohol and cancer specifically noted the substantial mechanistic evidence supporting a causal role for acetaldehyde in alcohol-related esophageal cancer [19].
Figure 4. Chemical Structures of Deoxyguanosine, the DNA Base That Is the Target for Acetaldehyde, As Well As the Acetaldehyde-Derived DNA Lesions Referred To in Table 1 The atoms in red represent the acetaldehyde-derived chemical modifications.
doi:10.1371/journal.pmed.1000050.g004
Table 1. Acetaldehyde-Derived DNA Damage in ALDH2-Deficient Alcoholics
doi:10.1371/journal.pmed.1000050.t001
#### Five Key Papers in the Field
Harada et al., 1981 [2] The first documentation of the relationship between ALDH deficiency and the flushing reaction.
Yoshida et al., 1984 [9] Identification of the amino acid variant responsible for ALDH deficiency.
Yokoyama et al., 1996 [12] The first evidence demonstrating that ALDH2-deficient individuals have a dramatically elevated risk of esophageal cancer when they drink alcohol.
Yokoyama et al., 2003 [25] Demonstrates that an updated flushing questionnaire containing two simple questions is approximately 90% sensitive and specific for identifying ALDH2-deficient individuals.
Baan et al., 2007 [19] Summary of the conclusions from the 2007 International Agency for Research on Cancer Working Group on the Consumption of Alcoholic Beverages. This is the first report to conclude that ethanol in alcoholic beverages is carcinogenic to humans. The report also adds the female breast and colorectum to the list of sites for alcohol-related carcinogenesis and notes substantial mechanistic evidence linking acetaldehyde to esophageal cancer risk based on studies from ALDH2-deficient individuals.
While the UADT is exposed to acetaldehyde from alcoholic beverages [20] and tobacco smoke, increasing evidence points to the metabolism of ethanol by microorganisms in the oral cavity as an important source of acetaldehyde in saliva and, by extension, in the esophagus. Acetaldehyde levels in saliva are 10–20 times higher than in blood, due to the local formation of acetaldehyde by oral microorganisms [21]. Importantly, ALDH2 heterozygotes had two to three times the acetaldehyde levels in their saliva compared to fully active ALDH2 individuals after a moderate dose of oral ethanol [22].
### Social and Cultural Factors Modulate Alcohol Drinking by ALDH2 Heterozygotes Top
Alcohol consumption is a social activity, and as such can be strongly influenced by cultural and social forces. In Japan, where the risk of alcohol-related esophageal cancer in ALDH2 heterozygotes has been most well documented, going out drinking after work with colleagues is an essential element of Japanese business society, and the idea of group harmony is particularly powerful. The percentage of heavy drinking men who are low-activity ALDH2 heterozygotes has risen substantially in the last few decades, in parallel with the proliferation of business society in Japan and increases in per capita alcohol consumption. Harada et al. [23] first reported that the frequency of inactive ALDH2 was very low (only 2%) in Japanese alcoholics in 1982. In a later study using archival DNA samples, Higuchi et al. [24] determined that in 1979, 3% of Japanese alcoholics were ALDH2 heterozygotes, compared with 8% in 1986 and 13% in 1992. In a more recent study, approximately 26% of heavy drinking (consuming more than about 400 g of ethanol per week) men in Tokyo were ALDH2 Lys487 heterozygotes [35]. In other East Asian countries, estimates of the percentage of alcoholics who are low-activity ALDH2 heterozygotes range from 17% in Taiwan in 1999 [26] to 4% in Korea in 2007 [27]. Taken together, these observations indicate that the inhibitory effect of heterozygous ALDH2-deficiency on alcohol consumption can be strongly influenced by local social and cultural factors which may change over time.
There are many East Asians now living in Western societies, particularly at universities and in metropolitan areas. A sub-population of special concern is ALDH2-deficient university students who may face peer pressure for heavy drinking and binge drinking. Furthermore, anecdotal evidence indicates that some young people view the facial flushing response as a cosmetic problem and use antihistamines in an effort to blunt the flushing while continuing to drink alcohol [28]. This practice is expected to increase the likelihood of developing esophageal cancer.
### Education and Early Detection Can Reduce the Global Health Burden of Esophageal Cancer Top
Clinicians who treat patients of East Asian descent need to be aware of the risk of esophageal cancer from alcohol consumption in their ALDH2-deficient patients. Importantly, clinicians can determine whether an individual of East Asian descent is ALDH2 deficient simply by asking whether they have experienced the alcohol flushing response. In the Japanese population, ALDH2 deficiency can be identified accurately based on the answers to a flushing questionnaire consisting of two questions (see Box 1) about previous episodes of facial flushing after drinking alcohol [25]. The two questions can be easily included as part of a standard clinical interview. In a Japanese male population, the flushing questionnaire had a 90% sensitivity and 88% specificity [25] and a positive predictive value of 87% (based on the tabulated data in [25]). The flushing questionnaire gave a similarly high sensitivity (88%) and specificity (92%) when administered to Japanese women [29].
#### Box 1. Clinical Tests To Assess ALDH2 Deficiency Due To the ALDH2 Lys487 Allele
1. The Flushing Questionnaire
The flushing questionnaire consists of two questions: (A) Do you have a tendency to develop facial flushing immediately after drinking a glass (about 180 ml) of beer?; (B) Did you have a tendency to develop facial flushing immediately after drinking a glass of beer in the first one or two years after you started drinking? For both questions, the choice of answers are: yes, no, or unknown.
If an individual answers yes to either question A or B, they are considered to be ALDH2 deficient [25]. The addition of question B is important because some individuals can become tolerant to the facial flushing effect.
The questionnaire that was tested referred to a small (about 180 ml) glass of beer. However, it seems likely that similar results would be obtained if the question were asked about beer or other beverages containing a similar amount of alcohol (about two-thirds of a glass of wine or shot of hard liquor).
2. The Ethanol Patch Test
The ethanol patch test is performed as follows: 0.1 ml of 70% ethanol is pipetted onto a 15 × 15 mm lint pad fixed on an adhesive tape. The patch is attached to the inner surface of the upper arm for a 7-minute period and then removed. A patch area that shows erythema 10–15 minutes after removal is judged as positive. The sensitivity, specificity, and positive predictive value for inactive ALDH2 are more than 90% in Japanese youth [34].
Once ALDH2-deficient patients have been identified, they should be informed about their elevated risk of developing esophageal cancer risk from drinking alcohol. As can be seen from Figure 5, ALDH2 deficiency increases esophageal cancer risk at all three drinking levels, but the slope of the line relating alcohol consumption to esophageal cancer risk is steeper in ALDH2-deficient individuals. Clinicians might therefore use this graph to explain the increased risk when counseling their ALDH2-deficient patients to reduce alcohol consumption.
Figure 5. Odds Ratios for Esophageal Cancer at Different Amounts of Alcohol Consumption In Relation To the Flushing Response
Alcohol consumption amounts: low, 1–8.9 units/week; moderate, 9–17.9 units/week; high, ≥18 units/week; where 1 unit = 22 g of ethanol. The referent (OR = 1) is never/rare drinkers (<1 unit/week) of either genotype. Odds ratios were adjusted for age, frequency of drinking strong alcohol beverages, pack-years of smoking, and intake of fruit and green-yellow vegetables, based on a multiple logistic regression model. Error bars are 95% confidence intervals. The graph is based on the data in [25].
doi:10.1371/journal.pmed.1000050.g005
The ORs in Figure 5 are adjusted for smoking. However, patients should also be informed that smoking further increases the esophageal cancer risk in a synergistic manner with alcohol [30]. As noted above, cigarette smoking dramatically increases acetaldehyde levels in saliva, and ALDH2-deficient individuals have a reduced capacity to clear salivary acetaldehyde.
For patients at high risk of esophageal cancer, doctors should also consider endoscopy for early cancer detection. A health risk assessment tool to select candidates for endoscopic cancer screening, including data on alcohol flushing as well as alcohol consumption, smoking, and dietary habits, is currently being developed and validated [31]. Using a version of the health risk assessment that includes the flushing questionnaire as a major component, it has been estimated that approximately 58% of esophageal cancers in the Japanese population could be detected by screening only the individuals with the top 10% risk scores [31].
When detected early, esophageal cancer can be treated by endoscopic mucosectomy, a standard and relatively non-invasive procedure. However, once the cancer has grown large enough to penetrate the submucosal layer, the likelihood of lymph node metastasis increases significantly [32]. Only about 20% of esophageal cancer patients survive three years after diagnosis [3], emphasizing the importance of disease prevention.
ALDH2-deficient university students may have their first experiences with heavy drinking while at university. Therefore, it is particularly important for university health professionals to be aware of the relationship between ALDH2 deficiency, facial flushing, and alcohol-related cancer risk. Informing ALDH2-deficient young people of their risk of esophageal cancer from alcohol drinking represents a valuable opportunity for cancer prevention. However, most of the data on the accuracy of the flushing questionnaire have come from individuals over 40 years old. To assess ALDH2 deficiency in young people with little experience of alcohol consumption, an ethanol patch test (see Box 1) can be used [13]. In the patch test, ethanol is applied to the skin, where it is metabolized to acetaldehyde. (Both ADH and ALDH can be detected in skin fibroblasts [33].) If the acetaldehyde is not further metabolized to acetate, it causes vasodilation, which is detected visually as localized erythema. Like the flushing questionnaire, the ethanol patch test is simple and inexpensive to perform, and the sensitivity, specificity, and positive predictive value for inactive ALDH2 have been shown to be more than 90% in Japanese youth [34].
### How Many Cancers Could Be Prevented by Reducing Alcohol Consumption in ALDH2-Deficient Individuals? Top
Finally, it is important to consider how many esophageal cancer cases might be prevented if ALDH2-deficient individuals reduced alcohol consumption. To address this question, the tabulated data of [35] were used to recalculate the population-attributable risk by Bruzzi’s method [36]. The results of this calculation indicate that if moderate or heavy drinking ALDH2 heterozygotes were instead only light drinkers, 53% of esophageal squamous cell carcinomas might be prevented in the Japanese male population.
### Supporting Information Top
*Alternative Language Summary S1. Translation of the article summary into Japanese by AY.
(23 KB DOC).
### References Top
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以下是纽约时报的报道：
March 21, 2009
Drinkers’ Red Face May Signal Cancer Risk
By NICHOLAS BAKALAR
People whose faces turn red when they drink alcohol may be facing more than embarrassment. The flushing may indicate an increased risk for a deadly throat cancer, researchers report.
The flushing response, which may be accompanied by nausea and a rapid heartbeat, is caused mainly by an inherited deficiency in an enzyme called ALDH2, a trait shared by more than a third of people of East Asian ancestry — Japanese, Chinese or Koreans. As little as half a bottle of beer can trigger the reaction.
The deficiency results in problems in metabolizing alcohol, leading to an accumulation in the body of a toxin called acetaldehyde. People with two copies of the gene responsible have such unpleasant reactions that they are unable to consume large amounts of alcohol. This aversion actually protects them against the increased risk for cancer.
But those with only one copy can develop a tolerance to acetaldehyde and become heavy drinkers.
“What we’re trying to do here is raise awareness of this risk factor among doctors and their ALDH2-deficient patients,” said Dr. Philip J. Brooks, an investigator with the National Institute on Alcohol Abuse and Alcoholism, and an author of the report published on Monday in the journal PLoS Medicine. “It’s a pretty serious risk.”
The malignancy, called squamous cell esophageal cancer, is also caused by smoking and can be treated with surgery, but survival rates are very low. Even moderate drinking increases the risk, but it rises sharply with heavier consumption. An ALDH2-deficient person who has two beers a day has six to 10 times the risk of developing esophageal cancer as a person not deficient in the enzyme.
Reducing drinking can significantly reduce the incidence of this cancer among Asian adults. The researchers calculate that if moderate- or heavy-drinking ALDH2-deficient Japanese men reduced their consumption to under 16 drinks a week, 53 percent of esophageal squamous cell cancers in that group could be prevented.
There is some anecdotal evidence that young people treat the flushing as a cosmetic response to be countered with antihistamines while continuing to drink. Ignoring the symptom and continuing to drink is likely to increase the incidence of esophageal cancer, researchers said.
To determine risk, doctors can ask their patients two simple questions. First, do you flush after drinking a glass of beer? Second, in the first one or two years after you began drinking, did you flush after having a beer?
The second question covers the possibility that a person has become tolerant to the effect.
Dr. Brooks said that the two questions give doctors an easy way to find out if the patient is ALDH2-deficient. There is also a patch test in which an ethanol-soaked pad is applied to the skin. If it causes reddening after 10 or 15 minutes, there is a high likelihood that the person is ALDH2-deficient.
看不懂英文的话，这里有丁香园的翻译：
| Blushing Drinkers at Risk for Esophageal Cancer喝酒脸红的人患食管癌风险增加 Article Tools Sponsored By By NICHOLAS BAKALAR Published: March 20, 2009 People whose faces turn red when they drink alcohol may be facing more than embarrassment. The flushing may indicate an increased risk for a deadly throat cancer, researchers report. 那些喝酒脸红的人可能面临的不只只是酒量差的尴尬。研究者发现，脸红可能预示着患喉癌的风险增加。 The flushing response, which may be accompanied by nausea and a rapid heartbeat, is caused mainly by an inherited deficiency in an enzyme called ALDH2, a trait shared by more than a third of people of East Asian ancestry — Japanese, Chinese or Koreans. As little as half a bottle of beer can trigger the reaction. 脸红的同时可能还会伴有恶心和心跳加快。脸红主要由一种酶的遗传缺陷所致，这种酶叫做ALDH2，大约有三分之一的亚洲人种存在这种缺陷—-日本人，中国人及朝鲜人。对于这种人，仅半瓶啤酒就可以引起这种脸红反应。 The deficiency results in problems in metabolizing alcohol, leading to an accumulation in the body of a toxin called acetaldehyde. People with two copies of the gene responsible have such unpleasant reactions that they are unable to consume large amounts of alcohol. This aversion actually protects them against the increased risk for cancer. 这种缺陷会使酒精代谢遇到问题，造成体内一种名为乙醛的毒素聚集。携带2个缺陷基因就会造成这种反应，这种人无法大量饮酒。但这却可以避免这些人饮酒从而减少患癌症的风险。 But those with only one copy can develop a tolerance to acetaldehyde and become heavy drinkers. 而那些携带一个拷贝数的人却可以耐受乙醛，从而大量饮酒。 “What we’re trying to do here is raise awareness of this risk factor among doctors and their ALDH2-deficient patients,” said Dr. Philip J. Brooks, an investigator with the National Institute on Alcohol Abuse and Alcoholism, and an author of the report published on Thursday in the journal PLoS Medicine. “It’s a pretty serious risk.” 国家研究所专门从事酗酒及酒精中毒研究的Philip医生说“我们现在试图做的是提高医生和那些ALDH2-缺陷患者对这种风险因子的警惕性”，他同时也是在星期四PLoS Medicine杂志上发表该文章的作者。“这是相当危险的。” The malignancy, called squamous cell esophageal cancer, is also caused by smoking and can be treated with surgery, but survival rates are very low. Even moderate drinking increases the risk, but it rises sharply with heavier consumption. An ALDH2-deficient person who has two beers a day has six to 10 times the risk of developing esophageal cancer as a person not deficient in the enzyme. 被称为食管鳞状细胞癌的恶性肿瘤同样也可由吸烟引起，虽然可以通过手术治疗，但是该病的生存率极低。即使适度饮酒也会增加患病风险，对于大量饮酒的人而言其风险急剧升高。和没有ALDH2缺陷的人相比，该基因缺陷的人每天喝2杯啤酒会使患食管癌的风险增加6-10倍。 Reducing drinking can significantly reduce the incidence of this cancer among Asian adults. The researchers calculate that if moderate- or heavy-drinking ALDH2-deficient Japanese men reduced their consumption to under nine drinks a week, 53 percent of esophageal squamous cell cancers in that group could be prevented. 对亚洲人群而言减少饮酒会显著减少这种癌症的患病率。研究者计算得出，如果一个适度或者大量饮酒的ALDH2缺陷的日本男性如果将酒量减至少于9杯/星期，他患食管鳞状细胞癌的风险可以减少53%。 There is some anecdotal evidence that young people treat the flushing as a cosmetic response to be countered with antihistamines while continuing to drink. Ignoring the symptom and continuing to drink is likely to increase the incidence of esophageal cancer, researchers said. 有无对照的证据说，一些喝酒脸红的年轻人认为脸红是一种过敏反应，服用抗组胺药物的同时可以继续喝酒。研究人员说，无视这种症状并且继续喝酒会增加食管癌的发病率。 To determine risk, doctors can ask their patients two simple questions. First, do you flush after drinking a glass of beer? Second, in the first one or two years after you began drinking, did you flush after having a beer? 为了测定这种风险，医生可以问他们的父母2个简单的问题。1，你们在喝一杯啤酒后脸红么？2，在你喝酒的1年或2年后，你喝酒还脸红么？ The second question covers the possibility that a person has become tolerant to the effect. 第2个问题涵盖了对脸红耐受的可能。 Dr. Brooks said that the two questions give doctors an easy way to find out if the patient is ALDH2-deficient. There is also a patch test in which an ethanol-soaked pad is applied to the skin. If it causes reddening after 10 or 15 minutes, there is a high likelihood that the person is ALDH2-deficient Brooks医生说，这两个问题可以帮助医生发现患者是否存在ALDH2缺陷。同样还可以通过乙醇浸润过得纸片贴于皮肤的皮肤接触实验来帮助诊断，如果接触酒精的部位10-15分钟后变红，这就说明这个人很可能为ALDH2-缺陷患者。 |
所以大家以后不要再说，喝酒脸红的人能喝了。