Potatoes: 

Jacob Schor, ND, FABNO

www.DenverNaturopathic.com

March 24, 2014

 

Potatoes: more dangerous than they look

 

There is something peculiar about potatoes.  It appears that their story of origin, the domestication by Neolithic Peruvians in some distant past, has an inherent weakness.  Early potatoes were too poisonous to eat.

 

Potatoes contain substantial amounts of two glycoalkaloids, namely solanine and chaconine that can wreck havoc on a person’s bowels.  These chemicals disrupt gut epithelial barrier integrity and aggravate or maybe cause inflammatory bowel disease (IBD). Frying potatoes concentrates glycoalkaloids and IBD incidence is highest in countries where fried potato consumption is also highest.[1]    That’s something to chew on.

 

[It is also worth noting, for the sake of curiosity, that Thomas Jefferson is credited with ‘inventing’ French fried potatoes [2]   and also as we’ve previously mentioned, he wrote about the batter fried fish that he ate in London and apparently served the same at Monticello.[3]  We might call Jefferson the ‘Fish and Chips President.’] 

 

It is potato skins in particular where these chemicals concentrate and while it makes good sense for individuals with IBD to avoid all potatoes, they should especially avoid potato skins and even more so fried potato skins [4] . 

 

Potatoes belong to the plant family Solanaceae, which contains several important foods including tomato and eggplant, along with several potent poisonous plants including mandrake, henbane and deadly nightshade. For IBD sufferers, avoiding all of these foods may provide some relief. 

 

The story goes that the Inca people of the Andes first cultivated potatoes in prehistoric times. Potatoes were brought to Europe by the Spanish invaders. Originally reviled as 'peasant food', potatoes were regarded with suspicion as an evil plant and a potential cause of leprosy. Over several centuries they became established throughout Britain, France and the continent, and in particular in Ireland, where its growth allowed the population to expand very rapidly between 1750 and 1850. In the late 1840s, trouble arrived in the form of the potato blight and the Irish famine. Potatoes can be rather poisonous if they are turning green or sprouting. The greening tuber produces toxic quantities of solanine.[5]   

 

It should be noted that an episode of the PBS program Arthur took on this subject; D.W. and tough guy Binky are tricked into eating a green potato chip and fearing an early demise both resolve to make the best of their remaining days. [6]   This cartoon, while amusing, may have done a disservice.  Green or sprouted potatoes can be a real problem and can lead to vomiting, diarrhea and death.[7]   Perhaps not in the small quantities that D.W. and Binky consumed, but perhaps it would be better to be reminded that green potatoes are dangerous than be told they are safe.  A particular case report of 78 British schoolboys sickened by eating old potatoes stands out [8] .

 

A 2009 paper attempted to calculate how close people come to routinely poisoning themselves with potatoes by calculating potato consumption versus toxic levels. Modern potatoes typically contain about 10-100 mg/kg of glycoalkaloids and tend not to contain more than 200 mg/kg. Poisoning causes GI ailments and neurological symptoms.  A critical dose is considered more than 1-3 mg/kg.  The researchers used databases of food consumption in the Czech Republic, Sweden and The Netherlands. Combining consumption, processing and other factors, they report that eating modern European potatoes may lead to acute intakes >1 mg/kg body weight in only about 0.01% of the population.  That’s only one person in a thousand.  People were consuming from only 25-50% of the toxic level.  Of course this is assuming that it takes 1 milligram/kg bw  a day to cause any symptoms, that all cases of poisoning  are reported,  that some people are not more sensitive than the general population. These are assumptions that few of us should be willing to bet on.[9]

 

There are other possible toxic reactions to solanaceae that are under appreciated. There is a reported case in 2008 of diabetes insipidus brought on by high dose solanine[10]  . This is complicated business to say the least [11] .   Highly edible foods don’t just show up in nature begging animals to eat them, they typically contain chemicals to discourage overconsumption.  So it’s no surprise that potatoes “… contain antinutritional and potentially toxic compounds including inhibitors of digestive enzymes, hemagglutinins, and glycoalkaloids. Solanum glycoalkaloids are reported to inhibit cholinesterase, and disrupt cell membranes.  Various things affect glycoalkaloids content including storage, light, radiation, mechanical damage, and food processing. While commercially available ELISA test kits permit easy assay of glycoalkaloid content and this could allow easy reporting of toxic content of food products,[12]    this is not yet seen in practice.

 

There are hundreds of wild potato species that grow in both North and South America, though most are in a small area of Peru.  There are ongoing debates as to where the first ‘real’ potato originated: Peru, Bolivia or Chile and whether this happened in one location or simultaneously in several. [13]   Today, it seems that, “More than 99 percent of all modern potato varieties planted today are the direct descendents of varieties that once grew in the lowlands of south-central Chile.”  [14] 

 

These wild potato ancestors of our modern potato contain far more solanine than our modern versions.  In other words they were quite poisonous.  Bill Bryson in his fascinating treatise, “At Home, a short history of private life” raises an interesting question about the story of potato origination:

“…. Making any wild potatoes safe to eat required reducing glycoalkaloid content to between one-fifteenth and one-twentieth of its normal level.   This raises a lot of questions, beginning most obviously with: How did they do it?  And while they were doing it, how did they know they were doing it?  And while they were doing it, how do you tell the poison content has been reduced by, say, 20 percent or 35 percent or some other intermediate figure?  How do you assess progress in such a process?  Above all, how did they know that the whole exercise was worth the effort and that they would get a safe and nutritious food stuff at the end?  ... The fact is, people in the ancient world were often doing things that are not just surprising but unfathomable.” [15]

 

In other words, the story of slowly breeding a potato over generations to be less toxic begins to sound implausible when you consider that all of the intermediate potatoes are still too toxic to eat and the only available test subjects were oneself and one’s family members.

 

Luckily Charles Mann writing in a 2011 issue of the Smithsonian provides us with a believable explanation:

 

 

“…. In the mountains, guanaco and vicuña (wild relatives of the llama) lick clay before eating poisonous plants. The toxins stick—more technically, “adsorb”—to the fine clay particles in the animals’ stomachs, passing through the digestive system without affecting it. Mimicking this process, mountain peoples apparently learned to dunk wild potatoes in a “gravy” made of clay and water. Eventually they bred less-toxic potatoes, though some of the old, poisonous varieties remain, favored for their resistance to frost. Clay dust is still sold in Peruvian and Bolivian markets to accompany them.”[16]

 

 

Thus an accompaniment of clay gravy allowed for the long-term consumption of poisonous varieties of potato and the slow evolutionary selection of low glycoalkaloid varieties, based on the simple calculation of how much clay was necessary to prevent symptoms of poisoning.

 

 

Our take home lesson from this story should go like this:

 

1.  People with inflammatory bowel disease (IBD), that is ulcerative colitis or Cohn’s disease (and probably other conditions we associate with increased bowel permeability (leaky gut syndrome) should limit their potato intake, in particular potato skins and equally so, fried potatoes.

 

2.  Potato skins are not the healthiest part of a potato; they may be the most toxic. We are in the habit of thinking that leaving the skin on potato is akin to whole-wheat flour, somehow healthier. This is wrong.  While potato skins may add flavor to French Fries, and other delectable foods, we should think twice about eating them, at least too often.

 

We might also add that human history, along with biology, is often more complex than one might think.

 

 

 

 

References:

 

1.  Patel B, Schutte R, Sporns P, Doyle J, Jewel L, Fedorak RN. Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease. Inflamm Bowel Dis. 2002 Sep;8(5):340-6.

 

2.  http://www.monticello.org/site/blog-and-community/posts/jefferson-era-recipe-fried-potatoes

 

3.  http://www.denvernaturopathic.com/chanukahfishandchips.htm

 

4.  Iablokov V, Sydora BC, Foshaug R, Meddings J, Driedger D, Churchill T, Fedorak RN. Naturally occurring glycoalkaloids in potatoes aggravate intestinal inflammation in two mouse models of inflammatory bowel disease. Dig Dis Sci. 2010 Nov;55(11):3078-85. doi: 10.1007/s10620-010-1158-9. Epub 2010 Mar 3.

 

5.  Lee MR. The Solanaceae: foods and poisons. J R Coll Physicians Edinb. 2006 Jun;36(2):162-9.

 

6.  http://en.wikipedia.org/wiki/List_of_Arthur_episodes_(season_3)

 

7.  Solanine poisoning. Br Med J. 1979 Dec 8;2(6203):1458-9.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1597169/pdf/brmedj00103-0006b.pdf

 

8.  McMillan M, Thompson JC. An outbreak of suspected solanine poisoning in schoolboys: Examinations of criteria of solanine poisoning. Q J Med. 1979 Apr;48(190):227-43.

 

9. Ruprich J1, Rehurkova I, Boon PE, Svensson K, Moussavian S, Van der Voet H, Bosgra S, Van Klaveren JD, Busk L. Probabilistic modelling of exposure doses and implications for health risk characterization: glycoalkaloids from potatoes. Food Chem Toxicol. 2009 Dec;47(12):2899-905. doi: 10.1016/j.fct.2009.03.008. Epub 2009 Mar 13.

 

10.  Huang WH, Hsu CW, Fang JT. Central diabetes insipidus following digestion Solanum indicum L. concentrated solution. Clin Toxicol (Phila). 2008 Apr;46(4):293-6. doi: 10.1080/15563650701385881.

 

11.  Friedman M. Potato glycoalkaloids and metabolites: roles in the plant and in the diet. J Agric Food Chem. 2006 Nov 15;54(23):8655-81.

 

12.Adv Exp Med Biol. 1999;459:121-43.

 

13.  Spooner DM1, McLean K, Ramsay G, Waugh R, Bryan GJ. A single domestication for potato based on multilocus amplified fragment length polymorphism genotyping.

Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14694-9. Epub 2005 Oct 3.

 http://www.pnas.org/content/102/41/14694

 

14.  http://www.eurekalert.org/pub_releases/2008-01/uow-uds012908.php

 

15.  Bryson, W. At Home:A short history of private life. Anchor Books, New York, 2010. Pg 49

 

16.   http://www.smithsonianmag.com/history/how-the-potato-changed-the-world-108470605/#GD1LYfhgtgOyzize.99