Coconut

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Code: f36
Latin name: Cocos nucifera
Source material: Fresh coconut meat
Family: Arecaceae
Common names: Coconut, Common Coconut
There have in the past been 60 other species classified under the genus Cocos, but the Coconut palm is actually monotypic, meaning that within the genus Cocos only one species, nucifera, is now recognised, though within this species are numerous varieties.
 

Allergen Exposure

Geographical distribution
The Coconut is native to tropical eastern regions, but today it is also grown in the tropical parts of the United States, in Central and South America, and in Africa. The largest-producing countries are Mozambique, Tanzania and Ghana. Coconut is a staple food in Asia. Coconuts are both a main source of income for many producing countries, and a source of many important products used in the industrialised world.

The Coconut palm is a long-lived, single-trunk plant up to 30 m tall, with a spiky to drooping crown of long leaves at the top. The fruit, as big as a man's head and 1-2 kg in weight, is a drupe with a thin, smooth, grey-brownish epicarp, a fibrous mesocarp and a woody endocarp. Inside, it contains a single seed, which is partly liquid (Coconut milk) and partly solid (Coconut meat).

Environment
Man can use every part of the Coconut. Coconut can be harvested when young, but the mature fruit is more familiar to the West. The white nut-meat can be eaten either raw or cooked, alone or in a great variety of dishes. The sap produces palm wine and vinegar. The apical buds are eaten as "palm-cabbage". Coconut milk derives from the unripe nuts and is used fresh or fermented. Desiccated Coconut consists of dried and shredded endosperm. Though desiccated Coconut meat in sweets and pastries is the most visible use of Coconut in the West, the oil is very widely used in processed foods such as margarine. Coconut is sensitive to oxidation due to the high oil content and should be stored in well-sealed containers.

At one time, Coconut oil received negative press because of its high level of saturated fat. However, recent research has shown that the fatty acids in unhydrogenated Coconut oil, the medium-chain triglycerides, do not raise serum cholesterol or contribute to heart disease, as do the long-chain triglycerides found in seed oils.
Coconuts are high in protein. Additionally, they have been classified as a "functional food", providing health benefits beyond those from the basic nutrients. The lauric acid in Coconut oil is converted into monolaurin in the body. Monolaurin is the antiviral, antibacterial, and antiprotozoal monoglyceride that destroys lipid-coated viruses and various pathogenic bacteria in the body. Studies have also shown some antimicrobial effects of free lauric acid. Coconut oil is also used by hypothyroid sufferers to increase body metabolism and to lose weight.

Non-edible parts of the plant are used for thatch, fertiliser, charcoal, lumber, caulking, components of furniture, tools, gas masks and air filters, and material for basket-weaving and many other handicrafts. Coconut oil may be burned for illumination and is often used for making natural soaps and other health products, detergents, etc.
 
Unexpected exposure
See under Environment and Other reactions.

Allergens
Coconut allergens appear to be 55, 35, and 36.5 kDa in size. The 35 kDa Coconut protein was shown to be immunologically similar to Soy glycinin (in the legumin group of seed storage proteins) (1).

In a 28-year-old man who experienced anaphylaxis following ingestion of Coconut ice-cream, protein bands of 15, 20, 35, 45 and 200 kDa were detected. IgE immunoblot showed intense reactivity to a 78 kDa protein, and weaker bands for 15-20, 22 and 30 kDa proteins (2).

In a study of a patient with anaphylaxis to Coconut and oral symptoms to tree nuts, IgE binding to 35 and 50 kDa protein bands in Coconut and Hazel nut extracts, respectively, was demonstrated (3).

The serum of a 64-year-old woman, who was monosensitised to Coconut, demonstrated multiple allergen-specific IgE-reacting bands to Coconut milk and Coconut pulp, as well as to dry commercial Coconut powder. The most prominent proteins involved had an apparent molecular weight of 18, 22 and 28 kD (4).

An IgE binding protein of about 18 kDa and 2 weaker bands of about 25 and 75 kDa were demonstrated in the serum of a 3-year-old boy who presented with abdominal pain, vomiting, oral allergy syndrome, and oedema of the eyelids immediately after ingesting a Coconut (5).

The following allergens have been isolated:
  • Coc n 7S globulin (6-7).
  • Coc n 11S globulin, known as Cocosin (6,8).
  • Coc n Profilin has been isolated from Coconut tree pollen (9).

A report was made of 2 Coconut-allergic patients, a 30-year-old man who experienced severe oropharyngeal itching, throat hoarseness, and gastric pain; and a 4-year-old girl who experienced anaphylaxis. An almost identical profile of IgE binding proteins in the Coconut extract was demonstrated in both patients. Both reacted strongly to a band of approximately 29 kDa, shown to be a 7S globulin (7). The 29 kDa band was digested by pepsin in less than 1 minute.

Coconut water contains the proteins glutelin and prolamin (10). Their allergenic potential has not been assessed.

Potential cross-reactivity

An extensive cross-reactivity among the different individual species of the genus could be expected (11).

A 35 kDa Coconut protein is immuno-logically similar to Soy glycinin (in the legumin group of seed storage proteins). In 2 patients allergic to Coconut, the clinical reactivity was reported to likely be due to cross-reacting IgE antibodies primarily directed against Walnut, the original clinical allergy reported, and most likely against a Walnut legumin-like protein (1). Coconut only partially inhibited IgE reactivity to 35 and 36 kDa bands on a Walnut immunoblot, suggesting that IgE resulting from primary Walnut exposure was responsible for a secondary cross-reaction to Coconut (12). Even though Coconut is a monocot and Walnut a dicot, a quite distant relationship, evidence of substantial IgE cross-reactivity between the 2 nuts was detected (12). Similarly, cross-reactive allergens between Hazel nut (a tree nut) and Coconut (a distantly related palm family member) have been reported (3).

In a report on 2 Coconut-allergic patients, a 30-year-old man who experienced severe oropharyngeal itching, throat hoarseness, and gastric pain, and a 4-year-old girl who experienced anaphylaxis, both reacted strongly to a band of approximately 29 kDa shown to be a 7S globulin, a protein with a high correlation with a 7S globulin from Elaeis guineensis (Oil Palm). Cross-reactivity was demonstrated among Coconut, Walnut, and Hazel nut by inhibition studies in patient 2 (7).

There may be a weak association between Latex allergy and allergy to Coconut. Among 137 patients with Latex allergy, 49 potential allergic reactions to foods were reported in 29 (21.1%). Foods responsible for these reactions included Banana (n=9, or 18.3%), Avocado (n=8, or 16.3%), shellfish (n=6, or 12.2%), fish (n=4, or 8.1%), Kiwi (n=6, or 12.2%), and Tomato (n=3, or 6.1%); Watermelon, Peach, and Carrot (n=2, or 4.1% each); and Apple, Chestnut, Cherry, Coconut, Apricot, Strawberry, and Loquat (n=1, or 2.0% each). Reactions to foods included local mouth irritation, angioedema, urticaria, asthma, nausea, vomiting, diarrhoea, rhinitis, and anaphylaxis (13).

Clinical Experience

IgE-mediated reactions
Coconut may uncommonly induce symptoms of food allergy in sensitised individuals (1,14-16). The prevalence of Coconut allergy has not been studied; however, the Food Allergy and Anaphylaxis Network (FAAN) Peanut and Tree Nut Allergy Registry in the USA, which collected data on 5,149 patients (mainly children), records that 4 individuals reported allergy to Coconut (17).

A baby of 8 months, fed from birth with maternal milk, developed severe gastro-intestinal symptoms due to the presence of Coconut oil in an infant formula. Diagnosis was made using SPT and oral challenges (18).

A report described 2 Coconut-allergic patients: a 30-year-old pollen-allergic man monosensitised to Coconut who presented with severe oropharyngeal itching, throat hoarseness, and gastric pain 10 minutes after the intake of fresh Coconut; and a 4-year-old girl with a previous allergy to Walnut (intense oropharyngeal itching and facial pruritic erythema after ingesting a small amount of Walnut), but not allergic to pollen, who developed anaphylaxis on Coconut ingestion. Within 15 minutes of eating a piece of fresh Coconut, she experienced intense oropharyngeal itching, followed by facial angioedema, cough, wheezing and dyspnoea requiring emergency treatment. Both patients were shown to have skin reactivity and serum IgE to Coconut. The adult patient did not report any adverse reactions Peanut or tree nuts. For him, Coconut-specific IgE was 18 kUA/l. The young girl's IgE was 18.3 kUA/l for Coconut, and IgE for Almond, Hazel nut, and Walnut were 2.40, 19.70, and 49.0 kUA/l, respectively, with cross-reactivity being demonstrated between these (7).

Monosensitisation to Coconut was described in a 64-year-old woman who experienced generalised urticaria, facial and uvula oedema, dysphagia and dyspnoea a few minutes after eating a Coconut biscuit. She also experienced bronchoconstriction, hypotension and hypoxemia minutes after eating a Spanish sweet containing, among other ingredients, Coconut. She was not sensitised to the other ingredients. SPT was strongly positive for Coconut pulp and Coconut milk, and a skin reaction (oedema and erythema) developed 4-6 hours later. No skin reactivity was demonstrated for, among other substances, Date, Palm pollen, Peanut, Almond, Pistachio nut, Walnut, Hazel nut, Sweet chestnut, Soybean, Cocoa, Chick pea, Lentil, Mustard or Latex. Coconut IgE antibody level was 20.8 kUA/l, but not detected for Tree nuts, legumes or Soybean (4).

A 3-year-old boy was described as experiencing abdominal pain, vomiting, oral allergy syndrome, and oedema of the eyelids immediately after ingesting a Coconut sweet. A year after this episode, he experienced the same symptoms after eating a small portion of fresh Coconut. SPT to Coconut  with fresh Coconut was strongly positive. SPT was weakly positive for Almond, and an oral challenge with Almond was negative. A patch test with Coconut was negative. Coconut-specific IgE was Class 3 (5).

Two patients aged 50 and 21, with tree nut allergy manifested by life-threatening systemic reactions, reported systemic reactions after the consumption of Coconut. The clinical reactivity in these 2 patients was ascribed to cross-reacting IgE antibodies directed primarily against Walnut, the original clinical allergy reported, and most likely against a Walnut legumin-like protein (1).

Anaphylaxis following the ingestion of Coconut has been reported in a 28-year-old atopic man following ingestion of Coconut ice cream. The reaction consisted of oral pruritis, vomiting and intense angioedema of the lips and uvula (2).

Concomitant anaphylaxis to Coconut and oral symptoms to Hazel nut have been reported, with positive SPT to Coconut (3).

Contact dermatitis to Coconut has been more commonly reported than Coconut food allergy. Coconut-derived products include Coconut diethanolamide, cocamide sulphate, cocamide DEA, and CDEA. These are commonly present in cosmetics, moisturisers, soaps, hand washing liquids and other cleansers, and shampoo. An itchy, blistering rash may arise a day or two after contact with the allergen and take several days to resolve - unless ongoing contact with the allergen is made, in which case it will persist (19).

It has been proposed that sensitisation to foods may occur through topical exposure. A study sought to describe the prevalence of allergenic foods and herbs in pediatric skin care products and found that Coconut was the most common food present. It was found in 44.4% of the products examined, and was particularly often used in soaps and body washes (75.9%) and in shampoos (76.9%) (20).

Other reactions
Various substances, e.g., Coconut diethanol-amide (CDEA), are manufactured from Coconut and Coconut oil. These substances are widely used as surface-active agents in hand gels, hand-washing liquids, shampoos and dish-washing liquids, and may result in contact dermatitis (19,21).

Pollen from the Coconut tree has been reported to result in rhinitis and asthma in Coconut pollen-sensitised individuals (22-24).
Occupational allergic conjunctivitis due to Coconut fibre dust was reported in a 46-year-old who had worked for 10 years in a Coconut fibre mattress factory. Conjunctivitis would develop 20-30 minutes after he began tufting mattress with Coconut fibre (25).

Compiled by Dr Harris Steinman, harris@zingsolutions.com

References

  1. Teuber SS, Peterson WR. Systemic allergic reaction to coconut (Cocos nucifera) in 2 subjects with hypersensitivity to tree nut and demonstration of cross-reactivity to legumin-like seed storage proteins: new coconut and walnut food allergens.
    J Allergy Clin Immunol 1999;103(6):1180-5
  2. Rosado A, Fernandez-Rivas M, Gonzalez-Mancebo E, Leon F, Campos C, Tejedor MA. Anaphylaxis to coconut.
    Allergy 2002;57(2):182-3
  3. Nguyen SA, More DR, Whisman BA, Hagan LL. Cross-reactivity between coconut and hazelnut proteins in a patient with coconut anaphylaxis. Ann Allergy Asthma Immunol 2004;92(2):281-4
  4. Martin E, Tornero P, De Barrio M, Pérez CI, Beitia J M, Baeza ML. Monosensitization to coconut.
    J Allergy Clin Immunol 2004:113:S315
  5. Tella R, Gaig P, Lombardero M, Paniagua MJ, Garcia-Ortega P, Richart C. A case of coconut allergy. Allergy 2003;58(8):825-6
  6. Balasundaresan D, Sugadev R, Ponnuswamy MN. Purification and crystallization of coconut globulin cocosin from Cocos nucifera.
    Biochim Biophys Acta 2002;1601(1):121-2
  7. Benito C, Gonzalez-Mancebo E, de D, Tolon RM, Fernandez-Rivas M. Identification of a 7S globulin as a novel coconut allergen.
    Ann Allergy Asthma Immunol 2007;98(6):580-584
  8. Carr HJ, Plumb GW, Parker ML, Lambert N. Characterization and crystallization of an 11S seed storage globulin from coconut (Cocos nucifera). Food Chemistry 1990;38(1):11-20
  9. Liu ZG, Wu YL., Zhang HY. Cloning, expression and immunocharacterization of pan-allergen profilin in Cocos nucifera.
    http://www.expasy.org/uniprot/A1Z292 2007: February 6
  10. Birosel DM, de Oliveira Ferro V, Holcberg IB, Pitelli AC. Isolation of proteins in coconut water. [Portuguese] Rev Farm Bioquim Univ Sao Paulo 1976;14(1):35-42
  11. Yman L. Botanical relations and immuno-logical cross-reactions in pollen allergy. 2nd ed. Pharmacia Diagnostics AB. Uppsala. Sweden. 1982: ISBN 91-970475-09
  12. Roux KH, Teuber SS, Sathe SK. Tree nut allergens. Int Arch Allergy Immunol 2003;131(4):234-44
  13. Kim KT, Hussain H. Prevalence of food allergy in 137 latex-allergic patients.
    Allergy Asthma Proc 1999;20(2):95-7
  14. Sastre J, Olmo M, Novalvos A, Ibanez D, Lahoz C. Occupational asthma due to different spices. Allergy 1996;51(2):117-20
  15. Jacquenet S, Moneret-Vautrin DA. Les allergènes de l'arachide et des fruits à coque / Allergy to peanut and all kinds of nuts Revue francaise d allergologie 2007;47(8):487-91
  16. Agarkhedkar SR, Bapat HB, Bapat BN. Avoidance of food allergens in childhood asthma.
    Indian Pediatr. 2005;42(4):362-6
  17. Sicherer SH, Furlong TJ, Munoz-Furlong A, Burks AW, Sampson HA. A voluntary registry for peanut and tree nut allergy: characteristics of the first 5149 registrants.
    J Allergy Clin Immunol 2001;108(1):128-32
  18. Couturier P, Basset-Stheme D, Navette N, Sainte-Laudy J. A case of coconut oil allergy in an infant: responsibility of “maternalized” infant formulas. [French] Allerg Immunol (Paris) 1994;26(10):386-7
  19. Fowler JF Jr. Allergy to cocamide DEA.
    Am J Contact Dermat 1998;9(1):40-1
  20. Newhall KK, Amoruso LS, Sinacore JM, Pongracic JA. Presence of common food allergens in commercially available pediatric skin care products.
    J Allergy Clin Immunol 2004:113:S235
  21. Pinola A, Estlander T, Jolanki R, Tarvainen K, Kanerva L. Occupational allergic contact dermatitis due to coconut diethanolamide (cocamide DEA).
    Contact Dermatitis 1993;29(5):262-5
  22. Karmakar PR, Chatterjee BP. Cocos nucifera pollen inducing allergy: sensitivity test and immunological study.
    Indian J Exp Biol 1995;33(7):489-96
  23. Chowdhury I, Chakraborty P, Gupta-Bhattacharya S, Chanda S. Antigenic relationship between four airborne palm pollen grains from Calcutta, India Ann Agric Environ Med. 1999; 6(1):53-56
  24. Pumhirun P, Towiwat P, Mahakit P. Aeroallergen sensitivity of Thai patients with allergic rhinitis. Asian Pac J Allergy Immunol 1997;15(4):183-5
  25. Wittczak T, Pas-Wyroslak A, Palczynski C. Occupational allergic conjunctivitis due to coconut fibre dust.
    Allergy 2005;60(7):970-1

 

As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.