Why You Should Never Drink Alcohol
Sorry in advance, but your body does not want a glass of 2015 Château Margaux
Alcohol has always been depicted as a reward, a way to unwind after a hard day, or a way to celebrate something great. It is the great connector among friends and colleagues at the end of a long workweek and is built into nearly every ritual of modern life. A drink to relax, a toast to success, a glass to take the edge off.
Living in California wine country, then relocating to the land of the local pub in London, I am implicated in this as well. Yet the more research I do on metabolic health, inflammation, and chronic disease, the clearer the picture becomes, and it is not a flattering one. Behind the marketing lies one of the most underestimated drivers of metabolic illness and chronic inflammation.
Once we have a drink, alcohol hijacks our biochemistry. It consumes a coenzyme called NAD+, which is required for mitochondrial energy production and repair. It generates reactive oxygen species (ROS), driving oxidative stress, lipid peroxidation, and inflammation.
Over time, this cascade contributes to insulin resistance, hepatic steatosis, endothelial dysfunction, and neuroinflammation. These are the same biological pathways that underpin Type 2 diabetes, cardiovascular disease, and cognitive decline.
So, is it only heavy drinking that does damage, or does a single drink matter? Research increasingly shows that even small amounts can shift metabolism in the wrong direction.
There is truly no safe dose.
One beer or a glass of wine still depletes NAD+ and activates the same oxidative cascade. The myth of ‘healthy moderation’ was built on outdated epidemiology, and newer studies reveal what biochemists have long known: ethanol is a mitochondrial toxin.
Alcohol also dismantles the gut-liver-brain axis, weakening the intestinal barrier, altering microbial balance, and allowing bacterial endotoxins to enter circulation. This translocation activates immune signaling through toll-like receptors and drives systemic inflammation.
With enough time, this biological stress amplifies metabolic syndrome, the cluster of insulin resistance, dyslipidemia, hypertension, and abdominal fat accumulation that underlies most chronic disease.
Metabolic syndrome is not simply a lifestyle diagnosis. It is a systemic breakdown in energy regulation. Alcohol accelerates that process by increasing triglycerides, promoting hepatic fat accumulation, and depleting NAD+ reserves needed for mitochondrial repair. By impairing mitochondrial efficiency, altering neurotransmitter signaling, and spiking blood sugar, alcohol produces the very anxiety, fatigue, and irritability it claims to relieve.
Restoration of our health comes from our body’s ability to repair, and alcohol erodes that capacity. In our modern culture, which has become the poster child for rampant stress and inflammation, not drinking may be the greatest act of love we can show ourselves.
This piece builds on the threads from my earlier essays — The Cell Danger Response and Restoring Harmony in Our Immune System, both of which explore how chronic stress, oxidative load, and energy imbalance shape our biology. Alcohol sits at the center of that conversation because it amplifies every pathway that drives inflammation and mitochondrial dysfunction. The more we understand these mechanisms, the more clearly we see that resilience isn’t found in moderation; it’s built through restoration.
References
Fairfield, B., & Schnabl, B. (2021). Gut dysbiosis as a driver in alcohol-induced liver injury. JHEP Reports, 3(1), 100220. https://doi.org/10.1016/j.jhepr.2020.100220
Kang, H., Park, Y. K., & Lee, J. Y. (2021). Nicotinamide riboside attenuates inflammation and oxidative stress by activating SIRT1 in alcohol-stimulated macrophages. Laboratory Investigation, 101(9), 1225–1237. https://doi.org/10.1038/s41374-021-00599-1
Lee, J., Lee, J.-Y., & Kang, H. (2025). Excessive alcohol consumption: A driver of metabolic dysfunction and inflammation. Frontiers in Toxicology, 7, 1670769. https://doi.org/10.3389/ftox.2025.1670769
León, B. E., Kang, S., Franca-Solomon, G., Shang, P., & Choi, D. S. (2021). Alcohol-induced neuroinflammatory response and mitochondrial dysfunction on aging and Alzheimer’s disease. Frontiers in Behavioral Neuroscience, 15, 778456. https://doi.org/10.3389/fnbeh.2021.778456
World Health Organization. (2023, January 4). No level of alcohol consumption is safe for our health. https://www.who.int/news/item/04-01-2023-no-level-of-alcohol-consumption-is-safe-for-our-health
It is never too late to stop drinking alcohol, even in end-stage liver disease.
In advanced liver disease, abstaining from alcohol can reduce ongoing oxidative damage, stabilise metabolic pathways, and improve the efficacy of medical interventions. It may not reverse cirrhosis, but it can slow further deterioration, reduce complications, and enhance quality of life.
The body’s capacity for repair is remarkable and removing alcohol restores the biochemical conditions necessary for healing. In this context, choosing sobriety is not just a lifestyle change; it is a scientifically supported act of metabolic restoration.
In my clinic and in my own life, I have learned that prevention works best when people feel supported, not judged. We can talk honestly about alcohol risk and still enjoy our lives, our friendships, and our celebrations without guilt.