Reports of potato poisoning are uncommon, yet persistent incidents—particularly of mass poisonings1—are reported in the literature from time to time, going as far back as 1846. Though catalogued in the British medical journal, The Lancet, it’s actually in a section summarizing findings from other medical journals. In this case, a Dr. O’Brien reported in the Dublin Hospital Gazette seeing 10 patients in the span of 4 days with a range of uncomfortable GI and neurological symptoms. He attributed these to bad potatoes. The Lancet writer editorialized: “If these observations be correct, we should hear of this disease from other quarters.”2
The culprit is usually poor storage and handling. Popular wisdom has long held that green potatoes suggested high solanine content, but that has been challenged.3 When solanine levels are high, however, the skin and the eyes do have the highest concentrations. Poor storage and rough handling can increase solanine after the harvest. Just cutting and leaving potatoes for a day can lead to substantial increases in solanine levels. Because of this, food safety research is filled with techniques for proper handling of potatoes. As noted above, breeders have had to remove potatoes from market in 19704 and in 19865 because of high solanine content.
In 1996 Roddick’s lab published “Potato glycoalkaloids: Some unanswered questions.” He’d been studying glycoalkaloids for more than two decades. The article asserted: “if the potato were to be introduced today as a novel food, it is quite possible that its use would not be approved because of the presence of these potentially toxic compounds.”6
That’s a surprising statement, given that it’s the most consumed vegetable in the U.S., and among the most popular in the world. Variations on this theme appear periodically in the scientific literature.
In 2004, scientists from the Institute of Molecular Biology and Genetics in Ukraine, led by Yaroslav Korpan, also reviewed the science. Noting that glycoalkaloids are clearly toxic they questioned the informal standard of 200 milligrams per kilogram, citing some older work, from 1984:7 “Many authors have assumed without further evidence that levels below 200 mg/kg are safe. They ignore the fact that the 200 mg/kg (FW) level only relates to acute and/or subacute effects and not to possible chronic effects….”8 (Korpan’s apparent interest was as a designer of food sensors, including automating the monitoring of glycoalkaloids.)
In 2016 Mendel Friedman and his colleague Carol Levin reviewed the known toxicities of the potato in a chapter for the second edition of Advances in Potato Chemistry and Technology. Their conclusions, with the benefit of more than two decades of experience in the field, note first the systemic impacts of high levels of glycoalkaloids:
- anti-cholinesterase activity affects the central nervous system
- liver damage
- cell membrane disruption with adverse impacts on digestive system and metabolism
Symptoms at these higher doses include fever, increased pulse, low blood pressure, rapid respiration, and neurological disorders. Lower doses can cause gastrointestinal troubles like vomiting, diarrhea, and abdominal pain.9
Whether or not you have a nightshade sensitivity, it’s extremely unlikely you’ll be so unfortunate as to encounter such catastrophically high levels of glycoalkaloids. In the U.S. the FDA has an advisory guideline for solanine levels of about 20–25 mg/100 g fresh potato weight (or 200–250 ppm).10
But setting a standard is not easy. Friedman and Levin note that the Food and Agricultural Organization of the World Health Organization was unable to “make a recommendation owing to insufficient data.” And we can’t overlook the fact that so many people consume so many potatoes, often daily, with apparent minimal difficulty.11
Yet insufficient data remains an issue. Because of the paucity of human studies, Mendel and Levin report, “the susceptibility per individual variation and influence of other factors are not well established.” Glycoalkaloid poisoning may be underreported, probably because physicians are more likely to implicate food-borne pathogens (also underreported) or general viral infections as behind GI illness. “We therefore have no real basis to determine the frequency of poisoning caused by glycoalkaloids,” they caution.11
Other avenues of potential harm?
Poisoning is an acute experience. What about potato glycoalkaloids and chronic conditions such as inflammatory bowel disease (IBD)? There has not been a lot of research, and there are even studies suggesting potato juice can benefit GI distress.12
An academic lab in Canada has run several small studies examining potato glycoalkaloids and IBD. A 2002 article shows how the integrity of the membrane layer of the intestine affects the onset of IBD. A lot has changed since then, but its findings are still interesting. The scientist examined 3 model systems—one using cultured cells, one using sheets of mammalian intestine, and one mice strain genetically prone to IBD. Each system was subjected to potato glycoalkaloids at a level comparable to normal potato consumption. The mice showed an increase in the disruption and inflammation of the intestines. In the cultured cells and the intestinal sheets, the glycoalkaloids would “embed themselves and disrupt epithelial barrier integrity.” Higher levels of glycoalkaloids led to more disruption.13
In 2009 the same lab investigated the potential for commercially prepared fried potato skins to aggravate IBD. This time they used two different mouse models of IBD: a strain genetically predisposed to IBD, and a standard lab mouse treated with a chemical that induces IBD. The results: “consumption of potato skins containing glycoalkaloids can significantly aggravate intestinal inflammation in predisposed individuals.”14
In work published in 2007, the Institute of Food Safety at the Wageningen University and Research Centre in the Netherlands exposed lab-grown intestinal cells to concentrations of alpha-chaconine and alpha-solanine, which account for 95% of the total glycoalkaloids in potatoes. Observable changes were noted in cholesterol biosynthesis, growth signaling, and lipid and amino acid metabolism—to name just those covered by less technical language. (Also affected were mitogen-activated protein kinase (MAPK) and NF-kB cascades, cell cycle, and cell death/apoptosis.)15
Glycoalkaloids aren’t even the only problematic compounds in potatoes. The nortropane alkaloids, called calystegines, are another category of alkaloids found in potatoes (and tomatoes and eggplant). Less is known about these toxic alkaloids. They were not discovered until 1988, and detected in potatoes only in 1993. They can inhibit the enzymes involved in digestion and may influence other complex cellular operations. “No human toxicity data for calystegines have been reported,” according to Friedman and Levin. “It is really unknown whether past potato poisonings are a result of glycoalkaloid toxicity alone or a result of the combination of glycoalkaloids and calystegines.”11
Potatoes also contain lectins, proteins—sometimes called anti-nutrients—that bind to carbohydrates. (For more on that, keep reading or scroll directly to the section entitled The Lectin Hypothesis)
A final note, confusing things even further: the potato glycoalkaloids, the calystegines, and the potato lectin all have potential health benefits. The glycoalkaloids and the calystegines may act as anti-inflammatory agents for some people.16 All three may have some utility in fighting cancer.17 Calystegines and glycoalkaloids also have some promise as therapy for diabetes,18 infections, and as an immune system stimulant. Glycoalkaloids may also be useful in treating Alzheimer’s disease.19
That’s a lot of information, some of it contradictory.
I believe the best way to interpret it is to remember that for most people, nightshades like potatoes are an excellent and nutritional food source, and not worth avoiding if you don’t perceive any problem with them.
But don’t let someone say that they can’t cause health problems. The evidence is clear that they have the capacity do harm.
NEXT: The Lectin Hypothesis
- “Horrific Tales of Potatoes That Caused Mass Sickness and Even Death”
- “BRITISH AND AMERICAN MEDICAL JOURNALS”
- “Glycoalkaloid Development during Greening of Fresh Market Potatoes (Solanum tuberosum L.)”
- “The case of the poison potato”
- “High levels of glycoalkaloids in the established swedish potato variety magnum bonum”
- “Potato glycoalkaloids: Some unanswered questions”
- Karpov et al cite the following: Parnell, A. et al. (1984) The glycoalkaloid content of potato varieties. J. Natl. Inst. Agric. Bot. 16, 535 – 541. If you have access to this in your library I’m eager to get a copy of this work; it’s not available from any library I frequent.
- “Potato glycoalkaloids: true safety or false sense of security?”
- page 174-175, Advances in Potato Chemistry and Technology (Second Edition); “Chapter 7 – Glycoalkaloids and Calystegine Alkaloids in Potatoes”
- “Naturally occurring food toxins”
- page 175, Advances in Potato Chemistry and Technology (Second Edition); “Chapter 7 – Glycoalkaloids and Calystegine Alkaloids in Potatoes”
- “Spray-Dried Potato Juice as a Potential Functional Food Component with Gastrointestinal Protective Effects”
- “Potato Glycoalkaloids Adversely Affect Intestinal Permeability and Aggravate Inflammatory Bowel Disease”
- “Naturally Occurring Glycoalkaloids in Potatoes Aggravate Intestinal Inflammation in Two Mouse Models of Inflammatory Bowel Disease”
- “Differential Gene Expression in Intestinal Epithelial Cells Induced by Single and Mixtures of Potato Glycoalkaloids”
- “alpha-Solanine Isolated From Solanum Tuberosum L. cv Jayoung Abrogates LPS-Induced Inflammatory Responses Via NF-kB Inactivation in RAW 264.7 Macrophages and Endotoxin-Induced Shock Model in Mice” & “Anti-inflammatory properties of potato glycoalkaloids in stimulated Jurkat and Raw 264.7 mouse macrophages”
- “Glycoalkaloids and metabolites inhibit the growth of human colon (HT29) and liver (HepG2) cancer cells.”
- “Inhibition of human intestinal alpha-glucosidases by calystegines.”
- “Acetylcholinesterase inhibitors from plants”