Consumption of Nightshade Plants (Part 1) - by Loren Cordain, Ph.D., Professor
Editor's note: Dr. Cordain's latest paper on paleo nutrition discusses the consumption of the nightshade family of plants (potatoes, tomatoes, and chili peppers). We will publish this paper in three parts over the next three weeks in the free weekly edition of The Paleo Diet Update, in addition to making the inividual papers available for purchase in our web store the following week for a limited time. Afterwards, this paper will be available in its entirety from our web store.
Consumption of Nightshade Plants, Human Health and Autoimmune Disease
Previously, I have not specifically commented about the nightshade family of plants in any of my three books, however I have written a brief paper (Tomatoes, Vaccines and Autoimmune Disease) demonstrating a possible link between tomato consumption and autoimmune disease, which is available for purchase in our web store.
Nightshade is the common name for flowering plants belonging to the botanical family Solanaceae, which contain more than 75 genera and 2,000 species1. Some notorious non-edible nightshades include tobacco, petunias, jimson weed, mandrake, and deadly nightshade. The family comprises well known food plants such as potatoes, tomatoes, green peppers, chili peppers, eggplants and tomatillos. Note that chili peppers include all varieties of peppers from the genus Capsicum, including bell peppers, jalapeno, wax, cayenne, habanero, Anaheim, Thai, Tabasco, cherry, pepperoncini and Serrano among others. Chili peppers are commonly consumed as dried powders such as paprika, chili powder and cayenne, and are near universal ingredients in hot sauces, Tabasco sauces, and salsas. Some more obscure edible plants from the Solanaceae family are listed below in Table 1.
Table 1. Some obscure and infrequently consumed edible plant foods within the Solanaceae family (adapted from: United States Department of Agriculture, Agricultural Research Service, Beltsville Area, Germplasm Resources Information Network (GRIN).
http://www.ars-grin.gov/cgi-bin/npgs/html/tax_search.plCommon name or names Scientific name
Tamarillo, Tree tomato, Terong belanda Cyphomandra betacea
Goji Berry, Wolfberry Lycium barbarum
Purple ground cherry, Chinese lantern Quincula lobata
Chinese lantern, Winter cherry, Bladder cherry, Strawberry cherry Physalis alkekengi
Cut leaf ground cherry Physalis angulata
Hairy ground-cherry, Dwarf cape gooseberry Physalis grisea
Cape gooseberries, Golden berry, Husk cherry, Peruvian ground cherry, Poha berry, Giallo grosso Physalis peruviana
Tomatillo, husk tomato Physalis philadelphica (formerly Physalis ixocarpa)
Husk tomato, Strawberry tomato, Ground cherry Physalis pubescens
Sticky gooseberry, Sticky Physalis Physalis viscose
Gilo, Kumpa, Scarlet eggplant Solanum aethiopicum
American nightshade, Black nightshade Solanum americanum
Tzimbalo Solanum caripense
Kangaroo apple Solanum laciniatum
Indian nightshade Solanum lasiocarpum
Garden huckleberry Solanum melanocerasum
Pepino melon Solanum muricatum
Lulo, Naranjilla Solanum quitoense
Cocona, Orinoco-apple, Peach-tomato Solanum sessiliflorum
Wonderberry, Sunberry Solanum retroflexum (formerly Solanum X burbankii)
Ashwagandha, Withania, Winter cherry, Indian winter cherry, Indian ginseng Withania somnifera
Table 2 below shows the recent per capita consumption of commonly eaten nightshades. Potatoes come in first (126 lbs) followed by tomatoes (85.7 lbs, including both fresh and processed), peppers (15.5 lbs) and eggplant (0.8 lbs). These figures clearly show that nightshades are a staple food, universally consumed in the U.S. diet. This raises the question: Are there any health hazards associated with eating almost 230 pounds of nightshades on a yearly basis?
Table 2. U.S. per capita nightshade consumption. Data from USDA Economic Research Service2.
Item Pounds Year
Potatoes (total) 126.0 2007
Frozen 53.0 2007
Fresh 44.0 2007
Chips 16.0 2007
Dehydrated 13.0 2007
Fresh Tomatoes 18.5 2008
Processed Tomatoes (total) 67.2 2008
Tomato sauces 23.5 2008
Tomato paste 12.1 2008
Canned whole tomatoes 11.4 2008
Catsup 10.1 2008
Tomato juice 10.1 2008
Bell peppers 9.1 2008
Chili peppers 6.4 2008
Eggplant 0.8 2008
Total 228.0 2008
Potatoes
Let’s first examine potatoes. Potatoes generally maintain one of the highest glycemic index and load values of any food3-6. Regular consumption of high glycemic index carbohydrates may promote obesity and diseases of insulin resistance, including type 2 diabetes, cardiovascular disease, abnormal blood lipids, gout, acne, polycystic ovary syndrome, epithelial cell cancers (breast, colon and prostate), acanthosis nigricans (a skin disease), and male vertex balding7. Consequently in both of my books I do not recommend that potatoes be included as a regular component of Paleo Diets. Additionally, as you can see from Table 1, most of the potatoes consumed in the U.S. are highly processed in the form of french fries, mashed potatoes, dehydrated potato products, and potato chips. Processed potato foods typically are made with multiple additives (salt, vegetable oils, trans fats, refined sugars, dairy products, cereal grains, preservatives, and other food additives) that may adversely affect health in a variety of ways.
An additional nutritional property of potatoes that is rarely considered in regard to human health is their saponin content. Saponins derive their name from their ability to form "soap" like foams when mixed with water. Chemically, saponins are classified as either steroid glycosides or triterpenoid glycosides. A glycoside is any of a group of organic compounds occurring abundantly in plants that yield a sugar and one or more non-sugar substances upon hydrolysis (chemical decomposition in which a compound is split into other compounds by reacting with water). Steroid glycosides are commonly called glycoalkaloids.
Both categories of saponins are widely distributed throughout the plant kingdom including many cultivated crops. The primary function of saponins is to protect the plant from microbial and insect attack by dissolving cell membranes of these potential predators8. In mammals, including humans who consume saponin containing plants, these substances frequently create pores in the gut lining, thereby increasing intestinal permeability8-10. If they enter the bloodstream in sufficient concentrations, they cause hemolysis (destruction of the cell membrane) of red blood cells8-10.
Figure 1 shows how saponins disrupt cell membranes which may lead to a leaky gut. Saponins first bind cholesterol molecules in intestinal cell membranes due to the affinity of a saponin component (the aglycone moiety) for the membrane sterol (cholesterol)9. In the series of steps that follows, you can see how saponins cause portions of the cell membrane to buckle and eventually break free, forming a pore or a hole in the membrane.
Figure 1. The proposed mechanism by which dietary saponins may elicit pores in intestinal cells leading to a "leaky gut" (adapted from 9).
Potatoes contain two glycoalkaloid saponins: ?-chaconine and ?-solanine which may adversely affect intestinal permeability and aggravate inflammatory bowel disease11, 12. Even in normal healthy adults, a meal of mashed potatoes results in the rapid appearance of both ?-chaconine and ?-solanine in the bloodstream13. The toxicity of these two glycoalkaloids is dose dependent – meaning that the greater the concentration in the bloodstream, the greater is their toxic effect. At least 12 separate cases of human poisoning from potato consumption, involving nearly 2000 people and 30 fatalities have been recorded10. Potato saponins can be lethally toxic once in the bloodstream in sufficient concentrations because these glycoalkaloids inhibit a key enzyme (acetyl cholinesterase) required for the synthesis of acetylcholine, a neurotransmitter required for nerve impulse conduction10. The concentration of both ?-chaconine and ?-solanine in a variety of potato foods are listed in Table 3. Note that the highest concentrations of these toxic glycoalkaloids appear in potato foods containing the skins.
Table 3. Concentrations (mg/kg) of total glycoalkaloids (?-chaconine + ?-solanine) in a variety of potato foods (adapted from 10).
Food Item ?-chaconine + ?-solanine (mg/kg)
Fried skins 567-1450
Chips with skins 95 - 720
Chips (US potatoes) 23 - 180
Frozen baked potatoes 80 - 123
Frozen skins 65 - 121
Baked potato w/jacket 99 - 113
Dehydrated potato flour 65 - 75
Boiled peeled potato 27 - 42
Canned whole new potatoes 24 - 34
Frozen fried potato 4 - 31
Frozen French fries 2 - 29
Dehydrated potato flakes 15 - 23
French fries 0.4 - 8
Frozen mashed potatoes 2 - 5
Canned peeled potato 1 - 2
So the next logical question arises: Should we be eating a food that contains two known toxins which rapidly enter the bloodstream, increase intestinal permeability and potentially impair the nervous system?
In the opinion of these authors: ". . . if the potato were to be introduced today as a novel food it is likely that its use would not be approved because of the presence of these toxic compounds." 11
Other researchers state: "Available information suggest that the susceptibility of humans to glycoalkaloids poisoning is both high and very variable: oral doses in the range 1 - 5 mg/kg body weight are marginally to severely toxic to humans whereas 3 - 6 mg/kg body weight can be lethal. The narrow margin between toxicity and lethality is obviously of concern. Although serious glycoalkaloid poisoning of humans is rare, there is a widely held suspicion that mild poisoning is more prevalent than supposed." 10
The commonly accepted safe limit for total (?-chaconine + ?-solanine) in potato foods is 200 mg/kg, a level proposed more than 70 years ago, whereas more recent evidence suggests this level should be lowered to 60 – 70 mg/kg10. If you take a look at Table 2 you can see that many potato food products exceed this recommendation.
I believe that far more troubling than the potential toxicity of potato glycoalkaloids is their potential to increase intestinal permeability over the course of a lifetime, most particularly in people with diseases of chronic inflammation (cancer, autoimmune disease, cardiovascular disease and diseases of insulin resistance). A leaky gut has been recently proposed to be a universal initiating trigger for autoimmune diseases14 – a conclusion that I agree with15, as well as promoting cardiovascular disease16, 17 and diseases of insulin resistance18. When the gut becomes "leaky" it is not a good thing, as the intestinal contents may then have access to the immune system which in turn becomes activated thereby causing a chronic low level systemic inflammation known as endotoxemia16 – 18. In particular a component of the cell walls of gut gram negative bacteria called lipopolysaccharide (LPS) is highly inflammatory. Any LPS which gets past the gut barrier is immediately engulfed by two types of immune system cells (macrophages and dendritic cells). Once engulfed by these immune cells, LPS binds to a receptor (toll-like receptor-4) on these cells causing a cascade of effects leading to increases in blood concentrations of pro-inflammatory cytokines (localized hormones) including interferon gamma (INF-?),interleukin 1 (IL-1), IL-6, IL-8 and tumor necrosis factor alpha (TNF-?)16, 19. Two recent human studies have shown that high potato diets increase the blood inflammatory marker IL-620, 21. Without chronic low level systemic inflammation, it is unlikely that few of the classic diseases of civilization (cancer, cardiovascular disease, autoimmune diseases and diseases of insulin resistance) would have an opportunity to take hold and wreak their fatal effects.
A final note on potatoes – to add insult to injury, this commonly consumed food is a major source of dietary lectins. On average potatoes contain 65 mg of potato lectin per kilogram. As is the case with most lectins, they have been poorly studied in humans, so we really don’t have conclusive information how potato lectin may impact human health. However, preliminary tissue studies indicate that potato lectin resists degradation by gut enzymes, bypasses the cell wall barriers and can then bind various tissues22, 23. Potato lectins have been found to irritate the immune system and produce symptoms of food hypersensitivity in allergenic and non-allergenic patients24. Just say "no" to potatoes!!
Next week we will publish part 2 of this article: Tomatoes.
References:
Heiser CB. Nightshades, the Paradoxical Plants. W.H. Freeman and Company, San Francisco, CA, 1969.
USDA, Economic Research Service.
http://www.ers.usda.gov/Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002 Jul;76(1):5-56.
Leeman M, Ostman E, Björck I. Glycaemic and satiating properties of potato products. Eur J Clin Nutr. 2008 Jan;62(1):87-95.
Fernandes G, Velangi A, Wolever TM. Glycemic index of potatoes commonly consumed in North America. J Am Diet Assoc. 2005 Apr;105(4):557-62.
Henry CJ, Lightowler HJ, Strik CM, Storey M. Glycaemic index values for commercially available potatoes in Great Britain. Br J Nutr. 2005 Dec;94(6):917-21.
Cordain L, Eades MR, Eades MD. Hyperinsulinemic diseases of civilization: more than just Syndrome X. Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):95-112.
Francis G, Kerem Z, Makkar HP, Becker K. The biological action of saponins in animal systems: a review. Br J Nutr. 2002 Dec;88(6):587-605.
Keukens EA, de Vrije T, van den Boom C, de Waard P, Plasman HH, Thiel F, Chupin V, Jongen WM, de Kruijff B.. Molecular basis of glycoalkaloid induced membrane disruption. Biochim Biophys Acta 1995;1240: 216-228.
Smith DB, Roddick JG, Jones JL. Potato glycoalkaloids: some unanswered questions. Trends in Food Sci Technol 1996;7:126-131.
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.
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 Mar 3. [Epub ahead of print]
Hellenäs KE, Nyman A, Slanina P, Lööf L, Gabrielsson J. Determination of potato glycoalkaloids and their aglycone in blood serum by high-performance liquid chromatography. Application to pharmacokinetic studies in humans. J Chromatogr. 1992 Jan 3;573(1):69-78.
Fasano A. Surprises from celiac disease. Sci Am. 2009 Aug;301(2):54-61.
Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.
Stoll LL, Denning GM, Weintraub NL. Endotoxin, TLR4 signaling and vascular inflammation: potential therapeutic targets in cardiovascular disease. Curr Pharm Des. 2006;12(32):4229-45.
Rauchhaus M, Coats AJ, Anker SD. The endotoxin-lipoprotein hypothesis. Lancet. 2000 Sep 9;356(9233):930-3.
Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007 Jul;56(7):1761-72.
Sweet MJ, Hume DA. Endotoxin signal transduction in macrophages. J Leukoc Biol 1996;60: 8-26.
Kallio P, Kolehmainen M, Laaksonen DE, Pulkkinen L, Atalay M, Mykkänen H, Uusitupa M, Poutanen K, Niskanen L. Inflammation markers are modulated by responses to diets differing in postprandial insulin responses in individuals with the metabolic syndrome. Am J Clin Nutr. 2008 May;87(5):1497-503.
Naruszewicz M, Zapolska-Downar D, Ko?mider A, Nowicka G, Koz?owska-Wojciechowska M, Vikström AS, Törnqvist M. Chronic intake of potato chips in humans increases the production of reactive oxygen radicals by leukocytes and increases plasma C-reactive protein: a pilot study. Am J Clin Nutr. 2009 Mar;89(3):773-7.
Gabor F, Stangl M, Wirth M. Lectin-mediated bioadhesion: binding characteristics of plant lectins on the enterocyte-like cell lines Caco-2, HT-29 and HCT-8. J Control Release. 1998 Nov 13;55(2-3):131-42.
Qaddoumi M, Lee VH. Lectins as endocytic ligands: an assessment of lectin binding and uptake to rabbit conjunctival epithelial cells. Pharm Res. 2004 Jul;21(7):1160-6.
Pramod SN, Venkatesh YP, Mahesh PA. Potato lectin activates basophils and mast cells of atopic subjects by its interaction with core chitobiose of cell-bound non-specific immunoglobulin E. Clin Exp Immunol. 2007 Jun;148(3):391-401.
