Paradise Nut
You may drive out nature with a fork - it will always revert”. In our time the sentence of the Latin poet is more appreciated than ever. “Naturalness” is an attractive feature of any product, especially if it is to be used as food. Vitamins and trace elements are considered to be more valuable if they come from a natural source. For the important trace element selenium a natural source exists in the form of the seeds of the paradise nut tree. The name Paradise nut or Sapucaia nut is used for the genus Lecythis of which 26 species have been described (MORI 1990).
Together with the genus Bertholettia (only one species: B. excelsa, the Brazil nut) it forms the subfamily of the Lecythidoideae of the family Lecythidaceae. Many members of the Lecythidaceae have an interesting characteristic: They accumulate selenium in the seeds if they grow in seleniferous soil. Selenium accumulation has been found in the Brazil nut (PALMER, 1982), in the species Lecythis ollaria (KERDEL-VEGAS, 1966), Lecythis minor (DICKSON, 1969), Lecythis pisonis (ANDRADE 1999) and Lecythis tuyrana (BEHR, 2002). It is likely that selenium accumulation is a common characteristic of the entire genus Lecythis, or, to include the Brazil nut, of the entire subfamily Lecythidoideae.
Why and how does Selenium present in the soil end up in the seeds of paradise and Brazil nut trees? Selenium is actually an element which is detrimental to most plants. They absorb the selenium from the soil as selenate and process it in analogy to the common biochemical pathway of sulphur. Most plants cannot differentiate between selenium and sulphur and therefore incorporate selenium at random instead of sulphur into amino acids: They synthesise instead of cysteine to a certain degree selenocysteine and insteadxof methionine selenomethionine. Most plants do also not differentiate between normal sulphur containing amino acids and these seleno analogs and thus incorporate them in random substitution of the sulphur analogs into proteins (DAWSON, 1988).
There are certain differences between sulphur amino acids and selenium amino acids: The selenium atom is larger and - more important - it behaves chemically somewhat differently. The SeH bond in selenocysteine is more acidic (that is, it ionises at lower pH) than the S-H bond; also it is more prone to oxidation. Thus, in proteins Se-H groups form readily -Se-Se- crosslinking bridges. These, together with the higher degree of ionisation contorts proteins and makes them -from a certain Se concentration on -dysfunctional: The organism - be it plant or animal - dies if it has absorbed too much selenium (HUBER, 1967). Selenium accumulator plants have found a solution for this dilemma. They interrupt the normal biochemical pathway of selenium metabolism at a precursor of the seleno amino acids namely selenocystathionine: HOOC-CH(NH2)-CH2-CH2-Se-CH2-CH(NH2)-COOH The advantage of this compound is that it (like the sulphur analog cystathionine) is not incorporated into proteins. Thus, proteins cannot be damaged.
Rather, the uncommon amino acid is “compartmentalized” in certain parts of the plant in the free form rendering these parts less attractive to browsing animals. Selenium is thus used as a protective agent. And the selenium accumulator plants can thrive on seleniferous soils unlike all other plants. Paradise or Brazil nuts can be used as sources for nutritional selenium provided they do contain sufficient selenium to make the processing economical. This is rarely the case with Brazil nuts: Bertholettia excelsa cannot be cultivated (in pure stands the trees do not bear seeds), the nuts are collected from the wild and the provenance of individual lots is usually unknown. And this provenance can be any location of the entire Amazonian region where soils are often free of selenium.
Individual Brazil nuts may have a very high selenium content, but the average concentration in commercial lots is fairly low (SECOR 1989, CHANG 1995). In contrast, paradise nut species (in particular L. ollaria and L. minor) have more narrow distribution ranges. Provenances can thus be selected in view of the occurrence of selenium. Paradise nuts too are collected from the wild. Their cultivation has often been recommended (“Frutales de Venezuela” (HOYOS, 1989), “Some Fruits and Nuts for the Tropics” (KENNARD, 1960), “Edible Nuts of the World” (MENNINGER, 1977) and “Tropische Nutzpflanzen ” (BRUECHER, 1977). But so far the cultivation was not a success. It should be stressed that common nut species (walnut, almond, pecan) do not accumulate selenium in the seeds (CARLSON), it is an exclusive characteristic of the Lecythidoideae subfamily of the Lecithidaceae.
By pressing shelled paradise nuts a meal is obtained which may contain as much as several thousand milligrams selenium per kilogram. For practical purposes it is blended with a carrier to obtain a standard selenium concentration of 1000 mg/kg. While the Se concentration in the pure nut meal varies, it is fairly constant (and low) in the oil: Around 4 mg Se/kg. This is explained by the fact that the selenium in paradise nut is predominantly present as selenocystathionine which is water soluble and has a correspondingly low solubility in oil. The high molecular weight and low volatility of Selenocystathionine has also the consequence that paradise nut meal does not have the offensive odour commonly associated with organic selenium compounds.
The importance of an adequate nutritional selenium intake is generally known and therefore shall be summarized only shortly here. Selenium is essential for human and animal nutrition. It occurs in the body in appr. 35 proteins, generally in the form of selenocysteine. Many of the proteins are enzymes (glutathione peroxidases, iodothyronine deiodinases, thioredoxine reductase), the function of others (Selenoprotein P, Selenoprotein W) is unknown, they may simply be storage forms. Non-proteinaceous selenium occurs in form of certain metabolites (e.g. selenodiglutathione) which do also have an important function. Selenium is further found in low concentration in all (e.g. muscle) proteins where methionine (and probably also cysteine) is randomly substituted by the seleno analogs selenomethionine (and selenocysteine).
Selenium is not evenly distributed in the body. In times of deficiency the element is rapidly lost from muscle and liver and retained in brain, endocrine and reproductive organs, apparently because it is essential for the functioning of these organs. Even within organs certain selenoenzymes are expressed with preference over others in periods of undersupply (McKENZIE, 2002, p. 234).
How much selenium intake is sufficient?
paradise Nut Shell
LEVANDER and MORRIS (1984) determined the dietary selenium requirement to maintain a balance to be 80 mcg per person per day for men and 57 mcg for women or 1 mcg/kg body weight in general. At equilibrium, excretion equals intake. Is this balance requirement an optimal value? It is rather a minimum value, if the results of certain intervention studies are considered, e.g. of CLARK (1996). Cancer incidence reduction was observed at supplementation rates of 200 mcg Se per person per day. Apparently, higher intake while leading to higher excretion involves also an increased selenium metabolism. And selenium metabolites are assumed to play a critical role in cancer prevention (McKENZIE, 2002, p. 245). The upper limit of selenium intake (long term level of no adverse effect) was stated by COMBS & COMBS (1986) to be 775 mcg organically bound and 550 mcg of inorganic selenium per person per day.
According to SPALLHOLZ (1990) adverse effects can be observed at intakes above 400 mcg Se per person per day already. Therefore, considering the amount of selenium already present in the common diet and applying a safety margin, selenium supplements should not be consumed over longer periods at rates of more than 200 mcg per person per day.
What are the effects of dietary selenium?
Complete Paradise Nut Shell
Selenium detoxifies mercury by formation of a mercury selenide protein complex (SCHRAUZER). It also reduces the toxicity of cadmium (PARIZEK 1971) and arsenic (WANG 2001). Selenium diminishes the coronary infarction risk, already at fairly low supply rates (45 mcg per person per day). Therefore the preventive effect of selenium supplementation becomes visible only in populations with a low average dietary selenium intake (e.g. Finland, New Zealand, Germany). This observation is explained by the hierarchy of selenium usage: In Se deficiency the more vital organs retain selenium in preference to others. (HUTTUNEN 1997, KARDINAAL 1997). KIEM (1987) states that no human cell has a higher selenium concentration than blood platelets and he found that they retain selenium firmer than other blood components under conditions of depletion.
Most striking is the effect of selenium supplementation in the prevention of cancer. CLARK (1996 ) reports a 50% reduction of cancer incidence in a double blind prevention study in which half of the participating patients were administered 200 mcg selenium while the other half obtained placebos (all patients had a previous cancer history).
The effect of selenium became strikingly visible at an early stage: “Primarily because of the apparent reductions in total cancer mortality and total cancer incidence in the thioredoxine reductase), the function of others (Selenoprotein P, Selenoprotein W) is unknown, they may simply be storage forms. Non-proteinaceous selenium occurs in form of certain metabolites (e.g. selenodiglutathione) which do also have an important function. Selenium is further found in low concentration in all (e.g. muscle) proteins where methionine (and probably also cysteine) is randomly substituted by the seleno analogs selenomethionine (and selenocysteine).
Selenium is not evenly distributed in the body. In times of deficiency the element is rapidly lost from muscle and liver and retained in brain, endocrine and reproductive organs, apparently because it is essential for the functioning of these organs. Even within organs certain selenoenzymes are expressed with preference over others in periods of undersupply (McKENZIE, 2002, p. 234).
How much selenium intake is sufficient?
LEVANDER and MORRIS (1984) determined the dietary selenium requirement to maintain a balance to be 80 mcg per person per day for men and 57 mcg for women or 1 mcg/kg body weight in general. At equilibrium, excretion equals intake. Is this balance requirement an optimal value? It is rather a minimum value, if the results of certain intervention studies are considered, e.g. of CLARK (1996). Cancer incidence reduction was observed at supplementation rates of 200 mcg Se per person per day. Apparently, higher intake while leading to higher excretion involves also an increased selenium metabolism. And selenium metabolites are assumed to play a critical role in cancer prevention (McKENZIE, 2002, p. 245). The upper limit of selenium intake (long term level of no adverse effect) was stated by COMBS & COMBS (1986) to be 775 mcg organically bound and 550 mcg of inorganic selenium per person per day.
According to SPALLHOLZ (1990) adverse effects can be observed at intakes above 400 mcg Se per person per day already. Therefore, considering the amount of selenium already present in the common diet and applying a safety margin, selenium supplements should not be consumed over longer periods at rates of more than 200 mcg per person per day.
What are the effects of dietary selenium?
Selenium detoxifies mercury by formation of a mercury selenide protein complex (SCHRAUZER). It also reduces the toxicity of cadmium (PARIZEK 1971) and arsenic (WANG 2001). Selenium diminishes the coronary infarction risk, already at fairly low supply rates (45 mcg per person per day). Therefore the preventive effect of selenium supplementation becomes visible only in populations with a low average dietary selenium intake (e.g. Finland, New Zealand, Germany). This observation is explained by the hierarchy of selenium usage: In Se deficiency the more vital organs retain selenium in preference to others. (HUTTUNEN 1997, KARDINAAL 1997). KIEM (1987) states that no human cell has a higher selenium concentration than blood platelets and he found that they retain selenium firmer than other blood components under conditions of depletion.
Most striking is the effect of selenium supplementation in the prevention of cancer. CLARK (1996) reports a 50% reduction of cancer incidence in a double blind prevention study in which half of the participating patients were administered 200 mcg selenium while the other half obtained placebos (all patients had a previous cancer history). The effect of selenium became strikingly visible at an early stage: “Primarily because of the apparent reductions in total cancer mortality and total cancer incidence in the selenium group, the blinded phase was stopped early”. Crucial for the prevention effect seem to be certain selenium metabolites, e.g. selenodiglutathione.
This compound does not harm normal cells but causes apoptosis of tumor cells by inducing the tumor suppressor protein, p53 (LANFEAR 1994). “Selenium modulates immunity: Se deficiency impairs immunity, Se intakes above those habitually consumed in many Western countries boost immunity and high Se intakes lead to toxic effects and suppression of immunity” (McKENZIE 2002, p. 229). The influence of selenium on the immune system has many facets which cannot be discussed in detail here. Only one function shall be mentioned, the role of selenium, or rather the selenoenzyme glutathione peroxidase in the so-called “respiratory burst”.
The respiratory burst is a rapid generation of reactive oxygen species (ROS), most of all superoxide (O2-.) which certain lymphocytes direct against invading microorganisms to destroy them. For the optimal function of the respiratory burst a sufficient concentration of the glutathione peroxidase is decisive and indispensible. Hydrogen peroxide generated in the process threatens to damage other cell functions and most of all it blocks the enzyme which provides the superoxide in the first place. The respiratory burst cannot start unless the hydrogen peroxide is removed. The removal of the hydrogen peroxide is effected by glutathione peroxidase which thus initiates and controls the entire process.
Is organic selenium superior to inorganic selenium?
From an aesthetic point of view organic forms are always preferable to inorganic forms. While inorganic forms (selenate and selenite) are effective and are used extensively in animal feed, especially selenite has many disadvantages. Its higher reactivity promotes other undesirable reactions: Ascorbate reduces selenite to insoluble and inabsorbable elemental selenium. According to SCHEARER (1980) selenite causes cataracts in young rats, probably because of its promotion of peroxidation. The general instability of selenite explains the inferior uptake and retention in comparison to organic forms of selenium (WHANGER 2002).
Selenocystathionine, the form of selenium in paradise nuts has many advantages as a nutritional selenium form. Its comparatively large molecule protects the selenium and diminishes the likeliness of unwanted side reactions as for instance oxidation. As a non-proteinaceous amino acid the compound is easily integrated into the physiological pathways of selenium metabolism without prior incorporation into body proteins. Paradise nuts are readily available, their seed meal as well as seed oil offer themselves as attractive new raw materials for the production of food supplements and cosmetic products.
References:
ANDRADE, MAIA, J., STREICH, R., 1999: Seed composition of Amazonian Lecythidaceae species. J. Food Compositon and Analysis, vol 12, p 37-51,1999
ARONOW, L.; KERDEL-VEGAS, F., 1965: Seleno-Cystathionine, a pharmacologically active factor in the seeds of Lecythis ollaria. Nature, Vol. 205,1965 March 20, No. 4977,1185-1187
BEHR, W., 2002: Unpublished. The analysis of the defatted seeds of seeds of Lecythis tuyrana showed the selenium concentration to be 800 mcg/g.
BRÜCHER, H., 1977: Tropische Nutzpflanzen, Springer Verlag, 1977, S. 410
CARLSON, R.M., et al.: Selenium Concentrations in Deciduous Nut Tree Tissue Samples from Western Fresno and Merced Counties. Contribution of the Department of Pomology, University of California, Davis, CA 95616
CHANG, J.C, 1995: Selenium content of Brazil nuts from two geographic locations in Brazil. Chemosphere, 30(4), 801-802, 1995
CLARK, L.C., 1996: Effects of Selenium Supplementation for Cancer Prevention in Patients With Carcinoma of the Skin. JAMA, December 25, 1996, vol 276, No. 24,1957-1963
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DICKSON, J. D., 1969): Notes on Hair and Nail Loss After Ingesting Sapucaia Nuts (Lecythis elliptica). Econ. Bot., 23,133-134
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KENNARD; WINTERS, 1960: Some Fruits and Nuts for the Tropics, p.78, Miscellaneous Publication No. 801, US Dept. of Agriculture
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KIEM, J.; KOSLOWSKI, G., 1987: Platelet and erythrocyte kinetics studied with Selenium-74. Trace Element - Anal. Chem. in Med. and Biol. vol. 4, p.311,1987
LANFEAR, J. et al., 1994 : The selenium metabolite selenodiglutathionine induces p53 and apoptosis. Carcinogenesis 15, 1387-1392
LEVANDER, O.A.; MORRIS, V.C, 1984: Dietary selenium levels needed to maintain balance in North American adults consuming self-selected diets. The American Journal of Clinical Nutrition 39: May 1984, pp 809- 815
MENNINGER, A.E., 1977: Edible Nuts of the World. Horticultural Books, Inc. Stuart. Florida 33494, p. 37
McKENZIE, R.C., 2002: Selenium and the Immune System, p. 229 in “Nutrition and Immune Function” Ed. P.C. Calder, C.J. Field and H.S. Gill, CABI Publishing, ISBN 0-85199-583-7
MORI, S.A.; PRANCE, G.T., 1990: Flora Neotropica, Monograph 21 (II), Lecythidaceae-Part II, Published by The New York Botanical Garden, p. 316-320
PALMER, I.S.; HERR, A., 1982: Toxicity of Selenium in Brazil Nuts to Rats. Journal of Food Science, vol. 47,1595-1597
PARIZEK J. et al., 1971: The detoxifying effects of Selenium, in: Mertz, W.& Cornatzer W.E. ed. Newer trace elements in nutrition, N.Y., M. Dekker, Inc., p 85-122
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SCHRAUZER , G.N.: Selen - natürlicher Schutzstoff bei Quecksilberbelastungen Ganzheitliche Zahnheilkunde in der Praxis, Spitta-Verlag
SECOR, C.L., 1989: Variation of in the selenium content of individual Brazil nuts. J. Food Safety, 9:279-281
SPALLHOLZ, J.E. et al., 1990: Advances in understanding selenium’ s role in the immune system. Annals of the New York Academy of Sciences, 587,123-139
TRENAM, C.W. et al., 1992 : Skin inflammation - reactive oxygen species and the role of iron. Journal of investigative Dermatology 99, 675-682
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WHANGER, P.D., 2002: Selenocompounds in Plants and Animals and their Biological Significance. Journal of the American College of Nutrition, Vol. 21, No. 3, 223-232 (2002)
