glutathione (increasing NAD+) in Spinach/spirulina neutralizes acetaldehyde, toxic byproduct of alcohol digestion via enzyme systems: 40% of people have fatty liver disease

  

Capsaicin, the active compound in chili peppers,

shows promise in treating non-alcoholic fatty liver disease (NAFLD) by reducing fat accumulation, inflammation, and fibrosis. It acts by promoting fatty acid oxidation, inhibiting liver lipogenesis, improving gut microbiota, and activating AMPK signaling.

Yes, coffee can help reduce fatty liver, with studies showing it's associated with lower risk, reduced liver fat, and improved fibrosis/cirrhosis, especially with 2-4 cups daily, though benefits depend on black coffee  The results revealed that tea supplementation significantly prevented liver steatosis, decreased oxidative stress and inflammation, and modulated gut microbiota ...The oolong tea (semi-fermented), black tea (deep-fermented) and dark tea (post-fermented) have received increasing attention on the regulation of gut microbiota in recent years, because many microbes and metabolites were produced in the fermented process [27,28,29,30].

Yes, certain terpenes and terpenoids have shown potential to reduce liver fat

, alleviate non-alcoholic fatty liver disease (NAFLD), and improve hepatic lipid metabolism in preclinical studies. Compounds like d-limonene and beta-myrcene help by reducing oxidative stress, inhibiting fat accumulation, and regulating metabolism https://pmc.ncbi.nlm.nih.gov/articles/PMC9822439/

  In total, we found 43 terpenoids used in the treatment of NAFLD. Over a dozen terpenoid compounds of natural origin were classified into five categories according to their structure: monoterpenoids, sesquiterpenoids, diterpenoids, triterpenoids, and tetraterpenoids. We found that terpenoids play a therapeutic role in NAFLD, mainly by regulating lipid metabolism disorder, insulin resistance, oxidative stress, and inflammation. The AMPK, PPARs, Nrf-2, and SIRT 1 pathways are the main targets for terpenoid treatment.

NADH (reduced nicotinamide adenine dinucleotide) is primarily "neutralized"—or more accurately,

oxidized back to

$NA{D}^{+}$

—through processes that transfer its high-energy electrons to other molecules, allowing cellular respiration to continue.

Under aerobic conditions, the enzyme NADH dehydrogenase (Complex I) in the inner mitochondrial membrane accepts two electrons from NADH, converting it back to

$NA{D}^{+}$

while pumping protons to drive ATP synthesis.

Significance: This is the primary, most efficient method for NADH oxidation in aerobic cell

Alcohol produces DNA mutations primarily by breaking down into acetaldehyde, a toxic byproduct that causes direct damage, such as interstrand crosslinks (ICLs) and double-strand breaks.

acetaldehyde, which binds to DNA and inhibits its repair. 

Also high sugar consumption can create sufficient reactive oxygen species (ROS) to cause significant DNA damage

. Excessive glucose and fructose increase intracellular ROS through mitochondrial overload, metabolic pathways, and glycation, leading to strand breaks, base modifications (e.g., 8-OHdG), and mutation. Free radicals are highly reactive atoms or molecules with unpaired electrons (often oxygen-based, thus ROS)...

Fructose is often considered "alcohol without the buzz" because it drives harmful reactive oxygen species (ROS) production in the liver through similar mechanisms, including mitochondrial stress and uric acid generation

. While both induce oxidative stress, high fructose intake is exceptionally damaging to metabolic health, potentially causing more chronic, long-term metabolic disruption than some studies report for ethanol in specific model...

 

Reactive Oxygen Species (ROS): Metabolism of alcohol generates high levels of free radicals, causing oxidative stress that damages DNA.

 best natural food source of glutathione...The best natural, direct food sources of glutathione are fresh, uncooked vegetables like asparagus, avocado, spinach, and okra. 

 Acetaldehyde, a highly reactive and toxic substance generated during alcohol metabolism, primarily causes DNA mutations, chromosomal damage, structural and functional impairments of organ, and the development of tumors by forming various adducts with DNA and proteins

https://pmc.ncbi.nlm.nih.gov/articles/PMC12031026/ 

  human ADH is classified into five types, with classes I, II, and IV being involved primarily in ethanol metabolism under physiological conditions...Class IV ADH was recently detected in the esophagus and stomach and was found to be responsible primarily for first-pass ethanol clearance. ²⁷ Approximately one-third of Asian individuals do not express it....

 Low ALDH1A1 activity is associated with a mild alcohol flush reaction in European individuals but has little impact on drinking behavior.

 A genetic variant, ALDH2*2 (rs671), prevalent in East Asian populations, disrupts the ALDH2 tetramer and significantly reduces its ability to metabolize acetaldehyde. ^{33 34} Carriers experience discomfort (e.g., nausea and headache) after ethanol intake, which reduces their risk of AUD and acute alcohol-related disease development.

 Chronic alcohol consumption can induce the expression of CYP2E1, which may be associated with faster alcohol clearance in heavy drinkers. CYP2E1 is also involved in the oxidation of compounds such as benzene and acetone, and it exacerbates oxidative stress in hepatocytes by generating reactive oxygen species (ROS). ³⁹

 CAT [catalase] plays an important role in alcohol metabolism in the brain, and its metabolite acetaldehyde is considered to be a key factor in alcohol reinforcing effects, tolerance, and voluntary ethanol intake. These effects are likely related closely to the interaction of acetaldehyde with catecholamines to produce various condensation products

Natural food sources of catalase include

raw fruits, vegetables, and organ meats, with particularly high concentrations found in broccoli, spinach, kale, onions, potatoes, and root vegetables. Fruits like bananas, pineapples, and cherries, along with raw dairy and liver, are excellent sources to help reduce oxidative stress

 Mechanistically, alcohol-induced CYP2E1 overexpression enhances HBV replication by upregulating hepatocyte nuclear factor-4α, the key transcription factor for the HBV core promoter, ¹¹⁷ and increases HCV-related mitochondrial ROS, reducing antioxidant capacity and depleting mitochondrial glutathione, which heightens oxidative damage and cell death. ¹¹⁸ However, both ethanol (via CYP2E1) and HBV can induce oxidative stress, complicating differentiation of their roles in liver damage.

 MASLD (formerly known as non-alcoholic fatty liver disease [NAFLD]) has become the most common cause of CLD worldwide....According to a recent meta-analysis, the global prevalence of MASLD has surpassed 30% and continues to increase

 Alcohol causes fatty liver (hepatic steatosis) by overwhelming the liver's ability to process toxins, leading to fat buildup from increased production and decreased breakdown of fatty acids, plus reduced fat export, disrupting normal lipid metabolism through various molecular pathways that promote fat synthesis and hinder oxidation, often starting with shifts in the NADH/NAD+ balance and involving inflammatory signals like TNF-α

  The metabolism of alcohol creates a large amount of NADH, which inhibits the liver's ability to burn fat (fatty acid oxidation).

  increases the production of tumor necrosis factor-α (TNF-α),

 Your liver breaks down alcohol, but heavy drinking produces harmful byproducts (like acetaldehyde) and puts stress on liver cells, interfering with its normal functions, including fat processing. 

 Alcohol metabolism shifts the liver's balance (increasing NADH), promoting the creation of glycerol-3-phosphate, which combines with fatty acids to form triglycerides (fat). It also activates SREBP-1c, boosting enzymes for fatty acid synthesis. 

 Chronic alcohol consumption not only reduces the NAD +/NADH ratio....

NAD+ (Nicotinamide Adenine Dinucleotide) is

a coenzyme used in therapy to assist alcohol recovery by replenishing levels depleted by chronic alcohol abuse. It is administered via IV to potentially reduce withdrawal symptoms, curb cravings, and aid in cellular energy production, though it is not a cure and studies are limited....

NAD+ and glutathione (GSH) are complementary, synergistic molecules that drive a "circular economy" for cellular health, acting as a powerful duo for energy, detoxification, and anti-aging.

NAD+ acts as cellular fuel and helps regenerate glutathione, while glutathione reduces oxidative stress to protect NAD+

 NAD+ (nicotinamide adenine dinucleotide) cannot be consumed directly through food, but you can boost its levels by eating foods rich in precursors like tryptophan, vitamin

$B_3$

(niacin), and Nicotinamide Riboside (NR). Key dietary sources include fatty fish (salmon, tuna), poultry (turkey, chicken), dairy, eggs, peanuts, mushrooms, and green vegetables

 From ages 20 to 60, NAD+ drops by 50%, while glutathione synthesis decreases by 45%

Spirulina contains tryptophan, which the body uses to create NAD+ through a series of steps.

Supports Natural Synthesis: Research indicates that some microalgae, including spirulina, contain compounds that may help the body increase its own NAD+ production, similar to how fasting or exercise works.

Metabolic Health Benefits: By potentially boosting NAD+, spirulina helps improve mitochondrial function and metabolic health.

Synergistic Effects: While not a direct concentrated supplement like NMN or NR, spirulina supports the overall, long-term healthspan by maintaining NAD+ levels, which naturally decline with ag

Alcohol increases visceral fat primarily because the liver prioritizes breaking down alcohol over burning fat, leading to higher rates of fat storage around abdominal organs

. It provides high "empty" calories, triggers increased cortisol (a stress hormone promoting fat storage), and causes overeating. 

 Excessive drinking may activate the same part of the brain as hunger causing binge eating.

 Alcohol Reduces Resveratrol Exposure: A study found that alcohol consumption significantly reduces exposure to resveratrol (by up to 95%), likely due to a decrease in its absorption.

 Resveratrol can help mitigate the toxic effects of alcohol on the liver (such as fatty liver disease) by regulating enzymes and activating pathways like SIRT1 and AMPK, even though the alcohol itself reduces the bioavailability of the resveratrol.

 

Alcohol triggers hunger, often leading to the "drunchies," by tricking the brain into a starvation-like state, activating AGRP neurons that drive intense hunger signals

. It interferes with satiety hormones like leptin, lowers inhibitions causing impulsive eating, and can cause a drop in blood sugar, increasing cravings for carbohydrates.

  Alcohol stimulates Agouti-Related Protein (AGRP) neurons in the hypothalamus, which are typically activated during starvation or fasting, causing intense, artificial hunger.

 Alcohol intake is known to contribute to weight gain, ⁹⁹ and 98% of heavy drinkers participating in one study had at least one cardiovascular metabolic risk factor, with more than 40% having four or more such factors.

 dyslipidemia (hypertriglyceridemia and low levels of high-density lipoprotein cholesterol), elevated blood pressure, impaired glucose tolerance, and central obesity is now classified as metabolic syndrome, also called syndrome X.

 

 https://pmc.ncbi.nlm.nih.gov/articles/PMC3045098/

 

 The predominant underlying risk factors of the metabolic syndrome appear to be abdominal obesity[1] and insulin resistance;[2] other associated conditions can be physical inactivity,[3] aging[4] and hormonal imbalance.[5] An atherogenic diet (e.g., a diet rich in saturated fat and cholesterol) although not listed specifically as an underlying risk factor for the condition can enhance risk in people with the syndrome for developing cardiovascular disease.

 Waist circumference ≥40 inches in men

Dietary Approaches to Stop Hypertension (DASH) study[41] patients who consumed a diet low in saturated fat and high in carbohydrates experienced a significant reduction in blood pressure, even without weight reduction. The DASH diet emphasizes fruits, vegetables, low-fat dairy foods, whole grains, poultry, fish, and nuts, while reducing saturated fats, red meat, sweets, and sugar containing beverages. Reducing sodium intake can further reduce blood pressure or prevent the increase in blood pressure that may accompany aging. Low-fat, high-carbohydrate diets have been criticized because they may raise triglyceride levels and lower HDL cholesterol levels in some patients, thus aggravating the dyslipidemia of metabolic syndrome. To treat hypertriglyceridemia, or the decline of HDL-cholesterol levels on a low-fat diet, carbohydrate intake can be reduced and replaced with foods high in monounsaturated fats or low glycemic index carbohydrates. These changes create a diet similar to the Mediterranean-style diet,

 

  Physical training has been shown to reduce skeletal muscle lipid levels and insulin resistance, regardless of BMI. 

 Walking or light jogging for one hour per day will produce significant loss of abdominal (visceral) fat in men without caloric restriction

 In a study to determine the antitumor effects of terpenoids, it was found that paclitaxel, geraniol [ in BEE BALM aka Wild Bergamot] and perillyl alcohol are the terpenoids with better anticancer activities (Yang et al., 2020). The anti-inflammatory activity of paeoniflorin and its derivatives, 4-O-methylbenzoyl paeoniflorin, 4-O-methyl paeoniflorin, and other monoterpenes was reported (Bi et al., 2017). The results reported that most of these monoterpenes can inhibit the production of tumor necrosis factor-alpha (TNF-α), interleukins-6 (IL-6), and inflammatory factor nitric oxide (NO) induced by lipopolysaccharides (LPs).

 

 The essential oil of thyme has showed free radical scavenging and antibacterial activity [74], and it could detoxify alcohol toxicity. Thymol was the major component (44.4%–58.1%), followed by p-cymene (9.1%–18.5%), γ-terpinene (6.9%–18.9%), and carvacrol (2.4%–4.2%) in the tested oil samples [75]. The water extract of thyme possessed the ability of detoxifying the injuries of alcohol on liver and brain in mice. It could decrease nitric oxide and MDA level in liver and brain, and increase the total antioxidant capacity and GPx activity [76]. Therefore, Thymus vulgaris was recommended to treat alcohol toxicity through its potent antioxidant properties.

 

 https://pmc.ncbi.nlm.nih.gov/articles/PMC6274469/