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Toxic compounds in potatoes
Potatoes contain glycoalkaloids, toxic compounds, of which the most prevalent are solanine and chaconine. Cooking at high temperatures (over 170 °C or 340 °F) partly destroys these. The concentration of glycoalkaloid in wild potatoes suffices to produce toxic effects in humans. Glycoalkaloids occur in the greatest concentrations just underneath the skin of the tuber, and they increase with age and exposure to light. Glycoalkaloids may cause headaches, diarrhea, cramps and in severe cases coma and death; however, poisoning from potatoes occurs very rarely. Light exposure also causes greening, thus giving a visual clue as to areas of the tuber that may have become more toxic; however, this does not provide a definitive guide, as greening and glycoalkaloid accumulation can occur independently of each other. Some varieties of potato contain greater glycoalkaloid concentrations than others; breeders developing new varieties test for this, and sometimes have to discard an otherwise promising cultivar.
Breeders try to keep solanine levels below 0.2 mg/g (200 ppmw). However, when even these commercial varieties turn green, they can approach concentrations of solanine of 1 mg/g (1000 ppmw). Some studies suggest that 200 mg of solanine can constitute a dangerous dose. This dose would require eating 1 average-sized spoiled potato or 4 to 9 good potatoes (over 3 pounds or 1.4 kg) at one time. The National Toxicology Program suggests that the average American consumes 12.5 mg/person/day of solanine from potatoes. Dr. Douglas L. Holt, the State Extension Specialist for Food Safety at the University of Missouri - Columbia, notes that no reported cases of potato-source solanine poisoning have occurred in the U.S. in the last 50 years and most cases involved eating green potatoes or drinking potato-leaf tea.
Clinical signs: the symptoms observed in a given case will depend on the balance of the irritant effect of the intact glycoalkaloid vs. the nervous system signs caused by the aglycone. GI signs include anorexia, nausea, salivation, abdominal pain, emesis, constipation or diarrhea (with or without blood). Nervous system signs include apathy, drowsiness, progressive weakness/paralysis, prostration and unconsciousness. Nervous signs build to a maximum followed by death or recovery within 1 to 2 days.
J Agric Food Chem. 2005 Jul 27;53(15):6162-9. Related Articles, Links
J Agric Food Chem. 2005 Oct 19;53(21):8420.
Anticarcinogenic effects of glycoalkaloids from potatoes against human cervical, liver, lymphoma, and stomach cancer cells.
Friedman M, Lee KR, Kim HJ, Lee IS, Kozukue N.
Western Regional Research Center, Agricultural Research Service, U.S. Department of Agriculture, Albany, California 94710, USA. firstname.lastname@example.org
Methods were devised for the isolation of large amounts of pure alpha-chaconine and alpha-solanine from Dejima potatoes and for the extraction and analysis of total glycoalkaloids from five fresh potato varieties (Dejima, Jowon, Sumi, Toya, and Vora Valley). These compounds were then evaluated in experiments using a tetrazolium microculture (MTT) assay to assess the anticarcinogenic effects of (a) the isolated pure glycoalkaloids separately, (b) artificial mixtures of the two glycoalkaloids, and (c) the total glycoalkaloids isolated from each of the five potato varieties. All samples tested reduced the numbers of the following human cell lines: cervical (HeLa), liver (HepG2), lymphoma (U937), stomach (AGS and KATO III) cancer cells and normal liver (Chang) cells. The results show that (a) the effects of the glycoalkaloids were concentration dependent in the range of 0.1-10 mug/mL (0.117-11.7 nmol/mL); (b) alpha-chaconine was more active than was alpha-solanine; (c) some mixtures exhibited synergistic effects, whereas other produced additive ones; (d) the different cancer cells varied in their susceptibilities to destruction; and (e) the destruction of normal liver cells was generally lower than that of cancer liver cells. The decreases in cell populations were also observed visually by reversed-phase microscopy. The results complement related observations on the anticarcinogenic potential of food ingredients.
Regul Toxicol Pharmacol. 2005 Feb;41(1):66-72. Epub 2004 Dec 10.
Potato glycoalkaloids and adverse effects in humans: an ascending dose study.
Mensinga TT, Sips AJ, Rompelberg CJ, van Twillert K, Meulenbelt J, van den Top HJ, van Egmond HP.
National Poisons Control Centre, National Institute for Public Health and the Environment, The Netherlands. email@example.com
Glycoalkaloids in potatoes may induce gastro-intestinal and systemic effects, by cell membrane disruption and acetylcholinesterase inhibition, respectively. The present single dose study was designed to evaluate the toxicity and pharmacokinetics of orally administered potato glycoalkaloids (alpha-chaconine and alpha-solanine). It is the first published human volunteer study were pharmacokinetic data were obtained for more than 24 h post-dose. Subjects (2-3 per treatment) received one of the following six treatments: (1-3) solutions with total glycoalkaloid (TGA) doses of 0.30, 0.50 or 0.70 mg/kg body weight (BW), or (4-6) mashed potatoes with TGA doses of 0.95, 1.10 or 1.25 mg/kg BW. The mashed potatoes had a TGA concentration of nearly 200 mg/kg fresh weight (the presently recognised upper limit of safety). None of these treatments induced acute systemic effects. One subject who received the highest dose of TGA (1.25 mg/kg BW) became nauseous and started vomiting about 4 h post-dose, possibly due to local glycoalkaloid toxicity (although the dosis is lower than generally reported in the literature to cause gastro-intestinal disturbances). Most relevant, the clearance of glycoalkaloids usually takes more than 24 h, which implicates that the toxicants may accumulate in case of daily consumption.
Med Hypotheses. 1999 Jul;53(1):80-6.
Schizophrenia: is the potato the environmental culprit?
Emeritus Consultant Pathologist, The Wollongong Hospital, New South Wales, Australia.
The pathology and aetiology of schizophrenia are reviewed in the light of the most recent research into the genetic/sporadic occurrence of this disease complex of world-wide distribution but of variable incidence. Although the aetiology is still unknown, numerous hypotheses have been postulated including dietetic factors but never has the potato (Solanum tuberosum L.) been suspected. However, a strong case can be advanced incriminating this widely, in fact almost universally, consumed vegetable tuber with its variable content of steroidal glycoalkaloids (SGAs) with known toxic action on both animals and humans, including possible teratogenic and cell membrane-damaging properties, as a very likely aetiological contender in most but possibly not all cases.
Spirosolane-containing Solanum species and induction of congenital craniofacial malformations.
Keeler RF, Baker DC, Gaffield W.
United States Department of Agriculture, Poisonous Plant Research Laboratory, Logan, UT 84321.
Comparison by GC analysis of purified alkaloid extracts of Solanum species revealed no measurable free solasodine, other spirosolanes, or any non-spirosolane steroidal alkaloid aglycones in unhydrolyzed total alkaloid fractions of fruit of Solanum elaeagnifolium Cav. (silverleaf nightshade), Solanum sarrachoides (S. villosum Lam.--hairy nightshade), Solanum dulcamara L. (European bittersweet nightshade) or Solanum melongena L. (eggplant). All alkaloidal material was apparently present as glycoside. Conversely, sprouts of Solanum tuberosum L. (potato) contained 67% of its alkaloids as glycosides, which was freed only upon hydrolysis with the remaining 33% present as free solanidine. GC/MS analysis of hydrolysates of purified extracts of the test Solanum species revealed that solasodine was a principal or sole aglycone of the alkaloid glycosides in each of the test species except Solanum tuberosum. In the latter, solanidine was the sole aglycone. Among the test species, exclusive of S. tuberosum, only S. dulcamara contained aglycones other than solasodine. In addition to solasodine, S. dulcamara contained appreciable amounts of an unknown spirosolane, an aglycone provisionally identified as soladulcidine. The induction of congenital craniofacial malformations in hamsters by high oral doses of the four Solanum species that contained mainly solasodine glycosides--S. elaeagnifolium, S. dulcamara, S. sarrachoides and S. melongena was compared to inductions of malformations by Solanum tuberosum, that contained mainly solanidane glycosides. Compared to controls, Solanum elaeagnifolium and Solanum dulcamara fruit both induced a high percentage incidence of deformed litters (20.4 and 16.3, respectively) that was statistically significant (P less than 0.001 level) while percentage incidence of deformed litters induced by Solanum sarrachoides and Solanum melongena fruit (9.5 and 7.6 respectively) were both higher than controls (3.4%), in neither case was the incidence statistically significant (P less than .05). Deformed litter incidence induced by sprouts of Solanum tuberosum was 24.0%, (P less than 0.001).