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1. Central Annals of Public Health and Research
Cite this article: Testino G, Leone S, Patussi V, Balbinot P, Fanucchi T, et al. (2016) Alcohol Consumption and Cancer: A Literature Search and a Proposal.
Ann Public Health Res 3(1): 1036.
*Corresponding author
Gia nni T
e stino , Ce ntro Alc o lo g ic o Re g io na le – Re g io ne
Lig uria , Pa dig lio ne 10, IRCCS AOU Sa n Ma rtino -IST
(Na tio na l Institute fo r Re se a rc h o n Ca nc e r), Pia zza le
R. Be nzi 10, 16132 Ge no va , Ema il:
Submitted: 01 De c e mb e r 2015
Accepted: 18 Ja nua ry 2016
Published: 19 Ja nua ry 2016
Copyright
© 2016 T
e stino e t a l.
OPEN ACCESS
Keywords
• Alc o ho l
• Ca nc e r
• Ca rc ino g e ne sis
• Pre ve ntio n
Review Article
Alcohol Consumption and
Cancer: A Literature Search and
a Proposal
Gianni Testino1,2
*, Silvia Leone3
, Valentino Patussi2,4
, Patrizia
Balbinot1,2
, Tiziana Fanucchi2,4
, Alessandro Sumberaz1,2
, Emanuele
Scafato2,5
and Paolo Borro1,2
1
Centro Alcologico Regionale – Regione Liguria, IRCCS AOU San Martino-IST, Italy
2
World Health Organization Collaborating Centre for Research and Health Promotion on
Alcohol and Alcohol-related Health Problems, Istituto Superiore di Sanita, Italy
3
School of Toxicology, University of Genoa, Italy
4
Centro Alcologico Regionale Toscano, AOU Careggi, Italy
5
National Institute of Health, Italy
Abstract
The correlation between alcohol and cancer is well-known. Recently, the
International Agency for Research on Cancer (World Health Organization) included the
consumption of alcoholic beverages, as well as the ethanol and acetaldehyde present
in alcoholic beverages, in Group 1. A causal relationship has been established between
alcohol and the occurrence of several types of cancer, particularly those with onset in
the oral cavity, pharynx, larynx, esophagus, colon-rectum, liver, and breast. To date,
a safe amount has not been established. Instead, a dose-dependent correlation has
been demonstrated between cancer risk and alcohol intake in both males and females
who consume alcohol on a regular basis. In subjects who consumed or consume alcohol
in a risky / harmful way, or in patients with a history of alcohol dependence or alcohol
problems, screening and oncological prevention programs should be customized with
regard to the general population.
INTRODUCTION
The correlation between the consumption of alcoholic
beverages and the onset of some types of tumor is well known,
as is the fact that the ingestion of any type of alcoholic beverage
is associated with the possible development of cancer. In the
international literature there are numerous experimental and
epidemiologicalstudiesanddatathathaveindicatedthisforyears.
This causal relationship has been confirmed by the publication of
volumes 96 (2010) and 100E (2012) by the International Agency
for Research on Cancer (IARC - World Health Organization) [1-3].
In Table 1 the risk is shown in relation to grams / day. It is
worth pointing out that the risk is cumulative. One Alcoholic Unit
(AU) is represented by 10-12 grams of ethanol, which occurs on
average in 125 ml of wine at 12%, in 330 ml of beer at 4.5%, in
80 ml of other alcoholic drinks or cocktails at 18 %, or 40 ml of
spirits at 36%.
The National Institute for Health and Clinical Excellence
suggests this classification by using a common means of
identification such as the Alcohol Use Disorders Identification
Test (AUDIT) [4]: If the score is greater than 8, this means the
consumer is at risk; if the score is between 16 and 19, this means
harmful use; if the score is greater than 20, this means severe
alcohol dependence.
From the methodological point of view in this literature
search, we selected studies that we considered most significant
(PubMed). In the light of the selected data and personal
experience a proposal is put forward for monitoring cancer
in alcohol dependence (AD) patients and in those with risky /
harmful consumption.
The mechanisms of carcinogenesis
The mechanisms of carcinogenesis induced by alcohol are
numerous. The following are the most accredited [1,2,5-9]: 1)
The production of toxins and carcinogens such as acetaldehyde,
oxygen-freeradicalsandproductsarisingfromlipidperoxidation,
2) interference with the absorption of certain nutrients, 3)
altered metabolism of some nutrients, 4) inhibition of some
detoxification mechanisms, 5) activating enzyme (cytochrome
P450-2E1: CYP2E1), 6) increased oxidative stress, 7) immune
suppression, 8) changes in membrane fluidity, 9) alteration of
cell proliferation / apoptosis, 10) stimulus to the processes of

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Ann Public Health Res 3(1): 1036 (2016) 2/8
angiogenesis, 11) weight gain, 12) genetic polymorphisms of
alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase
(ALDH).
The metabolization of ethanol by ADH entails the production
of acetaldehyde and NADH, while from CYP2E1 acetaldehyde and
oxygen-free radicals (ROS) are formed. The NADPH is reoxidized
to NADH in the mitochondria with the further formation of ROS.
ROS and reactive species of nitrogen (RSN) subsequently
induce lipid peroxidation. Acetaldehyde, ROS and products
of lipid peroxidation determine direct genotoxic activity
through the formation of “adducts,” which involves mutations
and chromosomal alterations that favor the development of
neoplastic cell lines. The number of adducts varies in relation to
individual genetic patterns (especially genetic polymorphisms of
alcohol dehydrogenase and aldehyde dehydrogenase) [9,10].
The acetaldehyde and nitric oxide produced through the
induction of nitric oxide synthase by ethanol inhibits DNA repair
systems. These systems are also inhibited by IL-6 and nuclear
factor kB. These last two factors sub-regulate the genes that
control the mechanisms of anti-apoptosis.
It should be remembered that increased CYP2E1 activity
leads to the activation of pro-carcinogenic substances found
in environmental tobacco smoke and certain foods such as
polycyclic hydrocarbons, hydrazine and nitrous mine [9,11].
CYP2E1 reduces the tissue levels of retinol and retinoic acid,
which have particular relevance in the regulation of cell growth
and differentiation. The decisive factor is the influence of ethanol
and acetaldehyde on the transfer mechanisms of the methyl
groups. In case of hypomethylation there is an activation of the
oncogenes, whereas in case of hypermethylation a deactivation
of the tumor suppressor genes occurs.
To maintain a sufficient methylation capacity, it is also
appropriate to maintain a fair number of lipotropic substances
including nutrients such as choline, betaine and methionine,
which are essential for the formation, transport and transfer of
methyl groups to the “target molecules.” Ethanol promotes tumor
progression via the induction of angiogenesis. In fact, an increase
in endothelial growth factors and tumor angiogenesis has been
found [12,13]. Polymorphisms and genetic mutations greatly
affect the ratio of alcohol to cancer.
Genetic variations related to the metabolism of ethanol and
acetaldehyde, oxidative stress, lipid storage mechanisms, the
metabolism endotoxins and the mechanisms of fibro genesis
have all been identified. The carriers of these polymorphisms
are predisposed to cancer through social consumption [2].
More incisive genetic modifications are related to aldehyde
dehydrogenase (ALDH) and alcohol deydrogenase (ADH). An
altered function of ALDH results in a buildup of acetaldehyde,
which is highly toxic and carcinogenic. The normal allele is
represented by ALDH2 * 1, while the inactive variant is ALDH2 * 2.
The presence of the variant involves the accumulation of a higher
concentration of acetaldehyde. This favors the mechanisms of
carcinogenesis.
Single nucleotide polymorphism (SNP) may also be present
in the structure of ADH. The presence of ADH1B * 2, for example,
ensures an activity 40 times higher. In these individuals the
metabolism of ethanol will be more effective and faster. This
provides protection against cancer [9].
From these examples it can be deduced that a genetic pattern,
at an equal frequency of consumption and dosing, leads to
unpredictable individual variations.
The correlation of alcohol consumption and cancer
In the past twenty years, the meta-analyses linking the
consumption of alcohol with cancer have been particularly
numerous. The cancers related to consumption are: oral cavity,
pharynx, larynx, esophagus, colon-rectum, liver and breast. There
is a possible correlation with stomach, pancreas, lung, prostate
and bladder cancers.
Boffetta et al. (2006) [14] estimated that about 3.6% of
cancers in the world are related to the consumption of alcoholic
beverages (5.3% in males and 1.7% in females). Considering that
in different areas of the world there is no consumption of alcohol,
mainly for religious reasons, this percentage is particularly
significant in the Western world and in Eastern Europe.
Table 1: Chronic consumption of alcoholic beverages: Proposal of a
scheme for the identification of risk in a healthy subject.
Very low risk:
Woman 3g / day between 45 and
65 years
Man 9 g / day between 45 and 65
years
Low Risk: Woman <10 g / day
Man <20 g / day
Risky Consumption: Woman 10-40 g / day
Man 20 and 60 g / day
“Binge drinking” (60 grams in a
single occasion)
Doses greater than 12 grams over
65 years
Harmful Consumption: Woman over 40 g / day
Man over 60 g / day
Alcohol dependence (mild, moderate, severe)
Table 2: Oncological screening in alcohol.
Head and Neck
Oral Cavity -
Pharynx
Neurological examination
Larynx ENT Visit
Esophagus /
Stomach
Testing for Hp infection and /or endoscopy with
biopsies
Colon-Rectum Fecal occult blood testing and/or colonoscopy
Hepato-biliary
System
If cirrhosis; US every 6 months
If chronic alcoholic liver disease; US every 6 months
If chronic pancreatic alcoholic liver disease; US every
6 months
Testing for HBV, HCV, HIV infection
Lung Chest X-ray
Breast
US <40 years
Mammography and US > 40 years

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The most affected areas of the world among males are:
European area C (including the Russian Federation) with a
correlation of about 9%; European area A (covering Western
Europe); African area E; and Western Pacific B, with a correlation
of approximately 6.5%. Regional differences in terms of risk
can be attributed to several factors: regional variations in the
prevalence of consumption, recruitment procedures, other
carcinogenic substances present in alcoholic beverages, the local
genetic structure of different populations and other associated
risk factors.
The cancers most causally related to alcohol worldwide are:
30.4% of cancers of the oral cavity and pharynx, 18.5% of cancers
of the esophagus, 3.2% of cancers of the colon-rectum, 9.4% of
cancers of the liver, 23% of cancers of the larynx and 4.5% of
breast cancers in women. In addition, 3.5% of all cancer deaths
globally are alcohol-related: 25.9% of deaths from cancers of the
oral cavity and pharynx, 18.1% from cancers of the esophagus,
3.1% from cancers of the colon and rectum, 9.4% from cancers
of the liver, 21.4% from cancers of the larynx and 4.1% from
cancers of the breast [14].
It has been shown that in Europe (Denmark, Germany, Greece,
Italy, Spain and Great Britain) 10% of cases in males and 3% in
females can be attributed to alcohol consumption [15]. In both
sexes, the percentage is higher for cancers of the upper digestive
tract-plane (44% males, 25% females), followed by cancers of the
liver (33% males, 18% females), then colorectal cancer (17% in
males, 4% in females) and finally breast cancer (5%).
The percentage increases if the daily dose exceeds two units
/ day for men and 1 unit / day for women: 10% of colorectal
cancers, 27% of liver cancers and 38% of cancers of the upper
digestive tract.
Recently, Nelson et al. [16] found that in the USA, 3.5% of all
cancer deaths are attributable to alcohol. In particular, 26-35%
of all alcohol-related cancers are caused by a consumption of less
than 20 grams per day.
Meta-analyses by Bagnardi et al. (2001) [17], Corrao et al.
(2004) [18], Boffetta et al. (2006) [14] and Nelson et al. [16]
show, in addition, that an increased risk is dose dependent.
It has also been reported that 68% of cancers of the upper
aero-digestivetract are related to the contemporary consumption
of alcohol and smoking tobacco [19]. Selected studies have
demonstrated that the dose-response effect is also present in
non-smokers.
For medium dosages of 21.5 units / day in males and 16.4
units / day in females (population of alcoholics), Thyngesen et al.
(2009) [20] found an increased risk at other sites: the gallbladder,
the digestive organs and the peritoneum, pleura, lung, kidney,
prostate, cervix, ovary and skin. This study included 15258 males
and 3552 females, who were followed up for a period of about
40 years.
Saieva et al. [21] calculated that alcohol dependency in a
population increased the mortality rate by just under 5-fold
compared to the general population. Alcohol-dependent
women were the most affected; this was confirmed in a study
by Thyngesen et al. [20], which found that the possibility of the
occurrence of cancer can affect different areas of the body.
CANCER SITES
The Oral Cavity and Pharynx
In a previous review [13] we evidenced how alcohol is the
most recognized risk factor in the cancer of the oral cavity and
the pharynx, and together with tobacco it is the cause of most
cases in developed countries (75% of cases). The relative risk
(RR) is also significant in non-smokers [22].
In the oral cavity the detrimental effects of alcohol are well
known on both an extracellular and intercellular level. Via these
mechanisms, carcinogens can act on the proliferative activity
of stem cells on the basal layer. In patients with oropharyngeal
cancer a significant increase in the concentration of salivary
acetaldehyde has been detected. This is also related to poor
oral hygiene and to cigarette smoking. These behaviors increase
the production of acetaldehyde by means of bacterial flora [5].
Seotz and Meier [5] evidenced how smoking changes the flora
from being predominantly Gram –, progressively evolving to
being predominantly Gram + with a concomitant increase in the
concentration of acetaldehyde by 50-60%, as compared to non-
smokers. It is worth pointing out that smokers who are exposed
to even moderate amounts of alcohol can significantly increase
the concentrations of acetaldehyde, whereby the most affected
oral sites are the ventral tongue and the floor of the mouth
[8,9,13].
Altieri et al. [22] detected a dose-dependent risk, with an odds
ratios (OR) of 2.1 for multivariate 3-4 units / day, 5 for 5-7 units
/ day, 12.2 for 8-11 units / day and 21.1 for more than 12 units
/ day [13,19]. A meta-analysis by Tramacere et al. [23] recently
showed an increase in risk for a consumption of less than 1
unit / day, with a progressively dose-dependent increase. More
recently, Roswall and Weiderpass [24] reported the conclusions
of the World Cancer Research Fund (WCRF)/American Institute
of Cancer Research (AIRC) [25]. The WCRF identified five cohort
studies and the AIRC identified nine studies. They showed a RR
per drink/weekly of 1.24 (95% confidence interval, 1.18 to 1.30)
[24,25].
The Larynx
Numerous epidemiological studies have shown that alcohol is
an independent risk factor for laryngeal cancer [1,2].
Islami et al. [26] found in a recent meta-analysis that the risk
significantly increases for doses of little more than one unit / day.
This increase in risk is also present in non-smokers [27].
The risk of laryngeal cancer is influenced by genetic
variations: in particular the polymorphisms of genes that control
DNA repair capability (“nucleotide excision repair”) [28].
The Esophagus
Between 50% and 75% of all cases of esophageal cancer
are attributable, in both males and females, to alcohol. Ethanol
promotes, through alterations to the motility and tone of the
lower esophageal sphincter, gastro-oesophageal reflux and

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consequent esophagitis [13]. This disease is a condition of risk for
the development of Barrett’s esophagus (intestinal metaplasia),
dysplasia and adenocarcinoma. The chronic inflammation makes
the esophageal mucosa more susceptible to nitrosamines and
polycyclic aromatic carbohydrates [13]. These substances may
be present in alcoholic beverages or in pre-cancerous substances
converted in the liver. In addition, we remember the direct
carcinogenic action of acetaldehyde that is formed in the oral
cavity from the metabolization of ethanol by bacterial flora [13].
Several studies (prospective and case control) have shown a
significant association between esophageal cancer (particularly
squamous cells) and alcohol. The risk is dose dependent [1,2,13].
The relative risk (RR) increases significantly when there is an
association with smoking. If you correlate more than 20 cigarettes
/ day with 1-4 units / day, the RR increases to 5.1 times; if you
consume between 4 to 8 units / day, the RR increases to 12.3;
and if consumption is greater than 8 units / day, the RR increases
by 44.4-fold [29]. The synergistic effect of this combination is
important, because the majority of subjects who use alcohol are
also chronic smokers (about 75%).
Jarl and Gerdtham [30] affirm that the risk is reversible
following drinking cessation. They conclude that it is most
likely that about 16 years are required until all elevated risk has
disappeared.
The Stomach
The general population has shown a modest increase in
risk [2]. A high risk has been reported in the alcohol-dependent
population, especially in males [2]. The risk of gastric cancer
has also increased in social drinkers suffering from infection by
Helicobacter pylori (Hp). It is known, in fact, that this bacterium
possesses ADH and, therefore, there is an increase in the gastric
mucosa of acetaldehyde [6].
The Colon-Rectum
Several meta-analyses have evidenced a positive dose-
response relationship between alcohol consumption and
colorectal cancer [9,13]. These studies have shown an increase
in relative risk of about 10-20% with a chronic consumption of
about 50 g / day. Likewise, there is an association for both colon
and rectal cancer [1,2,13].
Concerning cancer of the colon-rectum, an RR of 7.4 with
a dosage of 20 g / day [9] was indicated. An important role is
played by the production of acetaldehyde by bacterial flora.
For this reason ALDH polymorphisms are particularly
relevant. It has been suggested that, in this area, alcohol may
promote cancer by disturbing the equilibrium characterized by
a balanced transfer of methyl groups in combination with an
appropriate concentration of folates. It has been proposed that
the role of alcohol may be particularly relevant in the presence
of precancerous conditions such as, for example, aberrant crypt
foci [29,31].
There is no consistent evidence of any influence from smoking
[1,2].
The Liver
The association of alcohol consumption and hepatocellular
carcinoma (HCC) is well known: different assessments made
by both American and Italian groups have indicated that such
a correlation is present in 32-45% of cases. The occurrence of
HCC in the context of early-stage chronic liver disease is possible
(especially in combination with other risk factors). However,
the chain of events is as follows: steatosis, steatohepatitis,
steatofibrosis, cirrhosis and HCC. Cirrhosis itself is a risk factor for
the onset of HCC, even in subjects who have achieved abstinence.
The possibility of the evolution, and especially the speed of the
above sequence is certainly influenced by genetic patterns [32]
and by risk factors or associated comorbidities.
Hassan et al. [33] found this to be true for the intake of large
amounts of alcohol (80 g / day of ethanol) in association with
HCV or HBV-related hepatitis, with an OR of 53.9 (in cases of
isolated hepatitis an OR of 19.1, and in cases of isolated alcohol
consumption an OR of 2.4). In cases with a correlation between
alcohol (> 80 g / day) and diabetes mellitus (both insulin
dependent and non-insulin dependent), there was an OR of 9.9
(for isolated diabetes an OR of 2.4).
In many experiments a model of alcohol-induced
hepatocarcinogenesis has been proposed [8]. This model consists
of a first phase (initiation, direct genotoxicity) and a second
phase characterized by promotion / progression (angiogenesis
induction). In the first phase we witness a mechanism of direct
genotoxicity caused by oxidative stress and the formation
of adducts, in association with a reduction in anti-oxidant
mechanisms [7,34]. Moreover, an aberrant methylation has been
evidenced, Toll-like-receptor alterations and shorter telomere.
In particular, the telomere length decreases in relation to an
increase in drink-units per day [35].
The close correlation between the consumption of alcoholic
beverages and DNA fragmentation suggests that oxidative stress,
which is a result of ethanol metabolism, may be responsible
for direct genotoxic action [36]. A discontinuation of alcohol
consumption was estimated to reduce the annual risk by 6-7%
[36].
The Pancreas
With regard to pancreatic cancer, smoking, in combination
with certain mutations or polymorphisms, is certainly the main
risk factor. The relative risk (RR) is affected by alcohol at 21
units or more of alcohol per week [37]. Recently, Bagnardi et al.
[38] confirmed, through a meta-analysis (572 epidemiological
studies) this correlation only in the presence of huge alcohol
intake. An increase of 19% compared to non-drinkers was
found. This correlation was confirmed even after the removal of
the most important confounding factors: smoking, obesity and
diabetes mellitus.
The Lung
A significant increase in risk in the general population
has been reported in 16 cohort studies [2]. Populations with
risky / harmful alcohol consumption and alcohol-dependent
populations were found to be at high risk in 7 case studies. Korte

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et al. [39] showed the relative risk as being between 1.53 and
1.86 in case-control studies for doses of higher than 5 drinks /
day. Freudenheim et al. [40] reported an increased risk for doses
of higher than or equal to 30 g / day. An increased risk for doses
of higher than 15 g / day in the absence of cigarette smoke has
also been demonstrated.
The Prostate
A correlation between alcohol and prostate cancer was
reported in 2 out of 9 case. This Danish study by Piu et al. reported
by IARC [2] revealed a significant increase in prostate cancer as
compared to the general population.
The relation between alcohol consumption and prostate
cancer was recently confirmed by some authors [41,42]. Bagnardi
et al. [38] reported a significant increase in risk in heavy drinkers.
This correlation was not found in the Asian population [43]. To
date there is no unanimous opinion on this correlation: more
studies are needed before reaching a final conclusion.
The Bladder
To date, the correlation between alcohol consumption and
bladder cancer has not been identified [38]. On the other hand,
the consumption of alcohol promotes bladder cancer in smokers
and probably also in moderate doses [44].
The Breast
4-5% of all breast cancers are alcohol related, and breast
cancer accounts for 60% of alcohol-related tumors in women.
Numerous epidemiological studies have shown a positive
correlation between alcohol consumption and the incidence of
cancer. A risk has also been defined for moderate consumption.
It has been shown that for a 10 g / day increase in ethanol
consumption, there is a 10% increase in the RR [45,46].
In fact, Chen et al. [47] found that the RR increased (though
slightly) at doses of lower than 10 g / day, as well as in a subgroup
characterized by the absence of estrogen receptors, whereas in
a subgroup with a higher prevalence of progesterone receptors
there was an augmented RR at doses of less than 5 g / day. This
experience also confirmed there is no safe dose.
Kwan et al. [48] showed that in overweight women (especially
in those who are post-menopausal) who had already developed
breast cancer, the risk of suffering a relapse significantly
increased with a consumption of 3-4 units / week. Recently,
Romieu et al [49] confirmed the increased risk of alcohol on
breast cancer development. In particular this risk has been
evidenced in women who started drinking before their first full-
term pregnancy. Ethanol consumption was positively associated
with the risk of both estrogen receptor (ER) positive and ER
negative breast cancer risk [13,50,51].
Pathogenic mechanisms are certainly to be found in the
oxidative stress caused by the actions of acetaldehyde and by
changes in nutrition (folate, Vit. B6 and B12), but the main cause
is due to interactions with estrogen. It is known that estrogens
are metabolized by ADH, therefore competing with ethanol.
Particularly high concentrations of acetaldehyde were observed
in association with high levels of estrogen during the menstrual
cycle. The consumption of alcohol is probably involved in the
early stages of carcinogenesis caused by an increase in insulin-
like growth factor 1, which is linked to an increase in the binding
protein 3 of this growth factor.
Alcohol is one of the few risk factors that can be eliminated
in the prevention of cancer and in particular of breast cancer
[13,52].
The evaluation of the international agency for cancer
research (IARC)
The IARC (World Health Organization) issued the final
data on the relationship between alcohol / cancer in 2007 in
Lyon, which were published in Monograph 96, 2010 [1] and
confirmed in Monograph 100 E 2012 [2]. The IARC classification
provides four target groups: Group 1: Substances carcinogenic
for humans; Group 2A: Substances probably carcinogenic for
humans; Group 2B: Substances with the possibility of being
carcinogenic for humans; Group 3: Substances not classifiable
as being carcinogenic for humans (still under study); Group 4:
Substances probably not carcinogenic for humans.
In particular: 1) alcoholic beverages are carcinogenic for
humans (Group 1). The consumption of alcohol has a causal
relationship with cancers of the oral cavity, pharynx, larynx,
colon-rectum, liver and breast, 2) the free acetaldehyde in alcohol
promotes tumors of the esophagus and of the head and neck
(Group 1). In relation to “point 1” it is interesting to note that the
Agency has clearly used the word “consumption,” thus correlating
alcohol and cancer not only in alcohol-dependent populations.
Several authors have studied the role of free acetaldehyde. The
most authoritative studies on this are by Lachenmeier et al.
[53,54]:
Theauthorsdetectedfreeacetaldehydeinalltypesofalcoholic
beverage. They also found products where the free acetaldehyde
was equal to 0, as distillation reduces the levels of acetaldehyde.
Free acetaldehyde is able to act directly through contact [51]: this
justifies the position in Group 1 of cancers of the head, neck and
esophagus. The Agency stresses that aldehyde dehydrogenase
genetic polymorphisms are particularly important.
The Lachenmeier study [55] identified other substances in
alcoholic beverages included in Group 1: arsenic, formaldehyde,
acrylamide, cadmium, benzene and others. In addition, an
evaluation of the MOE (Margin of Exposition: this parameter
relates the toxicological threshold to the exposure) revealed an
impressive datum: a certain amount of ethanol, or its equivalent
per day in units, is just as potent a carcinogen as other substances
more likely to cause alarm in the general public.
CONCLUSIONS AND PROPOSALS
The conclusions to be drawn from the experimental and
epidemiological evidence fully confirm the correlation between
alcohol and cancer. In view of the relatively high frequency of
certain types of cancer (esophagus, colon, liver, breast) and the

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persistent chronic use of alcohol in our society, the link between
alcohol and cancer should be taken into great consideration in
both prevention programs, and for reaching an early diagnosis.
The aim of prevention and health promotion programs should
be to minimize the use of alcohol in the general population,
reaffirming that the consumption of alcoholic beverages is risky,
as alcohol is a toxic, carcinogenic substance, which involves not
only alcoholics, but also social drinkers.
Some international institutions agree that there is no “safe”
daily amount; however, “low risk” may be considered as follows:
20 g / day for males and 10 g / day for females [56].
It should be stressed, however, regarding the relationship
between alcohol and cancer, several authors and international
organizations have expressed the view, which we fully share,
that the most responsible attitude of health professionals should
be to not to specify “safe” dosages of alcohol. To date, in fact, the
scientific evidence suggests a ratio of alcohol / dose-dependent
cancer with no defined safe threshold [57-59].
The European Code Against Cancer affirms: “if you drink
alcohol of any type, limit your intake. Not drinking alcohol is
better for cancer prevention” [60]. In view of the high incidence
of cancer in people with risky / harmful alcohol consumption
and alcohol dependence, common screening and oncological
prevention programs for the general population should be
discussed again and put in place [61]. In addition, it should
be noted that for a high percentage of cases (over 80% in our
experience), there is a correlation with smoking.
All asymptomatic subjects with past or present risky /
harmful alcohol consumption, and all subjects with a history
of alcohol dependence or alcohol problems should undergo (at
a frequency yet to be determined by the proper guidelines and
compatibility with available economic resources): ENT check-
ups, hepato-biliary-pancreatic ultrasonography, chest X-rays,
breast ultrasonography, mammography, fecal occult blood
testing and / or colonoscopy, testing for Helicobacter pylori
infection and / or esophago-gastro-endoscopy (Table 2).
It should be emphasized that subjects should always undergo
an appropriate internal medical assessment, taking into account
the fact that alcohol can cause the development of around 60
different diseases and 11 different cancers [3, 62-64].
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