A Health-Destroying Toxin We Can't Avoid And Must Detoxify

By Carolyn Pierini, CLS (ASCP), CNC

Summer may bring increased exposure to more than just the sun. Summer gives us longer days, BBQs, pool parties, campfires, more alcohol and sweet beverages, road trips with the car windows and top down and home improvements. Harmless as they seem, these factors and more increase our exposure to multiple environmental toxins. One particular toxin that affects millions in the population is acetaldehyde.

Acetaldehyde belongs to the larger chemical family of aldehydes, which are pervasive environmental toxins. The human body possesses enzymes that convert it to a less-harmful substance and therefore is protected from small exposures. However, acetaldehyde at toxic levels can make its way into the brain from sources such as alcohol consumption, Candida sp. (yeast) overgrowth, breathing air contaminated with acetaldehyde from cigarette and other smoke, smog, vehicle and factory exhaust, synthetic fragrances and many commercially manufactured materials. Acetaldehyde and its close relative formaldehyde are used in the synthesis of chemicals such as plastics, dyes, fabrics, adhesives, fuels, plywood, particleboard, insulating foam, fragrances, preservatives and more. Besides being an occupational hazard, these materials are found throughout the home especially in new carpets, furniture and floors and can out-gas aldehydes into the air for years, creating continuous exposure. Aldehydes are among the top chemicals released into the environment daily.

The following article provides an overview of acetaldehyde and the danger it poses.

Acetaldehyde Exposure


One of the main significant acetaldehyde exposure routes is through alcohol (ethanol) consumption. Ethanol metabolism starts with the conversion of alcohol to acetaldehyde, which is at least 30 times more toxic than alcohol. Ideally, acetaldehyde is then oxidized to acetic acid and ultimately into Acetyl-CoA, which will be used for cellular energy. Unfortunately, in many if not most people, this conversion is slow and not always efficient due to genetic variations of the enzymes that perform this step, insufficient nutrient cofactors or exposure to related chemicals utilizing the same metabolic enzymes and nutrients. The result may be high acetaldehyde levels, which can cause significant damage to the liver where the bulk of alcohol metabolism occurs.1 Other alcohol metabolism sites that expose tissue to acetaldehyde’s damaging effects are the pancreas, gastrointestinal tract and in particular, the brain.2-3 Alcohol may result in “drunkenness”—the central nervous system effects of relaxation, loss of coordination and inhibition of judgment—but acetaldehyde is responsible for the “hangover,” the toxic side effects that can eventually damage the brain.


Another important exposure route to toxic acetaldehyde levels is through its production by the opportunistic yeast, Candida albicans. In small numbers, this yeast may be kept in check in the gut by the immune system and friendly bacteria such as Lactobacillus sp. and Bifidobacterium sp. But in many people, increasing carbohydrates, especially sweets, will cause chronic Candidiasis. Candida produces acetaldehyde in the GI tract by sugar fermentation. The typical American diet along with drug and antibiotic therapies, hypochlorhydria (low stomach acid), chronic stress, environmental toxins, etc. have altered gut integrity and immunity and predisposed millions of people to yeast overgrowth or the “Candida Syndrome.”4 A person with this condition who also drinks beer, wine or liqueurs not only produces acetaldehyde from the alcohol but also delivers more sugar for yeast production of acetaldehyde, creating a double-barreled dose. Acetaldehyde produced in the gut can eventually reach more parts of the body, flooding the system and increasing the risk for damage.5


Through the burning of tobacco, petroleum fuels, natural gas, wood and trash, aldehydes, including acetaldehyde, are present in the air we breathe. Vehicle and factory exhaust can create a chronic but significant exposure source to those who live near heavily trafficked areas or who spend hours commuting on freeways. Acetaldehyde contributes to photochemical “smog” formation when it reacts with other volatile substances in the air. Open car windows increase exposure, as does breathing in acetaldehyde-containing fumes near gas pumps. Cigarette smokers and others around them are exposed through inhaling smoke. According to the Environmental Protection Agency (EPA), wood smoke from campfires, wood-burning stoves and residential fireplaces is more toxic than cigarette smoke. But the acetaldehyde level released from burning items such as plastics, styrofoam and batteries is even higher.6 While acetaldehyde exposure from auto exhaust and cigarettes may be less than that from alcohol, research shows that low dose chronic exposure may still be sufficient to gradually damage proteins, enzymes and other cellular structures in the brain and other organs.7

Furthermore, most fragrances today are made from synthetic chemicals, many of which are toxic. Air fresheners, scented candles, cleaning products, cologne or perfume and more can create a source of chronic exposure to many toxic chemicals including acetaldehyde. Children and babies are particularly susceptible. Additionally, the Environmental Working Group (EWG) lists acetaldehyde as one of the contaminants released from polyethylene plastic bottles.8

Detrimental Effects

Acetaldehyde is classified as a probable human carcinogen linked to nose and throat irritation and cancer as well as a toxicant to the neurological (neurotoxin), respiratory, endocrine and immune systems. Animal research also shows that this chemical crosses the placental barrier causing skeletal deformities, reduced birth weights and infant death.9

Acetaldehyde significantly compromises brain function. It is considered to be the substance that directly contributes to the toxic effects and the chemical dependency to alcohol and cigarettes. Addictive, opiate-like biochemicals are formed in the brain when acetaldehyde combines with the key neurotransmitters, dopamine and serotonin. In acetaldehyde’s presence, dopamine is converted into salsolinol and serotonin into beta-carboline, both of which are very addictive tetrahydroisoquinolines (TIQs).10-11 Moreover, metabolites of salsolinol are neurotoxic to dopaminergic neurons inducing cell death and eliciting symptoms nearly identical to idiopathic Parkinson’s disease.12-13

Acetaldehyde damages the membranes of red blood cells (RBC) making them less flexible in passing through tiny capillaries, and it can alter hemoglobin, the oxygen transporter in the RBC.14 These two effects reduce available oxygen to the cells, especially in the brain.

Acetaldehyde disables the protein tubulin from assembling into microtubules in the brain.15 Microtubules structurally and nutritionally support the dendrites, the feathery-looking extensions from the nerve cells’ main body, which connect many nerve cells to each other. Without the microtubules, the dendrites atrophy and die. This can be seen in chronic alcoholism and Alzheimer’s disease.

Acetaldehyde and Nutrient Deficiencies

In addition to its toxic effects, acetaldehyde induces deficiencies of nutrients used for its detoxification. As an example, vitamin B1 (thiamine) is depleted through alcohol and acetaldehyde detoxification.16 B1 is essential in carbohydrate metabolism for energy production, of which the brain uses 20 percent. Acetaldehyde-induced B1 depletions exacerbate the already low B1 levels common in the population due to diuretics and other drugs, over-consumption of simple carbohydrates (dysglycemia) and adrenal stress. In addition to its many functions, thiamine, the “nerve vitamin,” is critical to nerves and neurotransmitters. Even mild, chronic B1 deficiency can produce brain-related symptoms such as emotional instability, confusion, depression, fatigue, irritability, headaches, sensitivity to noise, insomnia, decreased short-term memory, brain-fog and a feeling of impending doom.17-18

Relevant to this time of year, B1­deficiency-related lactic acidosis can make people more vulnerable to bug bites, since many insects, particularly mosquitoes, are attracted to mild acids.19

Furthermore, people with chemical sensitivities to aldehydes may also be sensitive to seemingly unrelated substances like sulfites (preservatives) from wines and foods, and the smell of chlorine from pools and bleach.

The under appreciated essential trace mineral molybdenum is also involved with acetaldehyde metabolism. A molybdenum deficiency not only affects this process but also other enzymes in the body that require molybdenum as a cofactor—for example, sulfite oxidase, responsible for converting irritating sulfites into harmless sulfates for use in liver detoxification and cartilage. Sulfur-containing amino acids, as important free radical scavengers, also use this molybdenum-dependent pathway. Molybdenum has been shown to reduce sulfite sensitivity by increasing sulfite oxidase activity.20 Sulfites also destroy vitamin B1’s biological activity, contributing to a deficiency. Nutrient depletion leads to sensitivity to other chemicals that use these same pathways. This has been demonstrated in patients with Candidiasis as the excess stress put on the enzyme systems to detoxify acetaldehyde often leave them with sensitivities to multiple chemicals especially fragrances. Supplementing with the appropriate cofactors may improve an individual’s ability to handle Candida-generated acetaldehyde.21

Acetaldehyde Relief

Acetaldehyde toxicity can be acute or chronic. In order to stop this toxicity, levels of key nutrients that metabolize and clear acetaldehyde must be adequate. Some of these nutrients are cofactors to the enzymes that metabolize acetaldehyde and others, such as sulfur-containing compounds, are necessary to scavenge or “mop up” any stray un-metabolized acetaldehyde. Supplementation with specific nutrients offers an important level of prevention and protection from toxicity. In one animal study, pretreatment of the animals with B1, vitamin C and the sulfur-containing amino acid cysteine completely blocked the LD-90 dose of acetaldehyde (the dose that would normally kill 90 percent of the animals).22 In another study, cysteine lowered in the digestive tract the amount of acetaldehyde produced by smoking and alcohol consumption. Both of these risk factors are considered the main causes of upper digestive tract cancer in 75 percent of developed countries with acetaldehyde as the probable cause.23


1. Zakhari S. Overview: How is alcohol metabolized by the body? Alcohol Research & Health. 2006;29(4):245-254.

2. Edenberg H J. The genetics of alcohol metabolism: Role of alcohol dehydrogenase and aldehyde dehydrogenase variants. Alcohol Research & Health. 2007;30(1):5-13.

3. Vonlaufen A, Wilson JS, Pirola RC, Apte MV. Role of alcohol metabolism in chronic pancreatitis. Alcohol Research & Health. 2007;30(1):38-54.

4. Galland LD. Nutrition and Candida albicans, 1986 A year in Nutritional Medicine, ed. J. Bland. New Canaan. Keats Pub. 1986 pg. 203-238.

5. Truss CO. Metabolic Abnormalities in Patients with Chronic Candidiasis: The Acetaldehyde Hypothesis. J Orthomolecular Psychiatry. 1984;13(2):66-93.

6. www.fs.fed.us/t-d/pubs/htmlpubs/htm04232327/page01.htm (US Forest Service-Dept of Agriculture). What’s Burning in your Campfire? Garbage In, Toxics Out.

7 Sorrell MF, Tuma DJ. The Functional Implications of Acetaldehyde Binding to Cell Constituents. Ann NY Acad Sci. 1987;492:50-62.

8. www.EWG.org, accessed on 5/10/10.

9. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Acetaldehyde. Source: http://www.epa.gov/iris/subst/0290.htm Nov. 2002.

10. Blum K, Payne J. Alcohol and the Addictive Brain. NYC: The Free Press, 1991, pp. 99-216.

11. Epp LM, Mravec B. Chronic polysystemic candidiasis as a possible contributor to onset of idiopathic Parkinson’s disease. Bratisl Lek Listy. 2006;107(6-7):227-30.

12. Maruyama W, Naoi M. Cell death in Parkinson’s disease. J Neurol 2002;249(suppl 2):183-89.

13. Martinez-Alvarado P, et al. Possible role of salsolinol quinone methide in the decrease of RCSN-3 cell survival. Biochem Biophys Res Commun 2001;283(5):1069-76.

14. Tsuboi KK, Thompson DJ, Rush EM, Schwartz HC. Acetaldehyde-Dependent Changes in Hemoglobin and Oxygen Affinity of Human Erythrocytes. Hemoglobin. 1981;5(3):241-50.

15. Tuma DJ, Jennett RB, Sorrell MF. The Interaction of Acetaldehyde with Tubulin. Ann NY Acad Sci 1987;492:277-286.

16. Takabe M, Itokawa Y. Thiamin depletion after ethanol and acetaldehyde administration to rabbits. J Nutr Sci Vitaminol (Tokyo). Oct. 1983;29(5):509-14.

17. Lonsdale D, Shamberger. Red cell transketolase as an indicator of nutritional deficiency. Am J Clin Nutr 1980;33:205-11.

18. Williams RR, et al. Induced Thiamin (vitamin B1) Deficiency in Man. Arch Int Med. 1942;69:721-38.

19. Fradin MS. Mosquitoes and Mosquito Repellents: A Clinician’s Guide. Ann Intern Med. June 1998;128(11):931-940.

20. Molybdenum. Monograph. Altern Med Rev. 2006;11(2):156-161.

21. Schmitt WH, et al. Molybdenum for Candida albicans Patients and other Problems. The Digest of Chiropractic Economics. Jan-Feb. 1991;31(4):56-63.

22. Sprince H, Parker CM, Smith GG, Gonzales LJ. Protective Action of Ascorbic Acid and Sulfur Compounds against Acetaldehyde Toxicity: Implications in Alcoholism and Smoking. Agents and Action. May 1975;5(2):164-73.

23. Salaspuro V. Interaction of alcohol and smoking in the pathogenesis of upper digestive tract cancers-possible chemoprevention with cysteine. Univ. Helsinki, Institute of Clinical Medicine. Doctoral dissertation. April 2006.

24. Horrobin DF. The Importance of Gamma-Linolenic Acid and Prostaglandin E1 in Human Nutrition and Medicine. J Holistic Med. 1981;3:118-39.