Alcohol and Anabolic Steroids

The use of anabolic steroids is often associated with the pursuit of physical performance and aesthetic changes, while alcohol consumption is frequently seen as routine and socially acceptable. However, combining the two raises a warning sign. More recent studies show that, although there are still gaps in understanding the exact mechanisms of this interaction, the concurrent use of alcohol and anabolic steroids may increase the burden on the liver and be part of a broader context of risk behaviors, with consequences that go beyond liver health and include cardiovascular, hormonal, and psychiatric effects.

The non-medical use of anabolic androgenic steroids has grown in various contexts, far beyond professional sports. Today, this use is seen among gym-goers, amateur bodybuilders, and individuals motivated by aesthetic changes or improved physical performance. At the same time, alcohol remains one of the most widely consumed psychoactive substances in the world. When these two exposures overlap, an important public health concern arises: the potential combined effect on the body, especially on the liver¹.

Anabolic steroids alone are already associated with a range of adverse effects. Among the most well-known are hormonal changes, infertility, acne, gynecomastia, increased blood pressure, and mood changes. The liver is also a major concern. Recent reviews show that prolonged use at supraphysiological doses can lead to elevated liver enzymes, cholestasis, hepatic vascular alterations, and even benign or malignant liver tumors in some cases².

Alcohol, in turn, also has toxic effects on the liver and is associated with a broad spectrum of damage, ranging from steatosis to more severe forms of liver disease³. When a potentially hepatotoxic substance such as anabolic steroids is used in an organism already exposed to harmful alcohol consumption, clinical concern becomes even greater.

One of the most well-known studies on the topic analyzed data from the Drug-Induced Liver Injury Network (DILIN) in the United States, focusing on patients with drug-induced liver injury. The authors observed that among individuals with heavy alcohol consumption, anabolic steroids were prominent among the identified causes of drug-induced liver injury. This finding is relevant because it suggests that heavy alcohol use may be more common in groups where anabolic steroids already represent a risk factor for liver damage.

At the same time, the study raised an important point: the authors did not find clear evidence that heavy drinkers necessarily had worse final outcomes—such as liver-related death or the need for transplantation—compared to non-drinkers in that cohort. This does not mean the combination is safe. In practice, the findings suggest that the relationship between alcohol and anabolic steroid–related liver injury is complex and likely involves both biological and behavioral factors.

This point deserves attention. Part of the association between alcohol and anabolic steroids may reflect a broader context of risk behaviors, such as using substances without prescription, high-dose cycles, combining different compounds, and limited medical supervision²⁴. In other words, it is often not just the sum of two potentially harmful agents, but a pattern of use that already increases vulnerability to multiple health problems.

Recent literature also reinforces that the adverse effects of anabolic steroids extend far beyond the liver. A meta-analysis published in 2025 showed that abuse of these substances among athletes and physically active individuals is associated with significant increases in blood pressure and LDL cholesterol, highlighting their cardiovascular impact⁴. This broadens the discussion: individuals who use anabolic steroids and consume excessive alcohol may be exposing themselves to a combination of hepatic, metabolic, and cardiovascular risks simultaneously.

Another recent review highlighted that androgen abuse is associated with increased mortality and multisystem adverse effects, including cardiovascular toxicity, infertility, hypogonadism, hepatotoxicity, and mental health disorders³. This helps dispel the idea that anabolic steroids produce only “aesthetic” or “hormonal” effects. In reality, these substances can have wide-ranging impacts on the body, especially when used outside a medical context.

It is also important to distinguish between supervised therapeutic use and non-prescribed use. Recent studies show that individuals who use anabolic steroids without medical indication experience more adverse events than those undergoing clinically supervised testosterone therapy. This reinforces that risk is particularly concentrated in recreational, aesthetic, or performance-oriented use—often done without clinical monitoring, regular testing, or appropriate dosing, and sometimes involving unsafe combinations.

From a mental health and behavioral perspective, this combination also warrants caution. Recent reviews describe associations between anabolic steroid abuse and mood changes, aggression, impulsivity, and other psychiatric effects. Since alcohol is also linked to reduced self-control and increased exposure to accidents, violence, and risky decisions, the combination of these substances should not be viewed solely as a liver issue, but as a broader health concern.

From a prevention standpoint, the main message is clear: although more studies are needed to precisely define the biological interaction between alcohol and anabolic steroids, the existing body of evidence is sufficient to treat this combination with seriousness. It is not a trivial combination, especially when it involves heavy alcohol consumption, prolonged steroid use, oral compounds, and lack of medical supervision.

In summary, current evidence indicates that:

• Non-medical use of anabolic steroids is associated with risk of liver injury and other significant systemic adverse effects;
• Heavy alcohol consumption remains an important factor in liver damage;
• The combination of alcohol and anabolic steroids deserves special attention, both because of potential biological overload and the broader context of risk behaviors in which it often occurs.

Informing the public about these risks is essential to counter the normalization of anabolic steroid use and excessive alcohol consumption. In public health, waiting for absolute certainty about every mechanism before issuing warnings is often a mistake. When signals of harm are already consistent, prevention remains the best course of action.

References:

• 1. Dakhoul, L., Ghabril, M., Gu, J., Navarro, V., Chalasani, N., & Serrano, J. (2018) Heavy Consumption of Alcohol is Not Associated With Worse Outcomes in Patients With Idiosyncratic Drug-induced Liver Injury Compared to Non-Drinkers.
  2. Petrovic A, Vukadin S, Sikora R, Bojanic K, Smolic R, Plavec D, et al. Anabolic androgenic steroid-induced liver injury: An update. World J Gastroenterol. 2022;28(26):3071-3080.
  3. Grant B, Hyams E, Jenkins N, Jayasena CN. Androgen abuse: Risks and adverse effects in men. Ann N Y Acad Sci. 2024;1538(1):56-70.
  4. Liu M, Yu Y. Adverse effects of anabolic androgenic steroid abuse in athletes and physically active individuals: A systematic review and meta-analysis. Subst Use Misuse. 2025;60(6):873-887.
• Journal Impact Factor: 7,683
• D.O.I.: https://doi.org/10.1016/j.cgh.2017.12.036

Pancreas Under Pressure: The Silent Enemy of Alcohol Excess

For a long time, science has tried to unravel a major mystery: why does only a small minority of people who drink large amounts of alcohol develop acute pancreatitis?¹ The answer tells an intriguing story about how our bodies react to excess. It is important to emphasize that alcohol-related acute pancreatitis is strongly associated with chronic, heavy alcohol consumption. Moderate or occasional drinking does not cause pancreatitis. Prolonged heavy drinking leads to changes that make the pancreas vulnerable to an acute crisis.

Alcohol itself, or even the substances produced when the body processes it, cannot cause the disease on their own.² Instead, intense and prolonged alcohol consumption acts silently, reducing the pancreas’s natural chemical signaling and causing its fluids to become highly concentrated, acidic, and thick.

This situation is worsened because long periods of alcohol use are often accompanied by poor nutrition and low water intake.¹ This dehydration and relative fasting contribute to the formation of “sludge” or small protein plugs that temporarily block the tiny ducts through which pancreatic and bile fluids should flow. The danger may also arise when a person stops drinking, because after interrupting alcohol consumption and returning to normal eating—especially heavier or fatty foods—the body sends a strong signal and overstimulates the pancreas, which had been operating at a reduced pace.³ It is not the interruption of drinking or the return to normal eating that causes the crisis; rather, the crisis is triggered by the heavy alcohol intake that occurred beforehand.

Imagine a hose running at maximum pressure but with its end blocked. This is essentially what happens in the pancreas: it is forced to produce and secrete digestive juices intensely against blocked ducts.¹ Unable to flow out, these enzymes begin to act within the organ itself, effectively digesting pancreatic tissue, damaging cells, and triggering a cascade of severe inflammation. To make matters worse, continuous alcohol use weakens the pancreas’s natural defense mechanisms against this stress—an effect that is even stronger in people who also smoke.⁴

Symptoms of acute pancreatitis (severe abdominal pain, nausea, vomiting) may not appear immediately after the last drink. Pain can occur hours—or even one or two days—after excessive alcohol intake. During this interval, the person may have already stopped drinking and even tried to eat normally before symptoms become severe enough to require hospitalization. Returning to a normal diet, especially one high in fat, may simply worsen the symptoms of an already developing pancreatitis.

Acute pancreatitis is a serious medical emergency, and although medicine continues to search for treatments that can halt the disease at its origin, rapid diagnosis combined with intensive hospital support remains the most effective and safest way to stabilize the patient and save their life.

References

1. Nordback, I., Paajanen, H., & Pandol, S. (2026). Understanding How Alcohol Induces Human Acute Alcoholic Pancreatitis. The American journal of pathology, 196(1), 68–77. https://doi.org/10.1016/j.ajpath.2025.03.008
2. Apte MV, Pirola RC, Wilson JS: Alcohol and the pancreas. Pancreapedia: Exocrine Pancreas Knowledge Base; 2016. Disponível em: https://pancreapedia.org/reviews/alcohol-and-pancreas, acessado em 1 de dezembro de 2024
3. Deng, X., Wood, P. G., Eagon, P. K., & Whitcomb, D. C. (2005). Rapid adaptation of pancreatic exocrine function to short-term alcohol feeding in rats. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 5(2-3), 183–195. https://doi.org/10.1159/000085270
4. Pallagi, P., Tóth, E., Görög, M., Venglovecz, V., Madácsy, T., Varga, Á., Molnár, T., Papp, N., Szabó, V., Kúthy-Sutus, E., Molnár, R., Ördög, A., Borka, K., Schnúr, A., Kéri, A., Kajner, G., Csekő, K., Ritter, E., Csupor, D., Helyes, Z., … Hegyi, P. (2024). Heavy metals in cigarette smoke strongly inhibit pancreatic ductal function and promote development of chronic pancreatitis. Clinical and translational medicine, 14(6), e1733. https://doi.org/10.1002/ctm2.1733

Parenting Styles and Substance Use: What a Study with Brazilian Families Shows

The use of alcohol, cigarettes, marijuana, and e-cigarettes among adolescents does not depend only on individual choices: parents’ behavior and the way they raise their children play a decisive role. A recent study conducted with more than four thousand adolescents in the state of São Paulo showed that, although there is a strong similarity between substance use patterns in parents and their children, this “cycle” is not inevitable. In particular, more structured and affectionate parenting styles can reduce the risk of heavy use of multiple substances during adolescence.

Adolescence is a period of greater vulnerability for initiating the use of psychoactive substances such as alcohol, tobacco, marijuana, and, more recently, e-cigarettes. These behaviors are associated with physical and mental health problems, academic difficulties, and a higher risk of dependence in adulthood. At the same time, many adolescents live with parents who also use these substances, raising the question: to what extent does parents’ use “transfer” to their children?

The study, published in the journal Addictive Behaviors, analyzed 4,280 dyads (pairs) consisting of adolescents aged 12 to 17 and their parents or guardians in four municipalities in the state of São Paulo¹. The researchers used a statistical approach called latent class analysis to identify substance use profiles among parents and adolescents, considering alcohol, binge drinking (episodes of heavy drinking), cigarettes, marijuana, and e-cigarette use. Instead of examining each drug separately, the study focused on behavioral patterns, such as abstainers, primarily alcohol users, and multiple-substance users.

Three main groups were identified among both parents and adolescents: an abstinent or very low-use group, a higher alcohol-use group, and a polysubstance use group, involving the combined use of several substances. Among parents, about half were in the low-risk group, while approximately one in eight was classified as a polysubstance user. Among adolescents, most were abstinent, but a smaller group reported recent alcohol consumption, binge drinking episodes, and use of other products, including vapes.

One of the study’s key findings was the strong correlation between parent and child profiles. When parents were abstinent, there was about a 90% probability that the adolescent would also not use substances. On the other hand, when parents belonged to the polysubstance group, the likelihood that the adolescent would also be a polysubstance user was approximately three times higher compared to children of abstinent parents. Even so, more than half of adolescents in families where parents used multiple substances remained abstinent, showing that intergenerational transmission is not automatic.

To better understand why some adolescents “escape” this family risk pattern, the study examined the role of parenting styles. Four classic styles were considered: authoritative (high warmth and high control), authoritarian (low responsiveness and high control), permissive (high warmth and low control), and neglectful (low responsiveness and low control). These styles were measured based on adolescents’ perceptions of how close their parents are, how much they communicate, set rules, and monitor behavior.

The results showed that the authoritative style had an important protective effect. Among adolescents with polysubstance-using parents, those who perceived their caregivers as authoritative were less likely to fall into the polysubstance group and more likely to remain abstinent. In other words, even when parents use substances at high levels, a parenting style that combines affection, supervision, and clear rules can significantly reduce the risk of heavy multiple-drug use during adolescence.

The authoritarian style also showed some protective effect against polysubstance use, reducing the likelihood that adolescents with high-risk parents would become polysubstance users. However, this style was associated with a greater likelihood of specific transmission of alcohol use—that is, it increased the probability that children of parents who drink would also consume alcohol. Permissive and neglectful styles did not show consistent protective effects, and in some cases estimates were limited by the small number of adolescents in certain profile combinations.

An important point is that, even in contexts with more protective parenting styles, parental alcohol consumption remained associated with a higher risk of alcohol use among adolescents. This suggests that, in the case of alcohol, the influence of modeling and normalization within the household may be particularly strong, possibly because it is a legal, widely available, and socially accepted substance.

From a public health perspective, the study highlights two key messages. First, substance use patterns are partly “inherited” within families, both in terms of risk and protection. Abstinent or low-consuming parents tend to have children who also do not use drugs, indicating that healthy behaviors can be transmitted across generations. Second, even when parents engage in risky use, more structured parenting styles—characterized by presence, warmth, and clear limits—can reduce the likelihood that adolescents will develop patterns of polysubstance use.

These findings reinforce the importance of prevention programs that involve families, not just adolescents. Interventions that strengthen parenting skills, promote dialogue, encourage consistent rules, and address beliefs about alcohol and other drugs can have a meaningful impact on reducing substance use among young people. At the same time, the study underscores that policies and actions aimed at reducing risky substance use among adults also indirectly benefit the next generation.

In summary, the article shows that:

• There is strong alignment between substance use profiles of parents and children, especially in the case of abstinence.
• Polysubstance-using parents increase the risk of polysubstance use among adolescents, but this risk is not inevitable.
• Authoritative and, to some extent, authoritarian parenting styles can mitigate intergenerational transmission of polysubstance use, although they do not eliminate the effect of parental alcohol consumption on children’s alcohol use.
• The combination of parental modeling and the quality of relationship and supervision appears crucial to understanding why some adolescents use substances while others, in similar contexts, remain abstinent.

Informing parents, educators, and policymakers about these mechanisms is essential for developing more effective prevention policies and programs aimed at reducing alcohol and other drug use during adolescence.

References

1. Sanchez Z, Caetano S, Valente JY, Soares-Santos LE, Cogo-Moreira H. Does the apple fall far from the tree? When parenting styles disrupt the intergenerational pattern of substance use. Addictive Behaviors. 2026;174:108567. doi:10.1016/j.addbeh.2025.108567

Alcohol, Calories, and Obesity: What Does the Scientific Evidence Say

The consumption of alcoholic beverages provides significant calories to the diet and may influence the risk of weight gain and obesity. Recent scientific studies show that this relationship is complex: while low alcohol intake is not always associated with weight gain, higher levels of consumption are linked to a greater likelihood of overweight and obesity, especially abdominal obesity.

Obesity is currently one of the main public health challenges worldwide. It is associated with cardiovascular diseases, diabetes, cancer, and reduced life expectancy. Among the various factors contributing to weight gain, alcohol consumption has received increasing attention from the scientific community.

Alcohol provides approximately 7 kcal per gram, an energy value close to that of fat (9 kcal/g) and higher than that of carbohydrates and proteins, both with 4 kcal/g. These calories can contribute to a positive energy balance, especially when consumption is frequent or in large amounts¹.

A comprehensive review published in the journal Critical Reviews in Food Science and Nutrition, which analyzed 127 observational studies, investigated the relationship between alcohol intake and excess weight¹. The results indicated that, in cross-sectional studies, alcohol consumption was associated with a higher likelihood of overweight and abdominal obesity. When the analysis considered the amount consumed, high intake (above 28 g of alcohol per day) was associated with a greater probability of overweight and abdominal obesity compared to non-drinkers or light drinkers. In contrast, light consumption did not show a consistent association with obesity in cohort studies.

Another meta-analysis, published in the Journal of Epidemiology and Public Health, specifically evaluated adults and found that alcohol consumption was associated with approximately a twofold increase in the likelihood of obesity in the studies included in the analysis². The study also highlighted that age influences this risk, as metabolism and physical activity patterns tend to change over the course of life.

Beyond the caloric aspect, more recent research suggests that the relationship between alcohol and obesity may go beyond simply counting calories. An article published in the journal Molecular Psychiatry discusses how alcohol and obesity share similar biological mechanisms, involving brain reward circuits, appetite regulation, gut hormones, and systemic inflammation³. This means that alcohol consumption may influence eating behavior, the feeling of satiety, and even preferences for higher-calorie foods.

Another relevant point is that alcohol can affect liver metabolism and promote fat accumulation in the liver, especially when consumed excessively. When combined with excess weight, the risk of liver disease increases significantly³. Studies show that the combination of obesity and high alcohol consumption can accelerate the development of liver diseases.

It is important to note that results vary according to the pattern of consumption. Light or occasional drinking does not show a consistent association with obesity in longitudinal studies¹. On the other hand, heavy and regular consumption is more frequently associated with weight gain and abdominal obesity, a type of body fat that carries greater cardiometabolic risk.

From a public health perspective, these findings reinforce that alcohol should be considered not only for its effects on the liver, brain, and risk of dependence, but also as a relevant source of calories in the diet. Reducing excessive consumption may contribute not only to a lower risk of alcohol-related diseases, but also to better body weight control.

In summary, scientific evidence indicates that:

• Alcohol provides significant calories and may contribute to a positive energy balance.
• High consumption is associated with a greater likelihood of overweight and obesity, especially abdominal obesity.
• Light consumption shows inconsistent results regarding obesity risk.
• Alcohol and obesity share biological mechanisms related to appetite regulation and reward.

The relationship between alcohol and obesity depends on dose, frequency, drinking pattern, and individual characteristics. Informing the public about this evidence is essential for making informed health decisions.

References

1. Golzarand M, Salari-Moghaddam A, Mirmiran P. Association between alcohol intake and overweight and obesity: a systematic review and dose-response meta-analysis of 127 observational studies. Crit Rev Food Sci Nutr. 2021. doi:10.1080/10408398.2021.1925221
2. Wulandari AN, Hanida AN. Meta-Analysis: Relationship between Alcohol Consumption and Age on Obesity in Adults. J Epidemiol Public Health. 2022;7(2):153–166. doi:10.26911/jepublichealth.2022.07.02.01
3. Leggio L, Farokhnia M, Kenny PJ, Pepino MY, Simmons WK. Crosstalk between alcohol use disorder and obesity: two sides of the same coin? Mol Psychiatry. 2025;30:5938–5952. doi:10.1038/s41380-025-03259-8

How Harmful Alcohol Consumption Impacts People with Heart Disease: Evidence from the PROSA Project

Alcohol consumption is a common behavior in the general population and, in some contexts, is still associated with the idea of potential cardiovascular benefits when consumed in moderation. However, recent scientific evidence shows that harmful alcohol use represents an important risk factor in people with heart disease. A Brazilian study published in 2025, conducted within the framework of the PROSA Project (Health and Alcohol Project), analyzed the relationship between lifestyle patterns and harmful alcohol consumption in patients with heart disease, bringing relevant findings for clinical practice and public health.

Harmful alcohol consumption is associated with increased morbidity and mortality, especially among individuals with cardiovascular diseases. Although light to moderate drinking has historically been described as potentially protective in some populations, this relationship does not hold when considering patterns of abusive alcohol intake, particularly in patients with established heart disease.

The PROSA Project study, published in the Arquivos Brasileiros de Cardiologia, evaluated more than 4,000 individuals¹, including patients with heart disease and volunteers without cardiopathy, using standardized instruments to measure both alcohol consumption and lifestyle behaviors. Harmful consumption was identified using the AUDIT-C test, while lifestyle was assessed through a specific score that considered factors such as smoking, physical inactivity, excess weight, anxiety, and depression.

The results showed that patients with heart disease and lifestyle behaviors classified as fair or unhealthy were more likely to engage in harmful alcohol consumption, even after adjusting for age and sex. In addition, the study demonstrated that improvements in lifestyle over time were associated with a significant reduction in abusive alcohol consumption, reinforcing the dynamic and potentially modifiable nature of this behavior.

Another relevant finding was the higher prevalence of abusive consumption among men and younger individuals, whereas prevalence was lower in older age groups. These data suggest that behavioral and psychosocial factors play a central role in alcohol consumption patterns among cardiac patients, more so than isolated clinical aspects of heart disease.

The study also highlights that abusive alcohol consumption in patients with heart disease may worsen preexisting conditions, increase the risk of arrhythmias, heart failure, and other cardiovascular events, as well as compromise treatment adherence and quality of life. Therefore, systematic lifestyle assessment emerges as an important tool to identify individuals at higher risk and to guide preventive interventions.

In conclusion, the evidence indicates that harmful alcohol consumption in people with heart disease is strongly associated with unfavorable lifestyle behaviors. Rather than being an isolated factor, alcohol is part of a broader set of habits that, when unhealthy, significantly increase cardiovascular health risks. Early identification of these behaviors and the promotion of lifestyle changes may effectively contribute to reducing abusive alcohol consumption and improving clinical outcomes in patients with heart disease.

References:

1. Martinelli-Filho M, Spaggiari CV, Baroni RV, Gomes CIG, Hueb TO, Martins SAM, et al. Consumo abusivo de álcool em cardiopatas: análise de risco pelo comportamento de estilo de vida – Projeto PROSA (Projeto Saúde e Álcool). Arquivos Brasileiros de Cardiologia. 2025;122(10):e20240744. doi:10.36660/abc.20240744