See "Acetaldehyde + Lovastatin" http://curezone.com/blogs/fm.asp?i=1990595
are there other endogenous or exogenous substances that may also have peripheral effects because of salient carbonyl groups in their configurations?
The ability of the carbonyl ketones in the female hormone progesterone to remove free acetaldehyde from circulation may provide some protection against interference with other vital substances such as CoQ10 and vitamin K.
Cyclic hormonal fluctuations [1] and pregnancy [2] certainly predispose the female metabolism to elevated colonization levels by Candida albicans, a source of acetaldehyde [3]. If progesterone is removing some of the toxic background acetaldehyde being emitted by budding yeast metabolism, then one might expect acetaldehyde-related interference to increase subsequent to menopause when progesterone levels drop drastically.
Vitamin K, a quinone which may be a target for acetaldehyde interference (ref. as above), is required for the gamma-carboxylation of osteocalcin, a bone-related protein circulating in the blood. Circulating levels of undercarboxylated osteocalcin are higher in postmenopausal women resulting in increased risk for fractures [4]. This is thought to be a result of inadequate vitamin K nutritional status. However, vitamin K quinones, denatured by interaction with acetaldehyde that is no longer being scavenged by progesterone, could produce the same effects as an overt nutritional deficiency.
Unlike the other fat-soluble vitamins, bodily stores of vitamin K are rapidly depleted [5], and a rapid onset of deficiency is possible. As a result the body's vitamin K status is exquisitely sensitive to anything that may be interfering with its molecular configuration. Genetically deficient aldehyde dehydrogenase activity is linked to impairment of osteoblastogenesis [6]. Chronic pulsed low-dosage exposure to acetaldehyde, even when aldehyde dehydrogenase activity is normal, can create the same deleterious effects as overtly impaired aldehyde disposal. This implies that circulating yeast-released acetaldehyde levels could lead to osteoporotic degradation [7] independently, even with or without the proposed protective effects of progesterone.
Even as estrogen-related compounds contribute to increased background yeast levels [8], that may persist even after menopause, there are other clues that progesterone may be acting in ways other than its usual function. The remission of nerve myelin deterioration, characteristic of multiple sclerosis, during pregnancy when progesterone levels are high, and the usage of dimethyl fumurate to alleviate this same disease suggest some link between these two compounds and the disease process:
See "Acetaldehyde + Dimethyl Fumarate" http://curezone.com/blogs/fm.asp?i=1989754
Although current thought is looking at autoimmunity and immunosuppressive connections between therapeutic substances, could the common factor be something completely different -- the ability of these molecular configurations to bind acetaldehyde and remove its toxic presence?
Advanced invasive candidiasis is not a prerequisite for exposure to toxic acetaldehyde. Even "commensal" levels of colonization can provide exposure levels capable of precipitating diseases as varied as the genetically susceptibility of the individuals involved. Candida antibody studies have already shown a correlation between the presence of candida species antibodies and multiple sclerosis [9].
Prednisone is a glucocorticoid precursor, hepatically transformed into prednisolone, used in diverse indications: asthma, COPD, CIPD, rheumatic disorders, allergic disorders, ulcerative colitis/Crohn's disease, adrenocortical insufficiency, cancer-associated hypercalcemia, thyroiditis, laryngitis, tuberculosis, lipid pneumonitis, multiple sclerosis, nephrotic syndrome, myasthenia gravis, lupus, migraines,...a long list indeed!
There are three carbonyls exposed in this molecule that would provide binding sites for acetaldehyde. Would something else that scavenged acetaldehyde provide relief in all of these different conditions?
One of the arguments used against "cure-all" herbals is that it is impossible for a single substance to be effective in so many different conditions. But prednisone is an example of a substance with just that profile -- but burdened with major side effects as well [10]. Drugs and the bioactive substances of herbal remedies converge at the molecular level and are indistinguishable, having both favorable modes of action and adverse side effects.
Even the common prostaglandin synthesis inhibitor, aspirin, has an ester side chain carbonyl that acetaldehyde might find attractive:
Given that acetaldehyde is going to be a factor in everyone with a yeast load and that yeast is virtually universally carried by everyone at some level or another, some of the therapeutic effects of aspirin may be a result of its acetaldehyde-binding ability. Its ability to lower acetaldehyde levels slightly after alcohol consumption suggests that it may have a partial action in this manner [11]. Consuming massive amounts of aspirin to try and combat acetaldehyde release is not a viable strategy, however, because of its impact upon essential prostaglandin metabolism and known toxicity risks [12] associated with high intake levels.
[1] Kalo-Klein A et al., "Candida albicans: cellular immune system interactions during different stages of the menstrual cycle.", Am J Obstet Gynecol. 1989 Nov;161(5):1132-6.
http://www.ncbi.nlm.nih.gov/pubmed/2686440
[2] Nohmi T et al., "Suppression of anti-Candida activity of murine neutrophils by progesterone in vitro: a possible mechanism in pregnant women's vulnerability to vaginal candidiasis.", Microbiol Immunol. 1995;39(6):405-9.
http://www.ncbi.nlm.nih.gov/pubmed/8551972
[3] Gainza-Cirauqui ML et al., "Production of carcinogenic acetaldehyde by Candida albicans from patients with potentially malignant oral mucosal disorders.", J Oral Pathol Med. 2012 Aug 22.
http://www.ncbi.nlm.nih.gov/pubmed/22909057
[4] Szulc P et al., "Serum undercarboxylated osteocalcin is a marker of the risk of hip fracture in elderly women.", J Clin Invest. 1993 Apr;91(4):1769-74.
http://www.ncbi.nlm.nih.gov/pubmed/8473517
[5] Suttie JW et al., "Vitamin K deficiency from dietary vitamin K restriction in humans.", Am J Clin Nutr. 1988 Mar;47(3):475-80.
http://www.ncbi.nlm.nih.gov/pubmed/3348159
[6] Huang QY et al., "Genetics of osteoporosis.", Mol Genet Metab. 2006 Aug;88(4):295-306. http://www.ncbi.nlm.nih.gov/pubmed/16762578
[7] Hoshi H et al., "Aldehyde-stress resulting from Aldh2 mutation promotes osteoporosis due to impaired osteoblastogenesis.", J Bone Miner Res. 2012 Sep;27(9):2015-23.
http://www.ncbi.nlm.nih.gov/pubmed/22508505
[8] Tarry W et al., "Candida albicans: the estrogen target for vaginal colonization.", J Surg Res. 2005 Dec;129(2):278-82.
http://www.ncbi.nlm.nih.gov/pubmed/16111702
[9] Benito-Leon J et al., "Association between multiple sclerosis and Candida species: evidence from a case-control study", European Journal of Clinical Microbiology & Infectious Diseases
Volume 29, Number 9 (2010), 1139-1145.
http://www.ncbi.nlm.nih.gov/pubmed/20556470
[10] Kauh E et al., "Prednisone affects inflammation, glucose tolerance, and bone turnover within hours of treatment in healthy individuals.", Eur J Endocrinol. 2012 Mar;166(3):459-67.
http://www.ncbi.nlm.nih.gov/pubmed/22180452
[11] Truitt EB Jr et al., "Aspirin attenuation of alcohol-induced flushing and intoxication in Oriental and Occidental subjects.", Alcohol Alcohol Suppl. 1987;1:595-9.
http://www.ncbi.nlm.nih.gov/pubmed/3426738
[12] Temple AR, "Acute and chronic effects of aspirin toxicity and their treatment.", Arch Interm Med. 1981 Feb 23;141(3 Spec No):364-9.
http://www.ncbi.nlm.nih.gov/pubmed/7469627